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Clinical Procedures in Emergency Medicine 4th edition (October 24, 2003) by James R. Roberts (Editor), Jerris Hedges (Editor) By W B Saunders
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Frontmatter Title Page Copyright Page Dedication How This Book Should be Viewed by the Practicing Clinician Contributors Foreword
Section I - Vital Signs and Patient Monitoring Techniques Section II - Respiratory Procedures Section III - Cardiac Procedures Section IV - Vascular Techniques and Volume Support Section V - Anesthetic and Analgesic Techniques Section VI - Soft Tissue Procedures Section VII - Gastrointestinal Procedures Section VIII - Musculoskeletal Procedures Section IX - Genitourinary Procedures Section X - Obstetric and Gynecologic Procedures Section XI - Neurologic Procedures Section XII - Ophthalmologic, Otolarynologic, and Dental Procedures Section XIII - Special Procedures Appendix: Commonly Used Formulas and Calculations
Section I - Vital Signs and Patient Monitoring Techniques 1 - Vital Signs Measurement 2 - Use of Monitoring Devices for Assessing Ventilation and Oxygenation
Section II - Respiratory Procedures 3 - Basic Airway Management and Decision-Making 4 - Tracheal Intubation 5 - Pharmacologic Adjuncts to Intubation 6 - Cricothyrotomy and Translaryngeal Jet Ventilation 7 - Tracheostomy Care and Tracheal Suctioning 8 - Mechanical Ventilation 9 - Thoracentesis 10 - Tube Thoracostomy
Section III - Cardiac Procedures 11 - Techniques for Supraventricular Tachycardias 12 - Defibrillation and Cardioversion 13 - Assessment of Implanted Pacemaker/AICD Devices 14 - Basic Electrocardiographic Techniques 15 - Emergency Cardiac Pacing 16 - Pericardiocentesis 17 - Artificial Perfusion During Cardiac Arrest 18 - Resuscitative Thoracotomy
Section IV - Vascular Techniques and Volume Support 19 - Pediatric Vascular Access and Blood Sampling Techniques 20 - Arterial Puncture and Cannulation 21 - Peripheral Intravenous Access 22 - Central Venous Catheterization and Central Venous Pressure Monitoring 23 - Venous Cutdown 24 - High-Flow Infusion Techniques 25 - Indwelling Vascular Devices: Emergency Access and Management 26 - Intraosseous Infusion 27 - Endotracheal Drug Administration 28 - Autotransfusion (Autologous Blood Transfusion) 29 - Transfusion Therapy: Blood and Blood Products
Section V - Anesthetic and Analgesic Techniques 30 - Local and Topical Anesthesia 31 - Regional Anesthesia of the Head and Neck 32 - Nerve Blocks of the Thorax and Extremities 33 - Intravenous Regional Anesthesia 34 - Procedural Sedation and Analgesia
Section VI - Soft Tissue Procedures 35 - Principles of Wound Management 36 - Methods of Wound Closure 37 - Foreign Body Removal 38 - Incision and Drainage 39 - Burn Care Procedures
Section VII - Gastrointestinal Procedures 40 - Esophageal Foreign Bodies 41 - Nasogastric and Feeding Tube Placement 42 - Balloon Tamponade of Gastroesophageal Varices 43 - Decontamination of the Poisoned Patient 44 - Peritoneal Procedures 45 - Abdominal Hernia Reduction 46 - Anorectal Procedures
Section VIII - Musculoskeletal Procedures 47 - Prehospital Splinting 48 - Management of Amputations 49 - Extensor and Flexor Tendon Injuries in the Hand, Wrist, and Foot 50 - Management of Common Dislocations 51 - Splinting Techniques 52 - Podiatric Procedures 53 - Injection Therapy of Bursitis and Tendinitis 54 - Arthrocentesis 55 - Compartment Syndrome Evaluation
Section IX - Genitourinary Procedures 56 - Urologic Procedures
Section X - Obstetric and Gynecologic Procedures 57 - Emergency Childbirth 58 - Culdocentesis 59 - Examination of the Sexual Assault Victim 60 - Drugs and Radiation In Pregnancy
Section XI - Neurologic Procedures 61 - Management of Increased Intracranial Pressure and Intracranial Shunts 62 - Spinal Puncture and Cerebrospinal Fluid Examination 63 - Special Neurologic Tests and Procedures
Section XII - Ophthalmologic, Otolarynologic, and Dental Procedures 64 - Ophthalmologic Procedures 65 - Otolaryngologic Procedures 66 - Emergency Dental Procedures
Section XIII - Special Procedures 67 - Procedures Pertaining to Hypothermia 68 - Procedures Pertaining to Hyperthermia 69 - Ultrasound-Guided Procedures 70 - Bedside Laboratory and Microbiologic Procedures 71 - Standard Precautions and Infectious Exposure Management 72 - Educational Aspects of Emergency Department Procedures
Appendix: Commonly Used Formulas and Calculations TEMPERATURE-CONVERSIONS FROM CELSIUS TO FAHRENHEIT WEIGHT-CONVERSION FROM POUNDS TO KILOGRAMS ESTIMATION OF A CHILD'S WEIGHT CALCULATION OF THE MEAN ARTERIAL PRESSURE QT AND QTC INTERVALS PREDICTED PEAK EXPIRATORY FLOW RATE ENDOTRACHEAL INTUBATION AND MECHANICAL VENTILATION RENAL FUNCTION ACID-BASE, FLUID, AND ELECTROLYTE BALANCE ARTERIAL BLOOD GAS ANALYSIS ACID-BASE BALANCE THE TRAUMATIC LUMBAR PUNCTURE DIAGNOSTIC PROBABILITY Acknowledgment
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CLINICAL PROCEDURES IN EMERGENCY MEDICINE
4th Edition James R. Roberts MD, FACEP, FAAEM, FACMT Professor and Vice Chair, Department of Emergency Medicine, Drexel University College of Medicine; Director, Division of Medical Toxicology, Hospital of the Medical College of Pennsylvania and Hahnemann Hospital, Philadelphia, Pennsylvania; Chair, Department of Emergency Medicine, Director, Division of Medical Toxicology, Fitzgerald Mercy Hospital and Mercy Hospital of Philadelphia, Mercy Catholic Medical Center, Philadelphia, Pennsylvania
Jerris R. Hedges MD, MS Professor and Chair, Department of Emergency Medicine, Oregon Health and Science University; Director, Emergency Services, OHSU and Doernbecher Children's Hospital, Portland, Oregon
ASSOCIATE EDITORS Arjun S. Chanmugam MD, MBA Residency Director, Department of Emergency Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland
Carl R. Chudnofsky MD Associate Professor, Thomas Jefferson University, Philadelphia, Pennsylvania; Chair, Department of Emergency Medicine, Albert Einstein Medical Center, Philadelphia, Pennsylvania
Catherine B. Custalow MD, PhD Assistant Professor, Department of Emergency Medicine, University of Virginia Health Sciences Center, Charlottesville, Virginia
Steven C. Dronen MD Director of Emergency Services, Fort Sanders Sevier Medical Center, Sevierville, Tennessee
SAUNDERS An Imprint of Elsevier
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SAUNDERS An Imprint of Elsevier The Curtis Center Independence Square West Philadelphia, PA 19106-3399 CLINICAL PROCEDURES IN EMERGENCY MEDICINE ISBN 0-7216-9760-7 Copyright © 2004, 1998, 1991, 1985, 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 photocopy, recording, or any information storage and retrieval system, without permission in writing from the publisher.
Notice Emergency Medicine is an ever-changing field. Standard safety precautions must be followed but as new research and clinical experience broaden our knowledge, changes in treatment and drug therapy may become necessary or appropriate. Readers are advised to check the most current product information provided by the manufacturer of each drug to be administered to verify the recommended dose, the method and duration of administration, and contraindications. It is the responsibility of the treating physician, relying on experience and knowledge of the patient, to determine dosages and the best treatment for each individual patient. Neither the publisher nor the author assumes any liability for any injury and/or damage to person or property arising from this publication. The Publisher
First Edition 1985. Second Edition 1991. Third Edition 1998. Library of Congress Cataloging-in-Publication Data Clinical procedures in emergency medicine/[edited by] James R. Roberts, Jerris R. Hedges.-4th ed. p. cm. Includes bibliographical references and index. ISBN 0-7216-9760-7 1. Emergency medicine. I. Title: Emergency medicine. II. Roberts, James R., III. Hedges, Jerris R. [DNLM: 1. Emergency Treatment. 2. Emergencies. WB 105 C641 2004] RC86.7.C55 2004 616.02'5-dc21 2003050537 Acquisitions Editor: Todd Hummel Senior Project Manager: Peter Faber Book Designer: Steven Stave 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 Michael P. Spadafora, MD (1953–1999). A great guy whose talent, charisma, and friendship will be missed by many. You taught me more than I ever taught you, Michael, and life's just not the same without you. To David K. Wagner, MD, Lewis R. Goldfrank MD, and Jerris R. Hedges, MD. Their prowess, prescience, and dynamism were obvious the first time I met them. And to Michael I. Greenberg, MD. As a toxicologist he was first my student, then my colleague, and now my mentor. J.R.R. This Fourth Edition of Clinical Procedures in Emergency Medicine is dedicated to all the future generations of emergency physicians. As our specialty becomes an international discipline, this text in English, Italian, and Spanish is now found in many lands. Countless practitioners have expanded their knowledge and shared this information with their trainees. If a copy of this text can make a profound difference in at least one new emergency physician's career, we have served the future well. J.R.H. This book is dedicated to all those who practice emergency medicine and to those that support them in their endeavors. A.S.C. To my wife Marcy, without a doubt the very best thing that has ever happened to me. Her kindness, patience, and devotion to family is surpassed by none. To my children, Adam, Arielle, and Allison, whom I love more than any words could ever express. And to my mother Eleanor, whose strength and courage in the face of adversity is an inspiration to everyone lucky enough to know her. C.R.C. To my son, Nicholas, and in memory of my daughter, Lauren; to Peter Pons, my favorite teacher; and to our residents so that when they are far away from this place of learning, they may confidently pick up the scalpel and perform these lifesaving procedures without hesitation—both quickly and competently. C.B.C. This effort is dedicated to the idealistic spirit that drives emergency physicians to seek excellence in the care of their patients. It is my hope that this book will be a valuable tool in their quest to bring order to the chaos of life in the ED. I could not work on projects such as this without the support and unfailing generosity of my wife, Beverly. I offer my thanks to Bev for all she has given to me and to the specialty of Emergency Medicine. S.C.D.
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How This Book Should be Viewed by the Practicing Clinician
The editors and authors of this textbook strongly believe that the complex practice of medicine, the vagaries of human diseases, the unpredictability of pathologic conditions, and the functioning and responses of the human body cannot be defined, explained, or rigidly categorized by any written document. Therefore, it is not the purpose of this text to serve as an authoritative source on any medical condition or clinical intervention, nor an attempt to define a standard of care that should be practiced by all clinicians. We provide the physician with a literature-based database, and a reasonable clinical guide that is combined with practical suggestions. We offer a general reference source on a variety of conditions and procedures that may confront clinicians who are experienced in emergency medicine practice. This text cannot replace physician judgment, cannot describe every possible aberration or clinical scenario, and cannot define rigid standards for clinical actions or procedures. Every medical encounter must be individualized and every patient must be approached on a case-by-case basis. Some of the procedures described are common, while others are uncommon, rarely encountered, or best performed, given specific circumstances, by another practitioner with different training, experience, or logistical constraints. The procedures described herein do not constitute the expertise or the knowledge base to be possessed by all clinicians. Finally, many of the described complications associated with implementing complex medical and surgical procedures may be encountered, even when every aspect of the intervention has been performed correctly. Editors and authors
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Contributors
James T. Amsterdam DMD, MD, MMD Professor and Vice-Chair, Emergency Medicine, University of Minnesota, Minneapolis, Minnesota; Head, Emergency Medicine Department, Health Partners/Regions Hospital, St. Paul, Minnesota Alexander B. Baer MD Clinical Instructor, Fellow, Division of Medical Toxicology, University of Virginia Health System, Charlottesville, Virginia Heather Bailey MD, FAAEM Assistant Professor of Emergency Medicine, Department of Emergency Medicine, Drexel University College of Medicine, Philadelphia, Pennsylvania; Associate Program Director of Emergency Medicine and the Director of Critical Care Education, Medical College of Pennsylvania Hospital, Philadelphia, Pennsylvania Aaron E. Bair MD Assistant Professor, University of California, Davis Medical Center, Sacramento, California William E. Baker MD Assistant Professor, Department of Emergency Medicine, New York Medical College, Valhalla, New York; Associate Director, Surgical Section, Emergency Department, Lincoln Medical and Mental Health Center, Bronx, New York Kip Benko MD Clinical Instructor, Affiliated Residency in Emergency Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania; Staff Physician, Mercy Hospital of Pittsburgh, Pittsburgh, Pennsylvania Edward S. Bessman MD Assistant Professor, Department of Emergency Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland; Chairman, Department of Emergency Medicine, Johns Hopkins Bayview Medical Center, Baltimore, Maryland Courtney A. Bethel MD Clinical Assistant Professor of Emergency Medicine, Drexel University, College of Medicine—Medical College of Pennsylvania and Hahnemann Medical School, Philadelphia, Pennsylvania;
Staff Physician, Mercy Catholic Medical Center, Philadelphia, Pennsylvania Barbara K. Blok MD Assistant Professor, Department of Emergency Medicine, Johns Hopkins University, Baltimore, Maryland Michael E. Boczar DO Clinical Assistant Professor, Department of Emergency Medicine, University of Michigan, Ann Arbor, Michigan; Vice Chairman, Department of Emergency Medicine, Hurley Hospital, Flint, Michigan Thomas A. Brabson DO, MBA Assistant Professor, Thomas Jefferson University School of Medicine, Philadelphia, Pennsylvania; College of Osteopathic Medicine, Albert Einstein Medical Center, Philadelphia, Pennsylvania William J. Brady Jr. MD Associate Professor, Vice Chair, Program Director, Department of Emergency Medicine, University of Virginia, Charlottesville, Virginia G. Richard Braen MD Professor and Chairman, Department of Emergency Medicine, Assistant Dean of Graduate Medical Education, University of Buffalo, School of Medicine and Biomedical Sciences, Buffalo, New York James H. Bryan MD Assistant Professor, Oregon Health and Science University, Portland, Oregon; Staff Physician, Veterans Affairs Medical Center, Portland, Oregon Kenneth H. Butler DO, FACEP Associate Residency Director, Emergency Medicine Residency Program, University of Maryland, Baltimore, Maryland Stacie E. Byers DO Assistant Residency Director, Department of Emergency Medicine, Albert Einstein Medical Center, Philadelphia, Pennsylvania Theodore C. Chan MD Associate Professor of Clinical Medicine, Department of Emergency Medicine, University of California, San Diego Medical Center and School of Medicine, San Diego, California Dane M. Chapman MD, PhD Associate Professor of Emergency Medicine, Washington University School of Medicine, St. Louis, Missouri; Attending Physician, St. Louis Children's Hospital, St. Louis, Missouri; Page Hospital, Page, Arizona; Tuba City Indian Medical Center,
Tuba City, Arizona Theodore A. Christopher MD Associate Professor, Department of Emergency Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania; Chairman, Department of Emergency Medicine, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania Carl R. Chudnofsky MD Associate Professor, Department of Emergency Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania; Chairman, Department of Emergency Medicine, Albert Einstein Medical Center, Philadelphia, Pennsylvania Wendy C. Coates MD Associate Professor, UCLA School of Medicine, Los Angeles, California; Director, Medical Education, Department of Emergency Medicine, Harbor—UCLA Medical Center, Torrance, California Pino D. Colone MD, FACEP Clinical Instructor, Department of Emergency Medicine, University of Michigan Hospital, Ann Arbor, Michigan; Emergency Department Faculty, Department of Emergency Medicine, Hurley Medical Center, Flint, Michigan Catherine B. Custalow MD, PhD Assistant Professor, Department of Emergency Medicine, University of Virginia Health Sciences Center, Charlottesville, Virginia William C. Dalsey MD, MBA, FACEP Chairman, Emergency Medicine, Kimball Medical Center, Lakewood, New Jersey Anthony J. Dean MD Assistant Professor of Emergency Medicine, University of Pennsylvania School of Medicine, University of Pennsylvania Medical Center, Philadelphia, Pennsylvania William R. Dennis MD Assistant Residency Director, Education Coordinator, Naval Medical Center, Portsmouth, Virginia Lynette Doan-Wiggins MD Clinical Assistant Professor, Department of Surgery, Section of Emergency Medicine, Loyola University Stritch School of Medicine, Maywood, Illinois; Faculty, Emergency Department, Loyola University Medical Center, Maywood, Illinois Denis J. Dollard MD Assistant Clinical Professor, Department of Emergency Medicine, Drexel University College of Medicine;
Director, Department of Emergency Medicine, Mercy Hospital of Philadelphia, Philadelphia, Pennsylvania Steven C. Dronen MD Director of Emergency Services, Fort Sanders Sevier Medical Center, Sevierville, Tennessee Timothy B. Erickson MD Associate Professor, Emergency Medicine Residency Program Director, and Director, Division of Clinical Toxicology, University of Illinois at Chicago, Chicago, Illinois Brian Euerle MD Assistant Professor, University of Maryland School of Medicine, and Attending
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Physician, Emergency Department, University of Maryland Medical Center, Baltimore, Maryland Dan L. Field MD Clinical Faculty, University of California, Davis, School of Medicine, Davis, California; University of California, San Francisco, School of Medicine, San Francisco, California; Staff Physician, The Permanente Medical Group, Department of Emergency Medicine, Kaiser Foundation Hospital, Sacramento, California Lisa Mackowiak Filippone MD Instructor, Department of Emergency Medicine, Drexel University College of Medicine, Medical College of Pennsylvania Campus; Director, Division of Emergency Medicine Ultrasound, and Attending Physician, Mercy Hospital of Philadelphia, Philadelphia; Attending Physician, Mercy Fitzgerald Hospital, Darby, Pennsylvania Jonathan Fisher MD, MPH Director of Undergraduate Education, Department of Emergency Medicine, Albert Einstein Medical Center, Philadelphia, Pennsylvania Brenda Foley MD Clinical Faculty of Emergency Medicine, Residency Program, Albert Einstein Medical Center, Philadelphia, Pennsylvania; Attending Physician, Department of Emergency Medicine, Delaware County Memorial Hospital, Drexel Hill, Pennsylvania Neal R. Frankel DO Staff Emergency Physician, Emergency Department, Saint Joseph's Medical Center, Towson, Maryland Diane L. Gorgas MD
Associate Residency Director, Associate Professor, The Ohio State University College of Medicine, Columbus, Ohio Steven M. Green MD Professor of Emergency Medicine and Pediatrics, Loma Linda University, Loma Linda, California Brett S. Greenfield DO Attending Physician, Department of Emergency Medicine, Virtua Health System, West Jersey Hospitals-Voorhees Division, Voorhees, New Jersey Richard J. Harper MD Assistant Professor, Oregon Health and Science University, Department of Emergency Medicine, Portland, Oregon; Chief, Department of Emergency Medicine, Portland Veterans Affairs Medical Center, Portland, Oregon Richard A. Harrigan MD Associate Professor of Emergency Medicine, Temple University Hospital and School of Medicine, Philadelphia, Pennsylvania Jerris R. Hedges MD, MS Professor and Chair, Department of Emergency Medicine, Oregon Health and Science University; Director, Emergency Services, Oregon Health and Science University and Doernbecher Children's Hospital, Portland, Oregon Alan C. Heffner MD Assistant Residency Director, Department of Emergency Medicine, Naval Medical Center Portsmouth, Portsmouth, Virginia Christopher P. Holstege MD Director, Division of Medical Technology, and Assistant Professor, Department of Emergency Medicine, University of Virginia, Charlottesville, Virginia Laura R. Hopson MD Clinical Instructor, University of Michigan Health System, Ann Arbor, Michigan J. Stephen Huff MD Associate Professor of Emergency Medicine, Medicine and Neurology, University of Virginia, Charlottesville, Virginia Ana Maria Ibrado MD, PhD Attending Physician and Clinical Operations Officer, Emergency Department, Providence Hospital, Washington, DC Charlene Babcock Irvin MD Assistant Professor, Wayne State University School of Medicine, Wayne State University, Detroit, Michigan; Research Director and Assistant Vice Chief,
Department of Emergency Medicine, St. John Hospital and Medical Center, Detroit, Michigan Kenneth V. Iserson MD, MBA Professor of Emergency Medicine, University of Arizona, Tucson, Arizona F. Michael Jaggi DO, FACEP, FACP Chairman, Department of Emergency Medicine, Hurley Medical Center, Flint, Michigan; Assistant Professor of Emergency Medicine, University of Michigan, Ann Arbor, Michigan Tim Janchar MD Clinical Faculty, Emergency Department, Virginia Mason Hospital, Seattle, Washington Lewis J. Kaplan MD, FACS Associate Professor of Surgery, Director, Emergency General Surgery, Yale University School of Medicine, New Haven, Connecticut Eric D. Katz MD Assistant Professor, Assistant Residency Director, Division of Emergency Medicine, Washington University, St. Louis, Missouri John J. Kelly DO, FACEP Associate Professor, Department of Emergency Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania; Adjunct Associate Professor, Department of Emergency Medicine, Drexel University College of Medicine-Medical College of Pennsylvania and Hahnemann University, Philadelphia, Pennsylvania; Adjunct Faculty, Department of Emergency Medicine, Philadelphia College of Osteopathic Medicine, Philadelphia, Pennsylvania; Associate Chairman, Department of Emergency Medicine, Albert Einstein Medical Center, Philadelphia, Pennsylvania Kevin P. Kilgore MD, FACEP Assistant Professor of Emergency Medicine, University of Minnesota School of Medicine, Minneapolis, Minnesota; Senior Staff Physician, Emergency Medicine Department, Regions Hospital, St. Paul, Minnesota Thomas D. Kirsch MD, MPH Faculty, Emergency Medicine Residency Program, Maricopa Medical Center, Pheonix, Arizona Kevin J. Knoop MD, MS Special Assistant for Graduate Medical Education and Research, Attending Physician, Emergency Medicine Department, Naval Medical Center, Portsmouth, Virginia Theodore K. Koutouzis MD Attending Physician, Memorial Hospital,
Jacksonville, Florida Baruch Krauss MD, EdM, FAAP Assistant Professor of Pediatrics, Harvard Medical School, Boston, Massachusetts; Faculty, Division of Emergency Medicine, Children's Hospital, Boston, Massachusetts John R. Krimm DO, FACEP, FAAEM Department of Emergency Medicine, Philadelphia College of Osteopathic Medicine, Philadelphia, Pennsylvania; Attending Faculty, Department of Emergency Medicine and Emergency Medicine Residency Program, Albert Einstein Medical Center, Philadelphia, Pennsylvania; Department of Emergency Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania Diann M. Krywko MD Assistant Clinical Professor, Emergency Medicine, University of Michigan Medical Center, Ann Arbor, Michigan; Clinical Instructor, Emergency Medicine, Hurley Medical Center, Flint, Michigan Richard L. Lammers MD Associate Professor of Emergency Medicine, Michigan State University, East Lansing, Michigan; Research Director, Kalamazoo Center for Medical Studies, Kalamazoo, Michigan
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Richard Lanoix MD Assistant Professor, Co-Program Director, New York Medical College, Valhalla, New York; Co-Program Director, Lincoln Medical and Mental Health Center, Bronx, New York Patricia L. Lanter MD Assistant Professor, Dartmouth College, Hanover, New Hampshire; Attending Physician, Dartmouth Hitchcock Medical Center, Lebanon, New Hampshire David C. Lee MD Clinical Assistant Professor, Department of Surgery, New York University, New York, New York; Director of Research, Department of Emergency Medicine, North Shore University Hospital, Manhassat, New York Shan W. Liu MD Resident, Department of Emergency Medicine, Harvard Associated Emergency Medicine Residency, Boston, Massachusetts Marie M. Lozon MD Clinical Associate Professor of Emergency Medicine and Pediatrics, University of Michigan Medical School, Ann Arbor, Michigan; Director,
Children's Emergency Services, University of Michigan Health System, Ann Arbor, Michigan Jeffrey Luk Medical Student, UMDNJ—Robert Wood Johnson Medical School, Piscataway, New Jersey Michael Lutes MD Chief Resident, Department of Emergency Medicine, University of Michigan/St. Joseph Mercy Hospital, Ann Arbor, Michigan Sharon E. Mace MD, FACEP, FAAP Associate Professor, Emergency Medicine, Ohio State University School of Medicine, Columbus, Ohio; Director, Observation Unit, and Director, Pediatric Education/Quality Improvement, Cleveland Clinic Foundation, Department of Emergency Medicine, Cleveland, Ohio David E. Manthey MD Director, Undergraduate Medical Education, and Assistant Professor, Wake Forest University Baptist Medical Center, Winston-Salem, North Carolina John A. Marx MD Clinical Professor of Emergency Medicine, University of North Carolina, Chapel Hill, Chapel Hill, North Carolina; Chair, Department of Emergency Medicine, Carolinas Medical Center, Charlotte, North Carolina Douglas L. McGee DO Assistant Professor, Thomas Jefferson University, Philadelphia, Pennsylvania; Philadelphia College of Osteopathic Medicine, Philadelphia, Pennsylvania; Director, Emergency Medicine Residency Program, Albert Einstein Medical Center, Philadelphia, Pennsylvania Robert M. McNamara MD, FAAEM Professor and Chair, Department of Emergency Medicine, Temple University School of Medicine, Philadelphia, Pennsylvania Marc Mickiewicz MD Clinical Instructor, Emergency Medicine, Vanderbilt University, Nashville, Tennessee Dave Milzman MD, FACEP Clinical Professor of Emergency Medicine, Adjunct Faculty, Department of Physiology, Georgetown University School of Medicine, Washington, DC; Research Director, Providence Hospital, Clinical Professor of Emergency Medicine, George Washington University Emergency Medicine Residency Program, Washington, DC Bohdan M. Minczak MD, PhD
Attending Faculty, Department of Emergency Medicine, Albert Einstein Medical Center, Philadelphia, Pennsylvania; Clinical Assistant Professor, Department of Emergency Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania; Associate Professor, Department of Biomedical Sciences, Philadelphia College of Osteopathic Medicine, Philadelphia, Pennsylvania John P. Mulligan MD Department of Emergency Medicine, Johns Hopkins Hospital, Baltimore, Maryland David W. Munter MD, MBA Assistant Clinical Professor, Department of Military and Emergency Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland; Executive Director, Tricare Mid-Atlantic Region, Norfolk, Virginia Kathleen A. Neacy MD Clinical Instructor, Department of Emergency Medicine, University of Minnesota Medical School, Minneapolis, Minnesota; Faculty, Emergency Medicine Residency, Regions Hospital, St. Paul, Minnesota Edward A. Panacek MD, MPH Professor of Medicine, Division of Emergency Medicine, University of California, Davis; Director, Office of Clinical Trials, University of California, Davis Medical Center, Sacramento, California Steven J. Parrillo DO, FACOEP, FACEP Attending Faculty, Albert Einstein Medical Center, Department of Emergency Medicine, Philadelphia, Pennsylvania; Assistant Professor, Philadelphia College of Osteopathic Medicine, Philadelphia, Pennsylvania Heather M. Prendergast MD Assistant Professor of Emergency Medicine, Attending Physician, University of Illinois Medical Center, University of Chicago at Illinois, Chicago, Illinois Emanuel P. Rivers MD, FACEP, FACP Associate Professor of Emergency Medicine, Case Western Reserve University, Cleveland, Ohio; Attending Physician, Henry Ford Medical Center, Detroit, Michigan Ralph J. Riviello MD, FACEP Assistant Professor, Department of Emergency Medicine, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania James R. Roberts MD, FACEP, FAAEM, FACMT Professor and Vice Chair,
Department of Emergency Medicine, Drexel University College of Medicine; Director, Division of Medical Toxicology, Hospital of the Medical College of Pennsylvania and Hahnemann Hospital, Philadelphia, Pennsylvania; Chair, Department of Emergency Medicine, Director, Division of Medical Toxicology, Fitzgerald Mercy Hospital and Mercy Hospital of Philadelphia, Mercy Catholic Medical Center, Philadelphia, Pennsylvania Brent E. Ruoff MD Associate Professor, Emergency Medicine, Washington University Medical School, St. Louis, Missouri; Clinical Chief, Emergency Medicine, Barnes-Jewish Hospital, St. Louis, Missouri Carolyn Joy Sachs MD, MPH Associate Professor, David Geffen School of Medicine, UCLA Medical Center, Los Angeles, California Leonard E. Samuels MD Assistant Professor of Emergency Medicine, Drexel University College of Medicine, Philadelphia, Pennsylvania; Interim Clinical Service Chief, Emergency Department, Hahnemann Hospital, Philadelphia, Pennsylvania Robert E. Schneider MD Clinical Associate Professor, Department of Emergency Medicine, University of North Carolina School of Medicine, Chapel Hill, North Carolina; Academic Faculty, Carolinas Medical Center, Charlotte, North Carolina Cecile G. Silvestre MD, FACEP Assistant Professor, Department of Emergency Medicine, and Associate Residency Director, George Washington University Medical Center, Washington, DC; Prince George's Hospital Center, Cheverly, Maryland Peter E. Sokolove MD Associate Professor of Clinical Medicine, Division of Emergency Medicine, University of California, Davis, School of Medicine, Sacramento, California; Residency Program Director, University of California, Davis Medical Center, Sacramento, California
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Mark Spektor DO Assistant Professor, Assistant Program Director, Division of Emergency Medicine, State University of New York—Downstate, Kings County Hospital Center, Brooklyn, New York Sarah A. Stahmer MD Associate Professor of Emergency Medicine and Director, Emergency Medicine,
Ultrasound, UMDNJ—Robert Wood Johnson Medical School, Camden, New Jersey; Associate Director for Graduate Medical Education, Program Director, Emergency Medicine, Cooper Hospital/University Medical Center, Camden, New Jersey Rachel Stanley MD Clinical Assistant Professor of Emergency Medicine and Pediatrics, University of Michigan, Hurley Medical Center, Flint, Michigan Daniel B. Stone MD, MBA Assistant Professor of Clinical Medicine, Division of Emergency Medicine, Northwestern University School of Medicine, Chicago, Illinois Christopher M. Strear MD Attending Physician, Emergency Medicine, Legacy Emmanuel Hospital and Health Center, Portland, Oregon Khosrow Tabassi MD Faculty, Department of Emergency Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland Jacob W. Ufberg MD Assistant Professor and Assistant Residency Director, Department of Emergency Medicine, Temple University School of Medicine, Philadelphia, Pennsylvania; Attending Physician, Department of Emergency Medicine, Temple University Hospital, Philadelphia, Pennsylvania Benjamin D. Vanlandingham MD Chief Resident, Department of Emergency Medicine, University of Arizona, Tucson, Arizona L. Albert Villarin Jr. MD, FACEP Assistant Professor, Emergency Medicine, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania; Director—Medical Informatics, Emergency Medicine, Albert Einstein Medical Center, Philadelphia, Pennsylvania Diamond Vrocher MD Department of Emergency Medicine, University of Michigan, Ann Arbor, Michigan Malinda Waddell RN, MN, FNP President, Forensic Nurse Specialists, Inc., Long Beach, California Jim Edward Weber DO, FACEP Assistant Professor of Emergency Medicine, University of Michigan, Ann Arbor, Michigan; Director of Research, Hurley Medical Center, Flint, Michigan John G. Younger MD, MS Assistant Professor,
Department of Emergency Medicine, University of Michigan, Ann Arbor, Michigan Richard D. Zane MD Instructor, Harvard Medical School, Boston, Massachusetts; Vice Chair, Department of Emergency Medicine, Brigham and Women's Hospital, Boston, Massachusetts
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Foreword
The emergency physician has the unique responsibility of offering his or her skills at all times to all people (young and old, friendly and hostile, rich and poor). No other health providers are always collectively there at the entrance to the hospital. As emergency physicians, our responsibilities have grown and our horizons have been expanded because of our commitment to people. We have built a system that creates a caring environment from the home to the street and to the hospital, and a system that also integrates firefighters, police officers, paramedics, nurses, clerks, students, pharmacists, and physicians into this caring service. Each new clinical problem and each creative intervention has led to innovations in thought and technical advances. The Fourth Edition of Roberts and Hedges' text, Clinical Procedures in Emergency Medicine, takes another step in the pursuit of excellence in the provision of that care. The authors' detailed critical analyses of the studies pertinent to the use of each technique allow for a rigorous approach as to how, why, and when each procedure is indicated. The past 30 years in the history of emergency medicine have seen a remarkably rapid evolution in care. Organized medicine has often been criticized for its inability to change thought patterns and approaches to care, but the ability to change current patterns is the recognized strength of emergency physicians. We have undertaken our responsibilities, created new relationships, and developed new perspectives on clinical medicine in an area where previously no one dared to serve. In the past, medical providers have also been criticized for not evaluating their clinical techniques and technology effectively. This text exemplifies and describes the tremendous progress in thought and technology that mark the success of emergency medicine in America today. The rapid growth of prehospital care, the ever-increasing roles of emergency care, and the diversity of clinical issues and research dilemmas in emergency medicine have led to the development of a new type of physician in the emergency department. This text defines the breadth of academic and clinical emergency medicine and the enormous technical skill and intellectual responsibility required by each emergency physician. These chapters are written by emergency physicians and other physicians working closely with emergency patients who have highly specialized knowledge in particular aspects of emergency medicine. Almost a third of these authors are new contributors to this edition. A reevaluation of the clinical and academic roles of the emergency physician has led to the refinement of this Fourth Edition. As the basic science and clinical practice of emergency medicine have further developed, this book has grown to represent a complete view of our specialty. This text offers a balanced analysis of the interventions at our disposal in the emergency department for the care of those with urgent and emergent problems. The authors attempt to simplify and clarify while focusing on knowledge and process with regard to the equipment we use in the environment where we practice. This text permits any practitioner the opportunity to perform his or her first emergency procedures with a foundation that emphasizes evidence and limits bias and ignorance. This text has filled a void in medical practice. Procedural interventions in the emergency department had previously been largely undefined and certainly inadequately analyzed. The emergency physician who is trained in these techniques can develop the requisite technical skills and combine them with the warmth and humanity essential to render concerned, committed, and compassionate emergency care. Knowledge of these skills and their indications, as well as the risks and benefits of practice, will permit emergency physicians to achieve the highest level of service and will foster their potential to initiate quality research. This book is also about motivating physicians to appreciate the clinical norms and expectations of our procedures. The editors have recognized for years many of the problems defined in the report To Err is Human released by the Institute of Medicine of the National Academy of Sciences in 1999. This text has moved the physician from anecdote to a rigorous analysis of procedures. The reader will not only feel more secure about performing an essential procedure, but he or she will also become more confident about not performing a procedure that entails more risk than benefit to an individual patient. The editors and authors have attempted to enhance education and limit the errors of commission as well as omission while improving the safety and occupational health of the emergency physician. This book attempts to prepare the clinician for his or her role in the emergency department. Recognizing that the emergency department environment is by definition unpredictable and often chaotic, these authors have prepared us to change the human response in an attempt to make errors more difficult to commit. Understanding the remarkable spectrum of responsibility of the emergency physician is our essential task. We shall succeed as health providers if we understand our patients and their needs, the pathophysiology of emergency medicine and its therapeutics, and our procedures and their pitfalls. The Fourth Edition of Roberts and Hedges' Clinical Procedures in Emergency Medicine provides enough thought-provoking information about medical technology to prepare the emergency physician to care for the emergency department patient in a humane and intellectually sound manner. Although few physicians other than emergency physicians will use all the techniques and technology detailed in this text, many other physicians can and will profit immensely from its use. The techniques are well defined, well illustrated, and well referenced by clinicians who obviously use them daily. This text remains unique with respect to the depth and breadth with which the editors and authors critically evaluate the tools of our trade. The two leaders of our field, Roberts and Hedges, have been joined by four new associate editors. The addition of these respected emergency physicians
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expands the text's excellent foundation of editorial contributions and ensures continued successful presentation of procedural techniques to help guide our clinical care. The understanding and application of the principles defined in this edition should be considered essential for each emergency physician in his or her attempt to continuously improve the delivery of the best possible health care to our patients. Lewis R. Goldfrank MD Director, Emergency Medicine, Bellevue Hospital Center, New York University Medical Center; Professor, Clinical Medicine and Surgery, New York University School of Medicine; Medical Director, New York City Poison Center, New York, New York
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Section I - Vital Signs and Patient Monitoring Techniques
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Chapter 1 - Vital Signs Measurement Diane L. Gorgas
Documentation of temperature, pulse, respiration, and blood pressure is generally recommended for all emergency department (ED) patients, except those with the most minimal complaints. These measurements provide a unique, objective, capsule assessment of the patient's clinical condition. Vital signs indicate the severity of illness and may dictate the urgency of required intervention. Although a single set of values may suggest disease, the greatest utility of vital signs is their measurement over time. Deteriorating vital signs are an important indicator of a deteriorating physiologic condition, whereas improving values provide reassurance that an unstable patient is responding to therapy. Hence, when a patient undergoes treatment over an extended time, selected vital signs, particularly previously abnormal ones, should be repeated. In some circumstances, the monitoring of select vital signs should be continuous. Vital signs should be measured and recorded at intervals dictated by the patient's clinical state (e.g., before and after fluid resuscitation, invasive procedures, or administration of medications with cardiopulmonary effects) or with any sudden change in the patient's clinical status. In addition, an abnormal vital sign can direct the clinician toward a group of diagnoses or a particular organ system for further evaluation. An abnormal vital sign may constitute the patient's entire complaint, as in the febrile infant, or be the only indication of the potential for serious illness, as in the patient with resting tachycardia. For these reasons, accurate determination and interpretation of vital signs are mandatory. Unfortunately, in many EDs, vital signs are not recorded reliably, accurately, [1] or with optimal frequency. [2] This can lead to delayed diagnosis or misinterpretation of the severity of an illness or injury. Assessment of a patient's status and vital signs should begin in the prehospital setting in cases where Emergency Medical Service (EMS) transport is involved. EMS transport-induced stress can alter vital signs because of epinephrine and norepinephrine surges that commonly occur during transport. This has been shown to lead to increased heart rates of >10%. [3] Although prehospital vital signs need to be interpreted carefully, they should still be obtained and in the vast majority of situations, they are. The exception occurs in the pediatric population, especially those younger than 2 years of age. The lack of routine measurement of vital signs by EMS personnel in this group is largely due to the paramedic's or technician's lack of confidence in accurately measuring vitals signs in newborns, infants, and toddlers. [4] In the ED, the accurate assessment and management of abnormal vital signs must reflect the priorities of resuscitation. Determination of airway patency with respiratory rate (RR) and pattern assumes first importance. Establishing the presence and quality of an arterial pulse is the second vital sign to be assessed, followed by blood pressure. Blood pressure and pulse are often evaluated in conjunction, as a measure of blood volume. Although body temperature is the last vital sign to be monitored during resuscitation, it has special importance for patients suffering from thermal regulation failure (see Chapter 67 and Chapter 68 ). The current chapter is organized according to the priorities of patient resuscitation and evaluation. Additional "vital signs" recently introduced into emergency medicine are pulse oximetry, capillary refill, and the analogue or similar pain scale. The use of pulse oximetry is discussed subsequently (see Chapter 2 ). Capillary refill in general is considered part of the assessment of overall perfusion and most closely linked to circulatory volume and blood pressure in children. In accordance, capillary refill is covered under the blood pressure section. Assessment of pain as a vital sign is gaining acceptance. Mental status has also been proposed as a vital sign, as it can be viewed as a summation of measurable vital signs (blood pressure, heart rate, RR, and temperature). Significant aberrations in any of these quantifiable vital signs will cause mental status changes.
BACKGROUND Early pulmonary medicine was dominated by the concepts of Herophilus (4th century B.C.) and Galen (131 to 200 A.D.), whose belief in the humoral theory of medicine dictated that the lungs functioned as a cooling device and site for generation of body humors. The pulmonary circulation was correctly described in the 13th century by Ibnan-Nafis; however, his observations passed unnoticed. Respiratory physiology did not progress until the significance of the pulmonary circulation was recognized by Harvey in 1628. It was not until the 1700s that advances in physics and chemistry allowed the identification of gases involved in respiration. [5] Sphygmology, or palpation of the pulse, was first appreciated by Herophilus. He believed that interpreting the pulse required a knowledge of both music and geometry and defined the characteristics of the pulse as size, frequency, force, and rhythm. Chinese clinicians (2nd century B.C.) timed the pulse by the RR of the examiner, believing that 4 pulsations/respiration was normal for adults. The study of pulses was greatly influenced by Galen, who expanded the subject into a rather complex and obscure art form, writing 18 books on the subject. [6] Blood pressure was first measured directly in 1733 by Hales, who recorded the arterial pressures in a mare by cannulation with a brass pipe and a blood-filled glass column.[7] Frank used large-bore catheters connected to a rubber membrane in a 1903 manometer. [8] The invention of inflatable cuff manometers (Riva-Rocci, 1896) and the discovery of the arterial phase sounds (Korotkoff, 1905) allowed for the development of indirect blood pressure measurement. [7] [8] The earliest recorded references to fever are from 6th century B.C. Akkadian cuneiform inscriptions, which appear to have adapted an ancient Sumerian icon of a flaming brazier to denote both fever and the local warmth of inflammation in a single ideogram. Clinical thermometry was introduced by Sanctorius in 1625. Mercury column thermometers were introduced by Fahrenheit in 1714. Although their routine use was supported by Boerhaave, thermometry was not established as routine clinical practice until the 1870s. [9]
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TABLE 1-1 -- Normal Values for Vital Signs of Infants and Children (Mean ± SD) Age Parameter
0–2 mo
3–12 mo
1–6 yr
7–12 yr
13–18 yr
Breaths/min
—*
—*
24 ± 3
19 ± 2
17 ± 3
Pulse/min
126 ± 20
131 ± 20
88 ± 9
70 ± 8
64 ± 7
Systolic BP†
72 ± 10
95 ± 15
93 ± 13
100 ± 10
112 ± 12
Diastolic BP
51 ± 9
53 ± 10
55 ± 10
63 ± 10
67 ± 10
*For data on children 0 to 36 months, see Table 1-2 . †As an estimate, for children 1 to 10 years: 2 × age (in years) + 90 mm Hg = 50th percentile for systolic BP.
NORMAL VALUES The range of normal, resting vital signs for specific age groups must be recognized by the clinician to enable identification of abnormal values and their clinical significance. Normal ranges for vital signs also may be influenced by sex, race, pregnancy, and residence in an industrialized nation. These ranges have not been validated in ED patients, who may have many reasons for vital sign abnormalities, including anxiety; pain; and other forms of distress, in addition to altered physiology from disease states. Published vital sign norms for children are not as well accepted as for adult patients. Table 1-1 and Table 1-2 report normal vital signs for children by age group as mean and standard deviations. In Table 1-1 , the values for pulse and blood pressure for 0- to 2-month-olds are adapted from studies of newborn populations (i.e., younger than 7 days). [10] [11] [12] During the newborn period, normal arterial blood pressure rises rapidly. Values for pulse and respiration in children older than 3 years reflect an average of male and female values for 0- to 1-, 3-, 9-, and 16-year-old populations. [13] The values for blood pressure reflect an average of male and female values for the 1- to 6-month and 3-, 9-, and 16-year-old populations. [12] Newer studies have reassessed reference values for RRs in children. [14] [15] [16] [17] [18] Table 1-2 reflects the age-related changes and the effect of the state of wakefulness in the RRs of children up to 3 years of age. [15] Hooker and colleagues measured resting RRs in pediatric ED patients up to age 18 years. [14] They noted considerable patient variability and somewhat higher RRs than are shown in Table 1-2 . For the adult population, normal values for blood pressure are well established. Although there is an increase in systolic blood pressure with age, normotensive or normal systolic blood pressure is defined as 90 to 140 mm Hg, and normotensive or normal diastolic blood pressure is defined as 60 to 90 mm Hg. Although most patients have similar blood pressures in both arms, Pesola and coworkers found that 18% of their hypertensive
Age (mo)
TABLE 1-2 -- Normal Respiratory Rates (Breaths/Min) for Children to Age 3 Years (Mean ± SD) Awake Asleep
0–60 are found to be hypoxic 80% of the time.[28] Procedure RR is the number of inspirations per minute. Generally, it is best measured with the patient unaware that breathing is being observed because awareness makes the patient conscious of the breathing pattern, which may alter the rate. Commonly, examiners count respirations while appearing to count the pulse. The RR is most accurately determined by counting for a full minute. Because the frequency is much less than the pulse, and breathing is less regular, an inaccurate measurement is more likely to occur if a 15-second interval is used. Infants, in addition to being principally nasal breathers, are predominantly diaphragmatic breathers, and an infant's RR is easily determined by observing or palpating excursion of the chest or the abdominal wall. [29] Complications There are no inherent complications from measuring respiration by observation. Problems related to the measurement of RR are generally due to failure to recognize a patient in obvious respiratory distress or failure to monitor RR in a patient who may be at risk for respiratory depression (e.g., in the case of sedative-hypnotic or narcotic overdose). Interpretation Respiratory Rate
A limited number of studies have examined RRs. Hutchinson evaluated RRs in 1897 healthy males at rest and found that 91% had RRs between 16 and 24 breaths/min. He also noted that 30% had exactly 20 breaths/min. [30] Hooker and colleagues note that current texts vary considerably in their definitions of a normal RR and cite published values that range from 8 to 20 breaths/min. [31] Hooker and associates, in a study that specifically investigated normal RRs in an ED, measured RRs in 110 afebrile ambulatory patients without respiratory complaints (53 females and 57 males). [31] They report a mean rate of 20.1 breaths/min. For patients whose RR was measured again before release from the ED, no significant difference was noted between initial and subsequent RRs. When analyzed by gender, females had a mean RR of 20.9 breaths/min and males had a mean RR of 19.4 breaths/min, a statistically significant difference. The researchers concluded that a normal RR in the adult patient population was 16 to 24 breaths/min. [31] This study also suggested a significant variability in the accurate measurement of RR by different examiners. Rates obtained by nurses versus medical students varied significantly, as did those obtained by medical students versus residents versus attending clinicians. [1] Other studies have provided additional information on normal resting and sleep state RRs in children younger than 7 years. [14] [15] [16] [17] [18] RRs obtained with a stethoscope were higher than those obtained by observation (mean difference, 2.6 breaths/min in awake and 1.8 breaths/min in asleep children). Smoothed percentile curves demonstrated a larger dispersion at birth (5th percentile, 34 breaths/min; 95th percentile, 68 breaths/min), while at 36 months of age (5th percentile, 18
breaths/min; 95th percentile, 30 breaths/min) dispersion was less. RR will generally increase in the presence of fever. It is often difficult to determine if tachypnea is a primary finding or simply associated with hyperpyrexia. Taylor et al.[32] studied 572 children younger than 2 years of age, 42 (7%) of whom were subsequently diagnosed with pneumonia and found that age-appropriate limits for resting tachypnea in the presence of fever could be defined. A sensitivity and specificity of 74% and 77% for pneumonia was achieved when children 6 months of age had a RR >59/min, those aged 6–11 months had a RR >52/min and those 1–2 years had a RR >42/min. Therefore, even in the face of physiologic compensation for fever, an interpretation of RR alone can help predict the presence of pulmonary disease. Respiratory Pattern and Amplitude
Abnormal respiratory patterns may be characteristic of metabolic or central nervous system pathologic conditions. Hyperventilation and hypoventilation may result from an
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extensive differential diagnosis including primary pulmonary disorders, such as pneumonia or chest wall pain. Respiratory disturbances also occur secondary to other disease processes. For example, Kussmaul respiration describes the hyperventilation pattern seen in diabetics with ketoacidosis. Abnormal respiratory patterns in adults can be used in differential diagnosis or in determining the location of central nervous system lesions. The recognition of subtle tachypnea can be difficult in the emergency setting, although this can be the solitary harbinger of disease. Measurement of an accurate RR in this patient population is crucial. Another instance of pathology that can confuse the routine measurement of RR is diaphragmatic breathing or retractions. The variability in counting respiratory effort versus effective respirations is generally not appreciated in a single recorded value. Respiratory patterns in children must be observed carefully. In infants, periodic breathing, which may be normal, must be distinguished from apnea. By definition, periodic breathing consists of three or more respiratory pauses >3 seconds in duration, with 20 seconds. It may be associated with bradycardia and hypoxia. [29] Periodic breathing and apnea are believed to be disorders on a continuum, both stemming from abnormal physiologic control of respiration. However, periodic breathing is considered a benign disorder, whereas infants with symptomatic apneic episodes resulting in an apparent life-threatening event (ALTE) are thought to be at increased risk for sudden infant death syndrome. [33]
PULSE The pulse is examined primarily to establish cardiac rate and rhythm. However, palpation of peripheral pulses yields clues to cardiac disease, such as aortic insufficiency, and information about the integrity of the peripheral vascular supply. Doppler ultrasound provides a noninvasive method of assessing blood flow in the ED. It has utility in the location of a pulse, in the assessment of fetal heart tones beyond the first trimester, for evaluation of peripheral lower extremity vascular insufficiency, and for the evaluation of blood pressure in infants or in patients with low-flow states. Physiology Blood flowing into the aorta with each cardiac cycle initiates a pressure wave. Blood flows through the vasculature at approximately 0.5 m/sec; however, pressure waves in the aorta move at 3 to 5 m/sec. Therefore, palpated peripheral pulses represent pressure waves, not blood flow. Indications and Contraindications The evaluation of pulse presence and rate is indicated in most patients who present to the ED. Patients with minor complaints, believed unlikely to be related to a circulatory problem, do not require this measurement. The necessity of repeated evaluations is dictated by the clinical complaint and status of the patient. Detailed pulse assessment is essential in all patients with potential peripheral vascular insufficiency. Although an association between the absence of a radial pulse (or the absence of both radial and femoral pulses) and hypotension has been demonstrated for hypovolemic trauma patients, the variability in individual response prohibits the use of this parameter as an absolute gauge of blood pressure. [34] No contraindications exist to assessment of pulse, but a few cautionary notes about the examination of the carotid pulse should be kept in mind: Concurrent bilateral carotid artery palpation should be avoided, as this maneuver could endanger cerebral blood flow. In addition, massage of the carotid sinus, found at the bifurcation of the external and internal carotid arteries at the level of mandible angle, may result in reflex slowing of the heart rate (see Chapter 11 ). To avoid inadvertent carotid sinus massage, the carotid pulse should be palpated at or below the level of the thyroid cartilage. A rare risk of precipitating a cerebrovascular event by vigorous palpation of the carotid artery is present in adults with atherosclerotic disease. This risk may be minimized by prior auscultation of the carotid artery. If a bruit is present, the carotid pulse may be gently palpated, but avoid vigorous palpation. Equipment Assessment of the pulse may be performed by the clinician at the bedside with any timepiece that has a second-hand display. This allows simultaneous assessment of all characteristics of the pulse: its rate, rhythm, gross perfusion pressure, and upstroke. If continuous monitoring is deemed necessary, bedside cardiac monitors can constantly monitor heart rate and rhythm and may be more accurate indicators of a perfusing rhythm than cardiac auscultation. Pulse oximetry (see Chapter 2 ), although primarily intended to measure oxygen saturation, also may be used to monitor the pulse rate. In a critical care situation, more sophisticated invasive monitoring techniques are available (see Chapter 20 ) for arterial pressure measurement and rate assessment. Procedure Pulses are palpable at numerous sites, although for convenience the radial pulse at the wrist is routinely used. The examiner should use the tips of the first and second fingers to palpate the pulse. The two advantages to this technique are (1) the fingertips are quite sensitive, enabling the pulse to be easily located and counted, and (2) the examiner's own pulse may be erroneously counted if the thumb is used instead of the first and second fingers. Pulses are also easily palpated at the carotid, brachial, femoral, posterior tibial, and dorsalis pedis arteries. Palpation of the pulse at the brachial artery may facilitate the appreciation of pulse contour and amplitude. It is located at the medial aspect of the elbow and is more easily palpated when the elbow is held slightly flexed. [35] Pulse rate is ideally determined by counting the pulse for 1 minute, particularly if any abnormality is present. Common convention in acute care settings is the counting of a regular pulse for 15 seconds and multiplying the resultant number by 4 to determine beats/min. In newborns, direct heart auscultation and umbilical palpation are the methods of choice to determine heart rate. Instantaneous changes in newborn heart rates are best
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indicated for the resuscitation team by the examiner tapping out each heartbeat. pulses, is recommended over palpation of more peripheral arteries.
[ 36]
In unstable children, palpation of central arteries, particularly femoral and brachial
In most circumstances the palpated heart rate will approximate the actual heart rate within 2%. [37] Interpretation Pulse Rate
Individual physiology must be considered in pulse interpretation. In infants and children, pulse rate must be interpreted with reference to age. Pulse varies with respiration, increasing with inspiration and slowing with expiration. This is known as a sinus dysrhythmia and is physiologic. Although bradycardia is defined as a heart rate of 10 mm Hg in systolic blood pressure. Others report that only 1.4% of elderly patients had a systolic brachial blood pressure difference of >10 mm Hg, although 6.5% had a difference exceeding 7.5 mm Hg. [98] Panayiotou noted that for most stroke patients, the difference between the paretic and normal arm was only 4 to 5 mm Hg.[99] However, differences of 9 to 12 mm Hg were noted for some patients. Hence, differential brachial blood pressures must be interpreted within the clinical context of the patient's presentation. Pulsus Paradoxus
Normal respiration decreases the systolic blood pressure by approximately 10 mm Hg during inspiration. Pulsus paradoxus occurs when there is a >12 mm Hg decrease in the systolic blood pressure during inspiration. Pulsus paradoxus may occur in patients with chronic obstructive pulmonary disease, pneumothorax, severe asthma, and pericardial tamponade. [100] Other conditions such as an atrial septal defect, aortic insufficiency, and poor left ventricular compliance have been associated with pulsus paradoxus without pericardial fluid. To measure a paradoxical pulse, the patient should be lying comfortably, at a 30° to 45° angle, and breathing normally in an unlabored fashion (unusual conditions in a patient suspected of cardiac tamponade, severe asthma or chronic obstructive pulmonary disease, or pneumothorax). [101] The blood pressure cuff is inflated well above systolic pressure and is slowly deflated until one first hears the systolic sounds that are synchronous with expiration ( Fig. 1-3 ). Initially, one will hear the arterial pulse only during expiration, and it will disappear during inspiration. The cuff is then further deflated until arterial sounds are heard throughout the respiratory cycle. A paradoxical pulse can be palpated if it is very large. During palpation the pulse may completely disappear during inspiration. When present, this technique is a quick bedside confirmation of the possibility of severe tamponade. Palpation for this purpose is best done at peripheral arteries, such as the radial or femoral. An alternative approach to measurement of pulsus paradoxus is to use a finger arterial pressure monitor (Finapres; Ohmeda, Englewood, CO) and to subtract the peak systolic blood pressure during expiration from the lowest systolic
Figure 1-3 A, Measurement of pulsus paradoxus. Note that the systolic pressure varies during the respiratory cycle. (From Stein L, Shubin H, Weil M: Recognition and management of pericardial tamponade. JAMA 225:504, 1973. Copyright 1973, American Medical Association. Reproduced by permission.) B, Technique for the measurement of pulsus paradoxus.
blood pressure during inspiration. [102] The pulsus paradoxus obtained with this technique was found to have less variability (when compared to intra-arterial measurements) than with manual measurements. Furthermore, pulsus paradoxus obtained using the finger pressure monitor correlates well with the pulmonary index score in asthmatic children. [103] Changes in the pulsus paradoxus were found to correlate with other markers of clinical status and admission decisions. If the difference between these inspiratory and expiratory pressures is >12 mm Hg, the paradoxical pulse is high. [104] Most patients with proven tamponade have a difference of =20 to 30 mm Hg during the respiratory cycle. [105] [106] This may not be true of patients with very narrow pulse pressures (typical of advanced tamponade), who have a "deceptively small" paradoxical pulse of 5 to 15 mm Hg. The relative decrease in pulsus paradoxus occurs because the paradoxical pulse is a function of actual pulse pressure, and the inspiratory systolic pressure may be below the level at which diastolic sounds disappear. [101] For this reason, the ratio of paradoxical pulse to the pulse pressure is a more reliable
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measure. A paradoxical pulse >50% of the pulse pressure is abnormal. [101] Pulsus paradoxus has been correlated with the amount of impairment of cardiac output by tamponade. In uninjured patients with pericardial effusion, a pulsus paradoxus >25 mm Hg (in the absence of relative hypotension) was both sensitive and specific for moderate or severe versus mild tamponade. [104] A similar study of
right ventricular diastolic collapse by echocardiography found that an abnormal pulsus paradoxus had a sensitivity of 79%, specificity of 40%, positive predictive value of 81%, and negative predictive value of 40%. [107] The absence of a paradoxical pulse does not rule out tamponade (see Chapter 16 ). In the pediatric population, pulsus paradoxus has been studied to determine the disease severity of obstructive and restrictive pulmonary disease, [108] most commonly asthma. A value of 15 mm Hg or greater correlates well with clinical score, peak expiratory value, flow rate, oxygen saturation, and subsequent need for admission. [109] Despite the disease entities that a widened pulsus paradoxus may suggest, it is a difficult task to perform adequately using only a syphgmomanometer. In a study by Jay et al., emergency clinicians and critical care specialists were unable to reliably measure pulsus paradoxus in a trained reference subject either by palpation or by syphgmomanometer. The variance of actual versus measured pulsus paradoxus was greater with increasing pulsus paradoxus values into the pathologic range, lowering significantly the positive predicative value of the test. [110] The author's conclusion was that new aids should be developed and used to reliably predict this important vital sign. Shock Index
The ratio of the pulse rate over the systolic blood pressure has been suggested as a measure of clinical shock. The shock index (SI) has a normal range of 0.5 to 0.7. A number of clinical scenarios have been studied using the shock index as a predictor of severe illness or injury. A shock index >0.85 to 0.90 suggests acute illness in medical patients, as well as a marked increase in potential for gross hemodynamic instability in a trauma patient. [111] [112] [113] [114] In a study evaluating first-trimester pregnancy, those patients with a shock index >0.83 were 15 times more likely to be diagnosed with an ectopic pregnancy in the ED. [111] [115] However, some studies have found that the presenting pulse rate alone had nearly the same predictive power for severity of illness as the shock index. Further, Rady and coworkers demonstrated that although the SI appeared to correlate with left ventricular stroke work index, it had little correlation with systemic oxygen transport in hemorrhagic and septic shock.[112]
DOPPLER ULTRASOUND FOR EVALUATION OF PULSE AND BLOOD PRESSURE Principles of Doppler Ultrasound Doppler ultrasound is based on the Doppler phenomenon: The frequency of sound waves varies depending on the speed of the sound transmitter in relation to the sound receiver. Doppler devices transmit a sound wave that is reflected by flowing erythrocytes, and the shift in frequency is detected. Frequency shift can only be detected for blood flow >6 cm/sec. Indications and Contraindications
Doppler ultrasound is commonly used in the ED for the measurement of blood pressure in low-flow states, evaluation of lower extremity peripheral perfusion, and assessment of fetal heart sounds after the first trimester of pregnancy. Doppler sensitivity allows the detection of systolic blood pressure down to 30 mm Hg in the evaluation of a patient in shock. In the patient with peripheral vascular disease in whom there is concern about the adequacy of peripheral perfusion, the ankle/brachial index provides a rapidly obtainable, reproducible, and standardized assessment. [116] Fetal heart sounds provide a baseline assessment of any patient with =12 weeks' gestation in whom there is possible abdominal trauma or fetal distress due to a pregnancy complication. The use of Doppler ultrasound in the evaluation of deep venous thrombosis is a valuable tool; however, it requires specific training and experience to attain proficiency. Discussion of this topic is beyond the scope of this chapter. Equipment
A nondirectional Doppler device has a probe that houses two piezoelectric crystals. One crystal transmits the signal and the other receives it. Reflected signals are converted to an electrical signal and fed to an output that transforms them to an audible sound. Two commonly used Doppler units are the pocket Doppler stethoscope (model BF4A, Medsonics, Inc, Los Altos, CA) and the ultrasonic Doppler flow detector (model 811, Parks Medical Electronics, Aloha, OR) ( Fig. 1-4 and Fig. 1-5 ). Probes with a frequency of 2 to 5 MHz are best for detecting fetal heart sounds. Frequencies of 5 to 10 MHz are appropriate for limb arteries and veins. The probes should be monitored periodically for electrical damage and integrity of the crystal. Sphygmomanometers used in conjunction with the Doppler device should be calibrated periodically, as described in the section on blood pressure evaluation.
Figure 1-4 Pocket Doppler stethoscope (model BF4A). (Courtesy of Medsonics Inc, Los Altos, CA.)
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Figure 1-5 Ultrasonic Doppler flow detector with speaker and probes (model 811). (Courtesy of Parks Medical Electronics, Aloha, OR.) Procedure
The Doppler probe is placed against the skin using an acoustic gel as an interface. The gel ensures optimal ultrasound signal transmission and reception and protects the crystals. In an emergency, water-soluble lubricant (e.g., Surgilube or K-Y jelly) may be substituted for commercial acoustic gel. The probe is angled at 45° along the length of the vessel to optimize frequency shifts and signal amplitude. In the evaluation of peripheral perfusion, a sphygmomanometer cuff is placed proximal to the arterial pulse and inflated. The probe is placed over the arterial pulse and the cuff is slowly deflated. The pressure at which flow is first heard is the systolic pressure. In the evaluation of peripheral vascular disease, the ankle/brachial index is determined. Both brachial arteries are examined at the medial aspect of the antecubital fossa. The probe is angled until the most satisfactory signal is obtained. The cuff is inflated and slowly deflated until the systolic pulse is heard. The procedure is repeated for the posterior tibial and dorsalis arteries of both lower extremities. In the evaluation of fetal heart tones, variable positioning of the fetus may require examination at several locations over the uterus and angling of the probe to search for the optimal signal. It is best to begin in the mid-suprapubic area and to explore the uterus via angulation of the probe. Once tones are located, the probe can be moved along the abdomen to reach a position closer to the origin of the sound. Fetal heart tones are distinguished from placental flow by the discrete quality of the fetal heart tones and the rate of placental flow, which matches the maternal pulse. Interpretation
As noted earlier, in low-flow states, Doppler ultrasound can detect a blood pressure as low as 30 mm Hg. The ankle/brachial index of each limb is calculated by dividing the higher systolic pressure of the posterior tibial or the dorsalis pedis artery of the limb by the higher of the systolic pressures in the brachial arteries. In normal individuals, the index should be >1.0. Patients with claudication have values between 0.6 and 0.8. Values 25 beats/min constitutes a positive tilt test, and an orthostatic pulse increase of 3 seconds and suggested a fluid deficit of >100 mL/kg. [164] The presence of delayed capillary refill >2 seconds when combined with any two or more of absent tears, dry mucous membranes, or ill general appearance can predict clinical dehydration (>5% deficit of body weight) in children (age 1 month to 5 years) with a 87% sensitivity and 82% specificity. [167] The role of serial capillary refill interval measurements for assessing the response to rehydration in adults is unknown. However, the test does not appear to be useful for assessing acute blood volume loss. In adults, the capillary refill interval was found to be less sensitive and less specific than orthostatic vital signs for detecting a 450-mL blood loss during blood donation. [123]
TEMPERATURE Accurate measurement of body temperature is an essential part of clinical medicine. When taken in the context of other vital signs, abnormalities of core body temperature are excellent guides to the severity of illness. Detection of abnormal body temperature facilitates proper diagnosis and evaluation of presenting complaints. [168] [169] [170] [171] [172] [173] [174] [175] [176] The inability to maintain normal body temperature is indicative of a vast number of potentially serious disorders, including infections, neoplasms, shock, toxic reactions, and environmental exposures.[168] [171] Fever in neutropenic, immunocompromised, and intravenous drug-abusing patients may be more reliable than laboratory tests or physician assessment in diagnosing serious illness. [171] Infants are particularly sensitive to thermal stress and may demonstrate lower body temperatures during asphyxia or necrotizing enterocolitis. [172] [173] [174] Normalization of body temperature following intervention may have important prognostic and therapeutic implications. [171] Physiology Under normal conditions, the temperature of deep central body tissues (i.e., core temperature) remains at 37 ± 0.6°C (98.6 ± 1.08°F). [175] [176] Core body temperature can be maintained within a narrow range while environmental temperature varies from as much as 13 to 60°C (55 to 140°F), [177] whereas surface temperature rises and falls with environmental and other influences. Maintenance of normal body temperature requires a balance of heat production and heat loss. Heat loss occurs by radiation, conduction, and evaporation. Approximately 60%, 18%, and 22% of heat loss, respectively, occurs by these methods. Heat loss is increased by wind, water, and lack of insulation (e.g., clothing). Sweating, vasodilation, and decreased heat production serve to decrease temperature, whereas piloerection, vasoconstriction, and increased heat production serve to increase body temperature. Heat production is increased by shivering, fat catabolism, and increased thyroid hormone production. Temperature control occurs by feedback mechanisms operating through the preoptic area of the hypothalamus. Heat-sensitive neurons in this area increase their rate of firing during experimental heating. Receptors in the skin, spinal cord, abdominal viscera, and central veins primarily detect cold and provide feedback to the hypothalamus, which signals an increase in heat production. Stimuli that change the core body temperature result in reflex changes in mechanisms that increase either heat loss or production. [177]
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Indications and Contraindications Clinicians generally measure body temperature to determine if it is outside the normal range and as an indication of pathologic conditions that can affect core body temperature. Because actual core body temperature measurement requires the placement of invasive monitors, such as an esophageal or a pulmonary artery probe, clinicians commonly use estimates of core body temperature, which conveniently and safely assess abnormalities of core temperature. Unfortunately, all noncore body sites and methods have inherent accuracy limitations, which clinicians have come to accept in assessing most patients. Oral temperature measurement requires a cooperative adult or child, generally older than 5 years. Patients who are grossly uncooperative, hemodynamically unstable, septic, or in respiratory distress (with a RR >20) require another method of temperature measurement. [178] This group includes children younger than 5 years and patients who are intubated. Special techniques of measuring actual core body temperature may be indicated in certain patients (e.g, those with profound hypothermia, frostbite, or hyperthermia). Measurement of core body temperature is indicated in these individuals because it accurately measures treatment effects. This is the group of patients who will also benefit most from continuous temperature measurements.[179] Measurement Sites Core Body Temperature
It has been demonstrated that the following sites accurately reflect core body temperature and its changes: esophageal (in the distal third of the esophagus), the tympanic membrane (using direct thermistor contact at the anterior inferior quadrant of the tympanic membrane), [180] [181] and the pulmonary artery temperature. [182] Other sites may represent core body temperature under certain conditions. For example (1) the rectum, when the temperature is obtained at least 8 cm from the anus using an indwelling thermistor and the body temperature is relatively constant, and (2) the bladder when measured with an indwelling thermistor. [128] [183] Data on core temperature in pediatric patients is limited and it is unclear if bladder, rectal, or oral temperature is a good measurement of core body temperature in children. [184] Peripheral Body Sites Approximating Core Body Temperature
Oral temperature measurement with a digital electronic probe is commonly used for ambulatory patients. [185] Advantages include convenience, timing, safety, and availability. Disadvantages include various factors that affect clinical accuracy and sensitivity. Electronic oral temperature probes must be covered with disposable covers, although these have been shown not to be completely effective in preventing probe contamination with microorganisms. [186] Although there are no absolute contraindications for oral temperature assessment, patients with factors shown to produce unreliable results (see later) require temperature measurement at other sites.[178] [187] [188] Rectal temperature is often considered the criterion standard of body temperature for ambulatory patients and is often routine for children younger than 3 years. [189] Advantages include accuracy, sensitivity, and availability. One intensive care unit study found rectal probe temperatures to demonstrate limited variability or bias when compared with pulmonary artery temperatures.[190] Disadvantages include longer intervals for measurement, safety concerns, and inconvenience. Neutropenia and recent rectal surgery represent relative contraindications to rectal temperature measurement. [191] Placement of a rectal probe thermometer may produce autonomic changes in patients with acute myocardial infarction. [192] Body temperature measured as a function of infrared radiation (IR) detected from the ear, including the auditory canal and tympanic membrane (TM), is easy to use, hygienic, convenient, and quick. [193] The noncontact IR ear thermometer has been studied under a variety of clinical conditions. [194] Concerns have been raised over the accuracy of these thermometers in screening for fever in children younger than 3 years of age. [195] [196] Romano and colleagues found the Thermoscan Pro-1 IR thermometer to perform similar to rectal probe temperature, but the FirstTemp IR thermometer displayed considerably more variability. [190] Intensive care studies have compared infrared thermometry to pulmonary artery core temperatures and found a sensitivity of detecting fever to be 58% and a specificity of 94%. Double ear thermometry (measuring values at both right and left TMs and calculating the mean) increased the sensitivity and specificity to 61% and 95%.[197] Increased variability of tympanic temperatures vs oral temperatures was also found in the critical care population. [198] In the ED setting, infrared tymponometers have undergone limited scrutiny. In 100 children, TM, rectal, and axillary temperatures were obtained with statistically significant differences noted. [199] In a similar ED-based study, 95 geriatric (older than 60 years of age) patients had oral, TM, and rectal temperatures measured with fevers missed with both oral and tympanic readings, as compared to rectal readings. [200] In another study of 100 adult ED patients, the TM and rectal temperatures showed generally good agreement, but the TM temperature missed 4 of 10 patients with a fever (>38.5°C). [201] The authors also noted that the temperature difference between TM and rectal temperature readings was greater in the presence of cerumen impaction. Special patient populations deserve separate attention. First, when a neonatal population is examined, significant variability is noted with TM temperatures, making rectal thermometers the standard. [202] Second, a theoretical
disadvantage of TM temperatures might be a falsely elevated estimate of the core temperature in the presence of otitis media. However, in one study tympanic thermometers accurately reflected oral temperatures in children with otitis media. [203] Although not a likely ED concern, prehospital providers who might wish to measure IR tympanic temperature at low ambient temperatures should be aware that below 24.6°C the TM readings will greatly underestimate core temperature. [204] EMS personnel should also be aware that in a cohort of exhausted marathon runners, rectal and IR tympanic temperatures have only moderate correlation. [205] Hence when hyperthermia or hypothermia is clinically suspected and the IR tympanic temperature does not confirm an abnormal temperature, a rectal temperature should be considered. Axillary and tactile temperature assessment have been demonstrated to be unreliable and insensitive. They should not be used as screening methods for core temperature abnormalities in the ED. [206] [207] [208] Similarly, the use of liquid crystal chemophototropic strips applied to the skin of the forehead
21
are not accurate for single measurement or fever screening. [209] [210] Single-use Tempa-DOT thermometers, which show increasing temperature dot darkening with increasing temperature, have been adopted by many EDs. The sensitivity of these thermometers for fever identification remains to be determined. The most rudimentary method for temperature measurement, parental assessment by tactile touch, is associated with a measured fever approximately 75% of the time. [211] Clinician estimation of fever is almost identical (70%). [212] Equipment Mercury-in-glass thermometers remain popular despite requiring longer equilibration times and having cumbersome cleansing requirements. Electronic methods of temperature measurement are based on the thermocouple principle. Modern electronic thermometers signal once extrapolation of the temperature-time curve occurs. [212A] Current in vitro standards call for an accuracy of ±0.1°C (±0.18°F) over the range of 37 to 39°C (98.6 to 102.2°F). [213] Thermistor probes (i.e., small thermocouples with instantaneous readouts) for esophageal and vascular temperature measurement provide continuous temperature readouts when attached to a potentiometer. [9] Thermistor products are available for esophageal, bladder, and rectal probes (Mallinckrodt Medical, Inc, St. Louis; or Yellow Springs Instruments, Yellow Springs, OH) with appropriate readout monitors. Noncontact IR ear thermometers were introduced in 1985. These thermometers were initially used only in hospitals, but they are now sold over the counter for home use. The IR ear thermometers work by incorporating an IR sensor in the field of view of the IR emissions from the ear. Ear IR thermometers generally detect naturally occurring IR emissions over a brief time period, generally 2 standard deviation (SD) above the mean. Fever has been defined as an oral temperature =37.8°C (=100.0°F), [222] a rectal temperature =38.0°C (=100.4°F), [223] or an IR ear temperature =37.6°C (=99.6°F).[224] Based on the measurement of temperatures in normal, healthy infants, Herzog and Coyne recommend that fever should be defined as rectal temperature =38°C in infants younger than 30 days old; =38.1°C in infants 30 to 60 days (1 month); and =38.2°C in infants 60 to 90 days old (2 months). [225] Hypothermia has been defined as a core body temperature 105.8°F), with accompanying symptoms and signs.[226] A useful nomogram and formulae for conversion of °C to °F are provided in Figure 1-11 . Temperature probes that require the transfer of heat energy from local tissues to the temperature probe require a period of equilibration and reliable tissue contact at the intended body site. Acceptable equilibration times for mercury-in-glass thermometers for oral, rectal, and axillary sites are 7, 3, and 10 minutes, respectively. Used in a predictive mode, electronic digital thermometers generally require 30 seconds for oral or rectal temperature equilibration. The predictive mode uses temperature changes vs time to predict an equilibration temperature. Normal ranges and suggested febrile thresholds for common body sites and methods should be considered in the interpretation of temperature values ( Table 1-8 ). The interpretation of temperature measurements during clinical assessment must consider the use of antipyretics, level of activity, pregnancy, environmental exposure, and patient age. The duration of antipyresis with acetaminophen or aspirin is 3.5 to 4 hours. When both drugs are given together, the duration of action may be extended up to 6 hours.[227] Body temperature is increased during sustained exercise, during pregnancy and during the luteal phase of the menstrual cycle. Temperature also increases in later afternoon during diurnal variation. Body temperature is generally reduced with advanced age. The interpretation of temperatures obtained with pulmonary artery or esophageal thermistors is generally straightforward. Comparison of measured values to the expected normal range should be performed to determine if the patient has an abnormal core body temperature. In addition to improper placement of the thermistor, sources of temperature error include an improperly calibrated potentiometer or thermistor, damaged thermistor, or improper placement. The biomedical staff at the institution should periodically verify readout and calibration of these instruments.
Figure 1-11 Temperature conversion scale. To change Celsius (centigrade) to Fahrenheit, multiply the Celsius temperature by 9/5 and add 32. To change Fahrenheit to Celsius, subtract 32 from the Fahrenheit number and multiply by 5/9.
24
Body Site
TABLE 1-8 -- Normal Ranges and Suggested Febrile Thresholds for Human Body Temperature (in Healthy Resting Patient) Type of Thermometer Normal Range (°C) Fever (°C)
Core*
Electronic
36.4–37.9
38.0
Oral
Mercury-glass, electronic
35.5–37.7
37.8
Rectal
Mercury-glass, electronic
36.6–37.9
38.0
Ear
Infrared emission
35.7–37.5
37.6†
*Temperature obtained with a properly positioned pulmonary artery, esophageal, or tympanic membrane thermistor. †For unadjusted ear temperature using Thermoscan Pro-1 (Thermoscan, Inc, San Diego, CA).
Oral temperature measurements are affected by ingestion of hot or cold liquids, [191] tachypnea,[228] and cold ambient air.[229] Smoking appears to result in little change in oral temperatures. [188] [191] Therefore, before taking an oral temperature, the examiner should inquire about these features and possibly delay taking the temperature. Also, Erickson found a 2.7°C (4.9°F) reduction of oral temperature measurement when the probe was placed under the tip of the tongue instead of under the posterior sublingual pocket. [187] When using a mercury-glass thermometer, optimum placement time was found to be 7 minutes for oral temperatures in children. [230] Given the extrapolation that occurs with rapid reading thermocouple devices and IR detectors, it is not surprising that the sensitivity of these devices (whether oral or tympanic) for fever (as detected by oral mercury thermometers) is only 86% to 88%. [231] Hence, many practitioners have adopted the adage that when a temperature is suspected or crucial in decision making, but not evident with an oral thermocouple probe or IR tympanic thermometer, measurement with a glass, mercury thermometer is indicated. Axillary temperatures obtained in 108 children by Kresch had a sensitivity of only 33% and a specificity of 98% for fever. electronic thermometer in the axilla. [232] Hence, axillary temperatures should not be used to screen for fever.
[207]
Ogren obtained similar results using an
When rapid changes in body temperature occur, oral and tympanic temperature measurements appear to be more reliable than rectal temperature. In 20 adults examined during open-heart surgery, oral temperatures showed a better correlation with blood temperature during rapid cooling and rewarming. [218] In 12 adults, the average rectal temperature lag during warming was 5.3 minutes during water immersion and 3.8 minutes during exercise. [233] Sublingual (oral) temperature delay (1.3 and 0.9 minutes for the 2 experiments, respectively) was less than auditory canal delay (1.1 and 4.1 minutes, respectively) in temperature response. Infrequently, ED patients require constant monitoring of temperature (e.g., in cases of hypothermia or hyperthermia). This can usually be performed using a bladder or esophageal probe attached to a potentiometer. Patients with indwelling central venous or pulmonary arterial catheters may have electronic thermistors inserted into the central circulation to measure core body temperature. As noted earlier, rectal temperature measurements are less desirable for monitoring patients undergoing rapid core temperature changes. Periodic IR tympanic temperature monitoring may represent one useful option in the hypothermic patient. [234] The interpretation of ear IR temperatures requires a knowledge of the mode of thermometer operation and ambient temperature. Cerumen occlusion of the ear canal may produce a false low reading. [235] Most IR ear thermometers have different modes that allow users to predict the equivalent temperature at other body sites. IR ear thermometers appear moderately sensitive for fever. [195] [196] If these devices are used, the clinician must be aware of the potential for a false low temperature. When in doubt, the measurement should be repeated with a more standard method.
CONCLUSION Vital signs must always be interpreted in relationship to each other to obtain a more complete clinical picture. All vital signs are subject to errors in measurement and therefore must be verified when the initial result does not match the clinical presentation. Abnormal vital signs may lead the clinician to a diagnosis, and abnormalities should be explained within the context of the patient's illness.
Acknowledgment
The editors and author wish to acknowledge the significant contributions of Jody Riva Lewinter, Thomas E. Terndrup, Terry M. Williams, and Robert K. Knoop to this chapter in previous editions.
References 1. Edmonds 2. Alcock
ZV, Mower WR, Lovato LM, Lomeli R: The reliability of vital sign measurements. Ann Emerg Med 39:233, 2002.
K, Clancy M, Crouch R: Physiologic observations of patients admitted from A&E. Nurs Stand 16:33, 2002.
3. Dorges
V, Wenzel V, Kuhl A, et al: Emergency medical service transport-induced stress? An experimental approach with healthy volunteers. Resuscitation 49:151, 2001.
4. Gausche
M, Henderson DP, Seidel JS: Vital signs as part of prehospital assessment of the pediatric patient: A survey of paramedics. Ann Emerg Med 19:173, 1990.
5. Fishman
AP: Pulmonary Diseases and Disorders, 2nd ed. New York, McGraw-Hill, 1988.
6. Bedford 7. Major
DE: The ancient art of feeling the pulse. Br Heart J 13:423, 1951.
RH: The history of taking the blood pressure. Ann Med Hist 2:47, 1930.
8. O'Rourke 9. Brock
RA: Physical examination of the arteries and veins. In Hurst JW (ed): The Heart, 6th ed. New York, McGraw-Hill, 1986, p 138.
L: The development of clinical thermometry. Guys Hosp Rep 121:307, 1972.
10.
Ziegler RF: Electrocardiographic Studies in Normal Infants and Children. Springfield, IL, Charles C Thomas, 1951.
11.
Haddad HM, Hsia DY, Gellis SS: Studies on respiratory rate in the newborn: Its use in the evaluation of respiratory distress in infants of diabetic mothers. Pediatrics 17:204, 1956.
12.
Report of the Second Task Force on Blood Pressure Control in Children, 1987: Task Force on Blood Pressure Control in Children. Pediatrics 79:1, 1987.
13.
Iliff A, Lee VA: Pulse rate, respiratory rate, and body temperature of children between 2 months and 18 years of age. Child Dev 23:237, 1952.
14.
Hooker EA, Danzl DF, Brueggmeyer M, Harper E: Respiratory rates in pediatric emergency patients. J Emerg Med 10:407, 1992.
15.
Rusconi F, Castagneto M, Gagliardi L, et al: Reference values for respiratory rate in the first three years of life. Pediatrics 94:350, 1994.
16.
Pesola GR, Pesola HR, Nelson MJ, et al: The normal difference in bilateral indirect blood pressure recordings in normotensive individuals. Am J Emerg Med 19:43, 2001.
25
17.
Pesola GR, Pesola HR, Lin M, et al: The normal difference in bilateral indirect blood pressure readings in hypertensive individuals. Acad Emerg Med 9:342, 2002.
18.
Marks MK, South M, Carlin JB: Reference ranges for respiratory rate measured by thermistry (12–84 months). Arch Dis Child 69:569, 1993.
19.
Spodick DH, Raj P, Bishop RL, et al: Operational definition of normal sinus heart rate. Am J Cardiol 69:1245, 1992.
20.
Spodick DH: Survey of selected cardiologists for an operational definition of normal sinus heart rate. Am J Cardiol 72:487, 1993a.
21.
Spodick DH: Redefinition of normal sinus heart rate. Chest 104:939, 1993b.
22.
Key TC, Resnik R: Maternal changes in pregnancy. In Danforth DN, Scott JR (eds): Obstetrics and Gynecology, 5th ed. Philadelphia, JB Lippincott, 1986.
23.
Katz R, Karliner JS, Resnik R: Effects of a natural volume overload state (pregnancy) on left ventricular performance in normal human subjects. Circulation 58:434, 1978.
24.
Levitsky MG: Pulmonary Physiology. New York, McGraw-Hill, 1982.
25.
Engum SA, Mitchell MK, Schere LR, Gomez G, et al: Prehospital triage in the injured pediatric patient. J Pediatr Surg 35:85, 2000.
26.
Orr RA, Venkataraman ST, McCloskey KA, Janosky JE, et al: Measurement of pediatric illness severity using simple pretransport variable. Prehosp Emerg Care 5:127, 2001.
27.
Gorelick MH, Lee C, Cronan K, et al: Pediatric emergency assessment tool (PEAT): A risk-adjustment measure for pediatric emergency patients. Acad Emerg Med 8:156, 2001.
28.
Rajesh VT, Singhi S, Kataria S: Tachypnea is a good predictor of hypoxia in acutely ill infants under 2 months. Arch Dis Child 82:46, 2000.
29.
Bates B: A Guide to Physical Examination and History Taking, 4th ed. Philadelphia, JB Lippincott, 1987.
30.
Hutchinson J: Thorax. In Todd RB (ed): Cyclopaedia of Anatomy and Physiology, vol 4. London, Longman, Brown, Green, Congmans, & Roberts, 1849, p 1079.
31.
Hooker EA, O'Brien DJ, Danzl DF, et al: Respiratory rates in emergency department patients. J Emerg Med 7:129, 1989.
32.
Taylor JA, Del Beccaro M, Done S, Winters W: Establishing clinically relevant standards for tachypnea in febrile children younger than 2 years. Arch Pediatr Adolesc Med 149:283, 1995.
33.
Rigatto H: Apnea. Pediatr Clin North Am 29:1105, 1982.
Deakin CD, Low JL: Accuracy of the advanced trauma life support guidelines for predicting systolic blood pressure using carotid, femoral, and radial pulses: Observational study. BMJ 321:673, 2000. 34.
35.
Burnside JW, McGlynn TJ: Physical Diagnosis, 17th ed. Baltimore, Williams & Wilkins, 1986.
36.
Chameides L, Hazinski MF (eds): Textbook of Pediatric Advanced Life Support. Dallas, American Heart Association, 1994.
Runcie CJ, Reeve W, Reidy J, Dougall JR: A comparison of measurements of blood pressure, heart rate and oxygenation during interhospital transport of the critically ill. Intensive Care Med 16:317, 1990. 37.
38.
Oakley GDG: The athletic heart. Cardiol Clin 5:319, 1987.
39.
Spodick DH: Normal sinus heart rate: appropriate thresholds for sinus tachycardia and bradycardia. South Med J 89:666, 1996.
40.
Opthof T: The normal range and determinants of the intrinsic heart rate in man. Cardiovasc Res 45:173, 2000.
41.
Harris RL, Musher DM, Bloom K, et al: Manifestations of sepsis. Arch Intern Med 147:1895, 1987.
42.
Kelly R, Hayward C, Avolio A, O'Rourke M: Noninvasive determination of age-related changes in the human arterial pulse. Circulation 80:1652, 1989.
43.
Wilkinson IB, Cockcroft JR, Webb DJ: Pulse wave analysis and arterial stiffness. J Cardiovasc Pharmacol 32:S33, 1998.
Tabata BK, Kirsch JR, Rogers MC: Diagnostic tests and technology for pediatric intensive care. In Roger MC (ed): Textbook of Pediatric Intensive Care. Baltimore, Williams & Wilkins, 1987, p 1401. 44.
45.
Kirkendall WM, Feinleib M, Freis ED, Mark AL: AHA Committee Report: Recommendations for human blood pressure determination by sphygmomanometers. Circulation 62:1146A, 1980.
46.
Silverman MA, Walker AR, Nicolaou DD, Bono MJ: The frequency of blood pressure measurements in children in four EDs. Am J Emerg Med 18:784, 2000.
47.
Paradis NA, Martin GB, Goetting MG, et al: Aortic pressure during human cardiac arrest: Identification of pseudoelectromechanical dissociation. Chest 101:123, 1992.
48.
Grunau CF: Doppler ultrasound monitoring of systemic blood flow during CPR. JACEP 7:180, 1978.
49.
O'Keefe KM, Bookman L: The portable Doppler: A practical application in EMS care. JACEP 5:987, 1976.
Weiss BM, Spahn DR, Rahmig H, et al: Radial artery tonometry: Moderately accurate but unpredictable technique of continuous noninvasive arterial pressure measurement. Br J Anaesth 76:405, 1996. 50.
51.
Petrie JC, O'Brien ET, Littler WA, DeSwiet M: Recommendations on blood pressure measurement. BMJ 293:611, 1986.
52.
Hemingway T, Abdelnur D, Guss DA. The impact of arm position on blood pressure measurement [abstract]. Acad Emerg Med 9:377, 2002.
53.
Nelson WP, Egbert AM: How to measure blood pressure accurately. Prim Cardiol 10:14, 1984.
54.
American Society of Hypertension: Recommendations for routine blood pressure measurement by indirect cuff sphygmomanometry. Am J Hypertens 5:207, 1992.
55.
Marks LA, Groch A: Optimizing cuff width for noninvasive measurement of blood pressure. Blood Press Monit 5:153, 2000.
56.
Perlman LV, Chiang BN, Keller J, Blackburn H: Accuracy of sphygmomanometers in hospital practice. Arch Intern Med 125:1000, 1970.
57.
Katona Z, Bolvary G: Automatic sphygmomanometer. Adv Cardiovasc Phys 5:119, 1983.
58.
Yelderman M, Ream AK: Indirect measurements of blood pressure in anesthetized patients. Anesthesiology 50:253, 1979.
59.
Park MK, Menard SM: Accuracy of blood pressure measurement by the Dinamap monitor in infants and children. Pediatrics 79:907, 1987.
60.
Nwankwo MU, Lorenz JM, Gardiner JC: A standard protocol for blood pressure measurement in the newborn. Pediatrics 99:E10, 1997.
61.
Pavlik VN, Hyman DJ, Toronjo C: Comparison of automated and mercury column blood pressure measurements in health care settings. J Clin Hyperten (Greenwich) 2:81, 2000.
Lahmann KG, Gelman JA, Weber MA, Lafrades A: Comparative accuracy of three automated techniques in the noninvasive estimation of central blood pressure in men. Am J Cardiol 15:1004, 1998. 62.
63.
Pickering TG: Principles and techniques of blood pressure measurement. Cardiol Clin 20:207, 2002.
64.
Prineas RJ, Jacobs D: Quality of Korotkoff sounds: Bell vs diaphragm, cubital fossa vs brachial artery. Prev Med 12:715, 1983.
65.
Park MK, Guntheroth WG: Direct blood pressure measurements in brachial and femoral arteries in children. Circulation 61:231, 1970.
66.
Hartmann AF, Klint R, Hernandez A, Goldring D: Measurement of the blood pressure in the brachial and posterior tibial arteries using the Doppler method. J Pediatr 82:498, 1973.
67.
Pascarelli EF, Bertrand CA: Comparison of blood pressures in the arms and legs. N Engl J Med 270:693, 1964.
68.
Singer AJ, Kahn SR, Thode HC Jr, Hollander JE: Comparison of forearm and upper arm blood pressures. Prehosp Emerg Care 3:123, 1999.
69.
Hirschl MM, Binder M, Herknew H, Bur A, et al: Accuracy and reliability of noninvasive continuous finger blood pressure measurement in critically ill patients. Crit Care Med 24:1684, 1996.
70.
Enselberg CD: Measurement of diastolic blood pressure by palpation. N Engl J Med 265:272, 1961.
71.
Reder RF, Dimich I, Cohen ML, Steinfeld L: Evaluating indirect blood pressure measurement techniques: A comparison of three systems in infants and children. Pediatrics 62:326, 1978.
72.
Goldring D, Wohltmann H: Flush method for blood pressure determinations in newborn infants. J Pediatr 40:285, 1952.
73.
Park MK, Menard SM: Normative oscillometric blood pressure values in the first 5 years in an office setting. AJDC 143:860, 1989.
74.
Elseed AM, Shinebourne EA, Joseph MC: Assessment of techniques for measurement of blood pressure in infants and children. Arch Dis Child 48:932, 1973.
75.
Cohn JN: Blood pressure measurement in shock. JAMA 199:118, 1967.
76.
Millar-Craig MW, Bishop CN, Raftery EB: Circadian variation of blood-pressure. Lancet 1:795, 1978.
American Heart Association: Recognition of respiratory failure and shock: Anticipating cardiopulmonary arrest. In Chameides L, Hazinski MF (eds): Textbook of Pediatric Advanced Life Support. American Heart Association, Dallas, 1988, p 1. 77.
78.
Schwaitzberg SD, Bergman KS, Harris BH: A pediatric trauma model of continuous hemorrhage. J Pediatr Surg 23:605, 1988.
79.
Wo CCJ, Shoemaker WC, Appel PL, et al: Unreliability of blood pressure and heart rate to evaluate cardiac output in emergency resuscitation and critical illness. Crit Care Med 21:218, 1993.
80.
Abou-Khalil B, Scalea TM, Trooskin SZ, et al: Hemodynamic responses to shock in young trauma patients: Need for invasive monitoring. Crit Care Med 22:633, 1994.
81.
The 1988 Report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure. Arch Intern Med 148:1023, 1988.
26
82.
Reeves RA: Does this patient have hypertension? How to measure blood pressure. JAMA 273:1211, 1995.
83.
Chernow SM, Iserson KV: Use of the emergency department for hypertension screening: A prospective study. Ann Emerg Med 16:180, 1987.
84.
Mancia G, Grassi G, Pomidossi G, et al: Effect of blood pressure measurement by the doctor on patient's blood pressure and heart rate. Lancet 2:695, 1983.
85.
Pickering TG, James GD, Boddie C, et al: How common is white coat hypertension? JAMA 259:225, 1988.
86.
Chrysant SG: Treatment of white coat hypertension. Current Hypertens Rep 2:412, 2000.
87.
Verdecchia P, Palatini P, Schillaci G, et al: Independent predictors of isolated ('white coat') hypertension. J Hypertens 19:1015, 2001.
Pose-Reino A, Rodriguez-Fernandez M, Lopez-Barreiro, et al: Diagnostic criteria of white coat hypertension (WCH): Consequences for the implications of WCH for target organs. Blood Press 11:144, 2002. 88.
89.
Bailey RH, Bauer JH: A review of common errors in the indirect measurement of blood pressure. Arch Intern Med 153:2741, 1993.
90.
Maxwell MH, Waks AU, Schroth PC, Karam M: Error in blood pressure measurement due to incorrect cuff size in obese patients. Lancet 2:33, 1982.
91.
Baker RH, Ende J: Confounders of auscultatory blood pressure measurement. J Gen Intern Med 10:223, 1995.
92.
Linfors KW, Feussner JR, Blessing CL, et al: Spurious hypertension in the obese patient: Effect of sphygmomanometer cuff size on prevalence of hypertension. Arch Intern Med 144:1482, 1989.
93.
Manning DM, Kuchirka C, Kaminski J: Miscuffing: Inappropriate blood pressure cuff application. Circulation 68:763, 1983.
94.
Guagnano MT, Palitti VP, Murri R, et al: Many factors can affect the prevalence of hypertension in obese patients: Role of cuff size and types of obesity. Panminerva Med 40:22, 1998.
95.
Poppers PJ, Epstein RM, Donham RT: Automatic ultrasound monitoring of blood pressure during induced hypotension. Anesthesiology 35:431, 1971.
96.
Dewar R: The effect of hemiplegia on blood pressure measurements in the elderly. Postgrad Med J 68:888, 1992.
97.
Armstrong RS: Nurses' knowledge of error in blood pressure measurement technique. Int J Nurs Pract 8:118, 2002.
98.
Hashimoto F, Hunt WC, Hardy L: Differences between right and left arm blood pressures in the elderly. West J Med 141:189, 1984.
99.
Panayiotou BN, Harper GD, Fotherby MD, et al: Interarm blood pressure difference in acute hemiplegia. J Am Geriatr Soc 41:422, 1993.
100. McGregor 101. Spodick
M: Pulsus paradoxus. N Engl J Med 301:480, 1979.
D: Acute cardiac tamponade: Pathologic physiology, diagnosis, and management. Prog Cardiovasc Dis 10:64, 1967.
102. Steele
DW, Wright RO, Lee CM, Jay GD: Continuous noninvasive determination of pulsus paradoxus: Pilot study. Acad Emerg Med 2:894, 1995.
103. Wright
RO, Santucci KA, Jay GD, Steele DW: A novel measurement technique for pulsus paradoxus: Utility in acute childhood asthma [abstract]. Acad Emerg Med 2:430, 1995.
104. Curtiss
E, Reddy P, Uretsky B, Cecchetti A: Pulsus paradoxus: Definition and relation to the severity of cardiac tamponade. Am Heart J 115:391, 1988.
105. Symbas
P, Harlafhs N, Waldo W: Penetrating cardiac wounds: A comparison of different therapeutic methods. Ann Surg 183:377, 1976.
106. Shoemaker
107. Singh 108. Frey
S, Wann L, Klopfenstein H, et al: Usefulness of right ventricular diastolic collapse in diagnosing cardiac tamponade and comparison to pulsus paradoxus. Am J Cardiol 57:652, 1986.
B, Freezer N: Diagnostic value and pathophysiologic basis of pulsus paradoxus in infants and children with respiratory disease. Pediatr Pulmonol 31:138, 2001.
109. Wright 110. Jay
W, Carey S, Yao S: Hemodynamic monitoring for physiologic evaluation, diagnosis, and therapy of acute hemopericardial tamponade from penetrating wounds. J Trauma 13:36, 1973.
RO, Steele DW, Santucci KA, et al: Continuous noninvasive measurement of pulsus paradoxus in patients with acute asthma. Arch Pediatr Adolesc Med 150:914, 1996.
GD, Onuma K, Davis R, et al: Analysis of physician ability in the measurement of pulsus paradoxus by sphygmomanometry. Chest 118, 348, 2000.
111. Rady
MY, Smithline HA, Blake H, Nowak R: A comparison of the shock index and conventional vital signs to identify acute, critical illness in the emergency department. Ann Emerg Med 24:685,
1995. 112. Rady 113. King
MY, Nightingale P, Little RA, Edwards JD: Shock index: A re-evaluation in acute circulatory failure. Resuscitation 23:227, 1992.
RW, Plewa MC, Buderer NM, Knotts FB: Shock index as a marker for significant injury in trauma patients. Acad Emerg Med 3:1041, 1996.
114. Ardagh
MW, Hodgson T, Shaw L, Turner D: Pulse rate over pressure evaluation (ROPE) is useful in the assessment of compensated haemorrhagic shock. Emerg Med (Australia) 13:43, 2001.
115. Birkhahn
RH, Gaeta TJ, Bei R, Bove JJ: Shock index in the first trimester of pregnancy and its relationship to ruptured ectopic pregnancy. Acad Emerg Med 9:115, 2002.
116. Bernstein 117. Newman
EF, Fronek A: Current status of noninvasive tests in the diagnosis of peripheral arterial disease. Surg Clin North Am 62:473, 1982.
AB, Sutton-Tyrrell K, Vogt MT, Kuller LH: Morbidity and mortality in hypertensive adults with a low ankle/arm blood pressure index. JAMA 270:487, 1993.
118. Nassoura
ZE, Ivatury RR, Simon RJ, et al: A reassessment of Doppler pressure indices in the detection of arterial lesions in proximity penetrating injuries of extremities: A prospective study. Am J Emerg Med 14:151, 1996. 119. Lennihan 120. Burri
R Jr, Mackereth MA: Ankle pressures in vascular insufficiency involving the legs. J Clin Ultrasound 1:120, 1973.
C, Henkemeyer H, Passler HH, et al: Evaluation of acute blood loss by means of simple hemodynamic parameters. Prog Surg 11:109, 1973.
121. Ebert
RV, Stead EA, Gibson JG: Response of normal subjects to acute blood loss. Arch Intern Med 68:578, 1941.
122. Shenkin
HA, Cheney RH, Govons SR, et al: On the diagnosis of hemorrhage in man: A study of volunteers bled large amounts. Am J Med Sci 208:421, 1944.
123. Schriger
DL, Baraff LJ: Capillary refill: Is it a useful predictor of hypovolemic states? Ann Emerg Med 20:601, 1991.
124. Knopp
R, Claypool R, Leonardi D: Use of the tilt test in measuring acute blood loss. Ann Emerg Med 9:29, 1980.
125. Tomaszewski 126. Delp
C, Cline DM, Whitley TW, Grant T: Effect of acute ethanol ingestion on orthostatic vital signs. Ann Emerg Med 25:636, 1995.
MH, Manning RT: Major's Physical Diagnosis: An Introduction to the Clinical Process, 9th ed. Philadelphia, WB Saunders, 1981.
127. Prior
JA, Silberstein JS, Stang JM: Physical Diagnosis: The History and Examination of the Patient, 6th ed. St Louis, CV Mosby, 1981.
128. Hayes
HR, Briggs BA: MGH Textbook of Emergency Medicine. Baltimore, Williams & Wilkins, 1978.
129. Holcroft
JW: Impairment of venous return in hemorrhagic shock. Surg Clin North Am 62:17, 1982.
130. Guyton
AC: Textbook of Medical Physiology, 8th ed. Philadelphia, WB Saunders, 1991, p 263.
131. Gann
DS: Endocrine control of plasma protein and volume. Surg Clin North Am 56:1135, 1976.
132. Drucker 133. Moore
WR, Chadwick CDJ, Gann DS: Transcapillary refill in hemorrhage and shock. Arch Surg 116:1344, 1981.
FD: The effects of hemorrhage on body composition. N Engl J Med 273:567, 1965.
134. Watkins
GM, Rabelo A, Bevilacqua RG, et al: Bodily changes in repeated hemorrhage. Surg Gynecol Obstet 139:161, 1974.
135. Thomas
JE, Schirger A, Fealey RD, et al: Orthostatic hypotension. Mayo Clin Proc 56:117, 1981.
136. Currens
JH: A comparison of the blood pressure in the lying and standing positions: A study of 500 men and 500 women. Am Heart J 35:646, 1948.
136A. Hull
DH, Wolthius RA, Cortese T, et al: Borderline hypertension versus normotension: Differential response to orthostatic stress. Am Heart J 94:414, 1977.
136B. Stair 137. Klein
I: Clinical studies in incoordination of the circulation as determined by the response to arising. J Clin Invest 22:813, 1943.
GJ, Lerman BB, Tavel ME: Diagnosis and management of syncope. Chest 105:1246, 1994.
138. Kosowsky
JM, Han JH, Collins SP, et al: Assessment of stroke index using impedance cardiography: Comparison with traditional vital signs for detection of moderate acute blood loss in healthy volunteers. Acad Emerg Med 9:775, 2002. 139. McGee 140. Caird
S, Abernathy WB III, Simel DL: The rational clinical examination. Is this patient hypovolemic? JAMA 281:1022, 1999.
FI, Andrews GR, Kennedy RD: Effect of posture on blood pressure in the elderly. Br Heart J 35:527, 1973.
141. Carlson
JE: Assessment of orthostatic blood pressure: Measurement technique and clinical applications. South Med J 92:167, 1999.
27
142. Angueira
C, Marshall R, Goldner F: The tilt test: Effect of diabetes mellitus and antihypertensive medication on normal values. J Emerg Med 12:139, 1994.
143. Naschitz
JE, Sabo E, Gaitini L, et al: The Hemodynamic Instability Score (HIS) for assessment of cardiovascular reactivity in hypertensive and normotensive patients. J Hum Hypertens 15:177,
2001. 144. Stevens 145. Duke
PM: Cardiovascular dynamics during orthostatism and the influence of intravascular instrumentation. Am J Cardiol 17:211, 1966.
M, Abelmann WH: The hemodynamic response to chronic anemia. Circulation 39:503, 1969.
146. Aronow 147. Raiha
W, Lee N, Sales F, et al: Prevalence of postural hypotension in elderly patients in a long-term health care facility. Am J Cardiol 62:366, 1988.
I, Luutonen S, Piha J, et al: Prevalence, predisposing factors, and prognostic importance of postural hypotension. Arch Intern Med 8:930, 1995.
148. Hossain
M, Ooi WL, Lipsitz LA: Intra-individual postural blood pressure variability and stroke in elderly nursing home residents. J Clin Epidemiol 54:488, 2001.
References 149. Horam
WJ, Roscelli JD: Establishing standards of orthostatic measurements in normovolemic adolescents. Am J Dis Child 146:848, 1992.
150. Bergman 151. Fuchs
GE, Reisner FF, Anwar FAH: Orthostatic changes in normovolemic children: An analysis of the "tilt test." J Emerg Med 1:137, 1983.
SM, Jaffe DM: Evaluation of the "tilt test" in children. Ann Emerg Med 16:386, 1987.
152. Kaufmann 153. Stair
H: Consensus statement on the definition of orthostatic hypotension, pure autonomic failure and multiple system atrophy. Clin Auton Res 6:125, 1996.
T: Orthostatic tachycardia and ectopic pregnancy [letter]. Ann Emerg Med 11:284, 1982.
154. Adams
SL, Greene JS: Absence of a tachycardic response to intraperitoneal hemorrhage. J Emerg Med 4:383, 1986.
155. Jansen
RPS: Relative bradycardia: A sign of acute intraperitoneal bleeding. Aust NZ J Obstet Gynaecol 18:206, 1978.
156. Barriot
P, Riou B: Hemorrhagic shock with paradoxical bradycardia. Intensive Care Med 13:203, 1987.
157. Johnson 158. Baraff
DR, Douglas D, Hauswald M, Tandberg D: Dehydration and orthostatic vital signs in women with hyperemesis gravidarum. Acad Emerg Med 2:692, 1995.
LJ, Schriger DL: Orthostatic vital signs: Variation with age, specificity, and sensitivity in detecting a 450 mL blood loss. Am J Emerg Med 10:99, 1992.
159. Witting
MD, Smithline HA: Orthostatic change in shock index: comparison with traditional tilt test definitions. Acad Emerg Med 3:926, 1996.
160. Witting
MD, Wears RL, Li S: Defining the positive tilt test: A study of healthy adults with moderate acute blood loss. Ann Emerg Med 23:1320, 1994.
161. Koziol-McLain 162. Levitt
J, Lowenstein SR, Fuller B: Orthostatic vital signs in emergency department patients. Ann Emerg Med 20:606, 1991.
MA, Lopez B, Lieberman ME, et al: Evaluation of the tilt test in an adult emergency medicine population. Ann Emerg Med 21:713, 1992.
163. Hollister
AS: Orthostatic hypotension: Causes, evaluation, and management. West J Med 157:652, 1992.
164. Saavedra 165. Gorelick 166. Brown
JM, Harris GD, Li S, Finberg L: Capillary refilling (skin turgor) in the assessment of dehydration. AJDC 145:296, 1991.
MH, Shaw KN, Baker MD: Effect of ambient temperature on capillary refill in healthy children. Pediatrics 92:699, 1993.
LH, Prasad NH, Whitley TW: Adverse lighting condition effects on the assessment of capillary refill. Am J Emerg Med 12:46, 1994.
167. Gorelick
MH, Shaw KN, Murphy KO, Baker MD: Effect of fever on capillary refill time. Pediatr Emerg Care 13:305, 1997.
168. Marantz
PR, Linzer M, Feiner CJ, Feinstein SA: Inability to predict diagnosis of febrile intravenous drug abusers. Ann Intern Med 106:823, 1987.
169. Mellors
JW, Horwitz RI, Harvey MR, Horwitz SM: A simple index to identify occult bacterial infection in adults with acute unexplained fever. Arch Intern Med 147:666, 1987.
170. Keating
HJ, Klimek JJ, Levine DS, Kiernan FJ: Effect of aging on the clinical significance of fever in ambulatory adult patients. J Am Geriatr Soc 32:282, 1984.
171. Baker
RC, Tiller T, Bansher JC, et al: Severity of disease correlated with fever reduction in febrile infants. Pediatrics 83:1016, 1989.
172. Scopes
JW, Ahmed I: Range of critical temperatures in sick and premature newborn babies. Arch Dis Child 41:417, 1966.
173. Adamsons 174. Burnard
ED, Cross KW: Rectal temperature in the newborn after birth asphyxia. BMJ 2:1197, 1958.
175. Cranston 176. Dubois
WI, Gerbrandy J, Snell ES: Oral, rectal and oesophageal temperatures and some factors affecting them in man. J Physiol 126:347, 1954.
EF: The many different temperatures of the human body and its parts. West J Surg 59:476, 1951.
177. Benzinger 178. Durham 179. Dart
K, Gandy GM, James LS: The influence of thermal factors upon oxygen consumption of the newborn human infant. J Pediatr 66:495, 1965.
M: Tympanic thermometry in surgery and anesthesia. JAMA 209:1207, 1969.
ML, Swanson B, Paulford N: Effect of tachypnea on oral temperature estimation: a replication. Nurs Res 35:211, 1986.
RC, Lee SC, Joyce SM, Meislin HW: Liquid crystal thermometry for continuous temperature measurement in emergency department patients. Ann Emerg Med 14:1188, 1985.
180. Shiraki
K, Konda N, Sagawa S: Esophageal and tympanic temperature responses to core blood temperature changes during hyperthermia. J Appl Physiol 61:98, 1986.
181. Brinnel
H, Cabanac M: Tympanic temperature is a core temperature in humans. J Therm Biol 14:47, 1989.
182. Nicholson 183. Nierman 184. Earp
RW, Iserson KV: Core temperature measurement in hypovolemic resuscitation. Ann Emerg Med 20:62, 1991.
DM: Core temperature measurement in the intensive care unit. Crit Care Med 19:818, 1991.
JK, Finlayson DC: Relationship between urinary bladder and pulmonary artery temperatures: A preliminary study. Heart Lung 20:265, 1991.
185. Erickson
RS, Woo TM: Accuracy of infrared ear thermometry and traditional temperature methods in young children. Heart Lung 23:181, 1994.
186. Brooks
SE, Veal RO, Krammer M, et al: Reduction in the incidence of Clostridium difficile-associated diarrhea in an acute care hospital and a skilled nursing facility following replacement of electronic thermometers with single-use disposables. Infect Control Epidemiol 13:98, 1992. 187. Erickson
R: Oral temperature differences in relation to thermometer and technique. Nurs Res 29:157, 1980.
188. Woodman 189. Dressler
EA, Parry SM, Simms L: Sources of unreliability in oral temperatures. Nurs Res 16:276, 1967.
DK, Smejkal C, Ruffolo ML: A comparison of oral and rectal temperature measurement on patients receiving oxygen by mask. Nurs Res 32:373, 1983.
190. Romano
MJ, Fortenberry JD, Autrey E, et al: Infrared tympanic thermometry in the pediatric intensive care unit. Crit Care Med 21:1181, 1993.
191. Terndrup 192. Gruber
TE, Allegra JR, Kealy JA: A comparison of oral, rectal, and tympanic membrane-derived temperature changes after ingestion of liquids and smoking. Am J Emerg Med 7:15, 1989.
P: Changes in cardiac rate associated with the use of the rectal thermometer in patients with acute myocardial infarction. Heart Lung 3:288, 1974.
193. Terndrup 194. Green
TE: An appraisal of temperature assessment by infrared emission detection tympanic thermometry. Ann Emerg Med 21;1483, 1992.
MM, Danzl DF, Praszkier H: Infrared tympanic thermography in the emergency department. J Emerg Med 7:437, 1989.
195. Brennan
DF, Falk JL, Rothrock SG, Kerr RB: Reliability of infrared tympanic thermometry in the detection of rectal fever in children. Ann Emerg Med 25:21, 1995.
196. Hooker
EA: Use of tympanic thermometers to screen for fever in patients in a pediatric emergency department. South Med J 86:855, 1993.
197. Stavem
K, Saxholm H, Smith-Erichsen N: Accuracy of infrared ear thermometry in adult patients. Intensive Care Med 23:100, 1997.
198. Giuliano
KK, Giuliano AJ, Scott SS, et al: Temperature measurement in critically ill adults: A comparison of tympanic and oral methods. Am J Crit Care 9:254, 2000.
199. Kocoglu
H, Goksu S, Isik M, et al: Infrared tympanic thermometer can accurately measure the body temperature in children in an emergency room setting. Int J Pediatr Otorhinolaryngol 65:39,
2002. 200. Varney
SM, Manthey DE, Culpepper VE, Creedon JF Jr: A comparison of oral, tympanic, and rectal temperature measurement in the elderly. J Emerg Med 22:153, 2002.
28
201. Yaron
M, Lowenstein SR, Koziol-McLain J: Measuring the accuracy of the infrared tympanic thermometer: Correlation does not signify agreement. J Emerg Med 13:617, 1995.
202. Sganga 203. Robb
A, Wallace R, Kiehl E, et al: A comparison of four methods of normal newborn temperature measurement. MCN Am J Matern Child Nurs 25:76, 2000.
PJ, Shahab R: Infrared transtympanic temperature measurement and otitis media with effusion. Int J Pediatr Otorhinolaryngol 59:195, 2001.
204. O'Brien 205. Roth
D, Rogers I, Smith A, Lopez D: Infrared tympanic thermometers are unreliable in low ambient temperatures. Emerg Med (Australia) 10:313, 1998.
RN, Verdile VP, Grollman LJ, Stone DA: Agreement between rectal and tympanic membrane temperatures in marathon runners. Ann Emerg Med 28:414, 1996.
206. Bergeson 207. Kresch
PS, Springfield HJ: How dependable is palpation as a screening method for fever? Clin Pediatr 13:350, 1974.
MJ: Axillary temperature as a screening test for fever in children. J Pediatr 104:596, 1984.
208. Masters
JE: Comparison of axillary, oral, and forehead temperature. Arch Dis Child 55:896, 1980.
209. Reisinger 210. Lewit
KS, Kao J, Grant DM: Inaccuracy of the Clinitemp skin thermometer. Pediatrics 64:4, 1979.
EM, Marshall CL, Salzer JE: An evaluation of a plastic strip thermometer. JAMA 247:321, 1982.
211. Hooker
EA, Smith SW, Miles T, King L: Subjective assessment of fever by parents: Comparison with measurement by noncontact tympanic thermometer and calibrated rectal glass mercury thermometer. Ann Emerg Med 28:313, 1996. 212. Hung
AL, Kwon NS, Cole AE, et al: Evaluation of the physician's ability to recognize the presence or absence of anemia, fever, and jaundice. Acad Emerg Med 7:146, 2000.
212A. Intermittent-use 213. Abbey
JC, Anderson AS, Close EL, et al: How long is that thermometer accurate? Am J Nurs 78:1375, 1978.
214. Shinozaki 215. Terndrup 216. Blainey
218. Molnar
T, Deane R, Perkins FM: Infrared tympanic thermometer: Evaluation of a new clinical thermometer. Crit Care Med 16:148, 1988. TE, Rajk J: Impact of operator technique and device on infrared emission detection tympanic thermometry. J Emerg Med 10:683, 1992.
CG: Site selection in taking body temperature. Am J Nurs 74:1859, 1974.
217. Erickson
R: Thermometer placement for oral temperature measurement in febrile adults. Int J Nurs Stud 15:199, 1976.
G, Read R: Studies during open-heart surgery on the special characteristics of rectal temperature. J Appl Physiol 36:333, 1974.
219. Schiffman 220. Murray 221. Buck
electronic thermometers. Health Devices, vol 3, p 3, 1982.
RF: Temperature monitoring in the neonate: A comparison of axillary and rectal temperatures. Nurs Res 31:274, 1982.
HW, Tuazon CU, Guerrero IC, et al: Urinary temperature: A clue to early diagnosis of factitious fever. N Engl J Med 296:23, 1977.
SH, Zaritsky AL: Occult core hyperthermia complicating cardiogenic shock. Pediatrics 83:782, 1989.
222. Mackowiak
PA, Wasserman SS, Levine MM: A critical appraisal of 98.6°F, the upper limit of the normal body temperature, and other legacies of Carl Reinhold August Wunderlich. JAMA 268:1578, 1992. 223. Anagnostakis 224. Chamberlain 225. Herzog 226. Miller
D, Masaniotis N, Grafakos S, et al: Rectal-axillary temperature difference in febrile and afebrile infants and children. Clin Pediatr 32:268, 1993.
JM, Terndrup TE, Alexander DT, et al: Determination of normal ear temperature with an infrared emission detection thermometer. Ann Emerg Med 25;15, 1995.
LW, Coyne LJ: What is fever? Normal temperature in infants less than 3 months old. Clin Pediatr 32:142, 1993.
JW, Danzl DF, Thomas DM: Urban accidental hypothermia: 135 cases. Ann Emerg Med 9:456, 1980.
227. Steele
RW, Young FSH, Bass JW, et al: Oral antipyretic therapy: Evaluation of aspirin-acetaminophen combination. AJDC 123:204, 1972.
228. Tandberg
D, Sklar D: Effect of tachypnea on the estimation of body temperature by an oral thermometer. N Engl J Med 308:945, 1983.
229. Nichols
GA, Kulvi RL, Life HR, Christ NM: Measuring oral and rectal temperatures of febrile children. Nurs Res 21:261, 1972.
230. Nichols
GA, Kucha DH: Oral measurements. Nurs Res 72:1091, 1972.
231. O'Brien
DL, Rogers IR, Holden W, et al: The accuracy of oral predictive and infrared emission detection tympanic thermometers in an emergency department setting. Acad Emerg Med 7:1061,
2000.
232. Ogren
JM: The inaccuracy of axillary temperatures measured with an electronic thermometer. AJDC 144:109, 1990.
233. Edwards 234. Zehner
RJ, Belyavin AJ, Harrison MH: Core temperature measurement in man. Aviat Space Environ Med 49:1289, 1978.
WJ, Terndrup TE: Ear temperatures during rewarming from hypothermia (letter). Ann Emerg Med 23:901, 1994.
235. Doezema
D, Lunt M, Tandberg D: Cerumen occlusion lowers infrared tympanic membrane temperature measurement. Acad Emerg Med 2:17, 1995.
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Chapter 2 - Use of Monitoring Devices for Assessing Ventilation and Oxygenation Jerris R. Hedges William E. Baker Richard Lanoix Dan L. Field
Ensuring delivery of oxygen (O 2 ) to the cell is the primary critical action in emergency medicine. Without O 2 to fuel cellular energy production, the cells ultimately falter and the organism dies. Except during cardiopulmonary bypass, tissue perfusion depends on an adequate inspired O 2 content, ventilatory effort, alveolar gas exchange, blood O2 carrying capacity, and cardiac output. This chapter covers emergency department (ED) assessment of spontaneous ventilation and O 2 delivery and noninvasive means of monitoring and improving inspired O 2 concentration and spontaneous ventilation.
BACKGROUND Respiratory illness has been poorly understood until recent times. The Talmud, the ancient law book of the Israelites, blames the etiology of asthma-like illness on a malignant spirit. Later, Celsus (AD 25), an encyclopedist of the late Roman period, noted a favorable prognosis for a respiratory illness if the "expectoration is white as if mucus from the nose, but unfavorable if sputum is purulent, and accompanied by fever," descriptions that are consistent with chronic bronchitis and pneumonia. Celsus recommended bleeding, purgatives, emetics, and diuretics; this therapy was less preferable perhaps to his prescription for phthisis (tuberculosis), for which he recommended a leisurely sojourn down the Nile and drinking tea and honey. [1] The Greek word asthetaµa signified panting and was applied generally to difficult breathing and respiratory illness; the term eventually gave rise to the word asthma. The earliest comprehensive distinction between asthma and other respiratory diseases came from Aretaeus of Cappadocia, who first recognized and recorded the chronic recurrent nature of the disease. [2]
Neurologic
Muscles and Chest Wall
TABLE 2-1 -- Causes of Respiratory Failure * Oropharynx Lower Airway Lung Parenchyma
Drug overdose
Myopathy
Foreign body
Tracheobronchitis Adult respiratory distress syndrome
Stroke
Myasthenia gravis
Laryngospasm
Tracheal stenosis
Central hypoventilation
Kyphoscoliosis
Tonsillar hypertrophy
Bronchospasm
Guillain-Barré syndrome
Flail chest
Head trauma
Emphysema
Heart Pulmonary edema
Mitral stenosis
Pneumonia Interstitial pneumonitis
Poliomyelitis Botulism *Disease at any level of the respiratory system, central or peripheral nervous system, bellows mechanism, or heart may cause respiratory failure.
In 1698, Sir John Floyer wrote the first book devoted entirely to asthma and recorded the first description of pulsus paradoxus. Atropine therapy began in England in 1802, and in 1830 John Eberle deduced that "it is highly probable, therefore, that asthma consists essentially in a peculiar irritation of the pneumogastric nerves (vagus), in consequence of which the smaller bronchial tubes and air-cells are thrown into a state of spasmodic constriction." [3] The American Thoracic Society statement on asthma in 1962 is an often-quoted definition of the disease: "asthma is a disease characterized by an increased responsiveness of the trachea and bronchi to various stimuli and manifested by a widespread narrowing of the airways that changes in severity either spontaneously or as a result of therapy." The term asthma is not appropriate for bronchial narrowing, which results solely from widespread bronchial infection; from destructive diseases of the lung, as in pulmonary emphysema; or from cardiovascular disorders. Asthma is the most common chronic disease of childhood and among the most frequent complaint of adults, resulting in 2 million outpatient visits per year; it is also the most common cause of absence from school and work.[4] Asthma, depending on one's definition, affects between 7 and 20 million people in the United States and is especially prevalent among those living below the poverty level. [5] The National Center for Health Statistics estimates that asthma affects 9.7 million people in the U.S. population and chronic obstructive pulmonary diseases (COPDs) afflict up to 14 million adults, with similar economic consequences. [6] Although many investigators and studies distinguish between asthma (pure reactive airway disease) and COPDs, which include chronic bronchitis (airway inflammation with increased mucus secretion) and emphysema (airway destruction and loss of airway elasticity), clinically the distinction is blurred by the similarities in ED management. In fact, the current literature cites studies that can document little to distinguish the response of either entity to bronchodilators. [7] These diseases must, however, be separated from other causes of dyspnea and respiratory distress ( Table 2-1 ), many of which are associated with wheezing.
PULMONARY FUNCTION TESTING Airway maintenance and breathing are given primacy in the ABCs of emergency medicine. Clinical assessment always begins with the patient's ventilatory function. The clinician notes quickly the patient's mental status, level of distress, skin color, character of effort, use of accessory muscles, presence of diaphoresis, lung sounds, and vital signs. In conjunction with this clinical overview, a brief clinical history provides
30
the clinician with sufficient information on which to initiate therapy. Unfortunately, the clinician's initial clinical impression of the patient's ventilatory status is based on imprecise subjective findings that may not detect serious illness in all patients. The ability of experienced clinicians to detect compromised pulmonary function when compared with pulmonary function testing seems only moderately better than chance alone. [8] In the study by Godfrey and coworkers, the sensitivity of clinical impression did not improve when the clinicians underwent training on the common and more subtle signs of respiratory distress. [8] Patients also appear superior to clinicians in predicting their own pulmonary function [9] and in assessing day-to-day variation in disease, using pulmonary function testing as the standard. [10] Regardless of the initial clinical presentation, results of treatment in a subjectively asymptomatic patient with reactive airway disease will reach, at best, only 40% to 50% of predicted normal pulmonary function and 60% to 70% when all abnormal physical signs have resolved. [11] This potentially undetected degree of dysfunction may contribute to recrudescence. Objective measures of pulmonary dysfunction serve both to quantify results of therapy and as possible predictors of admission. Spirometry has been used for decades by pulmonary specialists to assess airway limitation. The spirometric measurements were originally validated based on comparisons with clinical and body plethysmographic data. The terminology of pulmonary function testing was derived from the various measured subsegments of spirometry ( Fig. 2-1 ). More recently, inexpensive handheld electronic meters have replaced formal spirometry in many clinical settings. These devices accurately measure or calculate the peak expiratory flow rate (PEFR), forced expiratory volume in 1 second (FEV 1 ), forced vital capacity (FVC), and percent FEV 1 /FVC.[12] The Wright peak flow meter ( Fig. 2-2 ) was originally designed by Wright and McKerrow for use in their pneumoconiosis unit in
Figure 2-1 Time-forced vital capacity (FVC) is the volume of gas forcibly expelled following a maximal inspiration. Forced expiratory volume in 1 second (FEV 1 ) is the volume of gas expelled during the first second of the forced expiration. The other lung volumes obtainable are the tidal volume (TV), which is the volume of gas moved during quiet respiration; the inspiratory reserve volume (IRV), which is the volume of gas that can be inspired in addition to the tidal gas volume; and the expiratory reserve volume (ERV), which is the volume of gas that can be forcibly expired at the end of a tidal expiration. Some gas cannot be expired and remains in the chest. This is known as the residual volume (RV).
Figure 2-2 Wright peak flow meter. After resetting the dial to zero, the patient inhales fully and exhales forcefully through the disposable paper mouthpiece. The best of three attempts is recorded. A tight seal of the lips around the mouthpiece is required.
1959. Subsequently, development of compact, less complex, and less expensive calibrated spring-mechanism peak flow meters have allowed for widespread use in acute care and home settings ( Fig. 2-3 ). These peak flow meters also have been successfully used as an adjunct in the assessment of pediatric patients. In the acute clinical situation, PEFR meter readings correlate well with formal spirometry, offer simplicity, and reduce the need for patient cooperation. [13] Indications and Contraindications In the ED, acute respiratory diseases such as asthma and chronic lung diseases make up the bulk of the situations requiring the objective assessment of ventilatory status. ED pulmonary function testing with either a peak flow meter or spirometer provides objective data on pulmonary status and patient response to therapy. These tests may assist the clinician in determining patient disposition [14] and may facilitate patient transfer at the time of admission by providing an objective and reproducible measure of the patient's failure to improve. Studies have found excellent correlations between PEFR and FEV 1 , [13] [15] as well as between Wright and mini-Wright meters. [16] One investigation has evaluated PEFR for aiding differentiation of congestive heart failure from chronic lung disease in the patient with moderate to severe dyspnea. [17] Although opportunities will be infrequent, clinicians evaluating neuromuscular diseases affecting ventilatory function, such as the Guillain-Barré syndrome, may find these techniques useful in both initial and ongoing assessment. Near or true respiratory arrest may be the only true contraindication to obtaining these measurements because of limited patient cooperation and delay of immediate therapy.
Figure 2-3 Mini-Wright peak flow meter. The indicator arrow is moved back to zero. The patient inhales fully and then exhales forcefully through the disposable paper mouthpiece. The best of three attempts is recorded. Patient cooperation and a tight seal of the lips around the mouthpiece are required.
31
Equipment A spirometer is a tube connected to a bellows-type device that communicates with a recording device. The subject breathes in and out through an orifice, causing expansion and contraction of the bellows, which in turn activates the recorder that traces a curve corresponding to the lung volume. This traditional volume method is complex and cumbersome. Handheld electronic spirometers now available use sensing devices either to translate the pressure of exhalation (e.g., Respiradyne, Kendall Healthcare Products Company, Ocala, FL, Fig. 2-4 ) or to detect the number of rotations of a small turbine (e.g., Pocket Spirometer, Micro Medical Instruments, Rochester, NY) by an optical system. Both systems are self-calibrating, take little practice to use, and can calculate PEFR, FEV 1 , and FVC. Some systems, such as the transducer-based Respiradyne, also give additional calculated information such as percent FEV 1 /FVC and forced mid-expiratory flow rate (FEF 25 z 75%). Results are displayed digitally and maintained in memory until cleared. Peak flow meters are simple mechanical devices that use the force of exhalation to rotate or push a membrane-coupled measuring arm or spring-loaded piston to statically record a position of maximum flow. Several brands of peak flow meters are commercially available including the Pulmo-Graph (De Vilbiss Healthcare Inc., Somerset, PA), Assess (HealthScan Products Inc., Cedar Grove, NJ), Wright Pocket (Ferraris Medical International, Holland, NY), and the Mini-Wright (Clement Clark International, Columbus, OH). Low-flow units designed for children are also available.
Procedure The operation of peak flow meters and electronic spirometers is similar in many ways. Disposable mouthpieces are inserted
Figure 2-4 The Respiradyne portable spirometer. The device is turned on or "cleared" from the last effort. The patient exhales forcefully into the handheld mouthpiece following maximal inhalation. The "sequence" button permits selection of the desired spirometry measurements. The best of several tries should be recorded.
or attached. If the mouthpiece is to be reused by patients sharing a common meter (during serial evaluations), the "mouth" end should be identified with pen or tape to limit the possibility of spreading infection between patients. The electronic devices must be switched on for a 30-second self-calibration period. Both the handheld spirometers and the peak flow meters can be operated with the same respiratory maneuver: a maximal inhalation followed by a maximum forced expiration into the mouthpiece. The key is to have the patient exhale as rapidly as possible in order to achieve a brief, forceful exhalation rather than a slow, prolonged exhalation. Three attempts are standard, and the highest value is recorded, provided the best two of three readings are within 10% of each other. [18] Children as young as 3 years have consistently achieved the level of cooperation necessary to perform PEFR testing. [19] Interpretation Although intraindividual peak flow variability is low, [20] variability between different brands of calibrated spring mechanism peak flow meters may be significant. Flow measurements of four brands studied at low to medium flows differed by as much as 100 L/min, [21] and accuracy waned with age of the device. [22] This information should be considered when interpreting PEFR values both clinically and in the literature. Likewise, measurement of serial PEFRs should be done on the same meter. Altitude minimally affects PEFR interpretation; readings at 1400 m underestimate PEFR by 5.3% to 6.9%. [20] As with FEV1 measurement, patient size affects PEFR and is most important when interpreting readings in children. Most charts of normal PEFRs in pediatric patients are based on height. As age and height are also related, some investigators have developed age-PEFR charts. [14] [23] Having a measuring tape secured to the wall alongside a chart of normal values in an accessible area enables the clinician to quickly interpret the PEFR of a child. Table 2-2 lists approximate peak flow and spirometric values for various degrees of obstruction in adults and Figure 2-5A and B demonstrate percentile charts of PEFR vs height in boys and girls. These charts were constructed from data obtained by Carson and coworkers in 2752 healthy children in Dublin. [23] Normal PEFRs do vary in children based on a number of variables including race, geographic location, and local environment. [23] [24] [25] The use of PEFR measurements to predict the need for admission early during ED treatment found that in severely compromised adults (i.e., with initial PEFRs 90%, a large increase in PaO 2 results in a small increase in saturation. Therefore, an error of a few percentage points could represent a large error in PaO 2 . This is inconsequential for most adult patients but is of extreme importance for neonates at risk of retinopathy caused by hyperoxemia. Venous Pulsations
Increased venous pulsations resulting from right heart failure, tricuspid regurgitation, or placement of a tourniquet or blood pressure cuff above the probe can interfere with accurate readings and lead to artificially lower O 2 saturations, because the pulse oximeter interprets any pulsatile measurement as arterial. [72] Placing the probe on a site above the heart may improve accuracy. Some pulse oximeters have the capability to synchronize pulsations at the probe site to electrocardiographic (ECG) signals, thus enhancing the signal-to-noise ratio. Anemia
Because pulse oximeter measurements depend on light absorption by hemoglobin, they become less accurate and reliable in conditions of severe anemia. However, accuracy is not diminished until the hemoglobin content is 5 L/min
35–50
Deliver higher flow rates than nasal prongs
Must be removed for airway care, eating, and drinking
Masks with reservoir bag
Up to 15 L/min
60
Higher FIO2 at lower flow rates
Risk of atelectasis and oxygen toxicity (with prolonged use)
Venturi masks
4
24–28
More precise control of final oxygen concentration
Same as above
6
31
8
35–40
10
50
40+ L/min
60–90
Reservoir nebulizers, including CPAP, T-tubes
Disadvantages
Simple, comfortable, inexpensive, allow Can cause local irritation and drying of mucous membranes eating and drinking (primarily for flow rates >4 L/min)
Can deliver increased humidity, positive Risk of barotrauma pressure
*The theoretical maximum FIO 2 . In clinical practice the FIO 2 will be lower.
inhalation circuit. To comply with safety regulations designed to prevent asphyxiation should the O valves located on the mask, somewhat limiting the concentration of O 2 delivered.
2
supply be interrupted, many manufacturers remove one of the
Procedure Supplemental O2 should be given to increase the PaO 2 to between 60 and 80 mm Hg or between 90% and 95% SaO2 . In attempting to deliver high concentrations of O2 to a nonintubated patient, the challenge is to provide enough O 2 at flow rates sufficient to meet the patient's demands. A simple method of assessing the adequacy of O2 delivery with a medium flow system is to add water mist to the O2 (through a humidifier) and to visually observe the pattern of mist flow at the mask. Mist should escape from the side holes of the mask during both inspiration and expiration. If mist is not visualized to escape during inspiration, ambient air is being inspired by the patient (effectively reducing inspired O 2 concentration) and a higher flow system is required. Bedside pulse oximetry can provide prompt monitoring of changes in SaO2 , allowing adjustments to be made without repeated arterial blood gas determination. Pulse oximetry values generally equilibrate within 5 minutes of an oxygen delivery adjustment.[114] Evidence of CO2 retention, such as decreasing mental status and failing respiratory drive, indicates the need for an arterial blood gas determination to document the PaCO 2 ; however, the decision to intubate generally should be made on clinical grounds. The need to humidify bedside low-flow O 2 is unproven. [110] [115] Table 2-8 lists the steps required to provide O 2 from cylinders.
Complications Three distinct areas of risk accompany supplemental O 2 use: (1) respiratory dysfunction, (2) cytotoxic injury, and (3) physical hazards. Respiratory dysfunction results from CO2 retention and atelectasis. Variations in CO 2 level provide the main stimulus to breathe in normal subjects. Patients with COPD have a decreased sensitivity to CO2 levels secondary to chronic exposure to higher CO 2 levels, and hypoxia provides backup support for the respiratory drive. Oxygen given in sufficient amounts can remove the remaining chemical stimulus to respiration and has the potential to cause respiratory shutdown. The complete abolition of the hypoxic drive has been reported to require a PaO 2 of 200 mm Hg. However, administration of 100% O2 to 22 patients with COPD in acute respiratory distress (mean baseline blood gas values: PaCO 2 = 65 mm Hg, PaO2 = 38 mm Hg) for 15 minutes resulted in only a transient decrease in minute ventilation. [116] The lowest values for minute ventilation were reached between 20 and 180 seconds from onset of inhalation, followed by a slow rise over the next 12 minutes to within 93% of the control value. The decrease was the result of falls in both tidal volume and respiratory rate; however, after 15 minutes, these parameters had returned to baseline levels. Despite little difference in TABLE 2-8 -- Operation of Oxygen Cylinders 1. Secure the tank in an upright position so that it will not move or fall while being manipulated. 2. Remove the cylinder seal ("E" tank) or cylinder cap ("G," "H" tank). 3. Turn the cylinder valve on and off quickly to clear ("crack") the valve. On the "E" tank, this is done with a wrench; on the "G" or "H" tank, it is done with the cylinder handle. 4. Check the yoke to ensure that it is compatible for use with oxygen and place it on the cylinder. Make sure the fittings are compatible. 5. Tighten the yoke, making certain that any necessary gasket is in place. 6. Close the needle valve. 7. Slowly open the cylinder valve until the pressure maximizes. 8. Observe that the cylinder contains an adequate supply of gas. 9. Connect the desired secondary delivery system (e.g., nasal cannula). 10. Open the needle valve so that the desired oxygen flow registers on the flow meters.
45
these parameters at the 15 minute point, PaCO 2 had risen a mean of 23 mm Hg, and PaO2 had risen a mean of 225 mm Hg.[117] The mechanism leading to atelectasis is less clear. Elevated O 2 levels may affect underperfused or underventilated pulmonary segments by decreasing hypoxic vasoconstriction. The increased perfusion could lead to greater absorption of the remaining gas, destabilizing the alveolar units and bringing on collapse. [118] Cytotoxic damage, theoretically secondary to free radical production, leads to tracheobronchitis and adult respiratory distress syndrome (ARDS) manifested by pulmonary edema and focal lung collapse with pulmonary fibrosis as a long-term consequence. The mechanism of damage has been shown experimentally to include oxidation of carbohydrates with disruption of cell surface receptors, DNA-RNA alterations, lipid peroxidation, and protein denaturation. Administration of an inappropriately high level of O 2 does not usually produce consequences within the time frame of the ED visit. The risk of O 2 toxicity depends on several factors, including O 2 tolerance (the state of biologic resistance to O 2 -induced damage, which is itself dependent on antioxidant defenses, age, and nutritional and hormonal factors), concentration of O 2 delivered, and duration of treatment. The goal is to deliver the least O 2 required to achieve adequate tissue levels. During resuscitation and most emergency care, 100% O2 can be delivered safely to most patients without fear of cytotoxic injury. Healthy adult volunteers have received 100% O 2 for up to 6 hours without evidence of pulmonary injury. Except in special circumstances, such as paraquat poisoning, O 2 at concentrations of =50% is safe for 2 to 7 days. [110] Physical risks associated with O 2 therapy include trauma associated with tank explosions, fire hazard, local irritation, and drying of mucous membranes.
NONINVASIVE PRESSURE SUPPORT VENTILATION Noninvasive pressure support ventilation can be used to deliver increased airway pressure in several modes: (1) pressure increases solely during inspiration (i.e., delivery of inspiratory positive airway pressure [IPAP]) to supplement ventilatory mechanics; (2) continuous steady positive airway pressure maintained throughout the ventilation cycle (i.e., expiratory positive airway pressure [EPAP], also known as continuous positive airway pressure [CPAP]) to improve alveolar oxygen exchange; or (3) a combination of both modalities to achieve both goals. During noninvasive pressure support ventilation, a tight, well-fitting mask is placed over the patient's mouth and nose or just over the nose. Mask CPAP treatment of cardiogenic pulmonary edema was first described more than 50 years ago [119] and has been shown to be a useful adjunct in the treatment of acute cardiogenic pulmonary edema. Mask CPAP results in early physiologic improvement and reduces the need for intubation and mechanical ventilation in patients with pulmonary edema.[120] [121] [122] It also reduces total hospital costs for patients with severe cardiogenic pulmonary edema. [123] Use of mask CPAP to deliver PEEP has aided the treatment of other forms of respiratory failure including those due to pulmonary infections, trauma, and obstructive lung disease. Historically, patients with respiratory failure secondary to Pneumocystis carinii pneumonia who required mechanical ventilation had in-hospital mortality rates as high as 86% to 94%; however, those who were judged to require mechanical ventilation, but who were instead treated with mask CPAP, had in-hospital mortality rates of 22% to 55%. [124] [125] [126] Mask CPAP may be efficacious in the treatment of respiratory failure secondary to other pulmonary infections. [127] [128] Further, mask CPAP (either by full-face or nasal mask) may obviate the need for intubation and mechanical ventilation in acute exacerbations of COPD. [129] [130] [131] The general use of IPAP for respiratory failure has recently been reviewed. [132] The use of combined IPAP and EPAP in the ED and critical care setting appears promising. [133] [134] [135] [136] This technique is also known as bi-level positive pressure ventilation, because it allows the clinician to deliver different inspiratory and expiratory pressures. This technology offers the opportunity to both support mechanical ventilation and improve oxygen exchange through an enhanced functional residual capacity. In essence, a mask device provides the ventilation and PEEP that was once possible only with the use of tracheal intubation and a standard ventilator. Indications and Contraindications Noninvasive pressure support ventilation is indicated to treat impending ventilatory failure and avoid intubation and standard mechanical ventilation, with their associated morbidity and mortality. Noninvasive pressure support ventilation seems best applied to patients whose respiratory failure is expected to quickly respond to medical therapy, as continuous long-term mask CPAP or ventilation requires close attention. Noninvasive pressure support ventilation for acute respiratory failure requires an alert patient capable of protecting the airway and handling secretions. Other contraindications include an inability to obtain a good mask fit, cutaneous irritation from the mask, and inability to cooperate with the therapy. Finally, intubation and standard ventilation is preferred for patients who require total ventilatory support, because the mask may slip and effective ventilation may cease. Equipment Although numerous systems that provide CPAP are on the market, they are infrequently used in the ED. A small, noninvasive bi-level positive pressure ventilation system (BiPAP System, Respironics Inc., Murrysville, PA) that permits use of a nasal (rather than facial) mask alone in lieu of tracheal intubation may be most useful in the ED.[136] Therefore, an overview of the use of the BiPAP System is given in the next section. The advantage of the BiPAP System is that it supplies air or O 2 at pressure and flow rates that are suitable for assisted inhalation and expiration by sensing the patient's spontaneous breathing efforts and automatically adjusting to compensate for variations in ventilatory requirements, even in the presence of airway leaks. Importantly, this device is not intended to be a life support ventilator, because it is used only to temporarily augment spontaneous breathing. Regardless of the system used, close attention to manufacturer guidelines is advised. Procedure Before initiation of this technique, the patient must be informed of the purpose of the nasal mask and cooperate.
46
It helps to discuss an alternative therapy should this technique not meet the patient's needs and to reassure the patient that the operator will stay with him or her until a comfort level with the mask and ventilator system is obtained. Baseline vital sign and oxygenation measurements are made. The patient should be treated in a closely monitored setting where his or her vital signs and respiratory status are closely monitored.
Despite intervention with this system, emergent intubation and mechanical ventilation may become needed. Equipment for airway support (e.g., O 2 source, tubing, bag-valve mask, laryngoscope, suction equipment, and various airways) should be immediately available. The BiPAP System components are assembled and connected to oxygen—generally at the same flow settings as the patient is currently receiving (generally at 10 to 15 L/min). The pressure tubing is attached to the airway pressure monitor and the pressure monitor is turned on; the main system is then turned on and a ventilation mode selected. Generally, the system will be used in the spontaneous ventilation mode (i.e., to support spontaneous ventilations) with an initial EPAP setting of 3 to 5 cm H2 O and an IPAP setting of 8 to 10 cm H 2 O. Ideally, a mask sizing gauge ( Fig. 2-19 ) is used to choose a mask size that does not place direct pressure on the bridge of the nose, the lateral ala nasi, the inferior nasal septum, or the lip. The mask may be initially held in place by the operator as the patient adjusts to the ventilatory support. With the mask in place, the BiPAP System settings are modified to optimize patient ventilatory status ( Fig. 2-20 ). As the patient becomes more comfortable, the mask is secured in place on the face using self-adhesive binding straps ( Fig. 2-21 ). If time permits, the headgear straps may be loosely attached before placement and the mask slipped over the head as a unit; the straps are then tightened.
Figure 2-19 Use of template to size nasal mask for BiPAP System. A, The nasal mask sizing gauge is placed over the patient's nose. The size that comes close to, but does not touch, the nose in three locations is selected. B, The sites to avoid direct contact: (1) just above the junction of the nasal bone and cartilage; (2) on the sides of both nares; and (3) just below the lowest point of the nose, above the lip. Remember to use the smallest size mask that will sufficiently cover the nasal area. Too small a mask will produce skin discomfort or injury. Too large a mask will increase air leak. (Courtesy of Respironics Inc., Murrysville, PA.)
The patient is encouraged to breathe with the mouth closed. The facial mask fit should be adjusted for comfort and to minimize air leak, especially about the eyes. When the patient has accepted the mask and the clinical status has stabilized, the patient may be permitted to speak and even to eat small amounts. Adjustments in the EPAP and IPAP settings are generally made in 2 cm H2 O increments. Near optimal settings can generally be attained within 10 minutes. Periodic blood gas measurements should be coupled with ongoing vital sign and pulse oximetry measurements. When available, a CO 2 device side-flow catheter can be placed under the nasal mask for monitoring exhaled CO 2 levels. Increases in IPAP settings generally increase tidal volume and decrease CO 2 levels, whereas
increases in EPAP generally increase functional residual capacity and increase O 2 levels. The concentration of inspired oxygen also can be modified by changing the O2 flow rate. High levels of EPAP or IPAP can induce PEEP-related reductions in cardiac preload. Further, although the system can adjust for some air leak about the mask, higher pressures require a tighter mask fit and can increase patient discomfort. If the patient's hypoxic drive is diminished, decreased spontaneous ventilatory effort may be noted. If this situation occurs, the BiPAP System should be changed to the "spontaneous/timed" mode, which permits spontaneous breaths but imposes a mandatory ventilation if an extended ventilatory pause is noted. When initiating this mode, the clinician generally sets the respiratory rate at 10 breaths/min. At this setting, when a breath does not occur within 6 seconds of the preceding breath, a mandatory breath is provided. If the patient requires a brief period of hyperventilation to help coordinate ventilatory efforts, the BiPAP System can be
47
Figure 2-20 Control panel of BiPAP System. Note control setting for ventilation mode in lower left corner (see text for use of settings). For spontaneously breathing patients in respiratory distress, the "spontaneous" mode is generally selected and IPAP and EPAP settings selected. (Courtesy of Respironics Inc., Murrysville, PA.)
Figure 2-21 BiPAP System nasal mask in place on patient. (Courtesy of Respironics Inc., Murrysville, PA.)
set to the "timed" mode and a respiratory rate of 15 to 20 breaths/min can be initiated. In this mode, the %IPAP time must be set by the operator. A %IPAP of 30% produces an inspiratory-to-expiratory (I:E) ratio of 1:2.3, whereas a %IPAP of 40% produces an I:E ratio of 1:1.5. Aerosolized medications can be delivered either through in-line "T-pieces" in the BiPAP System circuit or through standard mouthpiece units (see following section). Complications Complications from this therapy include facial irritation, abrasion, or even facial necrosis; conjunctivitis due to mask air leak; aspiration; and gastric distention. A wound care dressing on the bridge of the nose may reduce skin abrasion. [135] Nasogastric tubes have been used to relieve gastric distention, although a nasal mask system is less likely to produce gastric distention. Additionally, although the pressures used are generally low, all of the complications of positive pressure ventilation may be seen with this technique.
48
Conclusions Positive pressure ventilation modalities offer the promise of averting the need for intubation and mechanical ventilation in certain groups of patients with acute respiratory failure. The procedure for instituting these therapies is relatively simple and may even have potential in the pre-hospital setting. Additionally, although best studied in adults, these therapies have been applied to pediatric patients, [137] [138] and pediatric masks are available commercially.
Acknowledgment
The authors thank Rawle A. Seupaul for reviewing the chapter.
References 1. Castiglioni 2. Adams
A: A History of Medicine, 2nd ed. New York, Alfred A. Knopf, 1947, p 76.
F: The Extant Works of Aretaeus the Cappadocian. London, Sydenham Society, 1856, p 316.
3. McFadden
ER Jr, Ingram HR: Asthma: Perspectives, definition and classification. In Fishman AP, Pulmonary Diseases and Disorders. New York, McGraw-Hill, 1980, p 562.
4. Newacheck
PW, Budetti P, Halfon N: Trends in childhood chronic illness. Am J Public Health 76:176, 1986.
5. Evans
R III, Mullally DI, Wilson RW, et al: National trends in the morbidity and mortality of asthma in the US: Prevalence, hospitalization and death from asthma over two decades: 1965–1984. Chest 91:65S, 1987. 6. Collins 7. Gross
JG: Prevalence of Selected Chronic Conditions: United States, 1986–88, series 10 (No. 182). Washington, DC, Vital and Health Statistics, National Center for Health Statistics, 1993, p 29.
NJ: COPD: A disease of reversible air-flow obstruction. Am Rev Respir Dis 133:725, 1986.
8. Godfrey
S, Edward RHT, Campbell EJM: Repeatability of physical signs in airways obstruction. Thorax 24:4, 1969.
9. Mannino
DM, Etzel RA, Flanders WD: Do the medical history and physical examination predict low lung function? Arch Intern Med 153:1892, 1993.
10.
Shim CS, Williams MH: Evaluation of the severity of asthma: Patients versus physicians. Am J Med 68:11, 1980.
11.
Kelsen SG, Kelsen DP, Fleegler BF, et al: Emergency room assessment and treatment of patients with acute asthma: Adequacy of the conventional approach. Am J Med 64:622, 1978.
12.
Wiltshire N, Kendrick AH: Evaluation of a new electronic spirometer: The Vitalograph "Escort" spirometer. Thorax 49:175–178, 1994.
13.
Kelly CA, Gibson GJ: Relation between FEV 1 and peak expiratory flow in patients with chronic airflow obstruction. Thorax 42:335, 1988.
14.
Taylor MR: Asthma: Audit of peak flow rate guidelines for admission and discharge. Arch Dis Child 70:432, 1994.
15.
Nowak RM, Pensler MI, Sankar DD, et al: Comparison of peak expiratory flow and FEV 1 admission criteria for acute bronchial asthma. Ann Emerg Med 11:64, 1982.
16.
Brown LA, Sly RM: Comparison of mini-Wright and standard Wright peak flow meters. Ann Allergy 45:72, 1980.
17.
McNamara RM, Cionni DJ: Utility of the peak expiratory flow rate in the differentiation of acute dyspnea. Chest 101:129, 1992.
18.
Dahlquist M, Eisen EA, Wegman DH, Kriebal D: Reproducibility of peak expiratory flow measurements. Occup Med 8:295, 1993.
19.
Milnar AD, Ingram D: Peak expiratory flow rates in children under 5 years of age. Arch Dis Child 45:780, 1970.
20.
Hegewald MJ, Crappo RO, Jensen RL: Intraindividual peak flow variability. Chest 107:156, 1995.
21.
Simmons M, Wynegar BS, Hess D: Evaluation of the agreement between portable peak flow meters and a calibrated pneumotachometer. Respir Care 38:916, 1993.
22.
Shapiro SM, Hendler JM, Ogirala RG, et al: An evaluation of the accuracy of Assess and MiniWright peak flowmeters. Chest 99:358, 1991.
23.
Carson JW, Hoey H, Taylor MR: Growth and other factors affecting peak expiratory flow rate. Arch Dis Child 64:96, 1989.
24.
Hsu KH, Jenkins DE, Hsi BP, et al: Ventilatory functions of normal children and young adults—Mexican-American, white, and black: II. Wright peak flowmeter. J Pediatr 95:192, 1979.
25.
Graff-Lonnevig V, Harfi H, Tipirneni P: Peak expiratory flow rates in healthy Saudi Arabian children living in Riyadh. Ann Allergy 71:446, 1993.
26.
Banner AS, Shah RS, Addington WW: Rapid prediction of need for hospitalization in acute asthma. JAMA 235:1337, 1976.
27.
Nowak RM, Gordon KR, Wroblewski DA, et al: Spirometric evaluation of acute bronchial asthma. JACEP 8:9, 1979.
28.
Martin TG, Elenbass RM, Pingleton SH: Failure of peak expiratory flow rates to predict hospital admission in acute asthma. Ann Emerg Med 11:466, 1982.
29.
Emerman CL, Effron D, Lukens TW: Spirometric criteria for hospital admission of patients with acute exacerbation of COPD. Chest 99:595, 1991.
30.
Silver RB, Ginsburg CM: Early prediction of the need for hospitalization in children with acute asthma. Clin Pediatr 23:81, 1984.
31.
Ownby DR, Abarzua J, Anderson JA: Attempting to predict hospital admission in acute asthma. Am J Dis Child 138:1062, 1984.
32.
Martin TG, Elenbass RM, Pingleton SH: Use of peak expiratory flow rates to eliminate unnecessary arterial blood gases in acute asthma. Ann Emerg Med 11:70, 1982.
33.
Nowak RM, Tomlanovich MC, Sankar DD, et al: Arterial blood gases and pulmonary function testing in acute bronchial asthma: Predicting patient outcomes. JAMA 249:2043, 1983.
34.
Standards for Basic Intra-Operative Monitoring. Park Ridge, IL, American Society of Anesthesiologists, 1991.
35.
Aughey K, Hess D, Eitel D, et al: An evaluation of pulse oximetry in pre-hospital care. Ann Emerg Med 20:887, 1991.
36.
Hay WW Jr, Thilo E, Curlander JB: Pulse oximetry in neonatal medicine. Clin Perinatol 18:441, 1991.
37.
Kellermann AL, Cofer CA, Joseph S, Hackman BB: Impact of portable pulse oximetry on arterial blood gas test ordering in an urban emergency department. Ann Emerg Med 20:130, 1991.
38.
Bowton DL, Scuderi PE, Harris L, Haponik EF: Pulse oximetry monitoring outside the intensive care unit: Progress or problem? Ann Intern Med 115:450, 1991.
39.
Neff TA: Routine oximetry—A fifth vital sign [editorial]? Chest 94:227, 1988.
Aoyagi T, Kishi M, Yamaguchi K, Watanabe S: Development of an earpiece oximeter [in Japanese]. In Program and Abstracts of the 13th Annual Meeting of the Japanese Society for Medical Electronics and Biological Engineering. April 26, 1974, Osaka, Japan, p 90. 40.
41.
Severinghaus JW, Astrup PB: History of blood gas analysis: VI. Oximetry. J Clin Monit 2:270, 1986.
42.
Yelderman M, New W: Evaluation of pulse oximetry. Anesthesiology 59:349, 1983.
43.
Mendelson Y, Kent J, Shaharian A, et al: Evaluation of the Datascope Accusat pulse oximeter in healthy adults. J Clin Monit 4:59, 1988.
44.
Sinex JE. Pulse oximetry: Principles and limitations. Am J Emerg Med 17:59, 1999.
45.
New W: Pulse oximetry. J Clin Monit 1:126, 1985.
46.
Morris RW, Busehman A, Warren D, et al: The prevalence of hypoxemia detected by pulse oximetry during recovery from anesthesia. J Clin Monit 4:16, 1988.
47.
McKay WPS, Noable WH: Critical incidents detected by pulse oximetry during anesthesia. Can J Anaesth 35:265, 1988.
48.
Cooper JB, Cullen DJ, Nemeskal R, et al: Effects of information feedback and pulse oximetry on the incidence of anesthesia complications. Anesthesiology 67:686, 1987.
49.
The Technology Assessment Task Force of the Society of Critical Care Medicine: A model for technology assessment applied to pulse oximetry. Crit Care Med 21:615, 1993.
Maneker AJ, Petrack EM, Krug SE: Contribution of routine pulse oximetry to evaluation and management of patients with respiratory illness in a pediatric emergency department. Ann Emerg Med 25:36, 1995. 50.
51.
Geelhoed GC, Landau IL, Le Souef PN: Evaluation of SaO 2 as a predictor of outcome in 280 children presenting with acute asthma. Ann Emerg Med 23:1236, 1994.
52.
Tannen DA, Trocinski DR: The use of pulse oximetry to exclude pneumonia in children. Am J Emerg Med 20:521, 2002.
53.
Hedges JR, Amsterdam JT, Cionni DJ, et al: Oxygen saturation as a marker for admission or relapse with acute bronchospasm. Am J Emerg Med 5:196, 1987.
49
54.
Rosen LM, Yamamoto LG, Wiebe RA: Pulse oximetry to identify a high-risk group of children with wheezing. Am J Emerg Med 7:567, 1989.
55.
Witting MD, Lueck CH: The ability of pulse oximetry to screen for hypoxemia and hypercapnia in patients breathing room air. J Emerg Med 20:341, 2001.
56.
Kelly A-M, McAlpin R, Kyle E: How accurate are pulse oximeters in patients with acute exacerbations of chronic obstructive airways disease? Respir Med 95:336, 2001.
Poirier MP, Gonzalez Del-Rey JA, McAneney CM, DiGiulio GA: Utility of monitoring capnography, pulse oximetry, and vital signs in the detection of airway mishaps: A hyperoxemic animal model. Am J Emerg Med 16:350, 1998. 57.
58.
Bozeman WP, Myers RAM, Barish RA: Confirmation of the pulse oximetry gap in carbon monoxide poisoning. Ann Emerg Med 30:608, 1997.
59.
Severinghaus JW: Pulse oximetry uses and limitations. In ASA 40th Annual Refresher Course Lectures and Clinical Update Program. New Orleans, American Society of Anesthesiologists, 1989.
60.
Vaghadia H, Jenkins LC, Ford RW: Comparison of end-tidal carbon dioxide, oxygen saturation, and clinical signs for the detection of esophageal intubation. Can J Anaesth 36:560, 1989.
61.
Barker SJ, Tremper KK, Hyatt J: Effects of methemoglobinemia on pulse oximetry and mixed venous oximetry. Anesthesiology 70:112, 1989.
62.
Oski FA: Clinical implications of oxyhemoglobin curve in the neonatal period. Crit Care Med 7:412, 1979.
63.
Mendelson Y, Kent JC: Variations in optical absorption spectra of adult and fetal hemoglobins and its effect on pulse oximetry. IEEE Trans Biomed Eng 36:844, 1989.
64.
Pologe J, Raley D: Effects of fetal hemoglobin on pulse oximetry. J Perinatol 7:324, 1987.
65.
Severinghaus JW, Kelleher JF: Recent developments in pulse oximetry. Anesthesiology 76:1018, 1992.
66.
Scheller M, Unger R, Kelner M: Effects of intravenously administered dyes on pulse oximetry readings. Anesthesiology 65:550, 1986.
67.
Sidi A, Paulus D, Rush W, et al: Methylene blue and indocyanine green artificially lower pulse oximetry readings of oxygen saturation: Studies in dogs. J Clin Monit 3:249, 1987.
68.
Unger R, Scheller MS: More on dyes and pulse oximeters. Anesthesiology 65:550, 1986.
69.
Eide TR, Humayun-Scott B, Poppers PJ: More on dyes and pulse oximeters [reply]. Anesthesiology 67:148, 1987.
70.
Ralston AC, Webb RK, Runciman WB: Potential errors in pulse oximetry: III. Effects of interference, dyes, dyshaemoglobins and other pigments. Anaesthesia 46:291, 1991.
71.
White PF, Boyle WA: Nail polish and oximetry. Anesthesia and Analgesia 68:546, 1989.
72.
Sami HM, Kleinman BS, Lonchyna VA: Central venous pulsations associated with a falsely low oxygen saturation measured by pulse oximetry. J Clin Monit 7:309, 1991.
73.
Severinghaus JW, Koh SO: Effect of anemia on pulse oximeter accuracy at low saturation. J Clin Monit 6:85, 1990.
74.
Lee S, Tremper KK, Barker SJ: Effects of anemia on pulse oximetry and continuous mixed venous hemoglobin saturation monitoring in dogs. Anesthesiology 75:118, 1991.
75.
Smalhout B, Kalenda Z: Atlas of Capnography, vol. 1. Amsterdam, Kerckebosch/Zeist, 1975, p 28.
76.
Szaflarski NL, Cohen NH: Use of pulse oximetry in critically ill adults. Heart Lung 18:444, 1989.
77.
Birmingham PK, Cheney FW, Ward RJ: Esophageal intubation: A review of detection techniques. Anesth Analg 65:886, 1986.
78.
Bhende MS, Thompson AE, Howland DF: Validity of a disposable end-tidal carbon dioxide detector in verifying endotracheal tube position in piglets. Crit Care Med 19:566, 1991.
79.
Murray IP, Modell JH: Early detection of endotracheal tube accidents by monitoring carbon dioxide concentration in respiratory gas. Anesthesiology 59:344, 1983.
80.
Bailey PL, Pace NL, Ashburn MA, et al: Frequent hypoxemia and apnea after sedation with midazolam and fentanyl. Anesthesiology 73:826, 1990.
81.
American Medical Association Council on Scientific Affairs: The use of pulse oximetry during conscious sedation. JAMA 270:1463, 1993.
82.
Wright SW: Conscious sedation in the emergency department: The value of capnography and pulse oximetry. Ann Emerg Med 21:551, 1992.
83.
Tyburski JG, Collinge JD, Wilson RF: End-tidal CO 2 -derived values during emergency trauma surgery correlated with outcome: A prospective study. J Trauma 53:738, 2002.
84.
Szaflarski NL, Cohen NH: Use of capnography in critically ill adults. Heart Lung 20:363, 1991.
McEvedy BAB, Mcleod ME, Kerpalani H, et al: End-tidal carbon dioxide measurements in critically ill neonates: A comparison of sidestream and mainstream capnometers. Can J Anaesth 37:322, 1990. 85.
86.
Strunin K, William T: The FEF end-tidal carbon dioxide detector. Anesthesiology 71:621, 1989.
87.
Anonymous: Defibrillator monitors, capnographs and anaesthesia monitors, and intensive care ventilators. Intensive Care World 12:S3, 1995.
88.
Schena J, Thompson J, Crone RK: Mechanical influences on the capnogram. Crit Care Med 12:672, 1984.
89.
Carbon dioxide monitors. Health Devices 15:255, 1986.
90.
O'Flaherty D, Adams AP: The end-tidal carbon dioxide detector: Assessment of new method to distinguish oesophageal from tracheal intubation. Anaesthesia 45:653, 1990.
91.
Moorthy SS, Losasso AM, Wilcox J: End-tidal PCO 2 greater than PaCO 2 . Crit Care Med 12:534, 1984.
92.
Askrog V: Changes in (a-A)CO 2 difference and pulmonary artery pressure in anesthetized man. J Appl Physiol 21:1299, 1966.
93.
Hoffbrand BI: The expiratory capnogram: A measure of ventilation-perfusion inequalities. Thorax 21:518, 1966.
Tulou PP, Walsh PM: Measurement of alveolar carbon dioxide tension at maximal expiration as an estimate of arterial carbon dioxide tension in patients with airway obstruction. Am Rev Respir Dis 102:921, 1970. 94.
Kerr ME, Zempsky J, Sereika S, et al: Relationship between arterial carbon dioxide and end-tidal carbon dioxide in mechanically ventilated adults with severe head trauma. Crit Care Med 24:785, 1996. 95.
96.
Hatle L, Rokseth R: The arterial to end-expiratory carbon dioxide tension gradient in acute pulmonary embolism and other cardiopulmonary diseases. Chest 66:352, 1974.
97.
Luft UC, Loepsky JA, Mostyn EM: Mean alveolar gases and alveolar-arterial gradients in pulmonary patients. J Appl Physiol 46:534, 1979.
98.
Vukmir RB: Confirmation of endotracheal tube placement: A miniaturized infrared qualitative CO
99.
Murray IP, Modell JH, Gallagher TJ, Banner MJ: Titration of PEEP by the arterial minus end-tidal carbon dioxide gradient. Chest 85:100, 1984.
100. Garnett
CV, Aslam HB, Lambert MA: Capnography for monitoring non-intubated spontaneously breathing patients in an emergency room setting. J Accid Emerg Med 14:222, 1997.
MC: Noninvasive carbon dioxide monitoring. Crit Care Med 4:511, 1988.
103. Yamanaka
104. Miner
MK, Sue DY: Comparison of arterial-end-tidal pCO 2 difference and dead space/tidal volume ratio in respiratory failure. Chest 92:832, 1987.
JR, Heegaard W, Plummer D: End-tidal carbon dioxide monitoring during procedural sedation. Acad Emerg Med 9:275, 2002.
105. Smalhout 106. Cote
detector. Ann Emerg Med 20:726, 1991.
AR, Gervin CA, Gervin AS: Capnograph waveforms in esophageal intubation: Effect of carbonated beverages. Ann Emerg Med 8:387, 1989.
101. Egleston 102. Stock
2
B: A Quick Guide to Capnography and Its Use in Differential Diagnosis. Waltham, MA, Hewlett-Packard, 1983.
CJ, Liu LMP, Szyfelbein SK, et al: Intraoperative events diagnosed by expired carbon dioxide monitoring in children. Can Anaesth Soc J 33:315, 1986.
107. Adams 108. Gong
AP: Capnography and pulse oximetry. In Atkins RS, Adams AP (eds): Recent Advances in Anaesthesia and Analgesia. London, Churchill Livingstone, 1989, p 155.
H Jr: Air travel and oxygen therapy in cardiopulmonary patients. Chest 101:1104, 1992.
109. Ingrassia
TS III, Trastek VF, Rosenow EC III: Oxygen-exacerbated bleomycin pulmonary toxicity. Mayo Clin Proc 66:173, 1991.
110. Fulmer
JD, Snider GL: American College of Chest Physicians (ACCP)-National Heart, Lung, and Blood Institute (NHLBI) Conference on Oxygen Therapy. Arch Intern Med 144:1645, 1984.
111. Davies
RJ, Hopkin JM: Nasal oxygen in exacerbations of ventilatory failure: An underappreciated risk. BMJ 299:43, 1989.
112. Doyle
DJ: Computer program for predicting oxygen tank duration [letter]. Crit Care Med 16:915, 1988.
113. Bazuaye 114. Gruber
EA, Stone TN, Corris PA, Gibson GJ: Variability of inspired oxygen concentration with nasal cannulas. Thorax 47:609, 1992.
P, Kwiatkowski T, Silverman R, et al: Time to equilibrium of oxygen saturation using pulse oximetry. Acad Emerg Med 2:810, 1995.
50
115. Estey
W: Subjective effects of dry versus humidified low flow oxygen. Respir Care 25:1143, 1980.
116. Koslawski 117. Aubier
S, Rasmussen B, Wilkoff WG: The effect of high oxygen tensions on ventilation during severe exercise. Acta Physiol Scand 81:385, 1971.
M, Murciano D, Milic-Emili J, et al: Effects of the administration of O
2
on ventilation and blood gases in patients with chronic obstructive pulmonary disease during acute respiratory failure.
Am Rev Respir Dis 122:747, 1980. 118. Dantzker
DR, Wagner PD, West JB, et al: Instability of lung units with low VA/Q ratios during breathing. J Appl Physiol 38:886, 1975.
119. Poulton
PE: Left-sided heart failure with pulmonary oedema: Its treatment with the "pulmonary plus pressure machine." Lancet 2:981, 1936.
120. Bersten
AD, Holt AW, Vedig AE, et al: Treatment of severe cardiogenic pulmonary edema with continuous positive airway pressure delivered by face mask. N Engl J Med 325:1825, 1991.
121. Baratz
DM, Westbrook PR, Shah PK, Mohsenifar Z: Effect of nasal continuous positive airway pressure on cardiac output and oxygen delivery in patients with congestive heart failure. Chest 102:1397, 1992. 122. Kramer
N, Meyer TJ, Meharg J, et al: Randomized, prospective trial of noninvasive positive pressure ventilation in acute respiratory failure. Am J Respir Crit Care Med 151:1799, 1995.
123. Holt
AW, Bersten AD, Fuller S, et al: Intensive care costing methodology: Cost benefit analysis of mask continuous positive airway pressure for severe cardiogenic pulmonary oedema. Anaesth Intensive Care 22:170, 1994. 124. Prevedoros 125. Gachot
HP, Lee RP, Marriot D: CPAP: Effective respiratory support in patients with AIDS-related Pneumocystis carinii pneumonia. Anaesth Intensive Care 19:561, 1991.
B, Clair B, Wolff M, et al: Continuous positive airway pressure by face mask or mechanical ventilation in patients with human immunodeficiency virus infection and severe carinii pneumonia. Intensive Care Med 18:155, 1992.
Pneumocystis
126. Gregg
RW, Friedman BC, Williams JF, et al: Continuous positive airway pressure by face mask in Pneumocystis carinii pneumonia. Crit Care Med 18:21, 1990.
127. Sadovnikoff
N, Varon J: CPAP Mask management of varicella-induced respiratory failure. Chest 103:1894, 1993.
128. Brett
A, Sinclair DG: Use of continous positive airway pressure in the management of community acquired pneumonia. Thorax 48:1280, 1993.
129. Miro
AM, Shivaram U, Hertig I: Continuous positive pressure in COPD patients in acute hypercapnic respiratory failure. Chest 103:266, 1993.
130. Brochard
L, Isabey D, Piquet J, et al: Reversal of acute exacerbations of chronic obstructive lung disease by inspiratory assistance with a face mask. N Engl J Med 323:1523, 1990.
131. Soo
Hoo GW, Santiago S, Williams AJ: Nasal mechanical ventilation for hypercapnic respiratory failure in chronic obstructive pulmonary disease: Determinants of success and failure. Crit Care Med 22:1253, 1994. 132. Meyer
TJ, Hill NS: Noninvasive positive pressure ventilation to treat respiratory failure. Ann Intern Med 120:760, 1994.
133. Wysocki
M, Tric L, Wolff MA, et al: Noninvasive pressure support ventilation in patients with acute respiratory failure. Chest 103:907, 1993.
134. Lapinsky
SE, Mount DB, Mackey D, Grossman RF: Management of acute respiratory failure due to pulmonary edema with nasal positive pressure support. Chest 105:229, 1994.
135. Pennock
BE, Crawshaw L, Kaplan PD: Noninvasive nasal mask ventilation for acute respiratory failure. Chest 105:441, 1994.
136. Sacchetti
AD, Harris RH, Paston C, Hernandez Z: Bi-Level positive airway pressure system use in acute congestive heart failure: Preliminary case series. Acad Emerg Med 2:714, 1995.
137. Padman
R, Lawless S, Von Nessen S: Use of BiPap by nasal mask in the treatment of respiratory insufficiency in pediatric patients. Pediatr Pulmonol 17:119, 1994.
138. Fortenberry
JD, Del Toro J, Evey L, et al: Nasal mask bi-level positive pressure ventilation (BiPAP) in children with mild to moderate hypoxemic respiratory failure. Chest 104:133S, 1993.
51
Section II - Respiratory Procedures
52
53
Chapter 3 - Basic Airway Management and Decision-Making Diamond Vrocher Laura R. Hopson
Although it is common knowledge that airway management is the first priority in the management of any seriously ill or injured patient, its importance is often overlooked. Failure to treat airway management as the top priority can lead to serious errors in patient care and often presages a cycle of patient deterioration and misguided therapeutic intervention. Even when its importance is fully recognized, airway management can be one of the most difficult components of a resuscitation. Because of the sheer variety of airway difficulties that are possible, even the most skilled resuscitator can find the task challenging. Simply stated, it may be impossible to adequately manage an airway in an emergency situation in a timely enough fashion to prevent deterioration or assure a successful resuscitation. Blood, loosened teeth, vomitus, swollen or distorted landmarks, immobility of the jaw or cervical spine, and variations in anatomy all may present formidable barriers to successful management. When airway obstruction occurs in conjunction with reflex clenching of the jaws and possible cervical spine injury, conventional airway management tools may be ineffective. Time pressures imposed by the need to avoid cerebral anoxia force difficult decisions such as whether the neck can be moved, whether paralyzing agents should be administered, or whether a surgical airway is needed. Tools must be immediately available, skills must be well-honed, and decision-making must be sharp if optimal emergency airway management is to occur. Massive neck and upper airway swelling from angiotensin-converting enzyme (ACE)-inhibitor angioedema can essentially prohibit a successful airway, even by surgical means. Some solutions to the many obstacles faced in emergency airway management are presented in this and the following chapters. Minimally invasive approaches to airway establishment and emergency airway decision-making are described first in the current chapter with more advanced techniques covered in following chapters. Decision algorithms are presented to help assemble the pieces of the airway management puzzle into a logical framework.
DECISION-MAKING IN AIRWAY MANAGEMENT The resuscitator must have many tools at hand to deal with the acutely compromised airway. It is important to be proficient in many different techniques and to tailor their use to the needs of the individual patient. Rescuers should practice potential scenarios before facing patients with a compromised airway in the clinical situation. Failure to do so may lead to unnecessarily aggressive management in some situations or to irreversible hypoxic injury as a result of unnecessary hesitation in others. Deciding on who requires intervention in the field, and who can be supported adequately enough until definitive hospital management can be obtained, is a formidable task for even the most skilled clinician. Several parameters must be assessed quickly before an airway management choice can be made. The parameters to be considered are as follows: 1. 2. 3. 4. 5. 6.
Adequacy of current ventilation Potential for hypoxia Airway patency Need for neuromuscular blockade (muscle tone, teeth clenching, severe obstructive pulmonary disease, or asthma) Cervical spine stability Safety of technique and skill of the operator
Consideration of these factors should guide the clinician in selecting the optimal technique. This initial choice is often straightforward. Difficulty may arise precipitously when the initial choice fails. Time then becomes critical as the risk of irreversible hypoxic injury rises. Anxiety increases and error potential compounds under these circumstances. Forethought and practice are invaluable when making these decisions. Schemata offered in Figure 3-1 and Figure 3-2 outline a logical approach to airway management. Figure 3-1 presents the nonsurgical approaches with end points of either success or the decision to pursue surgical management. Note that a prolonged duration of hypoxia may hasten a decision in favor of surgical airway management. Figure 3-2 addresses choices once the decision has been made to manage the airway surgically. Consideration of patient condition, security of the airway approach, and the invasive nature of the procedure are factors to be weighed in the final decision.
ESTABLISHMENT OF AIRWAY PATENCY The first concern in the management of a patient in critical condition is adequacy of the airway. Partial or complete airway obstruction must be overcome quickly. In some cases, such as an airway obstructed by a tongue, simple maneuvers will suffice. In other cases, particularly those in which multiple agents are combining to block the airway, the task will be formidable. The tongue, dentures, swollen or distorted tissues, blood, and vomitus are common obstructing agents that compromise airway patency. Clearing obstructing agents may be made more difficult by muscular activity due to reflex stimulation or patient efforts to improve oxygenation. Moreover, the neck motion required for suction and intubation must be carefully managed in the setting of potential cervical spine instability. The wide availability of pulse oximetry monitors has greatly improved our ability to monitor oxygenation for patients at risk of airway or ventilatory compromise. [1] These monitors are accurate under most conditions, [2] and clinically subtle deterioration can be quickly recognized using the monitors. They are standard equipment in emergency departments (EDs), intensive care units, and operating rooms. Pulse oximetry is discussed in more detail in Chapter 2 . Airway Maneuvers Partial or complete airway obstruction resulting from lax musculature and tongue occlusion of the posterior pharynx may be overcome by a variety of maneuvers, including the neck-lift and head-tilt method, the jaw-thrust method, and the chin-lift method. In a study of 120 anesthetized patients whose airways
54
Figure 3-1 Nonsurgical airway management algorithm.
were obstructed by their tongues, Guildner concluded that the chin lift was the easiest to perform and produced the greatest airway patency of the three methods tested. [3] The chin-lift method has been shown conclusively to increase the airway diameter in pediatric patients. [4] Both the chin-lift and jaw-thrust methods have the additional advantage that neck extension is unnecessary ( Fig. 3-3 , Table 3-1 and Table 3-2 ). [3] Partial airway obstruction in the patient with a decreased level of consciousness is commonly due to posterior displacement of the tongue. This may be recognized readily in the presence of snoring or stridor, but an apneic patient or one who is moving minimal air may not exhibit any audible evidence of airway obstruction. Either a jaw-thrust or chin-lift maneuver should be performed on every unconscious patient. When uncertain about cervical spine status, the neck must be maintained in the neutral position. If the patient was found with a flexed or extended neck, the neck should first be restored to neutral position with gentle longitudinal traction. The chin-lift or jaw-thrust method is then performed. These maneuvers usually clear airways obstructed as a result of lax pharyngeal musculature or posterior displacement of the tongue. The neck-lift and head-tilt maneuvers described in cardiac life support courses should not be used when cervical spine injury is suspected, because the extension of the spine produced during the maneuver endangers the spinal cord. Partial or complete airway obstruction can be the result of upper airway hemorrhage, accumulation of the patient's own secretions, foreign body aspiration, vomitus, or fractured dentition. If foreign body aspiration is suspected, the rescuer should perform a subdiaphragmatic abdominal thrust (Heimlich maneuver). [4] When stability of the spine is a concern, application of the subdiaphragmatic thrust should be limited to the supine method described for unconscious victims. Potential risks of a subdiaphragmatic thrust include stomach rupture, esophageal perforation, and mesenteric laceration, compelling the rescuer to weigh the benefits of its application. [5] [6] [7] [8] [9] [10]
55
Figure 3-2 Surgical airway management algorithm. The Chin-Lift Maneuver
To perform the chin-lift maneuver, the rescuer places the tips of the fingers, volar surface superiorly, beneath the patient's chin. The jaw is lifted gently forward. The patient's mouth is opened by drawing down on the lower lip with the thumb of the same hand. [3] Mouth-to-mouth resuscitation or other means of positive-pressure ventilation is provided if the patient is not ventilating spontaneously. The Jaw-Thrust Maneuver
The jaw-thrust maneuver is the second choice, again because neck extension is not necessary. Forward traction on the mandible is achieved by using two hands to grasp the mandibular rami and pull them forward. The Subdiaphragmatic Abdominal Thrust
The subdiaphragmatic thrust is a method to relieve a completely obstructed airway. The technique was popularized by Dr. Henry Heimlich and is commonly referred to as the Heimlich maneuver.[11] The technique is most effective when a solid food bolus obstructs the larynx. Although a subject of controversy, a role for the maneuver has not been found for the resuscitation of near-drowning victims. [12] The conscious patient with an obstructed airway exhibits increased respiratory effort, anxiety, aphonia, and, occasionally, cyanosis. In the conscious patient, the maneuver is performed with the rescuer positioned behind the upright patient. The rescuer's arms are circled about the patient's midsection with the radial side of the clenched fist placed in the epigastrium of the patient. Care is exercised to position the fist midway between the umbilicus and the xiphoid of the patient. After proper positioning, the rescuer grasps the fist with the opposite hand and delivers an inward and upward thrust to the abdomen. A successful maneuver will cause the obstructing agent to be expelled from the patient's airway by the force of air exiting the lungs. [13] An unconscious, supine patient must be handled differently: The rescuer kneels next to the patient's pelvis facing cephalad. The palmar bases of the hands are
placed in an
56
Figure 3-3 Illustration of maneuvers for opening the airway. A, Neck lift. B, Chin lift. C, Jaw thrust. (From Guildner CW: Resuscitation—opening the airway: A comparative study of techniques for opening an airway obstructed by the tongue. JACEP 5:588, 1976. Reproduced by permission.)
overlapping fashion on the epigastrium at the same spot as that used in the upright patient. Inward, upward thrusts are delivered in this fashion with the same objective. [13] Abdominal thrusts are relatively contraindicated in pregnant patients and others with protuberant abdomens. A chest compression identical to chest compressions delivered during cardiopulmonary resuscitation (CPR) may be used instead. Chest compressions may create greater peak airway pressures than a Heimlich maneuver, although this is controversial. [14] A combined (simultaneous) chest compression and subdiaphragmatic abdominal thrust may produce even higher peak airway pressures. Hence, a combined maneuver should be considered in the case of total airway obstruction that is unresponsive to simple Heimlich maneuver. [15] Visceral injury can occur with the Heimlich maneuver. [5] [6] [7] [8] [9] [10] Excessive force or improper technique may be responsible in such cases. Nonetheless, the technique can be life-saving TABLE 3-1 -- Subjective Evaluation of Effectiveness of Techniques on Patients Not Making Any Respiratory Effort (n = 120) Neck Lift Chin Lift Jaw Thrust Effectiveness
No. %
No. %
No. %
Total obstruction Unable to ventilate
7
5.8
— —
1
0.8
8
6.7
2 1.7
2
1.7
58
48.3
9 7.5 23
19
47
39.2 109 90.8 94
78
Partial obstruction Inadequate ventilation Partial obstruction Adequate ventilation but with difficulty Good airway Easy ventilation
From Guildner CW: Resuscitation—opening the airway: A comparative study of techniques for opening an airway obstructed by the tongue. JACEP 5:588, 1976. Reproduced by permission. and should be used when needed. Attention to proper execution may limit complications. Positioning Positioning the patient who has sustained multiple trauma can be a problem. Spinal injury and airway access priorities dictate that the patient should be kept in the supine position while immobilized on a backboard. Turning the patient on the side allows upper airway hemorrhage, secretions, and vomitus to drain externally rather than to collect in the patient's mouth, which can lead to aspiration and airway obstruction. However, there is evidence suggesting that rotating the patient to the lateral decubitus position may not prevent aspiration. [16] Guidelines for patient positioning must take into account the status of the patient's spine and the use of gravity to enable secretions to drain rather than accumulate in the airway. The following is a judicious approach to airway management in a patient with spontaneous respiration: 1. Initial airway maintenance accomplished by the chin-lift maneuver and the application of cervical stabilization (see Chapter 47 ). 2. Immobilization of the patient on a spinal backboard. 3. With the position of the neck controlled, transportation of the patient on the side to facilitate airway drainage. Suctioning Patient positioning and airway opening and clearing maneuvers are often inadequate to achieve the degree of airway TABLE 3-2 -- Effectiveness of Techniques for Opening Airway in Patients with Complete Respiratory Obstruction Who Are Making Spontaneous Respiratory Effort (n = 30) Neck Lift Chin Lift Jaw Thrust Effectiveness (Tidal Volume)
No. %
No. %
No.
%
0–50 mL
13
43.3 —
—
1
3.4
50–250 mL
9
30
2
6.7
3
10
250–400 mL
6
20
7
23.3 7
23.3
>400 mL
2
6.7 21
70
63.3
19
From Guildner CW: Resuscitation—opening the airway: A comparative study of techniques for opening an airway obstructed by the tongue. JACEP 5:588, 1976. Reproduced by permission.
57
patency desired. Ongoing hemorrhage, vomitus, and particulate debris often require suction to clear and maintain the respiratory passage. Three basic types of suctioning tips are available ( Fig. 3-4 ). Each is suited to different types of airway obstruction problems. Dental tip suction is most useful for clearing particulate debris from the upper airway. Vomitus is most readily cleared with this tip because it is least likely to become obstructed itself by particulate matter. The tonsil tip (Yankauer) suction device is used most effectively to clear upper airway hemorrhage and secretions. Its design is
intended to prevent the obstruction of its tip by tissue and clot. The rounded tip is also less traumatic to soft tissues. The catheter tip works well for suctioning the trachea and bronchi through a tracheal tube, but it is inferior to the other tips for suctioning the oropharynx. The dental tip device should be used during the resuscitation period and should be ready at the bedside. The dental tip allows rapid clearing of both particulate matter and hemorrhage, thereby expediting airway control. A limiting feature of many suction catheters is the diameter of the tubing. Large particulate emesis may obstruct the standard ¼-inch diameter catheter. [17] A ?-inch diameter suction catheter (Conmed Corp) has been shown to significantly decrease suction time of viscous and particulate material, potentially decreasing the risk of aspiration. [18] Stabilization of the patient with multiple injuries may involve use of all three types of suction tips. The tonsil or dental tip should be attached to the suction source during the interval between patient evaluations because it is most likely to be the one needed on short notice. All suction apparatus must be immediately available, and everyone participating in a resuscitation should be familiar with the suction equipment and know how to turn it on during an emergency. In the resuscitation rooms, suction equipment should always be connected and ready to operate. Interposition of a suction trap at the base of the dental tip suction device prevents clogging of
Figure 3-4 Three types of suction tips: dental, tonsil, and catheter. (From Clinton JE, Ruiz E: Trauma Life Support Manual. Minneapolis, MN, Hennepin County Medical Center, 1982.)
the tubing with particulate debris. A trap that fits directly onto a tracheal tube has been described; use of this device still allows effective suctioning during intubation ( Fig. 3-5 ). [19] No specific contraindications to airway suctioning exist. Complications of suctioning may be avoided by anticipating problems and providing appropriate care before and during suctioning maneuvers. Nasal suction is seldom required to improve oxygenation (except in infants), because most adult airway obstruction occurs in the mouth and oropharynx. Vigorous nasal suction can induce epistaxis and further complicate an already difficult airway. Epistaxis may be avoided by limiting the force applied during suctioning. Vasoconstrictor drops or spray constrict the nasal mucosa and may reduce the injury potential in patients who require repeated nasopharyngeal suctioning. Prolonged suctioning should be avoided because it may lead to significant hypoxia, especially in children. Suctioning should not exceed 15-second intervals, and the provision of supplemental oxygen before and after suctioning should be routine (see also Chapter 7 ). Naigow and Powasner found that suctioning consistently induced hypoxia in dogs and that it was best avoided by hyperventilation with high-concentration oxygen before and after suctioning. [20]
Figure 3-5 The Ruben suction booster, which is designed to allow high-capacity suctioning through the endotracheal tube during intubation. Schematic diagram: A, Tracheal tube connection. B, Connection to suction. C, Introducer opening in the closed position. D, Opening that is kept closed when suction is needed through the tracheal tube. Note: All suction should be done under direct vision. (From Ruben H, Hansen E, MacNaughton FI: High-capacity suction technique. Anaesthesia 34:349, 1979. Reproduced by permission.)
58
Figure 3-6 Intracranial intubation. Lateral skull x-ray showing nasogastric tube placed into brain through skull fracture. (From Clinton JE, Ruiz E: Trauma Life Support Manual. Minneapolis, MN, Hennepin County Medical Center, 1982.)
Extreme care should be exercised when a basilar skull or facial fracture is suspected, because communication between nasal and intracranial cavities may exist and allow the inadvertent placement of nasal suction tubes in the cranial cavity ( Fig. 3-6 ). Generally, it is best to perform suctioning under direct visual inspection or with the aid of the laryngoscope. Forcing a suction tip blindly into the posterior pharynx can injure tissue or convert a partial obstruction to a complete obstruction. Artificial Airways Indications and Contraindications
Once the airway has been opened through various maneuvers and suctioning, the patient may require further temporary support to maintain airway patency. The semiconscious patient who is breathing with an adequate rate and tidal volume at the time of the chin-lift maneuver may develop hypoxia because of recurrent obstruction if the maneuver is discontinued. Oxygen supplementation and an artificial airway may be all the support that is necessary. The use of an artificial airway also allows more efficient use of rescuer skills and relief from fatigue that is caused by the continuous application of chin-lift or jaw-thrust maneuvers. Positive-pressure ventilation with a bag-valve-mask (BVM) device may be necessary to bolster the patient's inadequate ventilatory effort or to provide total ventilation in cases of apnea. By maintaining airway patency, artificial airways may facilitate both spontaneous and bag-mask ventilation. Airway Placement Technique
The simplest artificial airways are the oropharyngeal and nasopharyngeal airways ( Fig. 3-7 ). Both are intended to prevent the tongue from obstructing the airway by falling back against the posterior pharyngeal wall. The oral airway also may prevent teeth clenching. The oropharyngeal airway may be inserted by either of two procedures. One approach is to insert the airway in an inverted position along the patient's hard palate. When it is well into the patient's mouth, the airway is rotated 180 degrees and advanced to its final position along the patient's tongue, with the distal end of the airway lying in the hypopharynx. A second approach involves performance of a jaw-thrust maneuver, either manually or with a tongue blade, and the simple advancement of the airway into the mouth to its final position. No rotation is performed when the airway is placed in this manner. Once inserted, the oral airway may have to be taped in place to prevent expulsion by the patient's tongue. The oropharyngeal airway will keep the mouth partially open and prevent clenching of the teeth, which can obstruct an orogastric or orotracheal tube. The nasopharyngeal airway is likely an overlooked technique to assure a patent airway in an otherwise stable patient. The soft tube is placed by gently advancing the airway into a nostril, directing the tip along the floor of the nose toward the nasopharynx. When in final position, the flared external end of the airway should rest at the nasal orifice. Either of these two airways provides airway patency similar to that in a correctly performed chin-lift maneuver, but the nasal airway may be better
tolerated by the semiconscious patient. Since the nasal tube is about the same size as an endotracheal tube, some clinicians place the nasopharyngeal airway to gently dilate the nasal passages before attempting blind nasotrachael intubation, but this technique is neither standardized nor well studied ( Fig. 3-8 ).
Figure 3-7 Simple artificial airways: oropharyngeal and nasopharyngeal. (From Clinton JE, Ruiz E: Trauma Life Support Manual. Minneapolis, MN, Hennepin County Medical Center, 1982.)
59
Figure 3-8 Some clinicians place a nasopharyngeal tube to dilate the nasal passage prior to blind nasotrachael intubation. Complications
Few complications are encountered with the use of oral or nasal airways. The oropharyngeal airway may cause airway obstruction if during its placement the tongue is pushed against the posterior pharyngeal wall. Care in placement will prevent this. In the semiconscious patient with intact reflexes, the gag reflex may stimulate retching and emesis. If gagging is a persistent problem, the airway should be removed and a nasal airway or tracheal intubation should be considered. If the patient with airway compromise is comatose and lacks a gag reflex, the oropharyngeal airway should not be used as a definitive airway; tracheal intubation should be used instead. The nasopharyngeal airway may offer an advantage over the oropharyngeal airway in that the nasopharyngeal airway is less likely to induce gagging. When placing a nasopharyngeal airway, care must be exercised not to induce epistaxis, and extreme caution is indicated in patients with a suspected basilar skull fracture or facial injury. All potentially unstable patients with oral or nasal pharyngeal airways should be observed constantly, because these devices are temporary measures and cannot substitute for tracheal intubation.
BAG-VALVE-MASK VENTILATION Indications and Contraindications Although the BVM method of ventilation appears to be simple and effective, it can be difficult to perform correctly. BVM ventilation should be used by experienced individuals who are able to ensure a tight mask seal in situations requiring positive-pressure ventilation. The BVM often is used with an oropharyngeal or nasopharyngeal airway in place. [13] Predictors of difficult BVM ventilation are shown in Table 3-3 .[21] Inexperience is a relative contraindication to the use of a BVM. A rescuer who is not skilled with the BVM will achieve much better ventilation with mouth-to-mouth or mouth-to-mask breathing than with a BVM. Concern regarding transmission of infectious diseases has reduced the willingness of the lay public and health professionals to perform mouth-to-mouth ventilations. [22] However, only 12 cases of infectious TABLE 3-3 -- Risk Factors for Difficult Mask Ventilation [21] Presence of beard Body mass index >26 kg/m2 Lack of teeth Age >55 yr History of snoring disease transmission from mouth-to-mouth or mouth-to-tube ventilation have been confirmed in the last 30 years, making CPR ventilation a relatively safe procedure ( Table 3-4 ). [23] Although BVM ventilation may provide excellent respiratory support in the anesthetized, paralyzed patient in the operating room, the device frequently is of marginal value during CPR, during an ambulance run, or in the combative patient. The three major problems encountered with BVM ventilation are inadequate tidal volumes, inadequate oxygen delivery, and gastric distention. A tight mask seal is mandatory to prevent loss of tidal volume and to ensure oxygen delivery during ventilation. Achieving a tight mask seal requires excellent procedural technique, and is much easier to achieve in the controlled setting with an anesthetized, paralyzed patient. Another hazard of BVM ventilation occurs when vomitus, blood, or other debris is present in the mouth or pharynx. The foreign material may be insufflated down the trachea if it is not cleared before ventilation. Ventilation Technique Achieving adequate tidal volume with BVM ventilation requires a tight mask seal and appropriate compression of the bag. The ideal tidal volume for BVM ventilation is 5 to 6 mL/kg, or approximately 500 mL for an adult. [24] A variety of mask configurations are available to facilitate a tight seal, but none substitutes for the practiced skill of the rescuer. For the single rescuer, only one hand can be used to achieve the seal because the other must squeeze the bag. The rescuer must apply pressure anteriorly while simultaneously lifting the jaw forward. The thumb and index finger provide anterior pressure while the fifth and fourth fingers lift the jaw. In pediatric patients the E-C clamp technique is used: The thumb and index finger form a "C" while providing anterior pressure over the mask, while the third, fourth, and fifth fingers form an "E" to lift the jaw ( Fig. 3-9 ). Dentures generally should be left in place to help ensure a better seal with the mask. It has been suggested that effective BVM ventilation during CPR requires two hands and, therefore, two rescuers. Fig. 3-9B )
[ 25]
We suggest using the two-rescuer technique (see
TABLE 3-4 -- Reported Infections (Since 1965) Acquired by Mouth-to-Mouth or Mouth-to-Tube Ventilation During CPR [23] Organism
Cases
Mycobacterium tuberculosis
1
Neisseria meningitides
4
Shigella sonnei
1
Salmonella infantis
1
Helicobacter pylori
1
Herpes simplex virus
3
Neisseria gonorrhoeae
1
60
Figure 3-9 Bag-valve-mask ventilation is very difficult for one person to do (A), and it frequently fails to deliver adequate tidal volumes, especially during cardiopulmonary resuscitation. With the two-person method (B), one person uses both hands to hold the mask firmly against the face and extend the head. The other person uses both hands to squeeze the bag. Dentures are generally left in place to help provide a better-fitting mask. (From Jesudian MC, Harrison RR, Keenan RL, Maull KI: Bag-valve-mask ventilation: Two rescuers are better than one. Crit Care Med 13:122, 1985.)
whenever it is practical. The presence on the BVM device of a pop-off valve may further frustrate ventilation efforts in the patient with reduced compliance. All BVM devices should be attached to a supplemental oxygen source (with a flow rate of 15 L/min) to avoid hypoxia. A significant problem with the BVM method is the low percentage of oxygen achieved with some reservoirs. The amount of delivered oxygen is dependent on the ventilatory rate, the volumes delivered during each breath, the oxygen flow rate into the ventilating bag, the filling time for reservoir bags, and the type of reservoir used. The commonly used corrugated tube reservoir is dependent on ventilatory technique and does not alert the rescuer to changes in oxygen flow. A 2.5-L bag reservoir and a demand valve are the preferred supplementation technique during BVM ventilation. [26] Pediatric BVM devices should have a minimum volume of 450 mL. Pediatric and larger bags may be used for ventilation of infants with the proper mask size, but care should be taken to administer only the volume necessary to effectively ventilate the infant. Pop-off valves should be avoided because airway pressure under emergency conditions may often exceed the pressure of the valve. [13] BVM ventilation may be the preferred method of prehospital airway support in children under the age of 12 years. Although the final outcome of out-of-hospital pediatric resuscitation is generally poor, Gausche et al. [27] reported that neurologic outcome and ultimate
survival rates of prehospital pediatric resuscitations by Emergency Medical Service (EMS) providers with BVM ventilation were as good as with tracheal intubation. Complications Hypoventilation often occurs because of improper technique including poor sealing of the mask, failure to achieve airway patency, and delivery of insufficient tidal volume. Proper training is necessary to avoid these errors. Gastric distention can occur if air is insufflated down the esophagus, increasing the risk of regurgitation and aspiration. When assistance is available, the application of firm posterior pressure on the cricoid ring helps reduce gastric inflation during BVM ventilation. [28] [29] The technique must be used carefully in infants, whose airway is more pliable and subject to obstruction with excessive cricoid pressure. Even with proper BVM technique, aspiration can occur. The rescuer must be vigilant to recognize complications early and take corrective action. Under most situations, however, some gastric dilation will occur even with strict attention to detail. Minor gastric distention should not be considered substandard under the setting of prolonged BVM ventilation.
INTERMEDIATE AIRWAYS Intermediate airways are those interventions that go beyond the maintenance of a patent airway. They represent a midpoint between airway establishment and true airway control by maneuvers such as tracheal intubation and tracheotomy. Many devices are available and no one technique is universally used. No agreed-upon standard of care has been promulgated for these devices, and their use varies by location and clinician experience. The devices described in this section allow ventilation across the larynx but do not involve complete airway control. These devices include the esophageal obturator airway (EOA), the esophageal gastric tube airway (EGTA), the laryngeal mask airway (LMA), and the esophageal-tracheal Combitube (ETC) airway (Sheridan Catheter Corp., Argyle, NY). Two are designed to occlude only the esophagus (EOA and EGTA), one (LMA) seals the larynx at the hypopharynx level, and one (ETC) offers the versatility of use whether placed into the esophagus or the trachea. There are several newer supraglottic ventilation devices, including the cuffed oropharyngeal airway (COPA), the airway management device (AMD), and the laryngeal tube (LT). Each is designed for use in the unconscious patient who requires positive-pressure ventilation. The esophageal cuff or seal built into these devices reduces gastric content aspiration. The EOA and EGTA have a relatively high complication rate and therefore are becoming less common as other ventilation devices are becoming available. Esophageal Obturator Airway and Esophageal Gastric Tube Airway The EOA and the EGTA maintain airway patency in ways similar to the oral and nasal airways, but they also protect the airway by occluding the esophagus to reduce gastric distention
61
and regurgitation. The face mask permits use of these airways as positive-pressure ventilating devices. Air insufflated through the airway traverses the upper airway before crossing the larynx and entering the trachea. Ventilation from the EOA exits the airway through numerous ports in its hypopharyngeal portion ( Fig. 3-10A and B ). Ventilation from the EGTA is identical to mask ventilation, with the addition of esophageal occlusion. A port is available on the EGTA to vent the stomach. The attractiveness of the EOA and the EGTA for use in the apneic patient stems from their retention of much of the simplicity of the artificial airway with the addition of an important feature of more complicated airways—some protection against regurgitation and reduction of gastric distention. Indications and Contraindications
The EOA and EGTA are indicated when positive-pressure ventilation is needed but neither BVM ventilation nor tracheal intubation can be performed safely, effectively, and rapidly. The EOA can be placed more quickly than a tracheal tube, [30] [31] and there are fewer intubation failures with the EOA than the tracheal tube. [32] The EOA and EGTA cannot be used in the awake patient with an intact gag reflex, and they are not available in pediatric sizes. They are relatively contraindicated in the presence of active oropharyngeal bleeding, suspected esophageal injury, caustic ingestion, or a history of esophageal disease. As a precaution against pressure-related complications, it is recommended that these devices be left in place for no longer than 2 hours. It must be recognized that the EOA and the EGTA are temporary forms of airway control, most suitable for use in out-of-hospital settings. Placement of EOA/EGTA
The head is in the neutral position during placement of the EOA and the EGTA. Neck motion is unnecessary. The rescuer
Figure 3-10 A, Esophageal obturator airway. Correct placement of the esophageal airway with the cuff inflated in the esophagus caudad to the bifurcation of the trachea. (From Clinton JE, Ruiz E: Trauma Life Support Manual. Minneapolis, MN, Hennepin County Medical Center, 1982.) B, Esophageal obturator airway. (From Jacobs LM: The importance of airway management in trauma. J Natl Med Assoc 80:873, 1988.)
grasps and pulls the jaw forward. At this point, the rescuer inserts the assembled airway with the mask attached. The obturator tip is directed into the patient's posterior pharynx with gentle, steady pressure. The obturator is advanced down the esophagus until the mask rests flush against the face of the patient. Figure 3-10A illustrates the correct position at placement. The cuff should lie in the esophagus just distal to the carina of the trachea. The rescuer postpones inflation of the balloon until proper position is confirmed. The patient is ventilated with a tight mask seal on the face, and the lungs are auscultated. For effective ventilation, the mask seal must be tight. Breath sounds should be audible bilaterally. Unilateral breath sounds or failure of auscultation should lead the rescuer to reassess the airway placement. Pneumothorax or hemothorax may explain unilateral sounds, as may inadvertent main stem bronchus intubation. Tracheal intubation will result in the absence of breath sounds. The possibility of bronchial or tracheal intubation requires removal and replacement of the airway. Once satisfactorily placed, the esophageal balloon is inflated with 20 to 25 mL of air. Complications
The complications of the EOA and EGTA are well reported. Hypercarbia from inadequate ventilation occurs more commonly with EOA than tracheal intubation. [33] [34] Unrecognized tracheal intubation may occur in 2.9% to 5% of patients with up to a 100% mortality due to airway occlusion. [31] [35] Esophageal injury may also occur, ranging from small lacerations in 8.5% of patients [32] to esophageal rupture. [36] [37] [38] Under ideal circumstances, tracheal intubation should be performed before removal of the EOA, because vomiting often occurs following deflation of the balloon and EOA removal. If the EOA cuff has been overinflated, it may partially occlude the trachea and make intubation difficult. In such
62
cases, the balloon is partially deflated to facilitate tracheal intubation. The Laryngeal-Mask Airway The LMA (Intavent International SA, Henley-on-Thames, England) functions intermediately between an oropharyngeal airway and an endotracheal tube. It was developed for use in the operating room as an alternative for endotracheal intubation, but it has also been recommended for use in difficult intubations and for rescue ventilation in emergency resuscitations. [39] [40] The LMA is considered a temporary adjunct until tracheal intubation can be established. [39] Since the introduction of the original LMA, several variations have become available. The original LMA, which is available in both reusable (LMA Classic) and disposable (LMA Unique) varieties, consists of a tube fitted with an oval mask, rimmed with an inflatable cuff ( Fig. 3-11A ). The mask is intended to reside
Figure 3-11 Laryngeal mask airway (LMA). A, inflated LMA outside of the body. B, LMA in place with cuff overlying larynx. C, LMA placement into the pharynx. D, LMA placement using the index finger as a guide. (From Basket PJF, Brain AIJ: The use of the LMA. In Basket PJF, Brain AIJ (eds): Cardiopulmonary Resuscitation Handbook. London, Intavent Research, 1994.)
in the hypopharynx rather than on the face. It is inserted digitally until its tip meets resistance in the upper esophageal sphincter. The cuff is then inflated, forming a seal around the glottic opening (see Fig. 3-11B ). The result is a relatively secure airway. However, it cannot be considered to protect against gastric regurgitation. Leakage of the hypopharyngeal mask allows aspiration of emesis and gastric distention may occur with misplacement. One variation, the Proseal LMA, has a parallel drainage tube attached to the airway tube that is designed to reduce gastric insufflation and allow gastric drainage by a nasogastric tube, potentially decreasing the risk of aspiration. [41] Another variation, the intubating LMA (LMA Fastrach) is designed to facilitate blind tracheal intubation while allowing continuous positive-pressure ventilation. [42] The LMA and the intubating LMA (ILMA) have become part of the standard airway armamentarium for many rescuers, both in the hospital and prehospital setting. [43] Although the standard LMA can
63
act as a conduit for tracheal intubation, there are several advantages to the ILMA. [44] Insertion of the ILMA is easier than the standard LMA when the head and neck must be maintained in the neutral position, [45] and the ILMA allows for passage of a larger tracheal tube (up to 8-0). [40] Thus far, the Proseal LMA's role in the setting of difficult intubation or rescue ventilation has not been studied, and it is mainly used in the operative environment. Indications and Contraindications
The LMA is indicated for patients requiring an airway who cannot be endotracheally intubated or cannot be ventilated with a BVM. The most frequently cited example is a patient whose anatomy prevents visualization of the larynx. Contraindications include the inability to open the patient's mouth, vomiting, or the need for high pulmonary inflation pressures. [40] Placement of LMA
After selecting the appropriate size ( Table 3-5 )[40] the LMA is checked for possible air leaks by inflating and deflating the cuff. If the patient has a gag reflex, deep oropharyngeal topical anesthesia or conscious sedation must be administered. Although the sniffing position is preferred for the standard LMA, placement is 95% successful when the neck and head are held in the neutral position, as would be necessary with cervical spine immobilization. [45] The posterior surface of the mask is lubricated and the mask is oriented so its opening faces the tongue. With the index finger of the dominant hand placed on the proximal aspect of the mask, the mask is inserted into the mouth, firmly against the hard palate (see Fig. 3-11C ). The index finger (or thumb) may also be used as a guide during advancement (see Fig. 3-11D ). With one smooth motion, the mask is advanced until resistance is encountered. With the tip of the mask thus seated in the upper esophageal sphincter, the cuff is inflated. The lungs are auscultated to confirm correct placement. Preparation for ILMA placement is similar to LMA placement. The preferred patient position for ILMA is with the head and neck in a neutral position. [46] The posterior surface of the mask is lubricated, and the mask is oriented so the opening is facing the tongue. While holding the ILMA by the handle, slide the mask along the hard palate and then downward until resistance is felt at the base of the hypopharynx. The cuff is then inflated, and position is confirmed by auscultation of the lungs. [40] After successful placement of the LMA, several methods are available to achieve subsequent endotracheal intubation. The
Weight
TABLE 3-5 -- Laryngeal-Mask Airway (LMA), Disposable LMA, and Intubating LMA Size Recommendation Based on Weight [40] LMA Disposable LMA
ILMA
100 kg
6
—
—
Note that only the standard LMA is available for patients 98%, attempts at intubation should be halted for bag-mask ventilation whenever the O 2 saturation drops below 92%. Assessment of tube location is the top priority immediately after its passage. The best assurance of tracheal placement is for the clinician to see the tube pass through
the vocal cords. Techniques to assess tube placement are discussed earlier. Another method of reliably determining tracheal tube location uses the fiberoptic scope. Passage of the scope through the tube with visualization of tracheal rings confirms ET placement as well as the position within the trachea. The placement of a lighted stylet down the tracheal tube and successful transtracheal illumination also reliably predicts ET placement. [40] The clinician should be aware of the potential for vomiting following removal of a tube from the esophagus. Cricoid pressure should be applied during tube removal and maintained until intubation is successful. Alternatively, the first tube can be left in the esophagus to serve as temporary gastric venting until tracheal intubation is achieved. Suction must be readily available should vomiting occur. Although seldom associated with serious complications, unrecognized positioning of the ET tube tip in the right mainstem bronchus may cause hypoxia as well as unilateral pulmonary edema. [41] A chest radiograph should be taken shortly after the intubation to confirm tube positioning. Endobronchial intubation was clinically unrecognized without a chest film in 7% of prehospital intubations in one study. [42] Persistent asymmetrical breath sounds after correct tube positioning suggests unilateral pulmonary pathology (e.g., main stem bronchus obstruction, pneumothorax, or hemothorax). Prolonged efforts to intubate may also cause cardiac decompensation. Pharyngeal stimulation can produce profound bradycardia or asystole; when feasible, an assistant should follow the cardiac rhythm throughout the intubation. Atropine should be available to reverse vagal-induced bradycardia that may occur secondary to suctioning or laryngoscopy. Prolonged pharyngeal stimulation also may result in laryngospasm, bronchospasm, and apnea. Complications may also result from the application of cricoid pressure. Cricoid deformation is proportional to the force applied during the application of cricoid pressure. This deformation may result in expiratory obstruction in up to 56% of patients at 44 Newtons but only 2% at 30 Newtons. [43] However, BURP maneuvers may increase obstruction even at low pressure. One should check for loose or missing teeth before and after orotracheal intubation. Any avulsed teeth not found in the oral cavity warrant a postlaryngoscopy chest film to rule out aspiration of a tooth. Swallowed teeth are of no consequence. Broken teeth are the most common complication of laryngoscopy. [44] Laceration of the mucosa of the lips, especially the lower lip, may also occur. Tracheal or bronchial injuries are rare but serious, usually occurring in infants and the elderly as a result of decreased tissue elasticity. [45] Vomiting with aspiration of gastric contents is another serious complication that can occur during intubation. Case reports of both ARDS and chronic lung disease are thought to be due to the aspiration of activated charcoal. [46] [47] Patients who are obtunded, at risk for seizures, or vomiting should be considered for tracheal intubation before the administration of activated charcoal. Controversy exists regarding exacerbation of cervical spine injuries during orotracheal intubation in the trauma patient. A cadaveric study of intubation under fluoroscopy showed that the greatest degree of motion occurs at the
83
occiput-C1 junction and decreases with each sequential interspace. [48] Manual in-line immobilization did not significantly limit motion at any level in this study. Neither manual in-line immobilization nor traction significantly reduced motion at a surgically created ligamentous injury at the C4–C5 level. Complete immobilization of the cervical spine likely cannot be completely achieved by means readily available in the ED, but attempts should still be made to minimize movement with manual in-line stabilization and use of proper intubation technique. However, concern for a cervical spine injury should not deter the clinician from securing a patient's airway when clinically warranted. Exacerbation of a cervical spine injury remains largely a theoretical concern, while in contrast, inadequate ventilation and failure to adequately secure the airway occurs regularly in the emergency setting. Intubation may also be complicated by a persistent air leak. This is generally caused by failure of either the cuff or pilot balloons or by positioning the cuff balloon between the vocal cords. If the cuff balloon is leaking, the tracheal tube must be replaced (see Changing Tracheal Tubes later in this chapter). If the pilot balloon is determined to be leaking, however, this can usually be remedied without changing the tube. [49] An incompetent one-way balloon valve can be fixed by placing a stopcock into the inflating valve. Reinflation of the cuff followed by shutting off the stopcock should solve the problem. If the leak involves the pilot balloon itself, or if the distal inflation tube has been inadvertently severed, cut off the defective part and slide a 20-ga catheter into the inflation tube. Then connect the stopcock to the catheter, inflate the cuff, and close the stopcock. Tracheal stricture used to be a significant late complication of long-term intubation with low-volume high-pressure cuffs. The standard use of high-volume low-pressure cuffs has markedly decreased the incidence of this complication. [50] Tubes with high-pressure cuffs are obsolete and should be avoided. Summary
Orotracheal intubation is the primary method of definitive airway management. In the comatose patient, it is usually accomplished rapidly and without difficulty. The easy intubation is frequently successful in the hands of the novice; the difficult intubation often proves challenging even for the experienced clinician. Rapid-sequence induction has increased the use of orotracheal intubation as the first-line approach in various clinical situations and settings (see Chapter 5 ). Once the patient's breathing and protective reflexes are removed, however, the clinician has the supreme responsibility of safely reestablishing them. A mastery of the technique of orotracheal intubation is essential.
MODIFIED OROTRACHEAL INTUBATION Intubation with an Intermediate Airway in Place Esophageal Obturator/Gastric Tube Airway in Place
The unconscious patient requiring ventilatory assistance may benefit from temporary use of the esophageal obturator airway (EOA) or similar device, as described in Chapter 3 . Although the EOA may provide effective ventilation, it is, at best, a temporary measure. An ET tube generally provides more safe, convenient, and effective airway control. Therefore, the EOA should be replaced as soon as the patient's clinical condition permits and personnel skilled in ET intubation are available. Removal of the EOA from the esophagus often results in gastric regurgitation. Therefore, ET intubation must be performed around the EOA to protect the patient from aspiration. The process is begun by hyperventilating the patient through the EOA. The EOA mask is then removed, and the EOA tube is moved to the left side of the patient's mouth. Laryngoscopy and intubation are then performed in the usual fashion. The EOA balloon may cause resistance to passage of the tracheal tube, requiring the volume of the EOA balloon to be reduced. After passage of the orotracheal tube, the clinician deflates the EOA balloon completely and slides it out of the patient's esophagus. If resistance is met, the clinician must be sure that the esophageal cuff has been deflated completely. Esophageal-Tracheal Combitube (ETC) in Place
Combitubes placed in the esophagus will generally require replacement with a tracheal tube. The inflated pharyngeal balloon prevents tracheal intubation around this airway. This proximal balloon must be deflated before attempting tracheal intubation. If intubation is still not possible, the ETC may need to be removed; the stomach should first be emptied via a gastric tube placed through the esophageal port of the airway. Suction is readied, the distal balloon is deflated, and the patient is quickly intubated. Laryngeal Mask Airway in Place
The trachea can often be intubated with the laryngeal mask airway (LMA) left in place. The various approaches to intubation with an LMA in place are discussed in Chapter 3 (see Figs. 3-11 ). Bullard Laryngoscope A recent development for intubating the difficult airway is the Bullard laryngoscope, an anatomically shaped rigid fiberoptic laryngoscope that provides an indirect view of the larynx ( Fig. 4-13 ). Because no manipulation of the neck is necessary, it is especially well suited for the patient with potential cervical spine injury. Indeed, in the anesthetized patient, the Bullard laryngoscope has been found to cause less head extension and cervical spine extension than the conventional laryngoscope. [51] The addition of an intubating stylet attached to the laryngoscope has resulted in increased ease and speed of intubation, and the technique appears to be effective regardless of the patient's head and neck anatomy. [52] Because alignment of the oropharyngeal and laryngeal axes is not required, the Bullard laryngoscope offers the advantage provided by a conventional fiberoptic scope but requires less training to gain proficiency in its use. [53] Indications and Contraindications
The Bullard laryngoscope is indicated in patients with anticipated difficult airways who require definitive airway control. It can be used in awake as well as unresponsive patients. [54] Marked impairment of mouth opening is a contraindication to the use of a laryngoscope. However, because the Bullard laryngoscope follows the contour of the mouth and hypopharynx, only 2 cm of occlusal opening is necessary for the
84
Figure 4-13 Bullard laryngoscope. Anatomically shaped laryngoscope visualizing the glottis; tracheal tube is mounted on the attached stylet for easy tracheal passage. (Courtesy of Department of Emergency Medicine, Hennepin County Medical Center, Minneapolis, MN.)
introduction of the scope and an ET tube. The laryngoscope itself requires only 6 mm of mouth opening for insertion.
[55]
Procedure
The technique for introducing the Bullard laryngoscope blade is similar to that for direct laryngoscopy. The clinician, standing at the patient's head, opens the mouth with the left thumb while holding the head stable. As the scope blade is introduced into the oropharynx, the handle is rotated to follow the curve of the hypopharynx until the handle is fully vertical. The tip of the blade can be used to lift the epiglottis, but visualization of the larynx is usually possible without this maneuver. Only minimal force is exerted along the axis of the handle. Intubation of the larynx can be accomplished using a styletted ET tube or an ET tube with a directional tip (Endotrol; Mallinckrodt, Critical Care, Glens Falls, NY). The technique is generally successful when using the new Bullard intubating stylet. [52] Awake intubation using the Bullard laryngoscope can be performed comfortably using topical anesthesia and light IV sedation. [54] Adult and pediatric Bullard laryngoscopes are available, and the scope has been used successfully in neonates. [53] The Bullard scope can also be used in conjunction with nasotracheal intubation to visualize proper tube placement. Complications
The major difficulty in using the Bullard laryngoscope is the inability to visualize the larynx because of blood, emesis, or secretions. Another reason for failure is the inability to place the blade tip under the epiglottis. [52] Summary
The Bullard scope is useful in the difficult airway uncomplicated by blood and excessive secretions. In the all-too-common setting of blood and secretions, however, the inability to visualize the vocal cords significantly limits the utility of this device in emergency airway management.
NASOTRACHEAL INTUBATION Nasotracheal intubation was first described by Magill in the 1920s. The tube may be placed blindly or with the aid of a laryngoscope or bronchoscope. Blind nasotracheal intubation can be one of the more technically demanding airway approaches, with the outcome being heavily dependent on the skill and experience of the clinician. The primary advantage of the blind technique is that it minimizes neck movement and does not require opening the mouth. General Indications and Contraindications Nasotracheal intubation is technically more difficult than oral intubation, but it has definite advantages. It is especially suitable for the patient with a short, thick neck or other anatomic characteristics that would make orotracheal intubation difficult. It also requires minimal preparation. Blind nasotracheal intubation is possible with the patient in the sitting position, a distinct advantage when intubating the patient with congestive heart failure who cannot tolerate lying flat. In fact, patients in respiratory distress are the easiest to intubate blindly because their air hunger results in increased abduction of the vocal cords, which facilitates tube entry into the trachea. A nasotracheal tube has advantages that extend beyond the immediate difficulties of airway control. The patient cannot bite the tube or manipulate it with the tongue. Oral injuries may be cared for without interference by the tube. A nasotracheal tube is more easily stabilized and generally easier to care for than an orotracheal tube. It is better tolerated by the patient, permitting easier movement in bed, and produces less reflex salivation than do oral tubes. Nasal intubation should be avoided in patients with severe nasal or midface trauma. In the presence of a basilar skull fracture, a nasotracheal tube may inadvertently enter the cranial cavity. [56] The technique should be avoided in patients in whom thrombolytic therapy is being considered. Nasal intubation is relatively contraindicated if the patient is taking anticoagulants or is known to have a coagulopathy. Because the sound of air passing though the vocal cords guides proper tube placement, nasotracheal intubation is not recommended in patients without spontaneous respirations. Blind Placement Blind nasotracheal intubation is the most common form of nasotracheal intubation in the emergency setting. Danzl and Thomas reported a success rate of 92% in a large series of ED patients, but success rates are highly dependent on clinician skill. [57] Indications and Contraindications
Any patient requiring airway control who has spontaneous respirations is a candidate for blind nasotracheal intubation. Specific indications that favor this approach over others are (1) short, thick neck, (2) inability to open the mouth, (3) inability to move the neck, (4) gagging or resisting the use of the laryngoscope, and (5) oral injuries.
85
Apnea is the major contraindication to blind nasotracheal intubation. Attempts to place the tube without respirations as a guide are futile. Relative contraindications include basilar skull fracture and nasal injury. [56] [58] Furthermore, significant bleeding may occur if the patient is receiving anticoagulants or has a coagulopathy. Blind nasotracheal intubation should be avoided in patients with expanding neck hematomas. Patient combativeness, if not controlled with sedation, is also a contraindication. Some would argue that inability to open the mouth is a relative contraindication, because emesis may be induced and the vomitus could not be cleared. The clinician must exercise judgment in the individual case and be prepared to use neuromuscular blocking agents or bypass the upper airway with a surgical technique if such a complication develops. Procedure
The patient is placed in the "sniffing" position with the proximal neck slightly flexed and the head extended on the neck. In preparation for intubation, the clinician constricts the nasal mucosa of both nares, using either 0.25% to 1.0% phenylephrine drops, oxymetazoline (Afrin) spray, or 4% cocaine spray. Topical anesthesia of the nares, oropharynx, and hypopharynx with lidocaine spray (10%) is also indicated if time permits. If available, cocaine is ideal because it is both a vasoconstrictor and an anesthetic—caution is necessary in hypertensive patients. The most patent nostril is chosen. In the cooperative patient, this can be determined simply by occluding each nostril and asking the patient which one is easier to breathe through. The most patent nostril can also be identified by direct vision, or by gently inserting a gloved finger lubricated with viscous lidocaine, full length into the nostrils. If time is not an issue, an effective method to dilate the nasal cavity and administer the anesthetic is to pass a lidocaine gellubricated nasopharyngeal airway (nasal trumpet) into the selected nostril. This airway is left in place for several minutes, and progressively larger trumpets are introduced. After preparation of the nostril, a well-lubricated 7.0 or 7.5 ET tube is inserted along the floor of the nasal cavity. The tube is not directed cephalad, as one might expect from the external nasal anatomy, but rather is directed straight back toward the occiput, along the nasal floor. Twisting the tube may help bypass soft tissue obstruction in the nasal cavity. It is sometimes recommended that the tube's bevel be oriented toward the septum to avoid injury to the inferior turbinate. However, such an event is rare. At 6 to 7 cm, one usually feels a "give" as the tube passes the nasal choana and negotiates the abrupt 90° curve required to enter the nasopharynx. This is the most painful and traumatic part of the procedure and must be done gently. If resistance persists despite continued gentle pressure and twisting of the tube, the passage of a suction catheter down the tube and into the oropharynx may allow for successful passage of the tube over the catheter. [59] If this fails, the other nostril should be tried. In an attempt to avoid this difficulty from the outset, a controllable-tip tracheal tube (Endotrol, Mallinckrodt Medical Inc, St Louis) may be used. The tube allows the clinician to increase the flexion of the tube, facilitating passage past this tight curve. One study found that the Endotrol tube enhanced first-attempt success with blind nasotracheal intubation. [60] A study of paramedic-performed blind nasotracheal intubation reports success rates of 58% using standard ET tubes versus 72% success with directional tip control ET tubes. [61] As the tube advances through the oropharynx and hypopharynx and approaches the vocal cords, breath sounds from the tube become louder and fogging of the tube may occur. At the point of maximal breath sounds, the tube is lying immediately in front of the laryngeal inlet. The tube is most easily advanced into the trachea during inspiration, when the vocal cords are maximally open. As the patient begins to breathe in, the tube is advanced in one smooth motion. If a gag reflex is present, the patient usually coughs and becomes stridulous during this maneuver, suggesting successful tracheal intubation. The absence of such a response should alert the clinician to probable esophageal passage. If there is a delay in advancing the tube, oxygen can be added to the end of the tube to increase inspired oxygen. Once the tube is in the trachea, vocalization should cease. Persistent vocalizations suggest esophageal intubation. Breath sounds coming from the tube and tube fogging are other signs of ET placement. Reflex swallowing during blind nasotracheal intubation may direct the tube posteriorly toward the esophagus. If this occurs, the conscious patient should be directed to stick out the tongue to inhibit swallowing and prevent consequent movement of the larynx. Application of laryngeal pressure may also help avoid esophageal passage. Following intubation, both lungs are auscultated while positive-pressure ventilation is applied. If only one lung is being ventilated, the tube is withdrawn until breath sounds are heard bilaterally. The optimum distance from the external nares to the tube tip is about 28 cm in males and 26 cm in females. [62] After verification of tracheal placement, the cuff is inflated and the tube is secured.
Technical Difficulties
The nasotracheal tube may slide smoothly through the hypopharynx and into the trachea on the first pass. Unfortunately, this is not always the case; in an operating room series, the first attempt was successful in 15% change in respiratory rate, heart rate, or blood pressure), oxygen desaturation of 0.6. [7] PEEP is used to increase functional residual capacity (FRC) and move the zero pressure point of each alveolar unit more proximal in the airway so as to prevent early alveolar collapse. [8] By so doing, PEEP increases the available number of alveolar units that can participate in gas exchange. The
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primary effect of PEEP on gas exchange, however, is to improve oxygenation, not CO 2 removal. CO2 clearance is rather efficient and will be well preserved in situations where oxygenation is not. By opening one alveolar unit, the tendency of the adjacent unit is to open as well (i.e., alveolar codependency; Fig. 8-1 ). [9] Excessive PEEP will compromise hemodynamics. Therefore, there are two primary questions to ask when using PEEP to augment oxygenation: What is the "optimal PEEP," and is the current amount of PEEP compromising the patient's hemodynamics? There are several ways to determine the "optimal PEEP." One way is to increase the PEEP until there are no longer increases in the pO 2 . This method, however, may result in several untoward events. First, oxygen tension may steadily increase, but pCO 2 may increase as well from alveolar overdistension. With overdistension, the alveolar pressure may exceed pulmonary arteriolar pressure and actually decrease pulmonary blood flow and CO 2 clearance. Second, alveolar overdistension may increase total intra-thoracic pressure and therefore diminish venous return and hence cardiac output. Third, decreased venous return may result in cerebral venous hypertension as indicated earlier. The "optimal PEEP" for one organ system may be deleterious for another. For example, the optimal PEEP for ideal oxygenation may be the worst PEEP for cerebral venous drainage. A better method of determining the "optimal PEEP" relies on measuring oxygen delivery and oxygen consumption. PEEP may be increased until there is no further increase in oxygen delivery, and no increase in oxygen consumption. [10] This method does require a pulmonary artery catheter to be in place for determination of ?DO 2 and ?VO 2 . In many institutions, the application of PEEP above 10 cm H 2 O pressure in a
Figure 8-1 Alveolar interdependence. Note that alveoli are not round in shape; instead, they are polygons. Polygons have corners and may have two opposing surfaces that may adhere to one another via surface tension. Surfactant works to reduce this surface tension and allow alveoli to open with reduced shear stress at the junction of closed and open alveoli. Alveoli are connected via the pores of Kohn. This allows opening alveoli to pull a relatively closed alveolus open while equalizing pressure between adjacent alveoli. The central alveolus on the right is fairly closed in the upper diagram, but is pulled open by its neighbors as they expand and accept gas.
multiply injured patient necessitates a pulmonary artery catheter being placed to make such determinations regarding oxygen extraction. An alternative is to increase PEEP until a complication of PEEP occurs (e.g., pCO 2 elevation, hypotension), and then reduce PEEP if needed (inability to tolerate hypercapnia), or expand the patient's intravascular volume to combat decreased venous return. The authors favor the placement of a pulmonary artery catheter in these situations to accurately guide therapy and know the patient's ?DO 2 and ?VO 2 status. Another excellent method of determining the "optimal PEEP" is guided by assessing changes in plateau pressure with changes in PEEP. As PEEP is increased from a minimal level, the patient's peak airway pressure as well as plateau pressure will increase by the amount of the applied PEEP. However, when the "optimal PEEP" for the lung units is achieved, the plateau pressure will no longer increase; in fact, as the lung is optimally recruited, the peak and plateau pressure may decrease as there is more volume of lung available to receive a set V T . Once this level is exceeded, however, there will be further increases in plateau pressure beyond the incremental increase in PEEP as the units overdistend. Therefore, the clinician must readily identify the plateau in the plateau pressure trend. The same relationship may be displayed graphically in the dynamic pressure-volume loop ( Fig. 8-2 ). The lower limb of the loop represents the pressure required to open the alveolar units.[11] In the absence of PEEP (or inadequate PEEP), this limb is prolonged and flattened and has an inflection point far to the right of the origin of the loop ( Fig. 8-3 ). As PEEP is progressively increased, the inflection point travels to the left. When the "optimal PEEP" is achieved, there will be a rapid upstroke of the loop as the vast majority of the functional lung units are already open and ready to be ventilated (see Fig. 8-2 ). This strategy is known as the "open lung model" of MV. [11] PEEP is not without untoward side effects, and increased levels of PEEP can lead to hemodynamic compromise. [12] This occurs from increased intrathoracic pressures leading to cardiac compression and collapse, principally of the right
Figure 8-2 Dynamic pressure-volume loop. Note that as soon as there is delivered pressure to the airway, there is an increase in measured tidal volume. The lower arrow denotes inspiration while the upper arrow indicates exhalation. This indicates that the airways are open and do not need to be forced open by increasing the pressure in the airway. If this latter case were true, then the P-V loop would initially be flat along the X-axis.
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Figure 8-3 Inadequate PEEP and the P-V loop. Compare this curve to that in Figure 8-2 . Note that the loop is initially flat (lower segment) along the X-axis. Once the airway pressure is high enough to open the alveolar units, each increase in airway pressure is matched by a corresponding increase in tidal volume.
atrium. It is imperative that the patient be adequately resuscitated as volume depletion compounds this problem. Desired levels of PEEP simply may not be possible because of deleterious effects on cardiac output. Pressure Support Ventilation (PSV).
This mode augments spontaneous ventilation in the IMV/SIMV and CPAP modes. There is gas flow during inspiration for each spontaneous breath to help the patient overcome the resistance of the circuit and to achieve an acceptable V T . The range is from 0 up to 35 cm H2 O pressure; some ventilators may deliver PSV that achieves a greater range. The average starting point is 10 cm H 2 O. PSV is adjusted as needed so that the spontaneous V T approximates the set VT for mandatory breaths. Patients placed on the combined mode of CPAP/PSV must be spontaneously breathing. PSV-based ventilation must never be combined with neuromuscular blockade agent therapy, or death from apnea, hypercarbia, and hypoxia will result. PSV is commonly used to aid in weaning from IMV-based ventilation and is frequently part of a transition strategy from IMV to CPAP. [13] In this way, PSV is used to eliminate the work of breathing improved by the ETT and the ventilator tubing. The required amount of pressure support to overcome the tube-induced resistance has been well documented ( Table 8-1 ). [14] It is imperative not to lower the PSV during weaning below that required to overcome the resistance imposed by the diameter of the ETT or tracheostomy tube as the work of breathing may precipitously rise. Unlike AC or SIMV, PSV does not have a preset T i . In fact, the time at which the gas flow terminates for each PSV breath is determined by an algorithm that in most older ventilators is not manipulable. For instance, a patient breathing on CPAP/PSV on a Puritan-Bennett 7200 ventilator would have his or her maximal inspiratory flow required to achieve the set pressure support level measured. As the patient's airways progressively fill with gas, the patient draws in gas at a slower rate, and the machine needs less of a flow rate to maintain the airway pressure. When the machine flow rate decreases to 25% of the previously measured maximal inspiratory flow rate, all gas flow ceases. This termination occurs whether the patient is done inspiring or not. This algorithm may lead to significant patient-ventilator dysynchrony. [15] Newer ventilators, such as the Hamilton Gallileo, allow user adjustment for such dyssynchrony. A common resolution using such a PSV device is either patient sedation or an increased level of pressure support so that the patient receives his or her desired amount of gas before gas flow termination. Inspiration:Expiration (I:E) Ratio.
The normal I:E ratio in a spontaneously breathing, nonintubated patient is 1:4. [14] Intubated patients commonly achieve I:E ratios of 1:2. Shorter ratios may lead to
decreased exhalation by compromising exhalation time (T e ). In its extreme form, inverse ratio ventilation (IRV), the normal pattern of breathing is reversed. There is a longer time spent in inhalation to allow a longer time for oxygenation. Longer inspiratory times allow for better matching of alveolar regional time constants. [16] The decrease in expiratory time can lead to air trapping, elevated airway pressures, and rising pCO 2 . These problems lead to hypercapnia, respiratory acidosis, and auto-PEEP. [16] Auto-PEEP is additional pressure that is generated within the airways from trapped gas that should have been exhaled, but for various reasons (commonly obstruction to exhalation such as COPD), was not. Auto-PEEP can cause hemodynamic instability secondarily to decreased venous return just like high levels of PEEP. [17] Auto-PEEP may be detected in two ways: (1) evaluating the flow-time trace or (2) disconnecting the patient from the ventilator and listening for additional exhaled gas after an exhalation has already occurred. [11] The flow-time trace will demonstrate that the exhalation is not yet completed before the next breath has been initiated ( Fig. 8-4 ). Auto-PEEP is a real potential when one initiates IRV for the management of hypoxemic respiratory failure. One can initiate IRV most easily in pressure cycled ventilation (PCV) where the operator sets the T i directly. With VC ventilation, one can achieve a similar gas delivery by adjusting the flow rate of each breath to adjust the I:E ratio; that the Q needs to be adjusted on a breath-by-breath basis makes this impractical. ?Q.
This is the rate of gas delivery (L/min). The range of flows that can be achieved by current ventilation is from 10 to 160 L/min. Common flow settings are from 40 to 75 L/min. The higher the rate, the faster the ventilator will reach its set volume or pressure. A faster rate allows for a longer exhalation time, but due to the shortened inspiratory time, hypoxia can result. A slower rate allows for longer time in inhalation and improved oxygenation but a shortened expiratory time, which may lead to retained CO2 and auto-PEEP from inadequate Te ( Fig. 8-5 ). Waveforms Square.
Once the maximal inspiratory ?Q is achieved, the gas flow is constant until the set volume is delivered. When that point is reached, the gas flow is terminated. This waveform is best for patients with COPD and those suffering from head injury because gas delivered with this waveform allows for a longer T e and lower mean airway pressure (Paw -mean). The longer T e is beneficial for patients with restrictive airway disease such as COPD. Spending a longer time in exhalation allows for improved venous drainage from the brain. The drawback to this waveform is an increased P aw -peak, often requiring a lower V T or ?Q. This can lead to inadequate alveolar recruitment in patients with acute lung injury. Decelerating (Ramp).
Once the maximal inspiratory flow is reached, the rate of gas delivery immediately begins to slow in a preprogrammed fashion. Therefore, relative to the
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Type of Ventilation
TABLE 8-1 -- Initial Ventilator Settings Comments
Volume Cycled Ventilation (volume set, pressure varies) Mode: SIMV
If patient is paralyzed: IMV = AC ventilation
Rate: 10–12/min
Target normal ?VE
VT : no acute lung injury: 10 mL/kg acute lung injury or ARDS: decrease V T : 6–7 mL/kg
Increased survivorship in ARDS with decreased V T ventilation
FIO2 : 0.4–0.95
Titrate to pO2 > 60 mm Hg
PEEP: 5–20 cm H2 O pressure
Titrate to pO2 > 60 mm Hg and FIO2 = 0.6
PSV: 10–35 cm H2 O pressure
Target VT spont = VT set
Waveform: decelerating ramp
Use square wave form in COPD only
Peak Airway Pressure: 35 cm H 2 O associated with lung injury
Sigh: 0–2/min
Optional—use with decreased respiratory rate to maintain alveolar recruitment
Temperature: 35°C
Not efficacious in rewarming or cooling
Flow Rate (?Q): start at 60 L/min (range 45–75)
Titrate to Paw -peak and pO2 Decrease ?Q for hypoxemic patients Increase ?Q for patients with air hunger
Pressure Cycled Ventilation (pressure set, volume varies) Mode: SIMV
If patient is paralyzed: IMV = AC
Rate: 10–12/min
Decrease rate to allow longer time to exhale and to increase CO 2 clearance
PC: 2/3 of prior peak airway pressure or prior plateau pressure
Titrate to peak airway pressure-V T curve (hysteresis curve)
Ti : start at 2 sec and increase to increase mean airway pressure and pO 2
Increased T i will lead to IRV: will need heavy sedation and/or paralysis
FIO2 : 0.4–0.95
Titrate to pO2 > 60 mm Hg
PEEP: 5–20 cm H2 O pressure
Titrate to pO2 > 60 mm Hg and FIO2 = 0.6
PSV: 10–35 cm H2 O pressure
Target VT spont = VT set
Waveform: decelerating ramp
Use square wave in COPD only
Temperature: 35°C
Not efficacious in rewarming or cooling
Note: 1. Use inspiratory time cycled PVC to precisely control I:E ratio. IRV is used to manage hypoxia but may lead to hemodynamic instability owing to decreased venous return and decreased cardiac output. 2. Best to titrate ventilator settings to the shape of the pressure-volume curve (need ventilator with a graphics package, a.k.a. "open lung model"). Special Circumstances 1. Severe acute lung injury—consider permissive hypercapnia. If able to achieve pO 2 > 60 mm Hg on FIO2 = 0.6, the pCO2 may be allowed to be >40 mm Hg if pH > 7.25. Further attempts to raise ?VE to decrease pCO2 may induce additional lung injury.
2. Asthma—defect is decreased gas flow. In conventional ventilation use higher flow rate and lower respiratory rate to allow more time for exhalation. 3. Traumatic brain injury—Do not lower pCO 2 < 35 mm Hg, as it may induce severe cerebral vasoconstriction and lead to cerebral ischemia. The goal is normal pCO : 35–40 mm Hg. Acceptable to hyperventilate for a patient with an acute herniation syndrome as a bridging maneuver for definitive therapy.
2
4. PEEP—used to raise alveolar recruitment and increase pO 2 in patients with hypoxemic respiratory failure. Caution: excessive PEEP can lead to hypotension from diminished venous return. Initial treatment of this hemodynamic instability is with volume replacement and lowered PEEP if possible. AC, assist control; ARDS, acute respiratory distress syndrome; FIO2 , percent of inspired oxygen; I:E, inspiratory:expiratory; IMV, intermittent mechanical ventilation; IRV, inverse ratio ventilation; MAP, mean arterial pressure; Paw -peak, peak airway pressure; PEEP, positive end-expiratory pressure (5 cm H 2 O is considered physiologic); PSV, pressure support ventilation; PC, pressure control (setting); ?Q, flow rate; SIMV, synchronized intermittent mechanical ventilation; Ti , time in inspiration; ?VE , minute ventilation; VT , tidal volume. square waveform, longer time is spent in inhalation to deliver the set V T or achieve the target pressure, which allows for improved oxygenation. This waveform also achieves a lower Paw -peak and higher Paw -mean. Sine Wave.
Not useful in critically ill patients. Accelerating.
This is the flow pattern for neonatal gas intake and is generally not used in adult ventilation unless one must use the Siemens Servo 900 ventilator, which has only two options: square or accelerating. Sighs.
This is a large single breath or large multiple breaths, both designed to help maintain alveolar recruitment by ventilating a patient on a periodic basis at close to vital capacity. There is controversy regarding the utility of the sigh option with regard to alveolar overdistention. [18] Pause.
This is a variable used on the Siemens Servo 900 ventilator to alter the I:E ratio. This is technically complex for anyone not working with ventilator setup on a daily basis. It is much easier to directly adjust the T i /Te on more modern ventilators. A pause is useful to determine the Plateau Pressure on the Puritan Bennett 7200 or the Infrasonics Adult Star ventilator (as a point measurement). If a short pause is used to measure plateau pressure, the authors suggest no
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Figure 8-4 Identifying auto-PEEP with the flow-time trace. The X-axis is time while the Y-axis is flow rate in L/min. Deflections above the X-axis indicate inspiration, while deflections below represent exhalation. In this example, the flow pattern is ramp (decelerating). Note that as the respiratory rate increases (decreased time for exhalation), the flow has not yet returned to baseline (a), indicating incomplete exhalation when compared to the following breath (b).
longer than 0.5 seconds as the pause duration; remove the pause when the measurement is completed.
NEW MODES Airway Pressure Release Ventilation (APRV) APRV is essentially a high level CPAP mode that is terminated for a very brief period. The CPAP level may be as high as 40 or more cm H 2 O pressure. The long time during which the high-level CPAP is maintained achieves oxygenation while the short release period achieves CO 2 clearance ( Fig. 8-6 ). The long time during which the high-level CPAP is present results in substantial recruitment of alveoli of markedly different regional time constants at rather low gas flow rates and lower airway pressures (by comparison with conventional ventilation strategies). The establishment of
Figure 8-5 Effect of flow rate on inspiratory and expiratory times. Note that as the flow rate changes, there are corresponding alterations in the effective time for inspiration and exhalation. Deflections above the X-axis (time) indicate inspiration, while those below indicate exhalation. The delivered tidal volume for each cycle is the same, but the inspiratory and expiratory times are different.
intrinsic PEEP by the short release time enhances oxygenation. CO 2 clearance is aided by recruitment of the patient's lung at close to total lung capacity (TLC); elastic recoil creates large-volume gas flow during the release period. This is a fundamentally different mode from cyclic ventilation. This mode allows the patient to spontaneously breathe during all phases of the cycle. This mode is enabled to succeed by having a floating valve that is responsive to the patient's needs regardless of the location within the respiratory cycle. In other words, the patient is allowed to breathe in or out during the high-level CPAP phase as well as during the release phase. Accordingly, the sequence is called a phase cycle; there is no set inspiratory or expiratory time, and no readily identifiable respiratory rate in the traditional sense. During the high-CPAP phase, a patient may exhale 50 to 200 or more mL of gas as his or her lung volume becomes full of gas; this is not a full exhalation and the release of excess gas should not be counted as a breath. Given the spontaneous nature of the mode, there should be virtually no need for continuous infusions of neuromuscular blocking agents in patients placed on this mode of ventilation[19] ; exceptions to this observation do occur for the management of ICP but not for oxygenation or clearance of CO 2 . This may result in a shorter length of ICU stay and a reduced incidence of prolonged neuromuscular blockade syndrome. Furthermore, since patients may be ventilated at lower airway pressures than using cyclic ventilation, there is a reduced need for pressor support of hemodynamics to ensure oxygen delivery. [19] Moreover, there is a reduced sedative need as patients are more comfortable on this spontaneous mode than on cyclic ventilation. [19] Hemodynamic assessment using a pulmonary artery catheter in patients on APRV has been investigated. The pulmonary artery occlusion pressure (PaOP) must be read at the middle or end of the release phase to maintain the fidelity of the reading. Reading the PaOP at any other point in the cycle will give a significantly different value by comparison with the end expiratory reading obtained using pressure-cycled ventilation. [20] Transport of patients on APRV with a P aw -high (sustained peak P aw ) > 20 cm H2 O pressure should be with the patient attached to the ventilator instead of being hand ventilated. [21] Hand ventilation is unable to match the manner of gas delivery and pressure dynamics that the patient requires. Attempts at hand ventilation, even with an appropriately set PEEP valve, are frequently complicated by unexpected hypoxemia and hemodynamic instability. Proportional Assist Ventilation Ventilators that are capable of performing in this mode will be able to assess on a breath-by-breath basis how much work of breathing support the patient needs to achieve the targets and goals that the clinician sets. [22] The unique features of this type of ventilation promise to reduce inadvertent airway injury, and, in many ways, serve as a self-weaning ventilator mode. As the patient requires less support, the ventilator delivers less support. Current data are lacking to determine if this will realize a shortened length of ventilator support for those with acute respiratory failure. Permissive Hypercapnia As stated, excessive P aw -peak may be quite detrimental. One means of limiting P aw -peak, and thereby offer protection from
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Figure 8-6 Airway Pressure Release Ventilation (APRV)—airway pressure-time and flow-time traces. Note that the peak airway pressure (P aw -high) is maintained for a long period. This phase establishes oxygenation (Thigh ). There is a short period of release when most CO 2 is cleared (Tlow ). Note that the bottom trace is flow over time. The combined time for the T high and Tlow is known as a phase cycle. Note that the number of phase cycles is not the respiratory rate as patients breathe within the entirety of the T high . As the release phase is initiated, the flow rate is identified as negative and is of a high rate (here approximately 7.5 L/min), consistent with significant alveolar recruitment. During the high CPAP phase, the patient is allowed to exhale (negative deflections on the flow-time trace). Thus, APRV is quite dissimilar from traditional cyclic ventilation. This unique mode is made possible by a floating valve system.
the trauma of ventilation, is to decrease the delivered V T until an acceptable and less deleterious P aw -peak is achieved (=35 cm H 2 O). However, changes in Paw -peak may alter the pH-pCO 2 balance. If the pH is =7.25, and the patient can tolerate the elevated pCO 2 while still remaining well oxygenated, then the ?V E is not increased. Alternatively, the f may be decreased in similar fashion, but usually not 20 mm Hg can be detrimental in patients suffering from head injury or cerebral ischemia. [27] In patients with acute lung injury complicating traumatic brain injury or stroke, such a management strategy is optimally accompanied by a measure of cerebral perfusion to evaluate for hyperemia, or ICP monitoring to assess for intracranial hypertension from increased CO 2 tension. [28] Hypercapnia also shifts the oxyhemoglobin dissociation curve to the right, leading to increased early unloading of O 2 at the tissue level. Hypercapnia also creates an acidosis that may initiate myocardial depression, dysfunction of pH dependent enzyme kinetics, and distorted cellular metabolism. [29] Severe acidosis, pH 35 cm H2 O) commonly leads to alveolar overdistention and injury, causing release of inflammatory mediators and complications including pneuomothoraces, pneumatoceles, pulmonary interstitial emphysema, pneumomediastinum, acute lung injury and acute respiratory distress syndrome (ARDS). The peak airway pressure and alveolar overdistension are best evaluated using the pressure-volume curve, looking to abrogate any increases in airway pressure that are not accompanied by increases in delivered volume ( Fig. 8-8 ). Increases in airway pressure without accompanying increases in V T lead to a plateau of the P-V curve, known as the "bird's beak" profile. This profile is a reasonable indicator of alveolar overdistension and airway injury. Plateau Pressure.
This is the pressure reflected from the airways once the full set volume or targeted pressure change has been achieved. It is a reflection of pulmonary compliance, airway resistance and elastance. It is not directly manipulable, but may be impacted by V T , ?Q, PCV, Ti , and PEEP. It does provide a basis for the initiation of other modes of ventilation and is quite useful in that regard (see APRV earlier). Mean Airway Pressure (Paw -mean).
The area under the pressure-over-time curve ( Fig. 8-9 ) may be calculated and represents the mean airway pressure. The P aw -mean correlates most closely with the achieved pO 2 in volume-cycled or pressure-cycled ventilation modes. The longer the T i , the greater the P aw -mean. When a patient has hypoxemia and the clinician wants to change the ventilator orders, it is important to not reduce the Paw -mean as a result of the change in therapy since a decreased P aw -mean consistently leads to a decrease in pO2 .
Figure 8-8 Alveolar overdistension is reflected in the increase in airway pressure without any concomitant increase in tidal volume. This pressure-volume curve pattern approximates a "bird's beak" profile.
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Figure 8-9 Mean airway pressure and the pressure-time trace. Note that the greater the maximum airway pressure and the longer the T i , the greater the area under the curve (AUC) described by the positive-pressure (inspiratory) limb of the respiratory cycle. The increase in mean airway pressure (area under the curve) is the principal correlate of oxygenation in volume or pressure-cycled ventilation.
COMPLICATIONS OF MECHANICAL VENTILATION Pneumothorax.
Pneumothorax unassociated with thrauma in a mechanically ventilated patient typically stems from alveolar overdistension (continuous or episodic) that leads to alveolar rupture and escape of gas into the pleural space. [36] Patients on positive-pressure ventilation should have their pleural space drained to prevent progression to a tension pneumothorax with hemodynamic compromise. Loculated pneumothoraces may be successfully drained percutaneously under ultrasound or CT guidance. Successful drainage of airspace disease leads to enchanced liberation from MV. [23] Pneumothorax or tension pneumothorax may also result from aggressive and incorrectly performed bag-valve-mask ventilation. Patients with intrinsic lung disease such as COPD or asthma are more prone to pneumothorax than the average patient due to the abnormal structural integrity of their alveolar air spaces. [37] A simple pneumothorax may be drained by surgical tube thoracostomy with a small-bore tube (24 French [Fr]), a commercially available pneumothorax kit (Arrow), or a pigtail catheter placed into the pleural space using the Seldinger technique (see Chapter 10 ). Each of these catheters should be placed to a chest drainage collection unit that incorporates a water seal chamber as well as a variable suction control. Persistent airleaks initially require continuous suction (usually 20 cm H 2 O suction) to evacuate the pleural space and promote coaptation of the visceral and parietal pleurae. Reduction of suction and placement on water seal alone follows the resolution of the air leak. Chest tube removal may proceed directly from water seal if there is no pneumothorax on chest film, or may follow a test period of tube clamping and subsequent radiographic evaluation. The authors favor a 4-hour period of clamping as a recurrent pneumothorax is easily treated by unclamping a tube instead of placing a new one. Not all patients with a pneumothorax require invasive techniques to evacuate air from the pleural space. It is important to recognize that small pneumothoraces occurring in spontaneously breathing patients (i.e., negative-pressure ventilation) may be reevaluated in 4 to 6 hours with a repeat CXR, and drained only if they are expanding. This option is not advised for patients on any form of positive-pressure ventilation as a simple pneumothorax may rapidly become a tension pneumothorax with subsequent hypotension and death. Tension pneumothoraces may be recognized by tachycardia, hypotension, elevated P aw -peak (if mechanically ventilated, tachypnea if not), jugular venous distension (if not intravascularly depleted), thoracic resonance by percussion on the affected side, diminished or absent breath sounds on the affected side, and tracheal deviation away from the affected side. Clearly, not all signs or symptoms are present in all patients and treatment is dictated by the patient's clinical condition. Certain patients develop loculated pneumothoraces or fluid collections. If the collections are either single or immediately adjacent to one another and readily identified, they may be drained using ultrasound guidance at the bedside. [38] However, the loculations are frequently in inaccessible areas, or are difficult to image with ultrasound. Therefore, CT scanning of the thorax provides precise anatomic definition of the presence and number of loculated collections, as well as a guide for the interventional radiologist. The authors have successfully used CT-guided drainage of loculated pleural collections (air and fluid) to assist weaning of head-injured patients from mechanical ventilator support. [23] Biotrauma.
This term refers to the self-sustaining process of lung injury from MV that follows alveolar overdistension or rupture, alveolar hypoperfusion, and repetitive shear stresses across alveolar walls. Originally this problem was thought to be from too much pressure (barotrauma). [39] Current principles hold that elevated airway pressures are a straightforward reflection of excess volume delivered to a lung that cannot accept that much gas (i.e., volutrauma: excess volume is delivered). [13] When this process is active in a patient on MV, it is termed volume induced lung injury. Lung injury is an inhomogeneous process with areas of normal lung immediately adjacent to quite diseased and injured segments. [40] Thus, the healthy and compliant segments with shorter regional time constants will readily accept gas, while their neighbors with reduced compliance and longer regional time constants will not. The end result is overdistension of the compliant segments, alveolar injury, and the liberation of inflammatory cytokines, chemokines, and activation of endothelin and arachidonic acid pathways, as well as the expression of adhesion molecules along the vascular endothelium. [4] This leads to infiltration of inflammatory cells, their destructive lysosomal enzymes, and the induction of toxic oxygen metabolites. Avoiding this inflammatory cascade is an intelligent means of protecting a patient's lungs from volume induced lung injury. Such a notion has given rise to lung-protective ventilator strategies based on the low tidal volume ventilation (6 to 7 mL/kg body weight). Hemodynamic Compromise.
In all circumstances, the volume of venous return exactly matches the cardiac output volume. Any process that impedes venous return will decrease the available volume that establishes cardiac output. For patients on positive-pressure ventilation, each gas delivery increases the intrathoracic pressure while exhalation decreases that pressure. Therefore, venous return principally occurs during exhalation. If the ventilator orders are constructed in such a way as to lead to increased intrathoracic pressure during exhalation, then venous return will be
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reduced. Variables that can lead to this circumstance are increased PEEP, auto-PEEP, and inverse ratio ventilation. Recall that venous return depends not only on a relatively negative pressure within the thoracic cavity, but relies on a sufficient amount of time for flow into the thoracic vasculature and right side of the heart. Thus, significantly high respiratory rates may compromise venous return as well. An additional untoward side effect of impaired venous return is cerebral venous hypertension from impeded venous drainage. Since there are no valves between the cerebral parenchyma and the right atrium, increased pressure on the right atrium reduces cerebral venous flow and may contribute to cerebral ischemia in patients with traumatic brain injury or stroke, especially in the patient with compromised systemic hemodynamics. Such patients are prone to watershed infarction; cerebral venous hypertension may increase this risk. Ventilator Associated Pneumonia.
The association between the duration of endotracheal intubation and the promotion of pneumonia is quite clear. In fact, the likelihood of developing a pneumonia is four times greater for patients in a surgical ICU than those in a medical ICU. [41] Endotracheal intubation for >12 hours increases the risk threefold. [41] Early pneumonias (72 hours) typically stem from nosocomial pathogens that may be resistant to community antibiotics. [42] Such patients need to have empiric coverage for Pseudomonas, methicillin-resistant Staphylococcus aureus (MRSA), and the other SPACE microbes (Serratia, Pseudomonas, Acinetobacter, Citrobacter, and Enterobactericiae). Empiric coverage for fungi are not warranted except in special circumstances (recrudescent pneumonia in a patient already on broad-spectrum antibiotics for >7 days with negative cultures; solid organ transplant patient after implanatation for >4 months; poly-site positive fungal cultures or fungemia). Unequivocally, clinical estimation of pneumonia is correct at best 33% of the time. [43] The most sensitive and specific test to diagnose pneumonia in a patient with a radiographic infiltrate, fever, leukocytosis, and purulent secretions is bronchoscopy and bronchoalveolar lavage with quantitative cultures. [44] This strategy provides strong evidence of the exact pathogen(s), eliminates treating nonpathogenic microbes that are upper airway colonizers, and provides confidence in withholding antibiotic for the diagnosis of "no pneumonia," as many other diagnoses can present with a similar clinical picture ( Fig. 8-10 ). Nosocomial pathogens commonly have multiple resistance profiles, typically plasmid-mediated. Resistance pressure from the use of third-generation cephalosporins has led to the establishment of Vancomycin resistant enterococci (VRE) as well as extended spectrum ß-lactamase producing (ESBL) organisms of which Klebsiella is the prototype. [45] Plasmid-mediated resistance to fluoroquinolones parallels the rise of ESBL-producing organisms. [46] Empiric antibiotic selection should be derived from each hospital's local antibiogram based on likely pathogens. A ß-lactamase inhibitor combination paired with an aminoglycoside and vancomycin are the authors' empiric agents of choice based on their local antibiogram for Ventilator associated pneumonia. Should the reader's microbiology lab identify an ESBL-producing pathogen, the appropriate antibiotic class of choice is carbapenem. [47] Carbapenems consistently demonstrate excellent efficacy in eradicating ESBL-producing
microbes.
Figure 8-10 Confounders in the diagnosis of pneumonia. Fever, leukocytosis, radiographic infiltrate, and sputum production do not necessarily indicate the diagnosis of pneumonia. Multiple other causes should be considered as well so that one does not apply antibiotics when there is no infectious agent to address. ALI = acute lung injury, ARDS = acute respiratory distress syndrome.
ADJUNCTIVE THERAPIES ß2 -Agonists.
These agents stimulate ß-adrenergic receptors in bronchial smooth muscle, and induce muscle relaxation. This reduces airway resistance and improves gas flow through the conducting airways. [48] The ß2 -agonists also inhibit MAST cell degranulation, leading to ameliorated immune stimulation of the reactive airway. The most widely used agent in ICUs in the United States is albuterol. This agent may be administered via a side port of the ventilator circuit using a metered dose inhaler (MDI; cost-effective). Alternatively, albuterol may be delivered by placing an in-line nebulizer device between the circuit and the ETT, or on a side port on the ventilator tubing's inspiratory limb (ventilator tubing-dependent). Many patients may develop bronchoconstriction and wheezing when mechanically ventilated without a preexisting history of reactive airways disease. ß 2 -agonists should be administered to patients who have poor air movement, wheezing, or both. A physiologically appropriate means of detecting and following bronchospasm is the Peak-plateau gradient. A normal gradient is 24 hours. However, for the first 24 hours, NAC may provide significant benefit in liberating densely inspissated secretions from dependent portions of the airways. Recruitment Maneuvers.
These maneuvers are designed to apply consistent but well-regulated pressure to partly or completely closed alveoli to reintroduce gas into those segments. [49] The targeted segment(s) are those with poor compliance and long regional time constants. The area of interest is placed in a nondependent position (i.e., for left lower lobe benefit, place the left side of the patient up and right side down), and the patient is hand-ventilated using a bag-valve device attached to the endotracheal tube. An in-line pressure monitor is needed. The patient will usually require sedation to comply with the maneuver—fentanyl and midazolam are ideal. The clinician then applies pressure to the bag to achieve 35 cm H 2 O pressure and holds it for 4 to 6 seconds, after which the patient is allowed to exhale. This cycle is repeated for up to 5 minutes. A second examiner listens to the area of interest for an increase in breath sounds. The recruitment may be terminated when there are good breath sounds on two consecutive maneuvers. Recruitment maneuvers may be combined with chest physiotherapy for added benefit; chest physical therapy should, in general, precede the recruitment maneuver. Bronchoscopy.
See nosocomial pneumonia earlier. Bronchoscopy/Bronchoalveloar Lavage (BAL).
With MV, the normal bacterial, viral, and secretion clearance mechanisms of the mucociliary elevator are compromised. Accordingly, excellent pulmonary toilet is required to prevent secretion impaction, atelectasis, pneumonitis, pneumonia, intrapulmonary shunt, or ventilation perfusion mismatch. Despite seemingly adequate nursing or respiratory therapist care of a patient's airways, atelectasis, mucus plugging, and segmental or subsegmental airway obstruction and collapse may occur. Several initial maneuvers are indicated, including: alveolar recruitment, chest physiotherapy, postural drainage, and aerosolized bronchodilator therapy. Frequently, these maneuvers resolve the elevated P aw -peak and hypoxemia that are the markers of complications. When these initial therapies fail, a more invasive approach is warranted. The traditional approach to clearance of inspissated secretions is therapeutic bronchoscopy. The adult flexible fiberoptic bronchoscope has an outer diameter of 3.3 mm and a working channel for suctioning of 2.5 mm. Therefore, an ETT of size =8.0 is ideal as it will permit easy passage of the bronchoscope and allow for adequate MV of the patient. However, airway mucosal irritation is a powerful sympathetic stimulant. Tachycardia, systemic hypertension, and bronchospasm commonly complicate therapeutic bronchoscopy. In the setting of intracranial hypertension, the clinician must take steps to blunt any potential sympathetic stimulation. Mucosal irritation may be minimized by careful bronchoscopic technique that avoids impacting and suctioning the sidewalls. Additionally topical or systemic lidocaine will also blunt mucosal irritation. Preprocedure ß-blockade with a relatively short-acting agent like esmolol will blunt the tachycardia and elevated dP/dt that accompanies heightened sympathetic tone. This will diminish any increase in cerebral blood flow that accompanies sympathetic discharge. Adjuvant therapy with narcotic analgesia, with a short-acting agent like fentanyl, will enhance sedation and ameliorate pain from mucosal injury. When these measures fail, significant sedation and cerebral protection may be achieved with cautious administration of barbiturates like sodium pentothal. Pentothal therapy may also be complicated by systemic hypotension. Alternatively, for very short procedures, etomidate is an excellent and powerful sedative that has the unique advantage of inducing diminished ICP. Thus, excellent intravenous access for fluid or inotrope administration is mandatory when using barbiturates. A postprocedure CXR is indicated to assess the results of the bronchoscopy, and to assess for complications such as a pneumothorax or ETT malposition. When a specimen is obtained, it should be examined by Gram stain as well as culture for bacteria, viruses, fungi, or AFB when indicated. These results will help guide initial antibiotic therapy if the patient's clinical condition indicates infection (i.e., mucosal erythema, leukocytosis, fever, hypotension). The culture results are qualitative only and serve to identify which organism(s) are present, but not the bacterial burden. Accordingly, the utility of such results has been derided as being no more useful that an aspirate obtained by a closed suction system. However, a closed suction system does not allow directed suctioning of a particular side of the airway. In fact, the right side is more frequently suctioned than the left based on the straighter geometry of the right mainstem bronchus. To combat the geometry, "steerable" suction catheters that allow for directed lavage and suctioning are available. Furthermore, the suction catheter is enclosed within a sleeve that protects it from contamination during passage through the ETT and upper airways. With both the "steerable" catheter system and therapeutic bronchoscopy, the techniques may be modified so as to allow for quantitative assessment of the bacterial/viral/fungal burden. The technique is called bronchoalveolar lavage, and relies on wedging the tip of the fluid instillation/suction catheter into a broncho-pulmonary segment, instilling a known amount of fluid (usually 180 mL of NSS in 60-mL aliquots), and recovering that fluid for analysis. An adequate recovery is >50% of the instillate volume. Moreover, there are criteria for the diagnosis of infection (bacteria >300 CFU/mL). [50] The criteria are liberalized (>500 CFU/mL) if the lavage and aspirate were performed in a larger airway such as the bronchus intermedius, instead of a segmental orifice such as the superior segment
of the lower lobe. Another modality that may be useful in the diagnosis of pulmonary infection is the bronchoscopically directed "protected brush biopsy." [51] In this technique, the bronchoscope is advanced into the area of interest, and a sheathed brush is advanced through the working channel into the airway. Then the brush is extruded and worked back and forth against the airway to "biopsy" adherent microbes and airway mucosa. The brush is withdrawn into the sheath, and the entire assembly is withdrawn. The brush is then cut off and incubated in culture media. This technique has numerous advantages in that upper airway secretions may be suctioned without fear of contaminating the specimen and obtaining spurious results. By comparison, the standard BAL technique requires that the operator guide the bronchoscope into the affected region without suctioning so as to not contaminate the subsequently aspirated lavage sample. The downside to protected brush biopsy is that mucosal injury, bleeding, and pneumothorax occur more commonly than with bronchoscopically directed or steerable catheter BAL. Regardless of the technique used, the clinician must match the sample results with the patient's clinical picture.
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Gastric Content Aspiration and Pneumonia.
Additional consideration is needed to avoid gastric acid blockade in patients who require prolonged intubation and MV. Gastric acid inhibition has, in some studies, been associated with a higher rate of nosocomial pneumonia than in patients who received ulcer prophylaxis with sucralfate alone. [52] It is believed that the gastric acid milieu destroy refluxed bacteria and that most nosocomial pneumonias occur because of aspiration of gastric contents. It is important to recall that aspiration may occur simply by "wicking" of gastric secretions along an indwelling nasogastric tube that stents open the upper and lower esophageal sphincters, as well as by vomiting and passage of gastric contents along the sides of the cuffed endotracheal tube. Aspiration of gastric acid with intubation (the most common scenario) does not require antibiotic therapy, nor is it improved by the administration of glucocorticoids or the use of immediate bronchoscopy (unless there is large airway obstruction). The clinical syndrome of sterile gastric content aspiration is Mendelson syndrome. Heliox Therapy.
The interface of gas with airways creates a certain amount of friction. Heavier gases lead to greater amounts of friction than lighter gases. The more friction generated, the greater the work of breathing for a given gas. Severe asthma commonly entails significant work of breathing and may lead to respiratory failure from respiratory muscle fatigue. Altering the gas composition from N 2 :O2 to He:O 2 provides for a lighter gas that requires less work of breathing. Different percentage mixtures of He:O2 (Heliox) are prepared and commercially available (e.g., 70% O 2 and 30% helium). Successful resolution of impending respiratory failure has been achieved using this strategy. [53] Note that this is not a commonly used therapy, but an important adjunct to have available when the need arises. Negative-Pressure Ventilation.
This unique mode of ventilation is best achieved using the Hayak Oscillator, a device produced in Israel. Its appearance is quite similar to a Cuirasse vest, but the driving negative-pressure source is quite different. The Hayak Oscillator features independent controls for the application of negative pressure as well as positive pressure, frequency of cycling between negative and positive pressure (inspiration and expiration), a chest physiotherapy mode for sputum expectoration (useful for those with cystic fibrosis), as well as a cardiopulmonary resuscitation mode. It is not widely used in the United States, but has demonstrated use in the cystic fibrosis patient population and during upper airway surgery, when an indwelling ETT would be a significant obstruction. [54]
SPECIAL TOPICS Asthma.
Fortunately, most patients with asthma are easily managed with combination therapy such as ß 2 agonists, acetylcholine antagonists, and glucocorticoids. A true management challenge is the critically ill asthmatic. These patients are different from others with asthma exacerbation in that they require intubation and MV. [33] Unlike many other disease states, asthmatics are not immediately improved by positive-pressure ventilation; asthmatics often become acutely worse before any improvement from intubation and ventilation is realized. After intubation, the asthmatic's P aw -peak is usually elevated. This leads to various problems including, but not limited to, early termination of a volume cycled breath (excessive airway pressure limiting the breath), impaired gas exchange (increased V D /VT ), and the induction of "biotrauma" (see later). A slower respiratory rate allows for a longer time in exhalation. A prolonged T e is essential for the patient with restrictive disease. In volume-controlled ventilation, a lower respiratory rate with a low V T , as in the ARDSNet protocol may be used for the management of life-threatening asthma. [30] With pressure-controlled ventilation (as discussed earlier), the set pressure may generate an inadequate V T based on the restrictive component of the exacerbated asthma. It is essential that bronchodilator and anti-inflammatory therapy (i.e., glucocorticoids) be pursued in conjunction with positive-pressure ventilation for an optimal outcome.[34] A diligent search should be undertaken to discern any potential triggers (e.g., infection) that may be eliminated to hasten recovery and limit the duration of MV. Appropriate sedation is critical to ensure adequate gas exchange; it enables the patient to "synch" with the ventilator and not trigger early volume cycled breath termination. If sedation alone is inadequate to reduce the restriction imposed by the chest wall or intra-abdominal contents, pharmacologic relaxation is then indicated (although uncommonly required). Heliox therapy has also been used with success for the failing asthmatic as a means of avoiding intubation in select patients (see Heliox section). [35] APRV has been used for severe life-threatening asthma; insufficient data are currently available to recommend this as front-line therapy. Its role may be as a salvage mode for asthmatics with refractory hypoxemia. Ventilator Weaning Protocols and Pathways A well-designed weaning protocol is an invaluable aid in reducing the length of stay in the ICU. An appropriate protocol will enable the respiratory therapist and bedside nurse to initiate the weaning process each day before clinician evaluation. Computer order entry may create an ICU admission data set that automatically activates such a protocol once the entry criteria are met (i.e., the cause of respiratory failure is improving or has been eliminated, FIO 2 < 0.50, PEEP < 10 cm H2 O, and no pressors other than dopamine at 0.5 Pleural fluid lactate dehydrogenase (LDH) >2/3 upper limit of serum reference range Pleural fluid:serum LDH ratio >0.6 effusion, but also malignancy, TB, esophageal rupture, and collagen vascular disease. [72] Measurement of pleural pH is essential in the evaluation of suspected parapneumonic effusions since hydrogen ion concentration is a key factor in the management algorithm. The fluid must be collected anaerobically, but may be transferred from the initial 50- or 60-mL syringe into a heparinized blood gas syringe, [73] and then left at room temperature for up to 1 hour before laboratory analysis [74] without affecting the accuracy of the results. Because of these specifics regarding the collection and evaluation of pleural fluid pH, pleural fluid should routinely be transferred to a heparinized blood gas syringe and placed on ice while awaiting the decision for pH testing. The evaluation of a suspected parapneumonic effusion is described further as follows. Pleural amylase evaluation should occur in the setting of suspected esophageal rupture or pancreatitis. [75] Elevations of pleural fluid amylase >100 U/L are seen in various cases including malignancy, post cardiac bypass surgery, esophageal rupture, pancreatitis, and ruptured ectopic pregnancy. Routine measurement of pleural fluid amylase levels rarely provides useful information. White or milky fluid or concerns about thoracic duct injury should lead to analysis for pleural fluid triglycerides. Rarely, a longstanding benign effusion, such as one due to TB or rheumatoid disease, may have a similar gross appearance due to accumulation of cholesterol, lecithin, or globulin-rich fluid. This effusion is termed pseudochylothorax. Effusions with triglyceride concentrations of >110 mg/dL are uniformly chylous in nature. [76] The etiologies of chylous effusions include thoracic duct injury due to surgery, malignancy, trauma, and pleuritis. Patients with suspected parapneumonic effusions warrant rapid evaluation and outcomes risk assessment based on pleural anatomy, pleural fluid bacteriology, and pleural fluid chemistry. [77] All parapneumonic effusions require at least
Pleural Fluid Assay
TABLE 9-6 -- Selective Evaluation of Exudates Based on Clinical Suspicion Diagnosis Suspected
Amylase
Pancreatitis, esophageal rupture
Triglycerides
Chylothorax, intrathoracic TPN infusion
Glucose
Rheumatic effusion
Urea or creatinine
Urinothorax
Cytology
Malignancy
Albumin (with serum measurement)
CHF (after diuretics)
Adenosine deaminase, gamma interferon, PCR
TB (lymphocytic effusion)
Hematocrit
Hemothorax
pH
Parapneumonic effusion, empyema
CHF, congestive heart failure; PCR, polymerase chain reaction; TB, tuberculosis; TPN, total parenteral nutrition. diagnostic thoracentesis with the goal of identifying complicated parapneumonic effusions. Treatment before the organizational stage is ideal. Patients at high risk for poor outcome require complete drainage of the pleural space. This includes patients with large or loculated effusions, pleural thickening on CT scanning (the pleural peel), aspiration of frank pus, and pleural fluid pH of 24 h does not alter management recommendations. Secondary Spontaneous Pneumothorax Clinically Stable Patients with Small Pneumothoraces: * Clinically stable patients with small pneumothoraces should be hospitalized (good consensus). Patients should not be managed in the emergency department with observation or simple aspiration without hospitalization (very good consensus). Hospitalized patients may be observed (good consensus) or treated with a chest tube (some consensus), depending on the extent of their symptoms and the course of their pneumothorax. Some of the panel members argued against observation alone because of a report of deaths with this approach. Patients should not be referred for thoracoscopy without prior stabilization (very good consensus). The presence of symptoms for >24 h did not alter the panel members' recommendations. Clinically Stable Patients with Large Pneumothoraces: Clinically stable patients with large pneumothoraces should undergo the placement of a chest tube to reexpand the lung and should be hospitalized (very good consensus). Patients should not be referred for thoracoscopy without prior stabilization with a chest tube (very good consensus). The presence of symptoms for >24 h did not alter the panel members' recommendations. Terms
Definition
Spontaneous pneumothorax
No antecedent traumatic or iatrogenic cause
Primary spontaneous pneumothorax
No clinically apparent underlying lung abnormalities or underlying conditions known to promote pneumothorax (e.g., HIV disease)
Secondary spontaneous pneumothorax
Clinically apparent underlying lung disease
Pneumothorax size
Determined by distance from the lung apex to the ipsilateral thoracic cupola at the parietal surface as determined by an upright standard radiograph
Small pneumothorax
50 mm Hg in response to CSM. It shares many characteristics with sick sinus syndrome, suggesting that both are manifestations of the same disease. CSS causes cerebral hypoperfusion leading to dizziness and syncope. Analysis of patients with the syndrome indicates that it results from a baroreflex-mediated bradycardia in 29% of patients, hypotension in 37%, or both in 34%. [10] [11] Therefore, syncope, near-syncope, or a fall of unclear etiology in the elderly are important indications for diagnostic CSM. [12] The clinician can take advantage, however, of the similarity of the vagal effects of digoxin and the vagal maneuvers. Before starting digoxin administration in a patient, the practitioner can gauge the cardioinhibitory effect that will be achieved with the drug by first performing CSM. Significant slowing or block with CSM suggests a similar sensitivity to digoxin, and a smaller loading dose should be considered. Vagal maneuvers are also indicated in settings in which slowing conduction in the SA or AV node could provide useful information ( Fig. 11-2 Fig. 11-3 Fig. 11-4 Fig. 11-5 Fig. 11-6 Fig. 11-7 Fig. 11-8 Fig. 11-9 ). These settings include patients with wide-complex tachycardia in whom CSM aids in the distinction between SVT and ventricular tachycardia (VT). CSM can also elucidate narrow-complex tachycardia in which the P waves are not visible, or aid in detection of suspected rate-related bundle branch block or suspected pacemaker malfunction. After CSM, a wide-complex SVT may be converted to normal sinus rhythm, P waves may be revealed after increased AV node inhibition, or ventricular complexes may narrow as the ventricular rate slows. Because CSM slows atrial and not ventricular activity, AV dissociation may be more easily seen, indicating VT ( Fig. 11-2 ). In rapid atrial fibrillation, or atrial flutter with 2:1 block, either P waves or irregular ventricular activity with absent P waves may be revealed. Sinus tachycardia may also be more apparent once P waves are unmasked by slowing the SA node (see Fig. 11-4 ). Adenosine may be used for the same diagnostic purpose in these situations as well. [13] In order of decreasing frequency, the electrocardiogram (ECG) changes seen with CSM and vagal maneuvers include those shown in Table 11-3 . Equipment and Setup As a precaution against hypotension and life-threatening dysrhythmias, an IV line with normal saline is often started before attempting any vagal maneuver, including the use of pharmacologic agents or electrical cardioversion. The patient should be placed on a cardiac monitor and pulse oximeter.
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Figure 11-2 Ventricular Tachycardia. Carotid sinus massage (CSM) slows atria but not ventricles, thus establishing the presence of atrioventricular dissociation, supporting the diagnosis of ventricular tachycardia. The QRS measures 0.16 sec. Note the atrial rate slowing from 102 to 88 beats/min while the ventricular rate is unaffected. (From Lown B, Levine SA: Carotid sinus—Clinical value of its stimulation. Circulation 23:766, 1961. Reproduced by permission.)
Atropine and lidocaine, as well as a transvenous or transcutaneous pacemaker and defibrillator, should be readily available at the bedside. Oxygen and appropriate delivery systems plus standard airway management equipment should be readily available. The patient should be in the supine or slight reverse Trendelenburg position if it can be tolerated. Occasionally SVT will convert merely by lowering the back of the bed, presumably because the supine position results in a stretching of the carotid bulb, giving maximum baroreceptor sensitivity. The supine position may also prevent syncope in the event of a significant drop in heart rate or blood pressure. Carotid Sinus Massage Carotid sinus massage (CSM) is a bedside vagal maneuver technique involving digital pressure on the richly innervated carotid sinus. It takes advantage of the accessible position of this baroreceptor for diagnostic and therapeutic purposes. Its main diagnostic utility is in the differential diagnosis of syncope in the assessment of tachydysrhythmias and rate-related bundle branch blocks, and in clues to latent digoxin toxicity. Its main therapeutic application is for termination of SVTs due to paroxysmal atrial tachycardia (PAT). A diagnostic indication for CSM is evaluating digoxin toxicity. Toxicity from digoxin depends more on the response of the host than on the actual digoxin level. In cases of suspected digoxin toxicity, before the level is available, or when the digoxin level is in the "normal range," CSM may be a useful diagnostic adjunct. Significant inhibition of AV node conduction associated with ventricular ectopy (see Fig. 11-9 ), especially ventricular bigeminy, should lead to the suspicion of digoxin toxicity. [1] Other therapeutic uses of CSM have been made obsolete by current medical therapy. In 1961, Lown and Levine
Figure 11-3 Paroxysmal atrial tachycardia with variable block. Carotid sinus pressure uncovers P waves hidden in the ventricular complex. The upper strip resembles atrial flutter or atrial fibrillation with ventricular ectopic beats. The lower strip shows paroxysmal atrial tachycardia with variable block at an atrial rate of 166 beats/min. (From Lown B, Levine SA: Carotid sinus—Clinical value of its stimulation. Circulation 23:766, 1961. Reproduced by permission.)
described the dramatic effect CSM had in the 1920s on relieving acute pulmonary edema in a group of patients with hypertension and coronary artery disease. They reported: "Relief is immediate and coincides with the onset of bradycardia. In the majority, it is associated with a drop in blood pressure. The patient is promptly able to lie flat. Fear, dyspnea, and chest oppression disappear. ..." CSM also has been reported to relieve anginal pain. The technique may be useful when the diagnosis of angina is uncertain. [14] The advantage of the CSM technique over the use of nitroglycerin is unknown. Although CSM is no longer the first approach to either pulmonary edema or angina, it remains a therapeutic or adjunct diagnostic tool in some cases, or when modern pharmacological agents are unavailable. Because adenosine may not always be readily available, and because adenosine cannot be used to assess the sensitivity of the carotid sinus, CSM remains a useful bedside tool. Contraindications
CSM is contraindicated in patients likely to suffer neurologic or cardiovascular complications from the procedure. Patients with a carotid bruit should not have CSM because of the risk of carotid embolization or occlusion. A recent cerebral infarction is a theoretical relative contraindication, because marginal reduction of cerebral blood flow may produce further infarction. The presence of diffuse, advanced coronary atherosclerosis is associated with increased sensitivity of the carotid sinus reflex. This hypersensitivity is further augmented during an anginal attack or an acute myocardial infarction. Brown and coworkers found that the degree of carotid sinus hypersensitivity was directly proportional to the severity of coronary artery disease documented by cardiac catheterization. [18] Patients with acute myocardial ischemia or with recent
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Figure 11-4 Sinus tachycardia. The sinus P wave is obscured within the descending limb of the T wave. Carotid sinus massage (CSM) transiently slows the sinus rate and exposes the P wave. The rate then increases. The strips are continuous. (From Silverman ME: Recognition and treatment of arrhythmias. In Schwartz GR, Safar P, Stone JH, et al (eds): Principles and Practice of Emergency Medicine, vol. 2. Philadelphia, WB Saunders, 1978. Reproduced by permission.)
myocardial infarction are already at higher risk of VT or ventricular fibrillation (VF). A CSM-induced, prolonged asystole may further predispose them to these dysrhythmias. Therefore, CSM should be avoided in these patients when pharmacologic alternatives are available. Both digoxin and CSM act through a vagal mechanism to inhibit the AV node. Patients on digoxin may experience a greater inhibition of the AV node with longer AV block as a result. Patients with known digoxin toxicity should not have CSM, as AV inhibition may be profound. [19] However cautious CSM (as noted above) may be a useful diagnostic tool when the diagnosis is less certain. Simultaneous bilateral CSM is absolutely contraindicated, because cerebral circulation may be severely compromised. Before attempting CSM, the clinician should first auscultate for carotid bruits on both sides of the neck. The presence of a bruit is a contraindication to massage. Technique
The clinician should begin CSM on the patient's right carotid bulb, as some investigators have found a greater cardioinhibitory effect on this side difference was found in one study. [10]
[12] [ 15] [16]
; although no
Keeping the patient relaxed is helpful for two reasons: A tense platysma muscle makes palpation of the carotid sinus
Figure 11-5 Sinus tachycardia with high-degree atrioventricular block. Arrows indicate sinus P waves. Strips II-a to II-d are continuous. The basic rhythm is sinus, but marked first-degree atrioventricular block is present. High-degree (advanced) atrioventricular block associated with transient slowing of sinus rate is produced by carotid sinus stimulation (CSS). (From Chung EK: Electrocardiography, 2nd ed. New York, Harper & Row, 1980. Reproduced by permission.)
difficult, and an anxious patient will be less sensitive to CSM as a result of heightened sympathetic tone. With the head tilted backward and slightly to the opposite side, palpate the carotid artery just below the angle of the mandible at the upper level of the thyroid cartilage and anterior to the sternocleidomastoid muscle. Once the pulsation is identified, use the tips of the fingers to administer CSM for 5 seconds in a posteromedial direction, aiming toward the vertebral column. Although earlier practitioners used a longer duration of massage, a shorter period of massage minimizes the risk of complications and is adequate for diagnostic purposes in the majority of patients. [17] Pressure on the carotid sinus may be steady or undulating in intensity; the force, however, must not occlude the carotid artery. The temporal artery may be simultaneously palpated to ensure that the carotid remains patent throughout the procedure. If unsuccessful, CSM may be repeated after 1 minute. If the procedure is still unsuccessful, the opposite carotid sinus may be massaged in a similar fashion. Simultaneous Valsalva maneuvers may also enhance carotid sinus sensitivity. Complications
Neurologic complications of CSM are rare and are usually transient. In one review of neurologic complications in elderly
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Figure 11-6 Paroxysmal atrial tachycardia. Carotid sinus massage (CSM) abolishes the dysrhythmia and results in a period of sinus suppression with a junctional (J) escape beat, followed thereafter by a sinus rhythm. Prolonged periods of asystole may produce anxiety in the clinician who is waiting for the resumption of a sinus pacemaker. (From Silverman ME: Recognition and treatment of arrhythmias. In Schwartz GR, Safar P, Stone JH, et al (eds): Principles and Practice of Emergency Medicine, vol 2. Philadelphia, WB Saunders, 1978. Reproduced by permission.)
patients undergoing this procedure, Munro and others found 7 complications from a total of 5000 massage episodes, for an incidence of 0.14%. [20] Reported deficits included weakness in 5 cases and visual field loss in two others. In one case, the visual field loss was permanent. Patients in this study were excluded from CSM if they had a carotid bruit, recent cerebral infarction, recent myocardial infarction, or a history of VT or VF. The duration of massage was 5 seconds. Lown and Levine described one patient with brief facial weakness during several thousand tests. [1] Carotid emboli and hypotension have both been implicated as possible causes of the neurologic deficits. Unintentional occlusion of the carotid artery, if the contralateral circulation is impaired, may also be responsible for some neurologic complications. Cardiac complications include asystole, VT, or VF ( Fig. 11-10 ). A normal pause of 3 seconds, or a drop in systolic blood pressure >50 mm Hg in patients to whom CSM is administered while they are in a supine position, is diagnostic of the carotid sinus syndrome ( Fig. 11-11 ). Patients should be supine during testing to reduce the risk of cerebral hypoperfusion. [12] [22] Although the carotid sinus massage is one of the better known vagal maneuvers, a variety of other physical modalities are available to the clinician to affect a change in heart
Figure 11-7 Atrial flutter. Carotid sinus stimulation (CSS, downward arrow) produces marked slowing of the ventricular rate in atrial flutter. Note the obvious flutter waves with an atrial rate of 300 and a long period of ventricular standstill. Strips are continuous. (From Chung EK: Electrocardiography, 2nd ed. New York, Harper & Row, 1980. Reproduced by permission.)
rate. The anticipated rhythm response to different vagal maneuvers in the setting of different underlying rhythms is shown in Table 11-4 . Valsalva Maneuver
In general, mean bradycardia changes are greatest for the Valsalva maneuver and the diving response. [3] [22] [23] During the Valsalva maneuver, intrathoracic pressures are increased, leading to increased arterial pressure. This increased pressure is transferred to the peripheral vascular system. Venous return to the heart is decreased, resulting in a decreased stroke volume. This is followed by increased venous pressure. All of these pressure changes lead to an initial increase in heart rate and carotid sinus pressure. As the maneuver is sustained, vagal tone is increased leading to a compensatory decrease in SA and AV conduction (the desired diagnostic/therapeutic response). Contraindications
Patients must be able to cooperate with the clinician's commands. Remember that dyspneic or tachypneic patients may not be able to hold their breath for the period of time needed to complete the maneuver. Technique
The patient is placed supine and a cardiac monitor is attached. Ideally, intravenous (IV) access is secured, and atropine, lidocaine, and defibrillation equipment are available. Have the patient take a deep breath and hold it. Instruct the patient to bear down and try to exhale without allowing the air to leave the lungs. The patient should try to hold this position for 10 to 20 seconds. [24] [25] An adjunct method is to have the patient take a deep breath, hold the breath and try to push the clinician's
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Figure 11-8 Atrial fibrillation. Carotid sinus massage (CSM) slows the ventricular response transiently, revealing the fibrillating baseline. The ventricular rate subsequently accelerates. (From Silverman ME: Recognition and treatment of arrhythmias. In Schwartz GR, Safar P, Stone JH, et al (eds): Principles and Practice of Emergency Medicine, vol. 2. Philadelphia, WB Saunders, 1978. Reproduced by permission.)
hand off the patient's abdomen as the clinician gently pushes on the anterior wall of the abdomen. Apneic Facial Exposure to Cold ("Diving Response," Diving Bradycardia) Technique.
This technique represents a variation on the simple valsalva maneuver. It has been found useful in children who may be unable to volitionally do a valsalva maneuver. Classically the technique consists of facial immersion, without breathing, for 15 to 30 seconds in cold water (0°C to 15°C). Alternatively ice water can be dripped into the nostril of a small child. Be sure to monitor the oxygen saturation closely when applying this technique to a small child. The procedure is based on the classic diving reflex of bradycardia. Slowing of SVT to unmask the hidden, underlying rhythm is similar to the effects of CSM. The conversion of paroxysmal atrial tachycardia to sinus rhythm should be observed in 15 to 35 seconds. The procedure is convenient and noninvasive, and can be self-administered.[26] [27] [28] [29] [30] [31] Oculocardiac Reflex (OCR, Trigeminovagal Reflex)
This reflex is clinically significant during strabismus surgery in children, although the manifestations of this reflex are not consistent. The oculocardiac reflex (OCR) is induced by pressure on the eyeball. Afferent pathway follows the long and short ciliary nerves to the ciliary ganglion. From there, it travels to the gasserian ganglion body along the ophthalmic division of the trigeminal nerve (CN V). The afferent pathway ends in the main trigeminal sensory nucleus in the floor of the fourth ventricle. [4] [23] [24] Efferent impulses start at the vasomotor center and travel through the vagal nerve (CN X) and the sympathetic chain. Bradycardia results from increased parasympathetic tone.
Figure 11-9 Occult premature ventricular contractions. Carotid sinus massage (CSM) reveals ventricular extrasystoles, thereby explaining the cause of palpitation in this case. (From Lown B, Levine SA: Carotid sinus—Clinical value of its stimulation. Circulation 23:766, 1961. Reproduced by permission.)
Decreased sympathetic tone causes vasodilation. The cardiac effect stops when eye pressure is relieved. Atropine should be available to reverse life-threatening bradycardia.
[23]
Patients should be monitored to recognize ECG changes.
Contraindications
Common sense dictates that the clinician should try to elicit history of the following conditions prior to attempting the oculocardiac reflex: (a) recent retinal or lens surgery; (b) glaucoma; (c) thrombotic-related eye conditions, which all seem to be obvious possible contraindications. Care should be taken when pressing on the eye globe to prevent corneal or scleral injury. Technique
With the eyelid closed, non-rotating pressure is applied to the eyeball for 10 to 20 seconds. There is no advantage to the use of either eye. Ventricular slowing and possible decrease in blood pressure should be observed almost immediately when the pressure is applied. The cardiac effect of bradycardia will cease when pressure is removed. As with all vagal maneuvers, monitoring, IV access, atropine, lidocaine, and defibrillation should be available during the procedure. Summary Berk and colleagues have demonstrated in healthy volunteers that cold-water face immersion and the Valsalva maneuver can produce a greater vagal response than CSM.[15] Mehta and colleagues also found that the Valsalva maneuver was more effective than CSM for conversion of induced SVT. [16] [32] The pneumatic antishock garment has also been used to similarly increase vagal tone by stretching the carotid bulb. [33]
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TABLE 11-3 -- Order of Decreasing Frequency of Electrocardiogram Changes with Vagal Maneuvers 1. SA slowing, occurring in approximately 75% of cases (sinus arrest occurs approximately 3% of the time) 2. Atrial conduction defects, manifested by an increase in width of the P wave on the electrocardiogram 3. Prolongation of the PR interval and higher degrees of atrioventricular block, seen in approximately 10% of cases 4. Nodal escape rhythms 5. Complete asystole, defined as sinus arrest without ventricular escape lasting >3 seconds, occurring in 4% of cases 6. Premature ventricular contractions
SELECT PHARMACOLOGIC AGENTS Digoxin This time-honored drug was previously a mainstay for treatment of atrial fibrillation and atrial flutter. It is the only anti-dysrhythmic with inotropic properties, but is uncommonly used by the emergency clinician because of its long delay of onset. Digoxin is a cardiac glycoside found in a number of plants. It is commonly extracted from the leaves of the Digitalis lanata plant, and increases the intracellular Na+ by inhibiting Na-K-ATPase. This is the enzyme that regulates the quantity of Na+ and K+ inside the cell. Intracellular increases in the sodium ion concentration stimulate sodium/calcium exchange, leading to increased intracellular Ca+. The increased intracellular calcium can lead to increased contractility. Digoxin has both a direct action on cardiac muscles and an indirect action on the cardiovascular system. The indirect effects are mediated by the autonomic nervous system. The results of these actions are vago-mimetic effects on the SA node and the AV node. The consequences of these combined actions are: (1) increased force and velocity of myocardial contraction (positive inotropic effect); (2) slowing of the heart rate and AV nodal conduction (vago-mimetic effect); and (3) decrease in symptomatic nervous system effects (neurohormonal deactivating effect). [34] [35] [36] [37] [38] [39] Indications and contraindications.
Though its use in rate control of the ventricular response in chronic atrial fibrillation is well established, it is no longer the mainstay of therapy for narrow-complex tachycardias. Newer agents have replaced digoxin in the treatment and management of narrow-complex tachycardias. Its inotropic character is still widely used in the setting of heart failure.
Figure 11-10 A run of ventricular tachycardia is seen immediately after a supraventricular dysrhythmia is terminated by cardiac sinus massage (CSM). The patient remained asymptomatic, and a normal sinus rhythm was established spontaneously within a few seconds.
Use of digoxin should be avoided in the clinical settings of sinus node disease and AV blockade. It may cause complete heart block or severe sinus bradycardia. It should not be used in the presence of accessory bypass tract rhythms (Wolf-Parkinson-White [WPW]) or Long-Ganong-Levine [LGL] syndromes) as it may cause a rapid ventricular response or VF. Patients with idiopathic hypertrophic sub-aortic stenosis (IHSS), restrictive cardiomyopathy, constrictive pericarditis, or amyloid heart disease are particularly susceptible to digtoxicity. [40] Dosage: IV loading dose of 10 to 15 mcg/kg followed by individual parenteral dosing until desired rate is achieved.
[ 37] [38] [ 41] [42] [ 43] [44] [45] [46] [47]
Procainamide Another time-honored antiarrhythmic, procainamide slows conduction and decreases automaticity and excitability of atrial, ventricular, and Purkinje tissue. It also increases refractoriness in atrial and ventricular tissue. Procainamide prolongs the QT interval with little effect on Purkinje fibers or ventricular tissue. [38] [41] [46] Indications and contraindications.
The drug is used in the rhythm and rate management of SVT, SVT with aberrancy conduction (wide-complex SVT), atrial fibrillation/flutter associated with WPW conduction, and VTs. The advantage to using IV procainamide is the ability to convert to the oral form when rate control is achieved. The loading interval for procainamide is 20 minutes. This limits use of the drug to clinical situations when time is not a critical factor in patient care. Long-term management in the emergency department (ED) necessitates monitoring of the plasma concentrations of procainamide and its NAPA metabolite. Hypotension and conduction disturbances (torsades de pointes, heart blocks, and sinus node dysfunctions) are often signs of high plasma levels. Caution should be used in patients with histories of hypokalemia, long QT intervals, or torsades de pointes. Hematologic and rheumatologic disturbances are factors in long-term use. Dosages: Over 25 minutes, a loading infusion of 275 mcg/kg per minute is administered. This is followed by a maintenance infusion of 20 to 60 mcg/kg per minute.
[ 48]
[49]
Adenosine The use of vagal maneuvers has been eclipsed in recent years by the use of adenosine. The drug is an endogenous, ultrashort-acting vagal-stimulating nucleotide that occurs in all body cells. Its primarily action is to slow conduction time through the AV node. Extracellular adenosine is rapidly cleared from the circulation by the erythrocyte and vascular endothelium system,
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Figure 11-11 Hyperreactive carotid sinus reflex. Gentle pressure was applied to the carotid sinus for 3 seconds, resulting in a pause in sinus rhythm of approximately 7 seconds. This syndrome may be the cause of syncope. (From Bigger JT Jr: Mechanisms and diagnosis of arrhythmias. In Braunwald E (ed): Heart Disease, vol 1. Philadelphia, WB Saunders, 1980. Reproduced by permission.)
which transports adenosine intracellularly. Once inside the cell, rapid metabolism occurs via a phosphorylation or deamination cycle, producing inosine or adenosine monophosphate. Adenosine produces a short-lived pharmaceutical response because it is rapidly metabolized by the described enzymatic degradation. The half-life of adenosine is 180) is detected. [43] The algorithm used to analyze the acquired ECG waveform, the selected energy levels, and the actual sequence is preprogrammed by the manufacturer's medical director or can be modified by the clinician providing oversight in the use of this device. A fully automatic AED usually delivers a shock if indicated without user manipulation. These are used only in special situations. [4] Waveforms The first successful human defibrillation was performed using AC current. [23] Several years later DC current was shown to be more effective than AC current in accomplishing defibrillation. [44] Use of DC current also resulted in a significantly reduced incidence of postcardioversion dysrhythmias. [44] Only DC defibrillators are in clinical use today. Until recently, modern defibrillators delivered a "damped, monophasic, half-sinusoidal waveform" or a "trapezoidal truncated exponential decay" (voltage falling instantaneously) waveform. The trapezoidal waveform was modified to resemble a square waveform. The more square the waveform, the more effective it was for experimental defibrillation. [45] In a comparison of square waveforms and damped half-sinusoidal waveforms (voltage falling to zero gradually) for animal defibrillation, it was found that less peak current per kilogram was needed with the square waveforms, although the average current levels were equivalent. [46] This work was extended further, leading to the development of multiple new biphasic waveforms. These waveforms are achieved by manipulating the current (amperes), amplitude, duration, voltage, and ultimately the energy delivered to the myocardium. In light of the current research into the utility of the various energy waveforms that modern day defibrillators
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deliver, it would be useful to briefly describe/define terminology. Current output from a defibrillator is graphed with respect to time on an X-Y Cartesian plot. The form of the wave can be either "monophasic" or "biphasic." A characteristic monophasic wave is described as a rapid, positive, unidirectional increase in current flow to a predetermined peak with a return to baseline. If the return of the current to baseline is gradual, the waveform is termed a "damped" wave form (Monophasic Damped Sine-MDS waveform). These waves often resemble a sine wave ( Fig. 12-4 ). If the return of the current level to baseline is paroxysmal/sudden, the wave is termed a "monophasic truncated exponential waveform-MTE waveform" ( Fig. 12-5 ). If there is a rapid rise in current with respect to time with a slight plateau and then a subsequent paroxysmal/sudden reversal in current flow at a predetermined time until all of the energy is delivered with a return to baseline, this is termed a "biphasic" waveform because of the two "phases" in current flow, a positive and a negative phase. Essentially, for a biphasic waveform to occur, current travels from one pad or paddle to the other, then a reversal occurs so that current now flows from the second pad or paddle to the first. If the polarity/direction of the current flow is gradual, the wave is termed a "damped" waveform. If the current reversal is abrupt, the waveform is deemed a "truncated exponential waveform," hence the term "Biphasic Truncated Exponential Waveform—BTE waveform" ( Fig. 12-6 ). The highest current flow attained is termed the "peak" energy delivered. This, however, is not synonymous with the total amount of energy delivered. Energy is delivered throughout the duration or period of the wave. The current thinking is that if there is less peak energy and a smaller amount of energy delivered to the fibrillating myocytes, there will be less damage to the heart tissue. In addition, this may decrease the perpetuation of conditions favoring VF. This suggests that these waveforms will enhance defibrillation efficacy, decrease myocardial damage, and decrease post defibrillation arrhythmias. [47] [48] The first biphasic AED approved by the Food and Drug Administration used a biphasic truncated exponential (BTE) waveform (see Fig. 12-6 ). [4] Additional experiments are being done to further explore various biphasic, rectilinear, first-pulse waveforms. The motive behind these modifications is to find an optimal waveform that will deliver the least amount of energy to the myocardium, thus decreasing the structural damage to the myocytes [31] while achieving successful defibrillation. [47] [49] [50] Injury to myocardial tissue has been associated with the peak current, not the amount of energy actually
Figure 12-4 Monophasic damped sine waveform (MDS) (Energy delivered versus time/msec.) (Adapted courtesy of Cardiac Science, Inc., Irvine, CA.)
Figure 12-5 Monophasic truncated exponential waveform (MTE) (Energy delivered versus time/msec.) (Adapted courtesy of Cardiac Science, Inc., Irvine, CA.)
delivered to the myocytes. [51] With the biphasic defibrillators, lower energy levels (150 to 175 J) can be used without escalating the energy up to 300 J or 360 J. Experimental findings suggest that the clinical outcomes of these defibrillations are equivalent to those that used the escalating monophasic shocks. [52] There is data that also supports the claims that biphasic, low-energy defibrillations are efficient and cause less myocardial damage. [31] [53] However, the actual delivered energy is dependent on thoracic resistance/transthoracic impedance (TTI). Currently manufactured defibrillators are capable of determining TTI/resistance and can actually modify the waveform and thus the amount of energy delivered across the myocardium. A more detailed discussion of TTI is presented later in this chapter. In current clinical practice there is little clinical difference in the effectiveness of the currently available waveforms. The trend of the future will probably be to use biphasic, impedance-compensating defibrillators; however, currently, many monophasics are still in use. At this writing there is no convincing evidence to support the use of one defibrillator waveform over the other. Stored Energy Because the ability to defibrillate is dependent primarily on current delivered to the myocardium, stored in the battery and capacitor, the varying TTI, internal defibrillator energy
[ 54]
successful defibrillation depends on several factors—the energy
Figure 12-6 Biphasic truncated exponential waveform (BTE) (Energy delivered versus time/msec.) (Adapted courtesy of Cardiac Science, Inc., Irvine, CA.)
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loss, and the waveform configuration. In addition, the "patient-defibrillator circuit" comprised by the patient, the electrode gel, the electrodes, lead wires, and defibrillator contribute to the outcome of a defibrillation attempt. Each defibrillator is calibrated by measuring the current delivered as a function of time across a 50-ohm impedance. It is important to note that defibrillators do not always deliver the energy indicated on the device. With a "stored" energy of 400 J (1 J = 1 watt-sec), from 155 to 410 J may be delivered. It stands to reason that the current (for a square waveform) delivered to the myocardium is related to the energy delivered by the defibrillator, the combined electrical impedance in the device and chest, and the duration of current flow: Energy (J) = current (amperes) 2 × impedance (ohms) × duration (seconds)
Obviously, any increase in TTI will further reduce delivered current. With the development and refining of the biphasic waveform, and defibrillators that actually measure TTI/resistance and compensate for the patient defibrillator "circuit resistance," thus modifying the actual waveform of delivered energy, a more appropriate amount of current is delivered to the fibrillating myocardium. Furthermore, with better electrodes, more effective conductive material, and more efficient, smaller, lighter batteries, it is reasonable to assume that defibrillators of the future will be able to store energy for a longer time and be lighter and more portable. This may enhance compliance in the timely use of AEDs and early defibrillation. Device Switches Currently there are several manufacturers of electronic medical equipment. Although the equipment they manufacture may perform in a similar fashion (i.e., a defibrillator, an ECG monitor), it is vital that health care providers using the equipment be thoroughly familiar with the operation and layout of the controls in each particular unit. Furthermore, it is imperative that each piece of equipment be periodically tested to ensure optimal operation, battery charge, calibration, recording paper, and so forth. [4] Most, if not all, currently used defibrillators have the capability of operating independently (i.e., via battery power) without a wall source of energy (i.e., AC plug to operate the monitor, event recorder, and charged capacitor and defibrillator battery). Older models may often have separate power switches for the accompanying monitor, recorder, and defibrillator, while newer units have a multi-function switch or dial. More advanced units may have pacer capability, 12-lead ECG capability, an automatic VF/VT rhythm detection option, rate alarms, sphygmomanometry, and pulse oximetry offered as options (Fig. 12-7 (Figure Not Available) ). Some defibrillator monitors offer a radio-transmitter for telemetry monitoring. Currently used units have remote switches on the "quick-look" paddles to activate shock delivery. In addition, some units have energy- and event-recording switches on the paddles, giving the operator more control while in the proximity of the patient. With the discharge controls located on the paddle handles, this allows the operator the capability of positioning and holding the paddles in place while delivering the charge. Alternatively, there may be a separate control on the panel. The simultaneous activation of the control on both paddles is usually required for energy discharge. Figure 12-7 (Figure Not Available) Hewlett Packard HP Codemaster 100/Laerdal Catalog.
The same device can be used for cardioversion as well as defibrillation (see the second section of this chapter). Before attempting defibrillation, the clinician must be completely familiar with the location and operation of the controls. This knowledge will minimize time lost fumbling with the equipment during a resuscitation of VF when time to first shock is critical to the success of the defibrillation. Defibrillators also have a control permitting synchronous cardioversion. The clinician or other operator must be certain that the control is correctly set to the asynchronous mode to permit defibrillation; otherwise, the device in the synchronous mode would "wait" indefinitely for a repetitive series of R waves, not characteristic of VF, prior to discharging. Energy settings may be determined by a switch or a dial setting or may be read off of a meter permitting a continuous range of settings. In each case the operator must be aware of the need to charge the device initially and to recharge after each discharge. The mechanism of charging the device may be intrinsic to the setting of the dial or meter but more commonly requires the use of a separate charge button on the device control panel or paddle handle. Full-charge accumulation usually takes from 2 to 5 seconds following activation of the charging mechanism. Monitor controls permit alteration of lead-monitored, image size and often allow the selection of chest lead electrode versus paddle electrode monitoring. The latter is desirable when an initial "quick-look" rhythm evaluation is desired before placement of the chest lead electrodes. A hard copy paper recorder for documenting rhythms may operate in a real-time, delay, or standby mode. Paddles or Electrode Pads Previously, most commercial defibrillator devices were equipped with adult-sized paddle electrodes with diameters between 8 and 9 cm. Canine studies have shown that slightly larger (12.8 cm-diameter) paddles are more effective for defibrillation [55] and produce less myocardial injury. [31] Paddles that are slightly smaller (4.5 cm-diameter) produce greater damage at the same energies. The larger paddles may permit a greater amount of muscle to be depolarized while simultaneously decreasing the potentially damaging current density. If the paddles are too large with respect to the heart, the current
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density may be less and defibrillation may be rendered less effective (Fig. 12-8 (Figure Not Available) ). [42] Current recommendations from the Association for the Advancement of Medical Instrumentation are that a minimum electrode size of 50 cm 2 for each individual electrode be used. [56] The sum of the electrodes area should be a minimum of 150 cm2 .[2] Although larger electrodes have been reported to have lower impedance, excessively large electrodes may hinder transmyocardial current flow. [57] Some older defibrillators may still have a flat posterior ground shield rather than a second paddle for lateral chest wall placement. However, these are currently a rare find. The metal composition of the paddle electrode will affect TTI to the defibrillation discharge. Most modern defibrillators use stainless steel because of its durability, although copper alloys and several other metals provide a lower TTI. Defibrillation can also be performed with self-adhesive electrode pads (8 to 12 cm in diameter) applied to the skin. Pads slightly smaller in size have also been found to be effective in short-term, acute applications. [58] The self-adhesive monitor/defibrillator pads appear to perform as well as or better than handheld paddles. [59] Stults and colleagues, in a controlled prehospital study, found that the use of self-adhesive pads shortened the time to successful defibrillation, reduced the number of countershocks, reduced the amount of rhythm artifact, and improved survival until hospital admission when compared with the use of standard hand-held paddles. [42] However, the expense of self-adhesive defibrillator pads has limited their general acceptance. If future studies support their superiority in other clinical settings, it is likely that the pads will gain wider acceptance. Conductive Materials Transthoracic impedance varies with the type of conductive material applied between the paddles and the chest wall. [60] The average adult human impedance is reported to range from 70 to 80 ohms (O). [53] [61] [62] The variability in impedance is contributed to body weight, chest size, chest hair, patient diaphoresis, serial shocks, paddle size, paddle contact pressure, phase of respiration, and type of conductive material used—saline-soaked pads or a specialized conductive paste. For
paddles that are 8.0 cm in diameter, the TTI is 91 ± 20 O for bare contact, 71 ± 11 O for saline-soaked gauze, and 64 ± 15 O for Redux Paste. Clearly, electrode-skin agents reduce impedance and allow more current to be delivered to the heart, but Figure 12-8 (Figure Not Available) Current density/flow with respect to paddle placement. (Adapted courtesy of Medtronic Physio-Control, Redmond, WA.)
the ideal agent is the subject of some debate. Ewy and Taren recommend that Corgel, Redux Paste, American Writer, GE Gel, Electrode Jelly, or Trucon Electrode Paste be used to minimize impedance. Saline-soaked gauze pads may be used, although one must be careful not to allow the saline, coupling gels, or paste to flow into a "bridge" on the skin between the electrodes, creating a potential fire hazard. Although some form of coupling medium (e.g., paste, cream, gel, pad) should be used to reduce impedance, data conflict regarding which product is optimal. Although Redux Paste (Hewlett-Packard) has been associated with significantly lower TTI, a statistically significant increase in the success of defibrillation attempts has not been demonstrated with any specific product. Hummel and coworkers investigated conductive materials with regard to their potential to overheat and to spark. [63] They found that the products that offer lower impedance (e.g., Redux Paste, Signagel) remained stable and did not spark after four or five defibrillation discharges, which was seen with the higher impedance products (e.g., Redux Cream, Aquasonic 100, EKG Sol, Spectra 360, and Derma-Jel). [63] With the advent of self-adhesive pads that serve as leads and paddles, conductive material will probably become more standardized. Regarding diaphoresis and body hair, it is recommended that excessive perspiration be expediently wiped off if poor electrode contact is a problem. causes poor adhesion and the possibility of electrical spark and arcing, it should be quickly removed. [64]
[4]
If body hair
PROCEDURE Victims suffering from sudden cardiac death (SCD) should be defibrillated as quickly as possible ( Fig. 12-9 ). Current recommendations are that defibrillation be attempted up to three times prior to initiating CPR [4] [7] [65] unless additional personnel are on the scene and can perform CPR while the defibrillator device is being readied for use. Although survival from VF is highly dependent on many variables, the timeliness of defibrillation is the most important intervention determining the prognosis in cardiac arrest. [3] [9] Upon recognition that a victim is unresponsive, apneic, and pulseless, help should be summoned immediately. However, this should not cause delays in the timely implementation of defibrillation. Saline-soaked pads or an alternate conductive medium should be applied to the chest where the "quick-look" paddles are going to be placed. Alternatively, a conductive material may be spread onto the entirety of the paddle's conductive surface prior to placement onto the victim's chest. However, care should be taken to avoid excess gel/paste on the paddles, because this could cause arcing or inadvertent harm to the operator. The paddles should then be firmly (25 lbs of downward force) applied to the chest wall and held there by the operator. This will optimize skin-electrode contact and decrease resistance. Also, this will ultimately enhance the appropriate passage of current through the heart during defibrillation. One paddle should be positioned to the right of the upper sternum below the clavicle. The second paddle is placed just to the left of the nipple in the midaxillary line and is centered in the fifth intercostal space ( Fig. 12-10 ). Placement of both paddles close together on the anterior chest wall should be avoided. In some paddle sets, each paddle is labeled as either "sternum" or "apex" so that any rhythm detected on
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Figure 12-9 Ventricular fibrillation/pulses VT algorithm. (From Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 102(Suppl 1):I-147, 2000.)
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Figure 12-10 Anterolateral paddle electrode position. (From Suratt PM, Gibson RS: Manual of Medical Procedures. St Louis, CV Mosby, 1982. Reproduced by permission.)
the monitor can be properly aligned. This feature is irrelevant for defibrillation but is important for cardioversion (see the second section of this chapter). Anteroposterior paddle positioning is also acceptable and may deliver more current to the heart. In the patient with a normal cardiothoracic anatomy the anterior electrode can be placed to the left of the sternum over the precordium and the posterior electrode is placed just to the left of the spine directly posterior to the heart. In the tall, thin or emphysematous appearing patient the anterior paddle should be to the right of the sternum, as the heart is more retrosternal ( Fig. 12-11 ). With the monitor turned on and set to display the "paddle" electrodes, the rhythm is evaluated. If a flatline rhythm is detected, the operator must ensure that monitor gain is increased fully in order to rule out the presence of a "fine VF" tracing. Should the tracing remain flat during a brief pause in closed-chest cardiac massage, the paddles should be rotated 90° from the original position and the rhythm reassessed. The incidence of VF masquerading as asystole was approximately 2.5% in 1 prehospital study of patients with an initial flatline monitor rhythm. [33] Other conditions can cause a flatline rhythm during VF arrest. Cummins recommends that the rescuer also check all monitor cable connections to the patient and defibrillator, check the ECG size control, and check the power supply. [65] If VF is observed during any of these maneuvers, defibrillation should proceed without delay. Should a bradycardia or asystolic rhythm be detected, standard resuscitation measures, including basic CPR, correction of hypoxia, administration of catecholamines, correction of volume or cardiac filling deficiencies, and emergency cardiac pacing should be initiated when indicated. Although defibrillation should have no theoretical benefit for asystole, the use of countershock will result in the development of a QRS rhythm in a very small percentage of patients with flatline rhythms who receive such shocks. Presumably, such cases represent instances of fine VF simulating a flatline rhythm on the ECG. In cases of "fine VF" in which a patient is wearing an implanted (subcutaneous) pacemaker, the pacer spikes may initially appear to be a paced but nonconducted rhythm; attention to the baseline and lack of ST changes characteristic of capture should reveal the true nature of the dysrhythmia. [66] Because injury to the pacemaker pulse generator [66A] and to the myocardium can occur by transmission of current down the pacing electrode, the clinician must be careful to situate the defibrillator paddle at least 1 inch (2.5 cm) [67] away from the pulse generator.[4]
Figure 12-11 Anteroposterior paddle electrode position. Use this placement in tall, thin individuals with retrosternal cardiac location. (From Suratt PM, Gibson RS: Manual of Medical Procedures. St Louis, CV Mosby, 1982. Reproduced by permission.)
In the presence of VF, the paddles should be immediately charged to a stored energy of 200 J for adults. Keep in mind that separate power switches may be needed to turn on the defibrillator and to store the charge. A button or a dial on the control panel usually sets the amount of charge. In most devices, the preset level of charge (energy) can be stored if a button on the "apex" paddle is depressed. The clinician should always check to be certain that the defibrillator is not in the synchronous (cardioversion) mode. Once the paddles are charged, the clinician should instruct all personnel to " STAND BACK" from the patient and the stretcher to avoid stray discharge. The operator/clinician should then say aloud "I'M CLEAR, YOU'RE CLEAR, WE'RE ALL CLEAR" just prior to delivering the countershock. [4] However, there is no need for the individual who is bag-tube ventilating the patient to drop the bag and stand back if their only contact is a rubber or plastic bag. That individual is not touching conductive materials and will thus be protected from electrical shock. The defibrillator operator, in particular, must be sure that his or her only direct contact with the patient or stretcher is with dry paddle handles. The patient is allowed to exhale passively to minimize TTI, [68] while firm (25 lb) pressure is applied through the paddles to the thorax.[69] To minimize energy decay inside the device, the energy in the paddles is discharged through the chest as soon as possible after charging.
Simultaneous depression of both paddle discharge buttons is essential for discharge. Anticipation of
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patient extremity motion subsequent to discharge of the paddles will minimize operator and patient injury. Should no skeletal muscle contraction occur following simultaneous depression of the discharge buttons, the clinician should ensure that: firm chest wall contact has been made (some devices will not discharge without adequate contact), the device is set in the asynchronous mode, a charge has been stored, the defibrillator (not just the monitor) is turned on, and the battery is not depleted (when operating off the storage battery). If there is no muscle contraction even when these factors have been ruled out, a replacement defibrillator should be immediately brought into use. After the first shock, the paddles should remain in place for 5 to 10 seconds to enable the clinician to check for an organized rhythm while ventilation is continued. While waiting to analyze the rhythm, the rescuer should recharge the paddles for an immediate second defibrillation (200 to 300 J for adults) should VF persist. Should VF continue after the second shock, an immediate third defibrillation (360 to 400 J for adults) should be given. Immediate recharging of the defibrillator and rapid succession in the administration of the shocks decreases chest wall impedance. If the third defibrillation is unsuccessful, closed-chest cardiac massage should be continued, hypoxia corrected, and a-agonist catecholamine (epinephrine) [70] [71] or naturally occurring antidiuretic hormone vasopressin [72] administered intravenously to elevate the diastolic pressure and to improve coronary perfusion. [4] [70] [71] [73] Following circulation of the catecholamine or vasopressin agent, an attempt at defibrillation should be repeated. Currently there are no data to suggest that "high-dose" epinephrine use is associated with superior long-term survival compared to standard doses in either children or adults. [74] Superiority of epinephrine versus vasopressin has not been satisfactorily established. [4] Because excessive defibrillation energy may produce irreversible VF in the patient suffering toxic effects of digitalis, the lowest available energy level should be used for the initial defibrillation. If the initial energy dose is unsuccessful, the energy level can be increased cautiously for successive countershocks. Additional therapy (see the following section) can be undertaken to enhance defibrillation. Adequate ventilation, cardiac massage, correction of electrolyte disorders, ischemia, and acidemia are intrinsic to every resuscitation. In addition, evaluation of the patient for hypothermia and rapid core rewarming when indicated should not be overlooked. When practical, electronic monitoring devices and transvenous pacemakers should be turned off or, preferably, disconnected from the patient to avoid equipment damage. Recently manufactured patient monitoring devices, however, have built-in protective filter circuitry, which makes equipment damage an unlikely occurrence.
ENHANCING DEFIBRILLATION SUCCESS Early Defibrillation Energy requirements for conversion of VF may increase dramatically shortly after the onset of VF. [69] The rationale for early defibrillation is that in the absence of adequate coronary perfusion, cellular metabolism continues with the depletion of energy substrates and the accumulation of toxic metabolites. Electrophysiologic changes secondary to cellular ischemia/acidemia develop rapidly and contribute to continued asynchronous transmission of VF wavefronts. The American Heart Association Guidelines [4] support the belief that the most effective treatment for VF is early defibrillation [7] and that the probability of successful defibrillation decreases rapidly over time. [3] Clinical investigation of immediate defibrillation rather than drug therapy preceding defibrillation is limited. Martin and coworkers, in a retrospective analysis of prehospital VF resuscitation, found that survival until hospital discharge was increased when CPR followed by immediate defibrillation was used rather than CPR and drug therapy before countershock. [75] The group that received drug therapy first had a longer mean time until defibrillation (12 minutes additional), which was explained in part by the time required for IV line placement, drug administration, and drug circulation. The time lag until first shock may have confounded the results. Other studies describing treatment of prolonged VF suggest that CPR be performed for approximately 1 minute prior to administration of countershock. [17] The 2000 Guidelines suggest that administration of anti-arrhythmic medications may actually promote dysrhythmias. With the obvious controversies and confounders inherently present in these data, it is suggested that until further clinical studies are available, immediate defibrillation for VF appears to be the most appropriate course of action. Current-Based Defibrillation An alternative approach to defibrillation has been an attempt to use current-based (amperes) defibrillation. This approach would theoretically deliver the appropriate energy to the fibrillating myocardium by compensating for variations in thoracic impedance. Thus, patients with high impedance would not be victim to failed defibrillation secondary to insufficient energy delivery and patients with low impedance would not suffer myocardial damage due to excess current delivery. [48] [53] Based on monophasic damped sinusoidal (MDS) waveform research, it has been reported that 30 to 40 A is the optimal current necessary for defibrillation. Investigations are under way to determine values for biphasic waveform defibrillation. [76] Clinically, this is not an issue that the clinician has to adjust at the time of this writing. It may, however, modify future defibrillator design and enhance defibrillation outcome. Transthoracic Impedance (TTI) To accomplish successful defibrillation, sufficient current (amperes) must flow through the myocardium. Delivery of this current to the heart is dependent on the energy (joules) selected and the impedance or resistance (ohms [?]) to transmission of that energy from the paddles, through the chest wall and accompanying structures until the current traverses the heart itself. The greater the impedance or resistance, the less there is of delivered current. Reported values for human TTI using electrodes 8.0 cm in diameter range from 70 to 80 ohms with a mean of 75 ohms. [53] [61] [62] [77] We have previously discussed the factors that may affect TTI. The importance of paddle electrode composition and size, conductive materials applied paddle-to-chest-wall pressure, phase of ventilation, presence of excess chest hair, diaphoresis, and location of the paddle on the chest wall ( Table 12-2 ) all contribute to TTI. All of these factors must be considered and dealt with to facilitate successful defibrillation.
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Determinant
TABLE 12-2 -- Determinants of Transthoracic Impedance * Effect
Interelectrode distance (chest size)
Larger distance ? higher impedance
Energy selected
Higher energy ? lower impedance
Electrode size
Larger electrode ? lower impedance
Electrode-skin couplants
Failure to use a couplant ? very high impedance
Previous shocks
Previous shock ? lower impedance, especially after first shock
Phase of respiration
Inspiration ? higher impedance
Electrode-chest contact pressure (handheld paddles)
Firm pressure ? lower impedance
*Lower impedance is preferred. Higher impedance lessens the current delivered to the heart. (From Kerber RE: Electrical treatment of cardiac arrhythmias: Defibrillation and cardioversion. Ann Emerg Med 22:296, 1993.)
The TTI of DC discharge also decreases with higher energy shocks, with increasing number of previous countershocks delivered (see Table 12-2 )[77] [78] and with decreasing interval between the discharges. Unfortunately, each of the aforementioned maneuvers is also associated with an increased potential for myocardial injury. When considering normal defibrillation, the chest should be relatively dry, a conductive medium must be appropriately placed onto the chest, and a good seal must be established between the chest and the paddles. The paddles should be of appropriate size. Twenty-five pounds of force should be applied to the paddles and chest. Discharge of energy should be done at the end of an expiration. Energy selected should be appropriate for the initial shock—usually 200 Joules. [4] Nonetheless, one may be faced with the need to defibrillate a very obese patient who is unresponsive to standard paddle placement and maximum device energies. Should such a situation exist, the patient can be rolled on the side and anteroposterior defibrillation attempted. Should this prove unsuccessful, a second defibrillating device can be simultaneously charged and used to administer countershock immediately following discharge of the first defibrillator. It is interesting to note that a canine study of internal defibrillation indicated that two sequential shocks over different pathways reduced both total energy and peak voltage required to terminate VF.[79] Hence, sequential defibrillation using slightly different paddle placements may be beneficial independent of the concurrent reduction in TTI. Energy Choice Current International Liaison Committee on Resuscitation (ILCOR)/American Heart Association (AHA) guidelines recommend that energy for the first monophasic shock should be 200 J, and if unsuccessful, that the energy be escalated to 300 J or 360 J as needed. [4] [80] Many investigators have referred to a so-called defibrillation energy threshold for converting VF. Davy and coworkers suggest that no unique defibrillation energy threshold exists for the in vivo heart. [81] Experimentally, they found that successful defibrillation was related to delivered energy, which follows a typical "dose-response curve." However, there is evidence for a defibrillation current threshold. [54] Successful defibrillation is dependent on the simultaneous depolarization of a sizable mass of the myocardium resulting from the passage of current through the heart.
For a given thorax, defibrillation device, and defibrillation technique, more current is passed through the heart and, hence, more tissue is depolarized with larger energies. Once sufficient tissue has been depolarized, however, additional current is not desirable and may, in fact, produce additional tissue injury. Kerber and coworkers have suggested that the use of defibrillators that adjust defibrillation energy for the patient's TTI (measured by the device just before charging) may be one means to deliver an adequate current to the myocardium while minimizing potential harm as discussed earlier. [82] Such devices are not in routine use at present, but they may be helpful in the future for both the identification of high-impedance situations and adjustment of delivered energy. [48] Several studies have supported the concept that when current needs cannot be predicted nor current delivery measured, a weight-adjusted dosage of energy is preferred for converting VF. Indeed, a dose based on the patient's weight has been found clinically useful for treating children suffering VF. [83] Other prospective human adult studies have questioned the importance of dose strength to conversion of VF. [84] [85] Weaver and coworkers, using monophasic waveforms for defibrillation, alternated treatment protocols to determine prospectively the merits of 175 J (200 J of stored energy) versus 320 J (400 J of stored energy) countershocks for defibrillation. [80] On test days, VF patients were shocked initially with 1 or 2 175 J discharges, and all subsequent shocks needed were 320 J. On alternate days, only 320 J shocks were given. The investigators found that 73% (n = 76) of the patients were defibrillated following the first 2 shocks in the low-energy group, whereas 81% (n = 77) of the patients were initially defibrillated in the high-energy group (difference not statistically significant). Asystole occurred in 19% of patients receiving high energy and in 12% receiving low energy. Transient or persistent heart block occurred in 25% of patients shocked with high energy versus 11% of patients shocked with low energy. Survival until hospital discharge was inversely related to the number of shocks required; no patients who required >8 shocks survived. Weaver and associates concluded that low-energy (175 J delivered) countershocks were safe, effective, and less cardiotoxic. Obviously, many factors besides discharged energy play a role in successful defibrillation. Kerber found that defibrillation success rate is a unimodal function of transthoracic current. [86] The maximum defibrillation rate for their patients with a brief duration of VF (~35 seconds. [2] The AICD case is implanted in a subcutaneous pocket in the abdominal wall ( Fig. 13-5 and Fig. 13-6 ). The wires are run through a subcutaneous tunnel to the chest. A variety of surgical approaches to the heart are used. [19] The ventricular patches are sutured to the epicardium or parietal pericardium in roughly anterior and posterior positions on the left ventricle, depending on the surgical approach. The sensing electrodes may be placed in either the left or right ventricle. In those patients in whom the new transvenous lead is used, thoracotomy is not needed—the AICD case is still in the typical abdominal position, and a submuscular patch is placed in the chest wall. AICDs may be inactivated by a magnet, either purposely or inadvertently. They may also be interrogated via a radiotelemetry device (a procedure normally performed by a cardiologist).
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Figure 13-2 Automatic implantable cardioverter-defibrillator (AICD). (Courtesy of Medtronics Inc., Minneapolis, MN.)
INDICATIONS FOR IMPLANTABLE DEVICE USE Current indications for permanent pacemaker use include complete heart block, symptomatic type II second-degree block, second-degree block with episodic ventricular arrhythmias, sick sinus syndrome, symptomatic bradycardias with syncope or presyncope, hypersensitive carotid artery syndrome, type I block with infra-His bundle block, and certain subgroups of patients with triphasic and biphasic blocks at risk of developing sudden high-degree block. [14] [20]
Figure 13-3 Posteroanterior (A) and lateral (B) chest radiographs demonstrating typical appearance of AICD with ventricular patches.
The use of AICDs is generally limited to patients who are at high risk of sudden cardiac death from ventricular arrhythmias. Currently accepted indications are a documented episode of hemodynamically significant, sustained ventricular tachycardia or fibrillation; ventricular arrhythmia refractory to standard antiarrhythmic therapy as demonstrated electrophysiologically; persistent electrophysiologically inducible ventricular arrhythmia despite best available drug therapy; and recurrent syncope in a patient with electrophysiologically inducible ventricular arrhythmia in whom no effective drug is tolerated or available. [3] [16] [21]
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Figure 13-4 Posteroanterior (A) and lateral (B) chest radiographs demonstrating typical appearance of single-lead transvenous AICD.
Contraindications to AICD use are life expectancy of less than 6 months, New York Heart Association class IV heart failure, treatable causes of ventricular arrhythmias, or incessant or very frequent ventricular arrhythmias that result in rapid battery depletion.
Figure 13-5 Typical external appearance of AICD implanted in the abdominal wall. (Courtesy of Lawrence B. Stack, MD. From Munter DW, DeLacey WA: Automatic implantable cardioverter-defibrillators. Emerg Med Clin North Am 12:579, 1994. Used with permission.)
COMPLICATIONS OF PERMANENT PACEMAKERS Complications are commonly seen with permanent pacemakers. Failure rates in the first year postimplantation range from 7.4%
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Figure 13-6 Radiographic appearance of the implanted AICD in the abdominal wall.
to 15.0%, most occurring within the first 30 days. [1] After this initial period, approximately 6% of pacemakers fail each year. [22] Pacemaker failure can be categorized as failure to pace, failure to sense, failure to capture, inappropriate pacemaker rate, and other complications (e.g., vascular or infectious) ( Table 13-2 ). Failure to sense is the most common problem, accounting for 32% to 57% of failure cases. [3] [22] [23] Failure to Pace This condition is characterized by the lack of production of pacemaker spikes despite the lack of intrinsic cardiac electrical activity or an intrinsic cardiac rate falling below the threshold for pacing. Causes of failure to pace include lead fracture or disconnection, battery depletion, component failure, and oversensing. Lead fracture or disconnection may occur months to years after pacemaker implantation and may be due to inherent stress at the lead connection site. Blunt trauma may also cause lead fracture. [24] [25] [26] Battery depletion is normally a gradual process and is usually detected on routine checkups before complete failure of the pacemaker. regular follow-up may present with previously undetected battery depletion.
TABLE 13-2 -- Complications of Permanent Pacemaker Use Failure to pace (no pacemaker activity present) Lead fracture Lead disconnection Battery depletion Component failure Oversensing External interference Failure to sense (constant pacemaker spikes despite ongoing intrinsic cardiac electrical activity) Lead dislodgement Lead fracture Fibrosis around lead tip Battery depletion Pacer in asynchronous mode External interference Low-amplitude intracardiac signal Failure to capture (pacemaker spikes but no subsequent cardiac activity) Lead dislodgement including perforation Lead fracture Lead disconnection Poor lead position Fibrosis around lead tip Battery depletion Metabolic abnormalities Medications Inappropriate pacemaker rate (runaway pacemaker) Pacemaker reentrant tachycardia Resetting from external interference Battery depletion Other Infections: pocket, wires Lead displacement: cardiac perforation, tamponade, pericarditis, vascular perforation Vascular complications: thrombosis, superior vena cava syndrome Psychiatric: anxiety, panic attacks
[ 23]
Patients who have not had
Component failure may be due to various external influences including blunt trauma, therapeutic radiation, electrocautery, transthoracic defibrillation, diathermy, electroshock therapy for depression, magnetic resonance imaging (MRI), and extracorporeal shock-wave lithotripsy. [13] [23] [27] [28] [29] [30] Pacemakers may oversense or misinterpret nonQRS complex electrical activity (e.g., P waves, T waves, muscular activity, or chest thumping). [23] If this activity is interpreted as a QRS complex, the ventricular spike will be inhibited. If, however, the pacemaker is dual chambered and the electrical activity is misinterpreted as a P wave, it will stimulate firing of the ventricular electrode, which can lead to overpacing. External stimuli can also be misinterpreted and lead to oversensing. This interference can include electrocautery, MRI, diathermy, transcutaneous electrical nerve stimulation (TENS), electroshock therapy, ultrasound dental scalers, static electricity, or vibration (e.g., from a tractor or helicopter). [27] [31] [32] [33] [34] [35] Failure to Sense This condition is characterized by the presence of constant pacemaker spikes despite ongoing intrinsic cardiac electrical activity that should inhibit the device. Failure of the pacemaker to sense cardiac electrical activity can be due to lead
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dislodgement, lead fracture, normal development of fibrosis around the lead tip that occurs with time, battery depletion, external interference, or an intrinsically low-amplitude cardiac signal. Lead dislodgement, the most common reason for failure to sense, can be due to an enlarged right ventricle, poor initial lead positioning, blunt trauma, or patient manipulation of the generator unit in the chest wall pocket (pacemaker twiddler's syndrome). [23] [36] [37] [38] Fibrosis normally develops around the tip of the electrode, and this fibrosis can lead to abnormal sensing or higher required thresholds for pacing.
[36]
Several cardiac and metabolic abnormalities cause the intrinsic cardiac electrical activity to be of lower than normal amplitude, causing undersensing of the QRS complexes. Failure to Capture This condition is the appropriate presence and timing of pacemaker spikes, but without resultant cardiac activity. Reasons for failure to capture include lead dislodgement (e.g., myocardial perforation), lead fracture, lead disconnection, poor lead position, lead tip fibrosis, battery depletion, and metabolic abnormalities (e.g., hyperkalemia) or medications (e.g., lidocaine, flecainide) that make the myocardium less responsive to electrical impulses. Lead dislodgement is the most common reason for failure to capture. [23] Inappropriate Pacemaker Rate This condition, also known as a runaway pacemaker, is a rare complication that is usually seen in dual-chamber pacemakers. [39] [40] In dual-chamber pacers, it is caused by an endless loop reentry tachycardia, often initiated by a retrograde P wave. [40] In older or single-chamber pacemakers, it can be due to component failure or battery depletion. [41] Component failure is rare, as almost all pacemakers have circuitry to prevent high discharge rates.
Figure 13-7 A and B, Appearance of fracture of atrial "J" retention wire. A, Radiographic appearance of fracture of atrial "J" retention wire. B, Diagram of fracture site. (Courtesy of Telectronics Pacing Systems, Englewood, CO.)
Other Complications Infections including localized skin or pocket infections, more complicated infections along the route of the wires, or endocarditis occur in 1% to 15% of patients. [44] These infections are initially treated with broad-spectrum antibiotics against Staphylococcus aureus, but they often require removal of the pacemaker. [13] [44]
[ 42] [43]
Lead displacement, in addition to causing failure to sense or capture, can cause injury to the myocardium including cardiac perforation with resultant tamponade or restrictive pericarditis, [36] [45] [46] and it is usually seen early after pacemaker implantation. Fracture of the J-shaped retention wire within the lead can result in a protrusion of the wire outside the protective plastic coating. This protruding wire can then puncture the superior vena cava or right atrium, resulting in bleeding or cardiac tamponade. [47] Figure 13-7 illustrates this fracture. Vascular complications include thrombosis or superior vena cava syndrome. Many pacemaker patients have a benign thrombosis of the upper arm or shoulder, but only about 2% have a serious thrombotic or embolic event. [44] Superior vena cava syndrome is a rare complication. [48] Psychiatric complications include panic attacks and anxiety, which may prompt ED evaluation. [13] [44]
COMPLICATIONS OF AICDs The most common complication is the delivery of inappropriate shocks by the device when not indicated by a tachydysrhythmia. Up to 35% of AICD patients receive inappropriate shocks. [49] Causes of inappropriate shock delivery include misinterpretation of sinus tachycardia, atrial fibrillation, muscular activity (e.g., shivering), T waves, or extraneous sources (e.g., pacemaker spikes or vibrations) as a shockable tachydysrhythmia. [50] [51] Likewise an unsustained tachydysrhythmia also may be shocked. Component failure, such
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as electrode failure or migration, may result in false sensing and resultant shocking. Pacemaker magnet testing has produced inappropriate shocks resulting in ventricular fibrillation. [52] Other reported long-term complications include interference with cardiac pacemakers, particularly after AICD discharge [53] [54] ; component failures such as patch migration or distortion, [55] lead fracture, generator case rotation or fracture, and battery depletion; constrictive pericarditis and pericardial effusions, [56] [57] [58] cardiac fibrosis, and atrial or ventricular wall perforations after repeated shocks [58] [59] ; abdominal pocket infections [60] ; thrombosis and pulmonary embolism; erosion into the lung with hemoptysis [61] ; patient trauma sustained during falls after delivery of a shock, either due to the physical "jolt" of the shock [62] or to suspected postshock bradycardia and hypotension [63] [64] ; and psychiatric disorders, such as adjustment disorder, panic attacks, or major depression. [65] [66] The AICD may be inadvertently inactivated by any strong magnetic force including microwave ovens, industrial engines, metal detectors, magnets in speakers, refrigerator door magnets, bingo wands, and model airplane starters. [2] This inactivation is not normally noted until routine follow-up, but if the patient has a tachydysrhythmia, no shock will be delivered.
EVALUATION OF PACEMAKER PATIENTS Pacemaker patients presenting to the ED for any problem that may be associated with the device should have an evaluation that includes investigation of potential pacemaker malfunction. Historical Issues Pertinent information about the pacemaker unit should be obtained. The brand and manufacturer, type (NBE code), * implantation site, programmed rate, and any changes seen during follow-up at a pacemaker clinic should be noted. The time of implantation is important as certain types of complications such as lead failure, migration, or perforation typically occur within 3 months, whereas generator or battery failure usually occur later. [36] Some medications, such as lidocaine or flecainide, can raise myocardial thresholds to pacing,
[23]
and their use should be evaluated.
Patient symptoms that may be related to pacemaker failure should be ascertained. Chest pain may be due to cardiac ischemia, but pacemaker complications such as cardiac perforation, pericarditis, or infection may also be the cause. Recent trauma, especially to the chest or back, can cause failure of the generator unit, lead fracture, or lead displacement. Recent cardioversion or defibrillation, MRI, diathermy, lithotripsy, or electroconvulsive therapy for depression can have the same effect. [24] [25] [26] [27] [28] Symptoms of decreased cerebral perfusion, such as syncope, near-syncope, or orthostatic light-headedness, may indicate pacemaker malfunctioning that could lead to bradycardias. A runaway pacemaker can also cause these symptoms due to low cardiac output during the tachycardic phase. Palpitations are more typically due to intrinsic cardiac activity, but pacemaker failure to sense can cause an irregular rhythm due to inappropriate generation of pacer spikes, which may be perceived by the patient. The time and results of the last follow-up visit should be obtained if possible. Physical Examination The patient should be examined for potential pacemaker complications. The head and neck should be inspected for venous engorgement, which may indicate thrombosis or superior vena cava syndrome. [36] The chest wall, and especially the pacemaker pocket, should be inspected and palpated for erythema, edema, tenderness, and location of the pacemaker generator. The initial course of the lead wires should also be palpated. If the generator unit is malrotated or in a position other than the original pacemaker pocket, this may indicate "pacemaker twiddler's syndrome" (i.e., purposeful or inadvertent manipulation by the patient), [37] [38] which can lead to lead dislodgement or disconnection. The cardiac examination may be altered by the functioning of the pacemaker. A paradoxically split second heart sound is normal and is due to the origination of the pacemaker spike in the right ventricle. If the second heart sound is widely split, and widens more with inspiration, a left ventricular origin may be present due to cardiac perforation or lead migration. [36] A pericardial friction rub may be due to pericarditis, potentially from lead perforation. [45] A new murmur may be the result of infective endocarditis. [36] X-Ray A chest radiograph should be obtained and compared to old films, preferably ones taken shortly after implantation. Location of the generator and battery type should be ascertained. Lithium batteries are seen as a single radiopaque portion of the generator unit, whereas older pacemakers have four to five button batteries. Lead locations should be noted and migration should be sought. Lead presence outside the myocardial shadow is indicative of perforation. The connection site at the generator unit should be examined for disconnection. The lead wires should be traced and examined for fracture, or J retention wire fractures (see Fig. 13-7 ). Electrocardiogram The electrocardiogram (ECG) contains important information about pacemaker function and should be compared to old ECGs. An asynchronous mode pacemaker (i.e., VOO) will have regular pacer spikes followed by QRS activity. A left bundle-branch pattern is normal, as the lead is usually in the right ventricle. Absence of pacer spikes in the asynchronous mode is termed failure to pace. Absence of a QRS complex after a pacer spike represents failure to capture. Some pacemakers have a programmed feature called hysteresis, in which the intrinsic rate below which pacing is triggered is somewhat lower than the resultant pacing rate. Hence the pause following a spontaneous QRS complex may be longer than an R-R interval at normal pace. Pacemakers that sense intrinsic cardiac activity and are inhibited by same (i.e., VVI) should only generate pacer spikes if the patient's intrinsic rate falls below the programmed rate. In this case, pacer spikes followed by QRS complexes, again in a *North American Society of Pacing and Electrophysiology-British Pacing and Electrophysiology Group generic pacemaker code (NBE code).
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left bundle-branch pattern, should be noted. Failure to pace or capture may be seen. Pacer spikes occurring despite an intrinsic rate above the programmed rate represent failure to sense. Electrocardiograms from patients with dual chamber pacemakers (i.e., DDD) may demonstrate various rhythms. [36] These include the patient's intrinsic rhythm, atrial pacer spikes followed by a P wave and then an intrinsic QRS, or two pacer spikes sequentially followed by a P wave and then a QRS complex. Failure to pace, capture, or sense may again be noted. The electrical axis of the pacer spike and paced QRS complex should be compared to old ECGs. A change of the pacer spike axis may signal lead migration. [36] Normally, the paced QRS complex is a left bundle-branch pattern. A right bundle-branch pattern may be due to left ventricular lead placement, but a change from old ECGs from a left to a right bundle-branch pattern may be due to migration of the lead or perforation of the ventricular septum. Paced rates that are higher than the programmed rate can be due to pacemaker-mediated tachycardia, a reentrant tachycardia normally seen only in dual-chambered pacemakers, [39] [40] or runaway pacemaker, normally seen only in older pacemaker models and due to battery depletion or component failure. [41] External electrical sources can mimic pacemaker spikes and be misinterpreted as an inappropriate pacing rate. [36] General Management Patients who are found to have failure to sense or capture should undergo the basic evaluation outlined earlier; in addition, serum electrolyte assays should be performed to assess metabolic abnormalities. These patients and patients with infections, lead displacement, disconnection or fracture, or vascular complications will
require cardiology consultation for intervention as determined by the etiology of the malfunction. Patients who have failure to pace may undergo a magnet test in the ED to rule out battery depletion or oversensing. Patients with pacemaker-mediated tachycardia or runaway pacemaker need prompt cardiology evaluation, and those with unstable conditions require acute intervention in the ED, as outlined in the next section. Use of a Magnet in Pacemaker Assessment Indications
Magnet testing of a pacemaker is used on patients with "failure to pace" to assess for battery depletion, component failure, or oversensing. It is also indicated for pacemaker-mediated tachycardia or runaway pacemaker in an attempt to terminate the rhythm. Equipment and Setup
Typically, a ring magnet ( Fig. 13-8 ) is used for this procedure. Different brands of magnets are also available for specific pacemakers, but in almost all cases, a standard pacemaker ring magnet will suffice. The patient should undergo a baseline ECG and should be on a cardiac monitor. Placement of a magnet on a pacemaker closes a reed switch and reverts the pacemaker to an asynchronous, or fixed rate, mode. Technique
The location and orientation of the pacemaker generator should be ascertained by palpation. It is typically in the left or right upper chest wall ( Fig. 13-9 ). The magnet is placed
Figure 13-8 Ring magnet.
directly on the chest wall over the pacemaker generator ( Fig. 13-10 ). A repeat ECG is obtained to compare to the baseline ( Fig. 13-11 and Fig. 13-12 ). Some brands of pacemakers have either a several-second delay or a series of two to three rapid pacer spikes before reverting to the asynchronous mode. [36] If the patient has an underlying bradycardia associated with failure to pace that is corrected by magnet placement, the magnet should be left over the generator. Likewise, if a pacemaker-mediated tachycardia or runaway pacemaker is reverted to a normal rate or rhythm, the magnet should be left in place pending consultation with a cardiologist. Complications
Incorrect alignment of the magnet may cause only intermittent pacing in the asynchronous mode. Some pacemakers react erratically to a non-brand-specific magnet; if this is considered an issue, attempt to obtain a brand-specific magnet. Interpretation
In the case of failure to pace, three outcomes are possible: (1) The pacemaker will fire at its programmed rate (this is the expected outcome). In the case of failure to pace, this indicates that the pacemaker was oversensing and was inappropriately
Figure 13-9 Typical location of pacemaker pocket in upper chest wall.
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Figure 13-10 Application of ring magnet over pacemaker generator.
inhibited. The cause of the oversensing should then be investigated. (2) The pacer may not produce any spikes at all. This is indicative of component failure and requires cardiology consultation. (3) The pacemaker may produce spikes, but at a rate lower than the programmed rate, which is indicative of battery depletion; this also requires cardiology consultation. Management of Pacemaker-Mediated Tachycardia or Runaway Pacemaker Indications
These maneuvers are indicated for correction of an inappropriately high pacemaker rate.
Figure 13-11 Electrocardiogram of patient with a nonfiring pacemaker. Intrinsic cardiac rate is 80 beats/min, and no pacemaker activity is seen. Equipment and Setup
Intravenous access should be obtained and the patient should be placed on a cardiac monitor. A baseline ECG should be obtained. Because the definitive treatment often requires radiotelemetric reprogramming of the pacemaker, a cardiology consultation should be obtained. A ring magnet will be needed as well as a transcutaneous pacemaker unit with pads. If open lead disconnection is required, local anesthetic, sterile drapes, scalpel blade and handle, hemostats, and Mayo scissors or wire cutters will be needed, as well as either a transcutaneous pacemaker or portable pacemaker unit with alligator clip.
Technique
The initial procedure is to place a ring magnet over the pacer generator as described earlier. If the pacer then reverts to an asynchronous mode at the appropriate programmed rate, the magnet should be left in place. If magnet placement has no effect, then isometric pectoral exercises should be attempted. [13] [39] This is done by having the patient place his or her hand from the same side as the pacemaker generator onto the opposite shoulder and push against the shoulder as long and as hard as possible. This creates rapid muscle activity in the pectoral muscle surrounding the pacemaker generator, which may be interpreted as ventricular activity and inhibit the pacemaker, [39] [40] terminating the reentrant tachycardia. If this maneuver is unsuccessful and the patient's condition is stable, continue to monitor the patient and await cardiology consultation. If the patient's condition is unstable, the next maneuver is to attempt a standard chest (precordial) thump.[13] [39] This is performed by firmly striking the midsternum with a clenched fist from a distance of 30 to 38 cm. This procedure may be repeated once if needed. [39]
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Figure 13-12 Electrocardiogram of same patient with magnet applied over pacemaker, producing a paced rhythm. Pacer spikes are evident ( arrows) and the magnet rate is 85 beats/min. Note the left bundle-branch bundle typical of a pacer lead in the right ventricle.
If the chest thump is unsuccessful, attach transcutaneous pacemaker pads anteriorly and posteriorly, and attach the leads to the transcutaneous pacemaker generator. Pace the patient at an initial output of 2 to 5 mA and a rate of 40 beats/min. [39] This will stimulate chest wall movement that may be interpreted as ventricular activity and inhibit the pacemaker, terminating the reentrant tachycardia. Unipolar DDD pacemakers are normally inhibited at a low output. Bipolar DDD pacemakers often need higher outputs of up to 10 to 20 mA. [39] If increasing the output is unsuccessful, raise the transcutaneous pacing rate slightly to attempt to deliver chest wall stimulation outside the pacemaker's particular ventricular refractory period. [39] If these maneuvers are unsuccessful and the patient is hemodynamically unstable due to the pacer-induced tachycardia, the solution of last resort is to cut the pacer leads from the generator unit. The generator unit should be palpated to ascertain position and orientation. Apply transcutaneous pacemaker pads and connect them to the transcutaneous pacemaker. This is a precautionary measure, as cutting the leads may lead to profound bradycardia or asystole. A portable pacemaker generator should be available. Use povidoneiodine for sterile preparation of the site over the generator and apply sterile drapes. Instill local anesthesia in the skin and subcutaneous tissue overlying the generator in the area of the lead connections. Make a skin incision with a scalpel, and expose the lead wires with blunt dissection. Alternatively, make an incision through the previous scar and remove the pacemaker unit. [41] Cut the lead wires close to the generator using Mayo scissors or wire cutters. At this point, the patient may require transcutaneous pacing. An alternate procedure is to insert a needle into the cathode (negative) lead wire (this is the only wire on unipolar models, and it is identified on bipolar units either by marking or by a white band). [41] Connect an alligator clip to the needle, and connect the alligator clip to the negative terminal of the portable pacemaker generator. Ground the positive terminal via an alligator clip to the subcutaneous tissue of the incision, and pace the patient using the portable generator. [41] Complications Incorrect alignment of the magnet may cause pacing only intermittently in the asynchronous mode. Some pacemakers will react erratically to a non-brand-specific magnet; if this is a problem, attempt to obtain a brand-specific magnet. There are no potential complications from isometric pectoral muscle exercise. Chest thumps can result in sternal or rib fractures, myocardial contusion, pulmonary contusion, extrasystolic complexes, or ventricular tachydysrhythmias. [39] Transcutaneous pacing to stimulate chest wall movement is normally uncomfortable for the patient and can also result in diaphragmatic or arm muscle stimulation as well. Open disconnection of the pacemaker lead wires can be complicated by unanticipated bleeding, difficulty exposing the generator unit, and subsequent infection. A more common complication is the termination of the paced rhythm, resulting in a profound bradycardia or asystole that requires ongoing transcutaneous or portable generator pacing. [41] Interpretation Correction of the pacer-induced tachycardia by lead disconnection only is generally indicative of component failure or
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severe battery depletion, whereas termination by noninvasive procedures is more indicative of a pacemaker-induced endless loop reentrant tachycardia.
[ 39] [41] [ 67]
EVALUATION OF AICD PATIENTS Patients with an AICD who present to the ED can have noncardiac complaints unrelated to the AICD, cardiac complaints, or AICD-related problems, including AICD shocks. The evaluation should focus on potential AICD problems. Historical Issues Patients with AICDs have severe underlying cardiac disease, and will often present with cardiac chest pain, shortness of breath, or congestive heart failure. Potential AICD complications such as pericarditis, pericardial effusion, cardiac fibrosis, atrial or ventricular perforation, and infections of the wires or leads can all present with chest pain. Mortality in AICD patients is typically due to their underlying disease, and any complaints of chest pain must be pursued aggressively. Generator pocket infections or wound infections will produce complaints of pain and fever. The most common AICD-related complaint in patients presenting to the ED is that of one or more AICD shocks. Patients describe the shock as a feeling of being kicked or punched in the chest. [68] [69] The number of shocks received should be ascertained. Associated symptoms of syncope or near-syncope indicate a probable tachydysrhythmia and appropriate shock. Many patients fall down when they experience an AICD shock, and the presence of any fall-related trauma should be queried. Physical Examination The abdominal pocket and subcutaneous tunnel should be evaluated for signs of infection. Heart and lung sounds should be auscultated. A pericardial rub is indicative of pericardial fluid, which may be a result of pericarditis from the AICD. The patient should be examined for any signs of trauma if he or she fell. X-Ray A chest radiograph is generally not helpful, but one should be obtained and compared to old films to look for electrode fracture, displacement of sensing electrodes, and patch migration or distortion. Electrocardiograms An ECG should be obtained. Immediately after an AICD shock, the ECG often shows abnormalities such as ST-segment elevations or depressions. [59] [70] If these changes are due solely to the shock, they will resolve within 15 minutes. Otherwise, the ECG should be examined and compared to old studies for evidence of ischemia. Use of a Magnet for AICD Inactivation The patient who is experiencing inappropriate AICD discharges in the ED can be treated by magnet inactivation of the device similar to the approach described earlier for the pacemaker patient. Technique
The method for inactivating an AICD device is outlined in Table 13-3 . The orientation of the device in the abdominal pocket should be determined, with the lead connections normally cephalad. A ring magnet is then placed over the corner adjacent to the lead connections (usually the upper righthand corner of the device) ( Fig. 13-13 ). A series of beeping tones, which correspond to the sensed QRS complexes, will sound. In the absence of organized QRS activity, random beeps will sound.[68] When the magnet is left in place for 30 seconds, a continuous beep is heard. This indicates that the AICD is inactivated. The magnet should then be removed, and the AICD will remain inactivated. The AICD may be reactivated by applying the magnet for 30 seconds and removing it when the steady beep changes to intermittent beeping. Clinical Follow-Up The AICD patient who has component failure, such as patch migration or lead fracture or dislodgement; infection; vascular complications, such as thrombosis or perforation; or cardiac complications, such as perforation or pericarditis, requires cardiology consultation for admission. The AICD patient who received a single shock and had prodromal symptoms indicative of low cardiac output should be evaluated for myocardial infarction, electrolyte imbalance, or drug toxicity, as well as for any sustained trauma. If findings of this evaluation are normal, the patient is usually released home after discussion with the cardiologist. [2] The patient who received a single shock without related symptoms consistent with a ventricular tachydysrhythmia requires a more extensive evaluation including cardiac monitoring, determination of drug levels as appropriate, and electrolyte level measurement. [68] [69] [71] If the ED evaluation is normal, patients require cardiology consultation. The cardiologist normally interrogates the AICD using either phonogram or telemetry units. The decision to admit or release the patient with potential alterations of antiarrhythmic drug therapy is made based on the results of this testing. Patients whose condition is unstable, who report more than one shock in succession or more than two single shocks in a 1-week period, or who have evidence of ischemia, electrolyte imbalance, or drug toxicity often require admission to a monitored setting for further evaluation and continued monitoring. [2]
TABLE 13-3 -- Method for Inactivation of AICD 1. Determine the orientation of the device in the abdominal pocket, radiographically or by palpation. 2. Place a ring magnet over the upper righthand corner of the device. 3. A beeping tone will sound, which corresponds with the sensing of QRS complexes. 4. Leave the magnet in place for at least 30 sec. 5. When the beeping changes to a continuous tone, the device is inactivated. 6. Remove the magnet. From Munter DW, DeLacey WA: Automatic implantable cardioverter-defibrillators. Emerg Med Clin North Am 12:579, 1994. Used with permission.
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Figure 13-13 Placement of magnet on AICD.
THE PACEMAKER/AICD PATIENT IN CARDIAC ARREST Patients with pacemakers in cardiac arrest may require defibrillation or cardioversion, depending on their presentation. Although most pacemakers have circuitry that protects them from high current flows, various pacemaker-related problems can develop from defibrillation or cardioversion. These include damage to circuitry resulting in complete destruction, decrease in output, or runaway pacing; acute or chronic increases in the pacing threshold, which is normally temporary; undersensing lasting up to 10 days; reprogramming; resetting to a different mode, usually asynchronous; lead displacement; and myocardial thermal or electrical burns at the electrode-myocardium interface leading to ventricular fibrillation. [27] Due to these potential complications, Barold and colleagues have suggested guidelines for defibrillation and cardioversion in pacemaker patients. [27] The first of these is use of the anterior-posterior paddle position, if possible, preferably with specific anterior and posterior paddles. When impossible, the paddles should be placed along a line perpendicular to the line between the pulse generator and the tip of the ventricular lead. For a patient with a pacemaker generator in the left upper chest wall, the appropriate paddle placement would be left lateral chest wall and right midsternal border. For a patient with a pacemaker generator in the right upper chest wall, the appropriate paddle placement would be left upper chest wall and right lower chest wall. Second, the paddles should be placed at least 10 cm from the pulse generator or lead. Third, because of potential damage to the pacemaker or leads, a transcutaneous pacemaker and pads should be readily available if needed, and standby cardiology consultation should be arranged in case emergent reprogramming is needed. Fourth, the patient must be admitted to the hospital and pacemaker functioning must be monitored carefully with repeated threshold testing. Because of the lower current used by AICDs, the possibility of pacemaker damage from AICD discharge in patients with both is remote. [27] The AICD patient who is in cardiopulmonary arrest may be managed in the same manner as patients without the device, with minor modifications. Cardiopulmonary resuscitation (CPR) and transthoracic defibrillation will not harm the AICD. [68] The AICD may spontaneously discharge without warning if the patient's rhythm meets the preset criteria for shocking. In the case of an AICD shock, medical personnel performing CPR may experience a mild electrical shock, [72] but to date no reports of injury to medical personnel from such a shock have been noted. Some authors recommend leaving the AICD activated during cardiopulmonary arrest, [68] allowing it to discharge up to the maximum of four times allowed by the circuitry; but deactivation may be necessary to alleviate fears of medical personnel, to avoid AICD shock-induced arrhythmias, or if temporary cardiac pacing is needed. [2] Defibrillation does not harm the device or circuitry, and may be performed with the usual technique, although a theoretical possibility exists that the epicardial patches can shield the myocardium from the delivered energy. For this reason, paddle placement over the apex and right sternum may be indicated for AICD patients with anterior and posterior myocardial patches, with anterior and posterior paddle placement in AICD patients with a single patch over the cardiac apex. [72]
CONCLUSION Many patients have implanted pacemakers or AICDs. These patients have underlying cardiac disease and may present to the ED with various complaints. Complications associated with these devices are not uncommon. The evaluation of these patients must be directed toward the potential complications. Pacemaker function may be evaluated by ECG and magnet testing, but most problems will require cardiology consultation and intervention. Runaway pacemaker represents a true emergency and must be dealt with expeditiously. AICD complications can be initially evaluated in the ED, but they normally require specialized interrogation devices to analyze the problem. Patients with pacemakers or AICDs in cardiopulmonary arrest require modifications of standard paddle placement for defibrillation or cardioversion, and if an AICD is present, it may need to be deactivated with a magnet.
References 1. Vukmir
RB: Emergency cardiac pacing. Am J Emerg Med 11:166, 1993.
2. Munter
DW, DeLacey WA: Automatic implantable cardioverter-defibrillators. Emerg Med Clinic North Am 12:579, 1994.
3. Nisam
S, Barold S: Historical evolution of the automatic implantable cardioverter-defibrillator in the treatment of malignant ventricular tachydysrhythmias. In Alt E, Klein H, Griffin JC (eds): The Implantable Cardioverter/Defibrillator. Berlin, Springer-Verlag, 1992, p 3. 4. Zoll
PM: Historical development of cardiac pacemakers. Prog Cardiovasc Dis 14:421, 1972.
5. Hunter 6. Zoll
SW, Roth NA, Bernardez D, et al: A bipolar myocardial electrode for complete heart block. Lancet 79:506, 1959.
P, Linethat A, Gibson W, et al: Termination of ventricular fibrillation in man by externally applied electric countershock. N Engl J Med 254:727, 1956.
7. Gabry
MD, Brodman R, Johnston D, et al: Automatic implantable cardioverter-defibrillator: Patient survival, battery longevity and shock delivery analysis. J Am Coll Cardiol 9:1349, 1987.
8. Nisam
S: The automatic implantable cardioverter-defibrillator (AICD): A clinical and technical review. J Med Eng Technol 11:97, 1987.
9. Mirowski 10.
M, Reid PR, Morton M, et al: Successful conversion of out-of-hospital life-threatening arrhythmias with the implanted defibrillator. Am Heart J 103:147, 1982.
Mirowski M, Reid PR, Winkle RA, et al: Mortality in patients with implanted automatic defibrillators. Ann Intern Med 98:585, 1983.
269
11.
Ludmer PL, Goldschlager N: Cardiac pacing in the 1980s. N Engl J Med 311:1671, 1984.
12.
Bernstein AD: Classification of cardiac pacemakers. In El-Sherif N, Samet P (eds): Cardiac Pacing and Electrophysiology, 3rd ed. Philadelphia, WB Saunders, 1991, p 494.
13.
Coppola M, Yealy DM: Transvenous pacemakers. Emerg Med Clin North Am 12:633, 1994.
14.
Blumberg SM, Gross J: Permanent pacemaker implantation: Indications, techniques, and follow-up. Hosp Med 1991, p 24.
15.
Furman S, Hurzeler P, DeCaprio V: Appraisal and reappraisal of cardiac therapy. Am Heart J 93:794, 1977.
16.
Mirowski M: The automatic implantable cardioverter-defibrillator: An overview. J Am Coll Cardiol 6:461, 1985.
17.
Mirowski M, Mower MM, Veltri EP, et al: Recent clinical experience with the automatic implantable cardioverter-defibrillator. Cardiol Clin 3:623, 1985.
18.
Langer A, Hickman MS, Mower MM, et al: Considerations in the development of the automatic implantable defibrillator. Med Instrum 10:163, 1976.
19.
Siclari F, Klein H, Trapp J: Surgical techniques of defibrillator implantation. In Alt E, Klein H, Griffin JC (eds): The Implantable Cardioverter/Defibrillator. Berlin, Springer-Verlag, 1992, p 242.
20.
Harthorne JW: Indications for pacemaker insertion: Types and modes of pacing. Prog Cardiovasc Dis 23:393, 1981.
Veltri E, Griffin LSC, Tomaselli G, et al: Long-term clinical results with the implantable defibrillator. In Alt E, Klein H, Griffin JC (eds): The Implantable Cardioverter/Defibrillator. Berlin, Springer-Verlag, 1992, p 131. 21.
22.
Griffin JC, Schuenemeyer TD, Hess KR, et al: Pacemaker followup: Its role in the detection and correction of pacemaker system malfunction. Pacing Clin Electrophysiol 9:387, 1986.
23.
Hayes DL, Vlietstra RE: Pacemaker malfunction. Ann Intern Med 119:828, 1993.
24.
Grieco JG, Scanlon PJ, Pfiarre R: Pacing lead fracture after a deceleration injury. Ann Thorac Surg 47:453, 1989.
25.
Ohm OJ: Displacement and fracture of pacemaker electrode during physical exertion. Acta Med Scand 192:33, 1972.
26.
Tegtmeyer CJ, Bezirdjiam DR, Irani FA, et al: Cardiac pacemaker failure: A complication of trauma. South Med J 74:378, 1981.
Barold SS, Falkoff MD, Ong LA, et al: Interference in cardiac pacemakers: Exogenous sources. In El-Sherif N, Samet P (eds): Cardiac Pacing and Electrophysiology, 3rd ed. Philadelphia, WB Saunders, 1991, p 608. 27.
28.
Brown KR, Carter W, Lombardi GE: Blunt trauma-induced pacemaker failure. Ann Emerg Med 20:905, 1991.
29.
Brooks C, Mutter M: Pacemaker failure associated with therapeutic radiation. Am J Emerg Med 6:591, 1988.
30.
McCann WJ: Pacemaker malfunction associated with blunt trauma. New York State Med J 78:645, 1978.
31.
Dulk KD, Bouwels L, Lindemans F, et al: The Activitrax rate responsive pacemaker system. Am J Cardiol 61:107, 1988.
32.
French RS, Tillman JG: Pacemaker function during helicopter transport. Ann Emerg Med 18:305, 1989.
33.
Gordon RS, O'Dell KB, Low RB, et al: Activity-sensing permanent internal pacemaker dysfunction during helicopter aeromedical transport. Ann Emerg Med 19:1260, 1990.
34.
Irnich W: Interference in pacemakers. PACE 7:1021, 1984.
35.
Lindemans FW, Ranklin IR, Murtaugh R, et al: Clinical experience with an activity sensing pacemaker. PACE 9:978, 1986.
36.
Karkal SS, Syverud S: Permanent pacemaker malfunction: A primer for the emergency physician. Emerg Med Rep 12:61, 1991.
37.
Ellis GL: Pacemaker twiddler's syndrome: A case report. Am J Emerg Med 8:48, 1990.
38.
Newland GM, Janz TG: Pacemakers twiddler's syndrome: A rare case of lead displacement and pacemaker malfunction. Ann Emerg Med 23:136, 1994.
39.
Barold SS, Falkoff MD, Ong LS, et al: Pacemaker endless loop tachycardia: Termination by simple techniques other than magnet application. Am J Med 85:817, 1988a.
40.
Barold SS, Falkoff MD, Ong LS, et al: Magnet unresponsive pacemaker endless loop tachycardia. Am Heart J 116:726, 1988b.
41.
Campo A, Nowak R, Magilligan D, et al: Runaway pacemaker. Ann Emerg Med 12:32, 1983.
42.
Beeler BA: Infections of permanent transvenous and epicardial pacemakers in adults. Heart Lung 11:152, 1982.
43.
Heinberger TS, Duma RJ: Infections of prosthetic heart valves and cardiac pacemakers. Infect Dis Clin North Am 3:221, 1989.
44.
Phibbs B, Marriott HJL: Complications of permanent transvenous pacing. N Engl J Med 312:1428, 1985.
45.
Foster CJ: Constrictive pericarditis complicating an endocardial pacemaker. Br Heart J 47:497, 1982.
46.
Green SM: Pacemaker electrode perforation of the myocardium: An unusual etiology for recurrent abdominal pain. Am J Emerg Med 7:180, 1989.
47.
Collins KA: Accutrix Atrial J Pacing Leads: Clinical Update. Englewood, CO, Telectronics Pacing Systems, 1994.
48.
Ferguson R, McCaughan B, May J, et al: Venous occlusion: A rare complication of transvenous cardiac pacing. Aust NZ J Surg 62:977, 1992.
49.
Manolis AS, Tan-DeGuzman W, Lee MA, et al: Clinical experience in 77 patients with the automatic implantable cardioverter-defibrillator. Am Heart J 118:445, 1989.
50.
Marchlinski FE, Flores BT, Buxton AE, et al: The automatic implantable cardioverter-defibrillator: Efficacy, complications, and device failures. Ann Intern Med 104:481, 1986.
Roth JA, Fisher JD, Furman S, et al: Termination of slower ventricular tachycardia using an automatic implantable cardioverter-defibrillator triggered by chest wall stimulation. Am J Cardiol 59:1209, 1987. 51.
Kelly PA, Cannom MD, Garan H, et al: The automatic implantable cardioverter-defibrillator: Efficacy, complications and survival in patients with malignant ventricular arrhythmias. J Am Coll Cardiol 11:1278, 1988. 52.
53.
Calkins H, Brinker J, Veltri EP, et al: Clinical interactions between pacemakers and automatic implantable cardioverter-defibrillators. J Am Coll Cardiol 7:666, 1986.
54.
Slepian M, Levine JH, Watkins L, et al: Automatic implantable cardioverter-defibrillator/pacemaker interaction: Loss of pacemaker capture following AICD discharge. PACE 10:1194, 1987.
55.
Goodman LR, Almassi GH, Troup PJ, et al: Complications of automatic implantable cardioverter-defibrillators: Radiographic, CT, and echocardiographic evaluation. Radiology 170:447, 1989.
56.
Almassi GH, Chapman PD, Troup PJ, et al: Constrictive pericarditis associated with patch electrodes of the automatic implantable cardioverter-defibrillator. Chest 92:369, 1987.
57.
Kassanoff AH, Levin CB, Wyndham CRC, et al: Implantable cardioverter defibrillator infection causing constrictive pericarditis. Chest 102:960, 1992.
Singer I, Hutchins GM, Mirowski M, et al: Pathologic findings related to the lead system and repeated defibrillations with the automatic implantable cardioverter-defibrillator. Am Coll Cardiol 10:382, 1987. 58.
59.
Avitall B, Port S, Gal R, et al: Automatic implantable cardioverter-defibrillator discharges and acute myocardial injury. Circulation 81:1482, 1990.
60.
Almassi GH, Olinger GN, Troup PJ, et al: Delayed infection of the automatic implantable cardioverter-defibrillator: Current recognition and management. J Thoracic Cardiovasc Surg 95:908, 1988.
61.
Kao N, Messersmith MD, Klich J: Hemoptysis complicating AICD patch placement controlled by temporary selective bronchial balloon occlusion. Chest 99:1301, 1991.
62.
Partington MD, Dinapoli RP, David DH: Automatic defibrillator causes a pain in the neck. JAMA 263:375, 1990.
63.
Kou WH, Calkins H, Lewis RR, et al: Incidence of loss of consciousness during automatic implantable cardioverter-defibrillator shocks. Ann Intern Med 115:942, 1991.
64.
Niazi I, Kadri N, Mahmud R, et al: Absence of significant postdefibrillation bradyarrhythmias in patients with automatic implantable defibrillators. Am Heart J 115:830, 1988.
65.
Morris PL, Badger J, Chimielewski C, et al: Psychiatric morbidity following implantation of the automatic implantable cardioverter-defibrillator. Psychosomatics 32:58, 1991.
Vlay SC, Olson LC, Fricchione GL, et al: Anxiety and anger in patients with ventricular tachydysrhythmias: Responses after automatic implantable cardioverter-defibrillator implantation. PACE 12:366, 1989. 66.
67.
Tilden SJ, Koopot R, Sansbury D, et al: Runaway temporary pacemaker caused by a component defect. Crit Care Med 17:1231, 1989.
68.
Chapman PD, Veseth-Rogers JL, Duquette SE: The implantable defibrillator and the emergency physician. Ann Emerg Med 18:579, 1989.
69.
Craig SA, Hudson AD: Emergency department management of patients with automatic implantable cardioverter-defibrillators. Ann Emerg Med 19:421, 1990.
70.
Eysmann SB, Marchlinski FE, Buxton AE, et al: Electrocardiographic changes after cardioversion of ventricular arrhythmias. Circulation 73:73, 1986.
71.
Chapman PD, Troup P: The automatic implantable cardioverter-defibrillator: Evaluating suspected inappropriate shocks. J Am Coll Cardiol 7:1075, 1986.
72.
White RD, Feldman RA: The automatic implantable cardioverter-defibrillator (AICD): Description and guidelines for interaction during cardiac arrest. Ann Emerg Med 18:586, 1989.
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Chapter 14 - Basic Electrocardiographic Techniques Richard A. Harrigan Theodore C. Chan William J. Brady
The electrocardiogram (ECG) is a graphic recording of the electrical activity of the heart. The heart itself is unique among the muscles of the body in that it possesses the ability to generate regular electrical impulses to produce rhythmic cardiac contractions. These impulses can be measured and recorded at the body surface. The standard ECG is obtained by applying electrode leads over the chest and limbs to record the electrical activity of the cardiac cycle. Developed in the early 1900s, the ECG remains the most important initial diagnostic tool for the assessment of myocardial disease, ischemia, and cardiac dysrhythmias. Electrocardiography is performed widely throughout the health care field, including in ambulances, ambulatory clinics, emergency departments (EDs), and inpatient hospital units. Standard ECG machines are small, self-contained, and portable, allowing them to be used in virtually any setting. As a result, clinicians, nurses, and many other health care providers should be familiar with the procedure of standard 12-lead electrocardiography. Emergency clinicians should also be familiar with the alternative leads and other accessory techniques available in electrocardiography, as well as the pitfalls of lead misplacement, misconnection, and tracing artifacts.
BACKGROUND In 1903, Dutch physiologist Willem Einthoven first published his recordings of the cardiac cycle using a new device, the string galvanometer. [1] Einthoven's instrument consisted of a thin silver-coated quartz filament stretched across a magnetic field. When an electrical current passed through the string, it caused movement from side to side. The filament was connected to electrode leads placed on the limbs to measure differences in potential caused by the electrical activity of the heart. Einthoven magnified these measurements with a projecting microscope and recorded them photographically. [2] While others had previously recorded cardiac electrical activity, Einthoven's instrument laid the basis for modern clinical electrocardiography. His work described the standard frontal plane limb lead ECG using bipolar electrodes, and established standards for recording rate and amplitude. In addition, he described five separate electrical deflections, which he termed P, Q, R, S, and T, establishing basic ECG nomenclature. [3] Einthoven won the Nobel Prize in 1924 for his ECG recording machine, which has been called "probably the most sophisticated scientific instrument in existence when it was first invented." [4] Thomas Lewis visited Einthoven's laboratory and recognized the potential clinical utility of the ECG machine. Lewis became the leading authority on electrocardiography in the early 1900s and was instrumental in the development and clinical application of this new technology. [2] Using the ECG machine, Lewis determined that atrial fibrillation was due to a "circus conduction" involving the auricle of the heart. He published much of his clinical work on ECGs in his landmark texts, The Mechanism of the Heart Beat in 1911 and Clinical Electrocardiography in 1913.[5] [6] The development of smaller, portable bedside ECG recording machines after World War I led to their rapid dissemination and use in the clinical setting. In the early 1930s, Francis Wood and Charles Wolferth first reported the use of ECGs to differentiate cardiac and non-cardiac chest pain. [2] Along with Frank Wilson, their work also led to the development of the unipolar "exploring" electrode lead, which measured electrical activity anywhere in the body with a zero potential central terminal as a reference. These leads could be placed directly over the chest, forming the basis for the standard precordial leads. [7] In 1938, the American Heart Association, in conjunction with the Cardiac Society of Great Britain, established the standard six precordial chest lead positions (V1–6). [8] These precordial leads, along with Einthoven's original bipolar limb lead system (I, II, III) and the augmented unipolar limb leads developed by Emmanual Goldberger (aVR, aVL, and aVF) in 1942, comprise the standard 12-lead ECG used today.
INDICATIONS Numerous situations in the ED may require a 12-lead electrocardiogram—the typical ED patient undergoing electrocardiography has, in fact, approximately 3 indications for obtaining an ECG. [9] The most frequent indication for ECG performance in the ED is the presence of chest pain. Other reasons include dyspnea, syncope, diagnosis-based indications (e.g., acute coronary syndrome [ACS], suspected pulmonary embolism), and system-related indications (e.g., "rule out myocardial infarction" protocol, admission purposes, operative clearance). [9] Within a given diagnosis, the ECG may perform many functions. In the chest pain patient, for example, the ECG helps establish the diagnosis of ACS or, alternatively, some other noncoronary ailment. Moreover, it is used to select appropriate therapy, determine the response to ED-delivered treatments, establish the correct inpatient disposition location, and help predict the risk of both cardiovascular complication and death. The initial 12-lead ECG obtained in the ED can be a helpful guide for determination of cardiovascular risk and, as such, the choice of in-hospital admission location. Brush and colleagues have classified the initial ECG into high- and low-risk groups. The low-risk electrocardiographic group had absolutely normal ECGs, nonspecific ST-T wave changes (NSSTTW), or no change when compared with a previous ECG. High-risk ECGs had significant abnormality or confounding pattern, such as pathologic Q waves, ischemic ST segment or T-wave changes, left ventricular hypertrophy, left bundle-branch block, or ventricular paced rhythm. Patients with initial ECGs classified as low-risk had a 14% incidence of acute myocardial infarction (AMI), 0.6% incidence of life-threatening complications, and 0% mortality rate. Patients with initial ECGs classified as high-risk had a 42% incidence of AMI; 14% incidence of life-threatening complications, and 10% mortality rate. [10] Another approach to risk prediction involves a simple calculation of the number of electrocardiographic leads with ST-segment deviation (elevation
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or depression)—with an increasing number of leads being associated with higher risk. Along similar lines, the clinician can also predict risk with a summation of the total millivolts of ST segment deviation; once again, higher totals are associated with greater risk. [10]
BASIC EQUIPMENT The 12-lead ECG.
Although there is variability depending upon the workplace, most ECG machines today are three-channel recorders with computer memory. Such multi-channel systems, recording electrical events in several leads concurrently, offer advantages over the antiquated single-channel recorder systems—capturing transient events on multiple leads simultaneously; banking the data in computer memory for storage, comparison, and transmission; and allowing for data presentation on a single sheet of paper. [11] The ECG tracing is printed in a standardized manner on a standardized paper by the electrocardiograph, which has default settings regarding the speed with which the paper moves through the machine, as well as the amplitude of the deflections to be made on the tracing. ECG paper is divided into a grid, with a series of horizontal and vertical lines; the thin lines are 1 mm apart, and the thick lines are separated by 5 mm. At the standard paper speed of 25 mm/sec, each vertical thin line thus represents 0.04 sec (or 40 msec), whereas the thick vertical lines correspond to 0.20 sec (or 200 msec). Recordings from each of the 12 leads are typically displayed for 2.5 sec by default setting; the leads appearing horizontally adjacent to each other are separated by a small vertical hashmark to represent lead change. The standard ECG includes 12 leads derived from 10 electrodes placed on the patient; each is color-coded and represented by a two-character abbreviation ( Table 14-1 ). The placement of limb leads on the left and right arms (LA and RA, respectively) and the left and right legs (LL and RL, respectively) by color can be recalled with the help of several mnemonics: "Christmas trees below the knees" (the green and red leads are placed on the lower extremities); "white on right and green to go" (the white lead is placed on the right arm and the green lead is placed on the leg that controls the gas pedal, while the red lead is correspondingly placed on the leg that is closer to the brake); and "smoke over fire" (the black left arm lead is placed over the red left leg lead, as with telemetric monitoring pads). Use of these mnemonics may help prevent right/left confusion during lead placement, as well as the TABLE 14-1 -- Conventional Leads for the 12-Lead Electrocardiogram Location
Notation Color
Right arm
RA
White
Left arm
LA
Black
Left leg
LL
Red
Right leg
RL
Green
Precordial leads
V1
Brown/Red
V2
Brown/Yellow
V3
Brown/Green
V4
Brown/Blue
V5
Brown/Orange
V6
Brown/Violet
consequences of limb lead reversal and misinterpretation of the ECG (see "Lead Misplacement and Misconnection," later in this chapter). Standard 12 leads.
The standard 12-lead ECG depicts cardiac electrical activity from 12 points of view, or leads, which can be grouped according to planar orientation. Six leads (I, II, III, aVR, aVL, and aVF) are oriented in the frontal, or coronal, plane and derived from the four limb electrodes. The six precordial leads (V1, V2, V3, V4, V5, and V6) are oriented in the horizontal, or transverse, plane with each representing cardiac electrical activity from that perspective. Leads I, II, and III are termed limb leads; they are bipolar in that they record the potential difference between two electrodes ( Fig. 14-1 ). The fourth electrode located on the right leg serves as an electrical ground. The positive poles of these bipolar leads lie to the left and inferiorly, approximating the major vector forces of the normal heart. This early convention was established so that the tracing would feature primarily upright complexes. In contrast, augmented leads aVR, aVL, and aVF are unipolar leads, with the positive electrodes located at the respective extremities. These augmented leads serve to fill the electrical gaps between leads I, II, and III. Lead aVR stands alone with a polarity and resultant orientation opposite the other limb and augmented leads. This is due to the fact that its positive electrode is located in the opposite direction (superior and to the right) of the major vector force of the normal heart (inferior and to the left); thus, its complexes usually appear "opposite" to most or all of those in the other leads. Merging of the vector axes of the limb and augmented leads around a central axis yields a hexaxial system of representation of cardiac electrical activity in the frontal plane ( Fig. 14-2 ). The six precordial leads, oriented in the horizontal plane, represent six unipolar electrodes with vector positivity oriented toward the chest surface, with the central terminal of the hexaxial system serving as a negative pole. In contrast to
Figure 14-1 Bipolar limb leads. Leads I, II, and III are shown as a triangle, known as Einthoven's triangle. Left arm (LA), right arm (RA), and left leg (LL) placement is shown. These bipolar leads are oriented such that the positive poles lie inferiorly and to the left (given that the bottom apex of the triangle is directed toward the left leg)—as does the major electrical vector of the heart.
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Figure 14-2 Hexaxial system of limb and augmented leads in the frontal plane. Each lead is separated by 30° in this frontal plane representation of the limb and augmented leads. Augmented leads are shown in boldface. Arrows denote positive polarity. Note that the inferior leads (II, III, aVF) logically lie at the bottom of this figure, and the lateral leads (I, aVL) lie on the left side of the figure, where the lateral aspect of the heart is located were this to be superimposed on a patient.
the frontal plane leads, the angles between each of the precordial leads in the horizontal plane are not equal; however, they can vary depending upon lead placement and body habitus.
Lead placement.
The four limb electrodes are conventionally placed on the extremities as follows: RA on the right wrist; LA on the left wrist; RL on the right ankle; and LL on the left ankle. Electrodes may be affixed more proximally on the limbs if necessary (e.g., amputation, severe injuries), ideally with a notation made on the ECG. [12] Others note that the electrodes may be placed on any part of the arms or legs, providing they are distal to the shoulders or inguinal/gluteal folds, respectively. [13] The precordial leads should be placed as follows: V1—right sternal border, 4th intercostal space; V2—left sternal border, 4th intercostal space; V3—midway between V2 and V4; V4—left midclavicular line, 5th intercostal space; V5—left anterior axillary line, same horizontal level as V4; and V6—left midaxillary line, same horizontal level as V4 and V5. Note that V4 through V6 are placed at the same horizontal level, not all in the 5th intercostal space. If V5 and V6 are situated following the contour of the intercostal space rather than on the same horizontal level, they will be superiorly displaced as the ribs curve around the side of the thorax ( Fig. 14-3 ). Intercostal space number can be determined by first palpating the sternal angle (angle of Louis), which is the junction of the manubrium and body of the sternum. This transverse bony ridge is located about 5 cm caudad from the sternal notch in the adult. Immediately lateral and inferior to it is the second intercostal space; two spaces farther down lies the fourth intercostal space, where V1 and V2 should be placed. Alternatively, one can count down from the medial clavicle; beneath the clavicle lies the first rib, below which is the first intercostal space. If the patient's anatomy or injury precludes placement of a precordial lead as described earlier, it is permissible to
Figure 14-3 Precordial lead placement for the standard 12-lead ECG. If multiple or repeat ECG tracings are anticipated, the original lead placements should be marked on the patient's chest wall or stick-on leads should be left in place after the ECG wires are removed.
attach it within the radius of the width of one interspace of the recommended position, with appropriate notation on the tracing. If the situation demands further displacement, it is recommended that the lead be omitted with appropriate documentation on the tracing. [12] Pediatric lead placement.
In addition to the standard 12-lead tracing, leads V4R and V3R should also be recorded. These are mirror images of their left-sided counterparts (see "Additional Leads" later in this chapter). The chest of the tiny infant may not accommodate all the precordial leads; in such cases, the following array is recommended: V3R or V4R, V1, V3, and V6. Limb lead placement is as in adults. [14]
FEATURES OF THE ELECTROCARDIOGRAM Discussion of the interpretation of the ECG is beyond the scope of this chapter. Other features of the procedure itself, including a description of the other data found on the ECG tracing, will be detailed later. In addition to the patient demographic data that are entered by the operator, the tracing will often feature computations regarding rate, intervals, and axes along the top of the paper. On some tracings, a computer-generated "reading" will also be displayed at the top of the tracing. These interpretations are not infallible. A sample of nine of these programs was compared with the readings of eight cardiologists; the "gold standard" in this study was the clinical diagnosis made independently of the interpretations of these tracings, based on other objective data (e.g., echocardiography, cardiac catheterization). The performance of the programs was good, with correct interpretations in a median of 91% of cases, but the cardiologists were significantly better (median 96% correct). [15] Of note, this study did not evaluate interpretations
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of acute ischemia and cardiac rhythm disturbance—perhaps the most critical issues in ECG interpretation. Adjustable features.
Somewhere on the tracing, notation of the ECG paper speed (mm/sec), the calibration (mm/mV), and the frequency response in Hertz (Hz) will be evident (in Fig. 14-4 , these appear in the lower left corner of the tracing). Calibration, or standardization, refers to the amplitude of the waveforms on the tracing. It is usually set at a default value of 10 mm/mV, and is graphically depicted by a plateau-shaped waveform that appears at the extreme left side of the tracing, in front of the first complex (see Fig. 14-4A ). This calibration can be modified by the operator, or by the computer itself, as was the case in Figure 14-4B , where the patient appeared to have acquired voltage criteria for left ventricular hypertrophy, when in reality the tracing was unchanged from his baseline (see Fig. 14-4A ). Increasing the calibration to 20 mm/mV is helpful when trying to decipher P wave morphology. Decreasing the calibration to 5 mm/mV is helpful in cases wherein the amplitude of the QRS complex (usually in the precordial leads) is so large that it encroaches upon those of the adjacent leads. Standardization may not be uniform throughout a given tracing. At times the
Figure 14-4 A, Normal 10 mm/mV calibration. Note the box-shaped mark to the left of the complexes; this is a graphic representation of the calibration for the tracing. This parameter should be routinely noted before ECG interpretation. Note the change in B. B, Abnormal 20 mm/mV calibration. The calibration in this tracing was (inexplicably and unexpectedly) changed to 20 mm/mV by the ECG, not by the operator. When compared with a baseline ECG, it appeared that the patient had developed voltage criteria for left ventricular hypertrophy as well as ST segment elevation. A, which was recorded minutes later with correction of calibration to the standard 10 mm/mV, was unchanged from baseline tracings.
calibration will be adjusted automatically by the electrocardiograph based upon the waveform amplitudes it perceives. For example, it is possible to have normal calibration (10 mm/mV) in the limb and augmented leads, with half-standard calibration in the precordial leads (5 mm/mV); this may occur in instances of marked left ventricular hypertrophy. In this case, the calibration pulse at the lefthand side of the paper will have a downward stairstep appearance. Paper speed usually is set at a default of 25 mm/sec. It may be manipulated for purposes of deciphering a dysrhythmia, as described later in this chapter (see "Alteration in Amplitude and Paper Speed"). It is important that the clinician examine all ECG tracings for standardization and speed parameters before attempting clinical interpretation.
ADDITIONAL LEADS Although not considered standard of care in the routine evaluation of patients in the ED, additional electrocardiographic leads have been investigated for the evaluation of the patient with possible ACS. These additional, or nontraditional, leads
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include posterior leads (V7, V8 and V9), right ventricular leads (especially V4R), and procedural leads (transvenous pacemaker wire placement and pericardiocentesis). Acute posterior and right ventricular myocardial infarctions are likely to be underdiagnosed, as the standard 12-lead ECG does not assess these areas directly. The standard ECG coupled with these additional posterior leads constitutes the 15-lead ECG, the most frequently used extra-lead ECG in clinical practice. 15-Lead ECG.
In a study of all ED chest pain patients, Brady et al. reported that the 15-lead ECG provided a more accurate description of myocardial injury in those patients with AMI, yet failed to alter rates of diagnoses, use of reperfusion therapies, or change disposition locations. [16] Looking at a more select population of ED patients, Zalenski and associates investigated the use of the 15-lead ECG in chest pain patients with a moderate-to-high pretest probability of AMI, who were already identified as candidates for hospital admission. [17] In this 15-lead ECG study, the authors reported an 11.7% increase in sensitivity with no loss of specificity (i.e., no increase in false-positive findings) for the diagnosis of ST elevation AMI. They concluded that "the findings of ST elevation (STE) by use of these extra leads can strengthen the ED diagnosis of acute myocardial infarction on the initial tracing and may provide an indication for thrombolytic treatment." They further suggest that, in the diagnosis of posterior AMI, leads V8 and V9 are superior to reliance upon detecting the reciprocal ST segment depression seen in leads V1–V3. Possible indications for 15-lead ECGs in patients with suspected acute ischemic heart disease include (1) ST segment depression in leads V1 through V3; (2) all STE inferior and lateral AMIs; or (3) isolated STE in leads V1 and V2, or both. These indications, despite their apparent clinical utility, remain unproved, and the 15-lead ECG is currently not considered standard of care for evaluation in the ED. Posterior leads.
The posterior leads V8 and V9 are placed on the patient's back—V8 at the tip of the left scapula and V9 in an intermediate position between lead V8 and the left paraspinal muscles. An additional lead, V7, may also be placed on the posterior axillary line equidistant from lead V8 ( Fig. 14-5 ). The degree of ST segment elevation in the posterior leads is often less pronounced compared with the STE seen in the standard 12 leads in patients with STE AMI. This diminution of posterior lead STE results from both the relatively greater distance of these leads from the posterior surface of the heart as well as presence of air and soft tissue between the epicardium and electrocardiographic leads. Right-sided leads.
The right ventricular electrocardiographic leads are placed across the right side of the chest in a mirror image of the standard left-sided leads and are labeled V1R to V6R; alternatively, RV1 to RV6 is another commonly used nomenclature for this lead distribution ( Fig. 14-6 ). Lead V4R (right fifth intercostal space mid-clavicular line) is the most useful lead for detecting STE associated with right ventricular infarction and may be used solely in the evaluation of possible right ventricular infarction. The STE that occurs in association with right ventricular infarction is frequently quite subtle, reflecting the relatively small muscle mass of the right ventricle; at other times, the STE is quite prominent, similar in appearance to the ST segment changes seen in the standard 12 leads. Invasive procedural leads.
A patient may present with a severely compromising bradydysrhythmia and require a transvenous pacemaker. In such instances, the pacing wire must be
Figure 14-5 Posterior lead placement. Leads V7, V8, and V9 are placed on the same horizontal plane as V6, with V7 at the posterior axillary line, V8 at the tip of the left scapula, and V9 near the border of the left paraspinal muscles.
placed without the benefit of fluoroscopy. The wire can be advanced using electrocardiographic guidance. Such placement requires that the patient be connected to the limb leads of a grounded electrocardiographic machine and the pacing wire connected to the V lead. As the electrode enters the vena cava superior and high right atrium, the P wave and QRS complex
Figure 14-6 Right-sided lead placement. Right-sided leads RV1–RV6 are placed on the chest as a mirror image of the standard precordial leads.
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will be negative. While traversing the atrium, the P wave and QRS complex will become positive, with the latter becoming larger as the ventricle is approached. If a balloon-tipped flotation catheter is used, the balloon should be deflated once in the right ventricle, and advanced until contact is made with the endocardium and the ventricle is captured. Ventricular wall contact is indicated by marked ST segment elevation. In patients with suspected pericardial effusion who undergo urgent pericardiocentesis, an electrocardiographic lead may be placed on the syringe needle; this form of monitoring assists in the correct positioning of the catheter in the pericardial space. With advancement of the needle, ST segments are monitored. The sudden appearance of ST segment elevation indicates that the needle has moved too far internally (i.e., beyond the pericardial space) and has made contact with the epicardium.
ALTERNATIVE LEADS AND TECHNIQUES FOR RHYTHM ASSESSMENT Electrocardiographic rhythm assessment depends on a clear signal of both atrial and ventricular electrical activity over a period of time. While continuous 12-lead ECG rhythm monitoring has the advantage of recording cardiac activity over multiple leads (thus maximizing atrial and ventricular monitoring), it is often impractical. Moreover, correct identification of the cardiac rhythm on ECG can be difficult depending on the clinical setting. Rapid atrial or ventricular rates, especially those above 150 beats/min, often lead to simultaneous or near-simultaneous deflections that can alter the usual waveforms or cause smaller deflections to be buried within larger ones (such as P waves buried within the QRS complex). In addition, rapid rates result in smaller, narrower waveforms that make visual recognition on the ECG challenging. Finally, assessment of atrial activity is generally more difficult due to the smaller electrical impulse and resulting ECG waveform that is generated by the atria. A number of alternative techniques have been developed to improve rhythm assessment. These techniques include alterations in the standard 12-lead ECG, as well as the addition of non-standard leads to monitor cardiac, and particularly atrial, rhythm activity. Alteration in amplitude and paper speed.
Most 12-lead ECG machines today allow alteration of both amplitude and paper speed from the basic 10 mm/mV and 25 mm/sec standards, respectively. Increasing the amplitude, most commonly to double the standard or 20 mm/mV, can increase the prominence of smaller deflections, such as the P wave, and improve recognition of the atrial rhythm ( Fig. 14-7A–D Fig. 14-7A–D ). In addition, clinicians have also used photocopy enlargements of the standard ECG to enhance smaller deflections visually.[18] Increasing the paper speed, again most commonly to double the standard, or 50 mm/sec, has the effect of artificially slowing the rhythm. This technique is most advantageous when assessing patients with marked atrial or ventricular tachycardia. Increasing the paper speed exaggerates any existing irregularity (such as in atrial fibrillation) and can improve recognition of smaller deflections, such as P waves, in the presence of a significant tachycardia. Faster paper speeds also make it possible to measure short ECG intervals (such as P-R or R-R) more accurately ( Fig. 14-8A, B ). Accardi et al found that overall diagnostic accuracy improved when clinicians were provided ECGs recorded at the faster 50 mm/sec paper speed, as opposed to a standard 12-lead ECG, in patients with narrow complex tachycardias. Moreover, they reported this improved rhythm assessment likely would have resulted in fewer treatment errors.[19] Alternative leads.
Rhythm assessment often requires electrocardiographic monitoring over continuous periods of time, making the standard 12-lead ECG (requiring 10 electrodes), and even unipolar precordial V1 monitoring (requiring 5 electrodes), not feasible. A number of alternative lead systems requiring fewer electrodes have been described. Many of these systems use the limb bipolar leads (RA, LA, LL) in alternative positions over the chest. Leads I, II, or III are then recorded depending on the positions of the positive and negative electrodes. Lewis leads.
In 1910, Thomas Lewis first described alternative positions for the RA and LL leads to enhance detection of atrial fibrillation. The RA lead was placed over the right second costochondral junction, while the LL lead was placed in the right fourth intercostal space 2.5 cm to the right of the sternum—leaving the LA and RL leads in their usual positions. Lewis [20] reported enhancement of atrial activity when the RA served as the negative electrode and LL as the positive electrode (lead II) with this new configuration. Other alternative lead placements to enhance atrial activity detection have also been described ( Table 14-2 and Fig. 14-9 ). [21] [22] [23] Vertical sternal "Barker" leads.
In this alternative lead system, the positive electrode is placed at the xiphoid process and the negative electrode is placed just below the suprasternal notch on the manubrium. Herzog et al [18] reported that vertical sternal leads produce a larger P wave than other systems, including the Lewis leads. In addition, the vertical sternal leads are placed over bone, which may reduce muscle activity artifacts on recordings (see Fig. 14-9 ). Limb-precordium leads.
A sequential pattern of bipolar leads on the chest, termed limb-precordium leads, has been proposed in combination with the original Einthoven limb leads. In this system, standard limb leads are placed on the patient. The RA electrode is then repositioned sequentially at the fourth intercostal space just right of the sternum, fourth intercostal space just left of the sternum (low parasternal), 1st intercostal space just left of the sternum, and 1st intercostal space just right of the sternum (high parasternal). During this sequential mapping, tracings are recorded for leads I and II until atrial activity is identified. Brenes-Pereira reported that this mapping system allowed for the identification of P waves for a majority of patients when none was detected initially on a standard 12-lead ECG. [24] MCL leads.
Modified bipolar chest leads (MCL) are the most commonly used leads for cardiac rhythm monitoring. The positive electrode is placed on the chest at a precordial position (V) concordant with the MCL desired (e.g., the V 1 position for MCL 1 ). The negative electrode is placed on the left shoulder. On standard ECG machines, the LA electrode is placed at V 1 , RA at the left shoulder, LL at V 6 , and RL at a remote location on the chest to serve as ground. Lead I would then reflect MCL 1 and lead II, MCL 6 . MCL1 may be useful in distinguishing atrial activity, MCL 5 and MCL6 more commonly in ST/T wave monitoring, and both MCL1 and MCL6 may be useful in evaluating wide complex tachycardias (see Fig. 14-9 ). [25]
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Figure 14-7a A, Baseline ECG of patient before development of abnormal rhythm (10 mm/mV). Note the P wave morphologies, especially in leads I, II, and V1. B, ECG during ectopic atrial tachycardia (10 mm/mV). Note the change in P wave morphology, especially in lead V1. Esophageal leads.
The esophageal lead (E) was first described by Brown in the 1930s. [26] Since then, both unipolar and bipolar esophageal leads have been developed. [27] Because of its posterior location, this lead is often superior at detecting atrial deflections and recording the activity of the posterior surface of the left ventricle. The electrode, which is connected to the ECG machine by thin wires, is either swallowed, or passed through the nares, into the esophagus. Once in the esophagus, the location of
the electrode is determined either by fluoroscopy or by making a series of low-to-high esophageal recordings. The position of the electrode in the esophagus is adjusted by slowly pulling the electrode wire out the nares or mouth. For the normal adult, leads E 15–25 (electrode is located in the esophagus 15 to 25 cm from the nares) generally records atrial activity; E 25–35 , activity of the AV groove; and E 40–50 , activity of the LV posterior surface. The E lead should be recorded through lead channel I, simultaneously with the lead channel II and the other surface channels.
LEAD MISPLACEMENT AND MISCONNECTION Limb lead reversals.
Whereas the limb electrodes are not often misplaced, the cables that link them to the ECG machine are at times improperly connected. This can result in "ECG changes" that are in actuality artifacts. There are a multitude of possibilities for misconnection of the limb leads; some of the most probable are summarized here. It is helpful to categorize these possibilities into those that are recognizable without comparison to an old ECG versus those that are not. Recognizable without old ECG.
The most common of all misconnections is left and right arm lead reversal ( Fig. 14-10 ). The hallmark is a negative P wave and primarily negative QRS complex in lead I, creating a right or extreme axis deviation (depending upon the QRS complex in lead aVF). Dextrocardia should also be considered with this
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Figure 14-7b C, ECG during ectopic atrial tachycardia (20 mm/mV). The P waves are now easier to see in all leads. D, ECG after reversion to normal atrial focus (20 mm/mV). Contrast these accentuated P waves to those in C.
presentation; the pattern of precordial lead transition will differentiate between dextrocardia and arm lead reversal. Moreover, lead aVR is actually aVL in this circumstance, and thus may feature an upright QRS, which is highly unusual for aVR. [28] Transposition of the RA and LL cables is also easily recognized; all leads are upside down compared with the usual patterns, with the exception of aVL, which is unchanged. Anytime the RL lead is transposed with another extremity lead, one of the limb leads will appear as virtually a straight line, and thus is easily recognized if this finding is not incorrectly ascribed to poor electrode contact or function. An exception to this rule is if the leg leads are reversed (RL ? LL), in which case the ECG is virtually identical to one with correct placement of the leads. Reversal of the leg leads is largely insignificant in that the potentials at the left and right legs are essentially the same.[29] Recognizable with old ECG.
In addition to the reversal of the leg leads, one other limb lead reversal that is not readily recognizable without comparison to a prior tracing is transposition of the LA and LL leads. This causes reversal of lead I with II on the tracing, as well as aVL with aVF—both are difficult to discern at times without a baseline ECG for comparison. Furthermore, lead III will be upside down (although a negative QRS complex in III is not unusual), and aVR will be unchanged ( Fig. 14-11A, B ). [29] Clues to limb lead reversal are summarized in Table 14-3 . Precordial lead misplacement and misconnection.
Unlike the limb leads, the precordial electrodes are more prone to misplacement, especially when variations in body habitus (e.g., obesity, breast tissue, pectus excavatum, chronic lung disease) make proper lead placement more difficult. This may cause some variability in the amplitude and morphology of the complexes in the precordial leads; however, these changes are not usually grossly abnormal, and therefore can be difficult to detect. Variation often becomes evident when comparing the current tracing with an old ECG. [29] In such cases, it is useful to go to the bedside and examine where the electrodes were positioned relative to the recommended placement (see "Lead Placement" earlier in this chapter). One
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Figure 14-8 A, ECG with tachycardia at normal paper speed (25 mm/sec). Because of the rapid rate, the actual P waves are difficult to discern, thus making rhythm determination difficult. The computerized interpretation is sinus tachycardia with first-degree AV block. B, ECG with tachycardia at double paper speed (50 mm/sec). With increased paper speed, atrial P wave activity is accentuated, demonstrated atrial flutter with a 2:1 AV block.
cannot ensure, however, that the baseline ECG was done with proper lead placement. When comparing the precordial leads on the current ECG with a baseline tracing, ST segment and T wave changes should be viewed in light of the relative morphologies of the associated QRS complexes. If there is a marked difference between the two tracings in the amplitude and polarity of the QRS complex in a given precordial lead, the corresponding ST/T wave changes may be due to lead TABLE 14-2 -- Alternative Leads for Rhythm Assessment Lead I1 :
RA = negative electrode
LA = positive electrode
Lead II1 :
RA = negative electrode
LL = positive electrode
Lead III1 :
LA = negative electrode
LL = positive electrode
Alternative Lead
Negative Electrode Position
Positive Electrode Position
Lewis2
R 2nd costochondral junction
R 4th intercostal space, "1" right of sternum
Drury
2nd R costochondral junction
7th R costal cartilage
Center of sternum
Inferior angle of scapula 2" right of spine
3rd intercostal space along R sternal border
L leg
3rd intercostal space along R sternal border
R arm
Lu
1st intercostal space directly above V1
Approximately 3" directly below V4
Vertical Sternal ("Barker" Leads)
Below suprasternal notch at manubrium
Xiphoid process
Schoenwald
MCL1
L shoulder (1 cm inferior to L mid-clavicle)
V1 (4th intercostal space R sternal border)
MCL6
L shoulder (1 cm inferior to L mid-clavicle)
V6 (~6th rib mid-axillary line)
1
First, set the ECG machine to record the rhythm strip using this lead. If the recoding rhythm strip is lead I, the RA wire becomes the negative electrode that is placed as noted in table, and the LA wire becomes the positive electrode that is placed as noted in the table. If lead II or lead III is the lead that is set to record the rhythm strip, the positive and negative electrodes will vary. 2 Example: One way to record the Lewis lead: Set the ECG machine to record lead I, use the RA wire as the negative electrode, and place it in the R 2nd costochondral junction. Use the LA wire as the positive electrode and place it in the right 4th intercostal space, 1 inch right of the sternum. The Lewis lead may also be recorded on lead II and lead III, but the wires that serve as the positive and negative electrodes will vary.
placement, although cardiac ischemia cannot be completely excluded as the cause. Misconnection of the precordial cables is usually easy to detect. The expected progression of P, QRS, and T wave morphologies across the precordium will be disrupted ( Fig. 14-12A, B ). An abrupt change in wave morphology evolution—followed by a seeming return to normalcy in the next lead—is a good clue to precordial lead misconnection. [29]
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Figure 14-9 Alternative leads. The figure displays three of the more commonly used alternative lead strategies for atrial rhythm clarification (Lewis leads, vertical sternal or Barker leads, and MCL1), and ST/T wave monitoring (MCL6).
ARTIFACTS Electrocardiographic artifacts are commonly encountered, yet not always easy to recognize. They can be attributed to either physiologic (internal) or nonphysiologic (external) sources; the former includes muscle activity, patient motion, and poor electrode contact with the skin. Tremors, hiccups, and shivering may produce frequent, narrow spikes on the tracing, simulating atrial and ventricular dysrhythmias ( Fig. 14-13 ). [28] [30] A wandering baseline featuring wide undulations, as well as other "noise" on the ECG, can often be traced to patient movement and high skin impedance, leading to inadequate electrode contact to the skin. Minimizing skin impedance and artifacts may be achieved by (1) avoiding electrode placement over bony prominences, major muscles, or pulsating arteries; (2) clipping rather than shaving thick hair at electrode sites; and (3) cleaning and (most importantly) drying the skin surface before reapplying the electrode if the tracing features substantial artifacts. [28] [31] Nonphysiologic artifacts are most often due to 60-Hertz electrical interference, which is ascribable to various other sources of alternating current near the patient. This will manifest as a wide, indistinct isoelectric
Figure 14-10 Arm lead reversal (LA RA). The most common of limb lead reversals, the clues lie in leads I and aVR. Lead I features a negative P wave, as well as a principally negative QRS complex and T wave. This could suggest dextrocardia, but the precordial leads demonstrate normal transition, which is not consistent with dextrocardia. Note also the unusual appearance of aVR in this tracing.
baseline. Other sources of nonphysiologic artifact include loose connections, broken monitor cables, and mechanical issues with the machine (e.g., broken stylus, uneven paper transport). The 60-Hz artifact due to electrical current interference can be minimized by shutting off non-essential sources of current in the vicinity, as well as straightening the lead wires so that they are parallel to the patient's body in the long axis. [28] [30] [32] Differentiation of artifacts from true ECG abnormality is intuitively important; moreover, clinical consequences have been reported that are directly attributable to confusion of artifacts with disease. Unnecessary treatment and procedures—including cardiac catheterization, electrophysiologic testing, and even implantation of a pacemaker and an automatic defibrillator—have been reported. [33] Characteristics that may aid in differentiating artifacts from dysrhythmia include absence of hemodynamic instability during the event (or even absence of any symptoms); normal QRS complexes occurring during the dysrhythmia; instability of the baseline on the tracing during and immediately after the "dysrhythmic" event; association with body movement; and observance of "notches" amidst the complexes of the pseudodysrhythmia, which "march out" with the normal QRS complexes that precede and follow the disturbance. [34] [35]
CONCLUSION Electrocardiography is a simple, noninvasive, and invaluable bedside test. While used principally for the diagnosis and treatment of cardiovascular disorders, it has numerous other applications as well. Knowledge of standard lead placement and the features of the 12-lead ECG are essential. Several features—including adjustment of calibration, paper speed, and the addition of multiple accessory leads—can add to the diagnostic sensitivity of the procedure. Strategic repositioning of limb and precordial leads as described will aid in the assessment of difficult atrial rhythms. The addition of other thorax leads, such as V8 and V9 (posterior wall) and V4R (right ventricle), will increase the sensitivity of the ECG for ACS involving those difficult-to-assess areas of the heart. Pitfalls include failure to recognize lead misconnection and misplacement, as well as artifacts.
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Figure 14-11 A, Limb lead reversal (LA LL). A patient with a history consistent with ACS was brought to the ED after this ECG was recorded in a clinic. Leads I and aVL suggest an acute high lateral infarct but, surprisingly, there are no corresponding changes in leads V5 and V6. The deep T wave inversions in III and aVF were at first thought to be inferior ischemia or reciprocal changes (see also B). B, Correction of lead reversal (LA
LL). After the leads were reconnected, this tracing reveals an acute inferior wall MI, as well as deep T wave inversion in aVL—a
harbinger of acute inferior MI. Comparing this tracing with that in A, note the following: lead I become inferior.
lead II; lead aVL
aVF, and lead III is inverted. Thus, inferior changes become lateral, and lateral
Reversed Leads
TABLE 14-3 -- Clues to Improper Limb Lead Connections Old ECG Necessary for Detection? Key Findings
LA RA
No
PQRST upside down in lead I Precordial leads normal (not dextrocardia)
LA LL
Yes
III is upside down I
II; aVL
aVF; aVR no change
LA RL
No
III is straight line
RA LL
No
PQRST upside down in all leads except aVL
RA RL
No
II is straight line
LL RL
Cannot detect change
Looks like normal lead placement
LA LL
No
I is straight line
RA RL
aVL, aVR are same polarity and amplitude and II is upside down III
From Surawicz B, Knilans TK: Chou's Electrocardiography in Clinical Practice, 5th ed. Philadelphia, WB Saunders, 2001.
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Figure 14-12 A and B, Precordial lead reversal (V2 B shows a return to a normal V3 transition zone.
V3). Note the usual precordial progression of R wave growth in leads V2 and V3 is disrupted in the tracing displayed in A;
Figure 14-13 Artifact due to physiologic cause. The patient's monitor was alarming due to a perceived heart rate of >200 beats/min, and the computerized alert system called this ventricular tachycardia. The patient, who has Parkinson's disease, was without complaint. The ECG demonstrates a marked artifact, giving the appearance of atrial flutter in lead V1.
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References 1. Einthoven 2. Fye
W: The string galvanometer and the human electrocardiogram. Proc Kon Akademie voor Wetenschappen 6:107, 1903.
WB: A history of the origin, evolution, and impact of electrocardiography. Am J Cardiol 73:937, 1994.
3. Henson
JR: Descartes and the ECG lettering series. J Hist Med Allied Sci 26:181, 1971.
4. Burnett
J: The origins of the electrocardiograph as a clinical instrument. Med Hist Suppl 5:53, 1985.
5. Lewis
T: The Mechanisms of the Heart Beat. London, Shaw and Sons, 1911.
6. Lewis
T: Clinical Electrocardiography. London, Shaw and Sons, 1913.
7. Kossmann 8. Barnes 9. Brady
CE: Unipolar electrocardiography of Wilson: A half century later. Am Heart J 110:901, 1985.
AR, Pardee HEB, White PD, et al: Standardization of precordial leads: Supplementary report. Am Heart J 15:235, 1938.
W, Adams M, Perron A, Martin M: The impact of the 12-lead electrocardiogram in the evaluation of the emergency department patient [abstract]. Ann Emerg Med 40:S47, 2002.
10.
Brush JE, Brand DA, Acampora D, et al: Use of the initial electrocardiogram to predict in-hospital complications of acute myocardial infarction. N Engl J Med 312:1137, 1985.
11.
Surawicz B, Uhley H, Borun R, et al: Task force I: Standardization of terminology and interpretation. Am J Cardiol 41:130, 1978.
12.
Sheffield T, Prineas R, Cohen HC, et al: Task force II: Quality of electrocardiographic records. Am J Cardiol 41:146, 1978.
American Heart Association (AHA) Committee Report. Recommendations for standardization of leads and of specifications for instruments in electrocardiography and vectorcardiography. Circulation 52:11, 1975. 13.
14.
Resnekov L, Fox S, Selzer A, et al: Task force IV: Use of electrocardiograms in practice. Am J Cardiol 41:170, 1978.
15.
Willems JH, Abreu-Lima C, Arnaud P, et al: The diagnostic performance of computer programs for the interpretation of electrocardiograms. N Engl J Med 325:1767, 1991.
Brady WJ, Hwang V, Sullivan R, et al: A comparison of the 12-lead ECG to the 15-lead ECG in emergency department chest pain patients: Impact on diagnosis, therapy, and disposition. Am J Emerg Med 18:239, 2000. 16.
17.
Zalenski RJ, Cook D, Rydman R: Assessing the diagnostic value of an ECG containing leads V4R, V8, and V9: The 15-lead ECG. Ann Emerg Med 22:786, 1993.
18.
Herzog LDR, Marcus FI, Scott WA, et al: Evaluation of electrocardiographic leads for detection of atrial activity (P wave) in ambulatory ECG monitoring: A pilot study. PACE 15:131, 1992.
19.
Accardi AJ, Miller R, Holmes JF: Enhanced diagnosis of narrow complex tachycardias with increased electrocardiograph speed. J Emerg Med 22:123, 2002.
20.
Lewis T: Auricular fibrillation and its relation to clinical irregularity of the heart. Heart 1:306, 1910.
21.
Drury A, Iliescu CC: Observations upon flutter and fibrillation. Part VIII—The electrocardiograms of clinical fibrillation. Heart 8:171, 1921.
22.
Lu RMT, Steinhaus BM, Bailey W, Nademanee K: Clinical significance of a new p wave lead vector for pacemaker follow-up of atrial functions. PACE 19:1805, 1996.
23.
Schoenwald G: Chest leads for the demonstration of auricular activity. Middle Hospital J 39:183, 1939.
24.
Brenes-Pereira C: New bipolar leads for the study of atrial arrhythmias. Tex Heart Inst J 24:118, 1997.
25.
Drew BJ, Scheinman MM: Value of electrocardiographic leads MCL1, MCL6, and other selected leads in the diagnosis of wide QRS complex tachycardia. J Am Coll Cardiol 18:1025, 1991.
26.
Brown WH: A study of the esophageal lead in clinical electrocardiography. Am Heart J 12:1, 1936.
27.
Schnittger I, Rodriguez IM, Winkle RA: Esophageal electrocardiography: A new technology revives an old technique. Am J Cardiol 57:604, 1986.
28.
Surawicz B: Assessing abnormal ECG patterns in the absence of heart disease. Cardiovasc Med 2:629, 1977.
29.
Surawicz B, Knilans TK: Chou's Electrocardiography in Clinical Practice, 5th ed. Philadelphia, WB Saunders, 2001.
30.
Chase C, Brady WJ: Artifactual electrocardiographic change mimicking clinical abnormality on the ECG. Am J Emerg Med 18:312, 2000.
31.
Ostewr CD: Improving ECG trace quality. Biomedical Instrumentation Technology 34:219, 2000.
32.
Wagner G: Marriott's Practical Electrocardiography, 10th ed. Philadelphia, Lippincott Williams & Wilkins, 2001.
33.
Knight BP, Pelosi F, Michaud GF, et al: Clinical consequences of electrocardiographic artifact mimicking ventricular tachycardia. N Engl J Med 341:1270, 1999.
34.
Lin SL, Wang SP, Kong CW, Chang MS: Artifact simulating ventricular and atrial arrhythmia. Jpn Heart J 32:847, 1991.
35.
Littmann L, Monroe MH: Electrocardiographic artifact [letter]. N Engl J Med 342:590, 2000.
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Chapter 15 - Emergency Cardiac Pacing Edward S. Bessman
The purpose of cardiac pacing is to restore or ensure effective cardiac depolarization. Emergency cardiac pacing may be instituted either prophylactically or therapeutically. Prophylactic indications include those situations where there is high risk of atrioventricular (AV) block, including certain toxidromes and instances of acute myocardial infarction. Therapeutic indications include symptomatic bradyarrhythmias, asystole, and overdrive pacing. Several approaches to pacing exist, including transcutaneous, transvenous, transthoracic, epicardial, endocardial, and esophageal. Transcutaneous and transvenous are the two techniques most commonly used in the emergency department (ED). Since it can be instituted quickly and noninvasively, transcutaneous pacing is the technique of choice in the ED. Transvenous pacing should be reserved for patients who require prolonged pacing or who have a very high (greater than 30%) risk of heart block. Transcutaneous pacing is generally a temporizing measure that may precede transvenous cardiac pacing.
EMERGENCY TRANSVENOUS CARDIAC PACING The transvenous method of endocardial pacing is commonly used and is both safe and effective. In skilled hands, the semifloating transvenous catheter is successfully placed under electrocardiographic guidance in 80% of patients. [1] The technique can be performed in less than 20 minutes in 72% of patients and in less than 5 minutes in 30% of patients. However, in some instances anatomic, logistical, and hemodynamic impediments can prohibit successful pacing by even the most skilled clinician. As with other medical procedures, it should not be performed without a thorough understanding of its indications, contraindications, and complications. [2] Background The ability of muscle to be artificially depolarized was recognized as early as the 18th century. Initial efforts focused on the transcutaneous approach (see later in this section). Over the succeeding years, several scattered experiments were reported and in 1951 Callaghan and Bigelow first used the transvenous approach to stimulate the asystolic heart in hypothermic dogs. [3] Furman and Robinson demonstrated the transvenous endocardial approach in humans in 1958. [4] They treated two patients with complete heart block and Stokes-Adams seizures, reconfirming that low-voltage pacing could completely control myocardial depolarization. The catheter remained in the second patient for 96 days without complication. Other early clinical studies proved that transvenous pacing is a valuable procedure in medicine. [5] [6] [7] Fluoroscopic guidance was used for placement of the pacing catheter in all of these studies. In 1964, Vogel and colleagues demonstrated the use of a flexible catheter passed without fluoroscopic guidance for intracardiac electrocardiography. [8] One year later, this technique was used by Kimball and Killip to insert endocardial pacemakers at the bedside. [9] They noted technical difficulties including intermittent capture, difficulty passing the catheter, and catheter knotting in 20% of their patients. During the same year, Harris and associates confirmed the ease and speed with which this procedure could be accomplished. [10] Before 1965 all intracardiac pacing was done asynchronously, which meant that the pacing catheter could cause electrical stimulation during any phase of the cardiac cycle. Asynchronous pacing frequently resulted in the pacemaker firing during the vulnerable period of an intrinsic depolarization; this occasionally caused ventricular tachycardia or fibrillation. In 1967 a demand pacemaker generator that sensed intrinsic depolarizations and inhibited the pacemaker for a predetermined period of time was used successfully by Zuckerman and associates in six patients. [11] Since then there has been steady progress in the design and functionality of pacemakers. Table 15-1 summarizes the four-letter code that is used to describe modern pacemakers (there is a fifth letter for combined pacemaker-cardioverter/defibrillators). The most commonly used emergency transvenous pacemaker is represented by the code VVI, meaning that the ventricle is paced, the ventricle is sensed, and when a native impulse is sensed, the pacemaker is inhibited. Dual chamber pacing (DDD or DDDR) is the preferred methodology for permanent pacing but is less commonly used emergently because of the increased complexity of the procedure (see later in this section). Rosenberg and colleagues introduced an improved pacing catheter known as the Elecath semifloating pacing wire. [1] The Elecath was stiffer than the Flexon steel wire electrode that was in prevailing use. Rosenberg and coworkers achieved pacing in 72% of patients, with an average procedure time of 18 minutes. They also noted that 30% of their patients were paced in 5 minutes or less. [1] The technique of heart catheterization using a flow-directed balloon-tipped catheter was introduced by Swan and Ganz in 1970. [12] This concept was used successfully by Schnitzler and coworkers for the placement of a right ventricular pacemaker in 15 of 17 patients. [13] In 1981, Lang and colleagues compared the bedside use of the flow-directed balloon-tipped catheter with insertion of a semirigid electrode catheter in 111 perfusing patients. [14] These researchers found a significantly shorter insertion time (6 minutes and 45 seconds compared with 13 minutes and 30 seconds), a lower incidence of serious arrhythmias (1.5% compared with 20.4%), and a lower incidence of catheter displacement (13.4% compared with 32%) with the balloon-tipped catheter. They concluded that the balloon-tipped catheter was the method of choice for temporary transvenous pacing ( Table 15-2 ). Kruger and associates retrospectively reviewed the experience of general internists with transvenous pacemaker placement under electrocardiogram (ECG) guidance.[15] They reported a 4% risk of complications and a 14% incidence of electrode malfunction, and these percentages were noted to be similar to those reported by university cardiologists. They concluded that pacemaker placement by primary care clinicians was safe and effective when done under ECG guidance without fluoroscopy. Indications The purpose of cardiac pacing is to stimulate effective cardiac depolarization. In most cases the specific indications for cardiac pacing are clear; however, some controversial areas
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TABLE 15-1 -- Four-Letter Pacemaker Code First Letter
Second Letter
Third Letter
Fourth Letter
Chamber-Paced Chamber-Sensed Sensing Response
Programmability
A = atrium
A = atrium
T = triggered
P = simple
V = ventricle
V = ventricle
I = inhibited
M = multiprogrammable
D = dual
D = dual
D = dual (A-triggered and V-inhibited)
R = rate adaptive
O = none
O = none
O = none
C = communicating O = none
remain. The decision to pace on an emergent basis requires knowledge of the presence or absence of hemodynamic compromise, the etiology of the rhythm disturbance, the status of the atrioventricular (AV) conduction system, and the type of dysrhythmia. In general, the indications can be grouped into those that cause either tachycardias or bradycardias ( Table 15-3 ). Transcutaneous cardiac pacing has become the mainstay of temporary emergent cardiac pacing. It is often used pending placement of the transvenous catheter or as a means to determine whether potentially terminal bradyasystolic rhythms will respond to pacing. Bradycardias Sinus node dysfunction.
In a review of 200 initial pacemaker implants at Montefiore Hospital during 1975, 36.5% were used for sinus node dysfunction; 11.3% for sinus arrest; 20.2% for tachybrady (sick sinus) syndrome; and 5% for sinus bradycardia. [16] Patients without myocardial infarction who present with symptomatic sinus node dysfunction should be paced promptly if medical therapy fails. Escher and Furman note that pacing is indicated until the etiology of the dysrhythmia is clarified and stability is ensured.[17] In the asymptomatic patient, a more intensive cardiac evaluation is required in order to decide whether pacing will be beneficial. This evaluation frequently includes
24-hour Holter monitoring, noting sinus node recovery times, and occasionally coronary care unit monitoring.
TABLE 15-2 -- History of Transvenous Pacing Date Investigator
Event
1700 Early investigators
First restimulation studies
1951 Callaghan & Bigelow
First transvenous approach in dogs
1952 Zoll
Transcutaneous cardiac stimulator
1958 Falkmann & Walkins
Implanted pacing wires after surgery
1958 Furman & Robinson
First transvenous pacer in humans
1964 Vogel et al.
Flexible electrocardiographic catheter without fluoroscopy
1965 Kimball & Killip
First bedside transvenous pacing
1966 Goetz et al.
Demand pacemaker developed
1967 Zuckerman et al.
Use of demand pacemaker clinically
1969 Rosenberg et al.
Semifloating pacing catheter
1973 Schnitzler et al.
Balloon-tipped pacers
Sinus bradycardia occurs in an average of 17% of patients with acute myocardial infarction. [18] It occurs more frequently in inferior than in anterior infarction and has a relatively good prognosis when accompanied by a hemodynamically tolerable escape rhythm. However, sinus bradycardia is not a benign rhythm in this situation; it has a mortality rate of 2% with inferior infarction and 9% with anterior infarction. [19] Several mechanisms have been suggested to explain sinus node dysfunction with infarction. Among these, ischemia of the node or its neurologic controls [19] and reflex slowing secondary to pain play dominant roles. [20] Sinus node dysfunction frequently responds to medical therapy but requires prompt pacing if this fails. Asystolic arrest.
Transvenous pacing in the asystolic or bradyasystolic patient has little value. In one study of 13 patients who had suffered cardiac arrest, capture of the myocardium was noted in 4 patients, but there were no survivors. [21] Transvenous pacing alone may also not be effective in postcountershock pulseless bradyarrhythmias. [22] This failure of pacing has also been demonstrated with transcutaneous pacemakers, suggesting that failure of effective pacing is primarily related to the state of the myocardial tissue. [21] Pacing has no proven value in traumatic cardiac arrest. Other causes of failure to pace include catheter malposition and dislodgment of the pacing wire during closed-chest massage. [21] Cardiac pacing may be used as a "last ditch" effort in bradyasystolic TABLE 15-3 -- Indications for Cardiac Pacing * Bradycardias Without myocardial infarction Symptomatic sinus node dysfunction (sinus arrest, tachybrady [sick sinus] syndrome, sinus bradycardia) Second- and third-degree heart block Atrial fibrillation with symptomatic slow ventricular response With myocardial infarction Symptomatic sinus node dysfunction Mobitz II second- and third-degree heart block New left bundle-branch block (LBBB); right bundle-branch block (RBBB) with left axis deviation, bifascicular block, or alternating bundle-branch block Prophylaxis—cardiac catheterization, after open-heart surgery, threatened bradycardia during drug trials for tachydysrhythmias Malfunction of implanted pacemaker Tachycardias Supraventricular dysrhythmias Ventricular dysrhythmias Prophylaxis—cardiac catheterization, after open-heart surgery *Many indications are relative and are dependent upon a variety of symptoms and parameters.
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or asystolic patients but is rarely successful and is not considered standard practice. Early pacing is essential when done for this purpose if success is to be achieved [23] (see later in this section). Atrioventricular block.
Atrioventricular block is the classic indication for pacemaker therapy. In symptomatic patients without myocardial infarction and in the asymptomatic patient with a ventricular rate below 40, pacemaker therapy is indicated. [24] In patients with acute myocardial infarction, 15% to 19% progress to heart block: approximately 8% develop first-degree block, 5% develop second-degree block, and 6% develop third-degree block. [25] First-degree block progresses to second- or third-degree block 33% of the time, and second-degree block progresses to third-degree block about one third of the time. [26] Atrioventricular block occurring during anterior infarction is believed to occur because of diffuse ischemia to the septum and infranodal conduction tissue. These patients tend to progress to high-degree block without warning and a pacemaker is often placed prophylactically. Some pacemakers are prophylactically paced on a temporary basis, even in the absence of hemodynamic compromise. During inferior infarction, early septal ischemia is the exception and typically block develops sequentially from first-degree to Mobitz type I second-degree, then to third-degree atrioventricular (AV) block. These conduction abnormalities frequently result in hemodynamically tolerable escape rhythms because of sparing of the bundle branches. The hemodynamically unstable patient who is unresponsive to medical therapy should be paced promptly. Whether and when the stable patient should be paced is unclear, but placing a transcutaneous pacer is one option that can be tried before placing a transvenous pacing catheter. One study, which reviewed the indications for temporary and permanent pacemaker insertion in 432 patients with myocardial infarction, concluded that patients with
second- or third-degree AV block should be paced. This recommendation was made due to a higher incidence of sudden death or recurrent high-degree block over the following year that was found in patients who were not continuously paced. [27] Trauma.
Pacing is not a standard intervention; in traumatic cardiac arrest in selected cases, it may be considered. Several rhythm and conduction disturbances have been documented in the patient with nonpenetrating chest trauma. In these patients, traumatic injury to the specialized conduction system may predispose the patient to life-threatening dysrhythmias and blocks that can be treated by cardiac pacing. [28] Hypovolemia and hypotension can cause ischemia of conduction tissue and cardiac dysfunction. replacement may rarely respond to cardiac pacing in patients with such trauma. [30]
[29]
Marked bradyarrhythmias that persist even after vigorous volume
Bundle-Branch Block and Ischemia
Bundle-branch block occurring in acute myocardial infarction is associated with a higher mortality rate and a greater incidence of third-degree heart block than uncomplicated infarction. Atkins and associates noted that 18% of patients with myocardial infarction had bundle-branch block. [31] Of these patients, complete heart block developed in 43% who had right bundle-branch block and left axis deviation, in 17% who had left bundle-branch block, in 19% who had left anterior hemiblock, and in 6% who had no conduction block. The investigators concluded that right bundle-branch block with left axis deviation should be paced prophylactically. A study by Hindman and colleagues confirmed the natural history of bundle-branch block during myocardial infarction. [32] In their study, the presence or absence of first-degree AV block, the type of bundle-branch block, and the age of the block (new versus old) were used to determine the relative risk of progression to type II second-degree or third-degree block ( Table 15-4 ). Because of the increased risk, most should consider pacing the following conduction blocks: new-onset left bundle-branch block, right bundle-branch block with left axis deviation or other bifascicular block, and alternating bundle-branch block. [32] One authority recommends prophylactic pacing for all new bundle-branch blocks when myocardial infarction is evident. [33] Whether to place a transvenous pacemaker prophylactically in patients with left bundle-branch block before insertion of a flow-directed pulmonary artery catheter (PAC) remains controversial. Some researchers strongly advocate this procedure because of the risk of transient right bundle-branch block and life-threatening complete heart block in association with the placement of a PAC. [34] One study notes that this risk is low in patients with prior left bundle-branch block but continues to recommend temporary catheter placement for all cases of new left bundle-branch block. [35] One solution to this problem is to place a transcutaneous pacemaker before catheterization as an emergency measure should heart block develop. In these cases, a temporary transvenous pacemaker can be placed in a semi-elective manner when needed.[36] In any event, the trend toward decreased PAC use, particularly outside of the critical care setting, makes it unlikely that this will be an issue in the ED.[37]
TABLE 15-4 -- The Influence of Different Variables on Risk of High-Degree Atrioventricular Block in Patients with Bundle-Branch Block During Myocardial Infarction Patients Progressing to High-Degree AVB (%) Infarct location Anterior
25
Indeterminate
12
Inferior or posterior
20
PR interval >0.20 sec
25
=0.20 sec
19
Type of BBB LBBB
13
RBBB
14
RBBB + LAFB
27
RBBB + LPFB
29
ABBB
44
Onset of BBB Definitely old
13
Possibly new
25
Probably new
26
Definitely new
23
AVB, Atrioventricular block; BBB, bundle-branch block; LBBB, left bundle-branch block; RBBB, right bundle-branch block; LAFB, left anterior fascicular hemiblock; LPFB, left posterior fascicular hemiblock; ABBB, alternating bundle-branch block. (Reprinted by permission of the American Heart Association from Hindman MC, Wagner GS, JaRo M, et al: The clinical significance of bundle-branch block complicating acute myocardial infarction. 2. Indications for temporary and permanent pacemaker insertion. Circulation 58:690, 1978.)
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Tachycardias
Hemodynamically compromising tachycardias are usually treated by medical means or electrical cardioversion (see Chapter 12 ). Since 1980, there has been increased interest in pacing therapy for symptomatic tachycardias. Supraventricular dysrhythmias, with the exception of atrial fibrillation, respond well to atrial pacing. By "overdrive" pacing the atria at rates 10 to 20 beats/min faster than the underlying rhythm, the atria become entrained, and when the rate is slowed, the rhythm frequently returns to normal sinus. A similar procedure is done for ventricular dysrhythmias. [38] Overdrive pacing is especially useful for recurrent prolonged Q-T interval arrhythmias such as those seen with quinidine toxicity or torsades de pointes. [39] While an attractive thought, there is no reported experience with these techniques in the ED. Transvenous pacing may also be useful in patients with digitalis-induced dysrhythmias in whom direct current (DC) cardioversion may be dangerous or in patients in whom there is further concern about myocardial depression with drugs. [40] Cardiac Pacing in Drug-Induced Dysrhythmias
Significant dysrhythmias can occur from excessive therapeutic medication (often in combination therapy) and from overdose of cardioactive medications. Because these drugs have direct effects on the myocardial pacemaker and conduction system cells, cardiac pacing is usually of little therapeutic value. Both bradycardias and tachycardias may result. Tachycardic rhythms from amphetamines, cocaine, anticholinergics, cyclic antidepressants, theophylline, and others do not benefit from cardiac pacing. A drug-induced torsades de pointes may theoretically be overdriven by pacing, but data on this technique are lacking. Any drug that affects the central nervous system (opiates, sedative-hypnotics, clonidine, and others) may produce bradycardia. Rare causes of toxin-induced bradycardia include organophosphate
poisoning, various cholinergic drugs, ciguatera poisoning, and, rarely, plant toxins. Cardiac pacing is not used for bradycardias from these sources; rather, the underlying CNS depression is addressed. Severe bradycardia and heart block often accompany overdose of digitalis preparations, beta adrenergic blockers, and calcium channel blockers. While intuitively attractive, cardiac pacing is rarely successful in serious toxin-induced bradycardias. [41] [42] [43] [44] In beta-blocker overdose, pacing may increase heart rate but rarely benefits blood pressure or cardiac output. Worsening of the blood pressure may be seen from loss of atrial contractions with ventricular pacing. Likewise, calcium channel blocker overdose and digitalis-induced bradycardia and heart block rarely benefit from cardiac pacing. Pharmacologic interventions, such as digoxin-specific Fab, glucagon, calcium, and inotropic medications, and vasopressors remain the mainstay in the treatment of drug-induced dysrhythmias. Given the lack of success of pacing, possible downsides, and the greater effectiveness of specific antidotes, it is not standard to routinely attempt cardiac pacing in the setting of drug overdose. However, as a last ditch effort, cardiac pacing can be supported. Contraindications There are no absolute contraindications to transvenous cardiac pacing; however, the severely hypothermic bradycardic patient can often be managed without pacing. Severe hypothermia will occasionally result in ventricular fibrillation when pacing is attempted. Because ventricular fibrillation under these conditions is difficult to convert, caution is advised when considering pacing the severely hypothermic and bradycardic patient. Rapid warming is often recommended first, followed by pacing if the patient's condition does not improve. Equipment Several items are required to insert a transvenous pacemaker adequately. Like most special procedures, a prearranged tray is convenient. The usual components required to insert a transvenous cardiac pacemaker are listed in Table 15-5 . Pacing Generator
Many different pacing generators are available, but in general, they all have the same basic features. The on/off switch frequently will have a locking feature to prevent the generator from inadvertently being switched off. An amperage knob allows the operator to control the amount of electrical current delivered to the myocardium, usually 0.1 to 20 mA. The pacing control mode is the gain control for the sensing function of the generator. By increasing the sensitivity, one can convert the unit from a fixed rate (asynchronous mode) to a demand (synchronous mode) pacemaker. In the fixed-rate mode, the unit fires despite the underlying intrinsic rhythm; the unit does not sense any intrinsic electrical activity. In the full-demand mode, however, the pacemaker senses the underlying ventricular depolarizations, and the unit does not fire as long as the patient's ventricular rate is equal to or faster than the set rate of the pacing generator. A sensing indicator meter and rate control knob are also present. An example of a pacing generator is shown in Figure 15-1 . Pacing Catheters and Electrodes
Several sizes and brands of pacing catheters are available. In general, most range from 3 Fr to 5 Fr in size and are approximately 100 cm in length. Along the catheter surface are lines that are marked at approximately 10-cm intervals; these can be used to estimate catheter position during insertion. Two TABLE 15-5 -- Suggested Transvenous Cardiac Pacemaker Equipment Pacemaker Tray 10-mL syringe 1% lidocaine Alcohol wipes Povidone-iodine (Betadine) Several gauze pads 4 sterile drapes No. 11 scalpel blade 0.9 normal saline—2 ampules Sterile gloves Needle holder Two 22-ga needles Scissors (suture) Two 4-0 silk sutures on needles Sterile basin Electrical Hardware Insulated connecting wire with alligator clamps at each end (or a male-to-male adapter) Spare 9-V battery Medtronic pacing unit no. 5375 3 Fr Balectrode Pacing Kit (catalog no. 11—KBE1) 12-lead electrocardiographic machine (well grounded)
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Figure 15-1 Pacemaker energy source controls and connections.
basic types of pacing catheters are currently in use: (1) the flexible semifloating or floating catheter and (2) the rigid fixed-position catheter.
[ 39]
The flexible catheters are more advantageous than the rigid catheter by virtue of the flexible catheter's ability to be inserted in low flow states, as well as in their decreased tendency to perforate the ventricle. For emergency pacing, the 4 Fr semifloating bipolar electrode with or without the balloon tip is used most frequently ( Fig. 15-2 ). The balloon holds approximately 1.5 mL of air, and some of the injection ports have a locking lever to secure balloon expansion. Before insertion, the balloon is checked for air leakage by inflating it and immersing it in sterile water. The presence of an air leak is noted by a stream of bubbles arising at the surface of
the water. An inflated balloon helps the catheter "float" into the heart in low flow states but is obviously not advantageous in the cardiac arrest situation.
Figure 15-2 Balloon-tipped pacing catheter.
For all practical purposes, temporary transvenous pacing is accomplished with a bipolar pacing catheter. The terms unipolar and bipolar refer to the number of electrodes in contact with that portion of the heart that is to be stimulated. All pacemaker systems must have both a positive (anode) and a negative (cathode) electrode; hence, all stimulation is bipolar. In the typical bipolar catheter used for temporary transvenous pacing, the cathode (stimulating electrode) is at the tip of the pacing catheter. The anode is located 1 to 2 cm proximal to the tip, and the two electrodes may be separated by a balloon or an insulated wire. The distinction between the unipolar and bipolar pacing catheter is that a bipolar catheter has both electrodes in a relative close proximity on the catheter, and both may contact the endocardium. In the bipolar catheter, the electrodes are usually platinum rings that encircle the pacing catheter. When properly positioned, both electrodes will be within the right ventricle so that a field of electrical excitation is set up between the electrodes. With the bipolar catheter, the cathode does not need to be in direct contact with the endocardium for pacing to occur, although it is preferable to have direct contact. A unipolar system is also effective but is used infrequently for temporary transvenous pacing. In a unipolar system, the cathode is at the tip of the pacing catheter, and the anode is located in one to three places: (1) in the pacing generator itself, (2) more proximal on the catheter (outside the ventricle), or (3) on the patient's chest. A bipolar catheter system may be converted to a unipolar system by simply disconnecting the positive proximal connection of the bipolar catheter from the pacing generator and running a new wire from the positive (pacing generator) terminal to the patient's chest wall. Such a conversion may be required in the unlikely event of failure of one lead of the bipolar system. Theoretically, the field of electrical stimulation of a pacing catheter is equal to the distance between the electrodes. If the field of excitation is not close enough to the myocardium, depolarization will not occur. When a catheter is passed blindly in an emergency, it seems advantageous to ensure the best chance of capture by separating the electrodes by more than the standard 1 to 2 cm. A pacing catheter that uses this configuration (Davison pacing lead, Electro-Catheter Corporation, Rahway, NJ) is a hybrid of the standard bipolar and unipolar catheters. This catheter has the cathode at the tip, but the anode is situated 19 cm proximal to the tip. This configuration allows pacing with a very wide field of excitation. Pacing has been reported to occur with this catheter when the catheter is placed anywhere within the thoracic venous system. The catheter is a hybrid because both electrodes are present on the same catheter (bipolar), but both electrodes will not be positioned in the same cardiac chamber (unipolar). ECG Machine
An ECG machine can be used to record the heart's inherent electrical activity during pacer insertion and to aid in localization of the catheter tip without fluoroscopy. The ECG machine must be well grounded to prevent leakage of alternating current, which can cause ventricular fibrillation. Such leakage should be suspected if interference of 50 to 60 cycles per second (Hz) is noted on the ECG. The ECG machine should be placed in such a manner as to allow easy visibility of the rhythm during insertion. One method is to place the machine on the same side of the patient as the operator at the level of the midthorax ( Fig. 15-3 ). Note
288
Figure 15-3 Position of an electrocardiogram device during femoral vein insertion of a pacemaker catheter. Operator is on right side of patient facing cephalad.
that the operator stands at the head of the patient during internal jugular or subclavian vein passage of the catheter and at the midabdomen for femoral or brachiocephalic vein insertion. Introducer Sheath
An introducer set or sheath is required for venous access (see Chapter 22 ). Some pacing catheters are prepackaged with the appropriate equipment, whereas others require a separate set. The introducer set is used to enhance passage of the pacing catheter through the skin, subcutaneous tissue, and vessel wall. To allow passage of the pacing catheter, the sheath must be one size larger than the pacing catheter. A makeshift sheath can be made with an appropriate-sized intravenous (IV) catheter. For the 3 Fr balloon-tipped catheter, a 14-gauge, 1.5-to 2-inch IV catheter is suitable. The 4 Fr balloon-tipped catheter will also fit through a 14-gauge catheter or needle. A balloon-directed pulmonary artery catheter (Paceport pacing system, American Edwards Laboratories, American
Venous Channels Advantages Brachial
TABLE 15-6 -- Advantages and Disadvantages of Pacemaker Placement Sites Disadvantages
Very safe route
Often requires cutdown
Vessel easily accessible, either by cutdown or percutaneous approach
Easily displaced and poor patient mobility Not reusable if cutdown technique is performed Catheter is more difficult to advance than with central or larger vessels
Subclavian
Direct access to right heart (especially via left subclavian)
Pneumothorax and other intrathoracic trauma are possible
Rapid insertion time Reusable Good patient mobility Femoral
Direct access to right heart
Increased incidence of thrombophlebitis
Rapid insertion time
Can be dislodged by leg movement and poor patient mobility
Reusable Infection Internal jugular
Direct access to right heart (especially via right internal jugular)
Possible carotid artery puncture Dislodgment with movement of the head
Rapid insertion time
Thrombophlebitis
Reusable Hospital Supply Corporation) has been developed. It has a separate lumen that allows the passage of a transvenous pacing catheter. [45] This catheter is 7.5 Fr and has an opening 19 cm from the catheter tip that allows passage of the 2.4 Fr pacing wire. This stainless steel wire is Teflon-coated for easy passage and has a flexible tip. Combination pulmonary artery or pacemaker catheters are also available but are not widely used in the emergency setting. Overall, the key to success with this procedure is preparation. It is imperative that one examine all the components of the tray before starting the procedure and ensure that all wires, sheaths, dilators, and syringes fit as expected. Procedure Patient Preparation
Patient instruction is an extremely important aspect of any procedure. Frequently there is not enough time to give patients a detailed explanation. Nor to obtain written informed consent. Nonetheless, sufficient information should be provided so that the patient feels at ease. It is always prudent to obtain and document informed consent from the patient if possible prior to any invasive procedure, or to document that the circumstances did not allow informed consent. Patients should be assured that they will feel no discomfort after the venipuncture site has been anesthetized and that they will feel better when the catheter is in place and is functional. Continued reassurance is required during the procedure because patients are usually facing away from the operator and because their faces are often covered, they may be unsure of what is occurring. When appropriate sedation anxietolysis should be considered. All operators should wear surgical masks, caps, gloves, and gowns to decrease the risk of infection before catheter placement. This aseptic precaution should also be explained to the patient. Site Selection
The four venous channels that provide an easy access to the right ventricle are the brachial, subclavian, femoral, and internal jugular veins ( Table 15-6 ). The route selected is often one of
289
personal or institutional preference. The right internal jugular and the left subclavian veins have the straightest anatomic pathway to the right ventricle and are generally preferred for temporary transvenous pacing. In some centers a particular site is preferred for permanent transvenous pacemaker placement, and, if possible, this site should be avoided for temporary placement. The subclavian vein can be accessed by both an infraclavicular and a supraclavicular approach; the infraclavicular approach is most commonly reported for all temporary transvenous pacemaker insertions. This route is preferred because of its easy accessibility, close proximity to the heart, and ease in catheter maintenance and stability. The supraclavicular approach has been described in the literature for several years and has gained popularity among some clinicians. [46] [47] The left subclavian vein is preferred because of the less acute angle traversed when compared with the right-sided approach. However, a recent study reported safe and efficient emergency transvenous pacing via a right-sided supraclavicular approach. [48] Some clinicians believe the internal jugular approach is as easy as and safer than subclavian catheterization. [48] Either site is acceptable. The right internal jugular vein is preferred because of the direct line to the superior vena cava. Problems with this approach include dislodgment of the pacemaker with movement of the head, carotid artery puncture, and thrombophlebitis (see Chapter 22 ). During cardiopulmonary resuscitation, the use of the right internal jugular vein and the left subclavian veins for pacemaker insertion have been demonstrated to result in the highest rates of proper placement in the right ventricle. [49] The right internal jugular vein is the more direct route of the two and may be the most appropriate site. Because of the extremely low flow state during cardiopulmonary resuscitation, a larger (5 Fr), semirigid catheter may be a more appropriate choice than the 3 to 4 Fr catheters commonly used. Femoral veins, like neck veins, are reusable and easily catheterized. Problems include easy dislodgment, infection, and increased risk of thrombophlebitis. Brachial vein catheterization is easy to perform but results in a higher incidence of infection and vessel thrombosis. arm motion. This approach is seldom used in the emergency setting.
[52]
[50] [51]
In addition, the catheter is easily dislodged with
Skin Preparation and Venous Access
The skin over the venipuncture site is cleaned twice with an antiseptic solution such as povidone-iodine and isopropyl alcohol. A wide area is prepared because of the tendency for guidewires and catheters to spring from the hands of the unsuspecting operator. Preparation of the skin is shown in Chapter 22 . Similarly, wide draping is carried out in the standard manner to maintain a sterile field and to allow clear visibility of the venipuncture site. The infraclavicular approach is used in this chapter to illustrate venous access, although the mechanics are generally the same for other vascular approaches. The reader is referred to Chapter 22 for the specific techniques of venous access. Occasionally a patient who already has a central venous line in place requires the emergent placement of a pacing catheter. An existing central venous pressure (CVP) line can be used to place the pacing catheter if the catheter lumen is large enough to accept a guidewire. The CVP line should be withdrawn 1 to 2 in. to expose an area of sterile tubing. The tubing is transected through a sterile area while being held
Figure 15-4 Insertion of the pacing catheter through the introducer sheath.
firmly at the skin level. A guidewire can then be passed through the tubing, and the tubing can be withdrawn, leaving only the wire in the vein. The guidewire and the tubing should never be released because embolization may result. An introducer unit can then be passed over the guidewire, as is done in the Seldinger technique (see Chapter 22 ), and the pacing catheter can be placed ( Fig. 15-4 ). Bedside ultrasound (US) can be useful as an aid to securing central venous access and its use in the setting of emergency transvenous pacing has been reported (see Chapter 69 ). [53] [54] Pacemaker Placement Electrocardiographic guidance.
The patient should be connected to the limb leads of an ECG machine, and the indicator should be turned to record the chest (V) lead. With newer ECG machines, the pacemaker may be attached to any of the V leads (usually V 1 or V5 ) that are displayed during rhythm monitoring. As the tracing on the ECG machine is slightly delayed with the newer devices, advancement of the catheter after initial insertion must be carefully evaluated. The pacing wire should be
inserted about 10 to 12 cm into the selected vein. The distal terminal of the pacing catheter (the cathode or lead marked negative, "-") must be connected to the V lead of the ECG machine by a male-to-male connector or by an insulated wire with an alligator clip on each end ( Fig. 15-5 ). The pacing catheter is thus an exploring electrode that creates a unipolar electrode for intracardiac ECG recording. The ECG recorded from the
Figure 15-5 Using alligator clips to connect the negative lead of the pacemaker catheter to the V lead of an electrocardiographic machine.
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electrode tip localizes the position of the tip of the pacing electrode. If a balloon-tipped catheter is used, the balloon is inflated with air after the catheter enters the superior vena cava. The pacing catheter should be advanced both quickly and smoothly. The V lead should be monitored, and the P wave and QRS complex should be observed to ascertain the location of the pacing catheter tip. The use of an ECG to guide the placement of a pacing catheter is based on two concepts. First, the complex will vary in size depending on which chamber is entered. For example, when the tip of the pacing catheter is in the atrium, one will see large P waves, often larger than the corresponding QRS complex. Second, the sum of the electrical forces will be negative if the depolarization is moving away from the catheter tip and positive if the depolarization is moving toward the catheter tip. Therefore, if the catheter tip is above the atrium, both the P wave and the QRS complex will be negative (i.e., the electrical forces of a normally
Figure 15-6 A–K, Intracardiac electrocardiography: Electrical signals of atrial and ventricular depolarization and repolarization from different vascular and intracardiac locations (see text). (A–F and H–K from Bing OH, McDowell JW, Hantman J, et al: Pacemaker placement by electrocardiographic monitoring. N Engl J Med 287:651, 1972. G from Goldberger E: Treatment of Cardiac Emergencies, 3rd ed. St. Louis, CV Mosby, 1982, p 252.)
beating heart will be moving away from the catheter tip). As the tip progresses inferiorly in the atrium, the P wave will become isoelectric (biphasic) and will eventually become positive as the wave of atrial depolarization advances toward the catheter tip. The ECG resembles an aVR lead initially when in the left subclavian vein ( Fig. 15-6A ) or midsuperior vena cava ( Fig. 15-6B ). At the high right atrium, both the P wave and QRS complex are negative; the P wave is larger than the QRS complex and is deeply inverted ( Fig. 15-6C and D ). As the center of the atrium is approached, the P wave becomes large and biphasic ( Fig. 15-6E ). As the catheter approaches the lower atrium ( Fig. 15-6F ), the P wave becomes smaller and upright. The QRS complex is fairly normal. When striking the right atrial wall, an injury pattern with a P-Ta segment is seen ( Fig. 15-6G ). As the electrode passes through the tricuspid valve, the P wave becomes smaller, and the QRS complex becomes larger ( Fig. 15-6H ). 291
Placement in the inferior vena cava may be recognized by a change in the morphology of the P wave and a decrease in the amplitude of both the P wave and the QRS complex ( Fig. 15-6I ). Once the pacing catheter is in the desired position, the balloon is deflated by unlocking the port and removing the syringe. One should avoid drawing back on the syringe, because this may cause balloon rupture. If the operator suspects that the balloon may be ruptured, it should not be inflated. Instead, the pacing catheter should be withdrawn and the balloon checked for leaks. If a leak is found, a new pacing catheter should be used. After successful placement of the catheter within the right ventricle, the tip should be advanced until contact is made with the endocardial wall. When this occurs, the QRS segment will show ST segment elevation ( Fig. 15-6J ). Ideally, the tip of the catheter should be lodged in the trabeculae at the apex of the right ventricle; however, pacing may be successful if the catheter is in various other positions within the ventricle or outflow tract. If the pacer enters the pulmonary artery outflow tract, the P wave again becomes negative, and the QRS amplitude diminishes ( Fig. 15-6K ). If the catheter is in the pulmonary artery, the pacing catheter should be withdrawn into the right ventricle and readvanced. Sometimes a clockwise or counter-clockwise twist of the catheter will redirect its path in a more favorable direction. If catheter-induced ectopy develops, the catheter should be slightly withdrawn until the ectopy stops; then it should be readvanced. Occasionally an antidysrhythmic drug such as lidocaine may be needed to desensitize the myocardium. Once ventricular endocardial contact is made, the catheter is disconnected from the ECG machine. The proximal positive and negative leads are connected to their respective terminals on the pacing generator. The pacing generator is then set to a rate of 80 beats/min or 10 beats/min faster than the underlying ventricular rhythm, whichever is higher. The full-demand mode is selected, with an output of about 5 mA. The pacing generator is then turned on. If complete capture does not occur or if it is intermittent, the pacer will need to be repositioned. When proper capture occurs, the pacer is tested for optimal positioning. This is done by testing the thresholds for sensing and pacing and with chest radiographs, physical examination, and ECG. Catheter placement without an electrocardiograph.
Occasionally it is necessary to use a transvenous pacemaker in an emergency setting when a well-grounded ECG machine is not available. Blind insertion of the transvenous pacing catheter is a safe and effective alternative to placement with ECG guidance. In this technique, the pacing catheter is placed 10 to 12 cm into the venous port and is connected to the pacing generator as noted previously. The pacing rate is selected at twice the intrinsic heart rate, and the output is set at an amperage that is too low to capture the ventricle, usually less than 0.2 mA. The unit is then turned on to first sense but not to pace. On entering the ventricle, the pacer will sense on every other beat. The balloon can then be deflated, the amperage can be increased to 4 to 5 mA for initiating pacing, and the pacemaker can be advanced to capture the ventricle. If this does not occur within an additional 10 cm, the pacing catheter should be withdrawn to its original position and then advanced again. As with ECG placement, proper positioning must be ensured. In elective, nonemergent cases fluoroscopy is a valuable tool in the placement of transvenous pacemakers. Its use depends on the operator's preference, the patient's condition, and its availability. Generally transvenous pacemakers are not inserted under fluoroscopy without ECG monitoring because of the high incidence of ventricular dysrhythmias. [39] If the cardiac output is too low to "float" a pacing catheter or if the patient is in extremis, there may not be enough time to advance a pacing catheter using the previously described techniques. Such a situation would be asystole or complete heart block with malignant ventricular escape rhythms (although one can make a case for transcutaneous pacing in such conditions). In such emergent situations, the pacing catheter is connected to the energy source, the output is turned to the maximum amperage, and the asynchronous mode is selected. The catheter is then blindly advanced in the hope that it will enter the right ventricle and that pacing will be accomplished. The pacing catheter is rotated, advanced, withdrawn, or otherwise manipulated according to the clinical response. The right internal jugular approach is the most practical access route in this situation. In such instances, there is the theoretic advantage of using the previously described Davison catheter, because one is interested in rapid capture only until the patient is stabilized.
Ultrasound guidance.
As bedside US has become more widely available in the ED, new uses have been discovered. One promising technique involves using US to assist with the placement of emergency transvenous pacing catheters. [55] [56] The advantages of US over fluoroscopy are its safety and ready availability. Further experience will be necessary to confirm its utility. Dual Chamber Pacing
Synchronous pacing of the atria and ventricle through a dual-chamber pacing catheter that senses and paces both atria and ventricles (DDD mode) results in more physiologic pacing with further improvement in cardiac output. It also allows for variations in the atrial rate and improved coordination of atrial and ventricular contractions. This catheter is placed in the same manner as the ventricle-only pacing catheter (VVI mode) but requires greater skill and experience because of the need to properly place the catheter in both the atria and ventricle. When attaching the catheter to the pacing generator, it is important to ensure that the atrial catheter is connected to the atrial electrode and the ventricular catheter is connected to the ventricular electrode. There are devices that have dual-chamber pacemaking capability and can operate in a variety of modes, including DDD mode. However, it is seldom necessary to employ this modality in the ED. Testing Threshold
The threshold is the minimum current necessary to obtain capture. Ideally, this is less than 1.0 mA, and usually it is between 0.3 and 0.7 mA. If the threshold is in this ideal range, good contact with the endocardium can be presumed. To determine the threshold, the pacing generator should be placed in the full-demand mode at 5 mA with a rate of approximately 80 beats/min. The amperage (output) should then be reduced slowly until capture is lost. This current is the threshold. This maneuver should be carried out two or three times to ensure that this value is consistent; the amperage should then be increased to 2.5 times the threshold to ensure consistency of capture (usually between 2 and 3 mA). If one reduces the output to below the threshold and then slowly increases it, there may be a difference in the point at which capture returns. This difference is called hysteresis and
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represents the time interval between sensing and pacemaker firing. If the difference in capture current is greater than 20%, the pacing catheter should be repositioned, because serious dysrhythmias may result if the pacemaker fires during the vulnerable period of repolarization. [39] [57] Testing Sensing
The sensing function should be tested in patients who have underlying rhythms. The pacemaker system is again set in full-demand mode with complete capture, and the rate is decreased until it is suppressed by the patient's intrinsic rhythm. This is done several times to ensure accuracy of the sensing function. In bipolar systems, another method of evaluating the sensing mode is to take a unipolar ECG from each end of the bipolar lead on a chest lead at one-fourth standardization to permit observation of the entire complex. [39] The voltage of the QRS complex is multiplied by 4 and, if adequate, should be greater than the sensing threshold by greater than 1 mV ( Fig. 15-7 ). Another method is to set the ECG machine on lead I and connect the wires from the proximal electrode to the right arm lead and the left arm lead to the distal electrode. A lead I is created, which, when the QRS voltage is multiplied by 4, should also be at least 1 mV more than the sensing threshold. Securing and Final Assessment
After the pacemaker's position has been tested for electrical accuracy, the introducer sheath should be withdrawn ( Fig. 15-8 ) and the catheter secured to the skin with suture (e.g., 4-0 nylon or silk). A fastening suture should be sewn to the skin and the catheter tied securely in place. The excess pacing catheter should be coiled and secured in a sterile manner along with the introducer. A large sterile dressing should be applied. Pacemaker function should again be assessed, and a chest film should be taken to ensure proper positioning. Ideal
Figure 15-7 Testing unipolar sensing with a bipolar system. (From Goldberger E: Treatment of Cardiac Emergencies, 3rd ed. St. Louis, CV Mosby, 1982.)
positioning of the pacing catheter is at the apex of the right ventricle ( Fig. 15-9 ). A 12-lead ECG should be obtained after transvenous pacemaker placement. If the catheter is within the right ventricle, a left bundle-branch pattern with left axis deviation should be evident in paced beats ( Fig. 15-10 ). If a right bundle-branch block pattern is noted, coronary sinus placement or left ventricular pacing due to septal penetration should be suspected. With a properly functioning ventricular pacemaker, large cannon waves will be noted on inspection of the venous pulsations at the neck. This is caused by the atria contracting against a closed tricuspid valve. On auscultation of the heart,
Figure 15-8 Pulling back the introducer sheath (cannula). RA, right atrium; RV, right ventricle; LV, left ventricle.
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Figure 15-9 Normal pacemaker position on posteroanterior (A) and lateral (B) chest films. (From Goldberger E: Treatment of Cardiac Emergencies, 3rd ed. St. Louis, CV Mosby, 1982.)
a slight murmur secondary to tricuspid insufficiency from the catheter interfering with the tricuspid valve apparatus may be evident. [58] A clicking sound, heard best during expiration following each pacemaker impulse, may also be noted here and is believed to represent either intercostal or diaphragmatic muscular contractions caused by the pacemaker.[59] Note that this can also be a sign of cardiac perforation. [60] On auscultation of the second heart sound, paradoxical splitting may be noted. This represents a delay in closure of the aortic valve because of delayed left ventricular depolarization. As in any procedure, the patient should then be assessed for improvement in his or her clinical status. An evaluation of vital signs, mentation, improvement in congestive symptoms, and urinary output must be noted. In addition, complications secondary to the procedure should be sought and treated as needed. Complications The complications of emergency transvenous cardiac pacing are numerous and represent a compendium of those related to central venous catheterization, those related to right-sided heart catheterization, and those unique to the pacing catheter itself ( Table 15-7 ). Problems Related to Central Venous Catheterization
Inadvertent arterial puncture is a well-known complication of the percutaneous approach to the venous system. [61] This problem is usually recognized quickly because of the rapid return of arterial blood. Firm compression over the puncture site will almost always result in hemostasis in 5 minutes or less. Venous thrombosis and thrombophlebitis are also potential problems with central venous catheterization. Thrombophlebitis, which occurs early after insertion, is said to be a rare complication. Some experts believe that it can be managed without removal of the catheter or anticoagulation. [52] When thrombophlebitis occurs in long-term implanted pacemakers, removal and anticoagulation may be required. In one series, only 0.1% of permanent pacemakers were in this category, and in a small percentage of these, occult malignancies were found. [52] Complete thrombosis of the innominate vein is also a rare problem, with pulmonary embolism an even more uncommon event.[62] Femoral vein thrombosis, however, appears to be a much more common event associated with femoral vein catheterization. [50] [63] Studies using noninvasive techniques have shown a 37% incidence of femoral vein thrombosis, with 55% of these having ventilation-perfusion scan evidence of pulmonary embolism.[63] Thrombosis in the right atrium may also occur and has been treated successfully with thrombolytic agents. [64] Pneumothorax is consistently a problem with the various approaches to the veins at the base of the neck. The decision to place a chest tube in patients with this complication depends on the size of the pneumothorax and the clinical status of the patient (see Chapter 10 ). In addition, laceration of the subclavian vein with hemothorax,[65] thoracic duct laceration with chylothorax, air embolism, wound infections, pneumomediastinum, hydromediastinum, [66] hemomediastinum, phrenic nerve injury,[67] fracture of the guidewire with embolization, [68] [69] and catheter or guidewire knotting [70] [71] are all potential complications. [39] [65] Complications of Right-Sided Heart Catheterization
A common complication of the pacing catheter is dysrhythmia, with premature ventricular contractions being a common occurrence. One study noted a 1.5% incidence of serious dysrhythmias with a balloon-tipped catheter using ECG guidance, compared to a 32% incidence with the semirigid catheter using fluoroscopic guidance, suggesting that the balloon catheter was the preferred type of catheter. [14] Another study noted a 6% incidence of ventricular tachycardia during insertion. [50] The ischemic heart is more prone to dysrhythmias than the nonischemic heart. [72] The therapy for catheter-induced ectopy involves withdrawing the catheter from the ventricle. This usually stops the ectopy; however, if after repeated attempts it is found that the catheter cannot be passed without ectopy, myocardial suppressant therapy may be used to desensitize the myocardium. Misplacement of the pacing catheter has been well studied. Passage of the catheter into the pulmonary artery can be diagnosed cardiographically by observing the return of an inverted P wave and the decrease in the voltage of the QRS complex. Misplacement in the coronary sinus may occur and should be suspected in the patient in whom a paced right bundle-branch
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Figure 15-10 Electrocardiogram pattern of right venticular pacemaker.
pattern on the ECG is seen with right ventricular pacing ( Fig. 15-11 ). Rarely, a right bundle-branch pattern can be seen with a normal right ventricular position; therefore, all right bundle-branch patterns do not represent coronary sinus pacing. [73] Further evidence for coronary sinus location can be obtained by viewing the lateral chest film. Normally, the catheter tip should point anteriorly toward the apex of the heart; however, with coronary sinus placement, the catheter tip is displaced posteriorly and several centimeters away from the sternum ( Fig. 15-12 ). Other potential forms of misplacement include left ventricular pacing through an atrial septal defect or a ventricular septal defect, septal puncture, extraluminal insertion, and arterial insertions. [74] Perforation of the ventricle is a well-described complication that can result in loss of capture, [75] hemopericardium, and tamponade. [76] [77] Reported symptoms and signs of this problem include chest pain, pericardial friction rub, and diaphragmatic or chest wall muscular pacing. [78] At least one case of a post-pericardiotomy-like syndrome and two cases of endocardial friction rub have been reported without perforation. [79] [80] Pericardial perforation is suggested radiographically when the pacing catheter is outside or abuts the cardiac silhouette and is not in proper position within the right ventricular cavity ( Fig. 15-13 ).[81] ECG clues include a change in the QRS and T wave axis or a failure to properly sense. In suspected cases, a two-dimensional echocardiogram usually demonstrates the catheter's extracardiac position. Uncomplicated perforation can usually be treated by simply pulling back the catheter and repositioning it in the right ventricle. During the insertion of a temporary pacing catheter when a nonfunctioning permanent catheter is in place, there is a small risk of entanglement or knotting. This potential also exists with other central lines and Swan-Ganz catheters. Frequently these lines can be untangled under fluoroscopy using specialized catheters. Local and systemic infections, [52] balloon rupture, pulmonary infarction, [82] phrenic nerve pacing, [83] and rupture of the chordae tendineae are also potential complications.[82] Complications of the Pacing Electrode
The complications related to the pacing electrode can be separated into three groups: mechanical, organic, and electrical. Mechanical failures include displacement, fracture of the catheter, and loose leads. Displacement can result in intermittent or complete loss of capture or improper sensing, malignant dysrhythmias, diaphragmatic pacing, or perforation. Displacement should be suspected with changes in amplitude, with vector changes greater
than 90 degrees, or with a change in threshold. [84] Frequently catheter fractures may be detected by a careful review of the chest film or may be suspected because of a change in the sensing threshold. As with displacement, intermittent or complete loss of capture may result. Organic causes of pacemaker failure result in changes in the threshold or sensing function. [85] Progressive inflammation, fibrosis, and thrombosis may result in more than a doubling of the original threshold. [86] This may occur in 3 to 4 weeks and should be expected in prolonged temporary pacemakers. Physiologic and pharmacologic factors that affect the threshold have been studied. Sleeping, eating a heavy meal, lowered aldosterone concentration, potassium infusions, [87] and myxedema[88] all increase the threshold by raising the resting membrane potential. The threshold for cardiac pacing tends to decrease with exercise, sympathetic amines, glucocorticoids, and toxic levels of procainamide. [89]
295
Year Author
No. of Patients
1969 Rosenberg et 111 al[1]
Catheter
TABLE 15-7 -- Complications of Transvenous Cardiac Pacing Route Result
Flexon steelwire vs unipolar semifloating (ECG)
96 Subclavian
12 inconsistent pacing, 3 local infection, 2 pneumothorax, 1 subclavian artery puncture; 16% complication rate
5 Basilic 1 External jugular
1973 Schnitzler et al[13]
17
3 Fr bipolar semifloating balloon (ECG)
Antecubital vein
1973 Weinstein et al[51]
100
6 Fr bipolar (fluoroscopy) Femoral
1973 Lumia & Rios*
142 insertions in Bipolar (fluoroscopy) 113 patients
1980 Pandian et al.†
20
61 Brachial 81 Femoral
2 PVCs, stable pacing, no thrombophlebitis 2 ventricular tachycardia, 2 perforations, 2 required repositionings, 1 questionable thrombophlebitis and pulmonary embolism, 1 local infection 12 ventricular tachycardia and fibrillation in 9 patients, 3 perforations in 2 patients; local hematoma, abscess, and bleeding in 30%; 16.9% complication rate
5 Fr bipolar (fluoroscopy) Femoral
25% deep venous thrombosis
1980 Nolewajka et 29 al[63]
6 Fr cordis (fluoroscopy)
Femoral
34% venous thrombosis by venogram with 60% of these with pulmonary embolism by VQ scan
1981 Lang et al[14]
Balloon, semifloating vs semirigid
Subclavian
Serious dysrhythmia: 1.5% balloon-tipped, 20.4% semirigid
111
1982 Austin et al [50] 113 insertions in 4–7 Fr bipolar 100 patients (fluoroscopy)
Catheter displacement: 13.6% ± 4.4 days balloon-tipped; 32% ± 1.9 day semirigid Brachial Femoral
Failure to sense or pace in 37%; repositioning in 37% of brachial insertions; repositioning in 9% of femoral insertions; fever, sepsis, local infection only in femoral insertions; 20% complication rate
ECG, electrocardiogram; PVC, premature ventricular contraction; VQ, ventilation-perfusion. *Lumia FJ, Rios JC: Temporary transvenous pacemaker therapy: An analysis of complications. Chest 64:604, 1973. †Pandian NG, Kosowsky BD, Gurewich V: Transfemoral temporary pacing and deep venous thrombosis. Am Heart J 100:847, 1980.
In some patients the atrial contribution to ventricular filling is extremely important. Transvenous ventricular pacing results in loss of the atrial kick and ultimately a decrease in left ventricular stroke volume. This phenomenon is called postpacer syndrome and occasionally is severe enough to preclude the use of a pacemaker. [90] A bichamber sequential pacemaker that stimulates the atria and ventricles in sequential fashion is a viable alternative for patients unable to tolerate the loss of the atrial kick. [91] Electrical problems with pacing include pacemaker generator failure, dysrhythmias, and outside interference. Electrical interference is of occasional importance during aeromedical transport. [92] Usually converting the unit to a fixed mode will permit continued pacing. Although ventricular tachycardia and ventricular fibrillation have been reported to result from pacemakers, these dysrhythmias are rare. Because of this, patients who present with such dysrhythmias should be evaluated for a nonpacemaker etiology. [93] Direct current cardioversion and electroshock therapy are safe procedures to carry out in patients who have pacemakers as long as the current does not go directly over the subcutaneous lead or generator pack. [94] Conclusion Temporary transvenous pacing is a rapid, safe, and reliable method for achieving effective electrical stimulation of the heart. Symptomatic bradycardias unresponsive to pharmacologic treatment and some tachycardias are indications for its use. In acute myocardial infarction, it serves both a therapeutic and a prophylactic function.
EMERGENCY TRANSCUTANEOUS CARDIAC PACING Transcutaneous cardiac pacing (TCP) is a rapid, minimally invasive method of treating severe bradycardias and asystole. Electrodes are applied to the skin of the anterior and posterior chest walls, and pacing is initiated with a portable pulse generator. In an emergency setting, this pacing technique is faster and easier to initiate than transvenous pacing. Pulse generators are sufficiently portable to be used in EDs, hospital wards, intensive care units, and mobile paramedic vehicles. Background In 1872, Duchenne de Boulogne reported a successful resuscitation of a child by attaching one electrode to a limb while a second electrode was rhythmically touched to the precordium of the thorax.[95] Successful overdrive pacing of the human heart, using a precordial electrode, was reported by VonZiemssen in 1882. [96]
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Figure 15-11 Coronary sinus pacing. Note the paced right bundle-branch block pattern.
In 1952, Zoll introduced the first practical means of TCP. Using a ground electrode attached to the skin and a subcutaneous needle electrode over the precordium, he reported the successful resuscitation of two patients in ventricular standstill. [97] One patient was paced for 5 days and subsequently was discharged from the hospital. Zoll later introduced a machine that delivered impulses lasting 2 msec through 3-cm-diameter metal paddles pressed firmly against the anterior chest wall. This device was the first commercial transcutaneous cardiac pacemaker. During the 1950s, Zoll and Leatham demonstrated the effectiveness of TCP in patients with bradycardia and asystole.[98] [99] [100] [101] Leatham used larger electrodes (4 × 6 cm) and a longer pulse duration (20 msec) to successfully pace two patients with bradydysrhythmias. [101]
Until the late 1950s, TCP was the only clinically accepted method of cardiac pacing. The original technique using bare metal electrodes had adverse effects, including local tissue burns, muscle contraction, and severe pain. [97] [101] With the development of the first implantable pacemakers from 1958 through 1960 and the improvement of transvenous electrodes during the early 1960s, TCP was rapidly discarded. [102] Refinements in electrode size and pulse characteristics have led to the reintroduction of TCP into clinical practice. [103] [104] Increasing the pulse duration from 2 to 20 msec or longer was found to decrease the current output required for cardiac capture. [105] [106] Longer impulse durations also make the induction of ventricular fibrillation less likely. [105] Larger surface area electrodes (80 to 100 cm 2 ) decrease the current density at the underlying skin and therefore decrease pain and the possibility of tissue burns. [103] Indications and Contraindications General indications for cardiac pacing are discussed earlier. TCP is the fastest and easiest method of emergency pacing. This technique is useful for initial stabilization of the patient in the ED who requires emergency pacing while arrangements or decisions for transvenous pacemaker insertion are being made. The equipment is readily mastered, the procedure is fast, and it is minimally invasive. [104] [107] Refinements in equipment have made TCP the emergency pacing procedure of choice. TCP also is gaining widespread prehospital use in helicopter ambulance programs and inhospital use in the cardiac catheterization laboratory, operating room, intensive care unit, and on general medical floors. [108] [109] [110] The technique may be preferable to transvenous pacing in patients who have received thrombolytic agents. No central venous puncture, with the attendant risk of hemorrhage, is required. Limited experience suggests that TCP also may be useful in the treatment of refractory tachydysrhythmias by overdrive pacing. [111] [112] [113] [114] [115] Although small pediatric electrodes for TCP have been developed, experience with pediatric TCP has been limited. [116] [117] TCP is indicated for the treatment of hemodynamically significant bradydysrhythmias that have not responded to atropine therapy. Hemodynamically significant implies hypotension, anginal chest pain, pulmonary edema, or evidence of decreased cerebral perfusion. This technique is temporary and is indicated for short intervals as a bridge until transvenous pacing can be initiated or until the underlying cause of the bradyarrhythmia (e.g., hyperkalemia, [107] drug overdose[118] ) can be reversed. Although often unsuccessful, TCP may be
297
Figure 15-12 Coronary sinus position. A, Posteroanterior view. B, Lateral view. (From Goldberger E: Treatment of Cardiac Emergencies, 3rd ed. St. Louis, CV Mosby, 1982.)
attempted in the treatment of asystolic cardiac arrest. In this setting the technique is efficacious only if used early after arrest onset (generally within 10 minutes). [120] TCP is not indicated for treatment of prolonged arrest victims with a final morbid rhythm of asystole. [ 117] [ 121] [ 122] [123]
[119]
Delay from the onset of arrest to the initiation of pacing is a major problem that limits the usefulness of TCP in prehospital care. Hedges and colleagues reported that everyday availability of pacing increased the number of patients who received pacing within 10 minutes of hemodynamic decompensation and increased long-term patient survival as well. [120] Prehospital pacing may be most useful in treatment of the patient with a hemodynamically significant bradycardia who has not yet progressed to cardiac arrest (e.g., heart block in the setting of acute myocardial infarction) or in the patient who arrests after the arrival of prehospital providers. [119] [120] In conscious patients with hemodynamically stable bradycardias, TCP may not be necessary. It is reasonable to attach electrodes to such patients and to leave the pacemaker in standby mode against the possibility of hemodynamic deterioration while further efforts at treatment of the patient's underlying disorder are being made. This approach has been used successfully in patients with new heart block in the setting
Figure 15-13 A pacing catheter that is outside or abuts the cardiac silhouette and is not properly positioned within the right ventricular cavity suggests myocardial perforation. (From Tarver RD, Gillespie KR: The misplaced tube. Emerg Med, Feb 29, 1988, p 97.)
of cardiac ischemia. [124] Generally when a transvenous pace-maker becomes available, transvenous pacing is preferred because of better patient tolerance. Equipment Few medical product lines have changed as rapidly as commercial transcutaneous pacemakers. Patent controversy, corporate acquisitions, and rapid product evolution have all contributed to this rapid change. [125] Despite this instability in the marketplace, transcutaneous pacemakers are now standard equipment in most EDs and are rapidly spreading to other inhospital and prehospital care settings. The pacemakers introduced in the early 1980s tended to be asynchronous devices with a limited selection of rate and output parameters. Units introduced more recently have demand mode pacing and more output options and are more likely to be combined with a defibrillator in a single unit. Combined defibrillator-pacers offer advantages in cost, ease, and rapidity of use when compared with stand-alone devices. An example of one combined unit is shown in Fig. 15-14 . A full-featured stand-alone pacemaker is illustrated in Fig. 15-15 . All transcutaneous pacemakers have similar basic features. Most allow operation in either a fixed rate (asynchronous) or a demand mode. Most allow rate selection in a range from 30 to 200 beats/min. Current output is usually adjustable from 0 to 200 mA. If an electrocardiography monitor is not an integral part of the unit, an output adapter to a separate monitor is required to "blank" the large electrical spike from the pacemaker impulse and allow interpretation of the much smaller ECG complex. Without blanking protection, the standard ECG machine is swamped by the pacemaker spike and is uninterpretable. This could be disastrous, because the large pacing artifacts can mask treatable ventricular fibrillation
298
Figure 15-14 Combined defibrillator-transcutaneous pacemaker unit (Zoll-PD). The unit defibrillates through standard hand held paddles and has additional cable connections for electrocardiograph monitoring electrodes and for pacing electrodes. (Courtesy of ZMI Corporation, Cambridge, Mass.)
( Fig. 15-16 ). Pulse durations on available units vary from 20 to 40 msec and are not adjustable by the operator. Two sets of patient electrodes are usually required for operation of the device. One set of standard ECG electrodes is used for monitoring. The much larger pacing electrodes deliver electrical impulses for pacing. One pacing electrode is placed over the mid-dorsal spine, and the other is placed over the left anterior chest. The posterior electrode serves as the ground. Newer combined defibrillator-pacemakers can use a single set of electrodes for ECG monitoring, pacing, and defibrillation. This approach makes use of the device simpler,
Figure 15-15 "Stand alone" transcutaneous pacemaker (Zoll NTP). This unit has a built-in monitor and strip chart recorder. (Courtesy of ZMI Corporation, Cambridge, Mass.)
although the ECG waveform and analysis may be suboptimal. Provisions generally are made for separate ECG monitoring electrodes for use as desired by the operator. Technique Pad Placement
The pacing electrodes are applied as shown in Figure 15-17 and are attached to the instrument cable. The anterior electrode (cathode, or negative electrode) is placed as close as possible to the point of maximal impulse on the left anterior chest wall. This electrode adheres to the skin and has a large surface area for electrical contact. The second electrode is placed directly posterior to the anterior electrode. Failure to capture may be due to misplacement of the electrodes, and failure to pace may be rectified with a small change in anterior electrode position. ECG electrodes (if used) are placed on the chest wall or limbs, or both, as required and connected to the instrument cable. Some clinicians prophylactically apply pacing electrodes to all critically ill patients with bradycardia to facilitate immediate TCP should decompensation occur. There is little risk of electrical injury to health care providers during TCP. Power delivered during each impulse is less than 1/1000 of that delivered during defibrillation. [126] Chest compressions (cardiopulmonary resuscitation) can be administered directly over the insulated electrodes while pacing. [127] Inadvertent contact with the active pacing surface results only in a mild shock. Pacing Bradycardic Rhythms
To initiate TCP, the pacing electrodes are applied, and the device is activated. In the setting of bradyasystolic arrest, it is reasonable to turn the stimulating current to maximal output and then decrease the output as appropriate after capture is achieved. In a patient who has a hemodynamically compromising bradycardia but is not in cardiac arrest, the operator should slowly increase the output from the minimal setting until capture is achieved. Rate and output selections are adjustable ( Fig. 15-18 ). Generally a heart rate of 60 to 70 beats/min will maintain an adequate blood pressure (by blood pressure cuff or arterial catheter) or the desired degree of mentation.
299
Figure 15-16 The top three rhythm strips (A–C) are taken from a standard wall-mounted electrocardiograph monitor. They all demonstrate large pacer spikes without capture. The underlying rhythm cannot be determined and could be treatable ventricular fibrillation. The bottom rhythm strip (D) demonstrates a tracing on the same patient with the external pacer monitor (special dampening). Note that the pacing spikes are much smaller, and it is easily seen that the underlying rhythm is asystole, without pacer capture. The presence of a T-wave after the QRS complex is a good indicator of ventricular capture.
Assessment of electrical capture can be made by monitoring the ECG on the filtered monitor of the pacing unit ( Fig. 15-19 ). Additionally, bedside US may prove useful in determining ventricular capture. [128] [129] Ideally, pacing should be continued at an output level just above the threshold of initial electrical capture. One study in 16 normal male volunteers who were paced without sedation noted cardiac capture at a mean current of 54 mA (range, 42 to 60 mA). [130] Most subjects could tolerate pacing at their capture threshold; only 1 subject required discontinuation of pacing at 60 mA because of intolerable pain. Heller and associates compared subjective pain perception and capture thresholds in 10 volunteers paced with 5 different transcutaneous pacers. [131] Capture rates (40% to 80%), thresholds (66.5 to 104 mA), and subjective discomfort varied from pacemaker to pacemaker. Failure to capture with TCP may be related to electrode placement or patient size. Patients with barrel-shaped chests and large amounts of intrathoracic air conduct electricity poorly and may prove refractory to capture. In one study, thoracotomy was found to nearly double the pacing threshold. [132] A large pericardial effusion or tamponade also will increase the output required for capture. [133] Failure to electrically capture with a transcutaneous device in these settings is an indication to consider immediate transvenous pacer placement. Patients who are conscious or who regain consciousness during TCP will experience discomfort because of muscle contraction. [124] [130] [131] Analgesia with incremental doses of an opioid agent, sedation with a benzodiazepine compound, or both, will make this discomfort tolerable until transvenous pacing can be instituted. Overdrive Pacing
Overdrive pacing [111] [112] [113] [114] [115] of ventricular tachycardia or paroxysmal supraventricular tachycardia is performed in patients who are stable enough to tolerate the brief delay associated with the necessary preparation for this technique. Little data exist on the efficacy or use of this procedure in the ED. The patient is sedated as explained earlier, pacing and monitoring electrode pads are placed in the standard position as detailed earlier, and brief trains (6 to 10 beats) of asynchronous pacing are applied. The pacer rate must be set approximately 20 to 60 pulses/min greater than the dysrhythmia rate. [134] Generally, an impulse rate of 200 pulses/min is used for ventricular tachycardias (rate generally 150 to 180 beats/min), and a rate of 240 to 280 pulses/min is used for paroxysmal
300
Figure 15-17 Correct placement of transcutaneous pacemaker electrodes (see text). (Courtesy of ZMI Corporation, Cambridge, Mass.)
supraventricular tachycardias (rate commonly 200 to 250 beats/min). Because rhythm acceleration is possible during overdrive pacing, it is essential that full resuscitation equipment, including a defibrillator, be available at the bedside. Complications The major potential complication of TCP is failure to recognize the presence of underlying treatable ventricular fibrillation. This complication is primarily due to the size of the pacing artifact in the ECG screen, a technical problem inherent in systems without appropriate dampening circuitry. A theoretical complication of TCP is the induction of dysrhythmias. In animal models using epicardial electrodes, the threshold current required to induce ventricular fibrillation decreases as electrical impulse duration increases. At a 10-msec impulse duration, ventricular fibrillation can be induced with currents as low as 25 mA delivered through epicardial electrodes. [105] Because TCP impulses are of even longer duration (20 msec) and of higher current (50 to 200 mA), there has been concern about possible induction of ventricular fibrillation during TCP. Studies of fibrillation thresholds using large precordial electrodes have shown the relationship of threshold-to-impulse duration to be the opposite of that seen with epicardial electrodes. With cutaneous precordial electrodes, the current required to induce ventricular fibrillation increases as pulse duration increases.[106] The apparent paradox may be explained by the differing nature of the electrodes. Epicardial electrodes are localized over a small area of the myocardium, whereas transcutaneous electrodes deliver a broad electrical charge to the myocardium as a whole. The implication is that longer impulse durations, although more dangerous with internal pacing, seem to decrease the chance of inducing ventricular fibrillation with
Figure 15-18 Rate and output selections.
TCP. Nonetheless, asynchronous TCP for tachydysrhythmias has been associated with rhythm acceleration and development of ventricular fibrillation.
[113]
Experience with prolonged TCP in humans has not been extensive. Zoll and colleagues reported 25 humans paced for up to 108 hours with impulses of 20-msec duration.[100] Pacer-induced dysrhythmias did not occur. Leatham and associates paced 1 patient for 68 hours with impulses of 20-msec duration. [101] The patient died 2 days after pacing was discontinued. Pathologic examination revealed no evidence of pacerinduced myocardial damage. Madsen and colleagues paced 10 healthy volunteers at threshold for 30 minutes and found no enzyme or echocardiographic abnormalities. [135] Studies of repetitive direct current countershocks in dogs have induced tissue damage with energy levels that are 1000 times greater than those required to pace the heart transcutaneously. In a canine study, 10 animals with chronic heart block that were paced for 60 minutes (20-msec duration at 80 beats/min with 8-cm-diameter cutaneous electrodes) did not develop pacer-related dysrhythmias. Serial cardiograms and cardiac enzymes revealed no evidence of ischemia or infarction. [136] Examination of the canine hearts after the dogs were sacrificed 72 hours after pacing did not reveal clinically significant myocardial damage. [137] A single primate paced for 1 hour with 20-msec impulses of 400 mA similarly had no evidence of tissue damage at autopsy and at microscopic examination after sacrifice 24 hours later. [138] Based on these studies, TCP appears unlikely to produce cardiac injury with short-term use in humans. Soft tissue discomfort with the potential for injury may still occur with current transcutaneous pacemakers. One study with the Zoll transcutaneous pacemaker found only 2 of 30 subjects (patients and volunteers) who were paced while conscious required discontinuation of pacing owing to discomfort. [130] Most reported the
discomfort as "mild or moderate and easily tolerable." Sedation would presumably improve a conscious patient's ability to tolerate TCP.
301
Figure 15-19 Assessing electrocardiogram capture with TCP. Note that the monitor has been adapted to accommodate the large pacing artifact so as not to obscure the underlying ventricular activity.
Nonetheless, prolonged use may still induce local cutaneous injury; Pride and McKinley reported one 7-week-old child who was paced for 45 hours without a pad change and who developed third-degree burns. [139] Conclusion Devices that pace the heart externally have been available for clinical use since 1952. Technologic improvements have minimized the complications associated with earlier use of the transcutaneous route and have enabled the reapplication of this relatively old pacing technique to a select subset of cardiac emergencies. The introduction of combined defibrillator-pacemakers promises to make pacing more available in prehospital and health care settings. Although the technique is still not universally available, it is rapidly becoming the standard of care for resuscitation protocols and equipment. Pacing instituted earlier in the course of bradycardiac rhythms, including the prehospital phase of care, may improve the poor survival rate currently associated with these rhythms.
References 1. Rosenberg 2. Francis
AS, Grossman JI, Escher DJW, et al: Bedside transvenous cardiac pacing. Am Heart J 77:697, 1969.
GS, Williams SV, Achord JL, et al: Clinical competence in the insertion of a temporary transvenous ventricular pacemaker. Circulation 89:1913, 1994.
3. Callaghan 4. Furman
JC, Bigelow WG: Electrical artificial pacemaker for standstill of heart. Ann Surg 134:8, 1951.
S, Robinson G: The use of intracardiac pacemaker in the correction of total heart block. Surg Forum 9:245, 1958.
5. Muller
OF, Bellet S: Treatment of intractable heart failure in the presence of complete atrioventricular heart block by the use of internal cardiac pacemaker. Report of two cases. N Engl J Med 265:768, 1961. 6. Siddons
H, Davies JG: A new technique for internal cardiac pacing. Lancet 2:1204, 1963.
7. DeSanctis
RW: Short-term use of intravenous electrode in heart block. JAMA 184:130, 1963.
302
8. Vogel
JHK, Tabari K, Averill KH, et al.: A simple technique for identifying P waves in complex arrhythmias. Am Heart J 67:158, 1964.
9. Kimball
JT, Killip T: A simple bedside method for transvenous intracardiac pacing. Am Heart J 70:35, 1965.
10.
Harris CW, Hurlburt JC, Floyd WL, et al: Percutaneous technique for cardiac pacing with a platinum-tipped electrode catheter. Am J Cardiol 15:48, 1965.
11.
Zuckerman W, Zaroff L, Berkovits BV, et al: Clinical experience with a new implantable demand pacemaker. Am J Cardiol 20:232, 1967.
12.
Swan HJ, Ganz W: Catheterization of the heart in man with use of a flow-directed balloon-tipped catheter. N Engl J Med 283:447, 1970.
13.
Schnitzler RN, Caracta AR, Damato AN: "Floating" catheter for temporary transvenous ventricular pacing. Am J Cardiol 31:351, 1973.
14.
Lang R, David D, Herman HO, et al: The use of the balloon-tipped floating catheter in temporary transvenous cardiac pacing. PACE 4:491, 1981.
15.
Kruger BK, Rakes S, Wilkerson J, et al: Temporary pacemaking by general internists. Arch Intern Med 143:1531, 1983.
16.
Furman S: Cardiac pacing and pacemaker. I. Indications for pacing bradyarrhythmias. Am Heart J 93:523, 1977.
17.
Escher DJ, Furman S: Emergency treatment of cardiac arrhythmias. Emphasis on use of electrical pacing. JAMA 214:2028, 1970.
Julian DG, Valentine DA, Miller GG: Disturbances of rate, rhythm, and conduction in acute myocardial infarction: A prospective study of 100 consecutive unselected patients with the aid of electrocardiographic monitoring. Am J Med 37:915, 1965. 18.
19.
Baba N: Experimental cardiac ischemia, observation of the sinoatrial and atrioventricular node. Lab Invest 23:168, 1970.
20.
Wolf S: Bradycardia of the dive reflex: A possible mechanism of sudden death. Trans Am Clin Climatol Assoc 76:142, 1964.
21.
Hazard PB: Transvenous cardiac pacing in cardiopulmonary resuscitation. Crit Care Med 9:666, 1981.
Niemann JT, Adomian GE, Garner D, et al: Endocardial and transcutaneous cardiac pacing, calcium chloride, and epinephrine in postcounter-shock asystole and bradycardias. Crit Care Med 13:699, 1985. 22.
23.
Syverud SA, Dalsey WC, Hedges JR: Transcutaneous and transvenous cardiac pacing for early bradyasystolic cardiac arrest. Ann Emerg Med 15:121, 1986.
24.
Conklin EF, Giannelli S, Nealon TF: Four hundred consecutive patients with permanent transvenous pacemakers. J Thorac Cardiovasc Surg 69:1, 1975.
25.
Simon AB, Steinke WE, Curry JJ: Atrioventricular block in acute myocardial infarction. Chest 62:156, 1972.
26.
Resuekov L, Lipp H: Pacemaking in acute myocardial infarction. Prog Cardiovasc Dis 14:475, 1972.
Hindman MC, Wagner GS, JaRo M, et al: The clinical significance of bundle-branch block complicating acute myocardial infarction. 2. Indications of temporary and permanent pacemaker insertion. Circulation 58:689, 1978a. 27.
28.
Bognolo DA, Rabow RI, Vijayanagar RR, et al: Traumatic sinus node dysfunction. Ann Emerg Med 11:319, 1982.
29.
White BC, Hoehner PJ, Petinga TJ, et al: HIS electrocardiographic characterization of terminal arrhythmias of hemorrhagic shock in dogs. JACEP 8:298, 1979.
30.
Millikan JS, Moore EE, Dunn EL, et al: Temporary cardiac pacing in traumatic arrest victims. Ann Emerg Med 9:591, 1980.
31.
Atkins JM, Leshin SJ, Blumquist G, et al: Ventricular conduction blocks and sudden death in acute myocardial infarction. N Engl J Med 288:281, 1978.
Hindman MC, Wagner GS, JaRo M: The clinical significance of bundle-branch block complicating acute myocardial infarction. 1. Clinical characteristics, hospital mortality, and one year follow-up. Circulation 58:679, 1978b. 32.
33.
Escher DJ: The use of cardiac pacemakers. In Braunwald E (ed): Heart Disease: A Textbook of Cardiovascular Medicine. Philadelphia, WB Saunders, 1980, p 749.
34.
Thompson JR, Dolton BC, Lapis DG, et al: Right bundle-branch block in complete heart block caused by Swan Ganz catheter. Anesthesiology 51:359, 1979.
Morris D, Mulvihill D, Lew WYW: Risk of developing complete heart block during bedside pulmonary artery catheterization in patients with left bundle-branch block. Arch Intern Med 147:2005, 1987. 35.
36.
Buran MJ: Transcutaneous pacing as an alternative to prophylactic transvenous pacemaker insertion. Crit Care Med 15:623, 1987.
37.
Connors AF, Speroff T, et al: The effectiveness of right heart catheterization in the initial care of critically ill patients. JAMA 276:889, 1996.
38.
DeSanctis RW, Kastor JA: Rapid intracardiac pacing for treatment of recurrent ventricular arrhythmias in the absence of heart block. Am Heart J 76:168, 1968.
39.
Goldberger E: Temporary cardiac pacing. In Goldberger E, Wheet MW Jr (eds): Treatment of Cardiac Emergencies, 3rd ed. St. Louis, CV Mosby, 1982, p 233.
40.
Weiner I: Pacing techniques in the treatment of tachycardias. Ann Intern Med 93:326, 1980.
41.
Hofer CA, Smith JK, Tenholder MF: Verapamil intoxication: A literature review of overdoses and discussion of therapeutic options. Am J Med 95:431, 1993.
42.
Taboulet P, Cariou A, Berdeaux A, et al: Pathophysiology and management of self poisoning with ß-blockers. J Toxicol Clin Toxicol 31:531, 1993a.
43.
Taboulet P, Baud FJ, Bismuth C, et al: Acute digitalis intoxication: Is pacing still appropriate? J Toxicol Clin Toxicol 31:261, 1993b.
44.
Ramoska EA, Spiller HA, Myers A: Calcium channel blocker toxicity. Ann Emerg Med 19:649, 1990.
45.
Simoons ML, Demey HE, Bossaert LL, et al: The Paceport catheter: A new pacemaker system introduced through a Swan Ganz catheter. Cathet Cardiovasc Diagn 15:66, 1988.
46.
Dronen S, Thompson B, Nowak R, et al: Subclavian vein catheterization during cardiopulmonary resuscitation. JAMA 247:3227, 1982.
47.
Laczika K, Thalhammer F, Locker G, et al: Safe and efficient emergency transvenous ventricular pacing via the right supraclavicular route. Anesth Analg 90:784, 2000.
48.
Mostert MD, Kenny GM, Murphy GP: Safe placement of central venous catheter into the internal jugular veins. Arch Surg 101:431, 1970.
49.
Syverud SA, Dalsey WC, Hedges JR, Hanslits ML: Radiographic assessment of transvenous pacemaker placement during CPR. Ann Emerg Med 15:131, 1986.
50.
Austin JL, Preis LK, Crampton RS, et al: Analysis of pacemaker malfunction and complications of temporary pacing in the coronary care unit. Am J Cardiol 44:301, 1982.
51.
Weinstein J, Gnoj J, Mazzara JT, et al: Temporary transvenous pacing via the percutaneous femoral approach: A prospective study of 100 cases. Am Heart J 85:695, 1973.
52.
Furman S: Pacemaker emergencies. Med Clin North Am 63:113, 1979.
53.
Fyke FE III: Doppler guided extrathoracic introducer insertion. Pacing Clin Electrophysiol 18:1017, 1995.
Nash A, Burrell CJ, Ring NJ, Marshall AJ: Evaluation of an ultrasonically guided venepuncture technique for the placement of permanent pacing electrodes. Pacing Clin Electrophysiol 21:452, 1998. 54.
55.
Macedo W Jr, Sturman K, Kim JM, Kang J: Ultrasonic guidance of transvenous pacemaker insertion in the emergency department: A report of three cases. J Emerg Med 17:491, 1999.
56.
Aguilera PA, Durham BA, Riley DA: Emergency transvenous cardiac pacing placement using ultrasound guidance. Ann Emerg Med 36:224, 2000.
57.
Thompson ME, Shaver JA: Undesirable cardiac arrhythmias associated with rate hysteresis pacemakers. Am J Cardiol 38:685, 1976.
58.
Nachnani GH, Gooch AS, Hsu I: Systolic murmurs induced by pacemaker catheters. Arch Intern Med 24:202, 1969.
59.
Kluge WF: Pacemaker sound and its origin. Am J Cardiol 25:362, 1970.
60.
Kramer DH, Moss AJ, Shah PM: Mechanisms and significance of pacemaker-induced extracardiac sound. Am J Cardiol 25:367, 1970.
61.
Herbst CA: Indications, management, and complications of percutaneous subclavian catheters. Arch Surg 113:1421, 1978.
62.
Sethi GK, Bhayana JN, Scott SM, et al: Innominate venous thrombosis: A rare complication of transvenous pacemaker electrodes. Am Heart J 87:770, 1974.
63.
Nolewajka AT, Goddard MD, Brown TG: Temporary transvenous pacing and femoral vein thrombosis. Am J Cardiol 45:459, 1980.
64.
May KJ, Cardone JT, Stroebel PP, et al: Streptokinase dissolution of a right atrial thrombus associated with a temporary pacemaker. Arch Intern Med 148:903, 1988.
65.
Johnson CL, Jazarchick J, Lynn HB: Subclavian venipuncture, preventable complications. Mayo Clin Proc 45:719, 1970.
66.
Arbitman M, Kart BH: Hydromediastinum after aberrant central venous catheter placement. Crit Care Med 7:27, 1979.
67.
Drachler DH, Koepte GH, Wey JG: Phrenic nerve injury from subclavian vein catheterization. JAMA 236:2880, 1976.
303
68.
Cope C: Intravascular breakage of Seldinger spring guide wires. JAMA 180:1061, 1962.
69.
Schwartz AJ, Harrow JC, Jobes DR, et al: Guide wires—A caution. Crit Care Med 9:347, 1981.
70.
Johansson L, Malmstrom G, Uggla LG: Intracardiac knotting of the catheter in heart catheterization. J Thorac Surg 27:605, 1954.
71.
Boal BH, Keller BD, Ascheim RS, et al: Complication of intracardiac electrical pacing—knotting together of temporary and permanent electrodes. N Engl J Med 280:650, 1969.
72.
Mehra R, Furman S, Crump J: Vulnerability of the mildly ischemic ventricle to cathodal, anodal, and bipolar stimulation. Circ Res 41:159, 1977.
73.
Abernathy WS, Crevey BJ: Right bundle-branch block during transvenous ventricular pacing. Am Heart J 90:774, 1975.
74.
Campo I, Garfield GJ, Escher DJW, et al: Complications of pacing by pervenous subclavian semifloating electrodes including extraluminal insertions. Am J Cardiol 26:627, 1970.
75.
Danielson GK, Shabetai R, Bryant LR: Failure of endocardial pacemaker due to myocardial perforation. J Thorac Cardiovasc Surg 54:42, 1967.
76.
Goswani M, Gould L, Gompiecht RF, et al: Perforation of the heart by flexible transvenous pacemaker. JAMA 216:2013, 1971.
77.
Kalloor GJ: Cardiac tamponade. Report of a case after insertion of transvenous endocardial electrode. Am Heart J 88:88, 1974.
78.
Jorgensen EO, Lyngborg K, Wennevold A: Unusual sign of perforation of a pacemaker catheter. Am Heart J 74:732, 1967.
79.
Kaye D, Frankl W, Arditi LI: Probable postcardiotomy syndrome following implantation of a transvenous pacemaker: Report of the first case. Am Heart J 90:627, 1975.
80.
Glassman RD, Noble RJ, Tavel ME, et al: Pacemaker-induced endocardial friction rub. Am J Cardiol 40:811, 1977.
81.
Tarver RB, Gillespie KR: The misplaced tube. Emerg Med Clin North Am 20:97, 1988.
82.
Foote GA, Schabel SI, Hodges M: Pulmonary complications of the flow-directed balloon-tipped catheter. N Engl J Med 290:927, 1974.
83.
Escher DJ, Furman S, Solomon N, et al: Transvenous pacing of the phrenic nerve. Am Heart J 72:283, 1977.
84.
Preston TA: Electrocardiographic diagnosis of pacemaker catheter displacement. Am Heart J 854:445, 1973.
85.
Smith ND: Pacemaker dysfunction. In Greenberg MI, Roberts JR (eds): Emergency Medicine: A Clinical Approach to Challenging Problems. Philadelphia, FA Davis, 1982, p 355.
86.
Preston TA, Fletcher RD, Lucchesi BR, et al: Changes in myocardial threshold, physiologic, and pharmacologic factors in patients with implanted pacemakers. Am Heart J 74:235, 1967.
87.
Walker WJ, Elkins JT, Wood LWW: Effect of potassium in restoring myocardial response to a subthreshold cardiac pacemaker. N Engl J Med 271:12, 1964.
88.
Basu D, Chatterjee K: Unusually high pacemaker threshold in severe myxedema. Decrease with thyroid hormone therapy. Chest 70:677, 1976.
89.
Gay RJ, Brown DF: Pacemaker failure due to procainamide toxicity. Am J Cardiol 34:728, 1974.
90.
Haas JM, Strait GB: Pacemaker-induced cardiovascular failure. Am J Cardiol 33:295, 1974.
91.
Guzy PM: Emergency cardiac pacing. Emerg Med Clin North Am 4:745, 1986.
92.
Sumchai A, Sternbach G, Eliastam M, et al: Pacing hazards in helicopter aeromedical transport. Am J Emerg Med 6:236, 1988.
93.
Leung FW, Oill PA: Ticket of admission: Unexplained syncopal attacks in patients with cardiac pacemaker. Ann Emerg Med 9:527, 1980.
94.
Youmans RC, Bourianoff G, Allensworth DC, et al: Electroshock therapy and cardiac pacemakers. Am J Surg 118:931, 1969.
95.
Duchenne de Boulogne: De l'électrisation localise et son application a la pathologique et a la therapeutique. Paris, Bailliere, 1872.
96.
VonZiemssen H: Studien über die Bewegungsvorgänge am menschlichen Herzen, sowie über die mechanische und elektrische Erregbarkeit des Herzens und des Nervus, 1882.
97.
Zoll PM: Resuscitation of the heart in ventricular standstill by external electrical stimulation. N Engl J Med 247:768, 1952.
98.
Zoll PM, Linenthal AJ, Norman LR, et al: Treatment of unexpected cardiac arrest by external electric stimulation of the heart. N Engl J Med 254:541, 1956.
99.
Zoll PM, Linenthal AJ, Norman LR: Treatment of Stokes-Adams disease by external stimulation of the heart. Circulation 9:482, 1954.
100. Zoll
PM, Linenthal AJ, Norman LR, et al: External electric stimulation of the heart in cardiac arrest. Arch Intern Med 96:639, 1955.
101. Leatham
A, Cook P, Davis JG: External electric stimulator for treatment of ventricular standstill. Lancet 2:1185, 1956.
102. Chardack 103. Zoll
WM, Gage AA, Greatbatch W: A transistorized self-contained, implantable pacemaker for the long-term correction of complete heartblock. Surgery 48:643, 1960.
PM: External noninvasive electric stimulation of the heart. Crit Care Med 9:393, 1981.
104. Dalsey 105. Jones
WC, Syverud SA, Trott A: Transcutaneous cardiac pacing. J Emerg Med 1:201, 1984.
M, Geddes LA: Strength duration curves for cardiac pacemaking and ventricular fibrillation. Cardiovasc Res Bull 15:101, 1977.
106. Varghese 107. Clinton
JE, Zoll PM, Zoll R, et al: External noninvasive cardiac pacing. J Emerg Med 2:155, 1985.
108. Berliner
D, Okun M, Peters RW, et al: Transcutaneous pacing in the operating room. JAMA 254:84, 1985.
109. Johnson 110. Noe
PJ, Bren G, Ross A: Electrophysiology of external cardiac pacing: A comparative study with endocardial pacing. Circulation 66:349, 1982b.
DQ, Vukov LF, Farnell MB: External transcutaneous pacemakers in air medical transport services [abstract]. Aeromedical J 2:23, 1987.
R, Cockrell W, Moses HW, et al: Transcutaneous pacemaker use in a large hospital. PACE 9:101, 1986.
111. Rosenthal 112. Sharkey
SW, Chaffee V, Kapsner S: Prophylactic external pacing during conversion of atrial tachyarrhythmias. Am J Cardiol 55:1632, 1985.
113. Altamura 114. Grubb
ME, Stamato NJ, Marchlinski FE, Josephson ME: Noninvasive cardiac pacing for termination of sustained, uniform ventricular tachycardia. Am J Cardiol 58:561, 1986.
G, Bianconi L, Boccadamo R, et al: Treatment of ventricular and supraventricular tachyarrhythmias by transcutaneous cardiac pacing. PACE 12:331, 1989.
BP, Temsey-Armos P, Hahn H, et al: The use of external, noninvasive pacing for the termination of ventricular tachycardia in the emergency department setting. Ann Emerg Med 21:174,
1992. 115. Grubb
BP, Samoil D, Temsey-Armos P, et al: The use of external, noninvasive pacing for the termination of supraventricular tachycardia in the emergency department setting. Ann Emerg Med 22:714, 1993. 116. Beland 117. Quan
MJ, Hesslein PS, Finlay CD, et al: Noninvasive transcutaneous cardiac pacing in children. PACE 10:1262, 1987.
L, Graves JR, Kinder DR, et al: Transcutaneous cardiac pacing in the treatment of out-of-hospital pediatric cardiac arrests. Ann Emerg Med 21:905, 1992.
118. Cummins
RO, Haulman J, Quan L, et al: Near-fatal yew berry intoxication treated with external cardiac pacing and digoxin specific FAB antibody fragments. Ann Emerg Med 19:38, 1990.
119. Barthell
E, Troiano P, Olson D, et al: Prehospital external cardiac pacing: A prospective, randomized, controlled clinical trial. Ann Emerg Med 17:1221, 1988.
120. Hedges
JR, Feero S, Shultz B, et al: Prehospital transcutaneous cardiac pacing for symptomatic bradycardia. PACE 14:1473, 1991.
121. Eitel
DR, Guzzardi LJ, Stein SE, et al: Noninvasive transcutaneous cardiac pacing in prehospital cardiac arrest. Ann Emerg Med 16:531, 1987.
122. Cummins 123. Hedges 124. Zoll
RO, Graves JR, Larsen MP, et al: Out-of-hospital transcutaneous pacing by emergency medical technicians in patients with asystolic cardiac pacing. N Engl J Med 328:1377, 1993.
JR, Syverud SA, Dalsey WC, et al: Prehospital trial of emergent transcutaneous pacing. Circulation 76:1337, 1987.
PM, Zoll RH, Falk RH, et al: External non-invasive temporary cardiac pacing: Clinical trials. Circulation 71:937, 1985.
125. Heller
MB: Of pacing, patents, and patients [editorial]. Am J Emerg Med 6:78, 1988.
126. Syverud 127. Dalsey
SA, Dalsey WC, Hedges JR: Transcutaneous cardiac pacing [letter]. Ann Emerg Med 13:982, 1984.
WC, Syverud SA, Hedges JR: Emergency department use of transcutaneous cardiac pacing for cardiac arrests. Crit Care Med 13:399, 1985.
128. Ettin
D, Cook T: Using ultrasound to determine external pacer capture. J Emerg Med 17:1007, 1999.
129. Holger
JS, Minnigan HJ, Lamon RP, Gornick CC: The utility of ultrasound to determine ventricular capture in external cardiac pacing. Am J Emerg Med 19:134, 2001.
304
130. Falk
RH, Zoll PM, Zoll RH: Safety and efficacy of noninvasive cardiac pacing: A preliminary report. N Engl J Med 309:1166, 1983.
131. Heller
MB, Kaplan RM, Peterson J, et al: Comparison of performance of five transcutaneous pacing devices [abstract]. Ann Emerg Med 16:493, 1987.
132. Kemnitz
J, Winter J, Vester EG, Peters J: Transcutaneous cardiac pacing in patients with implantable cardioverter defibrillators and epicardial patch electrodes. Anesthesiology 77:258, 1992.
133. Hedges
JR, Syverud SA, Dalsey WC, et al: Threshold enzymatic and pathologic changes associated with prolonged transcutaneous pacing in a chronic heart block model. J Emerg Med 7:1, 1989.
134. Fisher
JD, Matos JA, Kim SC: Anti-tachycardia pacing and stimulation. In Josephson ME, Wellens HJJ (eds): Tachycardias: Mechanisms, Diagnosis, and Treatments. Philadelphia, Lea & Febiger, 1984, p 413. 135. Madsen
JK, Pedersen F, Grande P, et al: Normal myocardial enzymes and normal echocardiographic findings during noninvasive transcutaneous pacing. PACE 11:1188, 1988.
136. Syverud
SA, Dalsey WC, Hedges JR, et al: Transcutaneous cardiac pacing: Determination of myocardial injury in a canine model. Ann Emerg Med 12:261, 1983.
137. Kicklighter
EJ, Syverud SA, Dalsey WC, et al: Pathologic aspects of transcutaneous cardiac pacing. Am J Emerg Med 3:108, 1985.
138. Varghese
J, Bren G, Ross A: Absence of Tissue Injury after Prolonged Transcutaneous Pacing. The Scientific and Technical Basis of External Cardiac Pacing. Wilsonville, OR, Cardiac Resuscitator Corporation, 1982a. 139. Pride
HB, McKinley DF: Third-degree burns from the use of an external cardiac pacing device. Crit Care Med 18:572, 1990.
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Chapter 16 - Pericardiocentesis Richard J. Harper
Pericardiotomy under direct vision was first done in 1815, and in 1840 the first blind approach using a trocar was carried out successfully on a patient with tamponade from malignancy.[1] By the end of the 19th century, the trocar-and-cannula method of pericardiocentesis was commonly used. The subxiphoid approach was first described in 1911. Blind, electrocardiography (ECG)-assisted pericardiocentesis has a significant morbidity rate, reportedly as high as 15% to 20%. [2] [3] For this reason ultrasound diagnosis of pericardial effusion with fluoroscopic or ultrasound guidance has become the standard for elective pericardiocentesis because of its lower (0.5% to 3.7%)[4] [5] [6] incidence of complications. Even if tamponade physiology is present, echocardiographic diagnosis and guidance is essential. The ECG-assisted blind pericardiocentesis technique remains the standard procedure only for truly emergent pericardiocentesis when a lengthy delay may be associated with obtaining and organizing ultrasound or fluoroscopic assistance. Echocardiographic diagnosis and guidance are described elsewhere (see Chapter 69 ).
CAUSES OF PERICARDIAL EFFUSION AND TAMPONADE The medical literature concerning pericardiocentesis categorizes pericardial fluid collection as one of the following: acute hemopericardium (largely secondary to trauma) and pericardial effusion from other causes. This categorization is based on the fact that these two clinical entities are different in their time course, etiology, and treatment. Acute Hemopericardium Acute hemopericardium has several causes, including coagulopathies, cardiovascular catastrophes, and acute injury resulting from either blunt or penetrating trauma. All of these causes result in rapid accumulation of whole blood in the pericardial sac. The blood accumulates too fast for the relatively inelastic pericardial sac to stretch and accommodate the fluid. The result is cardiac tamponade produced by small fluid volumes and with an essentially normal pericardial size. Penetrating Trauma
Traumatic tamponade due to penetrating trauma may result from obvious external injury such as knife or gunshot wounds, or it may be insidious, as seen with iatrogenic cardiac perforation during cardiac or vascular procedures. In external penetrating trauma, tamponade is most commonly the result of a stab wound. [7] Approximately 80% to 90% of stab wounds to the heart demonstrate tamponade,[7] [8] compared with 20% of gunshot wounds. Stab wounds cause tamponade more often presumably because the pericardial rent is small enough to seal, trapping blood in the pericardial space. [7] [9] Larger pericardial wounds from gunshots generally drain into the pleural space and produce a hemothorax. [10] Cardiac tamponade is often suspected with anterior chest wounds, but it is imperative to remember that any penetrating wound of the chest, back, or upper abdomen may involve the heart. Iatrogenic causes of cardiac tamponade are relatively uncommon but well-known complications of invasive or diagnostic procedures. Pacemaker insertion (either transthoracic or transvenous) and cardiac catheterization, including valvuloplasty and angioplasty, are two of the main causes, from the inadvertent penetration of cardiac chambers or coronary vessels. [11] [12] [13] Penetration of vascular structures is common during transthoracic pacemaker placement. [14] Tamponade is also seen as a complication after cardiac surgery, although it is usually anticipated, and mediastinal or pericardial drainage helps to control and prevent it. [11] [15] Pericardiocentesis itself can cause tamponade by lacerating myocardium or coronary vessels. [16] [17] Cardiac tamponade may result from perforation of the right atrium or, less commonly, of the right ventricle or superior vena cava by a central venous pressure (CVP) catheter or subclavian hemodialysis catheter. [18] This event is usually not diagnosed early and is therefore often fatal. [19] Perforation may occur during placement or, more commonly, 1 to 2 days later, when the catheter erodes through tissue, particularly if a catheter made of stiff material is used or when the left internal jugular vein approach is used.[20] Tamponade from CVP line placement is seldom seen in the emergency department (ED) but must always be considered when there is sudden decompensation in a patient with a CVP line in place. Tamponade should always be considered when a patient deteriorates hemodynamically after an invasive diagnostic or therapeutic procedure involving the heart. Prevention involves proper placement of central venous catheters in the superior vena cava rather than the right atrium or ventricle. Blunt Trauma
Blunt trauma may cause hemopericardium, most often as the result of major chest injury with associated rib and sternal fractures. Cases have been reported, however, in which tamponade occurred in blunt trauma with no obvious signs of injury to the thorax. [21] Such incidents may be more common than are clinically recognized, judging by the reports of constrictive pericarditis and pericardial defects found months to years later in trauma patients who were not originally noted to have effusion. Pericardial effusion due to blunt trauma may also be a late finding, becoming symptomatic 12 to 15 days after trauma. [22] Severe deceleration injury may cause tamponade as a result of aortic or caval injury. [23] This appears to be an uncommon development, with two case series reporting tamponade in 3.6% (1 of 28 patients) and 2.3% (1 of 43 patients) of victims of aortic injury. [24] Theoretically, cardiopulmonary resuscitation (CPR) can cause pericardial effusion secondary to the blunt trauma of chest compressions, broken ribs, or intracardiac injections. Early studies reported pericardial effusion in 1% to 3% of CPR survivors. [25] Echocardiographic studies showed small cardiac effusions (but not tamponade) in 12% of survivors, only 4% of whom had received intracardiac injections. [26] Thus, although case reports of tamponade exist, [27] [28] CPR and intracardiac drug injections are unlikely to cause significant effusion, much less tamponade. Nontraumatic Hemopericardium
Nontraumatic but acute hemopericardium caused by a bleeding diathesis, aortic dissection and ventricular rupture behaves
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much like traumatic tamponade because of its acute nature. These types of hemopericardium are less obvious in etiology than hemopericardium caused by external trauma. Bleeding diathesis may cause spontaneous bleeding into the pericardial sac. The incidence of spontaneous pericardial tamponade in anticoagulated patients has been reported to range from 2.5% to 11%. [11] [29] Thrombolytic therapy has also been implicated in tamponade secondary to bleeding diathesis. Among 392 patients, only 4 (1%), all with large anterior myocardial infarctions, developed tamponade secondary to hemopericardium without ventricular rupture. [30] A dissection of the ascending aorta may extend around the base of the aorta into the pericardial sac, causing dramatic, rapid, and usually fatal tamponade. This pathologic abnormality may be due to conditions such as syphilis, Marfan syndrome, or atherosclerosis. Infection may create pseudoaneurysms of the aorta, which also can present as tamponade.[31] Ventricular rupture after myocardial infarction is a common source of acute hemopericardium. Although the prognosis is often grim, survival is possible with prompt recognition and definitive treatment. [32] [33] Nonhemorrhagic Effusions Nonhemorrhagic effusions usually accumulate slowly, allowing the pericardium to stretch and accommodate up to 2000 mL of fluid. [34] This slower accumulation, often over weeks to months, allows the circulatory system to adapt and permits more time for evaluation and treatment, even in a moderately hypotensive patient. [35] [36] In many cases of small nonhemorrhagic effusion, tamponade does not occur, and the effusion may resolve with treatment of the underlying disease or may be managed successfully by elective pericardiocentesis. Many disease processes, ranging from the common to the rare ( Table 16-1 ), can cause pericardial effusion. The cause of nonhemorrhagic tamponade may not be obvious on examination in the ED, and tamponade is frequently misdiagnosed as congestive heart failure or respiratory disease. Although neoplasm has generally been the most common underlying cause of nonhemorrhagic effusion, [29] [37] some reports[38] [39] have identified infectious complications of the human immunodeficiency
virus (HIV) as a common etiology of large nonhemorrhagic pericardial effusion and tamponade ( Table 16-2 ). HIV-related effusions have been ascribed to many opportunistic bacterial and viral infections, with mycobacterial infections being the most common. [38] [39] [40] Kaposi sarcoma and lymphoma[41] [42] have caused noninfectious pericardial effusions in HIV patients. Cancer is a prominent cause of nonhemorrhagic effusions; the pericardium is involved in 20% of patients with disseminated tumors [43] and 8% of all patients with cancer. [44] There is primary pericardial involvement in 69% of acute leukemias, in 64% of malignant melanomas, and in 24% of lymphomas; however, the incidence of actual tamponade in these malignancies is not known. Of metastases to the pericardium, 35% originate in the lung, 35% in the breast, 15% in lymphomas, and less than 3% in each of the other cancers. [44] Thus, any patient who is known to have one of these malignancies should be considered at risk for tamponade. Metastasis to the heart is usually a late finding in cancer, and other foci located elsewhere are usually evident. [45] Classic findings of tamponade, such as pulsus paradoxus, are frequently absent in cancer patients with tamponade, and their symptoms are usually attributed to their malignancy. [44]
Neoplasm
TABLE 16-1 -- Causes of Pericardial Effusion Mesothelioma Lung Breast Melanoma Lymphoma
Pericarditis
Radiation (especially after Hodgkin's disease) Viral Bacterial Staphylococcus Pneumococcus Haemophilus Fungal Tuberculosis Amebiasis Toxoplasmosis Idiopathic
Connective tissue disease
Systemic lupus erythematosus Scleroderma Rheumatoid arthritis Acute rheumatic fever
Metabolic disorders
Myxedema Uremia Cholesterol pericarditis Bleeding diatheses
Cardiac disease
Acute myocardial infarction Dissecting aortic aneurysm Congestive heart failure Coronary aneurysm
Drugs
Hydralazine Phenytoin Anticoagulants Procainamide Minoxidil
Trauma
Blunt Major trauma Closed-chest CPR Penetrating Major penetrating trauma Intracardiac injections Transthoracic and transvenous pacing wires Pericardiocentesis Cardiac catheterization CVP catheter
Miscellaneous
Serum sickness Chylous effusion Löffler syndrome Reiter syndrome Behçet syndrome Pancreatitis Postpericardiotomy Amyloidosis Ascites
Data from Guberman BA, Fowler NO, Engel PJ, et al: Cardiac tamponade in medical patients. Circulation 64:633, 1981; and Pories WJ, Caudiani VA: Cardiac tamponade. Surg Clin North Am 55:573, 1975.
Radiation pericarditis, particularly after treatment for Hodgkin's disease, is a common cause of effusion. receive 4000 rad to the heart.
[34]
Effusion occurs in approximately 5% of those patients who
Approximately 15% to 20% of patients on dialysis for renal failure develop pericarditis, and 35% of those with pericarditis
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TABLE 16-2 -- Etiology of Pericardial Effusion in Two Studies * Krikorian[29] (120 Patients) (%) Guberman[37] (56 Patients) (%) Neoplastic disease
—
32
Pericardial invasion
16
—
Radiation pericarditis
7.5
4
Etiology uncertain
18
—
Traumatic hemopericardium
9
—
Hemopericardium, nontraumatic
2.5
—
Rheumatic disease
12
2
Uremia/dialysis
5
9
Bacterial infection
2.5
12.5
Congestive heart failure
1.5
—
Uncertain etiology
12.5
—
Idiopathic pericarditis
13.5
14
Cardiac infarction
—
—
Iatrogenic diagnostic procedures
—
7.5
Myxedema
—
4
Aneurysm
—
4
Anticoagulation and cardiac disease
—
11
Postpericardiotomy
—
2
*Note: Various complications related to human immunodeficiency virus (HIV) infections are now probably the most common causes of large nonhemorrhagic pericardial effusions. Effusions related to bacterial, viral, and mycobacterial infections and Kaposi sarcoma and lymphoma are common.
develop tamponade. [46] [47] Up to 7% of patients on chronic dialysis may have effusions, sometimes of 1 L or more. [45] Some series have reported tamponade in 34% of uremic patients who have effusions. [47] Pericardial effusion in renal failure may be managed with dialysis alone in many cases. Thirty percent of myxedema patients may have pericardial effusions, but few have tamponade. [37] Most of the other etiologies listed in Table 16-1 are isolated case reports, and their exact incidences have not been determined. Other Causes of Pericardial Tamponade An interesting but rare cause of cardiac tamponade is pneumopericardium. Pneumopericardium is most commonly seen with pneumothorax and pneumomediastinum as a complication of respiratory therapy in infants, but it may also occur from similar barotrauma in adults. [48] Pneumopericardium also occurs spontaneously in asthma,[49] after blunt chest injury, [50] [51] and even after high-speed motorcycle rides. [52] Pneumopericardium is usually benign, but tension pneumopericardium has been reported as a cause of life-threatening tamponade after blunt chest trauma [51] [53] and after pericardiectomy. [54] The appearance of life-threatening pneumopericardium and tamponade has also been described immediately [55] and 6 days after penetrating chest trauma. [56]
PATHOPHYSIOLOGY OF TAMPONADE The pericardium is a tough, leathery sac normally containing about 25 to 35 mL of serous fluid. [57] It is not rapidly elastic, although it does demonstrate stress relaxation within minutes of increased intrapericardial pressure, providing a slight ability to accommodate sudden increases in fluid. [58] As fluid accumulates, the first 80 to 120 mL is easily accommodated without significantly affecting pericardial pressure ( Fig. 16-1 ). [59] However,
Figure 16-1 Production of cardiac tamponade by injections of saline into the pericardial sac. Although pericardial space can acutely accommodate 80 to 120 mL of fluid without a significant increase in pericardial pressure, note steep increases in pressure and drop in blood pressure at about 200 mL of saline. Once critical volumes are reached, very small increases cause significant hemodynamic compromise. (From Fowler NO: Physiology of cardiac tamponade and pulsus paradoxus. II: Physiological, circulatory, and pharmacological responses in cardiac tamponade. Mod Concepts Cardiovasc Dis 47:116, 1978. Reproduced by permission of the American Heart Association, Inc.)
if an additional 20 to 40 mL is rapidly accumulated, the intrapericardial pressure almost doubles, often leading to sudden decompensation. With effusions that develop over weeks to months, the pericardium lengthens circumferentially to a huge size and can accommodate liters of fluid. Pericardial compliance, which helps determine the pressure-volume response curve ( Fig. 16-2 ), [57] varies considerably in different individuals and various disease states. The
Figure 16-2 Relationship of intrapericardial pressure to volume of pericardial fluid. Note that pressure drops rapidly when a small amount of fluid is removed. (From Pories W, Gaudiani V: Cardiac tamponade. Surg Clin North Am 55:573, 1975. Reproduced by permission.)
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pressure-volume relationship demonstrates hystersis; the withdrawal of a quantity of fluid drops the pressure more than the addition of the same amount of fluid raised the pressure. As pericardial fluid accumulates, the increased intrapericardial pressure is transmitted across the myocardial wall and causes compression of the atria and perhaps the vena cava and pulmonary veins. This reduces right ventricular filling in diastole, producing decreased stroke volume and cardiac output. [60] Pulse pressure narrows as reflex sympathetic stimulation increases. Severe tamponade is produced with intrapericardial pressures of 15 to 20 mm Hg. [61] As stroke volume decreases, heart rate increases to maintain cardiac output. Sympathetic discharge causes both arterial and venous vasoconstriction. [61] [62] Vasoconstriction increases venous pressure, which helps to restore the normal venousatrial and atrioventricular filling gradients. These compensatory mechanisms are often effective and may permit establishment of a new homeostasis with normal cardiac output. With chronic effusion and in early tamponade, cardiac contractility is not affected, and myocardial perfusion is normal. [60] [63] [64] As pressure continues to increase, coronary perfusion pressure drops, so in its later stages, tamponade causes myocardial ischemia. Before hypotension occurs, left ventricular blood flow has already decreased 37%.[65] For comparable degrees of hypotension, experimental animals in hemorrhagic shock have five times greater coronary blood flow than animals in cardiac tamponade. [65] Severe experimental tamponade is followed by large increases in creatine kinase MB and microscopic evidence of cardiac injury resulting from ischemia. [66] As intrapericardial pressure continues to rise, the heart's compensatory mechanisms fail. Myocardial ischemia and perhaps lactic acidosis from poor tissue perfusion may be the triggering events that disrupt the delicate equilibrium. [67] Atrial
Figure 16-3 Summary of physiologic changes in tamponade. RV, right ventricle. (From Shoemaker WC, Carey JS, Yao ST, et al: Hemodynamic monitoring for physiological evaluation, diagnosis, and therapy of acute hemopericardial tamponade from penetrating wounds. J Trauma 13:36, 1973; and Spodick D: Acute cardiac tamponade: Pathologic physiology, diagnosis, and management. Prog Cardiovasc Dis 10:65, 1967. Reproduced by permission.)
pressure rises rapidly ( Fig. 16-3 ). The atria and pulmonary circulation, being at much lower pressure than the systemic arterial pressure, are more vulnerable to the rising intrapericardial pressure. A "pressure plateau" occurs in which right atrial pressure, right ventricular diastolic pressure, pulmonary artery diastolic pressure, and pulmonary capillary wedge pressure are virtually identical. This equalization of pressures leads to the echocardiographic hallmark of tamponade: right ventricular collapse. At this point hypotension is severe, bradycardia is common, and pulseless electrical activity (PEA) may occur. Unless intrapericardial pressure is immediately decreased, pulmonary blood flow ceases, and cardiac arrest follows. [67] Total blood volume affects cardiac compensation, and it is possible to encounter a "low-pressure" cardiac tamponade. [68] The hypovolemic patient with tamponade has a decreased venous pressure, which not only decreases cardiac output, but also may obscure the diagnosis, because distended neck veins or an elevated CVP are not present. In a patient with a chronic pericardial effusion, the onset of hypovolemia can lower filling pressure enough to precipitate tamponade, and conversely, providing additional volume may temporarily offset increased pericardial pressure. Ventilation and blood CO 2 levels have significant effects on cardiac tamponade. This is of particular significance, because trauma patients with tamponade may also have respiratory impairment. Pericardial pressure decreases 3 to 6 mm Hg with a hypocarbia of 24 torr and increases 2 to 4 mm Hg when the PCO 2 reaches 57 torr. [69] This degree of hypercarbia induced pericardial pressure rise can decrease cardiac output by 25%. Similarly, fluctuations in intrapleural pressure induced by intermittent positive-pressure ventilation are transmitted to the pericardial space and can reduce cardiac output another 25%. [70] The clinical implications of these findings are that patients suspected of having tamponade should normally be allowed to breathe spontaneously under careful monitoring and should not be ventilated
with positive pressure unless it is absolutely necessary, as their hemodynamic status may deteriorate precipitously.
DIAGNOSIS OF CARDIAC TAMPONADE Patient Profile and Symptoms Pericardial effusion is rarely diagnosed based on physical findings. In contrast, pericardial tamponade can be diagnosed based on clinical criteria, but specific clinical signs are often absent. Particularly in the setting of acute hemorrhagic tamponade, the time from the first signs of tamponade to full arrest may be brief. [71] Classic clinical findings have been described for tamponade. However, these findings are often obvious only when the patient is unstable due to tamponade. Ideally, tamponade is diagnosed early, when the patient suffers no more than dyspnea, weakness, or perhaps right heart failure. It is common to attribute respiratory symptoms (e.g., dyspnea on exertion) to a more common condition such as heart failure or pulmonary pathology and to overlook pericardial effusion until the classic late signs (e.g., hypotension) appear. [72] Acute pericardial tamponade may resemble tension pneumothorax, acute hemothorax, hypovolemia, pulmonary edema, or pulmonary embolism. Severe right ventricular contusion
309
can mimic the findings of tamponade.[73] The patient is often agitated or panic-stricken, confused, uncooperative, restless, cyanotic, diaphoretic, and acutely short of breath. In the late stages, the patient is moribund. Hypotension in the presence of severe cyanosis and distended neck veins is a helpful but late finding. Physical Signs The classic physical findings of tamponade were first characterized by Beck in 1935. He described two triads, one for acute and one for chronic compression. [74] The chronic compression triad consists of high CVP; ascites; and a small, quiet heart. The triad in acute compression consists of high CVP, decreased arterial pressure, and muffled heart sounds. Unfortunately, in most major trauma series, only about one third of patients demonstrate the complete acute triad, [67] [75] although almost 90% have one or more signs. [7] The simultaneous occurrence of all three physical signs is a very late manifestation of tamponade and is usually seen most consistently shortly before cardiac arrest (see Fig. 16-3 ). Careful hemodynamic monitoring reveals earlier changes that indicate the progression of tamponade ( Table 16-3 ). [76] In grade I tamponade, cardiac output and arterial pressure are normal, but CVP and heart rate are increased. In grade II tamponade, blood pressure is normal or slightly decreased, CVP is increased, and tachycardia persists. In grade III tamponade, the classic findings of Beck's acute triad occur. Although this sequence represents the natural history of acute tamponade, the time course varies. Some patients are stable at a given stage for hours; others proceed to cardiac arrest within minutes. [67] [76] Unfortunately, not all patients with early tamponade respond with a predictable pattern of change in vital signs. Brown and coworkers found that 6 of 18 patients with tamponade, defined through right heart catheterization, responded to tamponade with elevated systolic blood pressure. [77] After pericardiocentesis, these patients had a marked reduction in systolic blood pressure accompanied by increased cardiac output. All of these patients had previously been hypertensive. Pulsus Paradoxus (see also Chapter 1 )
Pulsus paradoxus is defined as an exaggeration of the normal inspiratory fall in blood pressure. [62] [75] A paradoxical pulse (pressure) is one of the classic physical signs of tamponade, but it is not pathognomonic. It is also caused by pulmonary emphysema, asthma, labored respirations, obesity, cardiac TABLE 16-3 -- Shoemaker System of Grading Cardiac Tamponade Stroke Mean Arterial CVP Heart Beck's Triad Index Pressure Rate
Grade Pericardial Volume (mL)
Cardiac Index
I
200
??
??
??
?? (up to 30–40 cm ? H 2 O)
Usually present
From Shoemaker WC, Carey SJ, Yao ST, et al: Hemodynamic monitoring for physiologic evaluation, diagnosis, and therapy of acute hemopericardial tamponade from penetrating wounds. J Trauma 13:36, 1973. failure, constrictive pericarditis, pulmonary embolism, and cardiogenic shock. [7] [35] [67] Measuring the paradoxical pulse is difficult and time-consuming, and any frightened, hypotensive patient with labored breathing can demonstrate this finding ( Fig. 16-4 ). If the difference between inspiratory and expiratory systolic blood pressures is greater than 12 mm Hg, the paradoxical pulse is abnormally high. [78] Most patients with proven tamponade will demonstrate a difference of 20 to 30 mm Hg or more during the respiratory cycle. [7] [35] [67] This may not be true of patients with very narrow pulse pressures (typical of grade III tamponade); they will have a "deceptively small" paradoxical pulse of 5 to 15 mm Hg. The decreased pulsus paradoxus with hypotension occurs because the paradoxical pulse is a function of actual pulse pressure, and the inspiratory systolic pressure may be below the level at which diastolic sounds disappear. [62] For this reason, the ratio of the paradoxical pulse to the pulse pressure is a more reliable measure. A paradoxical pulse greater than 50% of the pulse pressure is abnormal. [62] Pulsus paradoxus in tamponade has been correlated with the degree of impairment of cardiac output. In atraumatic patients, a 15% pulsus paradoxus in the face of relative hypotension was found in 97% of patients with moderate or severe tamponade and only 6% of patients with absent or mild tamponade. [78] A similar study of right ventricular diastolic collapse by echocardiography found that an abnormal pulsus paradoxus had a sensitivity of 79%, a specificity of 40%, a positive predictive value of 81%, and a negative predictive value of 40%. [79] The absence of a paradoxical pulse does not rule out tamponade. Although the mean paradoxical pulse was 49 mm Hg in one series of nonhemorrhagic tamponade,[37] 23% of the patients had a paradoxical pulse of less than 20 mm Hg, and 1 patient had no measurable paradoxical pulse. An abnormal pulsus paradoxus has been reported to be absent in tamponade when there is an atrial septal defect, aortic insufficiency, localized collections of pericardial blood, or extreme tamponade with hypotension. [68] It may also be absent when left ventricular diastolic pressure is intrinsically elevated owing to poor left ventricular compliance. This was seen in one half of uremic patients with tamponade. [47] [80] In traumatic tamponade, pulsus paradoxus is deemed unreliable. [68] [80] [81] [82] In one study, only 35% of trauma patients had an abnormal paradoxical pulse when elevated CVP and decreased heart sounds were present. [82] In another study of 197 traumatic cases, only 8.6% of the diagnoses of tamponade were made by finding an abnormal pulsus paradoxus. [83]
310
Figure 16-4 Normally systolic blood pressure drops slightly during inspiration. To measure pulsus paradoxus, the patient breathes normally while lying at a 45-degree angle. The blood pressure cuff is inflated well above systolic pressure and slowly deflated. When the pulse is first heard only during expiration, this is the upper value. The cuff is deflated until the pulse is heard during both inspiration and expiration, and this is the lower value. The difference in the two values is the amount of pulsus paradoxus. A difference of more than 12 mm Hg is abnormal.
Although the absence of a paradoxical pulse rules against severe tamponade, it does not completely rule it out. Whether time is taken to determine pulsus paradoxus depends on the patient's status. If the patient is moribund or rapidly deteriorating, taking time to check this parameter is obviously a poor choice of priorities. Venous Distention
Venous distention, reflecting increased CVP, is also a late sign in cardiac tamponade (see Fig. 16-3 ). It may be masked by venoconstriction as a result of vasopressors (e.g., dopamine), intrinsic sympathetic discharge, or hypovolemia. [35] [67] [76] [81] Neck vein distention may be obvious clinically, but the measured CVP is more reliable than the presence of venous distention. The CVP reading should take into account positive-pressure ventilation and the effects of a Valsalva maneuver. Most patients with significant tamponade will have a CVP of greater than or equal to 12 to 14 cm H 2 O.[81] Hypovolemia changes the intrapericardial pressure-volume curve in tamponade and will lower the CVP reading at any given stage in the tamponade process. Animal studies have documented that right atrial pressure can be normal in tamponade when hypovolemia is present. One case of low-pressure cardiac tamponade was reported in a patient with no jugular venous distention, no paradoxical pulse, and a right atrial pressure of 8 mm Hg. [68] Thus, although the initial CVP reading is useful and diagnostic if grossly elevated (e.g., 20 to 30 cm H 2 O),[54] [81] a series of CVP readings looking for an upward trend is the most sensitive diagnostic tool. [81] A rising CVP, especially when there is persistent hypotension, is extremely suggestive of tamponade in the trauma patient. In the rare case of the hypovolemic patient in whom tamponade is suspected but who demonstrates a low CVP, a fluid challenge will help clarify the situation and will also improve cardiac output at least temporarily. [68] Ancillary Testing Routine chest radiographs and electrocardiograms may be useful in increasing the level of suspicion for pericardial effusion and tamponade. Noninvasive diagnosis of effusion, however, must be made by computed tomography or, preferably, cardiac ultrasound. If available, bedside ultrasound is the fastest and most reliable for the emergency clinician to demonstrate a significant pericardial effusion, although it may not be diagnostic of tamponade. Chest Radiographs
Chest radiographs are not useful in the diagnosis of acute traumatic tamponade, because the cardiac size and shape do not change acutely. However, the radiographs may reveal hemothorax, bullet location, or even pneumopericardium. In the patient without trauma and with chronic effusion, a chest film often reveals an enlarged, sac-like "water bottle" cardiac shadow. Unfortunately, it is difficult to differentiate pericardial from myocardial enlargement, and radiographs cannot be used to distinguish between simple pericardial effusion and tamponade. One finding that is useful in identifying effusion on the plain chest film is the epicardial fat pad sign. The water density space between the radiolucent epicardial fat and the mediastinal fat represents the pericardial tissues and is normally less than 2 mm. An increase in this width suggests pericardial fluid or thickening ( Fig. 16-5 ). This sign may be seen in 41% of upright lateral and 23% of frontal chest films in proven pericardial effusion. [84] The diagnostic value may be enhanced by using a supine rather than upright cross-table, lateral chest radiograph. Obtaining a supine lateral film increases the sensitivity of the epicardial fat pad sign from 31% to 51%. [85] Electrocardiograms
Electrocardiograms may suggest, but should not be used to diagnose, pericardial effusion or cardiac tamponade. Most electrocardiogram changes, such as PR-segment depression, low-voltage QRS complexes, and electrical alternans, have acceptable specificity but poor sensitivity for pericardial effusion or tamponade.[35] [86] [87] Low voltage is defined as a QRS amplitude less than or equal to 5 mV in all limb leads (or a sum of the limb lead QRS amplitude less than or equal to 30 mV), and PR depression is defined as greater than or equal to 1 mV depression in at least 1 lead other than aVR. In a study correlating the electrocardiogram with echocardiographic evaluation, electrocardiogram signs had an overall sensitivity of only 1% to 17% and a specificity of 89% to 100% for pericardial effusion. [35] Others have demonstrated significantly higher sensitivity, i.e., in the range of 32 to 68% for voltage criteria. [88] PR-segment depression is the most common electrocardiogram finding in pericardial tamponade, and low voltage is most commonly associated with a moderate to large effusion. It is important to note that none of the ECG findings differentiate tamponade from effusion. Electrical alternans is caused by pendulum motion of the heart within the pericardial sac. [89] Alternans of the QRS complex has been seen in about 22% of medical tamponade cases[72] but in only 5% of cancer patients with tamponade. [44] Electrical alternans of both the P wave and the QRS complex (total electrical alternans) is a rare finding, but when seen is thought to be pathognomonic of tamponade ( Fig. 16-6 ). [35] [90] Like electrical alternans, low voltage may be a finding associated with tamponade, but not simple effusion. [91] Echocardiography
Echocardiography is the best available tool for diagnosing pericardial effusion and has the further advantage of being noninvasive. sensitive in the diagnosis of pericardial effusion and tamponade. [93] [94]
[92]
Echocardiography is very
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Figure 16-5 Epicardial fat pad sign. The water density space between the radiolucent epicardial fat and the mediastinal fat represents the pericardium and its contents and should be 2 mm or less. An increase suggests pericardial fluid or thickening. A, Left anterior-oblique chest film. B, Lateral chest film. In acute tamponade, the chest radiograph has very minimal diagnostic value.
The disadvantages of echocardiography are that it requires ultrasound equipment and is dependent on a skilled operator who is specifically trained in echocardiography. Even when immediately available, echocardiography may take at least 5 minutes, which may be too much time for a patient who is deteriorating rapidly. If the patient in not in full arrest and ultrasound is available, ultrasound should always be used to diagnose effusion and tamponade and to guide the procedure (see Chapter 69 ). Pericardial fluid is relatively easy
Figure 16-6 Overall, the electrocardiogram (ECG) has a low sensitivity for pericardial effusion or tamponade, but PR depression, low voltage, or electrical alternans may be seen. Lewis lead ECG showing total electrical alternans of both amplitude and configuration of P and QRS complexes. This is rarely seen but is highly suggestive of tamponade. Note that electrical alternans may not be evident in standard ECG leads. (From Sotolongo RP, Horton JD: Total electrical alternans in pericardial tamponade. Am Heart J 101:854, 1981. Reproduced by permission.)
to demonstrate with bedside ultrasound, but since many ill patients will demonstrate some pericardial fluid, bedside ultrasound may not be able to differentiate
incidental fluid from tamponade. Computed Tomography
At some institutions, computed tomography (CT) is much more readily available than echocardiography. However, it requires that the patient be transported to the site of the CT equipment and patient stability must be considered. If clinically indicated, CT is effective in defining the presence and extent of pericardial effusion in the stable patient. [95] In certain circumstances, CT can provide a more definitive diagnosis than echocardiography. In one series, eight equivocal echocardiograms were evaluated by CT. [96] Two patients thought to have pericardial effusion by ultrasound were found by CT to have pleural effusions. Another patient with pericardial effusion by ultrasound was found by CT to have an epicardial lipoma. CT defined three loculated pleural effusions not seen by ultrasound. A final two patients had hemopericardium visualized by CT but not ultrasound. In circumstances where the patient is stable and ultrasound produces equivocal results or is not available, CT may provide a definitive diagnosis of pericardial effusion.
INDICATIONS FOR PERICARDIOCENTESIS There are two indications for pericardiocentesis: (1) to diagnose the cause or presence of a pericardial effusion and (2) to relieve tamponade. The former is an elective procedure and ideally should be accomplished under ultrasound guidance. The latter may be semi-elective and performed with ultrasound guidance or emergent and performed blind with ECG assistance.
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Diagnostic Pericardiocentesis The use of pericardiocentesis for diagnosis of the etiology of nonhemorrhagic effusions is widespread, although opinions of its utility vary. [34] [97] [98] Neoplastic cells, blood, bacteria, viruses, and chyle can be sought. Measurement of pericardial fluid pH can be helpful, because inflammatory fluid is significantly more acidotic than noninflammatory fluid. [99] When a specific etiology is suspected, additional diagnostic testing may be useful (e.g., adenosine deaminase in tuberculosis, and carcinoembryonic antigen in suspected malignancy). [100] The diagnostic accuracy of pericardiocentesis varies greatly from series to series, depending on the vigor with which a definitive etiology was sought and the prevalence of certain etiologies in the patient population under consideration. In one large series, fluid was obtained in 90% of the taps, but a specific etiologic diagnosis was obtained in only 24% of the fluid specimens. [29] Certain diagnoses are unlikely to be made from pericardial fluid. Pericardial fluid has been shown to give false-negative cytologic results in several cases of lymphoma and mesothelioma. [29] In HIV patients, effusions caused by Kaposi sarcoma and cytomegalovirus have been diagnosed by pericardial biopsy after fluid studies were non-diagnostic. [101] [102] An alternative diagnostic tool is subxiphoid pericardiotomy. This technique, performed in the operating suite, obtains both fluid and a pericardial biopsy specimen. It is more likely to provide a definite diagnosis and has been performed safely without general anesthesia. [103] [104] In a prospective series of 57 patients, 36% obtained a definitive diagnosis; 40%, a probable diagnosis; 16%, a possible diagnosis; and 7% remained undiagnosed with subxiphoid pericardiotomy. [105] Although it is uncertain whether this technique is safer than ultrasound-guided pericardiocentesis, published reports show a low rate of complications in experienced hands. [105] Regardless of technique, the need to sample small effusions or obtain pericardial tissue has been questioned. A prospective series found a diagnostic rate of 6% with pericardial fluid and 5% with pericardial tissue when a small persistent effusion was sampled for the specific purpose of diagnosis. In contrast, when patients from the same population had therapeutic intervention for tamponade, the yields from fluid and tissue were 54% and 22%, respectively. [98] The use of pericardiocentesis as a diagnostic tool in traumatic tamponade is limited. When used diagnostically to determine the presence of pericardial bleeding in trauma, the procedure has a false-negative rate of between 20% and 40%. [81] [106] [107] [108] The reason for the high false-negative rate (defined as no blood aspirated) is well demonstrated by typical stab wounds of the heart. [8] [109] Ninety-six percent of the patients had blood in the pericardium, but it was clotted in 41% of the patients and partially clotted in another 24%. In only 19% was the blood completely fluid and thus capable of giving a true-positive result on pericardiocentesis. Therapeutic Pericardiocentesis Tamponade of Uncertain Etiology
The primary reason for performing pericardiocentesis in the ED is as part of the treatment for cardiac arrest or in peri-arrest situations. In particular, the presentation of PEA with elevated jugular venous pressure should cause immediate consideration of pericardiocentesis. In this setting, blind, ECG-guided pericardiocentesis can be life saving. However, the overwhelming majority of patients with PEA have neither significant effusion nor tamponade, and other etiologies for the PEA also should be sought. Pericardiocentesis also may be considered in other presentations of effusion with existing or incipient tamponade. Tamponade Caused by Nonhemorrhagic Effusions
Pericardiocentesis is often, at least temporarily, therapeutic in cardiac tamponade. Most nonhemorrhagic effusions are liquid and can be drained easily through a small needle. Removal of even a small amount of fluid can immediately and dramatically improve blood pressure and cardiac output. Pericardiocentesis relieves tamponade due to nonhemorrhagic effusions in 60% to 90% of cases. [29] [37] [44] Patients in whom it fails often have purulent pericarditis or malignant invasion of the pericardium. Pericardiocentesis without catheter placement may be much less useful for long-term management of these patients; 26% of the patients in the study by Guberman and coworkers eventually required pericardial resection. [37] In Krikorian's series, 24% of the patients were managed successfully with one pericardiocentesis, 37% needed multiple taps or an indwelling catheter, and 39% required surgical drainage. [29] Fifty-five percent of the last group had traumatic hemopericardium. Patients with renal failure and pericardial effusion may be better managed by dialysis than pericardiocentesis. In one series, 63% of these patients were successfully managed with dialysis alone, and only 6% needed surgical treatment over the long term. [29] Tamponade is less frequent with pericarditis when it occurs within the first months of dialysis, and such patients are much more likely to be successfully managed without invasive intervention. [46] When invasive treatment is needed for dialysis patients, pericardiocentesis is probably a poor choice; 9 of 10 patients who received it had complications in one series, and it was the only invasive treatment that resulted in death. [46] An algorithm for the urgent management of nonhemorrhagic cardiac tamponade is shown in Figure 16-7 . Use in Hemorrhagic Tamponade [ 110] [ 111] Pericardiocentesis is never the definitive treatment in hemorrhagic tamponade.
Although aspiration of a small quantity of fluid may cause dramatic improvement, blood usually reaccumulates. [35] [90] Thus, patients with pericardial hemorrhage ultimately require thoracotomy to explore and repair the cardiac injury. One of the greatest potential drawbacks of pericardiocentesis in traumatic tamponade is that it may delay thoracotomy. In one study of 25 trauma patients with cardiac injury,[110] all of those who were operated on within 2 hours of injury survived, regardless of age or type of wound. With greater delay, none survived. Sugg and colleagues, in a study of 459 similar patients, found a mortality rate of 43% when pericardiocentesis was the sole treatment, but only 16% when surgery was performed.[107] Most investigators agree that with early thoracotomy and little or no reliance on pericardiocentesis, the number of deaths due to stab wounds has decreased. [81] [108] [111] [112] Sugg and associates reported that 10 of 18 patients with traumatic tamponade who were managed by repeated pericardiocentesis alone died within 1 to 2 hours.[107] At autopsy, all patients had repairable wounds.
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Figure 16-7 Management of nontraumatic cardiac tamponade. IV, intravenous line; CVP, central venous pressure; ECG, electrocardiogram.
Nonetheless, while other temporizing treatments are instituted (see discussion later in this chapter) and arrangements for definitive surgical treatment are being made, pericardiocentesis may temporarily improve the patient's hemodynamic situation ( Fig. 16-8 ). Some clinical evidence supports the usefulness of pericardiocentesis as a temporizing measure. In a study of 174 patients with tamponade from penetrating trauma, 96 underwent operating room thoracotomy, 44 underwent ED thoracotomy, and 34 received only pericardiocentesis followed by observation. [83] Of those who underwent operating room thoracotomy, 68% were hemodynamically unstable, and preoperative pericardiocentesis decreased the mortality rate from 25% to 11%. Ninety-one percent of those who underwent ED thoractomy were unstable, and pre-thoracotomy pericardiocentesis decreased the mortality rate from 94% to 63%. For the unconscious and hypotensive or agonal patient, emergency thoracotomy is the preferred treatment (see Chapter 18 ). When a trauma patient's condition is relatively stable, but a high level of suspicion for a penetrating cardiac wound is present, an alternative to thoracotomy is the subxiphoid pericardial window. [103] [113] [114] The procedure has been done under local anesthesia. Although it is possible to perform the procedure in the ED, [114] most authors believe the procedure should be reserved for the operating suite. [115] [116] [117]
CONTRAINDICATIONS There is no absolute contraindication to pericardiocentesis. It should not be performed when better treatment modalities are immediately available (e.g., dialysis for uremic patients and immediate surgery for trauma patients). For diagnostic or non-emergent pericardiocentesis, echocardiographic or CT diagnosis is imperative. Ultrasound or fluoroscopic guidance should be used in all non-emergent situations.
EQUIPMENT FOR PERICARDIOCENTESIS Fluoroscopic or Ultrasound Guidance Pericardiocentesis is ideally performed in the cardiac catheter laboratory under fluoroscopic or echocardiographic guidance. In the ED, echocardiography is useful for directing pericardiocentesis. With ultrasound, the area of the heart with the greatest fluid accumulation can be accurately identified and its relationship to the body wall clarified. [118] [119] An entry site and angle of penetration can then be chosen that have the greatest likelihood of obtaining fluid while simultaneously avoiding vital structures. Ultrasonographic diagnosis and guidance is described elsewhere (see Chapter 69 ). Electrocardiographic Assistance Although the procedure can be performed with only a syringe and a spinal needle, electrocardiogram monitoring is desirable. An alligator clamp is used to connect the needle to any of the precordial leads (V leads) of a properly grounded electrocardiogram device ( Fig. 16-9 ). Generally the V lead (usually V 1 or V5 ), which permits a continuous display during rhythm monitoring, is used. When the alligator clamp connects the base of the pericardiocentesis needle to the V lead wire, the operator must set the machine to record the V lead as the rhythm strip. Other Equipment The traditional needle choice has been a 7.5- to 12.5-cm (3-to 5-inch), 18-ga spinal needle with an obturator. It is best to leave the obturator in the needle during initial passage through the skin to avoid obstruction of the needle lumen. More recently, the shorter Teflon-sheathed Intracath needle has been used. Alternatively, the clinician can use the guide
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Figure 16-8 Management of traumatic cardiac tamponade. IV, intravenous lines; CVP, central venous pressure; ECG, electrocardiogram; R/O, rule out.
wire (Seldinger) technique, inserting a plastic catheter over a flexible guide or J wire. With this technique, an 18-ga, thin-walled needle is used for placement of the wire. The catheter (after removal of the accompanying introducer) may be left in place for prolonged drainage, if needed. [120] [121] For drainage of blood, pus, or other viscous effusions, a large catheter such as a No. 7 to 9 Fr Cordis sheath should be inserted. [122] Alternatively, the guide wire technique can be used to insert a radiopaque, 16-ga, flexible, fenestrated, central venous catheter, which can then be connected to closed suction drainage
Figure 16-9 Equipment for emergent pericardiocentesis: long, 18-ga spinal needle; wire with alligator clips for connection to the electrocardiograph machine; and syringe (three-way stopcock optional). Sterile skin preparation and local anesthetic are also required.
and left in place for long periods of time. [123] Pigtail catheters with side and end holes or nephrostomy drainage catheters also can be used. [121] Multi-lumen catheter patency can be maintained by slow continuous flush with a heparinized saline solution. [121] Complete "sets" containing necessary equipment for placing a catheter using the guide wire technique are commercially available ( Fig. 16-10 ), including sets designed for pediatric use. [124] A three-way stopcock may be attached to the needle or catheter to allow removal of more than one filled syringe without much movement of the needle. The continuous
Figure 16-10 An example of the contents of a prepackaged pericardiocentesis set: finder needle, Seldinger wire, dilator, catheter guide, and pigtail catheter. Sterile skin preparation and local anesthetic are also required.
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motion of the heart may require minor changes in needle or catheter position during the procedure. Lengthy or repeat drainage is much safer if the steel needle is withdrawn and a plastic catheter is left in place.
PROCEDURE Temporizing Measures While preparing for pericardiocentesis in the unstable patient or attempting to stabilize the patient while the operating suite is readied for thoracotomy or subxiphoid pericardiotomy, temporizing measures should be considered. In the patient with suspected tamponade and without jugular venous distention, the administration of a fluid bolus may improve hemodynamics. [68] In the setting of non-penetrating tamponade, a fluid challenge has been recommended [59] [125] ; animal experiments have found this to be beneficial, with or without nitroprusside for afterload reduction. [126] However, a follow-up prospective evaluation in patients with tamponade found no benefit from either fluid challenge or nitroprusside; cardiac output remained unchanged at a mean of 5.1 L/min, in contrast to 9.1 L/min after pericardiocentesis. [127] In the trauma patient with penetrating cardiac injury, fluid resuscitation may produce improvement or deterioration. Animal experiments indicate that the response depends on whether fluid infusion produces recurrent bleeding from the cardiac wound. [128] One report found that dextran solution for volume expansion produced significant hemodynamic improvement in patients with subacute ventricular free wall rupture after acute myocardial infarction. [32] In summary, judicious volume expansion may produce temporary beneficial hemodynamic results, but this is not uniformly true. Vasopressors also have been recommended as a temporizing measure in tamponade. Dopamine, dobutamine, norepinephrine, and isoproterenol have been evaluated. Norepinephrine produced increased cardiac output in animal models of tamponade [129] [130] but failed to increase cardiac output in patients with malignant effusion. [129] Isoproterenol increased cardiac output in animal models but detrimentally affected cardiac blood flow. [129] Both dopamine and dobutamine have produced increased cardiac output and other improvements in hemodynamics in the setting of tamponade. [22] [127] Either of these agents may be helpful as a temporizing agent in tamponade, but dobutamine may be preferable on theoretical grounds because of its greater beta activity. [130] Preparation All necessary equipment must be checked and laid out in advance. Full resuscitation equipment must be on hand, including a defibrillator. The patient must have an IV line in place and be attached to a cardiac monitor. The non-emergent patient may require sedation, but in an emergency, pericardiocentesis is usually performed on patients who are already obtunded or unresponsive as a result of low cardiac output. Use of sedation in these patients not only is unnecessary, but also carries a high risk of hemodynamic or respiratory deterioration. Premedication of the patient with atropine may help to prevent vasovagal reactions. When possible, the presence of pericardial effusion and the optimal anatomic approach should be determined in advance by echocardiography. If surgery may be needed, preparations should already be under way to ensure prompt availability of both an operating room and a surgeon. If the patient's clinical condition permits, the chest should be elevated at a 45° angle to bring the heart closer to the anterior chest wall. If the abdomen is distended because of gastric contents or previous positive-pressure ventilation, a nasogastric tube should be used to decompress the stomach. The entire lower xiphoid and epigastric area should be carefully prepared with 10% povidone-iodine solution and sterilely draped, if time permits. If the patient is awake, the skin and the proposed route of the pericardial needle should be anesthetized by infiltration with 1% plain lidocaine or 0.5% bupivacaine. Note that the pericardium is very sensitive and should be anesthetized in patients who are awake. [120] Anatomic Approach The choice of anatomic approach in the past has been governed largely by conjecture and theory, not by actual study of patients with pericardial effusion. Traditionally the subxiphoid approach was preferred and recommended in most texts and articles as the optimal choice. However, two-dimensional echocardiography allows direct visualization in the individual patient of both the areas of maximal effusion and the location of vital structures. Studies of echocardiography-directed pericardiocentesis have found that the intercostal space near the heart apex is usually the best site for puncture, not the traditional subxiphoid approach. [119] [122] Careful cadaver studies have corroborated this finding, demonstrating greater safety with a parasternal approach in the fifth intercostal space and showing that the greatest number of injuries (usually to the right atrium) occurred with variants of the subxiphoid approach. [14] In contrast, studies of intracardiac injection using the same routes have found an increased incidence of pneumothorax when parasternal or intracostal approaches are used (see discussion of complications of pericardiocentesis). This risk may increase with underlying lung disease. Whenever time and the patient's condition permit, clinicians should rely on echocardiography to define the extent of and optimal approach to pericardial effusion. When time or circumstances prevent the use of ultrasound, the clinician should use the approach with which he or she is most familiar. Parasternal Approach
In this approach, the needle is inserted perpendicular to the skin in the left fifth intercostal space medial to the border of cardiac dullness ( Fig. 16-11 ). Older texts identify the puncture site as being at least 3 to 4 cm lateral to the sternal border to avoid the internal mammary artery. However, anatomic studies indicate that penetration immediately lateral to the sternum is less likely to cause this complication. [14] Subxiphoid Approach
In the traditional subxiphoid approach, the needle is inserted between the xiphoid process and the left costal margin at a 30° to 45° angle to the skin ( Fig. 16-12 ). Because the heart is an anterior structure, an angle greater than 45° may intercept the liver or stomach. In this approach, the needle enters the pericardium at the angle at which it becomes the diaphragmatic pericardium. Recommendations regarding needle aim vary widely, including among others the right shoulder, the
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Figure 16-11 Parasternal approach for pericardiocentesis. The patient is depicted in a supine position, although a preferable position would be sitting at a 45° angle, if the patient's clinical condition permits. Note ECG monitoring via alligator clamp attached to lead.
sternal notch, and the left shoulder. [120] [125] The only anatomic study conducted demonstrated that the subxiphoid approach is likely to injure the thin-walled right atrium when one aims for the right shoulder. [14] Aiming for the left shoulder directs the needle toward either the left ventricle or the anterior wall of the right ventricle ( Fig. 16-13 ). Apical Approach
In the less commonly used apical approach, the needle is inserted 1 cm lateral and in the intercostal space below the apical beat, within the area of cardiac dullness; it is aimed toward the right shoulder. [120] If the apex cannot be palpated, the needle is inserted just inside the area of cardiac dullness. This area is close to the lingula and left pleural space, and pneumothorax is more frequent; a concomitant pleural effusion may be inadvertently tapped. In theory, this technique is used because the coronary vessels are small at the apex, and if a ventricle is entered, it is the thick-walled left ventricle, which is more likely to seal off any ventricular injury. Data are insufficient to say whether these theoretical advantages are clinically important. With echocardiographic guidance, the apical approach may be more commonly
used.[131] Electrocardiogram Monitoring After the skin has been punctured but before the pericardial needle is advanced, the needle obturator is removed, and an aspirating syringe is attached. At this time, electrocardiogram monitoring is begun. Attach a sterile electrical cord with alligator clips (see Fig. 16-9 ) from the pericardial needle to any precordial lead (V lead) of the electrocardiogram machine. The V lead is then recorded, as the needle becomes an "exploring electrode." The machine must be properly tested and internally grounded. Small current leaks can induce dysrhythmias. [35] The purpose of the electrocardiogram monitoring is to prevent ventricular puncture. When the needle touches the epicardium, a current-of-injury pattern, often simulating a wide complex PVC with an elevated ST segment, is noted on the electrocardiogram ( Fig. 16-14 ). This current of injury may be local and could be missed if a lead other than a V lead is monitored or if a cardiac monitor (which has a lower
Figure 16-12 A and B, Xiphosternal approach for pericardiocentesis. The needle is aimed for the sternal notch or the left shoulder. Note the electrocardiography monitor. Although the patient is shown in a supine position, a preferable position would be sitting at a 45° angle, if the patient's condition permits. This general approach is also used for intracardiac injection of advanced cardiac life support drugs.
frequency response than the electrocardiogram machine) is used. Usually one notes ST-segment elevation on contact with the heart or pericardium in the absence of an effusion, but a premature contraction or other ventricular dysrhythmia also may be induced by direct mechanical stimulation of the ventricular epicardium by the needle. Contact with the atrium can cause atrial dysrhythmias, marked elevation of the PR segment, or atrioventricular dissociation. [16] If there is abnormal myocardial scarring secondary to infarction or other diseases or if there is malignant infiltration of myocardium, no current of injury may be generated. [17] Thus, electrocardiogram monitoring is not infallible in preventing myocardial penetration. In addition, the incessant motion of the heart makes it almost impossible to merely touch the epicardium. With continuous electrocardiogram monitoring, the operator slowly advances the needle and syringe while gently aspirating. The needle will penetrate the pericardium (this is usually not palpable) at about 6 to 8 cm below the skin in adults and 5 cm or less below the skin in children. [57] The awake patient may complain of sharp chest pain as the sensitive pericardium is entered. As soon as pericardial content is aspirated, the needle should not be further advanced. If a current of injury is noted (see Fig. 16-14 ), the needle is touching epicardium and can easily lacerate myocardium or coronary vessels. The needle should be withdrawn a few millimeters until the current of injury disappears. At this point, the needle should be safely positioned in the pericardial space, although heart motion
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Figure 16-13 Subxyphoid approach to catheter placement into pericordial space. A short needle (16- or 18-ga) is inserted into the left xiphocostal angle perpendicular to the skin and 3 to 4 mm below the left costal margin (A). After advancing the needle to the inner aspect of the rib cage, the needle's hub is depressed so that the needle points toward the patient's left shoulder. The needle is then cautiously advanced about 5 to 10 mm until fluid is reached (B). The fingers may sense a distinct "give" when the needle penetrates the parietal pericardium. Successful removal of fluid confirms the needle's position. The syringe is then disconnected from the needle, and the flexible tip of the guide wire is advanced into the pericardial space (C). The needle is withdrawn and replaced with a soft, multihole pigtail catheter (No. 6 to 8 Fr) using the Seldinger technique. After dilating the needle tract, the catheter is advanced over the guide wire into the pericardial space (D). Once the catheter is properly positioned, aspiration of fluid should result in rapid improvement in blood pressure and cardiac output, a decrease in atrial and pericardial pressures, and a decrease in the degree of any paradoxical pulse (E). Electrical alternans, if present, also decreases or disappears. (From Spodick DH: The technique of pericardiocentesis. J Crit Illness 2:91, 1987.)
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Figure 16-14 Current of injury. There is an obvious change in the electrocardiogram when the pericardiocentesis needle touches the epicardium. Following slight withdrawal (arrow), the ST-segment elevation diminishes.
may quickly bring it back into contact with the myocardium. This is particularly a risk if the presence of a large effusion has not been demonstrated by ultrasound. If the scenario permits, some clinicians would now use the properly placed needle to pass a wire, then catheter, into the pericardial space, rather than attempting to drain the fluid or blood with the needle alone (see Fig. 16-13 ). This is a technically difficult procedure. Fluid Aspiration and Evaluation Aspiration of blood during pericardiocentesis raises the possibility of cardiac puncture. If fluoroscopy is available, the injection of a small amount of contrast will quickly disclose intracardiac placement. In other circumstances, the needle may need to be repositioned and the aspirate reexamined. Laboratory tests may help distinguish circulatory blood from hemorrhagic pericardial fluid. The latter should have a lower hematocrit measurement than venous blood. Substantially different hematocrit values rule out the possibility that the needle was in a cardiac chamber. Hemorrhagic pericardial fluid usually is about 0.10 pH unit lower than simultaneously obtained arterial blood. [99] Bloody pericardial fluid may clot, particularly when bleeding is brisk, so clotting of the aspirated blood does not eliminate the possibility of a pericardial source. Nonclotting blood is indicative of defibrinated pericardial blood. Practically, however, there is rarely time for such analysis. If an indwelling catheter is to be placed, a guide wire is advanced through the needle (see Fig. 16-13 ). Then a dilator is passed over the wire to expand the needle tract. The guide wire should be maintained in sight and stabilized at all times. If intracardiac placement of the needle or guide wire is suspected, positioning must be verified by ultrasound or fluoroscopy or by using the techniques described earlier before the needle tract is dilated. Once the tract has been dilated, the pigtail catheter is placed over the guide wire. If the dilator is not used, particularly with the subxiphoid approach, the pigtail catheter tip may hang in the subcutaneous (SQ) tissue, making placement difficult. After the catheter is placed, or if a decision is made to do a single aspiration, as much fluid as possible should be aspirated from the pericardium. The removal of even 30 to 50 mL may result in marked clinical improvement in patients with tamponade. The catheter may be placed for continuous or intermittent drainage. A chest film should be obtained after the procedure to rule out iatrogenic pneumothorax. Patients should be monitored closely for 24 hours for signs of reaccumulating fluid or iatrogenic complications from the procedure. Repeat ultrasound examination is recommended. Diagnostic evaluation of nonhemorrhagic fluid is similar to the analysis of pleural fluid (see Chapter 9 ).
COMPLICATIONS The failure of pericardiocentesis to yield fluid ("dry tap") may be considered a complication, as the procedure has failed to achieve its desired result. If a dry tap is considered a complication, it is by far the most frequent one during blind pericardiocentesis. In addition, the pericardial needle can injure any organ within its reach, causing pneumothorax, myocardial or coronary vessel laceration, and hemopericardium. [112] Air embolism may be caused by air entering the heart. [132] The pericardial needle can also induce dysrhythmias from direct irritation of the epicardium or from small currents leaking from the connected electrocardiogram machine. [2] Assessing the frequency of complication from pericardiocentesis is not straightforward. Changes in diagnosis of effusion by ultrasound or CT and guidance of the procedure by ultrasound or fluoroscopy have greatly reduced the likelihood of complication. [6] [131] [133] [134] [135] No recent data is available related to complications of blind or electrocardiogram-guided emergency pericardiocentesis. The complication rate is expected to be quite different. For example, Wong and colleagues reported that most complications occurred in patients who were found retrospectively to have no effusion. [3] The procedure is also performed frequently in moribund patients, and distinguishing between a poor outcome resulting from a poorly performed procedure as opposed to the underlying condition can be difficult. A summation of the results of 5 recent reports on echocardiographically guided pericardiocentesis [6] [131] [133] [134] [135] includes 564 procedures with a 98% success rate. No deaths were reported. There were five incidents of pneumothorax, four reported cardiac punctures, one significant dysrhythmia, one hemothorax, one pericardial-pleural shunt and one instance of purulent pericarditis. The major complications will be discussed individually. Cardiac Arrest and Death Cardiac arrest and death is extremely rare in echocardiographically guided pericardiocentesis. In blind or ECG-guided pericardiocentesis, the patient is usually in full arrest and attribution of death to procedure or pre-procedure condition is nearly impossible. For example, in one series of 52 patients, the only death occurred in a patient in cardiogenic shock who had a nonproductive pericardiocentesis and who, on postmortem examination, had severe arteriosclerotic heart disease, not tamponade.[3] An additional case of cardiac arrest (successfully resuscitated) in this series was in a patient with a nonproductive pericardiocentesis; the cause of the arrest was not discussed. [3]
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In a series of 352 pericardiocenteses performed under fluoroscopic guidance, only 2 deaths resulted. [4] Ultrasound or CT confirmation of effusion was used in all but 15 cases. The two deaths occurred during or after the procedure, but whether they should be attributed to the procedure is unclear. One patient with aortic rupture penetrating into the pericardial space died of cardiac arrest immediately after the puncture. The other death, in a post myocardial infarction patient with left ventricular aneurysm, was due to ventricular fibrillation that occurred about 15 minutes after the procedure. Cardiac Chamber, Vessel, or Lung Laceration Cardiac chamber, vessel, or lung laceration occurs more frequently during blind or ECG-guided procedures. Nonfatal cardiac puncture, pneumothorax, suppurative pericarditis, costochondritis, and pneumoperitoneum have been reported. [47] Most cardiac perforations occur in the right ventricle, but left ventricular [4] as well as atrial punctures have been reported. [16] In Krikorian and Hancock's series, 13 of 123 patients developed hemopericardium as a result of pericardiocentesis, 1 as a result of a lacerated coronary artery. [29] One patient died from a punctured ventricle. Surgical control was necessary for four patients who developed tamponade, whereas eight patients with hemopericardium did not develop tamponade and were managed conservatively. Several cases of induced tamponade occurred in patients with platelet counts >50 × 10 9 /L. Guberman and coworkers reported 3 right ventricular lacerations in 46 patients; 1 laceration was fatal. [37] Wong and colleagues found five right ventricular punctures, four in patients with nonproductive pericardiocentesis, but none causing any adverse sequelae. [3] In a series of dialysis patients, 9 of 10 receiving pericardiocentesis had serious complications, including 3 deaths and 2 myocardial lacerations. [46] Duvernoy and coworkers[4] reported 23 penetrations (all right ventricular except 2 in which both the right and left ventricles had been perforated), along with 4 cases of significant arterial bleeding in a series of 352 procedures. Researchers differ in their opinions as to the adverse effects of ventricular puncture. Most ventricular punctures during the procedure occur in the lower aspect of the right ventricle. Because right ventricular pressure is lower, [57] puncture should cause less bleeding; however, the right ventricular wall is also thinner and more vulnerable to laceration. In a series of patients with ultrasound-directed pericardiocentesis, ventricular puncture still occurred in 1.5% but was without consequence due to small needle size. [122] In another study, right ventricular laceration occurred in one patient despite the use of echocardiography, producing tamponade and necessitating emergency surgery. [98] Of the 23 perforations in the series by Duvernoy and colleagues, [4] only 3 were considered "major" complications, with 2 of the patients requiring thoracotomy. A small number of pneumothoraces and pneumopericardia have been reported in various series but have been without clinical consequence other than drainage. A single case of tension pneumothorax has been reported after pericardiocentesis, but a cause-and-effect relationship was unclear. [136] Dysrhythmias Serious dysrhythmias induced by pericardiocentesis are rare. Premature ventricular contractions (PVCs) occur commonly during the procedure and are benign in most cases. Most case series report no dysrhythmias. [3] [37] [47] [122] Krikorian and Hancock reported only 1 episode of ventricular tachycardia and several "hypotensive vasovagal reactions," which were associated with bradycardia and responded to atropine and fluid loading. [29] Duvernoy and colleagues [4] reported 1 case of ventricular tachycardia and 1 case of atrial fibrillation among 352 procedures. Maggiolini reported transient third-degree heart block in a single patient. [133] Adverse Physiologic Consequences There have been a few case reports of adverse consequences even when pericardiocentesis inflicts no injury. Most of these have to do with the fact that during pericardiocentesis, the stroke volume of the previously collapsed right ventricle increases 77% with the first 200 mL of fluid removed. [60] Generally, this increase in stroke volume is greater initially than that demonstrated by the left ventricle. This can have significant consequences for both right and left ventricular function. In three of six patients in whom large effusions were removed by pericardiocentesis, there was right ventricular dilation and overload, with abnormal septal motion and either no increase in right ventricular ejection fraction or a decrease. [137] These patients returned to normal hemodynamic status slowly. Sudden pulmonary edema also has been reported after pericardiocentesis, presumably due to a sudden increase in venous return to the left ventricle at a time when peripheral vascular resistance is still high from compensatory cate-cholamine secretion. [138] [139] [140] Supporting evidence for this explanation is that right ventricular stroke volume increases more after relief of tamponade than the stroke volume increase of the left ventricle. [63] Circulatory collapse with persistently low arterial blood pressure has been reported in a patient who was drained of 700 mL of clear fluid at a rate of 100 mL/min. [141] These authors suggest that ketamine anesthesia may have played a role, but the relative ischemia created by tamponade, coupled with the sudden increase in left-sided preload, created a persisting imbalance. They recommend that pericardial drainage rate not exceed 50 mL/min. Given the rare occurrence of pulmonary edema or primary cardiac compromise, it is unclear that this recommendation is justified. A case of brief profound bradycardia and rebound hypertension has also been reported after surgical relief of tamponade. large series of patients receiving pericardiocentesis.
[142]
Such responses have not been noted in
SUMMARY In nontraumatic patients, tamponade should always be considered in the differential diagnosis of shock, especially in patients who are on anticoagulants, have had recent myocardial infarction, a history of pericardial disease, malignancy, or suspected aortic dissection or when a CVP catheter is in place. Tamponade should also be considered in the differential diagnosis when hypotension persists following closed-chest CPR or attempts at cardiac pacing. Its association with PEA should alert the clinician to the potential that tamponade exists. In any patient with blunt or penetrating chest or upper abdominal trauma, the possibility of traumatic tamponade
320
must also be considered. If clinical deterioration occurs in the ED pending operative care, temporizing pericardiocentesis should be considered if other therapy fails. When such a patient arrives with no obtainable blood pressure or in profound shock and unconscious, immediate thoracotomy and pericardiotomy are indicated after intubation. [111] [143] [144] Pericardiocentesis may cause a dangerous delay in this situation and has a low success rate. Management of tamponade requires a sound understanding of pathophysiology; an ever-vigilant evaluation; and the knowledge of when the patient's clinical condition requires blind or ECG-guided pericardiocentesis as contrasted to the safer alternative of echocardiographically guided diagnosis and therapy.
Acknowledgment
The editors and author wish to acknowledge the contributions of Michael Callaham to this chapter in previous editions.
References 1. Kilpatrick 2. Bishop 3. Wong
Z, Chapman C: On pericardiocentesis. Am J Cardiol 16:622, 1965.
LH, Estes EH, McIntosh HD: The electrocardiogram as a safeguard in pericardiocentesis. JAMA 162:264, 1956.
B, Murphy J, Chang CJ, et al: The risk of pericardiocentesis. Am J Cardiol 44:1110, 1979.
4. Duvernoy 5. Bastian
O, Borowiec J, Helmius G, Erikson U: Complications of percutaneous pericardiocentesis under fluoroscopic guidance. Acta Radiol 33:309, 1992.
A, Meissner A, Lins M, et al: Pericardiocentesis: Differential aspects of a common procedure. Intensive Care Med 26:573, 2000.
6. Tsang
T, Barnes M, Hayes S, et al: Clinical and echocardiographic characteristics of significant pericardial effusions following cardiothoracic surgery and outcomes of echo-guided pericardiocentesis for management. Chest 116:322, 1999. 7. Symbas 8. Borja
P, Harlafhs N, Waldo W: Penetrating cardiac wounds: A comparison of different therapeutic methods. Ann Surg 183:377, 1976.
A, Lansing A, Randell H: Immediate operative treatment for stab wounds of the heart. Ann Thorac Cardiovasc Surg 59:662, 1970.
9. Clarke
D: The heart and great vessels. In Dudley H (ed): Hamilton Bailey's Emergency Surgery, 11th ed. Bristol, England, Wright Publishers, 1986, p 235.
10.
Blair E, Tapuzla C, Dean R: Chest trauma. In Hardy J (ed): Critical Surgical Illness. Philadelphia, WB Saunders, 1971, p 175.
11.
Thomas T: Emergency evacuation of acute pericardial tamponade. Ann Thorac Surg 10:566, 1970.
12.
Isner JM: Acute catastrophic complications of balloon aortic valvuloplasty. J Am Coll Cardiol 17:1436, 1991.
Friedrich SP, Berman AD, Baim DS, Diver DJ: Myocardial perforation in the cardiac catheterization laboratory: Incidence, presentation, diagnosis and management. Catheter Cardiovasc Diagn 32:99, 1994. 13.
14.
Brown C, Gurley H, Hutchins G, et al: Injuries associated with percutaneous placement of transthoracic pacemakers. Ann Emerg Med 14:223, 1985.
15.
Frater R: Intrapericardial pressure and pericardial tamponade in cardiac surgery. Ann Thorac Surg 10:563, 1970.
16.
Kerber R, Ridges J, Harrison D: Electrocardiographic indications of atrial puncture during pericardiocentesis. N Engl J Med 282:1142, 1979.
17.
Sobol S, Thomas H, Evans R: Myocardial laceration not demonstrated by continuous electrocardiographic monitoring occurring during pericardiocentesis. N Engl J Med 292:1222, 1979.
18.
Barton B, Hermann G, Weil R: Cardiothoracic emergencies associated with subclavian hemodialysis catheters. JAMA 250:2660, 1983.
19.
Sheep RE, Guiney WB: Fatal cardiac tamponade: Occurrence with other complications after left internal jugular vein catheterization. JAMA 248:1632, 1982.
20.
Edwards H, King T: Cardiac tamponade from central venous catheters. Arch Surg 117:965, 1982.
21.
Ramp J, Harkins J, Mason G: Cardiac tamponade secondary to blunt trauma. J Trauma 14:767, 1974.
22.
Gabram SG, Devanney J, Jones D, Jacobs LM: Delayed hemorrhagic pericardial effusion: Case reports of a complication from severe blunt chest trauma. J Trauma 32:794, 1992.
23.
Fey G, Deren M, Wesolek J: Intrapericardial caval injury due to blunt trauma. Conn Med 63:259, 1999.
24.
Kirsh M, Behrendt D, Orringer M: The treatment of acute traumatic rupture of the aorta. Ann Surg 184:308, 1976.
25.
Atcheson S, Fred H: Complications of cardiac resuscitation. Am Heart J 89:263, 1975.
26.
Glasser S, Harrison E, Amey B: Echocardiographic incidence of pericardial effusion in patients resuscitated by emergency medical technicians. JACEP 8:6, 1979.
27.
Noffsinger AE, Bilsard KS, Balko MG: Cardiac laceration and pericardial tamponade due to cardiopulmonary resuscitation after myocardial infarction. J Forensic Sci 36:60, 1991.
28.
Reardon MJ, Gross DM, Vallone AM, et al: Atrial rupture in a child from cardiac massage by his parent. Ann Thorac Surg 43:557, 1987.
29.
Krikorian J, Hancock E: Pericardiocentesis. Am J Med 65:808, 1978.
Renkin J, de Bruyne B, Benit E, et al: Cardiac tamponade early after thrombolysis for acute myocardial infarction: A rare but not reported hemorrhagic complication. J Am Coll Cardiol 17:280, 1991. 30.
31.
Olson L, Edwards W, Olney B, et al: Hemorrhagic cardiac tamponade: A clinicopathologic correlation. Mayo Clin Proc 59:785, 1984.
Coma-Canella I, Lopez-Sendon J, Gonzalez Garcia A, Jadraque LM: Hemodynamic effects of dextran, dobutamine and pericardiocentesis in cardiac tamponade secondary to subacute heart rupture. Am Heart J 114:78, 1987. 32.
33.
Balakumaran K, Verbaan CJ, Essed CE, et al: Ventricular free wall rupture: Sudden, subacute, slow, sealed and stabilized varieties. Eur Heart J 5:282, 1984.
34.
Hancock E: Management of pericardial disease. Mod Concepts Cardiovasc Dis 48:1, 1979.
35.
Eisenberg MJ, de Romeral LM, Heidenreich PA, et al: The diagnosis of pericardial effusion and cardiac tamponade by 12-lead ECG. Chest 110:318, 1996.
LeWinter M, Pavelec R: Influence of the pericardium on left ventricular end-diastolic pressure-segment length relations during early and later phases of experimental chronic volume overload in dogs. Circ Res 50:401, 1982. 36.
37.
Guberman B, Fowler N, Engel P: Cardiac tamponade in medical patients. Circulation 64:633, 1981.
38.
Reynolds MM, Hecht SR, Berger M, et al: Large pericardial effusions in the acquired immunodeficiency syndrome. Chest 102:1746, 1992.
39.
Kwan T, Karve MM, Emerole O: Cardiac tamponade in patients infected with HIV. Chest 104:1059, 1993.
40.
Lewis W: AIDS: Cardiac findings from 115 autopsies. Cardiovasc Dis 32:207, 1989.
41.
Stotka JL, Good CB, Downer WR, Kapoor WN: Pericardial effusion and tamponade due to Kaposi's sarcoma in acquired immunodeficiency syndrome. Chest 95:1359, 1989.
42.
Zakowski MF, Ianuale-Shanerman A: Cytology of pericardial effusions in AIDS patients. Diagn Cytopathol 9:266, 1993.
43.
Stein L, Shubin H, Weil M: Recognition and management of pericardial tamponade. JAMA 225:503, 1973.
44.
Press O, Livingston R: Management of malignant pericardial effusion and tamponade. JAMA 257:1088, 1987.
45.
Hanfling S: Metastatic cancer in the heart. Circulation 22:474, 1960.
46.
Rutsky E, Rostand S: Treatment of uremic pericarditis and pericardial effusion. Am J Kidney Dis 10:2, 1987.
47.
Kwasnik E, Kostes J, Lazarus J: Conservative management of uremic pericardial effusions. J Thorac Cardiovasc Surg 76:629, 1978.
48.
Hurd T, Novak R, Gallagher T: Tension pneumopericardium: A complication of mechanical ventilation. Crit Care Med 12:200, 1984.
49.
Toledo T, Moore W, Nash D: Spontaneous pneumopericardium in acute asthma: Case report and review of the literature. Chest 16:118, 1972.
50.
Hacker P, Dorsey D: Pneumopericardium and pneumomediastinum following closed chest injury. JACEP 8:409, 1979.
51.
Capizzi PJ, Martin M, Bannon MP. Tension pneumopericardium following blunt injury. J Trauma 39:775, 1995.
52.
Frascone R, Cicero J, Sturm J: Pneumopericardium occurring during a high-speed motorcycle ride. J Trauma 23:163, 1983.
53.
McDougal C, Mulder G, Hoffman J: Tension pneumopericardium following blunt chest trauma. Ann Emerg Med 14:167, 1985.
54.
Khan R: Air tamponade and tension pneumopericardium. J Thorac Cardiovasc Surg 68:328, 1974.
321
55.
Robinson M, Markovchick V: Traumatic tension pneumopericardium: A case report and literature review. J Emerg Med 2:409, 1985.
56.
Lynn R: Delayed post-traumatic pneumopericardium producing acute cardiac tamponade. Can J Surg 26:62, 1983.
57.
Baue A, Blakemore W: The pericardium. Ann Thorac Surg 14:81, 1972.
58.
Lee M, Fung Y, Shabetai R: Biaxial mechanical properties of human pericardium and canine comparisons. Am J Physiol 253:H75, 1987.
59.
Shabetai R, Fowler N, Guntheroth W: The hemodynamics of cardiac tamponade and constrictive pericarditis. Am J Cardiol 26:480, 1970.
60.
Grose R, Greenberg M, Steingart R, Cohen M: Left ventricular volume and function during relief of cardiac tamponade in man. Circulation 66:149, 1982.
61.
Spodick D: The normal and diseased pericardium: Current concepts of pericardial physiology, diagnosis, and treatment. J Am Coll Cardiol 1:240, 1983.
62.
Spodick D: Acute cardiac tamponade. Pathologic physiology, diagnosis, and management. Prog Cardiovasc Dis 10:64, 1967.
63.
Manyari D, Kostuk W, Purves P: Effect of pericardiocentesis on right and left ventricular function and volumes in pericardial effusion. Am J Cardiol 52:159, 1983.
Crystal G, Bashour F, Downey H, Parker P: Myocardial blood flow and oxygen consumption during moderate cardiac tamponade: Role of reflex vasoconstriction. Proc Soc Exp Biol Med 160:65, 1979. 64.
Wechsler A, Auerbach B, Graham T: Distribution of intramyocardial blood flow during pericardial tamponade correlated with microscopic anatomy and intrinsic myocardial contractility. J Thorac Cardiovasc Surg 68:847, 1974. 65.
66.
Wertheimer W, Bloom S, Hughes R: Myocardial effects of pericardial tamponade. Ann Thorac Surg 14:494, 1972.
67.
Shoemaker W, Carey S, Yao S: Hemodynamic monitoring for physiologic evaluation, diagnosis, and therapy of acute hemopericardial tamponade from penetrating wounds. J Trauma 13:36, 1973.
68.
Antman E, Cargill V, Grossman W: Low-pressure cardiac tamponade. Ann Intern Med 91:403, 1979.
69.
Koller J, Smith R, Sjostrand U, Breivik H: Effects of hypo-, normo-, and hypercarbia in dogs with acute cardiac tamponade. Anesth Analg 62:181, 1983.
70.
Moller C, Schoonbee C, Rosendorff C: Haemodynamics of cardiac tamponade during various modes of ventilation. Br J Anaesth 51:409, 1979.
71.
Freshman SP, Wisner DH, Weber CJ: 2-D echocardiography: Emergent use in the evaluation of penetrating precordial trauma. J Trauma 31:902, 1991.
72.
Markiewicz W, Borovik R, Ecker S: Cardiac tamponade in medical patients: Treatment and prognosis in the echocardiographic era. Am Heart J 111:1138, 1986.
Goldberg SP, Karalis DG, Ross JJ Jr: Severe right ventricular contusion mimicking cardiac tamponade: The value of transesophageal echocardiography in blunt chest trauma. Ann Emerg Med 22:745, 1993. 73.
74.
Beck C: Two cardiac compression triads. JAMA 104:715, 1935.
75.
DiPasquale J, Pluth J: Penetrating wounds of the heart and cardiac tamponade. Postgrad Med 49:114, 1971.
76.
Shoemaker W, Carey J, Jao S: Hemodynamic alterations in acute cardiac tamponade after penetrating injuries of the heart. Surgery 67:754, 1970.
77.
Brown J, MacKinnon D, King A, Vanderbush E: Elevated arterial blood pressure in cardiac tamponade. N Engl J Med 327:463, 1992.
78.
Curtiss E, Reddy P, Uretsky B, Cecchetti A: Pulsus paradoxus: Definition and relation to the severity of cardiac tamponade. Am Heart J 115:391, 1988.
79.
Singh S, Wann L, Klopfenstein H, et al: Usefulness of right ventricular diastolic collapse in diagnosing cardiac tamponade and comparison to pulsus paradoxus. Am J Cardiol 57:652, 1986.
80.
Shabetai R: Changing concepts of cardiac tamponade. Mod Concepts Cardiovasc Dis 52:19, 1983.
81.
Shoemaker W: Algorithm for early recognition and management of cardiac tamponade. Crit Care Med 3:59, 1975.
82.
Trinkle J, Marcas J, Grover F: Management of the wounded heart. Ann Thorac Surg 17:230, 1974.
83.
Breaux E, Dupont J, Albert H: Cardiac tamponade following penetrating mediastinal injuries: Improved survival with early pericardiocentesis. J Trauma 19:461, 1979.
84.
Carsky E, Azimi F, Maucer R: Epicardial fat sign in the diagnosis of pericardial effusion. JAMA 244:2762, 1980.
85.
Heinsimer JA, Collins GJ, Burkman MH, et al: Supine cross table lateral chest roentgenogram for the detection of pericardial effusion. JAMA 257:3266, 1987.
86.
Meyers DG, Bagin RG, Levene JF: Electrocardiographic changes in pericardial effusion. Chest 104:1422, 1993.
87.
Smedema J, Katjitae I, Reuter H, et al: Twelve-lead electrocardiography in tuberculous pericarditis. Cardiovascular Journal of Southern Africa 12:31, 2001.
88.
Parameswaran R, Maniet A, Goldberg S, Goldberg H: Low electrocardiographic voltage in pericardial effusion. Chest 85:631, 1984.
89.
Sotolongo R, Horton J: Total electrical alternans in pericardial tamponade. Am Heart J 101:853, 1981.
90.
Spodick D: Electrical alternans of the heart: Its relation to the kinetics and physiology of the heart during cardiac tamponade. Am J Cardiol 10:155, 1962.
Bruch C, Schmermund A, Dagres N, et al: Changes in QRS voltage in cardiac tamponade and pericardial effusion: reversibility after pericardiocentesis and after anti-inflammatory drug treatment. J Am Coll Cardiol 38:219, 2001. 91.
92.
Berger BC: Pericardiocentesis using echocardiography. Cardiovasc Clin 15:269, 1985.
93.
Ansinger R, Rourke T, Hodges M: Role of echocardiography in emergencies. Minn Med 63:855, 1980.
Levine MJ, Lorell BH, Diver DJ, Come PC: Implications of electrocardiographically assisted diagnosis of pericardial tamponade in contemporary medical patients: Detection before hemodynamic embarrassment. J Am Coll Cardiol 17:59, 1991. 94.
Duvernoy O, Larsson SG, Persson K, et al: Pericardial effusion and pericardial compartments after open heart surgery. An analysis by computed tomography and echocardiography. Acta Radiol 31:41, 1990. 95.
96.
Yousem D, Traill TT, Wheeler PS, Fishman EK: Illustrative cases in pericardial effusion misdetection: Correlation of echocardiography and CT. Cardiovasc Intervent Radiol 10:162, 1987.
97.
Memon A, Zawadski Z: Malignant effusions: Diagnostic evaluation and therapeutic strategy. Curr Probl Cancer 5:1, 1981.
98.
Permanyer-Miralda G, Sagrista-Sauleda J, Soler-Soler J: Primary acute pericardial disease: A prospective series of 231 consecutive patients. Am J Cardiol 56:623, 1985.
99.
Kindig J, Goodman M: Clinical utility of pericardial fluid pH determination. Am J Med 75:1077, 1983.
100. Koh
KK, Kim EJ, Cho CH, et al: Adenosine deaminase and carcinoembryonic antigen in pericardial effusion diagnosis, especially in suspected tuberculous pericarditis. Circulation 89:2728, 1994.
101. Just
M, Raventos A, Romeu J, et al: Cardiac tamponade and Kaposi's sarcoma. Med Clin 102:495, 1994.
102. Nathan
PE, Arsura EL, Zappi M: Pericarditis with tamponade due to cytomegalovirus in the acquired immunodeficiency syndrome. Chest 99:765, 1991.
103. Prager
R, Wilson C, Bender H: The subxiphoid approach to pericardial disease. Ann Thorac Surg 34:6, 1981.
104. Alcan
K, Zabetakis P, Marino N: Management of acute cardiac tamponade by subxiphoid pericardiotomy. JAMA 247:1143, 1982.
105. Corey
GR, Campbell PT, Van Tright P, et al: Etiology of large pericardial effusions. Am J Med 95:209, 1993.
106. Bolanowski
P, Swaminathan A, Neville W: Aggressive surgical management of penetrating cardiac injuries. J Thorac Cardiovasc Surg 66:52, 1973.
107. Sugg
W, Rea W, Ecker R: Penetrating wounds of the heart: An analysis of 459 cases. J Thorac Cardiovasc Surg 56:531, 1968.
108. Arom
K, Richardson J, Webb G: Subxiphoid pericardial window in patients with suspected traumatic pericardial tamponade. Ann Thorac Surg 23:545, 1977.
109. Ivatury 110. Boyd
R, Shah P, Ito K, et al: Emergency room thoracotomy for the resuscitation of patients with "fatal" penetrating injuries of the heart. Ann Thorac Surg 32:377, 1981.
T, Strieder J: Immediate surgery for traumatic heart disease. J Thorac Cardiovasc Surg 50:305, 1965.
111. Siemens 112. Beall
R, Polk H, Gray L: Indications for thoracotomy following penetrating thoracic injury. J Trauma 17:493, 1977.
A, Gasior R, Bricker D: Gunshot wounds of the heart: Changing patterns of surgical management. Ann Thorac Surg 11:523, 1972.
113. Osuch
J, Khandekar J, Fry W: Emergency subxiphoid pericardial decompression for malignant pericardial effusion. Am Surg 51:298, 1985.
114. Courcy 115. Miller
P, Stair T, Brotman S: Subxiphoid pericardial window in traumatic pericardial tamponade. Am J Emerg Med 2:153, 1984.
F, Bond S, Shumate C, et al: Diagnostic pericardial window. A safe alternative to exploratory thoracotomy for suspected heart injuries. Arch Surg 122:605, 1987.
116. Brewster 117. Duncan
S, Thirlby R, Snyder W: Subxiphoid pericardial window and penetrating cardiac trauma. Arch Surg 123:937, 1988.
AO, Scalea TM, Sclafani SJA, et al: Evaluation of occult cardiac injuries using subxiphoid pericardial window. J Trauma 29:955, 1989.
322
118. Callahan 119. Clarke
D, Cosgrove D: Real-time ultrasound scanning in the planning and guidance of pericardiocentesis. Clin Radiol 38:119, 1987.
120. Treasure 121. Patel
T, Cottler L: Practical procedures: How to aspirate the pericardium. Br J Hosp Med 24:488, 1980.
A, Kosolcharoen P, Nallasivan M, et al: Catheter drainage of the pericardium. Practical method to maintain long-term patency. Chest 92:1018, 1987.
122. Callahan 123. Stewart 124. Park
J, Seward J, Nishimura R, et al: Two-dimensional echocardiographically guided pericardiocentesis: Experience in 117 consecutive patients. Am J Cardiol 55:476, 1985b.
J, Seward J, Tajik A: Cardiac tamponade: Pericardiocentesis directed by two-dimensional echocardiography. Mayo Clin Proc 60:344, 1985a.
J, Gott V: The use of a Seldinger wire technique for pericardiocentesis following cardiac surgery. Ann Thorac Surg 35:467, 1983.
SC, Pahl E, Ettedgui JA, et al: Experience with a newly developed pericardiocentesis set. Am J Cardiol 66:1529, 1990.
125. Fowler
N: Recognition and management of pericardial disease and its complications. In Hurst J (ed): The Heart, 4th ed. New York, McGraw-Hill, 1978.
126. Gascho
JA, Martins JB, Marcus ML, Kerber RE: Effects of volume expansion and vasodilators in acute pericardial tamponade. Am J Physiol 240:H49, 1981.
127. Kerber
RE, Gascho JA, Litchfield R, et al: Hemodynamic effects of volume expansion and nitroprusside compared with pericardiocentesis in patients with acute cardiac tamponade. N Engl J Med 307:929, 1982. 128. Pierart
J, Gyhra A, Torres P, et al: Causes of increasing pericardial pressure in experimental cardiac tamponade induced by ventricular perforation. J Trauma 35:834, 1993.
129. Martins
JB, Manuel WJ, Marcus ML, Kerber RE: Comparative effects of catecholamines in cardiac tamponade; experimental and clinical studies. Am J Cardiol 46:459, 1980.
130. Zhang
H, Spapen H, Vincent JL: Effects of dobutamine and norepinephrine on oxygen availability and tamponade-induced stagnant hypoxia: A prospective, randomized, controlled study. Crit Care Med 22:299, 1994. 131. Caspari 132. Kizer
G, Bartel T, Mohlenkamp S, et al: Contrast medium echocardiography-assisted pericardial drainage. Herz 25:755, 2000.
K, Goodman P: Radiologic manifestations of venous air embolism. Diagn Radiol 144:35, 1982.
133. Maggiolini
S, Bozzano A, Russo P, et al: Echocardiography-guided pericardiocentesis with probe-mounted needle: Report of 53 cases. J Am Soc Echocardiogr 14:82, 2001.
134. Salem
K, Mulji A, Lonn E: Echocardiographically guided pericardiocentesis—The gold standard for the management of pericardial effusion and cardiac tamponade. Can J Cardiol 15:1251, 1999.
135. Tsang
T, El-Najdawi E, Seward J, et al: Percutaneous echocardiographically guided pericardiocentesis in pediatric patients: Evaluation of safety and efficacy. J Am Soc Echocardiogr 11:1072,
1998. 136. Ewer
M, Ali M, Frazier O: Open chest resuscitation for cardiopulmonary arrest related to mechanical impairment of the circulation. Crit Care Med 10:198, 1982.
137. Armstrong
W, Feigenbaum H, Dillon J: Acute right ventricular dilatation and echocardiographic volume overload following pericardiocentesis for relief of cardiac tamponade. Am Heart J 107:1266,
1984. 138. Vandyke
WJ, Cure J, Chakko C, Gheorgeiade M: Pulmonary edema after pericardiocentesis for cardiac tamponade. N Engl J Med 309:595, 1983.
139. Glasser
F, Fein AM, Feinsilver SH, et al: Non-cardiogenic pulmonary edema after pericardial drainage for cardiac tamponade. Chest 94:869, 1988.
140. Downey
RJ, Bessler M, Weissman C: Acute pulmonary edema following pericardiocentesis for chronic cardiac tamponade secondary to trauma. Crit Care Med 19:1323, 1991.
141. Hamaya
Y, Dohi S, Ueda N, Akamatsu S: Severe circulatory collapse immediately after pericardiocentesis in a patient with chronic cardiac tamponade. Anesth Analg 77:1278, 1993.
142. Prida
X, Cody R: Profound bradycardia following release of cardiac tamponade. Chest 83:148, 1983.
143. Mattox
K, Beall A, Jordan G: Cardiography in the emergency center. J Thorac Cardiovasc Surg 68:886, 1974.
144. Fulton
R: Penetrating wounds of the heart. Heart Lung 7:262, 1978.
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Chapter 17 - Artificial Perfusion During Cardiac Arrest Jim Edward Weber F. Michael Jaggi Emanuel P. Rivers
The modern era of cardiopulmonary resuscitation (CPR) was introduced by Kouwenhoven and colleagues in 1960 in a classic paper that brought together the concepts of mouth-to-mouth ventilation, closed-chest compression, and external defibrillation. [1] Although CPR and advanced cardiac life support (ACLS) interventions have saved many lives, overall survival after cardiac arrest remains low. [2] [3] [4] [5] [6] [7] [8] Evolving data from both laboratory and clinical studies suggest that restoration of heart function after cardiac arrest is related to the generation of adequate coronary perfusion. [9] [10] Despite this insight, artificial perfusion is the principal weak link in the resuscitation armamentarium. Subsequently, periodic revision of the recommended standards for CPR and the development of alternative methods of CPR are revisited by international resuscitation organizations as new science becomes available. [11] This chapter updates the current understanding of the mechanism of blood flow during CPR, reviews standard and alternative techniques of CPR, and summarizes methods for improving vital organ perfusion during cardiac arrest.
BACKGROUND The mechanism of blood flow during CPR has been the subject of debate since the 1960s. Two mechanisms for blood flow have prevailed over time: the "cardiac pump" model and the "thoracic pump" model. Controversy continues over the nature of the pump at work during external chest compression. Future studies might help resolve this controversy, but now it seems that the driving force for blood flow produced by standard external chest compression is a combination of intrathoracic pressure fluctuations and direct cardiac compression. The current concept of blood flow during CPR is based on a combination of these models and provides the theoretical basis for the newer CPR techniques. Kouwenhoven and colleagues first proposed the traditional cardiac pump mechanism of blood flow. [1] Pressure on the chest compresses the heart between the sternum and the vertebrae, forcing blood into the arterial circulation (Fig. 17-1 (Figure Not Available) ). [12] Closure of the atrioventricular valves during chest compression was thought to prevent retrograde blood flow. With the release of chest compression, the heart expands and fills with blood. This model assumes that compression of the ventricles raises intraventricular pressure, rather than intrathoracic pressure, above that of the aorta and pulmonary artery, creating a pressure gradient that generates forward blood flow. The validity of this model has been questioned almost since its introduction. Several studies of simultaneous compression and ventilation have suggested that increases in intrathoracic pressure alone can produce forward flow of blood. Weale and Rothwell-Jackson, in 1962, showed that chest compression induces almost equivalent increases in arterial and venous pressures in animals, thus challenging the cardiac pump hypothesis. [13] They hypothesized that closed-chest compression creates a generalized increase in intrathoracic pressure that is transmitted equally to the heart and intra- and extrathoracic vessels, because the atrioventricular valves remain open (Fig. 17-2 (Figure Not Available) ). [12] Additional evidence for the thoracic pump model has been provided by the reported success of cough CPR. During cough CPR, perfusion is maintained by intermittent increases in intrathoracic pressure by self-induced coughing. Although multiple studies have been published in support of each of these models, [14] it is possible that neither fully explains blood flow during CPR. An alternative explanation is that both mechanisms play a role. Maier and associates studied the effect of varying the rate, force, and duration of compressions in CPR on large dogs.[15] These investigators demonstrated that the relative contribution of the thoracic pump and direct cardiac compression models to blood flow varied with the CPR technique used. Direct cardiac compression predominated when chest compressions were delivered at higher rates (high-frequency CPR), and the thoracic pump mechanism predominated in low-momentum compression techniques, such as simultaneous compression and ventilation (SCV) CPR. In addition, Babbs and coworkers noted that the optimal technique of CPR varied with the size of the experimental animal and the size of the pad performing chest compressions. [16] Large animals in arrest were more likely to benefit from SCV CPR than smaller animals. Direct cardiac compression was proposed to play a greater role in smaller animals. Interestingly, sustained intrathoracic pressure elevations can occur during CPR in the setting of increased airway resistance. [17] The inability to adequately exhale during CPR can lead to the auto-positive end-expiratory pressure (auto-PEEP) phenomenon. The presence of auto-PEEP can adversely impact cardiac filling and cardiac output. In summary, the mechanism of forward blood flow during closed chest compression appears to be multifactorial. Key factors include body size, chest configuration (particularly anteroposterior diameter), previous thoracic surgery, molding of the chest with continued CPR, size of hand or paddle performing chest compressions, and rate and force of chest compressions. Knowledge of the mechanisms of blood flow during CPR allows the clinician to use alternative techniques that may provide better perfusion pressures during cardiac arrest. The optimal technique for CPR may not be the same in every patient. For example, obese patients with large anteroposterior diameters may benefit more from SCV; thin patients may benefit from faster compression rates. The key to clinical implementation of these changes is being able to assess perfusion during ongoing CPR. Advances in this area are discussed later in this chapter.
INDICATIONS AND CONTRAINDICATIONS CPR is generally indicated for all patients in cardiac arrest. One contraindication to initiating or continuing CPR is when the provider has reason to believe that resuscitation will be a futile intervention. Often, for such patients, an advance directive that outlines the patient's preferences regarding resuscitative efforts is available. At other times, the patient's condition or
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Figure 17-1 (Figure Not Available) Cardiac pump model of cardiopulmonary resuscitation. During the relaxation phase, negative intrathoracic pressure enhances blood return to the heart. During closed-chest compression, the heart is squeezed between the sternum and the spine, a pressure gradient is developed between the ventricles and great vessels, and antegrade flow occurs because of the one-way arrangement of heart valves. RV, right ventricle; LV, left ventricle. (From Luce JM, Cary JM, Ross BK, et al: New developments in cardiopulmonary resuscitation. JAMA 244:1366, 1980. Copyright 1980, American Medical Association.)
response to resuscitative efforts will guide subsequent therapy. Details regarding the ethics and associated laws surrounding the initiation or continuation of resuscitative efforts for specific circumstances are beyond the scope of this text. A special caution is warranted regarding new implantable left ventricular assist systems that serve as bridges until cardiac transplant or as mechanisms to enhance cardiac function in nonsurgical heart failure patients. These new devices can be operated by a hand pump in the setting of battery failure. When this condition is identified by the external hydraulic line or when described by family members, these Figure 17-2 (Figure Not Available) Thoracic pump model of cardiopulmonary resuscitation. Closed-chest compression causes a generalized increase in intrathoracic pressure that squeezes all structures, including the pulmonary reservoir, which is filled during the relaxation phase. A pressure gradient is developed, and blood flows into the head, because the thick-walled carotid artery remains patent while the thin-walled jugular vein is squeezed shut, or because of a venous valve. RV, right ventricle; LV, left ventricle. (From Luce JM, Cary JM, Ross BK, et al: New developments in cardiopulmonary resuscitation. JAMA 244:1366, 1980. Copyright 1980, American Medical Association.)
patients should be resuscitated using the hand pump or a backup electronic pump. Although these patients can be resuscitated with standard cardiac drugs or cardioversion/defibrillation as warranted, they should not receive chest compressions.
STANDARD CPR TECHNIQUE Guidelines for the performance of CPR have been recommended by the American Heart Association and are revised
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Adult
TABLE 17-1 -- Guidelines for Cardiopulmonary Resuscitation Child Infant
Neonate
Compression rate (per min)
100
100
=100
120
Compression depth
4–5 cm
1/3–1/2*
1/3–1/2*
1/3*
Compression duration
50% of cycle
50% of cycle
50% of cycle
50% of cycle
Compression mode
Both hands
Heel of one hand
Apposed thumbs†
Apposed thumbs
Compression-to-ventilation ratio
15:2 (1 or 2 rescuers)
5:1 (1 or 2 rescuers)
5:1 (1 or 2 rescuers)
5:1 (1 or 2 rescuers)
From American Heart Association: Guidelines 2000 for cardiopulmonnary resuscitation and emergency cardiovascular care. Circulation 102(suppl): I1, 2000. *Anteroposterior diameter of chest. †May be performed with ring and middle fingers one fingerwidth below intramammary line if rescuer hands are too small.
periodically to reflect ongoing research. [11] Current guidelines are summarized in Table 17-1 . Traditionally, external chest compression was performed two fingerbreadths above the xiphoid-sternal notch, compressing the sternum 4.0 to 5.0 cm in the normal-sized adult. A simplified method of achieving correct hand position, particularly for lay rescuers, is "in the center of the chest, right between the nipples." The pressure is released completely after each compression, and an equivalent amount of time is allotted for relaxation as for compression. The chest compression rate was previously 80 to 100 per minute. Rescuers working within the range of 80 to 100 compressions per minute will naturally drift to the lower end of the range, especially when fatigued. Therefore, the newly recommended compression rate for adult victims is 100 compressions per minute. Two ventilations are given after each 15 chest compressions in one-rescuer CPR, and 2.0 seconds are allowed for each breath in order to provide good chest expansion. For adult victims, it is now recommended that 2 rescuers also use a compression-ventilation of 15:2. The compression-ventilation ratio of 5:1 results in interruptions, which subsequently lead to a marked reduction in blood flow and blood pressure. Once the patient is endotracheally intubated, the rescuer need not stop compressions for the ventilatory pause. Rather, ventilation should be performed asynchronously at a rate of 12 to 15 per minute. In children (1 to 8 years), compressions are performed with the heel of one hand over the lower half of the sternum, ensuring that compressions do not occur on or near the xiphoid process. The sternum is depressed approximately one third to one half of the depth of the child's chest, which corresponds to a compression depth of approximately 2.5 to 4.0 cm, at a rate of approximately 100 compressions per minute. One or two rescuers providing compressions should pause after every fifth compression and provide effective ventilation. Chest compressions in infants (younger than 1 year old) currently are performed 1 fingerwidth below the intramammary line. The sternum is depressed with 2 to 3 fingers to a depth of approximately one-third to one-half of the infant's chest (1.25–2.5 cm). The recommended compression rate in infants is at least 100 per minute. A 5:1 compression-to-ventilation ratio is maintained for both one- and two-rescuer CPR. The preferred two-rescuer technique for performing chest compressions in the infant is the two thumb-encircling hands technique. [18] [19] Using the same location, sternal depression is performed using the two apposed thumbs while the infant's chest is encircled with the back supported by the fingers of both hands. If the rescuer's hands are too small to encircle the chest, compressions may be performed with the ring and middle fingers one fingerwidth below the intramammary line. Previous guidelines suggested that sternal compression depth for a neonate was 1.3 to 2.0 cm. Because these recommendations were considered complex and difficult to remember, a relative gauge that is sufficient to generate a palpable pulse or about one-third of the anteroposterior depth of the chest is preferred. Use of an absolute gauge for compression depth is discouraged. Chest compressions should be coordinated with ventilation at a ratio of 5:1 with a compression rate of 120 per minute.
MECHANICAL DEVICES FOR STANDARD CPR Mechanical resuscitators that can provide standard chest compressions and ventilations during adult CPR have been developed. Early clinical studies have demonstrated that mechanical CPR devices are comparable to standard manual CPR. [20] [21] [22] Three human studies that compared mechanical with standard CPR demonstrated improvement in the concentration of end-tidal carbon dioxide (Pet CO2 ) during mechanical external chest compression. However, no survivors were reported in any study. [20] [22] [23] In addition, one animal study showed improvement in the coronary perfusion pressure and Pet CO2 concentrations, but again, revealed no survival advantage. [24] Nonetheless, the decay in quality of chest compressions with time periods as short as 5 minutes is well recognized. [25] The nomenclature has been changed to differentiate the various types of mechanical adjuncts to reflect automatic versus manual devices and piston-type versus belt-type devices. Piston-type chest compression devices provide an acceptable alternative to standard manual CPR in circumstances that make manual chest compressions difficult. Advantages of mechanical devices include controlled, constant chest compressions; the elimination of operator fatigue; and the freeing of personnel to perform other functions. The most commonly used device is the Thumper Cardiopulmonary Resuscitator (Michigan Instruments, Inc., Grand Rapids, MI). The Thumper The Thumper is a gas-powered mechanical device that is in relatively broad use. This device consists of a compressed gas-powered plunger mounted on a backboard and a time-cycled volume ventilator ( Fig. 17-3 ).
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Figure 17-3 The Thumper Cardiopulmonary Resuscitator.
The Thumper delivers chest compressions at rates consistent with American Heart Association guidelines with a compression duration that is 50% of the cycle length. Every fifth compression is followed by ventilation with an adjustable tidal volume. The Thumper can be driven by wall oxygen at 50 psi or by standard portable oxygen tanks. Setup of the Thumper
The Thumper can be positioned from either side of the patient. Care should be taken to ensure that the base plate is positioned horizontally under the patient's posterior thorax with the patient lying near the center of the backboard. After the arm/column assembly and piston are fitted on the base plate, the piston pad position should be adjusted so that the pad lies over the lower one third of the sternum. The compressor piston is positioned after the oxygen hose has been connected; therefore, CPR is not interrupted during assembly of the Thumper. The piston column is calibrated with rings, each indicating 1.25 cm of piston excursion. Before
Type of CPR
Mechanism
TABLE 17-2 -- Summary of Alternative Cardiopulmonary Resuscitation Data Hemodynamic Outcomes Complications Recommendations Reference Findings
IAC
Augments AP
? ROSC
? Survival*
Abdominal injury
High frequency
Cardiac compression
? MAP, CO, CPP
No survival studies
= Traditional CPR Experimental
[15] [39] [40] [41]
Vest
Thoracic pump
? CO, CPP, ROSC
? Survival†
No reported harm Acceptable alt.
[4] [42] [43] [44] [45] [46]
AC-DC
Cardiac + thoracic
? CPP
Discrepant (see text)
Local trauma
[7] [46] [47] [48] [49] [50] [51] [52] [ 53] [54] [ 55] [56] [ 57] [58]
Acceptable alt.
Acceptable alt.
[35] [36] [37]
??[59] [60] [61] [62] [63] [64] [65] [66] [67]
Chest compression Cardiac pump only
Similar to traditional
Similar to traditional
Similar to traditional
Acceptable alt.‡
[72] [73] [74] [75] [76] [ 77] [78] [ 79] [80]
Impedance threshold
? Intrathoracic pressure
PetCO2 , ? CPP
Under study
No add'l risk
Acceptable alt.§
[82] [83] [84]
Lifestick
Cardiac + thoracic
? ROSC
No improvement ? Sternal FX
Experimental
[85] [86] [87]
AC/DC, active compression/decompression; AP, aortic pressure; CO, cardiac output; CPP, coronary perfusion pressure; Pet CO2 , end-tidal CO 2 ; IAC, interposed abdominal compression; MAP, mean arterial pressure; ROSC, return of spontaneous circulation; Sternal FX, sternal fracture. *No survival benefit demonstrated in pre-hospital setting. †Survival defined as 6 hrs postarrest. No ? in survival to discharge. ‡For lay rescuers unable or unwilling to perform mouth-to-mouth breathing. §Only for use with active compression-decompression device.
the device is started, the piston height should be adjusted so that one ring is just visible on the piston column. With the Thumper operational, chest compressions should be adjusted to a depth of 5 to 6.25 cm or 20% to 25% of the patient's anteroposterior chest diameter, once the machine is in operation. The device should not be set to function at a predetermined chest compression force. The ventilation hose can be connected to an endotracheal tube, an esophageal obturator, or a facemask. The Thumper uses a Patient Demand Valve (PDV) attached to the arm/column assembly and an associated tidal volume control that provides ventilation. The delivered tidal volume can be set from 400 mL to 1200 mL. The ventilation rate is preset to be synchronized with the Thumper chest compressions to provide ventilation on every fifth upstroke. The ventilator inspiratory-to-expiratory ratio is fixed at 1:2. It is pressure limited to 55 cm H 2 O of airway pressure. Use of the Thumper requires operation of 3 key switches: (1) RUN/STOP control, (2) the compression depth control, and (3) ventilation volume control. When a pause in compressions is required for other procedures, the operator can easily stop compressions by turning off the RUN/STOP control. Subclavian or jugular central lines can be placed with the Thumper in position, although it is recommended that the device be turned off during needle advancement to avoid arterial or lung injury. Defibrillation should be performed during the compression phase, when thoracic impedance is minimized.
ALTERNATIVE CPR TECHNIQUES Because controversy continues as to the type of pump mechanism at work during chest compression, modifications of the standard CPR technique have been used in an effort to maximize coronary perfusion. [26] [27] [28] [29] [30] [31] [32] [33] [34] Proposed pumps include direct cardiac compression, intrathoracic pressure augmentation, abdominal pressure augmentation, or various combinations. The outcomes and recommendations of these alternative techniques are summarized in Table 17-2 .
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Interposed Abdominal Compression CPR The use of abdominal compressions during CPR evolved from the hypothesis that venous return might be improved and from laboratory observations that compression of the abdomen during cardiac arrest resulted in aortic pressure fluctuations similar to those with chest compressions. The technique of interposed abdominal compression (IAC)-CPR interposes abdominal compressions between chest compressions ( Fig. 17-4 ). [35] [36] [37] CPR is performed using American Heart Association guidelines; however, during the relaxation phase, the abdomen is compressed. IAC-CPR has been studied extensively as a potential alternative to standard CPR using animal, human, and mathematical models. [38] Four prospective randomized human clinical trials have compared IAC-CPR with standard CPR. [39] [40] [41] [42] Three of the studies involved in-hospital cardiac arrest victims, and reported improved return of spontaneous circulation (ROSC), [41] improved 24-hour survival, [41] [42] and improved survival to discharge [41] using IAC-CPR. No survival advantage using IAC-CPR has been demonstrated in the pre-hospital setting. [39] IAC-CPR appears to be safe despite theoretical concerns over abdominal injury. Only one human case report described traumatic pancreatitis after IAC-CPR that was attributable to abdominal compression. [43] At the current time, IAC-CPR is not considered the technique of choice for external CPR because outcome benefits have been reported by only one center and the abdominal compression techniques used have not been consistent among studies. Also, use of IAC-CPR requires additional training and one additional rescuer to perform the technique. However, because of overall encouraging in-hospital results, supportive hemodynamic data, and apparent safety, the use of IAC-CPR is currently recommended as an acceptable alternative to standard CPR for
Figure 17-4 An artist's conception of basic rescuers performing interposed abdominal compression cardiopulmonary resuscitation. For clarity, both rescuers are shown on the same side of the victim. With two rescuers, the first compresses the chest and performs ventilation while the second compresses the abdomen. With three rescuers, ventilation, chest compression, and abdominal compression are performed by each individual. Ideally, the rescuer performing chest compressions is on the victim's right side and the rescuer performing abdominal compressions is on the victim's left side. (From Voorhees WD, Niebauer MJ, Babbs CF: Improved oxygen delivery during cardiopulmonary resuscitation with interposed abdominal compressions. Ann Emerg Med 12:128, 1983. Reproduced by permission.)
in-hospital resuscitation when sufficient personnel trained in the technique are available.
[ 11]
High-Frequency (High-Impulse) CPR Rapid manual CPR uses standard CPR techniques, but chest compressions are performed at a rate of 120 per minute. Animal data have shown that rates of 120 result in increased cardiac output, aortic pressure, coronary perfusion pressure, and blood flow as well as 24-hour survival. [15] [44] Swart and coworkers demonstrated that at a compression rate of 100 per minute, shorter compression duration (i.e., duty cycles less than 50% or "high-impulse" CPR) also improved resuscitation hemodynamics.[45] Kern and colleagues found that patients who had CPR with chest compression rates of 120 per minute had significantly higher levels of end-tidal CO2 excretion (a surrogate for cardiac output) compared to patients with chest compression rates of 80 per minute. [46] Because survival studies have not been performed to clarify the effect of higher compression rates, high-impulse CPR should be considered an experimental technique and is not recommended for routine use in patients with cardiac arrest. Vest CPR The CPR vest was designed to take advantage of the thoracic pump mechanism of blood flow. [47] [48] [49] [50] Niemann and colleagues demonstrated hemodynamic improvement and 24-hour survival in animals receiving vest/binder CPR compared with standard CPR. [48] In contrast, Kern and coworkers found no improvement in resuscitation or 24-hour survival when vest CPR was compared with mechanical CPR. [49] Similarly, vest CPR proved to be of no benefit in one prehospital cardiac arrest study.[50] A recent study has reported improved 6-hour survival, but there was no improvement in survival to discharge. [7] Randomized studies have not demonstrated harm with vest CPR. However, technical difficulties exist with the current device because of its size and subsequent energy requirements. The additional training and equipment requirements with CPR vests also add to the complexity of resuscitation. Despite these limitations, vest CPR is considered an acceptable alternative to standard CPR in the hospital or during ambulance transport, assuming there are an adequate number of well-trained personnel to properly perform CPR ( Fig. 17-5 ). Active Compression-Decompression After publication of the initial case report in which a patient was resuscitated from cardiac arrest with the aid of a plunger, active compression-decompression (ACD)-CPR became one of the most heavily researched areas of advanced life support. [51] Standard CPR involves a forceful or active chest compression phase with elastic recoil of the chest wall during the relaxation phase (passive decompression). ACD-CPR involves both active compression and active decompression of the thorax using a device that consists of a circular suction cup with a handle and a force gauge that is applied to the midsternal chest ( Fig. 17-6 ). [5] At least 21 studies have evaluated the role of ACD-CPR in human cardiac arrest. [5] [51] [52] [53] [54] [55] [56] [57] [58] [59] [60] [61] [62] [63] ???[64] [65] [66] [67] [68] [69] [70] [71] Laboratory evidence has shown that ACD-CPR can decrease the venous system pressure to a greater extent than the arterial pressures during the
328
Figure 17-5 A comparison of vest cardiopulmonary resuscitation (CPR) and standard manual CPR. With vest CPR, a pneumatic system inflates and deflates a bladder surrounding the chest. The compression phase results in circumferential compression as opposed to point compression during manual CPR. The vest CPR system is equipped with defibrillator electrodes that monitor the patient's electrocardiogram as well as allow defibrillation without removal of the vest.
active decompression phase, resulting in improved venous return and increased CPR-diastolic coronary perfusion pressures. However, most human studies failed to
demonstrate long-term survival benefits. One study group demonstrated a neurologically intact survival benefit with the use of ACD-CPR. [58] However, these results should be interpreted with caution because the study investigators were unable to control for the use of ACD-CPR by basic life-support providers, and the resuscitation study team was unblinded to the technique used for external cardiac compression. Stiell and colleagues performed the most methodologically robust prospective study to date, and failed to demonstrate any significant benefits of ACD-CPR in either the basic or advanced life-support setting. [54] Despite the abundance of studies that have evaluated the role of ACD-CPR, meta-analysis of data is difficult because of inconsistent outcome definitions, inability to control for background confounders, differences in randomization schemes, and variability in prehospital response time for basic and advanced life support. The use of ACD-CPR requires additional equipment and training. Additional concerns with ACD-CPR include difficulties with application of the technique, increased energy expenditure requirements, and mounting evidence of increased local trauma. [70] [71] However, since one center has demonstrated improvement in long-term outcomes, and most studies have not demonstrated harm, ACD-CPR has been approved as an acceptable alternative to standard CPR when rescue personnel are adequately trained to use this technique. Chest Compression-Only CPR Factors affecting widespread application of basic life support (BLS) techniques involve education of laypersons and acceptance of mouth-to-mouth ventilation. Current BLS techniques are difficult for laypersons to learn, retain, and correctly perform. [72] Surveys among laypersons, BLS instructors, and clinicians have reported resistance to performing mouth-to-mouth breathing for a stranger. [73] [74] [75] Correspondingly, the American Heart Association simplified the current requirements for and teaching of CPR. [11] Data from 6 well controlled animal studies suggest that chest compression-only BLS performed by the lay public may be equally effective as standard BLS-CPR with rescue breathing using 24- to 48-hour survival as an outcome measure. [76] [77] [78] [79] [80] [81] Three important clinical trials corroborate these experimental data. Bossaert and colleagues found that when good-quality chest compression-only CPR was performed on prehospital cardiac arrest patients, there was no difference in long-term survival when compared with chest compression and ventilation CPR (15% vs. 12%). [82] Van Hoeyweghen and coworkers
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Figure 17-6 The active compression-decompression (ACD) device uses a suction cup positioned at mid-chest at the level of the nipples. The device is pushed downward into the chest during the compression phase of CPR. The force of compression can be approximated by the gauge within the handle. During the decompression phase, the handle is actively pushed up and away from the chest while the suction keeps the device attached. This active withdrawal characterizes the decompression phase of CPR. The value of this adjunct is uncertain.
retrospectively found that only 10% of prehospital cardiac arrest patients who received chest compression-only CPR survived long term. This compares with a 16% survival rate for patients receiving good-quality chest compressions and ventilations, and a 7% survival rate when no bystander CPR was performed. [83] Hallstrom and colleagues reported that slightly more prehospital cardiac arrest patients survived in the chest compression-only CPR group than in the standard CPR group (14.6% vs. 10.4%).[84] Long-term survival following cardiac arrest with chest compression alone has been reported. Fifteen of the CPR-only cohorts from the Ontario Prehospital Advanced Life Support Study were discharged alive from the hospital, representing 3.6% of all study survivors. [85] However, some patients had hemodynamic compromise, rather than a true arrest, and this may have falsely inflated reported survival rates. Continued efforts to improve and simplify BLS have led to the rationale for a "staged" approach for teaching BLS. [86] While CPR with compressions and ventilations remains the ideal method of maintaining blood flow until the arrival of emergency medical system personnel, chest compressions with an open airway at a rate of approximately 100 per minute is recommended if rescuers are unwilling or unable to perform mouth-to-mouth rescue breathing. [11] Impedance Threshold Valve CPR The reduction of intrathoracic pressures during ACD-CPR led to the recognition that occlusion of the airway during the chest wall decompression phase resulted in an additional decrease in negative intrathoracic pressure, and increased blood return to the chest. [65] Based on this mechanism, a small inspiratory impedance threshold valve (ITV) inserted into any respiratory circuit was developed to occlude the airway selectively during the decompression phase of CPR, without resistance to exhalation or active ventilation. [87] [88] The ITV has been shown to significantly increase vital organ flow when used with either standard CPR or ACD-CPR in a porcine model, and to decrease defibrillation energy thresholds when used together with ACD-CPR. [89] In patients undergoing ACD-CPR, the ITV cohort had significantly increased end-tidal CO 2 , systolic, diastolic, coronary perfusion pressures, and ROSC rates compared with patients treated with ACD-CPR alone. [88] The potential benefits of the ITV are promising. However, comparative data with standard CPR and long-term survival data remain under study. Presently, the ITV is acceptable as an adjunct for use with a cardiac compression-decompression device to augment hemodynamic parameters. However, there are no data at this time to support the use of ITV with standard CPR. Phased Chest and Abdominal Compression-Decompression (Lifestick CPR) Lifestick CPR (Lifestick Resuscitator, Datascope Corporation, Fairfield, NJ) combines the hemodynamic advantages of IAC-CPR and ACD-CPR ( Fig. 17-7 ). The device has adhesive chest and abdominal pads that are connected to an adjustable rigid frame with a handle at each end. The chest and abdomen are compressed in an alternating pattern by a single operator in a seesaw manner. Tang and colleagues recently demonstrated higher resuscitation rates, 48-hour survival, and cerebral recovery with the Lifestick resuscitator compared to conventional chest compressions using a porcine model. [90] Correspondingly, using a mathematical model of adult human circulation, Babbs and colleagues demonstrated improved blood flow and systemic perfusion pressures with phased chest and abdominal compression-decompression compared to standard CPR. [91] Arntz and colleagues recently studied the feasibility, safety, and efficacy of the Lifestick compared with conventional resuscitation in a small cohort of 50 patients. [92] A
Figure 17-7 Lifestick Resuscitator used for active compression-decompression cardiopulmonary resuscitation (ACD-CPR).
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significantly lower incidence of sternal fractures were found at autopsy with the Lifestick when compared to subjects receiving conventional CPR (3 vs. 9; p < 0.05). In addition, a higher proportion of patients with asystole or ventricular fibrillation achieved ROSC in subjects resuscitated with the Lifestick. However, no survival advantage was reported with the Lifestick over conventional CPR. [92] This method may prove to be a practical alternative to standard CPR in the future. However, large-scale clinical data are currently lacking, and the Lifestick Resuscitator remains experimental.
ASSESSMENT OF ONGOING CPR The prognosis for resuscitation of patients in cardiac arrest depends on the no-flow interval before CPR is initiated, the time interval from collapse to defibrillation (if the rhythm is ventricular fibrillation), and the initial cardiac rhythm. Once the resuscitation efforts are initiated, there is no ideal criterion to judge the efficacy of CPR. In most animal and clinical studies, outcome (i.e., resuscitation or death) is the only criterion used. Recent studies have focused attention on assessing the effectiveness of ongoing resuscitation efforts, and identifying indices predictive of successful outcomes. Pulses Once considered a mainstay of CPR, the pulse check has been scrutinized for its reliability. [93] [94] Although femoral artery pulses are frequently assessed by medical personnel during CPR, accurate identification of a central pulse in a collapsed and unresponsive patient is extremely difficult. The clinician should exercise caution when making critical resuscitative decisions based on the presence or absence of a pulse. Palpating the pulse is also not an accurate means of assessing the adequacy of CPR because the pulse is more likely to represent the systolic-to-diastolic pressure gradient rather than the coronary perfusion pressure (CPP). In addition, femoral pulses perceived to be arterial may actually be venous. Blood frequently flows in a retrograde fashion to the lower half of the body during chest compression, because there are no valves in the inferior vena cava. The presence of carotid pulses may indicate forward blood flow with chest compression, but the extent of blood flow and, more importantly, tissue perfusion cannot be gauged by the presence or absence of a pulse. Emerging data support the difficulties associated with pulse check interpretation. Flesche and colleagues studied the ability of trained medical professionals to accurately palpate central pulses in manikins as well as human models. [95] They found that fewer than 10% of medical students and trained rescuers detected an existing pulse in manikins, and it required 6 seconds to identify a pulse in healthy volunteers. Detecting pulses in collapsed and artificially ventilated patients is inherently more difficult. The carotid pulse check should under no circumstance be permitted to cause a delay in the decision to initiate CPR in an obviously lifeless person. Excessive time in locating a pulse and inaccurate determination of the presence of a pulse was reported to cause delays in chest compression or automated external defibrillator (AED) attachment in 10% of cardiac arrest patients. [11] Because of these difficulties, recent guidelines suggest that the "pulse check" should not be taught to lay rescuers. Central Venous Oxygen Saturation The ability to accurately predict ROSC and successful resuscitation based on surrogate markers of perfusion has been intensively studied. Mixed venous oxygen saturation obtained from pulmonary artery (S VO2 ) and central venous oxygen saturation (Sc VO2 ) have been shown to reflect the balance of systemic oxygen delivery (supply) to consumption (demand) in multiple disease states. [96] [97] [98] [99] [100] [101] The ultimate goal of artificial circulatory support is to maintain oxygen delivery as to avoid the complex cascade of events that results in cellular dysoxia and end-organ injury. Although no single marker of perfusion is ideal, oxygen transport variables and mixed venous oxygen saturation provide the clinician with valuable physiologic information. Combined with other clinically important data (e.g., Pet CO2 ), mixed venous oxygen saturation can provide prognostic information as well as help guide the clinician in the post-resuscitative period. Pulmonary artery catheter placement is not necessary to analyze mixed venous blood. A number of studies have supported the use of central venous (right atrial or superior vena cava) blood for mixed venous blood (pulmonary artery) during spontaneous circulation, closed chest CPR, and circulatory failure. [102] [103] [104] [105] Emerman et al. reported no significant differences among pulmonary artery, central, and femoral venous blood gases during closed-chest CPR in animal models. [105] The close association between Sc VO2 and SVO2 allows placement of a central venous catheter as opposed to the more technically demanding pulmonary artery catheter. The fundamentals of oxygen transport are beyond the scope of this text and are described in detail elsewhere. [106] Rivers and colleagues evaluated continuous central venous oxygenation saturations in 100 patients who experienced 68 episodes of cardiac arrest. [107] Central venous saturations were measured continuously by a fiberoptic catheter in the central venous location. ROSC was defined as an aortic blood pressure of at least 60 mm Hg for more than 5 minutes. Patients with a return of spontaneous circulation had a higher initial and statistically higher mean and maximal central venous oxygen saturation than those without a ROSC. No patient attained ROSC without reaching a central venous saturation of at least 30%. Furthermore, a central venous oxygen saturation of greater than 72% was 100% predictive of a ROSC. Coronary Perfusion Pressure As early as 1906, researchers noted the importance of achieving adequate diastolic pressure. [108] During diastole, the aortic pressure exceeds the right atrial pressure, resulting in blood flow to the coronary arteries. CPP represents the pressure gradient between aortic and right atrial pressures as measured during the relaxation phase of standard CPR.[109] [110] The resuscitation literature provides abundant evidence that CPP is the best hemodynamic predictor of ROSC. [10] [110] [111] [112] [113] [114] [115] [116] [117] A CPP of greater than 20 mm Hg in canine models and of greater than 10 mm Hg in swine is very accurate in predicting ROSC after electrical defibrillation. [115] [118] [119] The utility of monitoring CPP during human CPR has also been demonstrated. [ 9] Paradis and colleagues measured the CPP of 100 patients undergoing CPR. Only patients with maximal CPPs of 15 mm Hg or more had ROSC, and the fraction of
331
patients with ROSC was directly proportional to the CPP. Patients achieving a CPP of >25 mm Hg had a >80% likelihood of ROSC. The traditional method of measuring CPP requires placement of a central venous line as well as an aortic arch catheter. The technical demands and time required for line placement, combined with the need for monitoring and signal amplification, make this modality somewhat limited in the everyday practice of emergency medicine. Rivers and colleagues, in an attempt to examine the validity of interchanging arterial sites, concluded that femoral artery relaxation-phase pressure was not statistically different from aortic relaxation-phase pressure. [120] Thus, substitution of a femoral artery catheter for the aortic arch line may encourage the clinical applicability of this potentially useful data. In summary, the aortic diastolic pressure and CPP appear to be the best available criteria for assessing perfusion during CPR and correlate with survival in animal models. Although in the non-research setting, technical and time constraints associated with data retrieval may limit CPP usefulness outside of the research setting, these hemodynamic parameters appear helpful in directing resuscitative efforts. End-tidal Carbon Dioxide Monitoring in Cardiac Arrest The importance of PetCO2 monitoring was first recognized by Ruldolf Eisenmenger in 1929. [121] In a canine CPR model using the "biomotor," Eisenmenger very eloquently described the physiologic importance of monitoring Pet CO2 and correlated subsequent values with the likelihood of "futility." Since then, researchers have made significant strides in defining the basic physiology of carbon dioxide production and removal in cardiac arrest states. [122] Carbon dioxide is a byproduct of cellular metabolism that is eliminated primarily through the lungs. Blood transport occurs primarily as the bicarbonate ion with protein-bound transport contributing to a lesser degree. The partial pressure difference of CO 2 between the pulmonary capillaries and the alveoli accounts for the rapid diffusion of CO 2 into the alveoli. Normally, levels of alveolar carbon dioxide and therefore Pet CO2 are determined by carbon dioxide production, alveolar ventilation, and pulmonary blood flow. During low-flow states, Pet CO2 levels reflect predominantly pulmonary blood flow; in cardiac arrest, the level is determined entirely by the cardiac output generated by
CPR.[123] [124] [125] [126] [127] [128] Falk and associates reported that Pet CO2 levels accurately reflected cardiac output in low-flow and no-flow states in 10 patients in an intensive care unit, thus correla ting Pet CO2 and cardiac output. [127] Correspondingly, Pet CO2 values during CPR may offer prognostic information as to the likelihood of achieving ROSC. Sanders et al. studied the end-tidal CO 2 values in both in-hospital and prehospital cardiac arrest. [129] Resuscitated patients had higher initial Pet CO2 levels (greater than 10 mm Hg). Over 20 minutes, Pet CO2 levels averaged 18 mm Hg in survivors and 6 mm Hg in those who could not be resuscitated. Varon and colleagues reported similar findings; no patient in their study survived either in-hospital or prehospital cardiac arrest with a Pet CO2 level of 5 to 10 seconds, radial artery puncture should not be performed. Be careful to avoid overextension of the hand with wide separation of the digits, because this may compress the palmar arches between fascial planes and give a false-positive result. [51] Barber and associates[47] reported a modified Allen test that is useful in unconscious or anesthetized patients who cannot clench their fists. An Esmarch bandage is used to exsanguinate the hand, and the test is performed as previously described. Time permitting, performance of some variation of the Allen test is desirable before ulnar or radial puncture for cannulation or blood gas sampling. The true predictive value of the Allen test is still questioned, as there are numerous reports of permanent ischemic sequelae, post-cannulation, following a normal Allen test.[49] [52] [53] Notably,
Figure 20-12 Allen test. Before puncturing the radial artery it is important to identify a competent ulnar artery. This can be done as follows: ( 1) The examiner compresses both arteries, and the patient repeatedly makes a tight fist to squeeze all the blood out of the hand. ( 2) The patient then extends the fingers, and the examiner observes the blanched hand. ( 3) Compression of the ulnar artery is released, and the examiner observes the hand filled with blood. If filling does not occur within 5 to 10 seconds, radial artery puncture should not be done. If brisk filling occurs, the test is then repeated with release of the radial artery to assess radial artery patency. If both radial and ulnar arteries demonstrate patency, the wrist may be used for arterial puncture. (From Schwartz GR [ed]: Principles and Practice of Emergency Medicine. Philadelphia, WB Saunders, 1978, p 354. Reproduced by permission.)
other studies have found no ischemic complications following radial artery catheterizations after abnormal Allen tests. [35] [54] Although there are no guarantees against digital ischemia following radial artery cannulation, [55] the finding of an abnormal Allen test should result in the search for an alternative site. If available, this alternative arterial site should be used and the abnormal Allen test documented for medicolegal reasons. Once adequate collateral flow has been ascertained, arterial puncture may be performed. At the wrist, the radial artery rests on the flexor digitorum superficialis, flexor pollicis longus, and pronator quadratus, and against the radius. [45] The pulsation of the artery should be isolated on the palmar surface of the wrist. The radial artery is more superficial closer to the wrist and provides a more consistent cannulation due to fixation and less mobility. Dorsiflexing the wrist at about a 60° angle over a towel or sandbag, preferably
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Figure 20-13 Percutaneous arterial cannulation at the wrist. The catheter unit is advanced 1 to 2 mm into the vessel lumen after blood first appears in the flash chamber. While the needle is fixed, the catheter is threaded over the needle. (From Beal JM [ed]: Critical Care for Surgical Patients. New York, Macmillan, 1982. Reproduced by permission.)
fixing the wrist to an arm board, will also significantly help isolate the artery. This degree of preparation should be considered standard when time for setup is allowable ( Fig. 20-13 ). [34] [35] Antegrade radial artery cannulation may be accomplished in infants and children when radial arteries are obstructed and retrograde blood flow is observed during a failed cut down attempt at standard retrograde arterial cannulation. [56] Additionally, displacement of perivascular interstitial fluid in neonates and bright light makes the course of the artery visible so that under direct vision, cannulation of the artery becomes as easy as venous cannulation. [57] Doppler ultrasound use on select patients with poor peripheral pulses may facilitate percutaneous radial artery cannulations and minimize the number of punctures needed for placement. [27]
The ulnar artery is seldom used because its smaller size makes it more difficult to puncture than the radial artery. At the wrist, the ulnar artery runs along the palmar margin of the flexor carpi ulnaris in the space between it and the flexor digitorum sublimes. [45] Caution is necessary because the artery runs next to the ulnar nerve as both pass into the hand just radial to the pisiform bone. The ulnar artery can also be made more accessible with dorsiflexion of the wrist. Brachial The brachial artery appears safe for arterial puncture, but it does not have the anatomic benefit of the collateral circulation found in the wrist. The brachial artery begins as the continuation of the axillary artery and ends at the head of the radius, where it splits into the ulnar and radial arteries. The preferred puncture site of the brachial artery is in or just proximal to the antecubital fossa. In this region the artery lies on top of the brachialis muscle and enters the fossa underneath the bicipital aponeurosis with the median nerve occupying the medial side of the artery ( Fig. 20-14 ). Both the radial and axillary arteries are preferred upper extremity sites to the brachial artery. There is an increased ischemic complication risk from reduced collateral circulation as well as the necessity of maintaining the arm in extension for puncture or prolonged cannulation. Despite all of these theoretical possibilities, the safe cannulation of the brachial artery has been demonstrated by some investigators.[58] Bazaral et al. found only one minor thrombotic occurrence in more than 3000 brachial artery
Figure 20-14 The right brachial artery and its branches. (From Christensen JB, Telford IR: Synopsis of Gross Anatomy. New York, Harper & Row, 1966. Reproduced by permission.)
catheterizations over 3 years in cardiac surgery patients. [59] A longer catheter (10-cm) is required for the brachial artery so that sufficient length is available to traverse the elbow joint. Axillary Axillary artery cannulation as described by Adler and coworkers [60] is also a safe means of monitoring arterial blood pressure for a long time. The left axillary artery is preferred in order to decrease the possibility of cerebral embolization of flush solution or thrombus. The path from the left subclavian to the left carotid artery is less direct than on the right side, whereas the vertebral arteries are equally vulnerable. To cannulate the axillary artery, the arm is placed in 90° abduction. The axillary pulse is then palpated high in the axilla between the insertion of the pectoralis major and the deltoid muscles. The artery may then be cannulated percutaneously, and a Seldinger guidewire technique with a longer catheter (18-ga, 10-cm) is strongly recommended. This site is seldom used and is unfamiliar to many clinicians. Due to positioning and extra time for setup, this site should be avoided in the ED. There are few reported complications from catheter placement in the axillary artery. [61] Dorsalis Pedis The dorsalis pedis artery continues from the anterior tibial artery and runs from approximately midway between the malleoli to the posterior end of the first metatarsal space, where it forms the dorsal metatarsal and deep plantar arteries. The lateral plantar artery, a branch of the posterior tibial,
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Figure 20-15 A 20-ga catheter in the dorsalis pedis artery, illustrating the relationship to surrounding tendons. The catheter is secured with Steri-Drape. Splinting is not needed. (From Johnstone RE, Greenhow DE: Catheterization of the dorsalis pedis artery. Anesthesiology 39:655, 1973. Reproduced by permission.)
passes obliquely across the foot to the base of the fifth metatarsal. The plantar arch is completed where the lateral plantar artery joins the deep plantar artery between the first and second metatarsals. On the dorsum of the foot, the dorsalis pedis artery lies in the subcutaneous tissue parallel to the extensor hallucis longus tendon, and between it and the extensor digitorum longus ( Fig. 20-15 ). [62] The artery should be cannulated in the mid-foot region. Although this vessel is amenable to cutdown, the vascular anatomy of the foot is quite variable. This is of no consequence if a pulse can be palpated, but Huber, in his dissection of 200 feet, noted the dorsalis pedis artery was absent in 12% of patients. [63] In 16% of patients, the dorsalis pedis artery provides the main blood supply to the toes. [64] Although the dorsal pedis and posterior tibial arteries form similar collateral foot circulation as in the hand, the nature of advancing vascular disease makes this a more difficult cannulation, with increased complication compared to the wrist. Nevertheless, this site has its major utility in pediatric monitoring cases. Attempts to predetermine collateral flow with a modified Allen test using the posterior tibial and dorsalis pedis arteries is not as easily performed in the foot as in the hand, nor is there good data to prove its validity. Monitoring problems also exist with this artery. The pressure wave obtained with an electronic transducer attached to the dorsalis pedis artery will be 5 to 20 mm Hg higher than that of the radial artery and, in addition, will be delayed by about one tenth of a second. [62] Femoral The femoral artery is the second most commonly used vessel for prolonged arterial cannulation. Based on its ease of cannulation and low record of complication, it has been called the vessel of choice for arterial access. [61] [65] [66] Along with the axillary artery, the femoral artery more closely resembles aortic pressure waveforms than those from any other peripheral site. [5] The femoral artery is the direct continuation of the iliac artery and enters the thigh after passing below the inguinal ligament. Arterial puncture must always occur distal to the ligament to prevent uncontrolled hemorrhage into the pelvis or peritoneum. [67] The artery may be easily palpable midway between the public symphysis and the anterior superior iliac spine. One can also place the thumb and fifth finger on the aforementioned distal sites and locate the artery underneath the middle knuckle. When puncturing this vessel, care must be taken to avoid the femoral nerve and vein, which create the lateral and medial borders, respectively ( Fig. 20-16 ). A longer, larger diameter catheter is required for accurate monitoring of the femoral artery due to the relatively greater depth at which it lies and greater vessel size. Only the Seldinger technique is recommended for this site, enabling placement of a 15- to 20-cm plastic catheter for prolonged monitoring. Use of catheter-through-the-needle or over-the-needle catheter devices should be avoided because cannulating the vessel is difficult due to its distance beneath the skin. Leakage around the catheter can occur with catheter-through-the-needle or over-the-needle catheter devices due to high arterial pressures and loose fit of the cannula in the hole in the vessel wall. Regardless of the device used, the needle should enter the skin at an angle of about 45° instead of the usual 15 to 20°. The extremely large ratio of arterial diameter to catheter diameter is thought to beneficially reduce the incidence of thrombosis, particularly total occlusion. However, occlusions have been reported with femoral cannulation for monitoring purposes. [68] A commonly postulated disadvantage of this site is the possibility of increased bacterial contamination because of its proximity to the warm, moist groin and perineum; however, no studies confirm this hypothesis. [69] The femoral area is inconvenient for any patient who is awake and mobile, or if the patient is able to sit in a chair. If the patient is that mobile, then risk/benefit from invasive monitoring should be reconsidered. Despite theoretic difficulties, some large hospitals use femoral arterial lines almost exclusively, and the intensive care nursing staff is often
more comfortable caring for these lines than those at other sites. Umbilical and Temporal In the neonate, arterial access can be accomplished through the umbilical artery for a short time. After this artery closes, the temporal artery provides a safe alternative. Prian described the use of the temporal artery, noting its accessibility and the lack of clinical sequelae if it undergoes thrombosis. [70] The cutdown method should be used with a 22-ga catheter after the artery's course has been traced with an ultrasonic flow detector. Because of the increasing accuracy of ear oximeters and the use of capillary blood gases for pH determination, prolonged arterial cannulation will become less frequent during infant care. Further discussion of infant arterial cannulation is provided in Chapter 19 .
COMPLICATIONS Long-term arterial cannulation is safe if care is taken to avoid complications. Almost all difficulties one may encounter can be avoided or their incidence markedly decreased by adhering to a few simple principles. Reported clinical sequelae of arterial puncture and cannulation range from simple hematomas to life-threatening infections and exsanguination. Other potential complications include ischemia, arteriovenous fistula, and pseudoaneurysm formation. The incidence of complications varies with the site selection, method of
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Figure 20-16 The right femoral vessels and some of their branches. The femoral nerve (not shown) lies lateral to the artery and may be deep to the artery. (From Warwick R, Williams PL [eds]: Gray's Anatomy, 35th ed. Edinburgh, Churchill Livingstone, 1973, p 676. Reproduced by permission.)
cannulation, and clinician's procedural skill and experience. Early detection of complications is greatly aided by enhanced vigilance and concern of the patient's clinicians and nurses. It is difficult to compare complication rates at various sites, because most published studies have primarily used the radial artery. No studies have compared the approach and complication rates of arterial catheters in the ED compared to ICU or to OR uses. Over 24 months, 2119 ICU patients had an arterial catheter placed at admission: 52% at the radial site and 45% at the femoral site. The most common complication was vascular insufficiency (4%), followed by bleeding (2.1%) and infection (0.6%). There was no difference reported for infection rates for femoral vs radial sites. [71] There are reports of complications from arterial puncture for procedures unrelated to long-term cannulation such as arteriography or simple arterial puncture for blood sampling as routinely performed in the ED. In a study of 2400 consecutive cardiac catheterizations over a 12-month period, complications occurred in 1.6% of patients including 17 needing vascular repair and 28 needing transfusion. [72] A commonly encountered problem is hematoma formation at the puncture site. Zorab [22] reported this complication in 50% of catheterizations. The bruising was of minimal clinical significance in Zorab's study, but leakage, when it occurs around the catheter or from the puncture site after the catheter's removal, can be dangerous. Compression neuropathy secondary to bleeding has been reported after brachial artery puncture in anticoagulated patients; in some cases, surgical decompression has been necessary. [9] The large amount of soft tissue surrounding the femoral artery makes bleeding in this area difficult to control. Large hematomas are
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not uncommon after femoral artery catheterization; indeed, Soderstrom and associates [65] reported two cases of bleeding that required transfusion after femoral puncture. More commonly, hematomas are painful, slow to resolve, and prone to infection. Multiple-site punctures and inadequate pressure applied for sufficient time account for most hematomas. Furthermore, hematomas may make further procedures in the groin difficult to complete. Thrombotic occlusion after radial arterial cannulation occurs in nearly 50% of infants and small children; however, ischemia from occlusion is rare because of collateral blood supply from the ulnar artery. [73] Insertion sites closest to the bend of the wrist increase the chances of maintaining patency. Nonpatency is 4 times more likely with insertion in sites =3 cm above the bend in the wrist. [74] Slogoff et al. [54] described 1700 cardiovascular surgical patients who underwent radial artery cannulation without any long-term, ischemic complications, despite evidence of radial artery occlusion after de-cannulation in more than 25% of patients. Serious complications after radial artery cannulation are extremely rare in the absence of contributing factors, such as preexisting vasospastic arterial disease, previous arterial injury, protracted shock, high-dose vasopressor administration, prolonged cannulation, or infection. [53] [75] Prevention of bleeding complications may be accomplished with frequent careful inspection of the puncture site and with the use of prolonged compression after removal of the catheter or needle. Firm pressure should be maintained for =10 minutes after removal of a peripheral artery catheter and longer after femoral cannulation or if the patient is anticoagulated. Five minutes of pressure is sufficient after puncture for a blood gas sample in an individual with normal coagulation. Exsanguination, a related complication, may occur if the arterial line apparatus becomes disconnected. This is more common in the obtunded or combative patient, and restraints are often required for patients with indwelling arterial cannulas. Exsanguination should not occur if tight connections are maintained throughout the system and if frequent, careful inspections of both the circuit and the patient are made. Meticulous attention to aseptic technique is necessary during insertion and catheter maintenance to minimize the risk of catheter-related infection. [76] [77] Serious infections rarely complicate arterial cannulation. Most simple interventions can reduce the risk for serious catheter-related infection. The strongest supportive evidence is from usage of full barrier precautions during catheter insertion, specialized nursing care, and newer generation catheters with antiseptic hubs or antimicrobial agent impregnated catheters. [76] The incidence of catheter-related infections increases with prolonged cannulation. [69] Catheters placed with sterile technique have an extremely low rate of infection up to 96 hours. Catheters changed over a guidewire every 96 hours have an infection rate of about 10% at the radial and femoral sites.[66] Most infections begin locally at the puncture site and remain localized, although systemic sepsis has been reported. [75] Radial and femoral sites have a similar incidence of complications, but axillary cannulations seem to have a much higher incidence of infection (although no large studies of cannulation at this site exist). [70] [78] Arterial cannulas are more prone to infectious complications than other vascular catheters. Many mechanisms have been proposed for this occurrence. [77] [ 79] The arterial pressure monitoring system usually consists of a long column of fairly stagnant fluid and is subject to frequent manipulation. Stamm and colleagues [78] found that patients were at greater risk for systemic infection if they had an arterial line and required frequent blood gas determinations than if they had the cannula alone. The sampling stopcock is a site of frequent bacterial contamination. The risk of infection also increases as the duration of cannulation is prolonged. Older studies recommend that catheters be changed after 4 days if continued monitoring is necessary. [78] [79] In addition, Makai and Hassemer [79] recommend changing the entire fluid-filled system, including transducer chamber-domes and continuous flow devices, every 48 hours. However, other risks for noninfectious concerns increase with more frequent catheter and site changes when based solely on length of catheterization of a site. Therefore, daily evaluation of the site is advised and catheter change should not be mandatory until 7 to 8 days, if the site remains clean. Shinozaki and coworkers [80] demonstrated a marked reduction in equipment contamination when the continuous flush device was located just distal to the transducer, as opposed to closer to the three-way stopcock used for sampling. This setup reduces the length of the static column of fluid between the sampling stopcock and the transducer. As mentioned previously, a drop of iodophor or antibiotic ointment applied to the puncture site decreases the incidence of local wound infection. [39] This technique has drawn a great deal of criticism, however. The current standard is a clean, dry dressing, not an occlusive type. An antibiotic or silver impregnated catheter is always recommended for long-term placements. Thrombosis of the vessel in which the cannula is placed is another frequently encountered problem. The incidence with which this occurs varies with the method used
to determine the presence of the clot. Bedford and Wollman [14] found a >40% occlusion rate when radial artery catheters were left in place for >20 hours. All of these occluded vessels eventually re-cannulized. Angiographic studies show deposition of fibrin on 100% of the catheters left in place for >1 day, although clinical evidence of ischemia secondary to occlusion with thrombus present occurs in 10 kg) and those with higher CVPs (>10 cm H2 O). With infants and children, needle puncture
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occurs at the apex of the triangle bordered by the two heads of the sternocleidomastoid muscle and the clavicle. Similar to the approach for adults, one passes a 22-ga needle attached to a 2- to 5-mL non-Luer-Lok syringe into the skin at a 45-degree angle and directs it caudally and laterally toward the ipsilateral nipple. The vessel is usually entered at a depth of 1 to 2 cm. The locator needle is then withdrawn, and a 17- to 19-ga needle is inserted into the skin until the IJ vein is penetrated. Posterior and anterior routes.
For the posterior approach, the skin is entered at the lateral edge of the sternocleidomastoid muscle one third of the way from the clavicle to the mastoid process (see Fig. 22-14 ). The locator needle is directed caudally and medially toward the sternal notch until blood is aspirated. To perform the anterior approach, the course of the carotid is identified and marked by the index and middle fingers (see Fig. 22-14 ). [82] The small needle should then enter the skin at the midpoint of the medial aspect of the sternocleidomastoid muscle. The needle is directed at an angle of 30 to 45 degrees to the coronal plane caudally toward the ipsilateral nipple. The proximity of the carotid artery in the anterior approach may prohibit venous cannulation without carotid puncture. [49] Doppler ultrasound can facilitate difficult IJ cannulation, a matter discussed in more detail later and in Chapter 69 .[83] External Jugular Vein Approach Positioning.
With the patient in the Trendelenburg position, the EJ vein is distended by instructing the patient to perform a Valsalva maneuver and then tamponading the vein just cephalad to the clavicle with a finger. Venipuncture.
The vein is approached from the side while slight traction is placed on the vein to stabilize it. The needle is advanced at a small angle from the skin plane (about 10 degrees) until the operator feels it "pop" into the lumen of the vein. The needle or catheter should be advanced slightly after feeling the pop to ensure intraluminal placement. As discussed later, use of the EJ vein as a site for central vein access requires the use of a guidewire. Femoral Vein Approach Positioning and needle orientation.
The patient must be supine. The femoral pulse is identified and the scout needle (at least 4.4 cm length) is inserted at 45 degrees to the skin in a cephalic direction just medial to the femoral pulsation. Because CPR can produce venous pulsations, unsuccessful venous aspiration medial to the pulsations should be followed by an attempt directly over the pulsations. Venipuncture.
During needle advancement, negative pressure is maintained within the syringe at all times while the needle is under the skin. The needle is directed posteriorly and advanced until the vein is entered, as identified by a flash of dark, nonpulsating blood. If the vessel is penetrated when the syringe is not being aspirated, the blood flash may be seen only as the needle is being withdrawn. The femoral vein lies just medial to the femoral artery at the level of the inguinal ligament. It is closer to the artery than many clinicians appreciate. As the vein progresses distally in the leg, it runs closer to, and almost behind, the femoral artery (see Fig. 22-3 ). This anatomical fact should be considered if the cannulating needle is introduced more than a few centimeters distal to the inguinal ligament. Basilic and Cephalic Approach Venipuncture.
The basilic and cephalic venous systems are entered through the large veins in the antecubital fossa (see Fig. 22-4 ). Tourniquet placement aids venous distention and initial venous puncture. When veins are not visible, they may be reached with a cutdown procedure, as described in Chapter 23 . The basilic vein, located on the medial aspect of the antecubital fossa, is generally larger than the radially located cephalic vein. Furthermore, the basilic vein generally provides a more direct route for passage into the axillary vein, subclavian vein, and SVC.
CATHETER PASSAGE TECHNIQUE Once there is a venous flashback into the syringe, it is detached from the needle, and a catheter is passed either via the Seldinger technique or, alternatively, over or through the needle. Removing the syringe must be done with care to avoid dislodging the needle tip from the lumen of the vein. If the syringe is tightly attached to the needle, a hemostat may be used to grasp and secure the needle hub during removal of the syringe. Needle tip displacement may also occur if blood specimens are drawn at this time. Hence, it is best to delay blood sampling until the catheter has been advanced. The needle hub should be occluded with the thumb to avoid air embolism.
SPECIAL CONSIDERATIONS FOR THE FEMORAL AND SMALLER VESSELS Femoral Vein Approach Once in the femoral vein, the needle is stabilized; often, a hemostat is helpful for holding the needle during removal of the syringe. A premeasured section of a 90-cm catheter may then be inserted using a through-the-needle system. One determines the appropriate length by holding the catheter over the patient's body and estimating the distance from the skin puncture site to the right atrium. Contamination of the catheter must be avoided while this maneuver is performed. Once the catheter is placed, it is secured with sutures and dressed in the same manner as other central lines. In situations requiring rapid volume infusion, in the absence of intra-abdominal trauma, the femoral vein may be cannulated with a sheath introduced via the guidewire technique. The introducer will allow rapid transfusion of large volumes of blood or crystalloid solution for fluid resuscitation. The femoral vessels may also be cannulated under direct visualization using a cutdown technique (see Chapter 23 ). External Jugular Vein Approach Central venous catheterization via the EJ vein is time consuming and often difficult. Use of the EJ vein for achieving
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Figure 22-15 Insertion of a catheter over a wire via the external jugular vein. Successful passage may require many attempts and manipulations of the J wire to navigate turns and valves. (From Blitt CD, Wright WA, Petty WC: Central venous catheterization via the external jugular vein, a technique employing the J-wire. JAMA 229:817, 1974. Reproduced by permission.)
central venous access requires use of a guidewire. After cannulation of the vein and intraluminal placement of the guidewire, the guidewire is advanced into the thorax by rotating and manipulating the tip into the central venous circulation ( Fig. 22-15 ). Guidewire advancement is the most difficult and time-consuming portion of the procedure, and this time constraint limits the usefulness of the technique in an emergency. A small-radius J-tipped wire, a distended vessel lumen, and exaggeration of patient head tilt, coupled with skin traction, may facilitate successful guidewire passage. Partially withdrawing the wire and twisting it 180° before readvancing the tip may also be helpful. Basilic and Cephalic Approach Passage of a catheter into the central circulation is difficult using the basilic and cephalic routes and failure is common. The cephalic vein may terminate inches above the antecubital fossa or bifurcate before entering the axillary vein, sending a branch to the EJ vein. The cephalic vein may also enter the axillary vein at right angles, defeating any attempt to pass the catheter centrally. Furthermore, both the basilic and cephalic systems contain valves that may impede catheterization. Abduction of the shoulder may help to advance the catheter if resistance near the axillary vein occurs. The incidence of failure to place the catheter in the SVC ranges from a high of 40% to a low of 2%. [40] [84] The greatest success rate (98%) reported was obtained with slow catheter advancement with the patient in a 45° to 90° upright position. [40] Flexible catheters were introduced into the basilic vein until the tip was judged to be proximal to the junction of the cephalic and basilic veins and distal to the junction of the IJ vein with the innominate vein. The wire stylet was withdrawn 18 cm, and the catheters were advanced slowly 1 cm at a time, with 2 seconds allowed between each 1-cm insertion. The natural flexibility of the Bard catheters contributed to negotiation into the SVC when the patient was upright. This time-consuming technique is contraindicated when the patient cannot tolerate an upright position.
ASSESSING LINE PLACEMENT Once the catheter has been passed, it must be carefully secured. All tubing and connections should first be checked for tightness to prevent air embolism, fluid loss, or bleeding. The technique for securing a catheter depends on the type of equipment and the site of puncture. In general, all catheters should be secured with sutures (or skin staples [85] ) and a sterile dressing placed. Most systems have some type of anchoring device to simplify securing of the catheter. Since dressings are inspected and changed periodically, it is prudent to place a simple dressing, avoiding excessive amounts of gauze and tape. An effective method for securing an IJ catheter is shown in Figure 22-16 . Care is taken to protect the skin against maceration. Transparent dressings made of polyurethane are popular and simple. They also yielded a lower rate of catheter colonization than newer hydrocolloid dressings in a prospective, randomized, controlled trial. [86] Before the infusion of fluids, the IV fluid reservoir should be lowered below the level of the patient's right atrium and the line checked for backflow of blood. The free backflow of blood is suggestive, but not diagnostic, of intravascular placement. However, backflow may occur with a hematoma or a hemothorax if the catheter is free in the pleural space. A pulsatile blood column may be noted if the catheter has been inadvertently placed into an artery. Less pronounced pulsations may also occur if the catheter is advanced too far and reaches the right atrium or ventricle. Pulsations also may be noted with changes in intrathoracic pressure due to respirations, although these pulsations should be at a much slower rate than the arterial pulse. A final method of checking intravascular placement is to attach a syringe directly to the catheter hub and aspirate venous blood. It is also advisable to
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Figure 22-16 Internal jugular line secured by looping around the ear. (From Boulanger M, et al: Une nouvelle voie d'abord de la veine jugulaire interne. Can Anaesth Soc J 23:609, 1976. Reproduced by permission.)
ensure that the catheter is easily flushed with a heparin solution, if no heparin sensitivity on the part of the patient exists. This carries the additional benefit of removing air from the system. Radiographs are also always indicated to verify catheter location and assess for potential complications, except for routine femoral line placements. In an awake patient, infusing fluids via a catheter tip positioned in the internal jugular vein may produce an audible gurgling sound or flowing sound in the patient's ear. [87] Radiographs Following placement of lines involving puncture of the neck or thorax, the lungs should be auscultated to detect an inequality of lung sounds suggestive of a pneumoor hemothorax. A chest film should be obtained as soon as possible, checking for hemothorax, pneumothorax, and catheter tip position. Because small amounts of fluid or air may layer out parallel to the x-ray plate with the patient in the supine position, the film should be taken in the upright or semi-upright position whenever possible. Proper catheter tip position is shown in Figure 22-17 . Misplaced catheters should be repositioned. In ill patients, a rotated or oblique projection on a chest radiograph may be obtained, and the clinician may be confused as to the proper position of the catheter ( Fig. 22-18 ). In such cases, a repeat radiograph is necessary. A misplaced catheter tip is usually obvious on a properly positioned standard posteroanterior (PA) chest radiograph, but occasionally the injection of contrast material may be required. For example, a catheter in one of the internal thoracic veins may simply appear more lateral than expected, but because of the close proximity of these veins and the superior vena cava, malposition may not be appreciated by this subtle finding. Postprocedure radiographs are not always warranted for routine replacement of catheters over guidewires. If such patients
Figure 22-17 A chest film showing the proper catheter tip placement in the superior vena cava (arrow). The tip should not lie within the right atrium or the right ventricle.
are stable and hemodynamically monitored, radiography may be safely deferred in the absence of apparent complications or clinical suspicion of malposition. not standard to perform a radiograph following femoral line placement.
[88]
It is
Redirection of Misplaced Catheters Improper catheter tip position occurs commonly. It has been reported that only 71% of subclavian catheters are located in the SVC on the initial chest film. [122] Complications of improper positioning include hydrothorax, hemothorax, ascites, [123] chest wall abscesses, [124] embolization to the pleural space, [125] and chest pain. [126] More commonly, improper location yields inaccurate measurements of the CVP or is associated with poor flow caused by kinking. [127] An unusual complication caused by improper tip position is cerebral infarction, which can occur following inadvertent cannulation of the subclavian artery. [128] Misdirection or inappropriate positioning of the tip of a central venous catheter is not uncommon. These events if promptly recognized and corrected represent inconsequential complications. Loop formation, lodging in small neck veins, tips directed caudally, and innominate vein position are common problems. Misplaced catheters should be repositioned as soon as logistically possible. If the catheter is being used for fluid resuscitation, the malposition may be tolerated for some time. If vasopressors or medications are infused, it is more critical to properly position the catheter tip. A number of options are available to remedy malpositioning. One strategy is to insert a 2 Fr Fogarty catheter through the lumen of the central line, advancing it 3 cm beyond the tip. The entire assembly is withdrawn until only the Fogarty catheter is in the subclavian vein. One milliliter of air is injected into the balloon, and the Fogarty catheter is advanced. It is hoped that the
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Figure 22-18 A chest radiograph should be routinely taken to assess position of a central catheter introduced via the chest or neck. A, In this case a poorly positioned patient produced a rotated and oblique film, and the catheter (black arrow) appeared, at first glance, to be in the correct position in the right subclavian vein. The supine position of the patient did not allow identification of an early hydrothorax (white arrow). B, A repeat radiograph shows the obvious intrapleural position of the catheter, and a large hydrothorax after infusion of 2 liters of saline.
blood flow will direct the assembly into the SVC. The balloon is deflated and the central line is advanced over the Fogarty catheter, which is then withdrawn.
[ 89]
One anecdotal strategy is to withdraw the catheter until only the distal tip remains in the cannulated vessel. This measurement is best appreciated by comparing the indwelling catheter length with another unused catheter. The clinician then simply readvances the catheter, hoping that it becomes properly positioned. Other manipulations with guidewires have been suggested, but often reinsertion with another puncture is required for the misplaced catheter to be positioned properly.
ULTRASOUND-GUIDED CENTRAL VENOUS ACCESS In maximizing the success and minimizing the complications of central venous access, there is no substitute for experience. However, some patients will present challenges to even the most seasoned clinician. Anatomic (skeletal or vascular) abnormalities, whether congenital or acquired, may be encountered and can thwart successful cannulation. When time permits, difficult cases may be simplified by using a Doppler ultrasound device to identify the location of major veins. The course of these vessels can be marked on the skin surface and used as an anatomic guide during needle placement. Alternatively, more sophisticated ultrasound imaging systems have been adopted for guiding venous cannulation. The most commonly described imaging tool is a handheld 7.5 MHz real-time mechanical sector transducer with an attached needle guide. The device is coupled with a small video display ( Fig. 22-19 ). To use the instrument, the nonsterile transducer is covered with acoustic coupling gel and placed inside a sterile sheath. Additional sterile gel is placed on the skin over the site being imaged, and the unit is used to determine the location, orientation, and diameter of the target vessel. When accessing the jugular or femoral systems, this is done by placing the transducer according to traditional puncture site landmarks. Imaging the subclavian vein from the IC approach is more difficult, but can be attempted by identifying the axillary vessels at their most proximal position under the distal clavicle and then following the vessels medially as they course beneath the clavicle. [90] Once the vessel is identified, the overlying skin may be marked for later venipuncture or a needle and syringe secured to the transducer for immediate cannulation. Under ultrasound guidance, the needle is advanced through the skin and SQ tissue toward the target vessel. Once the needle is in close proximity to the vessel, one will see compression of the vein. Once the vessel wall has been penetrated, the vein will refill with blood and assume its original shape. The transducer can then be detached and cannulation proceeds. Most prospective analyses of the device have examined IJ vein cannulations [91] [92] [93] and have uniformly suggested advantages to the technique. Ultrasound-guided attempts demonstrated greater overall success, as well as an increased rate of successful first punctures. Clinically significant complications were too infrequent to definitely conclude greater patient safety with the ultrasound technique; studies specifically examining complications demonstrated less frequent hematoma formation and inadvertent arterial puncture. [90] [91] Ultrasound guidance may assume greater prominence in central venous access in the future. However, given the generally favorable success rate and low complication rate of traditional access techniques, the relative infrequency of central venous cannulation in many EDs, and the considerable cost of the device, the routine role of ultrasound imaging guidance remains uncertain.
COMPLICATIONS The medical literature is replete with reports of the complications of large vein venipuncture. Some are minor and inconsequential, such as hematoma formation, while others are serious and life-threatening, such as hemothorax. No clinician can expect to routinely perform these procedures and be complication-free. Common complications for the different approaches are summarized in Table 22-6 and Table 22-7 . Key injuries categorized by organ system and by approach are discussed in the sections that follow. The FDA has released a three-volume video entitled "CVC Complications," which was sent to all hospitals where such catheters are placed. It is also commercially available from the Internet (at www.fda.gov). Published rates vary widely and complication rates depend on one's definition. One 3-year retrospective review
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Figure 22-19 A, Surface ultrasound-directed central vein identification. A handheld transducer allows noninvasive localization of veins, in this case the subclavian. The device shown includes a needle guide, which allows simultaneous visualization and penetration of a targeted vessel. B, Surface ultrasound image of the subclavian artery (left) and vein (right). (Courtesy of Irene R. Skolnick, Dymax Corp, Pittsburgh.)
of all central catheters placed in the ED (SC, IJ, and femoral lines) reported a mechanical complication rate of 3.5%, or 22 of 643 lines placed. [94] Complication was defined as pneumothorax, hematoma, line misplacement, hemothorax, or any issue with the CVC (excluding infection or thrombosis) that required an inpatient consultation. In general, failure and complication rates increase as the number of percutaneous punctures increase. Pulmonary Complications Pulmonary complications of subclavian and internal jugular venipuncture include pneumothorax, hemothorax, hydrothorax, hemomediastinum, hydromediastinum, tracheal perforation, and endotracheal cuff perforation. Pneumothorax is the most frequently reported complication, occurring in up to 6% of subclavian venipunctures. [95] Initially the importance of this complication was minimized, but reports of fatalities caused by tension pneumothorax, bilateral pneumothorax, and combined hemopneumothorax followed.[96] [97] One would expect a higher incidence of pneumothorax if the procedure were performed during CPR or positive-pressure ventilation. A small pneumothorax can quickly become a life-threatening tension pneumothorax under positive-pressure ventilation. The treatment of a catheter-induced pneumothorax is controversial, but certainly not all patients will require a formal tube thoracostomy. [98] Some authors conclude that many stable outpatients exhibiting a pneumothorax following central venous catheter insertion can often be successfully managed with observation alone (60% in their series) or catheter (pigtail/Heimlich valve) aspiration, reserving large tube thoracostomy for refractory cases or emergent settings ( Fig. 22-20 ). Critically ill patients, or those on mechanical ventilation will likely require invasive treatment of a catheter-induced pneumothorax. Hemothorax may occur following subclavian vein or artery laceration, pulmonary artery puncture, or intrathoracic infusion of blood. Hydrothorax occurs as a result of infusion of IV fluid into the pleural space. Hydromediastinum is an uncommonly reported complication that is potentially fatal. [99] Vascular/Bleeding Complications The most common vascular complication is inadvertant artery puncture. This is usually easily recognized and controlled with simple compression. Rarely an artery is lacerated to an extent that bleeding is significant and arterial repair is necessary. In cardiac arrest, low flow, or shock states, arterial puncture may not be obvious, and arterial cannulation and the intra-arterial administration of medications has occurred. When the systolic blood pressure rises, arterial pulsations become more obvious. In critically ill patients, however, this complication may escape detection for some time. The subsequent development of ischemia or thrombosis of an artery that has been cannulated or injected with detrimental medication reflects the blind nature of this procedure in an emergency. Air embolism is a very rare, but potentially serious complication from any central venous cannulation. Undoubtedly, minor and clinically inconsequential amounts of air enter the venous circulation during many cannulation procedures. Maintaining constant occlusion (with the operator's finger) of all needles that are located in central veins will minimize this occurrence. A 14-ga needle can transmit 100 mL of air per second with a 5-cm H 2 O pressure difference across the needle. [100] Air embolism may occur if the line is open to air during catheterization or if it subsequently becomes disconnected. The recommended treatment is to place the patient in the left lateral decubitus position to relieve air bubble occlusion of the right ventricular outflow tract. [101] If this is unsuccessful, aspiration with the catheter advanced into the right ventricle has been
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TABLE 22-6 -- Complications of Central Venous Access General Vascular Air embolus Adjacent artery puncture Pericardial tamponade Catheter embolus Arteriovenous fistula Mural thrombus formation Large vein obstruction Local hematoma Infectious Generalized sepsis Local cellulitis Osteomyelitis Septic arthritis Miscellaneous
Dysrhythmias Catheter knotting Catheter malposition Subclavian and internal jugular approaches Pulmonary Pneumothorax Hemothorax Hydrothorax Chylothorax Hemomediastinum Hydromediastinum Neck hematoma and tracheal obstruction Tracheal perforation Endotracheal cuff perforation Neurologic Phrenic nerve injury Brachial plexus injury Cerebral infarct Femoral approach Intra-abdominal Bowel perforation Bladder perforation Psoas abscess advocated.[102] Emergent cardiothoracic surgical consultation may also be warranted. Catheter embolization resulting from shearing of a through-the-needle catheter by the needle tip is a serious and generally avoidable complication. Embolization can occur when the catheter is withdrawn through the needle or if the guard is not properly secured. Because through-the-needle catheters are less commonly need, this problem is rare. However, when present, subsequent adverse events occur frequently following embolization and include arrhythmias, venous thrombosis, endocarditis, myocardial perforation, and pulmonary embolus. [54] The mortality rate in patients who did not have these catheters removed has been reported to be as high as 60%. [103] Transvenous retrieval techniques are usually attempted and followed by surgery if they are unsuccessful. [104] Entire guidewires may also embolize to the general circulation if the tip is not always secured by the operator. Perforation or laceration of vascular structures may cause hemothorax, hemomediastinum, and volume depletion. These are rarely serious complications, but fatalities have been reported. Surgical repair is occasionally required. [105] Arteriovenous fistula formation has also been reported. [106] Delayed perforation of the myocardium is a rare but generally fatal complication of central venous catheterization by any route. [107] [108] The presumed mechanism is prolonged contact of the rigid catheter with the beating myocardium. [109] The catheter perforates the myocardial wall and causes tamponade either by bleeding from the involved chamber or infusion of IV fluid into the pericardium. The right atrium is involved more commonly than the right ventricle. [76] All who insert such catheters or care for such patients, or both, should be aware of this deadly complication, which results in profound deterioration with hypotension, shortness of breath, and shock. Emergent echocardiography, pericardiocentesis, and operative intervention by a chest surgeon all may be required for patient salvage. This can also occur with misplacement of the central venous line in the pericardiophrenic vein. [110] Fortunately this complication is preventable by using a postinsertion chest film to confirm catheter tip position and repositioning any catheter if the tip is within the cardiac silhouette. Catheter knotting or kinking may occur if the catheter is forced or repositioned or if an excessively long catheter is used. [111] The most common result of kinking is poor flow of IV fluids, although rare complications as severe as SVC obstruction caused by a kinked catheter have been seen. [112] Thrombosis and thrombophlebitis occur rarely because of the large caliber and high flow rates of the vessels involved. [68] It is important to determine that the catheter tip rests in the SVC, especially during the infusion of irritating or hypertonic solutions. [112] Thrombi may also form secondary to prolonged catheter contact against the vascular endothelium. One autopsy study found a 29% incidence of mural thrombi in the innominate vein, SVC, and right ventricle of patients who had central lines in place an average of 8 days before death. [113] However, no complications were directly attributable to these small, firmly adherent thrombi. Thoracic duct laceration is a frequently discussed complication of left-sided subclavian venipuncture; however, it is extremely uncommon, and has been reported only as a complication of internal jugular, but not subclavian, cannulation. [95] Although poorly studied, it has been promulgated that patients with a coagulopathy may experience significant bleeding from central catheter placement, especially if arterial puncture/laceration has occurred. Traditionally, prophylactic blood component therapy (fresh frozen plasma, platelet infusions) has been suggested in patients with a coagulopathy prior to percutaneous placement of a central venous catheter. While intuitively reasonable, this concept has no support in the literature. Mumtaz et al. have challenged this concept as unproven and unnecessary, citing a 3% bleeding rate in coagulopathic patients who experienced only minor bleeding that could be controlled with digital pressure. Although central venous access may be safely performed in patients with underlying disorders of hemostasis, without correction of the coagulopathy, caution is urged. It would be prudent to target central access in patients with coagulopathies to areas of arterial compression. [42] Infectious Complications Infectious complications include local cellulitis, thrombophlebitis, generalized septicemia, osteomyelitis, and septic arthritis. [95] The incidence of septic complications varies from 0% to 25%.[114] [115] The frequency with which infectious complications are seen is directly related to the attention given to
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Structure
TABLE 22-7 -- Anatomic Structures That Can Be Injured by Central Venous Cannulation Anatomic Relation to Vein Error in Procedure Injury
Subclavian Vein Cannulation Subclavian artery
Posterior and slightly superior, separated by scalenus anterior—10 to 15 mm in adults, 5 to 8 mm in children
Insertion too deep or lateral
Hemorrhage, hematoma, possible hemothorax
Brachial plexus
Posterior to and separated from the subclavian vein by the scalenus anterior and the subclavian artery (20 mm)
Same as with subclavian artery
Possible motor or sensory deficits of hand, arm, or shoulder
Parietal pleura
Contact with posteroinferior side of the subclavian vein, medial to the attachment of the anterior scalenus muscle to the first rib
Needle penetrates beneath or through both walls of the subclavian vein
Pneumothorax
Phrenic nerve
Same as with parietal pleura
Placement of needle above or behind the vein or by penetration of both its walls
Paralysis of the ipsilateral hemidiaphragm
Thoracic duct
Cross the scalenus anterior and enter the superior margin of Same as with phrenic nerve the subclavian vein near the internal jugular junction
Soft tissue lymphedema or chylothorax on left
Carotid artery
Passes with jugular vein in carotid sheath, consistently medial and deep to the vein
Insertion site too medial or needle course not directed at ipsilateral nipple
Hematoma, possible cerebral thromboembolism or airway obstruction
Phrenic nerve
Passes along anterior surface of scalenus anterior, behind the vein
Insertion too deep
Paralysis of the ipsilateral hemidiaphragm
Brachial plexus
Separated from the internal jugular by the scalenus anterior
Insertion too deep or too lateral
Possible motor or sensory deficits of hand, arm, or shoulder
Femoral artery
Lies lateral to the vein in the femoral triangle
Needle passed too laterally
Hematoma
Psoas muscle
Directly posterior to the artery and vein
Needle passed too deep
Hematoma, psoas abscess
Bowel
Proximal and deep to femoral vein
Needle passed too deep and above inguinal ligament
Enterotomy, peritonitis
Synovial capsule of hip
Deep to the psoas muscle
Needle passed too deep, particularly in Arthritis small children
Internal Jugular Vein Cannulation
Femoral Vein Cannulation
From Knopp R, Dailey RH: Central venous cannulation and pressure monitoring. JACEP 6:358, 1977. aseptic technique in insertion and aftercare of the catheter. One study suggested a higher incidence of contamination with triple-lumen catheters [116] ; for the most part, however, an acceptably low incidence of bacteremia and sepsis (3.1%) using these devices has been encountered. [117] Femoral venous catheterization may be related to a greater risk of infection than subclavian catheterization. Merrer et al. reported overall infectious complications from femoral vs subclavian catheters to be 19.8% and 4.5% respectively. The most common organisms recovered from colonized femoral catheters, or involved with infectious complications from femoral catheters, were coagulase-negative staphylococci, Enterobacteriaceae, Enterococcus species, and Pseudomonas aeruginosa. [118] Neurologic Complications Neurologic complications are extremely rare and are presumably caused by direct trauma from the needle during venipuncture. Brachial plexus palsy and phrenic nerve injury with paralysis of the hemidiaphragm have been reported. [119] [120] Infusing medications into the internal jugular vein via a malpositioned catheter may result in a variety of neurologic complications from retrograde perfusion of intracranial vessels. [121] Subclavian Approaches Although both approaches to the subclavian are relatively safe ( Fig. 22-21 ), the IC approach is more likely to be associated with complications. In a randomized prospective comparison of SC and IC venipuncture in 500 ED patients, complication rates were 2.0% and 5.1%, respectively. [129] The most significant complications have been pneumothorax and subclavian artery puncture; the highest incidence of pneumothorax is 2.4%. [29] Adherence to recommended techniques for SC subclavian venipuncture decreases the risk of these complications because the needle is directed away from the pleural dome and subclavian artery. [12] The relatively superficial location of the vein when approached from above the clavicle (1.5 to 3.5 cm) lessens the risk of puncture or laceration of deep structures.
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Figure 22-20 A, A femoral vein catheter is more prone to deep vein thrombosis and infection than a subclavian/internal jugular line, but it is a standard access route in the emergency department. Strict attention to sterile procedure and limiting use for a few days will negate most of the negatives of this approach. A, Significant hemorrhage can occur after puncture of the femoral artery, but this area is readily compressed. The femoral route may be the route of choice in the patient with a coagulopathy who requires a central line. The femoral vein will accept: ( B) a triple-lumen catheter or ( C) a large sheath introducer.
Catheter tip malposition should be expected with some frequency, as high as 27.6% in one study examining the IC technique. [130] Because of the more direct path to the SVC, the SC approach may be advantageous in this regard. For those SC series in which malposition has been reported, the overall rate is 1.1%. [13] [28] [29] The highest incidence of malposition using the SC technique, 7%, occurred during the performance of CPR. [13] The incidence of failure to establish a functioning SC line ranges from 0% to 5%, [12] [28] [29] [131] with an overall rate of 4%. The failure rate reported for the IC technique ranges from 2.5% to 8%.[68] A recent case series of 178 SC attempts, often in patients with difficult anatomy, supports the high placement success (97.8%) and low significant complication rate (0.56%). [132] IJ Approach Many complications of IJ cannulation are similar to those of subclavian access. Infection, catheter malposition, thrombosis, and damage to surrounding structures are complications common to all puncture sites for central venous cannulation. The reported rates of thrombosis for internal jugular vein catheterizations range from a report of no significant thrombosis in 1 study to a high of 66% of patients exhibiting some thrombosis in a study of 33 medical intensive care unit patients. [133] No reports of significant pulmonary embolus directly attributable to an IJ catheter were found. Such wide variation in the reported incidence of complications is common, in part because of the different methods of detecting and reporting complications, variable experience with the different techniques, and the different patient populations. The number of complications increases, especially those due to thrombosis and infection, with longer duration of catheterization and increasing severity of the patient's illness. [17] Complications also seem to be higher with the use of the left IJ vein as opposed to the right. [49] [76] [77] Reported complications thought to be due at
least in part to the use of the left-sided approach include mediastinal migration of the catheters and at least one instance of fatal pericardial tamponade. One fairly common complication unique to the IJ approach is a hematoma in the neck. [33] With the IJ approach, pressure can be maintained easily on the area of swelling, and most hematomas will resolve spontaneously. If carotid arterial puncture is recognized and treated with compression, it rarely causes significant morbidity in the absence of marked
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Figure 22-21 A subclavian line can easily be advanced into the neck (internal or external jugular vein). Malpositioned catheters should be discovered and replaced as soon as possible. Infusing saline into this catheter is not harmful, but hyperosmotic and vasoactive medications should not be given through this catheter for prolonged periods of time.
atherosclerotic disease, although arteriovenous fistulas have been reported after IJ puncture. [134] Several neurologic complications unique to the IJ site of venipuncture have also been reported as a result of hematomas or of direct injury. [135] [136] These complications include damage to the phrenic nerves, an iatrogenic Horner syndrome, trauma to the brachial plexus, and even an instance of the passage of a catheter into the thecal space of the spinal canal. [137] [138] [139] [140] If the carotid artery is punctured, one may again attempt IJ or subclavian cannulation on the same side after appropriate, prolonged (15 to 20 minutes) compression. The IJ vein valve is frequently damaged when cannulated, often resulting in its incompetence. The clinical significance of this, if any, is unknown. [141] Arterial puncture is a contraindication to attempting the IJ route on the opposite side, because bilateral hemorrhage may occur with resultant airway compromise. The clinician should be prepared to rapidly intubate should this occur. Even in the face of a coagulopathy, however, the IJ approach has been found to be successful (up to 99.3% of cases) and safe (15 minutes) pressure should stop any arterial hemorrhage in a patient with normal clotting mechanisms. Prolonged arterial bleeding in patients, particularly those receiving thrombolytic or antiplatelet therapy, may warrant evaluation by a vascular surgeon or duplex imaging to evaluate for pseudoaneuyrsm formation, or both. A large study of military casualties found a 1.6% incidence of major hematomas, but these were mostly young, previously healthy patients. [144] The peritoneum can also be violated, with possible resulting perforation of the bowel. Bowel penetration is especially likely if the patient has a femoral hernia. Injury to the bowel is usually minimal and is unlikely to require specific treatment. Nonetheless, the potential bacterial contamination of the femoral puncture site may pose a significant problem. Aspiration of air on placement of a femoral line necessitates removal of the catheter and reinsertion at another site. A case has been reported in which a patient developed clinical signs of peritonitis that were found to be due to infiltration of IV fluids into the anterior abdominal wall from a femoral catheter. [145] A psoas abscess may result from penetration posteriorly of the underlying psoas fascia. The bladder, when distended, can also be punctured during femoral cannulation, although bladder puncture is unlikely to require therapy beyond removal of the aberrantly placed catheter. Strict aseptic technique should be maintained to prevent septic arthritis in the unlikely event that the hip capsule is punctured. This complication has been reported in infants. [146] The femoral nerve can also be injured by an errant needle puncture. [142] [145] Complications can be minimized if the patient has a pulse and the femoral vein is approached medial to the femoral pulsations. A helpful mnemonic is NAVEL, which describes the anatomy of the region from lateral to medial: nerve, artery, vein, empty space, and inguinal ligament. A controlled trial by Merrer and colleagues identified significantly increased risks of infectious and thrombotic complications with the femoral vs the subclavian approach. [118] Deep venous thrombosis (DVT) may also occur in or near cannulated lower extremity veins, and propagate to the IVC. Several prospective studies followed cohorts of patients with femoral lines, and found iliofemoral DVT in frequencies ranging from 6.6% to 10%. [147] [148] Most were clinically silent, without leg swelling or suspicion for pulmonary embolism. The relevance of long-term complication cannot be extrapolated to the short-term value of this procedure in the ED setting. However, such DVTs definitely pose embolic risk, and may lead to fatal pulmonary emboli. [149] IJ or subclavian cannulation may result in comparable rates of upper extremity DVT. [150] The true incidence of clinical sequelae from upper extremity DVT remains unclear, and lower extremity DVT is felt to be more often responsible for large or fatal pulmonary embolism. Therefore, some authors believe that the additional risk of lower extremity DVT in patients receiving longer-term femoral catheterization (perhaps sixfold above baseline) is not justified given the existence of alternative approaches. [147] Others disagree, stating that femoral vein catheterization is a standard intervention and a valuable, generally safe technique in the ED setting. Basilic-Cephalic Approaches Cannulation of the central venous system through the arm veins has the lowest major complication rate of all the approaches. Superficial local infections are common (10% to 20% incidence) and rarely lead to more serious problems, including sepsis. Catheter malposition is common, and studies have shown this to occur in 10% to 40% of placements.[84] [151] Cannulation of these veins requires immobilization of the entire extremity and shoulder to prevent catheter movement
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and kinking. Immobilization may be independently associated with complications.
CONCLUSION Cannulation of the central venous circulation is a necessary skill for emergency clinicians. Safe application of the various techniques available requires detailed knowledge of anatomy and operative technique, as well as a healthy respect for potential complications. Inexperienced clinicians should not undertake these techniques without supervision, although even in experienced hands, complications should be expected. While the IC subclavian approach is most commonly encountered in clinical practice, familiarity with the SC, IJ, femoral, and basiliccephalic approaches will provide the emergency clinician with a full complement of techniques for gaining access to the central venous circulation under a variety of clinical demands.
CENTRAL VENOUS PRESSURE MEASUREMENT Although described by Forssman in 1931, it was not until the early 1960s that measurement of CVP became commonplace as a means of assessing cardiac performance and guiding fluid therapy. [5] CVP measurements are most frequently used as a guide for determination of a patient's volume status and fluid requirements and for investigation of tamponade. [152] [153] Critical commentaries have been written by some researchers who regard CVP monitoring as ineffective, outmoded, and unreliable. [154] The astute clinician, however, can maximize the usefulness of this diagnostic tool by careful consideration of its indications and limitations. CVP is one of many variables that must be correlated in the development of an overall management plan for the care of critically ill patients. Physiology Simply stated, the CVP is the pressure exerted by the blood against the walls of the intrathoracic venae cava. Because the pressure in the great veins of the thorax is generally within 1 mm Hg of right atrial pressure, the CVP reflects the pressure under which blood is returned to the right atrium. [155] The pressure in the central veins has two significant hemodynamic effects. First, the pressure promotes filling of the heart during diastole, a factor that helps determine cardiac output. Second, the CVP is also the backpressure of the systemic circulation, opposing the return of blood from the peripheral blood vessels into the heart. [156] The CVP therefore affects both the ability of the heart to pump blood and the tendency for blood to flow from the peripheral veins. [27] [155] The CVP reading is determined by a complex interaction of intravascular volume, right atrial and ventricular function, venomotor tone, and intrathoracic pressure. [155] One can measure CVP accurately by placing the tip of a pressure monitoring catheter into any of the great systemic veins of the thorax or into the right atrium. [156] Because the risks of catheter placement in the atrium include atrial perforation and cardiac dysrhythmias, any large vein within the thorax is preferred. [157] The catheter is commonly connected to an electronic pressure transducer interfaced with a monitoring system capable of calculating a mean pressure value and displaying pressure waveforms. Indications and Contraindications for CVP Measurement The four major indications for CVP monitoring are as follows: 1. 2. 3. 4.
Acute circulatory failure Anticipated massive blood transfusion for fluid replacement therapy Cautious fluid replacement in patients with compromised cardiovascular status Suspected cardiac tamponade
The procedure is contraindicated when other resuscitation therapeutic and diagnostic interventions take priority over central venous access and CVP transducer setup and calibration. A common misconception is that CVP consistently reflects pressures found in the left side of the heart. The measurement that best reflects left ventricular pressure changes and reserve is the left atrial pressure, or the nearly equivalent pulmonary capillary wedge pressure (PCWP). The development of the flow-directed pulmonary artery catheter has allowed repeated measurements of PCWP, thus permitting reliable estimation of the left atrial pressure. The CVP is most helpful in patients without significant preexisting cardiopulmonary disease. Numerous studies highlight the apparent unreliability of right-sided hemodynamic monitoring in patients with underlying coronary artery or other cardiac disease or pulmonary disease. [131] [158] [159] [160] Ultimately, however, the differences noted are not a failure of CVP monitoring to reflect central hemodynamics. Rather, the disagreements noted by previous authors simply highlight the complexity of the relationship between ventricular and vascular compliance, blood volume, and filling pressures in all but very healthy patients. As when making pulmonary arterial and pulmonary arterial occlusion pressure measurements, the clinician is cautioned to be fully aware of the assumptions that such measurements make and to recognize the scenarios in which these assumptions do not hold true. Procedure Although CVP may be determined with a manometry column assembled at the bedside ( Fig. 22-22 ), the most common technique in practice is measurement with an electronic transducer interfaced to a monitoring system ( Fig. 22-23 ). Typical transducers include a nipple valve attached to a pressurized bag of saline to allow easy flushing of the system. To use these manometers, the transducer is attached to the patient's central line with a length of flexible yet fairly rigid-walled tubing filled with saline. A three-way stopcock is placed between the patient and the transducer to simplify line flushing and calibration. All air bubbles are flushed from the system by opening the stopcock to air and flushing saline through the line. Air bubbles should not be flushed into the patient. Even tiny bubbles left in the tubing will dampen the CVP wave and potentially cause underestimation of venous pressure.
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Figure 22-22 A, Simple manometry column used to measure CVP at the bedside. The stopcock is turned to direct the flow to the patient, bypassing the manometer. This is the position that is maintained to keep the catheter patent. The tubing is always flushed before connecting it to the patient's central venous pressure catheter. B, The stopcock is turned to fill the manometer to 25 cm H 2 O. C, The stopcock is opened to the patient, and the column of water in the manometer is allowed to fall and stabilize before a reading is taken. Note that the zero mark is horizontally aligned with the tricuspid valve (midaxillary line in a supine patient).
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Figure 22-23 General configuration of an intravascular pressure transducer. A working understanding of these devices, particularly regarding proper setup, zeroing, and line debubbling, will maximize their effectiveness and accuracy.
After the system has been flushed, the stopcock (with the transducer still open to air) is placed at the level of the patient's tricuspid valve. The monitor detecting the transducer's signal is then "zeroed," or calibrated. The transducer is calibrated at the level of the tricuspid valve, which can be approximated on the skin surface as a
point at the midaxillary line and fourth intercostal space. [155] Finally, the stopcock is set so that the transducer is in continuity with the patient's venous catheter. In spontaneously breathing patients, readings should be taken at the end of a normal inspiration. If the patient is receiving positive-pressure ventilation, the CVP changes during the respiratory cycle are reversed, rising with inspiration and decreasing with expiration. In these patients, readings should be taken near the end of expiration. [161] Thus, during both normal and mechanical ventilation, the lowest reading is a useful estimate of the mean CVP. A reading may be taken after proper assembly of the equipment and after accurate placement of the tip of the catheter has been established. To ensure optimal measurement, the patient should be in the supine position. Whenever the patient is repositioned, care must be taken to ensure that the transducer has been recalibrated to reflect the new position of the patient. Errors in CVP Measurement A number of extrinsic factors may alter the accuracy of the CVP reading ( Table 22-8 ). [27] In addition to the position of the patient, these include changes in intrathoracic pressure, [162] catheter tip malposition, obstruction of the catheter, and failure to calibrate or zero the line. Activities that increase intrathoracic pressure, such as coughing or straining, may cause spuriously high measurements. The patient should be relaxed at the time of the measurement and breathing normally. In mechanically ventilated patients, the CVP will be elevated to an extent directly proportional to the ventilatory pressures being delivered and inversely proportional to the mechanical TABLE 22-8 -- Faulty Central Venous Pressure Readings Increased intrathoracic pressure (ventilator, straining, coughing) Reference points in error Malposition of catheter tip Blocking or ball-valve obstruction of catheter Air bubbles in circuit Readings during wrong phase of ventilation Readings by different observers Vasopressors (presumed) compliance of the lung. Care should be exercised in interpreting filling pressures in this circumstance, as ventilator-induced elevations in CVP are not artifactual, but represent changes in the hemodynamic physiology of the patient. As in spontaneously breathing patients, CVP measurements are only meaningful in a relaxed, sedated, or sedated and paralyzed subject. Another reason for faulty readings is malposition of the catheter tip. If the catheter tip has not passed far enough into the central venous system, peripheral venous spasm or venous valves may yield pressure readings that are inconsistent with the true CVP. [27] If the catheter tip is passed into the right ventricle, a falsely high CVP is obtained. Recognition of a characteristic right ventricular pressure waveform on the patient's monitor should hopefully preclude this error. Such fluctuations may occasionally be seen in appropriately positioned CVP lines when significant tricuspid regurgitation or atrioventricular dissociation (cannon a waves) is present. Inaccurate low venous pressure readings are seen when a valve-like obstruction at the catheter tip occurs either by clot formation or by contact against a vein wall. As mentioned earlier, wave damping due to air bubbles in the transducer or tubing also leads to faulty readings. Using poorly zeroed lines may result in inaccurate measurements that may be interpreted as a change in the patient's status when none has actually occurred. The transducer should be zeroed to the same level for every measurement. Some investigators mention a falsely elevated CVP in patients who are receiving vasopressors, but controlled data on this aberration are lacking. One animal study suggests that fluid can be infused into one lumen of a multilumen catheter without affecting the CVP reading at another lumen. [163] Interpretation of the CVP measurement Because determination of the CVP can aid the clinician in assessment of the critically ill patient, it is paramount that the clinician knows the normal values and the variables that may affect these values and can recognize the pathologic conditions that correlate with abnormal values. Although various ranges for normal have been reported,[153] [164] [165] a summary of these values is as follows: Low: 12 cm H2 O
In the late stages of pregnancy (30 to 42 weeks), the CVP is physiologically elevated, and normal readings are 5 to 8 cm H 2 O higher in pregnant women.
443
A CVP reading 12 cm H 2 O indicates that the heart is not effectively circulating the volume presented to it. This situation may occur in the case of either a normovolemic patient with underlying cardiac disease such as left ventricular hypertrophy (with associated poor ventricular compliance) or a patient with a normal heart who is over-hydrated and over-transfused. A high CVP is also related to variables other than pump failure, which include pericardial tamponade, restrictive pericarditis, pulmonary stenosis, and pulmonary embolus. [164] Changes in blood volume, vessel tone, and cardiac function may occur alone or in combination with one another; therefore, it is possible to have a normal or high CVP in the presence of normovolemia, hypovolemia, and hypervolemia. One must interpret the specific CVP values with respect to the entire clinical picture. The response of the CVP to an infusion is more important than the initial reading. Fluid Challenge Monitoring of the CVP may be helpful as a practical guide for fluid therapy. [152] [153] Serial CVP measurements provide a fairly reliable indication of the capability of the right heart to accept an additional fluid load. Although the PCWP is a more sensitive index of left heart fluid needs (and in some clinical situations, PCWP measurement is essential), serial measurement of CVP can provide significant information.
A fluid challenge can help assess both volume deficits and pump failure. Although a fluid challenge can be used with either PCWP monitoring or CVP monitoring, only the fluid challenge for CVP monitoring is discussed here. Slight variations in methodology of fluid challenge are reported in the literature. Generally, aliquots of 50 to 200 mL of crystalloid are sequentially administered, and measurements of CVP levels are obtained after 10 minutes. [131] [164] The fluid challenge is generally carried out in the following manner [153] : Fluid is administered by a route other than that used for monitoring. An initial CVP reading is taken, and fluid is infused at a rate of 20 mL/min over a 10-minute period. The infused volume is allowed to equilibrate for 10 minutes, and a reading is taken. If the CVP is >5 cm of H2 O over the initial measurement, the fluid challenge is discontinued, and one assumes that the right ventricle is unable to handle an additional fluid load. Increases of between 3 and 5 cm H 2 O over the initial CVP value are equivocal, and additional measurements are taken over the next 30 minutes if this reading is obtained. An increase of 15% to 30% than that through a 5-cm, 14-ga catheter. The difference is greater if pressure is applied to the system. The improvement in flow rate through large-bore lines is greater for blood than for crystalloid solutions, because the viscous characteristics of blood greatly impede its passage through small-bore tubing. [10] A unit of blood can be transfused in 3 minutes using IV extension tubing inserted into the vein. Consequently, large-bore lines placed by venous cutdown are an excellent mechanism for the treatment of severe hypovolemia. High-flow infusion techniques are discussed elsewhere (see Chapter 24 ).
CONTRAINDICATIONS Venous cutdown is contraindicated when less invasive alternatives exist or when excessive delay would be required for the procedure to be performed. [12] Although highly skilled operators may perform a cutdown in 1.5 times normal or the activated PTT (aPTT) is >1.5 times the top normal value. If the PT is 2 units) of whole blood have already been given.
522
One may transfuse both Rh-positive and Rh-negative group O packed cells in patients who are in critical condition.
It is a common misconception that patients who are Rh-negative will have an immediate transfusion reaction if given Rh-positive blood. There is no particular advantage in the Rh factor determination because preformed, naturally occurring anti-Rh antibodies do not exist. Theoretically, individuals who are Rh-negative may become sensitized either through pregnancy or by previous transfusions, resulting in a delayed hemolytic transfusion reaction if Rh-positive blood is transfused. However, this scenario is very rare and is of no great clinical significance when compared with life-threatening blood loss. Many advise the routine use of the more widely available O Rh-positive packed cells in all patients for whom the Rh factor has not been determined, except in females of childbearing age, for whom future Rh sensitization may be an important consideration. Once resuscitated with Rh-positive packed cells, patients may receive their own type without a problem. Because individuals with O Rh-negative blood represent only 15% of the population and the blood may be in short supply, it is reasonable to save O Rh-negative blood for Rh-negative females of childbearing potential and to use group O Rh-positive packed cells routinely as the first choice for emergency transfusions. In a study of emergency blood needs, Schmidt and colleagues reported 601 units of Rh-positive type O blood transfused to 193 patients, including 8 Rh-negative women, before blood type was determined. No acute hemolytic reaction occurred, and no women were sensitized. Rh immune globulin prophylaxis is recommended only for Rh-negative women with childbearing potential receiving Rh-positive blood. If noncrossmatched blood is transfused, the laboratory should receive a plain (without a serum separator) red-top tube of venous blood as soon as possible to begin a formal crossmatch procedure. Whenever possible, this should be drawn before any blood is transfused. Brickman and coworkers have demonstrated that bone marrow aspirates obtained by an intraosseous needle can be used for crossmatching. [27] Rh immune prophylaxis with human immune globulins (RhoGAM) is indicated for Rh-negative pregnant women who may be bearing Rh-positive children and may have fetomaternal transplacental hemorrhage. These events include bleeding in early pregnancy, such as spontaneous or elective abortion, ectopic pregnancy, and other potential causes of antepartum hemorrhage such as trauma. Administration of Rh immunoglobulin in threatened abortions is advocated by some. The product suppresses the immune response of Rh-negative women to Rh-positive RBCs, and it is effective when given up to 72 hours after exposure to fetal erythrocytes. Dosing of Rh immunoglobulin is 50 µg intramuscularly (IM) for first-trimester bleeding and 300 µg IM for later bleeding. [28] In the setting of significant fetal-maternal transfusion (usually only in the third trimester), doses may be increased. In such circumstances, Rh immunoglobulin is prepared in the blood bank and the correct dose is suggested on an individual basis, following confirmation of Rh status, evidence of prior sensitization, and testing for fetal erythrocytes in the mother's blood. Transfusion Coagulopathy Within the past 10 years it has been appreciated that pathologic hemostasis occurs following massive blood transfusions. [29] [30] [31] The exact cause of the transfusion coagulopathy is not well understood. Although such abnormalities rarely develop within the time frame of the initial resuscitation in the emergency department (ED), an understanding of the problem leads to a more intelligent approach to transfusion practices and the anticipation of potential problems. The term massive transfusion is loosely defined but is usually considered to be the transfusion of >10 units of blood to an adult (equivalent to 1 blood volume) within 24 hours. In patients who are given a transfusion equal to 2 blood volumes, only approximately 10% of the original elements remain. Considering the significant alteration in blood and blood products that occurs during storage, one can readily appreciate the underlying problem associated with such massive transfusions. The development of transfusion coagulopathy is multifactorial and in large part is related to tissue injury and duration of shock. [32] Abnormalities in platelets and plasma clotting factors also play a
role. Platelets
Transfusion coagulopathy is related in part to dilution of the recipient's platelets by transfused blood, which is devoid of functioning platelets. Dilutional thrombocytopenia is a well-recognized complication of massive transfusion, and a platelet count should be obtained routinely if >5 units of blood are transfused. Generally, platelet therapy should be considered after the first 10 units of blood have been given, although the most useful parameter for estimating the need for platelet transfusions is the platelet count. Plasma Clotting Factors
Disseminated intravascular coagulopathy plays a secondary role in post-transfusion bleeding. Factors V and VIII are labile in stored blood and absent in packed cells. Fibrinogen is relatively stable in stored blood but is absent in packed cells. A deficiency of most clotting factors, especially factors V and VIII and fibrinogen, occurs with massive transfusions. This deficiency probably occurs on a "washout" (i.e., dilutional) basis, although the dynamics are poorly understood. The replacement of these factors may be required. Specific assays for the individual factors are available, but it is more practical to measure PTT, PT, and fibrinogen levels. FFP has been used to correct clotting factor abnormalities secondary to dilution from massive transfusions, but its effectiveness has not been firmly established. Cryoprecipitate has also been used to replace factor VIII and fibrinogen, but it is rarely required, because FFP contains some fibrinogen. FFP should be infused to correct the coagulopathy as indicated by clotting studies, but as a general guide, 1 to 2 units of FFP may be given empirically for each 5 to 6 units of blood in the massively traumatized or bleeding patient. Cryoprecipitate may be required if fibrinogen levels fall below 100 mg/dL and are not adequately supplemented with FFP.
ORDERING OF BLOOD Ordering a type and crossmatch procedure on a blood product implies that the decision has already been made to administer a transfusion. A "type and hold" or "type and screen" (no crossmatch) request alerts the blood bank to the possibility that a blood product will be required for the patient, so appropriate units can be acquired and kept on hand. A type and crossmatch procedure takes 45 minutes and restricts a unit of blood to a specific patient. This limits a valuable resource and should not be requested lightly. In the ED, a crossmatch procedure should be requested for a blood product only if the adult patient (1) manifests shock, (2) has symptomatic anemia
523
(usually associated with a hemoglobin 12 5–10 years old: Use adult dosing IM: 10–20
SEDATIVE/HYPNOTICS Lorazepam* (Ativan)
Sedation, motion control, anxiolysis
Anxiolytic and sedative adjunct to neuroleptic
1–4 mg IM/IV
0.05–0.1 mg/kg IM/IV (not to to exceed adult dosing)
IV: 2–3 IV: 45–60
IM: 10–20
IM: 60–120
PO: 15–60
PO/IM: 24 hours
Monitor for respiratory depression
TREATMENT OF EXTRAPYRAMIDAL SYMPTOMS Benztropine (Cogentin)
Reversal of EPS
EPS (dystonia, akathisia)
2 mg PO/IM
0.5–2 mg PO/IM
IM: 10
Anticholinergic effects (e.g., dry mouth, urinary retention, tachycardia).
Diphenhydramine (Benadryl)
Reversal of EPS
EPS (dystonia, akathisia)
25–50 mg PO/IM/IV
1 mg/kg PO/IM/IV
PO: 30–60
PO/IM/IV: 6–8 hours
Anticholinergic effects (e.g., dry mouth, urinary retention, tachycardia).
IM: 20–30 IV: 5–10 *There is no maximum dose of benzodiazepines. Massive doses may be required in severely agitated patients. EPS = extrapyramidal symptoms.
617
with the direct IV injection of the sedating medication ( Fig. 34-6 ). When the patient has been controlled, indwelling venous access can be accomplished. In the less stressful situation, the IM route may be acceptable. The use of IM ketamine to control a dangerous and violent patient without venous access has been described, but the role of ketamine in this situation is presently unclear. [125] There is no specific maximum dose for drugs used for chemical restraint.
Occasionally massive doses may be required. If benzodiazepine or neuroleptics, or both, are not effective, muscular paralysis and mechanical ventilation may be necessary to gain control of the patient. Benzodiazepines Historically, the first drugs used as adjuncts to phenothiazines for RT were barbiturates, allowing decreased dosing of chlorpromazine, thereby minimizing the incidence of hypotension. Benzodiazepines have now replaced barbiturates as adjuncts to neuroleptics in RT. The benzodiazepine of choice for RT in both adults and children is lorazepam (Ativan, adult dosing: 1–4 mg IM/IV; pediatric dosing: 0.05–0.1 mg/kg IM/IV) because of its bioavailability and rapid IM absorption, intermediate duration, and low side-effect profile ( Table 34-14 ). It is commonly given with a neuroleptic (e.g., haloperidol) to achieve rapid anxiolysis and anti-psychosis. [126] This combination has been shown to have a more rapid onset and fewer extrapyramidal symptoms (EPS) than with haloperidol alone, and is well-tolerated with no respiratory depression or hypotension. [127] Neuroleptics The first anti-psychotic agents used for rapid tranquilization were the low-potency phenothiazines (e.g., chlorpromazine [Thorazine], thioridazine [Mellaril]). These agents are highly sedating and manifest anticholinergic effects, alpha adrenergic blockade (leading to orthostatic hypotension), a lowered seizure threshold, and cardiac toxicity in overdose. During the 1990s, these agents have been replaced by the butyrophenones haloperidol (Haldol) and droperidol (Inapsine) (see Table 34-14 ). Haloperidol (adult dosing: 5–10 mg IM/IV [start at 2 mg in the elderly and patients receiving concomitant CNS depressants]; pediatric dosing—5–12 years old: 0.1 mg/kg IM/IV, >12 years old: use adult dosing) and droperidol (adult dosing: 2.5–10 mg [reduce dose for elderly patients and patients receiving concomitant CNS depressants]; pediatric dosing: 0.05–0.07 mg/kg IM/IV) are high-potency agents that, compared to the phenothiazines, are relatively free of anti-cholinergic effects, alpha-blocking properties, and cardiac toxicity, but cause more EPS. [128] The overall incidence of EPS (e.g., dystonic reactions, akathisia) with butyrophenones is low, occurring in less than 10% of RT patients within the first 24 hours, and such reactions can be effectively treated with IM or IV diphenhydramine (Benadryl, adult dosing: 25–50 mg PO/IM/IV; pediatric dosing: 1 mg/kg PO/IM/IV and/or benztropine; Cogentin, adult dosing: 2 mg PO/IM; pediatric dosing [>3 years old]: 0.5–2 mg PO/IM).[128] Acute dystonia in particular is a non-dose-dependent, idiosyncratic reaction. Both neuroleptics have minimal effect on respiratory drive and airway reflexes, and their safety and efficacy in the ED have been well-documented. [129] [130] [131] Droperidol has a faster onset time IM, shorter duration, and is more sedating than haloperidol. [129] [132] Neuroleptics will also exacerbate pre-existing Parkinsonism, and should be avoided in these patients. A much-feared idiosyncratic reaction, occurring in 1% of patients on neuroleptics, is neuroleptic malignant syndrome (NMS), characterized by potentially severe autonomic instability (hyperthermia, hypertension, and rigidity). NMS can rarely occur in the setting of RT with patients on chronic antipsychotic medications. Haloperidol has been reported to lower the seizure threshold in animals, but this remains a theoretical concern clinically as there are no reported cases in humans despite its use in post-ictal and alcoholic patients. Although droperidol has been used extensively in the ED over the last 10 years and clinicians experienced in its use consider it safe and effective, its use has decreased since the FDA issued "black box warning" in December 2001 regarding QT-related dysrhythmias. [133] Patients receiving droperidol must be carefully screened for a history of QT-related dysrhythmias and whenever possible receive a baseline ECG or rhythm strip to ensure a normal QT interval. However, there is little rational behind the "black box warning" to justify a change in ED practice with this agent. [134] Alternative Agents Ketamine has been effectively used as an alternative tranquilization agent [125] ; however, it may exacerbate intracranial hypertension in patients with head trauma or CNS infections.[92] A reserve option for situations of grave danger is paralysis with succinylcholine IV or IM (1–1.5 mg/kg IV; 4 mg/kg IM), followed by rapid airway control. [135]
Acknowledgment
The editors and author wish to acknowledge the contributions of Kevin R. Ward and Donald M. Yealy to this chapter in previous editions.
References 1. Cote
CJ, Karl HW, Notterman DA, Weinberg JA, McCloskey C: Adverse sedation events in pediatrics: A critical incident analysis of contributing factors. Pediatrics 105:805, 2000a.
2. Cote
CJ, Karl HW, Notterman DA, et al: Adverse sedation events in pediatrics: Analysis of medications used for sedation. Pediatrics 106:633, 2000b.
3. American 4. Green
SM, Rothrock SG, Lynch EL, et al: Intramuscular ketamine for pediatric sedation in the emergency department: Safety profile with 1022 cases. Ann Emerg Med 31:688, 1998b.
5. Krauss 6. Pena
College of Emergency Physicians: Clinical policy for procedural sedation and analgesia in the emergency department. Ann Emerg Med 31:663, 1998.
B, Green SM: Sedation and analgesia for procedures in children. N Engl J Med 342:938, 2000.
BMG, Krauss B: Adverse events of procedural sedation and analgesia in a pediatric emergency department. Ann Emerg Med 34:483, 1999.
7. Chudnofsky 8. American 9. National
CR, Wright SW, Dronen SC, Borron SW, Wright MB: The safety of fentanyl use in the emergency department. Ann Emerg Med 18:635, 1989.
Academy of Pediatrics Committee on Drugs: Guidelines for the elective use of conscious sedation, deep sedation, and general anesthesia in pediatric patients. Pediatrics 76:317, 1985.
Institutes of Health: Consensus conference—Anesthesia and sedation in the dental office. JAMA 8:1073, 1985.
10.
Cote CJ: Conscious sedation: Time for this oxymoron to go away! J Pediatr 139:15, 2001.
11.
Murphy MF: Sedation. Ann Emerg Med 27:461, 1996.
12.
American Society of Anesthesiologists: Practice guidelines for sedation and analgesia by non-anesthesiologists. Anesthesiology 84:459, 1996.
618
13.
JCAHO: Accreditation Manual for Hospitals. Oakbrook Terrace, IL, Joint Commission on Accreditation of Healthcare Organizations, 2001. Available at http://www.jcaho.org/standards_frm.html
American Academy of Pediatrics Committee on Drugs: Guidelines for monitoring and management of pediatric patients during and after sedation for diagnostic and therapeutic procedures. Pediatrics 89:1110, 1992. 14.
15.
American Society of Anesthesiologists: Practice guidelines for sedation and analgesia by non-anesthesiologists. Anesthesiology 96:1004, 2002.
16.
Green SM, Krauss B: Pulmonary aspiration risk during ED procedural sedation—An examination of the role of fasting and sedation depth. Acad Emerg Med 9:35, 2002.
American Society of Anesthesiologists: Practice guidelines for preoperative fasting and the use of pharmacologic agents to reduce the risk of pulmonary aspiration: Application to healthy patients undergoing elective procedures. Anesthesiology 90:896, 1999. 17.
18.
Bhavani-Shankar K, Moseley H, Kumar AY, et al: Capnometry and anesthesia. Can J Anaesth 39:617, 1992.
19.
Cote CJ, Liu LM, Szyfelbein SK, et al: Intraoperative events diagnosed by expired carbon dioxide monitoring in children. Can Anaesth Soc J 33:315, 1986.
20.
Kaneko Y: Clinical perspectives on capnography during sedation and general anesthesia in dentistry. Anesthesia Progress 42:126, 1995.
21.
Miner JR, Heegaard W, Plummer D: End-tidal carbon dioxide monitoring during procedural sedation. Acad Emerg Med 9:275, 2002.
Poirier MP, Gonzalez Del-Rey JA, McAneney CM, et al: Utility of monitoring capnography, pulse oximetry, and vital signs in the detection of airway mishaps: A hyperoxemic animal model. Am J Emerg Med 16:350, 1998. 22.
23.
Swedlow DB: Capnometry and capnography: The anesthesia disaster early warning system. Seminars in Anesthesia 3:194, 1986.
Tobias J: End-tidal carbon dioxide monitoring during sedation with a combination of midazolam and ketamine for children undergoing painful, invasive procedures. Pediatr Emerg Care 15:173, 1999. 24.
25.
Weingarten M: Respiratory monitoring of carbon dioxide and oxygen: A 10-year retrospective. J Clin Monit Comput 6:217, 1990.
26.
Williamson JA, Webb RK, Cockings J, Morgan C: The capnograph: Applications and limitations—An analysis of 2000 incident reports. Anaesth Intensive Care 21:551, 1993.
27.
Farmery AD, Roe PG: A model to describe the rate of oxyhaemoglobin desaturation during apnea. Br J Anaesth 76:284, 1996.
28.
Patel R, Lenczyk M, Hannallah RS, McGill WA: Age and the onset of desaturation in apnoeic children. Can J Anaesth 41:771, 1994.
29.
Chan MT, Gin T: What does the bispectral EEG index monitor? Eur J Anaesthesiol 17:146, 2000.
30.
Rosow C, Manberg P: Bispectral index monitoring. Anesthesiology Clinics of North America: Annual of Anesthetic Pharmacology 2:89, 1998.
31.
Sleigh J, Andrzejowski J, Steyn-Ross A, Steyn-Ross M: The bispectral index: A measure of depth of sleep? Anesth Analg 88:659, 1999.
32.
Vissers R, McHugh D: Bispectral index monitoring as a continuous, non-invasive measure of sedation during procedures in the ED. Acad Emerg Med 7:529, 2000.
33.
Kain ZN, Mayes LC, O'Connor TZ, Cicchetti DV: Preoperative anxiety in children: Predictors and outcomes. Arch Pediatr Adolesc Med 150:1238, 1996.
34.
Kain Z, Mayes L, Caramico L, Hofstadter M: Distress during induction of anesthesia and postoperative behavioral outcomes. Anesth Analg 88:1042, 1999a.
35.
Kain Z, Mayes L, Caramico L, et al: Postoperative behavioral outcomes in children: Effects of sedative premedication. Anesthesiology 90:758, 1999b.
36.
McCann ME, Kain ZN: The management of preoperative anxiety in children: An update. Anesth Analg 93:98, 2001.
37.
Chen E, Joseph MH, Zeltzer LK: Behavioral and cognitive interventions in the treatment of pain in children. Pediatr Clin North Am 47:513, 2000.
38.
Kennedy RM, Luhmann JD: The "ouchless emergency department." Getting closer: Advances in decreasing distress during painful procedures in the emergency department. Pediatr Clin North Am
46:1215, 1999. 39.
Binder LS, Leake LA: Chloral hydrate for emergent pediatric procedural sedation: A new look at an old drug. Am J Emerg Med 9:530, 1991.
40.
Olson DM, Sheehan MG, Thompson W et al: Sedation of children for electroencephalograms. Pediatrics 108:163, 2001.
Malviya S, Voepel-Lewis T, Prochaska G, Tait AR: Prolonged recovery and delayed side effects of sedation for diagnostic imaging studies in children. Pediatrics 105:E42, 2000. Available at http://www.pediatrics.org/cgi/content/full/105/3/e42. 41.
42.
D'Agostino J, Terndrup TE: Chloral hydrate versus midazolam for sedation of children for neuroimaging: A randomized clinical trial. Pediatr Emerg Care 16:1, 2000.
Greenberg SB, Faerber EN, Aspinall CL, Adams RC: High-dose chloral hydrate sedation for children undergoing MR imaging: Safety and efficacy in relation to age. AJR Am J Roentgenol 161:639, 1993. 43.
44.
Hubbard AM, Markowitz RI, Kimmel B, et al: Sedation for pediatric patients undergoing CT and MRI. J Comput Assist Tomogr 16:3, 1992.
45.
Malviya S, Voepel-Lewis T, Tait AR: Adverse events and risk factors associated with the sedation of children by nonanesthesiologists. Anesth Analg 85:1207, 1997.
Vade A, Sukhani R, Dolenga M, Habisohn-Schuck C: Chloral hydrate sedation in children undergoing CT and MR imaging: Safety as judged by American Academy of Pediatrics (AAP) Guidelines. AJR Am J Roentgenol 165:905, 1995. 46.
47.
Pereira JK, Burrows PE, Richards HM, et al: Comparison of sedation regiments for pediatric outpatient CT. Pediatr Radiol 23:341, 1993.
48.
American Academy of Pediatrics Committee on Drugs: Use of chloral hydrate for sedation in children. Pediatrics 92: 471, 1993.
49.
Bailey PL: Frequent hypoxemia and apnea after sedation with midazolam and fentanyl. Anesthesiology 73:826, 1990.
Karl HW, Coté CJ, McCubbin MM, et al: Intravenous midazolam for sedation of children undergoing procedures: An analysis of age and procedure-related factors. Pediatr Emerg Care 15:167, 1999. 50.
51.
Davies FC, Waters M: Oral midazolam for conscious sedation of children during minor procedures. J Accid Emerg Med 15:244, 1998.
52.
Massanari M, Novitsky J, Reinstein LJ: Paradoxical reactions in children associated with midazolam use during endoscopy. Clin Pediatr (Phila) 36:681, 1997.
McGlone RG, Fleet T, Durham S, Hollis S: A comparison of intramuscular ketamine with high dose intramuscular midazolam with and without intranasal flumazenil in children before suturing. J Emerg Med 18:34, 2001. 53.
54.
Connors K, Terndrup TE: Nasal versus oral midazolam for sedation of anxious children undergoing laceration repair. Ann Emerg Med 24:1074, 1994.
55.
Fatovich DM, Jacobs IG: A randomized, controlled trial of oral midazolam and buffered lidocaine for suturing lacerations in children (the SLIC trial). Ann Emerg Med 25:209, 1995.
56.
Feld LH, Negus JB, White PF: Oral midazolam preanesthetic medication in pediatric outpatients. Anesthesiology 73:831, 1990.
57.
Haas DA, Nenniger SA, Yacobi R, et al: A pilot study of the efficacy of oral midazolam for sedation in pediatric dental patients. Anesth Prog 43:1, 1996.
57A. McGlone
RG, Ranasinghe S, Durham S: An alternative to "brutacaine": A comparison of low-dose intramuscular ketamine with intranasal midazolam in children before suturing. J Accident Emerg Med 15:231, 1998. 58.
Younge PA, Kendall JM: Sedation for children requiring wound repair: A randomized controlled double-blind comparison of oral midazolam and oral ketamine. J Emerg Med 18:30, 2001.
Abrams R, Morrison JE, Villasenor A, et al: Safety and effectiveness of intransal administration of sedative medications (ketamine, midazolam, or sufentanil) for urgent brief pediatric dental procedures. Anesth Prog 40:63, 1993. 59.
60.
Ackworth JP, Purdie D, Clark RC: Intravenous ketamine plus midazolam is superior to intranasal midazolam for emergency pediatric procedural sedation. J Emerg Med 18:39, 2001.
61.
Theroux MC, West DW, Corddry DH, et al: Efficacy of intranasal midazolam in facilitating suturing of lacerations in preschool children in the emergency department. Pediatrics 91:624, 1993.
Roelofse JA, Joubert JJ, Roelofse PGR: A double-blind randomized comparison of midazolam alone and midazolam combined with ketamine for sedation of pediatric dental patients. J Oral Maxillofac Surg 54:838, 1996. 62.
63.
Tanaka M, Sato M, Saito A, Nishikawa T: Reevaluation of rectal ketamine premedication in children: Comparison with rectal midazolam. Anesthesiology 93:1217, 2000.
64.
Kennedy RM, Porter FL, Miller JP, Jaffe DM: Comparison of fentanyl/midazolam with ketamine/midazolam for pediatric orthopedic emergencies. Pediatrics 102:956, 1998.
65.
Sievers TD, Yee JD, Foley ME, et al: Midazolam for conscious sedation during pediatric oncology procedures: Safety and recovery parameters. Pediatrics 88:1172, 1991.
66.
Moro-Sutherland DM, Algren JT, Louis PT, et al: Comparison of intravenous midazolam with pentobarbital for sedation for head computed tomography imaging. Acad Emerg Med 7:1370, 2000.
619
67.
Bloomfield EL, Masaryk TJ, Caplin A, et al: Intravenous sedation for MR imaging of the brain and spine in children: Pentobarbital versus propofol. Radiology 186:93, 1993.
68.
Egelhoff JC, Ball WS Jr, Koch BL, et al: Safety and efficacy of sedation in children using a structured sedation program. AJR Am J Roentgenol 168:1259, 1997.
69.
Strain JD, Campbell JB, Harvey LA, Foley LC: IV Nembutal: Safe sedation for children undergoing CT. AJR Am J Roentgenol 151:975, 1988.
70.
Green SM: Propofol for emergency department procedural sedation—Not yet ready for prime time [editorial]. Acad Emerg Med 6:975, 1999.
71.
Beekman RP, Hoorntje TM, Beek FJ, Kuijten RH: Sedation for children undergoing magnetic resonance imaging: Efficacy and safety of rectal thiopental. Eur J Pediatr 155:820, 1996.
72.
Daniels AL, Cote CJ, Polaner DM: Continuous oxygen saturation monitoring following rectal methohexitone induction in paediatric patients. Can J Anaesth 39:27, 1992.
73.
Glasier CM, Stark JE, Brown R, et al: Rectal thiopental sodium for sedation of pediatric patients undergoing MR and other imaging studies. Am J Neuroradiol 16:111, 1995.
74.
Manuli MA, Davies L: Rectal methohexital for sedation of children during imaging procedures. AJR Am J Roentgenol 160:577, 1993.
75.
O'Brien JF, Falk JL, Carey BE, Malone LC: Rectal thiopental compared with intramuscular meperidine, promethazine, and chlorpromazine for pediatric sedation. Ann Emerg Med 20:644, 1991.
76.
Pomeranz ES, Chudnofsky CR, Deegan TJ, et al: Rectal methohexital sedation for computed tomography imaging of stable pediatric emergency department patients. Pediatrics 105:1110, 2000.
77.
Lerman B, Yoshida D, Levitt MA: A prospective evaluation of the safety and efficacy of methohexital in the emergency department. Am J Emerg Med 14:351, 1996.
78.
Schwanda AE: Brief unconscious sedation for painful pediatric oncology procedures: Intravenous methohexital with approriate monitoring is safe and effective. Am J Ped Hematol Oncol 15:370,
1993. 79.
Sedik H: Use of intravenous methohexital as a sedative in pediatric emergency departments. Arch Pediatr Adolesc Med 155:665, 2001.
79A. Havel
CJ, Strait RT, Hennes H: A clinical trial of propofol vs midazolam for procedural sedation in a pediatric emergency department. Acad Emerg Med 6:989, 1999.
79B. Hertzog
JH, Campbell JK, Dalton HJ, Hauser GJ: Propofol anesthesia for invasive procedures in ambulatory and hospitalized children: Experience in the pediatric intensive care unit. Pediatrics 103:E30, 1999. 79C. Hertzog
JH, Dalton HJ, Anderson BD, et al: Prospective evaluation of propofol anesthesia in the pediatric intensive care unit for elective oncology procedures in ambulatory and hospitalized children. Pediatrics 106:742, 2000. 79D. Lowrie
L, Weiss AH, Lacombe C: The pediatric sedation unit: A mechanism for pediatric sedation. Pediatrics 102:E30, 1998.
79E. Swanson
ER, Seaberg DC, Mathias S: The use of propofol for sedation in the emergency department. Acad Emerg Med 3:234, 1996.
80.
Dickinson R, Singer AJ, Carrion W: Etomidate for pediatric sedation prior to fracture reduction. Acad Emerg Med 8:74, 2001.
81.
Ruth WJ, Burton JH, Bock AJ: Intravenous etomidate for procedural sedation in emergency department patients. Acad Emerg Med 8:13, 2001.
82.
Yealy DM: Safe and effective . . . maybe: Etomidate in procedural sedation/analgesia [editorial]. Acad Emerg Med 8:68, 2001.
83.
Schenarts CL, Burton JH, Riker RR. Adrenocortical dysfunction following etomidate induction in emergency department patients. Acad Emerg Med 8:1, 2001.
84.
Billmire DA, Neale HW, Gregory RO: Use of IV fentanyl in the outpatient treatment of pediatric facial trauma. J Trauma 25:1079, 1985.
85.
Pohlgeers AP, Friedland LF, Keegan-Jones L: Combination fentanyl and diazepam for pediatric conscious sedation. Acad Emerg Med 2:879, 1995.
86.
Schechter NL, Weisman SJ, Rosenblum M, et al: The use of oral transmucosal fentanyl citrate for painful procedures in children. Pediatrics 95:335, 1995.
Schutzman SA, Liebelt E, Wisk M, Burg J: Comparison of oral transmucosal fentanyl citrate and intramuscular meperidine, promethazine, and chlorpromazine for conscious sedation of children undergoing laceration repair. Ann Emerg Med 28:385, 1996. 87.
88.
Kendall JM, Reeves BC, Latter VS: Multicentre randomised controlled trial of nasal diamorphine for analgesia in children and teenagers with clinical fractures. Br Med J 322:261, 2001.
89.
Wilson JA, Kendall JM, Cornelius P: Intranasal diamorphine for paediatric analgesia: Assessment of safety and efficacy. J Accid Emerg Med 14:70, 1997.
Bates BA, Schutzman SA, Fleisher GR: A comparison of intranasal sufentanil and midazolam to intramuscular meperidine, promethazine, and chlorpromazine for conscious sedation in children. Ann Emerg Med 24:646, 1994. 90.
91.
Litman RS: Conscious sedation with remifentanil and midazolam during brief painful procedures in children. Arch Pediatr Adolesc Med 153:1085, 1999.
92.
Green SM, Johnson NE: Ketamine sedation for pediatric procedures: Part 2, review and implications. Ann Emerg Med 19:1033, 1990.
93.
Green SM, Clem KJ, Rothrock SG: Ketamine safety profile in the developing world—Survey of practitioners. Acad Emerg Med 3:598, 1996.
94.
Green SM, Kupperman N, Rothrock SG, et al: Predictors of adverse events with ketamine sedation in children. Ann Emerg Med 35:35, 2000.
95.
JCAHO: Care of Patients: Examples of Compliance. Oakbrook Terrace, IL, Joint Commission on Accreditation of Healthcare Organizations, 1999, p 87.
96.
Green SM, Krauss B: The semantics of ketamine [editorial]. Ann Emerg Med 36:480, 2000.
97.
Green SM, Rothrock SG, Harris T, et al: Intravenous ketamine for pediatric sedation in the emergency department: Safety and efficacy with 156 cases. Acad Emerg Med 5:971, 1998a.
98.
Qureshi F, Mellis PT, McFadden MA: Efficacy of oral ketamine for providing sedation and analgesia to children requiring laceration repair. Pediatr Emerg Care 11:93, 1995.
99.
Green SM, Li J: Ketamine in adults: What emergency physicians need to know about patient selection and emergence reactions [editorial]. Acad Emerg Med 7:278, 2000.
100. Li
J: Ketamine: Emergency applications. In Plantz SH (ed): Emergency Medicine Text. Boston, Boston Medical Publishing, 1999. Available at http://www.emedicine.com/emerg/topic802.htm
101. Chudnofsky
CR, Weber JE, Stoyanoff PJ, et al: A combination of midazolam and ketamine for procedural sedation and analgesia in adult emergency department patients. Acad Emerg Med 7:228,
2000. 102. Howton
JC, Rose J, Duffy S, et al: Randomized, double-blind, placebo-controlled trial of intravenous ketamine in acute asthma. Ann Emerg Med 27:170, 1996.
103. Sherwin
TS, Green SM, Khan A, et al: Does adjunctive midazolam reduce recovery agitation after ketamine sedation for pediatric procedures? A randomized, double-blind, placebo-controlled trial. Ann Emerg Med 35:239, 2000. 104. Wathen
JE, Roback MG, Mackenzie T, Bothner JP: Does midazolam alter the clinical effects of intravenous ketamine sedation in children? A double-blind, randomized, controlled emergency department trial. Ann Emerg Med 36:579, 2000. 105. Annequin
D, Carbajal R, Chauvin P, et al: Fixed 50% nitrous oxide oxygen mixture for painful procedures: A French survey. Pediatrics 105:e47, 2000. Available at http://www.pediatrics.org/cgi/content/full/105/4/e47 106. Burton
JH, Auble TE, Fuchs SM: Effectiveness of 50% nitrous oxide/50% oxygen during laceration repair in children. Acad Emerg Med 5:112, 1998.
107. Hennrikus
WL, Shin AY, Klingelberger CE: Self-administered nitrous oxide and a hematoma block for analgesia in the outpatient reduction of fractures in children. J Bone Joint Surg Am 77:335,
1995. 108. Wattenmaker
I, Kasser JR, McGravey A: Self-administered nitrous oxide for fracture reduction in children in an emergency room setting. J Orthop Trauma 4:35, 1990.
109. Wilson
S: A survey of the American Academy of Pediatric Dentistry membership: Nitrous oxide and sedation. Pediatr Dent 18:287, 1996.
110. Gamis
AS, Knapp JF, Glenski JA: Nitrous oxide analgesia in a pediatric emergency department. Ann Emerg Med 18:177, 1989.
111. Krauss
B: Continuous-flow nitrous oxide: Searching for the ideal procedural anxiolytic for toddlers. Ann Emerg Med 37:61, 2001.
111A. Luhmann
JD, Kennedy RM, Jaffe DM, McAllister JD: Continuous-flow delivery of nitrous oxide and oxygen: A safe and cost-effective technique for inhalation analgesia and sedation of pediatric patients. Pediatr Emerg Care 15:388, 1999. 112. Luhmann
JD, Kennedy RM, Porter FL, et al: A randomized clinical trial of continuous-flow nitrous oxide and midazolam for sedation of young children during laceration repair. Ann Emerg Med
37:20, 2001. 113. American
Academy of Pediatrics Committee on Drugs: Reappraisal of lytic cocktail/demerol, phenergan, and thorazine (DPT) for the sedation of children. Pediatrics 95:598, 1995.
620
114. Nahata
MC, Clotz MA, Krogg EA: Adverse effects of meperidine, promethazine, and chlorpromazine for sedation in pediatric patients. Clin Pediatr 24:558, 1985.
115. Barsan
WG, Seger D, Danzl DF, et al: Duration of antagonistic effects of nalmefene and naloxone in opiate-induced sedation for emergency department procedures. Am J Emerg Med 7:155,
1989. 116. American
Academy of Pediatrics Committee on Drugs: Naloxone dosage and route of administration for infants and children: Addendum to emergency drug doses for infants and children. Pediatrics 86:484, 1990. 117. Medical 118. Glass
Letter: Nalmefene—A long-acting injectable opioid antagonist. Med Lett 37:97, 1995.
PSA, Jhaveri RM, Smith R: Comparison of potency and duration of action of nalmefene and naloxone. Anesth Analg 78:536, 1994.
119. Chudnofsky
CR, for the Emergency Medicine Conscious Sedation Study Group: Safety and efficacy of flumazenil in reversing conscious sedation in the emergency department. Acad Emerg Med
4:944, 1997. 120. Shannon
M, Albers G, Burkhart K, et al: Safety and efficacy of flumazenil in the reversal of benzodiazepine-induced conscious sedation. J Pediatr 131:582, 1997.
121. Sugarman 122. Hicks
JM, Paul RI: Flumazenil: A review. Ped Emerg Care 10:37, 1994.
JL, Smith SW, Lynch MT: Metabolic acidosis in restraint-associated cardiac arrest: A case series. Acad Emerg Med 6:239, 1999.
123. Ruttenber
AJ, Lawler-Heavner J, Yin M, et al: Fatal excited delirium following cocaine use: Epidemiologic findings provide new evidence for mechanism of cocaine toxicity. J Forensic Sci 42:25,
1997. 124. Stratton
SJ, Rogers C, Green K: Sudden death in individuals in hobble restraints during paramedic transport. Ann Emerg Med 25:710, 1995.
125. Roberts
JR, Geeting GK: Intramuscular ketamine for the rapid tranquilization of the uncontrollable, violent, and dangerous adult patient. J Trauma 51:1008, 2001.
126. Garza-Trevino
ES, Hollister LE, Overall JE, Alexander WF: Efficacy of combinations of intramuscular antipsychotics and sedative-hypnotics for control of psychotic agitation. Am J Psychiatry
146:1598, 1989. 127. Battaglia 128. Dubin
WR: Rapid tranquilization: Antipsychotics or benzodiazepines. J Clin Psychiatry 49:5, 1988.
129. Clinton 130. Dubin
J, Moss S, Rush J, et al: Haloperidol, lorazepam, or both for psychotic agitation? A multicenter prospective, double-blind emergency department study. Am J Emerg Med 15:335, 1997.
JE, Sterner S, Steimacheers Z, et al: Haloperidol for sedation of disruptive emergency patients. Ann Emerg Med 16:319, 1987.
WR, Feld JA: Rapid tranquilization of the violent patient. Am J Emerg Med 7:313, 1989.
131. Thomas
H, Schwartz E, Petrilli R: Droperidol versus haloperidol for chemical restraint of agitated and combative patients. Ann Emerg Med 21:407, 1992.
132. Grancher 133. FDA
online: Available at http://www.fda.gov/medwatch/SAFETY/2001/inapsine.htm, http://www.fda.gov/bbs/topics/ANSWERS/2001/ANS01123.html
134. Horowitz 135. Liu
RP, Ruth DD: Droperidol in acute agitation. Curr Ther Res 25:361, 1979.
BZ, Bizovi K, Moreno R: Droperidol-behind the black box warning. (commentary). Acad Emerg Med 9:615, 2002.
LM: Dose response to intramuscular succinylcholine in children. Anesthesiology 55:599, 1981.
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Section VI - Soft Tissue Procedures
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Chapter 35 - Principles of Wound Management Richard L. Lammers
Acute traumatic wound management is one of the most common procedures in the practice of emergency medicine. There are many areas of controversy in the medical literature, numerous personal preferences, and a plethora of protocols and individual approaches. Few agreed upon standards of care exist for many aspects of wound care.[1] Also, there are many myths and misconceptions surrounding the vagaries of wound preparation and wound care. The purpose of this chapter is to give the clinician a general approach to wound care and to suggest reasonable techniques; however, lack of data to support or refute many of the described clinical issues that confront clinicians daily renders much of the following discussion intuitively practical but somewhat theoretical. Wound care involves much more than closure of divided skin. The primary goal of wound care is not the technical repair of the wound; it is providing optimal conditions for the natural reparative processes of the wound to proceed. Primary wound healing is not an inevitable process. For centuries, victims of wounds commonly experienced inflammation, infection, and extreme scarring; in fact, these processes were considered part of normal wound repair. Only in the late 19th century did surgeons first realize that sepsis could be separated from healing. [2] The cornerstones of wound care are cleaning, debridement, closure, and protection. The primary technical objectives in wound care are as follows: 1. 2. 3. 4. 5. 6.
Preserving viable tissue and removing nonviable tissue Restoring tissue continuity and function Optimizing conditions for the development of wound strength Preventing excessive or prolonged inflammation Avoiding infection and other impediments to healing Minimizing scar formation
When presenting to emergency departments (EDs) with acute wounds, patients report that their top priorities in the management of their wounds include prevention of infection, return to normal function, good cosmetic outcome, and minimal pain during repair. [3] [4] This chapter reviews current strategies for achieving all of these goals.
BACKGROUND Wound Healing Emergency clinicians should have a basic understanding of the process of wound healing. Highlights of this complex phenomenon as they relate to clinical decision making are presented. Wounds extending beneath the epithelium heal by forming scar tissue. Inflammation, epithelialization, fibroplasia, contraction, and scar maturation constitute the stages of this nonspecific repair process. [2] [5] [6] Inflammation is a beneficial response that serves to remove bacteria, foreign debris, and devitalized tissue—a biologic debridement. Polymorphonuclear and mononuclear leukocytes concentrate at the site of injury and phagocytose dead and dying tissue, foreign material, and bacteria in the wound. [7] As white blood cells die, their intracellular contents are released into the wound. In excessive amounts, they form the purulence characteristic of infected wounds. Some exudate is expected even in the absence of bacterial invasion; however, infection with accumulation of pus interferes with epithelialization and fibroplasia and impairs wound healing. Wounds contaminated with significant numbers of bacteria or foreign material may undergo a prolonged or persistent inflammatory response and may not heal. Granuloma formation surrounding retained sutures is an example of chronic inflammation. [8] As white blood cells remove debris within the wound, epithelial cells at the surface of the wound begin to migrate across the tissue defect. In most sutured wounds, the surface of the wound develops an epithelial covering impermeable to water within 24 to 48 hours. Eschar and surface debris impair this process. The epithelium thickens and grows downward into the wound and along the course of skin sutures. Although there is some "adhesiveness" to the wound edges during the first few days, this is lost because of fibrinolysis. By the fourth or fifth day, newly transformed fibroblasts in the wound begin synthesizing collagen and protein polysaccharides, initiating the stage of scar formation known as fibroplasia. Collagen is the predominant component of scar tissue. Wound strength is a balance between the lysis of old collagen and the synthesis of new collagen "welding" the wound edges together. The amount of scar tissue is influenced by physical forces (e.g., the stresses imposed by movement) acting across the wound. In contrast, a wound that heals by secondary intention closes by contraction. Contraction is the movement of skin edges toward the center of the defect, primarily in the direction of underlying muscle. Significant gains in tensile strength do not begin until approximately the fifth day following the injury. Strength increases rapidly for 6 to 17 days, more slowly for an additional 10 to 14 days, and almost imperceptibly for as long as 2 years ( Fig. 35-1 ). The strength of scar tissue never quite reaches that of unwounded skin. Although the process of collagen formation is essentially completed within 21 to 28 days, the scar widens for another month, and collagen continues to remodel and strengthen the wound for up to 1 year. [2] [8] Decisions regarding the optimal time for suture removal and the need for continued support of the wound with tape are influenced by (1) wound tensile strength, (2) the period of scar widening, and (3) the cosmetically unacceptable effect of epithelialization along suture tracks. Scars are quite red and noticeable at 3 to 8 weeks following closure. However, the appearance of a scar should not be judged before the scar is well into its remodeling phase. The cosmetic appearance of wounds 6 to 9 months after injury cannot be predicted at the time of suture removal. [9] Therefore, any scar revision should be postponed until 6 to 12 months after injury. Zitelli states, "The most important factor in predicting the cosmetic result is wound location. In general, wounds on concave surfaces heal with better cosmetic results than wounds on convex surfaces. Besides location, other factors such as skin color, wound size, and wound depth are helpful in predicting the cosmetic results of wounds healing by secondary intention." [10] Small, superficial wounds in lax, light-colored skin, especially in areas in which the skin is thin, result in less noticeable scars. Wounds on convex surfaces look better after
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Figure 35-1 Graphic representation of the various phases of wound healing. Note that the tensile strength of scar tissue never reaches that of unwounded skin. Displayed values of tensile strength are approximate and demonstrate the general concept of wound healing.
primary closure than following secondary healing. Static and dynamic forces, and the propensity toward keloid formation, may influence the long-term cosmetic appearance of wounds more than the surgical skills of the clinician who repaired the wound. [9] Repigmentation occurs over 3 to 5 years, even in large wounds that heal by secondary intention. [10]
INITIAL EVALUATION The approach to the management of a particular wound depends on information gathered during history taking and on the results of physical examination. The decision on whether to close a wound immediately or after a period of observation is based on various factors that affect the risk of infection. Some wounds may appear benign but conceal extensive and devastating underlying tissue damage. The discovery that an extremity wound was produced by a roller or wringer device, a high-pressure injection gun, high-voltage electricity, heavy and prolonged compressive forces, or the bite of a human or a potentially rabid animal radically alters the overall management of the affected patient. The American College of Emergency Physicians' "Clinical Policy for the Initial Approach to Patients Presenting with Penetrating Extremity Trauma" provides a useful approach to the evaluation of all wounds. [11] History In the initial evaluation of a wound, the clinician should identify all of the extrinsic and intrinsic factors that jeopardize healing and promote infection. These include the mechanism of injury, the time of injury, the environment in which the wound occurred, and the patient's immune status. Although the clinician would like to believe that all patients are forthright and honest when offering historical data, such is not always the case. A common example of this is the workman who sustains a human bite to the hand during a bar fight on Saturday who steadfastly claims that the injury occurred on the job Monday morning to gain workman's compensation benefits. Wound Age: The "Golden Period"
In general, the likelihood of wound infection increases with the time that elapses before definitive wound care. [12] [13] [14] A delay in wound cleaning is the most important variable, and may allow bacteria contaminating the wound to proliferate. A delay in treatment of a contaminated wound for as little as 3 hours can result in infection. [15] [16] However, there is evidence suggesting that wounds in highly vascular regions such as the face and scalp can be closed without increased risk as long as 24 hours after injury. [17] Some investigators have been unable to establish any significant relationship between time of suturing and subsequent infection rates. [18] Contrary to popular belief, the "golden period"—the maximum time after injury that a wound may be safely closed without significant risk of infection— is not a fixed number of hours.[19] Likely this period is longer than commonly believed ( Fig. 35-2 ). Many factors affect infection risk, and closure decisions should not be based solely on temporal considerations. Peacock points out that "a clean razor slice of highly vascular skin of the face might be closed safely 48 hours after injury, whereas a stable-floor-nail penetration of the foot of an elderly person might not be closed safely 1 minute after injury."[6] Berk and colleagues concluded that there is little change in wound infection rates in most areas of the body for up to 19 hours after various traumatic injuries, and infection rates of simple wounds involving the head are essentially unaffected by the interval between injury and repair. [17] Hence, all data accumulated in the initial evaluation, both historical and physical, must be considered when making the decision to close a wound in a particular patient. In addition, the techniques of wound care in and of themselves may extend the golden period; a skillful clinician can often convert a dangerously contaminated wound into a clean wound that can be safely closed. [6] Other Historical Factors
Other factors that affect wound healing or the risk of infection include the patient's age and state of health. Patient age appears to be an important factor in host resistance to infection; those individuals at the extremes of age—young children and the elderly—are at greatest risk. [20] [21] Infection rates are reported to be higher in patients with medical illnesses (e.g., diabetes mellitus, immunologic deficiencies, malnutrition, anemia, uremia, congestive heart failure, cirrhosis, malignancy, alcoholism, arteriosclerosis, arteritis, collagen vascular disease, chronic granulomatous disease, smoking or chronic hypoxia, liver failure), in obese patients, and in patients taking steroids or immunosuppressive drugs or those receiving
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Figure 35-2 This laceration illustrates that there is no specific time frame (the so-called golden period) during which a laceration must be closed, or else relegated to an unsightly scar or a revision months later. A, This woman was punched in the face, suffered a laceration of the cheek, and presented to the ED 36 hours later. The wound was not infected, had contracted, and was beginning to heal by granulation. Under local anesthesia the wound was opened, irrigated, minimally debrided, and the skin edges were trimmed. B, Using a No. 15 blade, a 1-mm skin edge was incised. C, The trimmed edges were then cut by scissors. D, The wound was undermined to relieve tension on the skin. E, The wound was closed with 6-0 interrupted sutures that were removed in 5 days. No antibiotics were used and only a small linear scar resulted.
radiation therapy. Shock, remote trauma, distant infection, bacteremia, retained foreign bodies, denervation, and peripheral vascular disease also increase wound infection rates and slow the healing process. [7] [21] [22] [23] Additional information pertinent to decision making in wound management includes: Present medications (specifically, anticoagulants and immunosuppressive drugs) Allergies (especially to local anesthetics, antiseptics, analgesics, antibiotics, and tape) Tetanus immunization status Potential exposure to rabies (in bite wounds and mucosal exposures) Potential for foreign bodies embedded in the wound, especially when the mechanism of injury is unknown or was associated with breaking glass or vegetative matter[24] Previous injuries and deformities (especially in extremity and facial injuries) Associated injuries (underlying fracture, joint penetration) Other factors (availability for follow-up, patient understanding of wound care or compliance)
Physical Examination All wounds should be examined for amount of tissue destruction, degree of contamination, and damage to underlying structures. A common error in wound management is to assume that a traumatic wound is already contaminated and then, during the examination, to contaminate it further. Despite the fact that all traumatic wounds are contaminated to some degree, these injuries should be examined using aseptic technique. It is prudent for the examiner to wear clean or sterile
gloves and avoid droplet contamination from the mouth by maintaining distance or, preferably, by wearing a mask. [25] It has never been proven, however, that the use of sterile gloves (as opposed to clean ones) has any influence on infection rates for common lacerations, and many clinicians do not routinely
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use sterile gloves for all wound care. Wounds should be examined under good lighting and after bleeding is controlled. It is appropriate, and often necessary, to obtain a bloodless field with the use of tourniquets. Distal perfusion and motor/sensory function should be assessed and documented during the evaluation of extremity wounds, and before the use of anesthetics. Mechanism of Injury and Classification of Wounds
The magnitude and direction of the injuring force and the volume of tissue on which the force is dissipated determine the type of wound sustained. Three types of mechanical forces produce soft tissue injury: shear, tension, and compression forces. The resulting disruption or loss of tissue determines the configuration of the wound. Wounds may be classified into six categories: 1. Abrasions. Wounds caused by forces applied in opposite directions, resulting in the loss of epidermis and possibly dermis (e.g., skin grinding against road surface). 2. Lacerations. Wounds caused by shear forces that produce a tear in tissues. Tensile and compressive forces also cause separation of tissue. Little energy is required to produce a wound by shear forces (e.g., a knife cut). Consequently, little tissue damage occurs at the wound edge, the margins are sharp, and the wound appears "tidy." The energy required to disrupt tissue by tensile or compressive forces (e.g., forehead hitting a dashboard) is considerably greater than that required for tissue disruption by shear forces, because the energy is distributed over a larger volume. These lacerations have jagged, contused, "untidy" edges; consequently, they have a higher risk of infection. [21] 3. Crush wounds. Wounds caused by the impact of an object against tissue, particularly over a bony surface, which compresses the tissue. These wounds may contain contused or partially devitalized tissue. 4. Puncture wounds. Wounds with a small opening and whose depth cannot be entirely visualized. Puncture wounds are caused by a combination of forces. 5. Avulsions. Wounds in which a portion of tissue is completely separated from its base and is either lost or left with a narrow base of attachment (a flap). [26] Shear and tensile forces cause avulsions. 6. Combination wounds. Wounds with a combination of configurations. For example, stellate lacerations caused by compression of soft tissue against underlying bone create wounds with elements of crush and tissue separation; missile wounds involve a combination of shear, tensile, and compressive forces that puncture, crush, and sometimes avulse tissue. [25] Contaminants (bacteria and foreign material).
Numerous factors affect the risk of wound infection, but the primary determinants of infection are the amount of bacteria and dead tissue remaining in the wound. Also of importance is the ability of the patient's immune system to respond to bacterial invasion and the presence of local tissue ischemia or hypoxia. [28]
[27]
Essentially all traumatic wounds are contaminated with bacteria to some extent. The number of bacteria remaining in the wound at the time of closure is directly related to the risk of infection. A critical number of bacteria must be present in a wound before a soft tissue infection develops. In experimental wounds produced by shear forces, an inoculum of =10 6 aerobic bacteria per gram of tissue inevitably produces wound infection in time. When the mechanism of injury involves a compressive force, the infective dose of bacteria is =10 4 bacteria per gram of tissue. If bacterial counts after injury (or after wound management) are below this level, the wound has a very low probability of becoming infected. [12] [15] Surgical operations are categorized on the basis of the relative levels of bacterial contamination of the wounds. Most traumatic wounds fall into one of two categories: 1. Contaminated wounds. Traumatic wounds 10 5 bacteria/cm2 ) include the hairy scalp, the forehead, the axilla, the perineum, the foreskin of the penis, the vagina, the mouth, intertriginous areas, and the nails. In other regions, skin bacteria are sparse (10 2 to 103 bacteria/cm2 ) and are not a source of infection. [25] Wounds in regions of high vascularity, such as the scalp and the face, more easily resist bacterial incursions. The high vascularity of the scalp probably accounts for extremely low infection rates with scalp injuries, despite the large numbers of endogenous
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microflora. Distal extremity wounds, in contrast, are more at risk for the development of wound infections than are injuries of most other parts of the body. [20] Wounds in ischemic tissue are notoriously susceptible to infection. [38] Devitalized Tissue
Identifying devitalized tissue is an important part of the examination of a wound. Tissue damage lowers the resistance of the wound to infection. Devitalized or necrotic tissue enhances the possibility of infection in a wound by providing a culture medium in which bacteria proliferate, by inhibiting leukocyte phagocytosis, and by creating an anaerobic environment suitable for certain bacterial species. [25] [27] Underlying Structures
Identification of injury to underlying structures such as nerves, vessels, tendons, joints, bones, or ducts may lead the emergency clinician to forgo wound closure and consult a surgical specialist. Procedures such as joint space irrigation, reduction and debridement of compound fractures, neurorrhaphy, vascular anastomosis, and
flexor tendon repair are best accomplished in the controlled setting of the operating room, in which optimal lighting, proper instruments, and assistance are available. [25]
CLEANING The wound should be cleaned as soon as possible after evaluation. Although most wounds are contaminated initially with less than an infective dose of bacteria, given time and the appropriate wound environment, bacterial counts may reach infective levels. The goals of wound cleaning and debridement are the same: (1) to remove bacteria and reduce their numbers below the level associated with infection, and (2) to remove particulate matter and tissue debris that would lengthen the inflammatory stage of healing or allow the growth of bacteria beyond the critical threshold. [23] Patient Preparation Before examining, cleaning, exploring, or repairing wounds, medical procedures should be explained to patients to allay fears and encourage patient cooperation. In general, all wound care should be performed with the patient in a supine position, since fainting is a common occurrence once wound preparation has commenced ( Fig. 35-3 ). Even the most hardy or brave patient may faint at the sight of a needle, scalpel, or blood. Patient falls are a serious source of comorbidity and litigation. Likewise, relatives and friends should be allowed to stay with the patient only after their propensity for fainting has been assessed and they have been properly cautioned. The wise clinician will insist that any significant others who remain in the room to support the patient sit during the procedure and report any perceived dizziness or nausea. In general it is not suggested that parents or friends actively participate in the wound care procedures. Wound Handling Anyone cleaning, irrigating, or suturing wounds should wear protective eyewear and a mask, as virtually any patient may be seropositive for the human immunodeficiency virus (HIV). Although mucosal exposure to blood or tissue products that
Figure 35-3 What's wrong with this picture? The patient is sitting up during laceration repair. Shortly after this picture was taken the patient fainted and nearly fell off the chair. Even the bravest patients should be supine for surgical procedures.
are contaminated by HIV is considered a relatively low risk for subsequent infection, universal precautions are currently recommended. Thorough cleansing of bacteria, soil, and other contaminants from a wound cannot be accomplished without the patient's cooperation. Scrubbing most open wounds is painful, and the patient's natural response is withdrawal. Therefore, local or regional anesthesia often must precede the examination and cleaning of a wound. Approaches to wound anesthesia are discussed in detail in Chapter 30 Chapter 31 Chapter 32 Chapter 33 . Despite adequate anesthesia, the patient may be unable to cooperate because of apprehension. The clinician should explain the wound cleansing procedure and assure the patient that everything possible will be done to minimize pain. Reassurance may not alleviate the fears of young children, and both sedation and physical restraining devices must be used. Approaches to sedation using parenteral sedative-hypnotics and narcotic agents and the use of inhaled nitrous oxide are discussed in Chapter 34 . The two primary methods of wound cleaning are mechanical scrubbing and irrigation. Soaking a wound in a saline or antiseptic solution before the clinician arrives is of little value and is not recommended as a routine practice. Indeed, soaking a wound in saline may actually increase bacterial counts. [39] The following section discusses methods of scrubbing and irrigation. Mechanical Scrubbing Initially, a wide area of skin surface surrounding the wound should be scrubbed with an antiseptic solution to remove contaminants that in the course of wound management might be carried into the wound by instruments, suture material, dressings, or the clinician's gloved hand. Minimal aseptic technique requires the use of gloves during the cleaning procedure. It is important to remove all nonabsorbable particulate matter; any such material left in the dermis may become impregnated in the healed tissue and result in a disfiguring "tattoo" effect. [8] However, scrubbing the internal surface of a wound is controversial. Although scrubbing a wound with an antiseptic-soaked sponge does remove foreign particulates, bacteria, and tissue debris, an abrasive sponge may inflict more damage on tissue and provoke more inflammation.[40] [41]
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Some clinicians reserve mechanical scrubbing for "dirty" wounds contaminated with significant amounts of foreign material. If irrigation alone is ineffective in removing contaminants from a wound, the wound should be scrubbed. Because the amount of damage inflicted on tissues by scrubbing correlates to the porosity of the sponge, a fine-pore sponge (e.g., Optipore sponge [90 pores per linear inch]) should be used to minimize tissue abrasion. [40] [42] Detergents have an advantage over saline because they minimize friction between the sponge and tissue, thereby limiting tissue damage during scrubbing. Detergents also dissolve particles, helping to dislodge them from the wound surface. Unfortunately, many of the available detergents are toxic to tissues. [40] [43] Antiseptics During Cleaning For many years, antiseptic solutions have been used for their antimicrobial properties in and around wounds ( Table 35-1 ). Studies of antiseptics in wounds demonstrate that there is a delicate balance between killing bacteria and injuring tissue. [44] Intact skin can withstand strong microbicidal agents, whereas leukocytes and the exposed cells of skin and soft tissue can be damaged by these agents. [23] Many antiseptic solutions have been used for cleaning wounds. Povidone-iodine (Betadine) is widely available as a 10% stock solution. The undiluted solution is best kept out of the wound proper. Although studies on the efficacy and safety of povidone-iodine solution have shown variable results, [29] [39] [45] [46] [47] [48] it appears that dilute povidone-iodine solution in concentrations of 800 mm Hg.[86] A finger can be exsanguinated with a Penrose drain, but a separate drain should be used as a tourniquet ( Fig. 35-16 ). A few millimeters of difference in total stretch makes a large difference in the pressure applied by this type of tourniquet. [86] Alternatively, a finger can be exsanguinated with a moistened piece of gauze opened to its fullest length, folded in half, and rolled tightly around the elevated finger from tip to base. A Penrose drain is stretched around the base of the finger and secured with a hemostat, and the gauze is removed. A latex rubber surgical glove placed over a patient's hand also can serve as a finger tourniquet. The tip of the glove covering the injured digit is removed, and the latex rubber is then rolled proximally along the patient's finger to form a constricting band at the base ( Fig. 35-17 ). Another advantage of this technique is that contamination of the wound during closure is less likely. Rolled surgical gloves produce pressures ranging from 113 to 363 mm Hg, depending on the thickness, the amount of glove finger removed, the number of rolls, and the size of the glove in relation to the size of the patient's hand. [86] Pressure under a Penrose drain ranges between 100 and 650 mm Hg, but it can be more easily controlled. [87] Commercial ring-shaped exsanguinating digit tourniquets are available (Tourni-cot [Mar-Med Company]) ( Fig. 35-18 ). There is a danger of forgetting to remove such a small tourniquet and of accidentally incorporating it in the dressing. These techniques provide bloodless fields in which to examine, clean, and close extremity wounds. The maximum tourniquet time on a finger should not exceed 20 to 30 minutes.[86] [87] Debridement of questionably devitalized tissue in a wound is best accomplished without a tourniquet or pharmacologic vasoconstriction, because bleeding from tissues is often an indication of their viability. [80]
CLOSURE The various techniques of wound closure are presented in Chapter 36 . The remainder of this chapter addresses issues related to wound management (e.g., secondary closure, wound dressings, antibiotic use, aftercare instructions, and suture removal). Open vs Closed Wound Management Wounds that heal spontaneously (i.e., by secondary intention) undergo much more inflammation, fibroplasia, and contraction than those whose edges are reapproximated by wound closure techniques. [8] [87A] During wound healing, contraction covers the defect, yet it may have undesirable consequences—notably, deformity (contracture) or loss of function. Left to itself, the healing process may be unable to close a
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Figure 35-16 Use of Penrose drain for exsanguination (A) of a wounded digit. A second Penrose drain is applied (B) as a finger tourniquet, and the first drain is removed (C). During actual patient care, the clinician would use sterile technique including gloves.
defect completely in areas in which surrounding skin is immobile, such as on the scalp or in the pretibial area. [8] Exposed tendons, bone, nerves, or vessels may desiccate in an open wound. If the patient is careless with an otherwise adequate dressing that covers an open wound, the wound may be further contaminated. [88] The advantages of surgical closure of wounds are apparent: This procedure minimizes inflammation, fibroplasia, contracture, scar width, and contamination. On the other hand, risks are incurred when wounds are closed. Closure of contaminated wounds increases the
Figure 35-17 Use of a sterile glove to provide a clean field and serve as a finger tourniquet. The distal end of the glove is clipped (A), and the glove finger is rolled proximally over the digit (B, C). During actual patient care, the clinician would use sterile technique including gloves.
probability of wound infection, with impaired healing, dehiscence, and sepsis as possible complications. After cleaning and debridement, wounds left unsutured appear to have a higher resistance to infection than do closed wounds. Sutures in themselves are detrimental to healing and increase the risk of infection. [12] [88] [89] Each suture inflicts an intradermal incision, damaging surface epithelium, dermis, SQ fat, blood vessels, small nerves, lymphatics, and epithelial appendages such as hair follicles, sweat glands, and ducts. These appendages, once divided and separated by a stitch,
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Figure 35-18 As in Figure 35-7 , a sterile glove has been used to provide a sterile field for the thumb. In addition, a commercial rubber ring tourniquet device has been applied to enhance hemostasis. The accompanying tag has been left exposed to remind the operator of the tourniquet device.
usually undergo inflammation and resorption. [90] [91] Each suture is another piece of foreign material that provokes inflammation. [8] When a suture is removed, bacteria that have settled on the exposed portion of the suture are pulled into the suture track and deposited there. [90] Raised pretibial flap lacerations in elderly patients often necrose when sutured but survive and heal well by secondary intention if taped back into position. [92] If the wound is judged to be clean or is rendered clean by scrubbing, irrigation, and debridement, it may be closed. If the wound remains contaminated despite the best of efforts, it must be left open to heal by secondary intention. If the status of the wound is uncertain, the clinician must estimate the risk of infection. Another option available is delayed primary closure. Delayed Primary or Secondary Closure There is a common misconception that all wounds must either be sutured within a few hours or left open and relegated to slow healing and an unsightly scar. If there is a substantial risk that closure of a particular wound might result in infection, the decision to close or to leave the wound open can be postponed ( Fig. 35-19 ). The condition of the wound after 3 to 5 days will then determine the best strategy ( Fig. 35-20 ). Although cleaning and debridement should be accomplished as rapidly as possible, there is no urgency in closing a wound. Edlich and coworkers point out that "the fundamental basis for delayed primary closure is that the healing open wound gradually gains sufficient resistance to infection to permit an uncomplicated closure." [25] Despite its effectiveness, delayed primary closure is a technique that is unappreciated and likely underused by most clinicians. Open wound management is usually an outpatient procedure. The technique consists of the usual careful cleaning and meticulous debridement, followed by packing of the wound with sterile, saline-moistened, fine-mesh gauze. The packed wound is covered by a thick, absorbent, sterile dressing. Depending on the specifics of the wound and the ability of the patient to perform his or her own wound care, the packing may be changed daily at home or in the ED, or the wound
Figure 35-19 Incidence of wound infection over time when delayed closure is performed. Delayed closure is best accomplished on the fourth or fifth day to minimize the risk of infection. (From Edlich RF, Thacker JG, Rodeheaver GT, et al: A Manual for Wound Closure. St. Paul, MN, 3M Medical Surgical Products, 1979. Reproduced by permission. © 1979 by Minnesota Mining and Manufacturing Company.)
may be left undisturbed for several days. Sterile saline-soaked packing is standard, and there is no need to impregnate wounds with antiseptics. Prophylactic antibiotics are occasionally prescribed, but their use is neither mandatory nor of proven benefit. On the fourth postoperative day, the wound is reevaluated for closure. If no evidence of infection is present, the wound margins can be approximated (delayed primary closure), or the wound can be excised and then sutured (secondary
closure) with minimal risk of infection. Because the wound is closed before the proliferative phase of healing, there is no delay in final healing, and the results are indistinguishable from those of primary healing. Certain wounds should almost always be managed open or by delayed closure. These include wounds that are already infected and those heavily contaminated by soil, organic matter, or feces. Also included in this category are wounds associated with extensive tissue damage (e.g., high-velocity missile injuries, explosion injuries of the hand, or complex crush injuries) and most bite wounds. Lacerations to the bottom of the feet, such as those occurring when the patient steps on an unknown object while wading in a stream or running through a field, are ideal candidates for delayed closure. Human bite wounds should probably never be sutured. Clinicians disagree as to which animal bite wounds may be closed initially. Most would suture cosmetically deforming injuries, including facial bites, and bite wounds that can be completely excised.[42] [93] Others would suture nonextremity dog bites. [94] In severe soft tissue injuries, delayed closure allows time for nonviable tissue to demarcate from uninjured tissue. Debridement can then be accomplished with maximal preservation of tissue. [88]
PROTECTION Dressings At the conclusion of wound repair, dried blood on the skin surface should be wiped away gently with moistened gauze, and the wound should be covered with a non-adherent dressing.
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Figure 35-20 A, This dirty contused wound, now 18 hours old, is an ideal candidate for a delayed primary closure. B, At presentation the wound is anesthetized, scrubbed, irrigated, and debrided. C, The wound is packed with sterile gauze and covered by a dry dressing. No antibiotics were prescribed. D, Four days later the packing is removed, and the wound is minimally debrided. E, Interrupted sutures are placed as though this is a fresh, clean wound. At suture removal 10 days later, only a linear scar was evident.
Depending on the specifics of the wound and the type of repair, a dressing can consist of a simple dry gauze pad or a complex multilayer dressing. Some wounds, such as sutured scalp lacerations, do not routinely require any dressing. Although various specialized (and expensive) dressings are available, there are little data to support their use over readily available, properly applied gauze dressings. Function of Dressings
Dressings serve various functions. They protect the wound from contamination and trauma, absorb secretions from the wound, immobilize the wound and the surrounding area, exert downward pressure on the wound, and improve the patient's comfort. [19] [95] [96] Occlusive dressings on burns or abrasions prevent painful exposure of the wound to the air and dehydration of the wound surface. [97] Sutured wounds are susceptible to infection from surface contamination during the first 2 days after wound repair. Dressings effectively protect the wound from contamination during this vulnerable period. One of the primary functions of a gauze dressing is to absorb the serosanguineous drainage that exudes from all wounds. Absorbent dressings also reduce the development of stitch abscesses to some extent. Surface sutures produce small indentations at their points of entrance; tiny blood clots and debris overlie these indentations, allowing bacterial growth at the site. Small "stitch abscesses" can develop; these are initially undetectable but are nevertheless destructive to epithelium. Stitch abscesses rarely infect the entire wound but can slightly increase the width of the scar and produce noticeable, punctate suture marks. [19] The most common type of dressing is constructed in three layers: a nonadherent contact layer, an absorbent layer, and an outer wrap ( Fig. 35-21 ). [98] Ideally, this dressing provides nonadherence without maceration. Contact Layer: Dry, Semiocclusive, and Occlusive Dressings
Petrolatum gauze (e.g., Adaptic, Xeroform, Betadine, Aquaflo) can be applied next to the wound surface to prevent the wound
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Figure 35-21 A common three-layer dressing, consisting of antibiotic ointment, Adaptic, and gauze.
from sticking to the dry gauze in the absorbent layer and to protect the regenerating epithelium ( Table 35-2 ). (Nonadherent material should always be used to cover skin grafts.) Coarse weaves of gauze, usually available in the form of multilayered pads, absorb blood and exudate, but the dressing will adhere if the interstices of the fabric are relatively large. Capillaries, fibrin, and granulation tissue will penetrate and become enmeshed in the material. If the proteinaceous exudate from the wound dries by evaporation, the scab usually clings to the dressing. [98] [99] Some clinicians use this effect to "debride" the wound when the gauze is removed. However, it also destroys healing tissue, particularly the new epithelium. Debridement of the wound with wet-to-dry dressings is quick, but debridement with surgical instruments is more controlled and less traumatic. Adherence to the wound can be avoided if the dressing is nonabsorbent, occlusive, or finely woven. Some clinicians use fine mesh gauze (41 to 47 warp threads per square inch) rather than petrolatum gauze on abrasions, especially on those wounds that are heavily contaminated, because removal of this type of dressing debrides only the small tufts of granulation tissue that become fixed in the mesh pores, leaving a clean, even surface. Once a healthy, granulating surface is present and re-epithelialization is proceeding, nonporous dressings can be used. [99] Fine mesh gauze also is used next to exposed tissue in wounds being considered for delayed primary closure; a protective and absorptive bulky dressing is placed on top of the wound. Wounds covered with permeable dressings such as plain gauze tend to dry out. Drying of the wound surface damages a shallow layer of exposed dermis, which impedes epidermal resurfacing of abrasions, burns, and incisions. [96] Wound desiccation results in further epidermal necrosis, crust formation, and increased inflammation.[99] [100] If the wound is kept moist by covering it with an occlusive film soon after wound management and if the film is left in place for at least 48 hours, the epidermis will migrate over the surface of the dermis up to 100% faster than when a dry scab is allowed to form. [101] [102] [103] In one study, the occluded half of a surgical incision produced TABLE 35-2 -- Advantages of Occlusive Dressings 1. More rapid healing 2. Less pain from air exposure 3. Better cosmetic results 4. Fewer dressing changes
5. Better protection from bacteria Data from Eaglstein WH: Effect of occlusive dressings on wound healing. Clin Dermatol 2:107, 1984. a more linear, less pigmented scar. [104] Protection of wounds that are healing by secondary intention with occlusive or semiocclusive dressings has several advantages, [10] including more rapid healing, less pain from air exposure, better cosmetic result, few dressing changes, and protection from bacteria. This occlusive effect is achieved with various polyurethane-derived membranes, such as Epilock (Derma-Lock Medical Corporation), Op-Site (Smith and Nephew, Ltd.), Tegaderm (3M), Bioclusive (Johnson & Johnson), and Primaderm (ACCO, Inc.); those with soluble collagen or gelatin backing, such as DuoDerm (Convatec) and Biobrane (Woodroof Laboratories); and products with hydrogels, such as Vigilon. [99] One fear of using occlusive dressings is that microorganisms will proliferate in the moist environment beneath the occlusive film and increase wound infection rates. [96] [105] Occlusive dressings such as DuoDerm actually serve more as a barrier to external pathogenic bacteria [106] ; although surface bacteria under occlusive dressings can multiply,[107] chronic wounds, usually contaminated with large numbers of bacteria, are routinely treated with occlusive dressings successfully. [108] A paint-on collodion dressing over a wound closed with a buried subcuticular stitch provides considerably greater resistance to infection than wounds closed by the same technique but with no dressing. The use of collodion obviates the need for a gauze dressing, frequent dressing changes, and uncomfortable dressings in areas such as the groin, the axilla, and the neck. [109] However, the collodion does not allow drainage of the wound and so is rarely used. Another concern is that occlusive dressings will macerate underlying skin. Optimal wound appearance under a dressing is a moist red surface with capillary and epithelial growth. Collagen sponge dressings provide this appearance (if they are not accidentally dislodged), whereas both DuoDerm and Op-Site adhere to the wound site, macerate it, and produce a thick eschar that may be difficult to remove. However, underneath the eschar the surface is epithelialized. [110] Wounds covered with certain occlusive dressings or with silver sulfadiazine (Silvadene [Marion Laboratories]) applications appear to be blanketed with pus; this exudate actually represents the beneficial proliferation of macrophages and polymorphonuclear leukocytes. [103] [111] Adhesive-backed dressings (e.g., DuoDerm and Op-Site) have a tendency to adhere to and remove new epidermis, and they do not allow exudate to drain out the edges of the dressing. Between dressing changes, the wound should be coated with petrolatum or an antibiotic ointment before these products are applied. [10] Epilock has the advantage of thermally insulating the wound by virtue of its thickness, but unlike Tegaderm and Op-Site, it is opaque and does not allow inspection of the underlying wound surface. [111] Because Epilock allows drainage of exudate, it is better tolerated by patients if the overlying gauze bandage is changed daily.
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Other nonadherent-type dressings include Adaptic, Xeroform, Betadine, Dermicel, and the nonabsorbent Telfa. Petrolatum gauze does not appear to enhance epidermal healing. [112] Absorbent Layer
In dressing wounds with considerable drainage, sufficient gauze should be used to cover the wound and to absorb all of the drainage. Dressings on such wounds can be changed daily, which is frequent enough to avoid bacterial overgrowth beneath the dressing. [8] [99] Once a dressing becomes moist, pathogens can pass through it to the underlying wound. [96] Any dressing should be changed whenever it becomes soiled, wet, or saturated with drainage. Fluid accumulating under an occlusive dressing should be aspirated or the dressing changed every 1 to 2 days during the first week or until the exudate no longer accumulates. [113] A dressing that is used to absorb exudate or debride the wound must be changed more frequently than one designed solely to occlude. Outer Layer
Dressings and bandages can serve as surface splints (as can surgical tape) by reducing mechanical stresses on the wound during the early phases of healing. Even when subcuticular stitches have been placed, these "external splints" are useful in relieving tension across the wound. They are most needed between the 7th and 42nd days, the time of collagen synthesis and remodeling. [19] Compressive dressings may be helpful in preventing hematoma formation and eliminating dead space within a wound. They are particularly useful in wounds that have been undermined extensively and in facial wounds, in which SQ capillary bleeding and swelling can exert tension on fine skin sutures and jeopardize skin closure. Pressure dressings should be used to immobilize skin grafts. Surgical tape can serve as a pressure dressing in areas such as fingertips on which bandages cannot be easily applied. However, a pressure dressing should not be used as a substitute for good hemostasis. [8] Pressure dressings should be applied to all ear lacerations to prevent hematoma formation and subsequent deformation and destruction of cartilage. The ear should be enveloped in the dressing so that pressure from the outer bandage is distributed evenly across the irregular surface of the pinna. Moistened cotton is packed into the concavities of the pinna until the cotton is level with the most lateral aspect of the helical rim. Square pieces of gauze cut to fit the curvature of the ear are placed behind (medial to) the pinna. Several more gauze squares are placed on the lateral surface of the ear; the packing is then secured in place with a circumferential head bandage. The bandage must not encompass the opposite ear because it would just as easily cause pressure necrosis of that ear if left unprotected. Application of a pressure dressing for the ear is discussed further in Chapter 65 . Traumatic wounds are bandaged to compress or immobilize the wound or to secure and protect the underlying dressing. Most bandaging is performed on extremities, on which dressings are difficult to secure with tape alone. Rolls of cotton (Kerlix; Kling stretch gauze) are well suited for this purpose. The bandage is wound around the extremity, advancing proximally with circular, overlapping turns. Care should be taken to avoid allowing wrinkles in the bandage, which will later create pressure points, or making loose turns that shorten the effective life of the dressing. When joint surfaces are crossed, the cotton is anchored distally with several turns, unrolled obliquely across the joint several times in a figure-of-eight pattern, and anchored proximally by two complete turns. This process is repeated until the bandage is securely in place. The ends of the bandage are fastened to the skin by strips of adhesive tape. Bandages over the forearm and the lower extremities are particularly prone to slippage because of the constant motion of these parts and because of the marked changes in extremity diameter over a short distance. The roll of bandage can be rotated 180° after each circular turn, producing a reverse spiral and reducing the bandage's mobility ( Fig. 35-22 ). A "tube" of elastic cotton netting (e.g., Surgifix, Tubex, Surgitube, HygiNet) pulled over the bandage or unrolled from a metal applicator frame effectively stabilizes the entire dressing in these areas ( Fig. 35-23 ). Another useful technique consists of placing strips of tape on opposite sides of the extremity, leaving the ends free. The bandage is wrapped around the dressing, covering the portions of the tape that are attached to the skin. The free ends of tape are then incorporated in the bandage ( Fig. 35-24 ).[114] Certain chemically treated wide-mesh weaves have the properties of cling and stretch, holding snugly in place but expanding if edema develops. [98] An elastic cotton roll (Kerlix) allows the bandage to conform to body contours, provides some mobility to bandaged joints, and permits the wound to swell without the circumferential bandage constricting the extremity. The inelastic Kling bandage better immobilizes the part. Rigid immobilization with plaster splints or braces is needed to protect wounds in mobile areas, such as around large joints. Most scalp wounds do well when left uncovered. If a dressing is necessary, it must be held in place by a bandage. There are many techniques for bandaging heads. One method[115] is shown in Figure 35-25 . Methods of bandaging wounds in other locations of the body are described in detail in other texts. [79] [95] Dressings should be changed when they become externally contaminated, saturated with exudate, or when inspection and wound cleaning is required.
Figure 35-22 Snugness of the bandage is increased by 180° rotation of the bandage roll after each circular turn to create a reverse spiral. (From Norton LW: Trauma. In Hill GJ II: Outpatient Surgery. Philadelphia, WB Saunders, 1980. Reproduced by permission.)
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Figure 35-23 Finger dressing. A, The inner layer is nonadherent gauze or whatever is required for soft tissue care. The middle layer is 2 × 2 in. gauze sponges wrapped circumferentially and held in place with a small strip of tape. B, Begin No. 2 tube gauze at the base of the finger. It is useful to hold this end with one finger while the tube gauze applicator is pulled toward the fingertip. A twisting motion firms the wrap about the digit; generally about 90° is necessary. Excessive stretch or twisting can compromise circulation. C, When the fingertip is reached, make a 360° twist. D, Pass the applicator toward the finger base with an additional 90° twist. Repeat once more; thus, three layers are in place. E, Cut enough gauze to reach the base of the finger, and tape it there. As an alternative, pull the final layer beyond the tip, leaving it long enough to reach to and around the wrist (about three times the finger length). Split this gauze into two strands; bring them dorsally to the wrist, knot, and loosely wrap around the wrist. (Redrawn from Kaplan EN, Hentz VR: Emergency Management of Skin and Soft Tissue Wounds: An Illustrated Guide. Boston, Little, Brown, 1984, p 86. Reproduced by permission.)
Dressings vary in their absorbency, adhesiveness, occlusiveness, opacity, and insulating properties. Further research may identify types of dressings best suited for different phases of the healing wound. Currently, a two- or three-layer dressing is used for most traumatic wounds; the choice of material for the contact layer is determined by the characteristics of the individual wound. [116] Splinting and Elevation Although splints are readily applied to orthopedic or soft tissue injuries, immobilization of wounds and sutured lacerations is often neglected, despite the fact that these techniques
Figure 35-24 A, When a Kling or Kerlix wrap must be applied to an area such as the forearm, start by putting a strip of tape on opposite sides of the arm, leaving the ends free. B, Wrap the bandage around the arm, covering the portions of the tape that are attached to the skin. C, After completing one layer of wrapping, tuck the free ends of the tape down so that the nonadhesive side faces the first layer of wrapping and the sticky side faces out. Place another layer of wrapping around the arm. D, After completing a second layer of wrapping, the dressing will not slip because it is adhered to itself as well as to the skin. (From Lazo J: Non-slip dressing technique. Res Staff Physician 22:103, 1976. Reproduced by permission.)
may enhance healing and provide patient comfort. Immobilization of an injured extremity promotes healing by protecting the closure and by limiting the spread of contamination and infection along lymphatic channels. Wounds overlying joints are subjected to repeated stretching and movement, which delays healing, widens the scar, and could 643
Figure 35-25 A–E, Technique for bandaging the head. A strip of bandage (the "tie strip") 3 inches wide and 3 feet long is placed over the head in the frontal plane ( A). While the patient maintains downward tension on the first strip of bandage, the clinician places a full-length gauze bandage at the forehead level in a horizontal plane, winding the bandage around the head ( B). (The "Kling"-type bandage is preferred.) The main bandage is stabilized with several turns, passing near the patient's ear, then wrapped around one side of the tie in a full turn ( C). The main bandage is then taken across the front of the head, wrapped full-turn around the other side of the tie bandage ( D). The main bandage is wrapped around the head, from front to back, overlapping with each pass. The dressing is secured in place by tying the ends of the tie strip under the chin ( E). This dressing can be removed easily by untying the chin straps and gently pulling both ends of the tie strip upward (F).
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possibly disrupt the sutures. [25] Splints are almost always required for lacerations that overlie joints and are frequently necessary for protection of wounds involving fingers, hands, wrists, the volar aspects of forearms, the extensor surfaces of elbows, the posterior aspects of legs, the plantar surfaces of feet, and the extremities when skin grafts have been applied. Splinting is often underused by the emergency clinician in the treatment of lacerations. A plaster or aluminum splint may be incorporated into a bandage to reduce the mobility of the part. Splinting techniques for extremities are explained more fully in Chapter 51 and Chapter 52 . Elevation of injured extremities is important in all but trivial injuries. Elevation limits edema formation, an expected sequela of trauma and inflammation, and allows more rapid healing. [25] Elevation also reduces throbbing pain. Patients given this information are often more motivated to elevate the extremity as instructed. Slings can be used to elevate wounds involving the forearm or the hand. Ointments The safety and efficacy of topical antibiotic preparations used on wound surfaces are unproven and still debated. Many clinicians routinely suggest the use of antibiotic ointments over sutured wounds, while others opt for a simple dry dressing. No universal standard exists. Since a major benefit from the routine use of topicals has never been substantiated, one would intuit that there is no compelling reason to use them. However, the application of a topical preparation involves that patient in the ongoing care of the wound, and forces the patient to evaluate the healing process on a regular basis . These reasons alone make the use of topicals reasonable interventions. Some investigators warn of skin sensitization by preparations containing neomycin [91] and others, of the emergence of resistant strains of bacteria with any topical antibiotic. [117] Other studies have shown that use of a triple-antibiotic preparation containing neomycin, bacitracin, and polymyxin provides a broad spectrum of
protection against infection in abrasions without systemic absorption and toxicity or the emergence of resistant strains of bacteria. Unless this topical antibiotic ointment is used repeatedly or on inflamed skin, there is a relatively low risk of allergic sensitization ( Fig. 35-26 ). [118] There is evidence that the active agents in Neosporin ointment and Silvadene cream, as well as their inert bases and vehicles, improve wound healing. [97] [119] [120] In a prospective, randomized, double-blind study, Dire and colleagues found that bacitracin and Neosporin ointments reduced the infection rate over that seen with plain petrolatum ointment. [121] Mupirocin (Bactroban, GlaxoSmithKline, London), which is a topical antibiotic in a water-soluble base, is an alternative. Ointments can be used to reduce the formation of a crust that covers and separates the edges of the wound. Lacerations surrounded by abraded skin are especially predisposed to coagulum formation. In such cases the patient can be instructed to cleanse the wound frequently and to follow the cleansing with an application of ointment during the first few days. [25] Ointments also prevent the dressing from adhering to the wound. [6] Some researchers recommend using bacitracin applied in a thin coating, not for protection against infection, but for prevention of these mechanical problems. Note that the stronger topical corticosteroids have detrimental effects on healing. Application of 0.1% triamcinolone acetonide in an ointment retards healing in wounds by as much as 60%, whereas hydrocortisone probably does not interfere with epithelialization. [102] [112] Some clinicians believe that single and low doses of oral corticosteroids probably have no effect on wound healing but that repeated, large doses of steroids (=40 mg of prednisone per day) inhibit healing, particularly if used before the injury or during the first 3 days of the healing phase. [122] [123] There is some evidence that topical vitamin A may reverse some of the anti-inflammatory and immunosuppressive effects of corticosteroids. [124] The exact value of ointments in the treatment of lacerations has yet to be determined. However, their routine use after wound cleaning does encourage patient inspection of the wound. Ointments should not be used on wounds closed with tissue adhesive because the ointment will dissolve the adhesive. Wound Cultures Cultures taken at the time of wound preparation and closure in the ED serve no useful purpose and are not recommended. Results of such cultures cannot logically guide future antibiotic selection and often only confuse the picture. It is not standard to routinely culture all infected wounds presenting after closure, unless extenuating circumstances exist. Often such cultures reveal multiple organisms, and do not reflect either the principal infecting organism or the antimicrobials that are required to cure a wound infection. Systemic Antibiotics
Most traumatic soft tissue injuries sustain a low level of bacterial contamination. [88] The standard wound infection rate in unselected ED wounds is 2% to 5%. In a number of clinical studies of traumatic wounds, prophylactic antibiotics administered orally [20] [125] [126] and intramuscularly [13] [126A] [30] [127] in various regimens did not reduce the incidence of infection. In experimental models of contaminated incisions, antibiotics have no therapeutic value >3 hours after the injury. bacteria per
[ 128] [ 129]
When the wound is contaminated with >10
[9]
Figure 35-26 This patient used a neomycin-containing ointment on a minor wound, and developed redness, swelling, pruritis, and skin changes. The patient thought it was an infection but it was a contact dermatitis from the neomycin. Plain bacitracin ointment will not do this.
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gram of tissue (such as wounds in contact with pus or feces), infection will develop despite antibiotic treatment. [42] Most clinical investigations of antibiotic use in emergency patients have omitted heavily contaminated wounds in their series. Studies of antibiotic prophylaxis for animal bite wounds have produced variable results, and no large study providing stratification of the many prognostic factors has been done. [130] The use of antibiotics varies widely among clinicians, and because of limited scientific data, there is no clear practice standard. [131] In most soft tissue wounds where the level of bacterial contamination after cleaning and debridement is low, antibiotics have not been proven beneficial. Antibiotics may have marginal benefit when the level of contamination is overwhelming or if the amount of questionably viable tissue left in the wound is considerable (e.g., with crush wounds). Antibiotics should be considered for extremity bite wounds, puncture-type bite wounds in any location, intraoral lacerations that are sutured, orocutaneous lip wounds, wounds that cannot be cleaned or debrided satisfactorily, and highly contaminated wounds (e.g., those contaminated with soil, organic matter, purulence, feces, saliva, or vaginal secretions). They also should be considered for wounds involving tendons, bones, or joints; for wounds requiring extensive debridement in the operating room; for wounds in lymphedematous tissue; for distal extremity wounds when treatment is delayed for 12 to 24 hours; for patients with orthopedic prostheses; and for patients at risk of developing infective endocarditis. [25] If systemic antibiotics are considered necessary, they should be given intravenously or intramuscularly in the earliest stages of wound management. The choice of antibiotic, particularly for bite wound prophylaxis, is as controversial as the indications for usage. Many species of bacteria cause bite wound infections, making complete coverage impossible.[31] [132] [133] Some antibiotic regimens recommended for bite wounds include dicloxacillin or cephalexin for high-risk dog bite wounds, dicloxacillin or cephalexin plus penicillin for human or cat bite wounds, and amoxicillin-clavulanic acid or cefuroxime for any domestic animal bite. The duration of antibiotic prophylaxis also is in question. It is common practice to provide antibiotics for 72 hours, although data from surgical studies indicate that antibiotics administered beyond the first postoperative day provide no additional protection. [134] Short courses of antibiotics do not seem to increase the incidence of resistant strains of organisms. [135] In all cases, the use of antibiotics should remain subordinate to careful cleaning and debridement. If the infection risk is high enough to warrant antibiotics, secondary closure should be considered. See additional comments on animal bites at the end of this chapter. There are no data to support the routine use of prophylactic antibiotics for the majority of wounds encountered in the ED. [136] Antibiotics should not be used as a substitute for proper wound preparation or a measure to overcome factors suggesting delayed wound closure. The downsides of antibiotic use include needless expense; potential side effects (e.g., rash, anaphylaxis, diarrhea, vomiting); and the development of resistant bacteria, both in the wound and in general. If antibiotics are used, they should be given as soon as possible after wounding and continued for only 2 to 3 days in the absence of a developing infection. Immunoprophylaxis Although tetanus is rare, it still occurs in the United States (about 50 cases per year) and is a preventable disease. Therefore, any wound should be assessed for its potential to cause tetanus, and prophylaxis should be considered in the ED. Gergen and colleagues demonstrated that about 70% of Americans older than 6 years of age had protective levels of tetanus antibodies. [137] Levels declined as age increased, and elderly women had the lowest levels of protection. Hispanics (and likely other immigrants) were most likely to have inadequate immunity. Hence, efforts at preventing tetanus should be especially addressed in immigrants and the elderly. Recommendations for tetanus prophylaxis have evolved since the 1980s. The guidelines published by the Public Health Services Advisory Committee on Immunization Practices, Centers for Disease Control and Prevention, differ slightly from those of the American College of Surgeons in the use of tetanus immune globulin. [138] [139] Many cases of tetanus develop despite prior immunization; tetanus can result from chronic skin lesions and apparently minor or clean wounds. [140] In 10% to 20% of cases, no precedent wound can be identified. Patients' recall of past immunizations is imperfect, and immunity may rarely be inadequate after a complete series of tetanus toxoid.[141] Furthermore, there is no precise consensus on the definition of a "tetanus-prone wound," yet treatment decisions are based on the differentiation between clean and contaminated wounds. Some investigators warn of overtreatment [142] [143] and others maintain that the risk of therapy is minimal compared with the danger of tetanus. [144] [145] After comparing those risks and benefits, most clinicians would agree that a certain amount of overtreatment is acceptable. However, tetanus
boosters given more frequently than advised increase the incidence of adverse reactions to subsequent injections. While any break in the skin can be classified as "tetanus prone" traditional definitions of tetanus-prone wounds include injuries >6 hours old; wounds contaminated by feces, saliva, purulent exudate, or soil; wounds with retained foreign bodies or containing devitalized or avascular tissue; established wound infections; penetrating abdominal wounds involving bowel; deep puncture wounds; and wounds caused by crush, burns, or frostbite ( Fig. 35-27 ). When patients are questioned about their tetanus immunization status, they should be asked if they completed the primary immunization series, and if not, how many doses have been given. Patients who have not completed a full primary series of injections may require both tetanus toxoid and passive immunization with tetanus immune globulin. Tetanus immune globulin will decrease, but will not totally eliminate, the subsequent development of clinical tetanus. The preferred preparation for active tetanus immunization in patients 7 years of age and older is 0.5 mL of tetanus toxoid (plus the lower, adult dose of diphtheria toxoid); the dose of tetanus immune globulin is 250 to 500 units given intramuscularly. [137] Mild local reactions consisting of erythema and induration are common after tetanus toxoid injections. Compared to the rate of reactions to tetanus toxoid (about 20%), reactions are about twice as common if diphtheria immunization is coupled with tetanus immunization. Some patients with high antibody levels develop a hypersensitivity reaction of tenderness, erythema, and swelling, or serum sickness. Generalized urticarial reactions and peripheral neuropathy have also been reported.
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Figure 35-27 Tetanus immunization guidelines.
A significant percentage of elderly patients fail to develop protective antitoxin antibody titers after 14 days when given tetanus toxoid boosters. Because protective levels of tetanus antibodies tend to parallel levels of antibodies to diphtheria, it has been recommended that both immunizations be given simultaneously. Both tetanus and diphtheria immunization have been implicated as a cause of adverse reactions. Tetanus and diphtheria toxoid are products of human antisera, and serious reactions are rare. [146] The most common reaction is a painful, indurated, tender eruption at the injection site, occasionally accompanied by a fever and mild systemic symptoms. This is a hypersensitivity reaction (Arthus-type reaction), not an infection or immunoglobulin E (IgE)-mediated allergy. As such, this reaction does not require drainage or antibiotics, nor does it represent an absolute contraindication to further immunizations. Local reactions are more common in patients who have been given multiple immunizations, so it is unwise to give excessive immunizations "just to be safe." In tetanus-prone injuries, "hyperreactors" can be given tetanus immune globulin. A minor febrile illness, such as an upper respiratory infection, is not a reason to delay immunization. The only absolute contraindication to tetanus toxoid is a history of anaphylaxis or a neurologic event. In such cases, tetanus immune globulin can be given safely. Pregnancy is not a contraindication to either toxoid or immune globulin, although some suggest that the toxoid be used with caution during the first trimester. Given the excellent amnestic response to the toxoid, it is likely that the primary immunization series, coupled with intermittent boosters, conveys immunity for most of one's life. When a wound results from the bite or scratch of a wild or domestic animal, prophylaxis against rabies also must be considered ( Table 35-3 and Table 35-4 ). Further discussion of the prevention of rabies is provided elsewhere. [147] [148]
PATIENT INSTRUCTIONS Successful wound healing is partly dependent on the care given to the wound once the patient leaves the emergency center. Patient satisfaction depends not only on the cosmetic result, but also on the expectation of that result. [10] Therefore, the patient should receive thorough and clear instructions. The patient should be informed that no matter how skillful the repair, any wound of significance produces a scar. Most scars deepen in color and become more prominent before they mature and fade. The final appearance of the scar cannot be judged before 6 to 12 months after the repair. [9] [91] Patients may experience dysesthesias in or around a scar, particularly about the midface. Gentle rubbing or pressing on the skin may relieve the symptoms. If wounds extending to SQ levels lacerate cutaneous nerves, patients may be bothered by hypoesthesia distal to the wound. Dysesthesia and anesthesia usually resolve in 6 months to 1 year.[10] Because the wound edges are rapidly sealed by coagulum and bridged by epithelial cells within 48 hours, the wound is essentially impermeable to bacteria after 2 days.[19] [149] The patient should be instructed to protect the wound by keeping the dressing clean and dry for 24 to 48 hours. In this initial period the dressing should be changed only if it becomes externally soiled or soaked by exudate from the wound. If possible, the injured part should be kept elevated. After 48 hours, the patient may remove the dressing in uncomplicated wounds and check for evidence of infection: redness, warmth, increasing pain, swelling, purulent drainage, or the "red streaks" of lymphangitis. Not all patients are able to identify these signs of infection; it is prudent to have patients with complicated or infection-prone wounds examined in 2 days by a clinician or nurse. [150] Interestingly, patients may be more likely to fail to recognize a bona fide infection than to overdiagnose an infection when it is absent. [149] [150]
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TABLE 35-3 -- Rabies Postexposure Prophylaxis Guide—July 1984 [147] The following recommendations are only a guide. In applying them, take into account the animal species involved, the circumstances of the bite or other exposure, the vaccination status of the animal, and presence of rabies in the region. Local or state public health officials should be consulted if questions arise about the need for rabies prophylaxis. Animal Species
Condition of Animal at Time of Attack
Treatment of Exposed Person *
Healthy and available for 10 days of observation
None, unless animal develops rabies †
Rabid or suspected rabid
HRIG‡ and HDCV
Unknown (escaped)
Consult public health officials. If treatment is indicated, give HRIG‡ and HDCV
Regard as rabid unless proven negative by laboratory tests§
HRIG‡ and HDCV
Domestic Dog and cat
Wild Skunk, bat, fox, coyote, raccoon, bobcat, and other carnivores Other Livestock, rodents, and lagomorphs (rabbits and hares)
Consider individually. Local and state public health officials should be consulted on questions about the need for rabies prophylaxis. Bites of squirrels, hamsters, guinea pigs, gerbils, chipmunks, rats, mice, other rodents, rabbits, and hares almost never call for antirabies prophylaxis.
From Leads from the Mortality and Morbidity Weekly Report. JAMA 252:883, 1984. *All bites and wounds should immediately be thoroughly cleansed with soap and water. If antirabies treatment is indicated, both human rabies immune globulin (HRIG) and human diploid cell rabies vaccine (HDCV) should be given as soon as possible, regardless of the interval from exposure. Local reactions to vaccines are common and do not contraindicate continuing treatment. Discontinue vaccine if fluorescent antibody tests of the animal are negative. †During the usual holding period of 10 days, begin treatment with HRIG and HDCV at first sign of rabies in a dog or cat that has bitten someone. The symptomatic animal should be killed immediately and tested. ‡If HRIG is not available, use antirabies serum, equine (ARS). Do not use more than the recommended dosage. §The animal should be killed and tested as soon as possible. Holding for observation is not recommended.
Patients may fail to appreciate the presence of an infection in >? of cases. Therefore, in high-risk circumstances, a scheduled, rather than an as-needed, wound check should be advised. Patients should be informed that sutures themselves do not cause pain. A painful wound is often a sign of infection or suture reaction, and pain should prompt a wound check. If there is no sign of infection after 48 hours, the patient can care for the wound until it is time for removal of the sutures. A daily gentle washing with mild soap and water to remove dried blood and exudate is probably beneficial, especially on areas such as the face or the scalp. Although
[147] [150]
TABLE 35-4 -- Rabies Postexposure Prophylaxis Schedule, United States *
Vaccination Status
Treatment
Regimen
Not previously vaccinated
Local wound cleansing
All postexposure treatment should begin with immediate thorough cleansing of all wounds with soap and water
HRIG
20 IU/kg of body weight; if anatomically feasible, up to half the dose should be infiltrated around wounds and rest administered IM in gluteal area; HRIG should not be administered in same syringe or into same anatomic site as vaccine; because HRIG may partially suppress active production of antibody, no more than recommended dose should be given
Vaccine
HDCV or RVA, 1 mL, IM (deltoid area), one each on days 0, 3, 7, 14, and 28
Local wound cleansing
All postexposure treatment should begin with immediate thorough cleansing of all wounds with soap and water
HRIG
HRIG should not be administered
Vaccine
HDCV or RVA, 1 mL, IM (deltoid area † ), one each on days 0 and 3
Previously vaccinated ‡
HDCV, human diploid cell rabies vaccine; HRIG, human rabies immune globulin; RVA, rabies vaccine, adsorbed. From the Recommendations of the Immunization Practices Advisory Committee, MMWR 40(RR-3):1, 1991. *These regimens are applicable for all age groups, including children. ‡Any person with a history of preexposure vaccination with HDCV or RVA, prior postexposure prophylaxis with HDCV or RVA, or previous vaccination with any other type of rabies vaccine and a
documented history of antibody response to the prior vaccination. †The deltoid area is the only acceptable site of vaccination for adults and older children. For younger children, the outer aspect of the thigh may be used. Vaccine should never be administered in the gluteal area.
patients may bathe with sutures in place, prolonged immersion in water should be avoided. Undiluted hydrogen peroxide may theoretically destroy granulation tissue and newly formed epithelium, and it should not be repeatedly used as a cleaning agent on the healing wound itself. [49] Generally, a wound should be protected with a dressing during the first week, and the dressing should be changed daily. If the wound is unlikely to be contaminated or traumatized, it may be left uncovered. Many clinicians wrongly admonish patients against getting sutured wounds wet, and prohibit bathing, prompting some patients to keep the original dressing in place for inordinate
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amounts of time. Although widely prohibited, there is no evidence that swimming in uncontaminated water with sutures in place delays healing or promotes infection. There is no evidence that gently cleaning a sutured wound even within a few hours of closure adversely impacts infection or healing rates. [149] It is generally recommended that uncovered scalp wounds can be washed after 1 to 2 days, but many clinicians advise showering the same day. Vigorous scrubbing of wounds should be discouraged. The skin surrounding a wound should be gently cleaned in the ED after wound closure to minimize subsequent itching caused by dried blood. Some wounds heal with wide, unattractive scars despite ideal management and closure. Wounds more likely to have significant scars are those that cross perpendicular to joints, wrinkle lines, or lines of minimum tension (Kraissel lines); that retract >5 mm; and that are over convexities or in certain anatomic locations (e.g., anterior upper chest, back, shoulders) where hypertrophic scars are common. A wound crossing a concave surface may result in a bowstring deformity; one crossing a convexity may leave a scar depression. To avoid these complications, a Z-plasty procedure can be done at the time of initial wound management, or the scar can be revised later. The patient should be told to expect suboptimal outcomes in these situations. [37] If an injured extremity or finger is protected by a splint, it should be left undisturbed until the sutures are removed. Patients with intraoral lacerations should be instructed to use warm salt water mouth rinses at least three times a day. Patients may ask about the efficacy of various creams and lotions (e.g., vitamin E, aloe vera, cocoa butter) in limiting scar formation. At this time there are no data to evaluate the use of these substances. Patients should be told to avoid aspirin, as it has been shown to decrease the development of tensile strength and increase the likelihood of hematoma formation. [151]
SECONDARY WOUND CARE Reexamination Patients with simple sutured wounds may be released with appropriate instructions for home care and told to return for suture removal at an appropriate time. High-risk wounds should be examined in 2 to 3 days for signs of infection. All wounds should be inspected if the patient experiences increasing discomfort or develops a fever, or believes that the wound is infected. [95] Bite wounds and other infection-prone wounds should be inspected in 2 days. Wounds being considered for delayed primary closure are evaluated in 4 to 5 days. [87A] Wounds in which extensive dissection of SQ tissue has been performed may develop an intense inflammation similar in appearance to a low-grade, localized cellulitis. It is rarely necessary to open these wounds. The removal of one or two stitches may relieve some of the tension caused by mild swelling. With daily cleansing using water and a mild soap and with application of warm compresses, this type of wound reaction should subside within 24 to 48 hours. [95] A wound that has become infected should be evaluated for the presence of a retained foreign body.
Also, in most sutured wounds that become infected, the sutures must be removed to allow drainage. If a wound exhibits a minor infection, a few sutures, or all of them, may be removed, but grossly infected wounds should be packed open to allow for further drainage. The presence of sutures in a contaminated wound considerably limits the activity of various antibiotics. [152] Infection around a suture can lead to the formation of a stitch mark. [75] Infected wounds should be treated with daily cleansing, warm compresses, and antibiotics. Wounds that have been opened should be left to heal by secondary intention, which involves wound contraction, granulation tissue formation, and epithelialization. Suture Removal Sutures are usually removed by medical personnel, but reliable patients can be given the appropriate materials and instructions to remove simple interrupted sutures themselves. Because wounds do not heal at a standard rate, no strict guidelines can be set for time of suture removal. The optimal time for suture removal varies with the location of the wound, rate of wound healing, and amount of tension on the wound. Certain areas of the body such as the back of the hand heal slowly, whereas facial or scalp wounds heal rapidly. Speed of wound healing is affected by systemic factors such as malnutrition, neoplasia, or immunosuppression. At the time that suture removal is being considered, one or two sutures may be cut to determine whether the skin edges are sufficiently adherent to allow removal of all the sutures. [6] Removing sutures too early invites wound dehiscence and widening of the scar, whereas leaving sutures in longer than necessary may result in epithelial tracts, infection, and unsightly scarring. [153] Small stitch abscesses are common in wounds in which sutures remain more than 7 to 10 days. Localized stitch abscesses generally resolve following removal of the sutures and application of warm compresses. There is usually no need for antibiotic therapy with localized stitch abscesses. Percutaneous sutures stimulate an inflammatory reaction along the suture track. Factors that determine the severity of stitch marks include the length of time skin stitches are left in place, skin tension, the relationship of the suture to the wound edge, the region of the body, infection, and tendency for keloid formation. [75] [154] The skin of the eyelids, palms, and soles and the mucous membranes seldom show stitch marks. In contrast, oily skin and the skin of the back, the sternal area, the upper arms, the lower extremities, the dorsum of the nose, and the forehead are likely to develop the permanent imprints of suture material on the skin surface. [75] If sutures are removed within 7 days, generally no discernible needle puncture or stitch mark will persist. [154] However, at 6 days, the wound is held together by a small amount of fibrin and cells and has minimal strength (see Fig. 35-1 ). [90] The tensile strength of most wounds at this time is adequate to hold the wound edges together, but only if there are no appreciable dynamic or static skin forces pulling the wound apart. [6] Minimal trauma to an unsupported wound at this point could cause dehiscence. The clinician should decide on the proper time of suture removal after weighing these various factors. If early suture removal is necessary, wound repair can be maintained with strips of surgical skin tape. The key to wound tensile strength after suture removal is an adequate deep tissue layer closure. There are some general guidelines for suture removal. Sutures on the face should be removed on the fifth day following the injury, or alternate sutures should be removed
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on the third day and the remainder on the fifth day. On the extremities and the anterior aspect of the trunk, sutures should be left in place for approximately 7 days to prevent wound disruption. Sutures on the scalp, back, feet, and hands and over the joints must remain in place for 10 to 14 days, even though permanent stitch marks may result.[75] Some clinicians recommend the removal of sutures in eyelid lacerations in 48 to 72 hours to avoid epithelialization along the suture tract, with subsequent cyst formation. [155] Removing sutures is relatively simple and the removal technique is not known to affect infection rates or scarring. The wound should be cleansed, and any remaining crust overlying the wound surface or surrounding the sutures should be removed. The skin is wiped with an alcohol swab. Each stitch is cut with a scissors or the tip of a No. 11 scalpel blade at a point close to the skin surface on one side. The suture is grasped on the opposite side with forceps and is pulled across the wound ( Fig. 35-28 ). The amount of exposed suture dragged through the suture tract is thereby minimized. It is difficult to remove sutures with very short ends. At the time of suture placement, the length of the suture ends should generally equal the distance between sutures to permit easy grasping of the suture during subsequent removal yet avoiding entanglement during the knotting of adjacent sutures. Once the skin sutures are removed, the width of the scar increases gradually over the next 3 to 5 weeks unless it is supported. Support is provided by previously placed SQ stitches that brought the skin edges into apposition, by a previously placed subcuticular stitch, or by the application of skin tape ( Fig. 35-29 ). A nonabsorbable subcuticular suture can be left in place for 2 to 3 weeks to provide continued support for the wound. Although complications such as closed epithelial sinuses, cysts, or internal tracts can occur from prolonged use of this stitch, they are unusual and can be avoided by the placement of a buried subcuticular stitch using an absorbable suture. [19] If a subcuticular stitch with reliefs has been used, the suture is cut at the midpoint of the relief. Half of the suture is removed at the original point of entry into the skin and the other half through the original exit point ( Fig. 35-30 ). [156] If a nonabsorbable subcuticular suture cannot be removed or a portion of it ruptures during removal, the protruding end should be grasped with a hemostat, pulled taut, and cut with scissors as close to the skin as possible so that the end of the suture retracts under the skin. If time and effort have been invested in a cosmetic closure of the face, the repair should be protected with skin tape after the skin sutures have been removed. Wound contraction and scar widening continue for 42 days after the injury. [90] Because the desired result is a scar of minimal width, the tape
Figure 35-28 Technique for suture removal. Pull should be toward the wound line (A) rather than away from it (B), which causes the wound to tear apart. (Modified from Stuzin J, Engrav LH, Buehler PK: Emergency treatment of facial lacerations. Postgrad Med 71:81, 1982.)
should be used for 5 weeks following suture removal. With exposure to sunlight, scars in their first 4 months redden to a greater extent than surrounding skin. In
exposed cosmetic areas and when prolonged exposure to the sun is anticipated, this should be prevented with the use of a sunscreen containing para-amino benzoic acid (PABA).
COMPLICATIONS Infection is probably the most common cause of dehiscence. If the patient is careless or unlucky, reinjury can reopen a wound despite the protection of a thick dressing. If the suture size is too small, the stitch may break. A stitch that is too fine or tied too tightly may cut through friable tissue and pull out. Knots that have not been tied carefully may unravel. The suture material may be extruded or absorbed too rapidly. Finally, if a stitch is removed too early (i.e., before tissues regain adequate tensile strength), the wound loses needed support and falls open. If the wound edges show signs of separating at the time of suture removal, alternate stitches can be left in place and the entire length of the wound supported by strips of adhesive tape. There are several reasons why wounds fail to heal; some are related to decisions made at the time of wound closure, and others are consequences of later events. Some of the impediments to healing include ischemia or necrosis of tissue, hematoma formation, prolonged inflammation caused by foreign material, excessive tension on skin edges, and immunocompromising systemic factors. In attempting to repair wounds, clinicians sometimes inadvertently retard the healing process (e.g., with premature closure of contaminated wounds). With the development of new methods and solutions for cleansing wounds and the discovery of the optimal concentrations of solutions currently in use, tissue-toxic antiseptic solutions can be abandoned. Better suture materials are replacing the reactive sutures that often served as foreign bodies rather than tissue supports. Improved materials used for dressing wounds enhance wound healing. A primary cause of delayed healing is wound infection. Wound cleaning and debridement, atraumatic and aseptic handling of tissues, and the use of protective dressings minimize this complication. Inversion of the edges of a wound during closure produces a more noticeable scar, whereas skillful technique can convert a jagged, contaminated wound into a fine, inapparent scar. However, the patient's actions also affect wound healing. Delay in seeking treatment for an injury may significantly affect the ultimate outcome of the wound. Furthermore, in the first few days following an injury, the
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Figure 35-29 Support of the wound with surgical tape.
patient must take responsibility for protecting the wound from contamination, further trauma, and swelling. The final appearance of a scar is determined by several factors. Infection, tissue necrosis, and keloid formation widen a scar. Wounds located in sebaceous skin or oriented 90° to dynamic or static skin tension lines result in wide scars. Miscellaneous Aspects of Wound Care Many parameters and scenarios are involved in the preparation for repair and definitive treatment of wounds. Many specific questions are discussed in other sections of this text but a few specific caveats are included below for completeness.
Figure 35-30 At the time of suture removal, the suture is cut at the midpoint of the relief (A). The proximal portion is removed at the point of original entry into the skin (B), and the distal portion is removed through the original exit point (C). (From Grimes DW, Garner RW: "Reliefs" in intracuticular sutures. Surg Rounds 1:48, 1978. Reproduced by permission.) Digital nerves.
The key to the best possible outcome of a digital nerve injury is making, or suspecting, the diagnosis at the time of initial presentation. Usually injury to a digital nerve is obvious, but numerous factors will hinder the timely diagnosis, and the presence or extent of nerve injury may not be immediately discernible in the ED. Numbness in the area of digital innervation, concomitant injury to a digital artery (flash/pulsating bleeding), or an electric shock sensation when exploring a laceration should alert the clinician to a possible digital nerve injury. When the presence of a digital nerve injury is in question, a follow-up visit usually confirms or eliminates this injury, so it is not critical that all decisions be made at the first visit. With regard to wound preparation issues, lacerations to the hand and fingers should be approached with caution. Debridement should be minimal, and wound preparation should be gentle yet meticulous. Digital nerves that are transected distal to the metacarpophalangeal joint may be candidates for surgical repair. It is not known exactly how far distal in the finger can the nerve be lacerated for a repair to be successful, and proper referral is therefore essential. Often injuries proximal to the distal inter-phalangeal joint are not repaired, but many other factors will influence operative decisions. Repair of a digital nerve will frequently result in return of good sensory function (but it takes months) and repair can prevent painful neuromas from developing. Most hand surgeons will not repair digital nerves at the time of initial presentation. Instead, they advise wound cleaning, skin closure, splinting, and outpatient follow-up in 24 to 36 hours, followed by delayed nerve repair. Animal bites.
The use of prophylactic antibiotics is discussed in a previous section of this chapter. However, many aspects of the treatment of animal bites are controversial and no universal standards exist. Most bites are caused by dogs or cats, with most being sustained from family pets. Numerous organisms will accompany a bite from a dog or cat. If a bite appears clinically grossly infected within the first 24 hours, the offending organism is usually the gram-negative rod Pasteurella multocida. If the infection appears later than 24 hours, a host of bacteria, but predominantly Staphylococcus aureus and Streptococcus viridans, are the culprits. Pasteurella infections are common in cat bites. Cat bites, probably because they are puncture wounds that can not be completely cleaned, frequently become infected. The incidence of infection following dog bite lacerations is not significantly greater than lacerations in general. Many clinicians have advocated the primary closure of large dog bite lacerations. Markedly contused lacerations are good candidates for delayed primary closure. Wound cultures taken at the time of an animal bite are worthless. The use of prophylactic antibiotics for animal bites is controversial and various approaches are advocated (see earlier discussion). The best way to approach bite wounds is to adhere to the general principles and details of wound care as outlined in earlier discussions. No specific intervention has been demonstrated to be superior for the preparation of bite wounds. Care should be taken to search for underlying fractures or tooth fragments in deep animal bites. Gunshot wounds.
A certain subset of gunshot wounds may be definitively handled in the ED, with outpatient follow-up. The landmark studies by Ordog et al. [157] [158] document a very low infection rate in gunshot wounds treated on an outpatient basis. In a retrospective study of nearly 17,000 subjects, the vast majority of patients did well, with only a 1.8% infection rate. Standard wound care was given and
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prophylactic antibiotics were withheld, and satisfactory results were obtained even when the missile was left in place, and minor fractures were present ( Fig. 35-31 ). Since most gunshot wounds are puncture wounds, minimal deep wound cleaning is possible. Puncture wounds.
The approach to specific puncture wounds is discussed in other sections, but a few caveats are repeated here. As a general rule, it is impossible to completely clean a puncture wound. In fact, it may be counterproductive to attempt to do so in some areas of the body. Superficial soft tissue wounds having entrance and exit wounds in proximity may be debrided by passage of a sterile gauze back and forth through the wound tract. Coring out a puncture wound is usually overly aggressive initial treatment, but it may be an option if gross contamination or infection is present. In selected punctures, it may be possible to incise the skin and cutaneous tissue over the tract, converting a puncture into a linear laceration. If a through-and-through stream cannot be established, attempting to irrigate the tract of a puncture
Figure 35-31 Minor gunshot wounds may be treated as outpatients, even when bullet fragments remain and there are minor fractures. A and B, This through-and-through injury transversed the hypothenar eminence. No bullet remained and no bones were involved. C, Usually it is impossible to irrigate a puncture wound, but in this case note the saline at the exit site. D, After the entrance wound is debrided of the powder burn, a hemostat is passed through the wound. E, The instrument grasps gauze packing and pulls it into the wound. The gauze was pulled back and forth to debride the wound tract, and then a clean gauze was left in place. No antibiotics were given, the pack was removed at wound check in 24 hours, and the patient did well. Many gunshot wounds cannot be irrigated to this extent but the treatment principles are similar.
wound by inserting a needle into the depths of the wound and forcibly injecting irrigating solution has the potential to disseminate contamination and increase soft tissue swelling, and is discouraged. If gross contamination remains in a puncture wound, it is unlikely that antibiotics will prevent or totally treat an infection. This leaves the clinician with the reality that many puncture wounds usually do quite well with minimal intervention, while others do quite poorly because of their inaccessibility to wound cleaning techniques. Simply stated, it may be impossible to predict the outcome of most puncture wounds on the first encounter. The key to success with any puncture wound is to acknowledge the issues discussed earlier, relay them to the patient, and provide the necessary follow-up.
CONCLUSION The objective of traumatic wound management is the restoration of tissue continuity and strength in the least possible
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time, with maximal preservation of tissues and minimal scar formation, deformity, or loss of function. It is important that clinicians follow the basic principles of wound care when cleaning, debriding, closing, and protecting wounds and continue to refine their management of wounds as further improvements in techniques and materials become available.
References 1. Howell 2. Hunt
JM, Chisholm CD: Outpatient wound preparation and care: A national survey. Ann Emerg Med 21:976, 1992.
JK, Van Winkle W: Wound healing: normal repair. In Hunt JK, Van Winkle W (eds): Fundamentals of Wound Management in Surgery. South Plainfield, NJ, Chirurgecom, Inc, 1976.
3. Quinn
JV: Clinical wound evaluation. Acad Emerg Med 3:298, 1996.
4. Singer
AJ, Mach C, Thode HC, et al: Patient priorities with traumatic lacerations. Am J Emerg Med 18:683, 2000.
5. Edlich
RF, Custer J, Madden J, et al: Studies in the management of the contaminated wound III. Assessment of the effectiveness of irrigation with antiseptic agents. Am J Surg 118:21, 1969.
6. Peacock
EE: Wound healing and wound care. In Schwartz SI (ed): Principles of Surgery, 3rd ed. New York, McGraw-Hill, 1979.
7. Timberlake 8. Bryant
GA: Wound healing: The physiology of scar formation. Curr Concepts Wound Care 9:4, 1986.
WM: Wound healing. Clin Symp 29:1, 1977.
9. Hollander
JE, Blasko B, Singer AJ, et al: Poor correlation of short- and long-term cosmetic appearance of repaired lacerations. Acad Emerg Med 2:983, 1995.
10.
Zitelli JA: Secondary intention healing: An alternative to surgical repair. Clin Dermatol 2:92, 1984.
11.
American College of Emergency Physicians: Clinical policy for the initial approach to patients presenting with penetrating extremity trauma. Ann Emerg Med 23:1147, 1994.
12.
Krizek TJ, Robson MC: Evolution of quantitative bacteriology in wound management. Am J Surg 130:579, 1975.
13.
Morgan WJ, Hutchison D, Johnson HM: The delayed treatment of wounds of the hand and forearm under antibiotic cover. Br J Surg 67:140, 1980.
14.
Dreyfuss UY, Singer M: Human bites of the hand: A study of one hundred six patients. J Hand Surg 10A:884, 1985.
15.
Robson MC, Duke WF, Krizek TJ: Rapid bacterial screening in the treatment of civilian wounds. J Surg Res 14:426, 1973.
16.
Ogilvie WH: Prevention and treatment of wound infection. Lancet 2:935, 1940.
17.
Berk WA, Osbourne DD, Taylor DD: Evaluation of the "golden period" for wound repair: 204 cases from a third world emergency department. Ann Emerg Med 17:496, 1988.
18.
Hollander JE, Singer AJ, Valentine SM, et al: Risk factors for infection in patients with traumatic lacerations. Acad Emerg Med 8:716, 2001.
19.
Peacock EE, Van Winkle W: Surgery and Biology of Wound Repair. Philadelphia, WB Saunders, 1970.
20.
Haughey RE, Lammers RL, Wagner DK: Use of antibiotics in the initial management of soft tissue hand wounds. Ann Emerg Med 10:187, 1981.
21.
Hollander JE, Singer AJ, Valentine SM, et al: Risk factors for infection in patients with traumatic lacerations. Acad Emerg Med 8:716, 2001.
22.
Cruse PJE, Foord R: A five-year prospective study of 23,649 surgical wounds. Arch Surg 107:206, 1973.
23.
Viljanto J: Disinfection of surgical wounds without inhibition of normal wound healing. Arch Surg 115:253, 1980.
24.
Lammers RL: Soft tissue foreign bodies. Ann Emerg Med 17:1336, 1988.
25.
Edlich RF, Thacker JG, Buchanan L, Rodeheaver GT: Modern concepts of treatment of traumatic wounds. Adv Surg 13:169, 1979.
26.
Trott A: Mechanisms of surface soft tissue trauma. Ann Emerg Med 17:1279, 1988.
27.
Haury B, Rodeheaver G, Vensko J Jr, et al: Debridement: An essential component of traumatic wound care. Am J Surg 135:238, 1978.
28.
Hunt TK: The physiology of wound healing. Ann Emerg Med 17:1265, 1988.
29.
Sindelar W, Mason GR: Irrigation of subcutaneous tissue with povidoneiodine solution for prevention of surgical wound infections. Surg Gynecol Obstet 148:227, 1979.
30.
Hutton PAN, Jones BM, Low DJW: Depot penicillin as prophylaxis in accidental wounds. Br J Surg 65:549, 1978.
31.
Galvin JR, DeSimone D: Infection rate of simple suturing. JACEP 5:332, 1976.
32.
Alkan M, Gefen Z, Goldman L: Wound infection after simple suture at the emergency ward. Infect Control 5:562, 1984.
33.
Rosenberg NM, Debaker K: Incidence of infection in pediatric patients with laceration. Pediatr Emerg Care 3:239, 1987.
34.
Gosnold JK: Infection rate of sutured wounds. The Practitioner 218:584, 1977.
35.
Mann RJ, Hoffeld TA, Former CB: Human bites of the hand: Twenty years of experience. J Hand Surg 2:97, 1977.
36.
Roberts AH, Rye DG, Edgerton MI, et al: Activity of antibiotics in contaminated wounds containing clay soil. Am J Surg 137:381, 1979.
37.
Edlich RF, Rodeheaver GT, Morgan RF, et al: Principles of emergency wound management. Ann Emerg Med 17:1284, 1988.
38.
Robson MC: Disturbances of wound healing. Ann Emerg Med 17:1274, 1988.
39.
Lammers RL, Fourre M, Callaham ML, et al: Effect of povidone-iodine and saline soaking on bacterial counts in acute, traumatic contaminated wounds. Ann Emerg Med 19:709, 1990.
40.
Rodeheaver GT, Smith SL, Thacker JG: Mechanical cleansing of contaminated wounds with a surfactant. Am J Surg 129:241, 1975.
Custer J, Edlich RF, Prusak M, et al: Studies in the management of the contaminated wound: V. An assessment of the effectiveness of pHisoHex and Betadine surgical scrub solutions. Am J Surg 121:572, 1971. 41.
42.
Edlich RF, Rodeheaver GT, Thacker JG, et al: Technical factors in wound management. In Edlich RF, Rodeheaver GT, Thacker JG, et al (eds): Fundamentals of Wound Management in Surgery.
South Plainfield, NJ, Chirurgecom, Inc, 1977. 43.
Rodeheaver G, Turnbull V, Edgerton MT, et al: Pharmacokinetics of a new skin wound cleanser. Am J Surg 132:67, 1976.
44.
Van Den Broek PJ, Buys LFM, Van Furth R: Interaction of povidone-iodine compounds, phagocytic cells, and microorganisms. Antimicrob Agents Chemother 22:593, 1982.
45.
Rodeheaver G, Bellamy W, Kody M, et al: Bactericidal activity and toxicity of iodine-containing solutions in wounds. Arch Surg 117:181, 1982.
46.
Lineaweaver W, McMorris S, Soucy D, et al: Cellular and bacterial toxicities of topical antimicrobials. Plast Reconstr Surg 75:394, 1985.
47.
Gravett A, Sterner S, Clinton J, et al: A trial of povidone-iodine in the prevention of infection in sutured lacerations. Ann Emerg Med 16:167, 1987.
48.
Rodeheaver GT, Kurtz L, Kircher BJ, et al: Pluronic F-68: A promising new skin wound cleanser. Ann Emerg Med 9:572, 1980.
49.
Gruber RP, Vistnes L, Pardoe R: The effect of commonly used antiseptics on wound healing. Plast Reconstr Surg 55:472, 1975.
50.
Sebben JE: Surgical antiseptics. J Am Acad Dermatol 9:759, 1983.
51.
Bryant CA, Rodeheaver GT, Reem EM, et al: Search for a nontoxic surgical scrub solution for periorbital lacerations. Ann Emerg Med 13:317, 1984.
52.
Rodeheaver GT, Pettry D, Thacker JG, et al: Wound cleansing in high pressure irrigation. Surg Gynecol Obstet 141:357, 1975.
53.
Madden J, Edlich RF, Schauerhamer R, et al: Application of principles of fluid dynamics to surgical wound irrigation. Curr Top Surg Res 3:85, 1971.
54.
Singer AJ, Hollander JE, Subramanian S, et al: Pressure dynamics of various irrigation techniques commonly used in the emergency department. Ann Emerg Med 24:36, 1994.
55.
Morse JW, Babson T, Camasso C, et al: Wound infection rate and irrigation pressure of two potential new wound irrigation devices: The port and the cap. Am J Emerg Med 16:37, 1998.
56.
Pronchik D, Barber C, Rittenhouse S: Low- versus high-pressure irrigation techniques in Staphylococcus aureus-inoculated wounds. Am J Emerg Med 17:121, 1999.
57.
Hamer ML, Robson MC, Krizek TJ, et al: Quantitative bacterial analysis of comparative wound irrigations. Ann Surg 181:819, 1975.
58.
Brown LL, Shelton HT, Bornside GH, et al: Evaluation of wound irrigation by pulsatile jet and conventional methods. Ann Surg 187:170, 1978.
59.
Wheeler CB, Rodeheaver GT, Thacker JG, et al: Side effects of high pressure irrigation. Surg Gynecol Obstet 143:775, 1976.
60.
Hollander JE, Rickman PB, Werblud M, et al: Irrigation in facial and scalp lacerations: Does it alter outcome? Ann Emerg Med 31:73, 1998.
61.
Brown DG, Skylis TP, Sulisz CA, et al: Sterile water and saline solution: Potential reservoirs of nosocomial infection. Am J Infect Control 13:35, 1985.
62.
Kaczmarek ER, Sula JA, Hutchinson RA: Sterility of partially used irrigating solutions. Am J Hosp Pharm 39:1534, 1982.
653
63.
Pigman EC, Karch DB, Scott JL: Splatter during jet irrigation cleaning of a wound model: A comparison of three inexpensive devices. Ann Emerg Med 22:1563, 1993.
64.
Halasz NA: Wound infection and topical antibiotics: The surgeon's dilemma. Arch Surg 112:1240, 1977.
Edlich RF, Madden JE, Prusak M, et al: Studies in the management of the contaminated wound: IV. The therapeutic value of gentle scrubbing in prolonging the limited period of effectiveness of antibiotics in contaminated wounds. Am J Surg 121:668, 1971. 65.
66.
Sher KS: Prevention of wound infection: The comparative effectiveness of topical and systemic cefazolin and povidone-iodine. Am Surg 48:268, 1982.
67.
Lindsey D, Nava C, Marti M: Effectiveness of penicillin irrigation in control of infection in sutured lacerations. J Trauma 22:186, 1982.
68.
Lammers RL, Henry C, Howell J: Bacterial counts in experimental, contaminated crush wounds irrigated with various concentrations of cefazolin and penicillin. Am J Emerg Med 19:1, 2001.
69.
Angeras MH, Brandberg A, Falk A, Seeman T: Comparison between sterile saline and tap water for the cleaning of acute traumatic soft tissue wounds. Eur J Surg 158:347, 1992.
70.
Moscati R, Mayrose J, Fincher L, et al: Comparison of normal saline with tap water for wound irrigation. Am J Emerg Med 16:379, 1998.
71.
Seropian R, Reynolds BM: Wound infections after preoperative depilatory versus razor preparation. Am J Surg 121:251, 1971.
72.
Howell JM, Morgan JA: Scalp laceration repair without prior hair removal. Am J Emerg Med 6:7, 1988.
73.
Alexander JW, Fischer JE, Boyajian M, et al: The influence of hair-removal methods on wound infections. Arch Surg 118:347, 1983.
74.
Ha'eri GB, Wiley AM: The efficacy of standard surgical face masks: An investigation using tracer particles. Clin Orthop 148:160, 1980.
75.
Grabb WC: Basic techniques of plastic surgery. In Grabb WC, Smith JW (eds): Plastic Surgery: A Concise Guide to Clinical Practice. Boston, Little, Brown, 1979, p 3.
76.
Kirk RM: Basic Surgical Techniques. Edinburgh, Churchill Livingstone, 1978.
77.
Edlich RF, Rodeheaver GT, Horowitz JH, et al: Emergency department management of puncture wounds and needlestick exposure. Emerg Med Clin North Am 4:581, 1986.
78.
Chisholm CD, Shlesser JF: Plantar puncture wounds: Controversies and treatment recommendations. Ann Emerg Med 18:1352, 1989.
79.
Kaplan EN, Hentz VR: Emergency Management of Skin and Soft Tissue Wounds: An Illustrated Guide. Boston, Little, Brown, 1984.
80.
Brown PW: The hand. In Hill GJ II (ed): Outpatient Surgery. Philadelphia, WB Saunders, 1980, p 643.
81.
Westaby S: Wound closure and drainage. In Westaby S (ed): Wound Care. St. Louis, CV Mosby, 1986, p 32.
82.
Lemos MJ, Clark DE: Scalp lacerations resulting in hemorrhagic shock: Case reports and recommended management. J Emerg Med 6:377, 1988.
83.
MacDonald RT: Maintenance of ligature tension by a single operator with simultaneous removal of a hemostatic clamp. Am J Surg 143:770, 1982.
84.
Wavak P, Zook EG: A simple method of exsanguinating the finger prior to surgery [letter]. JACEP 7:124, 1978.
85.
Sanders, R. The tourniquet: Instrument or weapon? Hand 5:119, 1973.
86.
Shaw JA, DeMuth WW, Gillespy AW: Guidelines for the use of digital tourniquets based on physiological pressure measurements. J Bone Joint Surg 67A:1086, 1985.
87.
Lubahn JD, Koeneman J, Kosar K: The digital tourniquet: How safe is it? J Hand Surg 10A:664, 1985.
87A. Edlich
RF, Rogers W, Kasper G, et al: Studies in the management of the contaminated wound: I. Optimal time for closure of contaminated open wounds: II. Comparison of resistance to infection of open and closed wounds during healing. Am J Surg 117:323, 1969. 88.
Marshall KA, Edgerton MT, Rodeheaver GT, et al: Quantitative microbiology: Its application to hand injuries. Am J Surg 131:730, 1976.
89.
Edlich RF, Panek PH, Rodeheaver GT, et al: Physical and chemical configuration of sutures in the development of surgical infection. Ann Surg 177:679, 1973.
90.
Ordman LJ, Gillman T: Studies in the healing of cutaneous wounds I. The healing of incisions through the skin of pigs. Arch Surg 93:857, 1966.
91.
Walike JW: Suturing technique in facial soft tissue injuries. Otolaryngol Clin North Am 12:425, 1979.
92.
Crawford BS, Gipson M: The conservative management of pretibial lacerations in elderly patients. Br J Plast Surg 30:174, 1977.
93.
Chen E, Horning S, Shepherd SM, et al: Primary closure of mammalian bites. Acad Emerg Med 7:157, 2000.
94.
Callaham ML: Human and animal bites. Top Emerg Med 4:1, 1982.
Wolcott MW: Dressings and bandages. And Wolcott MW: Hands and fingers: Part I-Soft tissues. In Wolcott MW (ed): Ferguson's Surgery of the Ambulatory Patient, 5th ed. Philadelphia, JB Lippincott, 1974, p 35, 396. 95.
96.
Lawrence JC: What materials for dressings? Injury 13:500, 1982.
97.
McGrath MH: How topical dressings salvage questionable flaps: Experimental study. Plast Reconstr Surg 67:653, 1981.
98.
Noe JM, Kalish S: The problem of adherence in dressed wounds. Surg Gynecol Obstet 147:185, 1978.
99.
Eaglstein WH, Mertz PM, Falanga V: Occlusive dressings. Am Fam Physician 35:211, 1987.
100. Rovee
DT, Kurowsky CA, Labun J: Local wound environment and epidermal healing: Mitotic response. Arch Dermatol 106:330, 1972.
101. Winter
GD: Formation of scab and the rate of epithelialization of superficial wounds in the skin of the young domestic pig. Nature 193:293, 1962.
102. Hinman 103. Wayne 104. Linsky
CD, Maibach H: Effect of air exposure and occlusion on experimental human skin wounds. Nature 200:377, 1963.
MA: Clinical evaluation of Epi-Lock-a semiocclusive dressing. Ann Emerg Med 14:20, 1985.
CB, Rovee DT, Dow T: Effect of dressing on wound inflammation and scar tissue. In Hildick-Smith G, Dineen P (eds): The Surgical Wound. Philadelphia, Lea & Febiger, 1981, p 191.
105. Bothwell 106. Mertz 107. Katz
JW, Rovee DT: The effect of dressings on the repair of cutaneous wounds in humans. In Harkiss KJ (ed): Surgical Dressings and Wound Healing. London, Crosby-Lockwood, 1971, p 78.
PM, Marshall DA, Eaglstein WH: Occlusive wound dressings to prevent bacterial invasion and wound infection. J Am Acad Dermatol 12:662, 1985.
S, McGinley K, Leyden JJ: Semipermeable occlusive dressings: Effects on growth of pathogenic bacteria and reepithelialization of superficial wounds. Arch Dermatol 122:58, 1986.
108. Eaglstein
WH: Effect of occlusive dressings on wound healing. Clin Dermatol 2:107, 1984.
109. Stillman
RM, Bella FJ, Seligman SJ: Skin wound closure: The effect of various closure methods on susceptibility to infection. Arch Surg 115:674, 1980.
110. Chvapil
M, Chvapil TA, Owen JA: Comparative study of four wound dressings on epithelialization of partial-thickness wounds in pigs. J Trauma 27:278, 1987.
111. Stair
TO, D'Orta J, Altieri MF, et al: Polyurethane and silver sulfadiazene dressings in treatment of partial-thickness burns and abrasions. Am J Emerg Med 4:214, 1986.
112. Eaglstein 113. Falanga 114. Lazo
WH, Mertz PM: New method for assessing epidermal wound healing: The effects of triamcinolone acetonide and polyethylene film occlusion. J Invest Dermatol 71:382, 1978.
V: Occlusive wound dressings: Why, when, which? Arch Dermatol 124:872, 1988.
J: Non-slip dressing technique. Res Staff Physician 22:103, 1976.
115. Stavrakis
P: A better head dressing. Res Staff Physician 26:88, 1980.
116. Turner
TD: Which dressings and why? In Westaby S (ed): Wound Care. St. Louis, CV Mosby, 1986, p 58.
117. Ayliffe
GAJ, Green W, Livingston R, et al: Antibiotic-resistant Staphylococcus aureus in dermatology in burn wounds. J Clin Pharmacol 30:40, 1977.
118. Leyden
JJ, Sulzberger MB: Topical antibiotics and minor skin trauma. Am Fam Physician 23:121, 1981.
119. Eaglstein
WH, Mertz PM: "Inert" vehicles do affect wound healing. J Invest Dermatol 74:90, 1980.
120. Geronemus 121. Dire
R, Mertz PM, Eaglstein WH: Wound healing: The effects of topical antimicrobial agents. Arch Dermatol 115:1311, 1979.
DJ, Coppola M, Dwyer DA, et al: Prospective evaluation of topical antibiotics for preventing infections in uncomplicated soft-tissue wounds repaired in the ED. Acad Emerg Med 2:4, 1995.
122. Pollack
SV: Systemic drugs and nutritional aspects of wound healing. Clin Dermatol 2:68, 1984.
123. DiPasquale 124. Hunt
G, Steinetz BG: Relationship of food intake to the effect of cortisone acetate on skin wound healing. Proc Soc Exp Biol Med 117:118, 1964.
TK, Ehrlich HP, Garcia JA, et al: Effect of vitamin A on reversing the inhibitory effect of cortisone on healing of open wounds in animals and man. Ann Surg 170:633, 1969.
125. Grossman 126. Thirlby
JAI, Adams JP, Kunec J: Prophylactic antibiotics in simple hand injuries. JAMA 245:1055, 1981.
RC, Blair AJ, Thal ER: The value of prophylactic antibiotics for simple lacerations. Surg Gynecol Obstet 156:212, 1983.
126A. Roberts
AHN, Teddy PJ: A prospective trial of prophylactic antibiotics in hand lacerations. Br J Surg 64:394, 1977.
654
127. Day
TK: Controlled trial of prophylactic antibiotics in minor wounds requiring suture. Lancet 4:1174, 1975.
128. Burke
JF: The effective period of preventative antibiotic action in experimental incisions and dermal lesions. Surgery 50:161, 1961.
129. National
Academy of Sciences—National Research Council: Post-operative wound infections: The influence of ultraviolet irradiation of the operating room and of various other factors. Ann Surg
160:1, 1964. 130. Cummings 131. Waldrop
P: Antibiotics to prevent infection in patients with dog bite wounds: A meta-analysis of randomized trials. Ann Emerg Med 23:535, 1994.
RD, Prejean C, Singleton R: Overuse of parental antibiotics for wound care in an urban emergency department. Am J Emerg Med 16:343, 1998.
132. Goldstein
EJC, Citron DM, Yagvolgyi AE, et al: Susceptibility of bite wound bacteria to seven oral antimicrobial agents, including RU-985, a new erythromycin: Considerations in choosing empiric therapy. Antimicrob Agents Chemother 29:556, 1986. 133. Callaham 134. Leyden 135. Oates
M: Controversies in antibiotic choices for bite wounds. Ann Emerg Med 17:1321, 1988.
JJ: Effect of bacteria on healing of superficial wounds. Clin Dermatol 2:81, 1984.
JA, Wood AJJ: Antimicrobial prophylaxis in surgery. N Engl J Med 315:1129, 1986.
136. Cummings 137. Gergen
P, Del Beccaro MA: Antibiotics to prevent infection of simple wounds: A meta-analysis of randomized studies. Am J Emerg Med 13:396, 1995.
PJ, McQuillan GM, Kiely M, et al: A population-based serologic survey of immunity to tetanus in the United States. N Engl J Med 332:761, 1995.
138. American
College of Surgeons: Committee on Trauma: Early Care of the Injured Patient, 2nd edition. Philadelphia, WB Saunders, 1982, p 68.
139. Immunization
Practices Advisory Committee, Centers for Disease Control: Diphtheria, tetanus, and pertussis: Guidelines for vaccine prophylaxis and other preventive measures. MMWR 30:392,
401, 1981. 140. Passen 141. Stair
EL, Anderson BR: Clinical tetanus despite a protective level of toxin-neutralizing antibody. JAMA 255:1171, 1986.
TO, Lippe MA, Russell H, et al: Tetanus immunity in emergency department patients. Am J Emerg Med 7:563, 1989.
142. Giangrasso
J: Misuse of tetanus immunoprophylaxis in wound care. Ann Emerg Med 14:573, 1985.
143. Brand
D, Acampora D, Gottlieb LD, et al: Adequacy of antitetanus prophylaxis in six hospital emergency rooms. N Engl J Med 309:636, 1983.
144. White
JD, Stair TO: Antitetanus prophylaxis in the emergency department [letter]. Am J Emerg Med 2:280, 1984.
145. Lindsey 146. Jacobs
D: Tetanus prophylaxis—Do our guidelines assure protection? J Trauma 24:1063, 1984.
RL, Lowe RS, Lanier BQ: Adverse reactions to tetanus toxoid. JAMA 247:40, 1982.
147. Recommendations 148. Noah
DL, Drenzek CL, Smith JS, et al: Epidemiology of human rabies in the United States, 1980 to 1996. Ann Intern Med 128:922, 1998.
149. Goldberg 150. Seaman 151. Lee
of the Immunization Practices Advisory Committee: Rabies Prevention—United States, 1984. JAMA 252:883, 1984.
HM, Rosenthal SAE, Nemetz JC: Effect of washing closed head and neck wounds on wound healing and infection. Am J Surg 141:358, 1981.
M, Lammers R: Inability of patients to self-diagnose wound infections. J Emerg Med 9:215, 1990.
KH: Studies on the mechanism of action of salicylates. III. Effect of vitamin A on the wound healing retardation action of aspirin. J Pharm Sci 57:1238, 1968.
152. Rodeheaver
G, Edgerton MT, Smith S, et al: Antimicrobial prophylaxis of contaminated tissues containing suture implants. Am J Surg 133:609, 1977.
153. Peacock
EE: Control of wound healing and scar formation in surgical patients. Arch Surg 116:1325, 1981.
154. Crikelair
CT: Skin suture marks. Am J Surg 96:631, 1958.
155. Converse
JM, Smith B: The eyelids and their adnexa. In Converse JM (ed): Reconstructive Plastic Surgery: Principles and Procedures in Correction, Reconstruction, and Transplantation, vol 2, 2nd ed. Philadelphia, WB Saunders, 1977, p 858. 156. Grimes
DW, Garner RW: "Reliefs" in intracuticular sutures. Surg Rounds 1:46, 1978.
157. Ordog
GI, Wasserberger J, Balasubramanium S, et al: Civilian gunshot wounds—outpatient management. J Trauma 36:106, 1994.
158. Ordog
G, Sheppard GF, Wasserberger JS, et al: Infection in minor gunshot wounds. J Trauma 34:358, 1993.
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Chapter 36 - Methods of Wound Closure Richard L. Lammers Alexander T. Trott
Once the decision to close a wound has been made, the clinician must select the closure technique best suited for the location and configuration of the wound. Available techniques include hair typing (in the scalp) and use of tape, tissue adhesive, metal staples, and sutures. All traumatic wounds should be cleaned, and wounds containing devitalized tissue should be debrided before closure (see Chapter 35 ).
HAIR TYING OF SCALP WOUNDS Scalp wounds that gape have traditionally been closed with suture material or skin staples. One "folk method" of scalp wound closure that has received limited discussion and study is the technique of tying together "roped" strands of hair from opposite sides of the wound. [1] [2] The advantages of this technique are that no surgical instruments are required; no foreign material is placed in the wound; and it is relatively painless, because a local anesthetic injection is not needed. This technique may be of particular value in wilderness settings when wound repair equipment is unavailable and the wound is relatively clean. In certain superficial scalp wounds in children, this technique offers a particularly humane method of wound closure. Indications and Contraindications Closure by hair tying can be performed on small scalp wounds (i.e., 1 to 2 cm in length). Davies suggests the following six criteria for consideration of this technique : 1. 2. 3. 4. 5. 6.
[2]
The patient's hair must be of adequate length to form "roped" strands that can be tied across the wound. The wound edges should not be contused. There should be no gross wound contamination. There must be good wound hemostasis. The galea (occipitofrontalis aponeurosis) must not be divided. There must be no underlying skull fracture.
When these conditions cannot be met, the technique should not be undertaken. If local anesthesia must be used to permit evaluation of the deep structures of the wound, it may be best to simply repair the wound with sutures or staples. Procedure When possible, the area surrounding the wound should be cleansed with mild disinfectant, avoiding contact with the unanesthetized wound. The wound should be irrigated with normal saline. The wound should be gently explored using a gloved hand or cotton-tipped applicator to verify that the galea is not compromised and that no foreign material remains in the wound. Hair on each side of the laceration is then twisted to form "ropes" of hair ( Fig. 36-1A ). These "roped" strands are tied across the wound in a surgical knot, with several additional throws ( Fig. 36-1B ) to tightly appose the skin edges. Davies recommends spraying a plastic sealant on the knot to avoid loosening it. [2] Postclosure wound care is similar to that for routine scalp closure. The patient may gently shampoo the hair, but vigorous hair massage or combing in the area should be avoided. The knot is allowed to grow away from the wound edge and can be cut free in 2 to 4 weeks. Complications In 1 series of 25 children under 8 years of age whose scalp wounds were closed by hair tying, 48-hour follow-up showed no evidence of wound infection and 2 cases of mild (2 to 4 mm) wound separation. [2] The investigators noted that some children complained of the sensation that their hair was "being pulled" during wound closure, but all cooperated without restraints or anesthesia. The most common complaint noted at follow-up was that the hair-tie knot was untidy. There is little control over apposition of wound edges with this technique. Conclusion Closure of scalp wounds by hair tying offers an alternative for closure of small, superficial scalp wounds in children and for clean scalp wound repair in wilderness settings.
WOUND TAPE The use of surgical tape strips to close simple wounds has become routine in recent years. Tape strips can be applied by health care personnel in many settings, including emergency departments (EDs), operating rooms, clinics, and first-aid stations. Advantages include ease of application, reduced need for local anesthesia, more evenly distributed wound tension, no residual suture marks, minimal skin reaction, no need for suture removal, superiority for some grafts and flaps, and suitability for use under plaster casts. One main advantage of wound tapes is their greater resistance to wound infection compared with standard sutures and wound staples. [3] [4] [5] [6] Background and Tape Comparisons Tape closure of wounds has been reported since 1600 BC. [7] It was not until the late 1950s, however, with the introduction of woven tapes and nonsensitizing adhesive, that tapes gained widespread acceptance in the United States. [8] Since then, there have been rapid advances in the manufacture of tapes with increased strength, improved adhesiveness, and presterilized packaging. Currently there are several brands of tapes with differing porosity, flexibility, strength, and configuration. Steri-Strips (3M Corporation, St. Paul, MN) are microporous tapes with ribbed backing. They are porous to air and water, and the ribbed backing provides extra strength. Cover-Strips (Beiersdorf, South Norwalk, CT) are woven in texture and have a high degree of porosity. They allow not only air and water, but also wound exudates to pass through the tape. Shur-Strip (Deknatel, Inc., Floral Park, NY) is a nonwoven microporous tape. Clearon (Ethicon, Inc., Somerville, NJ) is a synthetic plastic tape whose backing contains longitudinal parallel serrations to
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Figure 36-1 A, Hair on each side of a laceration is twisted to form "ropes" of hair. B, The "roped" strands are tied across the wound in a surgical knot along with additional throws to oppose the skin edges.
permit gas and fluid permeability. An iodoform-impregnated Steri-Strip (3M Corporation) is intended to further retard infection without sensitization to iodine. tape products include Curi-Strip (Kendall, Boston), Nichi-Strip (Nichiban Co., Ltd, Tokyo), Cicagraf (Smith & Nephew, London), and Suture Strip (Genetic Laboratories, St. Paul, MN).
[ 3]
Other
Scientific studies of wound closure tapes have been limited, and because of different investigators' choices of products and methods, it is not always easy to compare results. Koehn showed that the Steri-Strip tapes maintained adhesiveness about 50% longer than Clearon tape. [9] Rodeheaver and coworkers compared Shur-Strip, Steri-Strip, and Clearon tape in terms of breaking strength, elongation, shear adhesion, and air porosity. [10] The tapes were tested in both dry and wet conditions. The Steri-Strip tape was found to have about twice the breaking strength of the other two tapes in both dry and wet conditions; there was minimal loss of strength in all tapes when wetted. The Shur-Strip tapes showed approximately two to three times the elongation of the other tapes at the breaking point, whether dry or wet. Shear adhesion (amount of force required to dislodge the tape when a load is applied in the place of contact (angle = 0°) was slightly better for the Shur-Strip tape than for the Steri-Strip tape and approximately 50% better than for the Clearon tape. Of these three wound tapes, the investigators considered Shur-Strips to be superior for wound closure. One comprehensive study of wound tapes compared Curi-Strip, Steri-Strip, Nichi-Strip, Cicagraf, Suture Strip, and Suture Strip Plus. [11] All tapes were 12 mm wide except for Nichi-Strip, which was 15 mm. Each tape was compared for breaking strength, elongation under stress, air porosity, and adhesiveness. Curi-Strip, Cicagraf, and Steri-Strip exhibited equivalent dry breaking strengths. However, when wet (a condition that can occur in the clinical setting), Cicagraf outperformed all tapes. All of the tested tapes had similar elongation-under-stress profiles with the exception of Suture Strip Plus. This tape did not resist elongation under low or high forces. Excessive elongation may allow wound dehiscence. Nichi-Strip was the most porous to air, and Cicagraf was almost vapor impermeable. Nichi-Strip and Curi-Strip had the best adherence to untreated skin. When the skin was treated with tincture of benzoin, however, Steri-Strip dramatically outperformed all other products. When all of the study parameters were considered, Nichi-Strip, Curi-Strip, and Steri-Strip achieved the highest overall performance rankings. Indications The primary indication for tape closure is a superficial straight laceration under little tension. If necessary, tension can be reduced by undermining or placing deep closures. Areas particularly suited for tape closure are the forehead, chin, malar eminence, thorax, and nonjoint areas of the extremities. Tape also may be preferred for wounds in anxious children when suture placement is not essential. In young children who are likely to remove tapes, tape closures must be protected with an overlying bandage. However, adhesive bandages (e.g., Band-Aids) should be avoided (see later). In experimental wounds inoculated with Staphylococcus aureus, tape-closed wounds resisted infection better than wounds closed with nylon sutures. [6] Therefore, tape closures may be considered on wounds with potential for infection, although infection rates are generally comparable to those of sutured wounds. Tape closures work well under plaster casts when superficial suture removal would be delayed. Tape closures effectively hold flaps and grafts in place, particularly over fingers, the flat areas of the extremities, and the trunk ( Fig. 36-2 ). [3] [4] Wounds on the pretibial area are difficult to close. This area is particularly problematic in the elderly because of tissue atrophy. One report found that wound tapes outperformed suture closure of the pretibial area with regard to time to healing and complications. [12] Tape closures can be applied to wounds following early suture removal to maintain wound edge approximation while reducing the chance of permanent suture mark scarring. Finally, because of the minimal skin tension created by tapes, they can be used on skin that has been compromised by vascular insufficiency or altered by prolonged use of steroids.
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Figure 36-2 A, A skin avulsion is an ideal wound to close with closure tapes. An elderly woman who was on steroids had extremely thin skin and suffered an anterior tibial skin avulsion that could not be replaced with sutures. B, The skin edges are uncurled, stretched, and anatomically replaced. C, The wound should heal when closure tapes keep the skin in place. A compression dressing, such as an elastic bandage or a Dome paste (Unna) boot dressing, can be applied to minimize flap movement and decrease fluid buildup under the flap. D, Tape should be placed in a semicircular or spiral pattern on digits to avoid constriction.
Contraindications There are disadvantages to tape closures. Tape does not work well on wounds under significant tension or on wounds that are irregular, on concave surfaces, or in
areas of marked tissue laxity. In many cases tape does not provide satisfactory wound edge apposition without concurrent underlying deep closures. Tape does not stick well to naturally moist areas, such as in the axilla, the palms of the hands, the soles of the feet, and the perineum. Tape also has difficulty adhering to wounds that will have copious exudates. Tape strips are also at risk for premature removal by young children. Tape closures are contraindicated in wounds that are irregular or under tension and in those that cannot be appropriately dried of blood or secretions. They are of little value on lax and intertriginous skin and in the scalp and other areas with high concentration of hair follicles. Tapes should never be placed circumferentially around digits because they have insufficient ability to stretch or lengthen. If placed circumferentially, the natural wound edema of an injured digit can make the tape act like a constricting band, which can lead to ischemia and possible necrosis of the digit. Semicircular or spiral placement techniques should be used if digits are to be taped ( Fig. 36-2C ). Equipment For a simple tape closure, the required equipment includes forceps and tape of the proper size. Most taping can be done in the ED with ¼-inch × 3-inch strips. In wounds larger than 4 cm, however, ½-inch-wide strips might be desirable. Most companies manufacture strips up to 1 inch wide and up to 4 inches long. Procedure Application of the tape must be preceded by proper wound preparation, irrigation, debridement, and hemostasis. Fine hair may be cut short or shaved, and the area of the tape application is thoroughly dried to ensure proper adhesion. Attempting to apply tapes to a wet area or over a wound that is slowly oozing blood will usually result in failure of the tapes to stick to the skin. On fingers, tapes can be applied to a wound that is kept dry by a tourniquet temporarily placed at the base of the finger.
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Figure 36-3a Proper technique for application of tapes for skin closure. A, After wound preparation (and placement of deep closures, if needed), dry the skin thoroughly at least 2 inches around the wound. Failure to dry the skin and failure to obtain perfect hemostasis are common causes of failure of tapes to stick to the skin. B, If desired, apply a thin coating of tincture of benzoin around the wound to enhance tape adhesiveness. Benzoin should not enter the eye, and it causes pain if it seeps into an open wound. C, Cut the tapes to the desired length before removing the backing. D, The tapes are attached to a card with perforated tabs on both ends. Gently peel the end tab from the tapes.
Tincture of benzoin and Mastisol are liquid adhesives that can be applied initially to increase tape adhesion. [6] The clinician should use sterile technique at all times. Wound tapes do not adhere unduly to surgical gloves. All tapes come in presterilized packages and can be opened directly onto the operating field. The technique of applying tapes is shown in Figure 36-3A–J Figure 36-3A–J . After the wound has been dried and a liquid adhesive has been applied and has dried, the tapes, with backing attached, are cut to the desired length. Tapes should be long enough to allow for approximately 2 to 3 cm of overlap on each side of the wound. After the tape is cut to length, the end tab is removed. The tape is gently removed from the backing with forceps by pulling straight back. Do not pull to the side because the tape will curl and be difficult to apply to the wound. One half of the tape is securely placed at the midportion of the wound. The opposite wound edge is gently but firmly apposed to its counterpart. The second half of the tape is then applied. The wound edges should be as close together as possible and at equal height to prevent the development of a linear, pitted scar. Additional tapes are applied by bisecting the remainder of the wound. A sufficient number of tape strips should be placed so that the wound is completely apposed without totally occluding the wound edges. Finally, additional cross tapes are placed to add support and prevent blistering caused by unsupported tape ends. [5] Taped wounds are left open, without occlusive dressings. Adhesive bandages (e.g., Band-Aids) and other dressings promote excessive moisture, which can lead to premature tape separation from the wound. The bandage also may adhere to the closure tapes, causing separation of the closure tape from the skin at the time of the removal. Tapes may remain in place for approximately 2 weeks, longer in some cases. The duration of application is a decision that varies with the requirements of each wound. The patient can be allowed to clean the taped laceration gently with a moist, soft cloth after 24 to 48 hours. However, if excessive wetting or mechanical force is used, premature separation may result. Patients may be instructed to gently trim curled edges of the closure tape with fine scissors to avoid premature removal of the tape. Complications Complications are uncommon with tape closure. The infection rate is approximately 5% in clean wounds closed with tape. [5] This compares favorably with rates for other standard
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Figure 36-3b E, Use forceps to peel the tape off the card backing. Pull directly backward, not to the side. F, Place one half of the first tape at the midportion of the wound; secure firmly in place. G, Gently but firmly oppose the opposite side of the wound, using the free hand or forceps. If an assistant is not available, the operator can approximate the wound edges. H, The tape should be applied by bisecting the wound until the wound is closed satisfactorily. I, Wound margins are completely opposed without totally occluding the wound. J, Additional supporting tapes are placed approximately 2.5 cm from the wound and parallel to the wound direction. Taping in this manner prevents the skin blistering that may occur at tape ends.
closures. Premature tape separation occurs in approximately 3% of cases. [10] Other complications include (1) skin blistering, which occurs if the tape is not properly anchored with the cross-stay strip or the tape is stretched excessively across the wound; and (2) wound hematoma, which results if hemostasis is inadequate. When tincture of benzoin is used, it should be applied carefully to the surrounding uninjured skin. If spillage occurs into the wound, the wound is at higher risk for infection. [13] Benzoin vapors cause pain when applied near an open wound that has not been anesthetized. Benzoin can also injure the mucous membranes of the eye. Summary Most investigators believe that the results of proper tape closure are as successful as those of suture closure. [5] [7] However, some investigators believe that tape closure leads to inferior cosmetic results. [14] In the aggregate, modern tape products and techniques serve a valuable role in minor wound
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management of selected patients in the ED. Generally, closure tapes are underused, and many wounds that are currently sutured in cosmetically unimportant areas could be adequately closed with tapes. As a general guide, tapes should be considered in those cases where sutures are not clearly required, but the wound is too wide for a simple dressing.
TISSUE ADHESIVE Adhesive tape can only be used on superficial wounds on relatively flat, hairless body surfaces. The tissue adhesive N-2-octylcyanoacrylate (Dermabond, Ethicon Inc.) is a bonding agent that can be used on superficial wounds, even in hair-bearing areas. Tissue adhesive (also called tissue glue) polymerizes when it comes in contact with water. This substance is biodegradable but remains in the wound until well after healing. [15] Procedure Tissue adhesive can be used to approximate wounds not requiring deep-layer closure. In preparation for closure, the wound should be anesthetized and cleaned, and when necessary, debrided. Bleeding must be controlled. As the wound edges are held together with forceps or fingers, a small, cylindrical plastic container is squeezed to expel droplets of tissue glue through a cotton applicator tip at the end of the container. The glue is applied in at least 3 to 4 thin layers along the length of the wound's surface ( Fig. 36-4 ). Alternatively, one can place the glue in strips perpendicular to the laceration (analogous to placement of closure tapes). The purple color of the solution facilitates placement of the droplets. The wound edges should be supported with edges approximated for at least 1 minute while the glue dries. The closure can be reinforced and protected with a bandage such as Elastoplast. The primary advantage of tissue glue is the speed of closure. Wounds can be closed in as little as one sixth of the time required for repair with sutures. Application is rapid and painless. Wounds closed with tissue glue have less tensile strength than sutured wounds in the first 4 days [16] [17] but 1 week after closure the tensile strength and overall degree of inflammation in wounds closed with tissue glue were equivalent to those closed with sutures. [15] [18] Cosmetic results are similar to those obtained with suture repair. [17] [19] [20] [21] [22] [23] [24] [25] Tissue glue serves as its own wound dressing and has an antimicrobial effect against gram-positive organisms. [26] [27] The material sloughs off in 7 to 10 days, thereby saving the patient from a clinician visit. Ointments or occlusive bandages should not be placed on wounds closed with tissue glue. Complications Percutaneous sutures provide a more secure immediate closure than tissue glue. [15] Although tissue glue is classified as nontoxic and does not cause a significant foreign body reaction, it should not be placed within the wound cavity. [17] [18] If the wound edges cannot be held together without considerable tension, tissue glue should not be used.[25] Tissue glue should not be used near the eyes, over or near joints, on moist or mucosal surfaces, or on wounds under significant static or dynamic skin tension. After polymerizing, tissue glue can
Figure 36-4 Tissue adhesive, 2-octyl cyanoacrylate in a commercially available application dispenser.
fracture with excessive or repetitive movement. Although gentle rinsing is permitted, if the adhesive is washed or soaked, it will peel off in a few days, before the wound is healed. [17] If hemostasis is inadequate or an excessive amount of glue is applied too quickly, the patient can experience a burning sensation from the heat of polymerization. One risk involving the use of tissue glue is its ease of use. Clinicians may fail to adequately clean wounds before closure with tissue glue. [27A] Tissue glue should not be used to close infected wounds. If the clinician's gloved fingers contact the tissue glue during application, the glove may adhere to the patient's skin. Tissue glue can be removed with antibiotic ointment, petrolatum jelly, or more rapidly with acetone. [25] Summary Tissue glue has been approved for use in the United States since 1998. Dermabond is packaged in sterile, single-use ampules. It is best suited for superficial wounds that are under little tension and that do not require prolonged support. Cosmetic results are generally equivalent to sutured wounds when used properly. 276
WOUND STAPLES Background Wound stapling devices date back to the early part of this century. Several Russian, Hungarian, and Japanese investigators pioneered various instruments, but it was not until the early 1960s that significant interest in the use of these devices developed in the United States. [28] [29] Since then there has been a steady improvement in technology, including the introduction of automatic and disposable devices, precocking mechanisms, and optimal staple configurations. Automatic stapling devices have become commonplace for closure of surgical incisions and are finding acceptance among clinicians for closure of traumatic wounds. Clinical studies of patients with stapled surgical incisions have consistently revealed that there is no significant difference between stapling and suturing when infection rates, healing outcome,
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and patient acceptance are compared. [30] [31] [32] [33] [34] Four important studies have demonstrated that selected traumatic wounds in both adult and pediatric patients can be closed successfully with staples in the ED setting. [35] [36] [37] Wound stapling and nylon suture closure of skin compared favorably in wound tensile strength, complication rates, patient tolerance, efficiency of closure, scar width, color, general appearance, suture or staple marks, infection rates, and cost. However, in one study more patients in the staple group reported discomfort with removal. [37] In animal models, staples cause less wound inflammation, preserve wound defense mechanisms, and offer more resistance to infection in contaminated wounds. [38] [39] [40] [41] The most significant advantage of wound stapling over suturing is speed of closure. On average, stapling is three to four times faster than suturing traumatic wounds. [35] [37] [42] The time for actual staple application is =30 seconds for a laceration 3 to 5 cm in length. [43] [44] [45] Cost has been cited as a disadvantage of staple closure, particularly when large, multistaple (25 to 35) surgical units are the only product available. [43] However, with the introduction of smaller devices more appropriate for the average laceration, the cost of stapling devices has been reduced significantly. [43] When clinician time and cost of instruments are considered, the cost difference is minimal[35] or favors stapling. [46] Indications and Contraindications Currently the indications for stapling are limited to relatively linear lacerations with straight, sharp edges located on an extremity, the trunk, or the scalp. Staples may be especially useful for superficial scalp lacerations in the agitated or intoxicated patient. Because of their superficial placement in the adult scalp (usually above the galea), staples are not ideal for deep scalp lacerations. Staples may not provide the same hemostasis that is possible with deep sutures. Also, they should not be placed in scalp wounds if computed tomography head scans are to be performed because staples produce scan artifacts. Similarly, staples should not be used if the patient is expected to undergo magnetic resonance imaging, because the powerful magnetic fields may avulse the staples from the skin surface. As they are currently configured and manufactured, staples should not be used on the face, neck, hands, or feet. Equipment Standard wound care should precede wound closure (see Chapter 35 ). In many cases, when debridement and dermal (deep) closures are unnecessary, only tissue forceps are needed to assist in everting wounds. Many stapling devices are commercially available. The most versatile and least expensive stapler is the Precise (3M Corporation). Different units that hold between 5 and 25 staples can be purchased. The 10-staple unit will suffice for most lacerations. Other devices include the Proximate 11 (Ethicon, Inc.), Cricket (US Surgical, Irvine, CA), and Appose (Davis & Geck, Columbus, OH). These staplers have a minimum of 15 staples and are 3 to 5 times more expensive than the Precise stapler. Procedure The wound is prepared in the manner described in Chapter 35 . Whenever necessary, deep, absorbable sutures are used to close deep fascia and to reduce tension in the superficial fascia and dermal layers. Before stapling, the wound edges should be everted, preferably by a second operator. The assistant precedes the operator along the wound and everts the wound edges with forceps or pinches the skin with the thumb and forefinger. This technique allows the staple to be precisely placed. Once the edges are held in eversion, the staple points are gently placed across the wound ( Fig. 36-5 ). By squeezing the stapler handle or trigger, the staple is advanced automatically into the wound and bent to the proper configuration ( Fig. 36-6 and Fig. 36-7 ). One must take care not to press too hard on the skin surface in order to prevent placing the staple too deeply and causing ischemia within the staple loop. When properly placed, the crossbar of the staple is elevated a few millimeters above the skin surface ( Fig. 36-8 ). Enough staples should be placed to provide proper apposition of the edges of the wound along its entire length. After the wound is stapled, an antibiotic ointment may be applied to minimize dressing adherence, and a sterile dressing is applied. If necessary, the patient can remove the dressing and gently clean the wound in 24 to 48 hours. Removal of staples requires a special instrument that is made available by each manufacturer of stapling devices. The lower jaw of the staple remover is placed under the crossbar ( Fig. 36-9 ). One brings down the upper jaw by squeezing the handle ( Fig. 36-10 ). This action compresses the crossbar, thereby releasing the staple points for easy removal. If the patient is referred for office removal of staples, it may be advisable to provide the patient with the staple removal device on ED release because many clinicians do not routinely stock the instrument. The interval between staple application and removal is the same as that for standard suture placement and removal.
Figure 36-5 The skin edges must be approximated and everted by hand or with forceps before they are secured with staples. Failure to evert the wound edges is a common error that may cause an unacceptable result. (Adapted with permission from Edlich RF: A Manual for Wound Closure. St. Paul, MN, 3M Medical-Surgical Products, 1979. Reproduced by permission.)
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Figure 36-6 By squeezing the stapler handle, a plunger advances one staple into the wound margins. (From Edlich RF: A Manual for Wound Closure. St. Paul, MN, 3M
Medical-Surgical Products, 1979. Reproduced by permission.)
Complications Complications can occur with staple-closed wounds, although the incidence is low and equivalent to that for sutured wounds. In 2 studies of traumatic wounds closed with staples, the infection rates were reported to be 0% and 5%. [37] [43] Staple acceptance and comfort have been reported to be equal to those of sutures, but in one study, removal of staples was somewhat more uncomfortable than removal of sutures. [37] Wound dehiscence has been reported, but the incidence is not considered significant. [37] A common error is failure to evert the skin edges before stapling ( Fig. 36-11A and B ). Eversion avoids the natural tendency of the device to invert the closure. Eversion may be accomplished with forceps or by pinching the skin with the thumb and index finger, a procedure that requires some practice. Staples do cause marks in the skin similar to sutures. In patients who tend to scar more easily, the resulting scar from the staples may be more pronounced than that produced by sutures, especially if the staples are left in place for prolonged periods.
Figure 36-7 An anvil automatically bends the staple to the proper configuration. (From Edlich RF: A Manual for Wound Closure. St. Paul, MN, 3M Medical-Surgical Products, 1979. Reproduced by permission.)
Figure 36-8 Care should be taken to ensure that a space remains between the skin and the crossbar of the staple. Excessive pressure created by placing the staple too deep causes wound edge ischemia, as well as pain on removal. Note that the staple bar is 2 to 3 mm above the skin line. (From Edlich RF: A Manual for Wound Closure. St. Paul, MN, 3M Medical-Surgical Products, 1979. Reproduced by permission.)
Conclusion Overall results are favorable when staples are used for surgical incisions and traumatic lacerations of the scalp, trunk, and extremities. Wound stapling does not differ significantly from suturing in infection rates, wound healing, and patient acceptance. Stapling is clearly superior in reducing time to closure. With the introduction of new devices, the cost of wound stapling is comparable to that of suturing. Because of the increased availability and versatility of stapling instruments, they are being used more frequently in ED wound management.
SUTURES In most situations, suturing is the closure method of choice. Currently in the United States, most traumatic wounds are closed with sutures.
Figure 36-9 The lower jaw of the staple remover is placed under the crossbar of the staple. (From Edlich RF: A Manual for Wound Closure. St. Paul, MN, 3M Medical-Surgical Products, 1979. Reproduced by permission.)
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Figure 36-10 By squeezing the handle gently, the upper jaw compresses the staple and allows it to exit the skin. (Adapted from Edlich RF: A Manual for Wound Closure. St. Paul, MN, 3M Medical-Surgical Products, 1979. Reproduced by permission.)
Equipment Instruments
In addition to the instruments used for debridement, a needle holder and suture scissors are required for suturing. The size of the needle holder should match the size of the needle selected for suturing—that is, the needle holder should be large enough to hold the needle securely as it is passed through tissue, yet not so large that the needle is crushed or bent by the instrument. The mechanical performance of disposable needle holders distributed by different surgical instrument companies varies considerably. [47] Instruments used to debride a grossly contaminated wound should be discarded
Figure 36-11 A very poor result occurred when staples (some marked with arrows) were used to close this deep scalp laceration (A). The wound edges were not everted (in fact, the skin overlapped significantly), and poor hemostasis was obtained because the galea was not closed by the superficial staples. Three days later during a wound check, the staples were removed, and the laceration was closed with 3-0 interrupted nylon sutures ( B). The clinician should attempt to obtain a cosmetic closure on all scalp lacerations, because as patients lose their hair, a previously hidden, unsightly scar emerges. In general, staples should not be used to close full-thickness scalp lacerations, especially wounds that are actively bleeding.
and fresh instruments obtained for the closure of the wound. Instruments covered with coagulated blood can be cleansed with hydrogen peroxide, rinsed with sterile saline or water, and then used for suturing. Suture Materials
A wide variety of suture materials are available. For most wounds that require closure of more than one layer of tissue, the clinician must choose sutures from two general categories: an absorbable suture for the subcutaneous (SQ) layer and a nonabsorbable suture for skin closure. Sutures can be described in terms of four characteristics: 1. 2. 3. 4.
Composition (i.e., chemical and physical properties) Handling characteristics and mechanical performance Absorption and reactivity Size and retention of tensile strength
Composition.
Sutures are made from natural fibers (cotton, silk), from sheep submucosa or beef serosa (plain gut, chromic gut), or from synthetic materials such as nylon (Dermalon, Ethilon, Nurulon, Surgilon), Dacron (Ethiflex, Mersilene), polyester (Ti-Cron), polyethylene (Ethibond), polypropylene (Prolene, Surgilene), polyglycolic acid (Dexon), and polyglactin (Vicryl, coated Vicryl). Stainless steel sutures are rarely, if ever, useful in wound closure in the ED setting because of handling difficulty and fragmentation. Some sutures are made of a single filament (monofilament); others consist of multiple fibers braided together ( Table 36-1 ). [48] Handling and performance.
Desirable handling characteristics in a suture include smooth passage through tissues, ease in knot tying, and stability of the knot once tied ( Table 36-2 ). Smooth sutures pull through tissues easily, but knots slip more readily. Conversely, sutures with a high coefficient of friction have better knot-holding capacity but are difficult to slide through tissues. Smooth sutures will loosen after the first throw of a knot is made, and a second throw is needed to secure the first in place. However, the clinician may
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Absorbable Sutures
TABLE 36-1 -- Examples of Suture Materials Nonabsorbable Sutures
Monofilament Plain gut
Dermalon (nylon)
Chromic gut
Ethilon (nylon)
PDS (polydioxanone)
Prolene (polypropylene)
Maxon (polyglyconate)
Silk Steel Surgilene (polypropylene) Tevdek (Teflon coated)
Multifilament Dexon (polyglycolic acid)
Ethibond (polyethylene)
Coated Vicryl (polyglactin)
Mersilene (braided polyester) Nurulon (nylon) Surgilon (nylon) TiCron (polyester)
want to tighten a knot further after the first throw is made. This is difficult with rougher types of sutures. Multifilament sutures have the best handling characteristics of all sutures, whereas steel sutures have the worst. In terms of performance and handling, significant improvements have been made in the newer absorbable sutures. Gut sutures have many shortcomings, including relatively low and variable strength, a tendency to fray when handled, and stiffness despite being packaged in a softening fluid. [49] [50] Multifilament synthetic absorbable sutures are soft and easy to tie and have few problems with knot slippage. Polyglactin 910 (coated Vicryl) sutures have an absorbable lubricant coating. The "frictional drag" of these coated sutures as they are pulled through tissues is less than that of uncoated multifilament materials, and the resetting of knots following the initial throw is much easier. This characteristic allows retightening of a ligature without knotting or breakage and with smooth, even adjustment of suture line tension in running subcuticular stitches. [51] Synthetic monofilament sutures have the trouble-some property of "memory"—a tendency of the filament to spring back to its original shape, which causes the knot to slip and unravel. Some nonabsorbable monofilament sutures are coated with polytetrafluorethylene (Teflon) or silicone to reduce their friction. This coating improves the handling characteristics of these monofilaments but results in poorer knot security. [50]
Knot Security
TABLE 36-2 -- Characteristics of Suture Materials Tensile Strength Tissue Reactivity Duration of Suture Integrity (days)
Tie Ability
Surgical gut
poor
fair
greatest
5–7
poor
Chromic gut
fair
fair
greatest
10–14
poor
Coated Vicryl
good
good
minimal
30
best
Dexon
best
good
minimal
30
best
PDS
fair
best
least
45–60
good
Maxon
fair
best
least
45–60
good
Ethilon
good
good
minimal
good
Prolene
least
best
least
fair
Silk
best
least
greatest
best
Suture Material Handling Absorbable
Nonabsorbable
Modified with permission from Hollander J, Singer A: Laceration management. Ann Emerg Med 34:361, 1999.
Three square knots will secure a stitch made with silk or other braided, nonabsorbable materials, and four knots are sufficient for synthetic, absorbable and nonabsorbable monofilament sutures. [52] Five knots are needed for the Teflon-coated synthetic Tevdek. [53] With the use of coated synthetic suture materials, attention to basic principles of knot tying is even more important. An excessive number of throws in a knot weakens the suture at the knot. If the clinician uses square knots (or a surgeon's knot on the initial throw, followed by square knots) that lie down flat and are tied securely, knots will rarely unravel. [54] Absorption and reactivity.
Sutures that are rapidly degraded in tissues are termed absorbable; those that maintain their tensile strength for >60 days are considered nonabsorbable (see Table 36-1 ). Plain gut may be digested by white blood cell lysozymes in 10 to 40 days; chromic gut will last 15 to 60 days. Remnants of both types of sutures, however, have been seen in wounds more than 2 years after their placement. [49] [52] [55] The Ethicon catgut is rapidly absorbed within 10 to 14 days but with less inflammation than that caused by chromic catgut. [56] Vicryl is absorbed from the wound site within 60 to 90 days [49] [52] and Dexon, within 120 to 210 days. [57] [58] When placed in the oral cavity, plain gut disappears after 3 to 5 days, chromic gut after 7 to 10 days, and polyglycolic acid after 16 to 20 days. [59] In contrast, SQ silk may not be completely absorbed for as long as 2 years. [52] The rate of absorption of synthetic absorbable sutures is independent of suture size. [57] Sutures may lose strength and function before they are completely absorbed in tissues. Braided synthetic absorbable sutures lose nearly all of their strength after about 21 days. In contrast, monofilament absorbable sutures (modified polyglycolic acid [Maxon, Davis & Geck] and polydioxanone [PDS, Ethicon]) retain 60% of their strength after 28 days. [60] [61] Gut sutures treated with chromium salts (chromic gut) have a prolonged tensile strength; however, all gut sutures retain tensile strength erratically. [49] [52] Of the absorbable types of sutures, a wet and knotted polyglycolic acid suture is stronger than a plain or chromic gut suture subjected to the same conditions. [50] [62] Polypropylene remains unchanged in tissue for longer than 2 years after implantation. [63] In comparison testing, Hermann found that sutures made of natural fibers such as silk, cotton, and gut were the weakest; sutures made of Dacron, nylon, polyethylene, and polypropylene were intermediate in tensile strength; and metallic sutures were the
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strongest.[50] Kaplan and Hentz used the comparison of suture strength vs wound strength as a measure of the usefulness of a suture. They stated that catgut is stronger than the soft tissue of a wound for no more than 7 days; chromic catgut, Dexon, and Vicryl are stronger for 10 to 21 days; and nylon, wire, and silk are stronger for 20 to 30 days. [64] All sutures placed within tissue will damage host defenses and provoke inflammation. Even the least reactive suture impairs the ability of the wound to resist infection. [63] The magnitude of the reaction provoked by a suture is related to the quantity of suture material (diameter × total length) placed in the tissue and to the chemical composition of the suture. Among absorbable sutures, polyglycolic acid and polyglactin sutures are least reactive, followed by chromic gut. Nonabsorbable polypropylene is less reactive than nylon or Dacron. [50] [65] [66] Significant tissue reaction is associated with catgut, silk, and cotton sutures; highly reactive materials should be avoided in contaminated wounds. Adams found absorbable polyglycolic acid sutures to be less reactive than those of nonabsorbable silk. [67] The chemical composition of sutures is an important determinant of early infection. The infection rate in experimental wounds when polyglycolic acid sutures are used
is less than the rate when gut sutures are used. It is surprising that plain gut sutures elicit infection less often in contaminated wounds than chromic gut sutures. [63] Lubricant coatings on sutures do not alter suture reactivity, absorption characteristics, breaking strength, or the risk of infection. [51] [63] Multifilament sutures provoke more inflammation and are more likely to produce infection than monofilament sutures if left in place for prolonged periods. [68] [69] Monofilament sutures elicit less tissue reaction than do multifilament sutures, and multifilament materials tend to wick up fluid by capillary action. Bacteria that adhere to and colonize sutures can envelop themselves in a glycocalix that protects them from host defenses, [70] or they can "hide" in the interstices of a multifilament suture and, as a result, be inaccessible to leukocytes.[68] Polydioxanone (PDS) provides the advantages of a monofilament suture in an absorbable form, making it a good choice as a subcuticular stitch. Polypropylene sutures have a low coefficient of friction, and subcuticular stitches with this material are easy to pull out. [71] Size and strength.
Size of suture material (thread diameter) is a measure of the tensile strength of the suture; threads of greater diameter are stronger. The strength of the suture is proportional to the square of the diameter of the thread. Therefore, a 4-0 size suture of any type is larger and stronger than a 6-0 suture. The correct suture size for approximation of a layer of tissue depends on the tensile strength of that tissue. The tensile strength of the suture material should be only slightly greater than that of the tissue, because the magnitude of damage to local tissue defenses is proportional to the amount of suture material placed in the wound. [52] [72] Synthetic absorbable sutures have made the older, natural suture materials obsolete. Polyglycolic acid (Dexon) and polyglactin 910 (coated Vicryl) have improved handling characteristics, knot security, and tensile strength. Their absorption rates are predictable, and tissue reactivity is minimal. [73] [74] The distinct advantages of synthetic nonabsorbable sutures over silk sutures are their greater tensile strength, low coefficient of friction, and minimal tissue reactivity. [63] [73] They are extensible, elongating without breaking as the edges of the wound swell in the early postoperative period. [72] [73] In contrast with silk sutures, synthetics can be easily and painlessly removed once the wound has healed. The monofilament synthetic suture Novofil has elasticity that allows a stitch to enlarge with wound edema and to return to its original length once the edema subsides. Stiffer materials lacerate the encircled tissue as the wound swells. [75] The suture materials most useful to emergency clinicians for wound closure are Dexon or coated Vicryl for SQ layers and synthetic nonabsorbable sutures (e.g., nylon or polypropylene) for skin closure. Fascia can be sutured with either absorbable or nonabsorbable materials. In most situations, 3-0 or 4-0 sutures are used in the repair of fascia, 4-0 or 5-0 absorbable sutures in SQ closure, and 4-0 or 5-0 nonabsorbable sutures in skin closure. Lips, eyelids, and the skin layer of facial wounds are repaired with 6-0 sutures, whereas 3-0 or 4-0 sutures are used when the skin edges are subjected to considerable dynamic stresses (e.g., wounds overlying joint surfaces) or static stresses (e.g., scalp). Needles
The eyeless, or "swaged," needle is used for wound closure in most emergency centers ( Fig. 36-12 ). The traditional closed-eye needle requires additional handling to enable one to thread the needle with the suture, and its increased width causes more damage when passing through tissue than does a swaged needle. Selection of the appropriate needle size and curvature are based on the dimensions of the wound and the characteristics of the tissues to be sutured. The needle should be large enough to pass through tissue to the desired depth and then to exit the tissue or the skin surface far enough that the needle holder can be repositioned on the distal end of the needle at a safe distance from the needle point ( Fig. 36-13 ). While it is inviting to use the fingers to grasp the needle tip to pull the needle through the skin, this practice is an invitation for a needle stick. The clinician should either reposition the needle holder or use forceps to disengage the needle from the laceration. In wound repair, needles must penetrate tough, fibrous tissues—skin, SQ tissue, and fascia—yet should slice through these tissues with minimal resistance or trauma and without bending. The type of needle best suited for closure of SQ tissue is a conventional cutting needle in a three-eighths or one-half circle ( Fig. 36-14 ). The use of double curvature needles (coated Vicryl with PS-4-C cutting needles, Ethicon) may enhance the clinician's ability to maneuver the needle in narrow, deep wounds. For percutaneous closure, a conventional cutting-edge needle may
Figure 36-12 The eyeless, or "swaged," needle. (From Suture Use Manual: Use and Handling of Sutures and Needles. Somerville, NJ, Ethicon, Inc., 1977, p 29. Reproduced by permission.)
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Figure 36-13 The needle should be large enough to pass through tissue and should exit far enough to enable the needle holder to be repositioned on the end of the needle at a safe distance from the point.
permit more precise needle placement and require less penetration force ( Fig. 36-15 ). [76] [77] Suturing Techniques Skin Preparation
Before closing the wound, the skin surrounding it is prepared with a povidone-iodine solution and covered with sterile drapes. Some surgeons do not drape the face but prefer to leave facial structures and landmarks adjacent to the wound uncovered and within view. A clear plastic drape (Steri-Drape, 3M Corporation) can be used to provide a sterile field and a limited view of the area surrounding the wound. If no drapes are used on the face, the skin surrounding the wound should be widely cleansed and prepared. Wrapping the hair in a sheet prevents stray hair from falling into the operating field ( Fig. 36-16 ). Some EDs keep a supply of oversized scrub hats to use as an alternative to wrapping. Closure Principles
Three principles apply to the suturing of lacerations in any location: (1) minimize trauma to tissues, (2) relieve tension exerted on the wound edges by undermining and layered wound closure, and (3) accurately realign landmarks and skin edges by layered closure and precise suture placement. Minimizing tissue trauma.
The importance of careful handling of tissue has been emphasized since the early days of surgery. Skin and SQ tissue that has been stretched, twisted, or crushed by an instrument or strangled by a suture that is tied too tightly may undergo necrosis, and increased scarring and infection may result. When the edges of a wound must be manipulated, the SQ tissues should be lifted gently with a toothed forceps or skin hook, avoiding the skin surface.
Figure 36-14 One-half and three-eighths circle needles, used for most traumatic wound closures.
When choosing suture sizes, the clinician should select the smallest size that will hold the tissues in place. Skin stitches should incorporate no more tissue than is needed to coapt the wound edges with little or no tension. Knots should be tied securely enough to approximate the wound edges but without blanching or indenting the skin surface. [78] Relieving tension.
Many forces can produce tension on the suture line of a reapproximated wound. Static skin forces that stretch the skin over bones cause the edges of a fresh wound to gape and also continuously pull on the edges of the wound once it has been closed. Traumatic loss of tissue or wide excision of a wound may have the same effect. The best cosmetic result occurs when the long axis of a wound happens to be parallel to the direction of maximal skin tension; this alignment brings the edges of the wound together.[75] Muscles pulling at right angles to the axis of the wound impose dynamic stresses. Swelling following an injury creates additional tension within the circle of each suture.[78] Skin suture marks result not only from tying sutures too tightly, but also from failing to eliminate underlying forces distorting the wound. Tension can be reduced during wound closure in two ways: undermining of the wound edges and layered closure.
Figure 36-15 Types of needles. A, The conventional cutting needle has two opposing cutting edges, with a third edge on the inside curvature of the needle. The conventional cutting needle changes in cross section from a triangular cutting tip to a flattened body. B, The reverse cutting needle is used to cut through tough, difficult-to-penetrate tissues, such as fascia and skin. It has two opposing cutting edges, with the third cutting edge on the outer curvature of the needle. The reverse cutting needle is made with the triangular shape extending from the point to the swage area, with only the edges near the tip being sharpened. (From Suture Use Manual: Use and Handling of Sutures and Needles. Somerville, NJ, Ethicon, Inc., 1977, p 31. Reproduced by permission.)
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Figure 36-16 A–D, Technique for wrapping the scalp to keep stray hair from falling into the operating field. A scrub hat is an acceptable alternative. Undermining.
The force required to reapproximate the wound edges correlates with the subsequent width of the scar. [79] Wounds subject to significant static tension require the undermining of at least one tissue plane on both sides of the wound to achieve a tension-free closure. Undermining involves the creation of a flap of tissue freed from its base at a distance from the wound edge approximately equal to the width of the gap that the laceration presents at its widest point ( Fig. 36-17 ). The depth of the incision can be modified, depending on the orientation of the laceration to skin tension lines and the laxity of skin in the area. A No. 15 scalpel blade held parallel to the skin surface is used to incise the adipose layer or the dermal layer of the wound. The clinician also can accomplish this technique by spreading scissors in the appropriate tissue plane. Undermining allows the skin edges to be lifted and brought together with gentle traction. [80] Because undermining may harm the underlying blood supply, this technique should be reserved for relatively uncontaminated wounds. [76] Other potential complications of this procedure include injury to cutaneous nerves and creation of a hematoma under the flap. [64] Layered closure.
The structure of skin and soft tissue varies with the location on the body ( Fig. 36-18A–D Fig. 36-18A–D ). Most wounds handled in an ED require approximation of no more than three layers: fascia (and associated muscle), SQ tissue, and skin surface (papillary layer of dermis and epidermis). [81]
Figure 36-17 The technique of undermining. The scalpel is used to find an appropriate site; a natural plane often exists at the epidermis-dermis junction. Undermining relieves tension on the wound and renders a better cosmetic result. This technique is simple to master, but sometimes overlooked.
Closure of individual layers obliterates "dead space" within the wound that would otherwise fill with blood or exudate. The presence of dead space enhances the development of infection; however, it is not necessary to close the adipose layer of soft tissue with a separate stitch. A "fat stitch" is not necessary, because little support is provided by closure of the adipose layer, and the additional suture material that is required may enhance the possibility of infection. [6] [82] Separate approximation of muscle and SQ layers hastens the healing and return of function to the muscle. However, one should suture fascia, not muscle. Muscle tissue itself is too friable to hold a suture. Layered closure is particularly important in the management of facial wounds; this technique prevents scarring of muscle to the SQ tissue and consequent deformation of the surface of the wound with contraction of the muscle. If a deep, gaping wound is closed without approximation of underlying SQ tissue, a disfiguring depression may develop at the site of the wound. Finally, layered closure provides support to the wound and considerably reduces tension at the skin surface. There are exceptions to the general rule of multilayered closure. Scalp wounds are generally closed in a single layer. For lacerations penetrating the dermis in fingers, hands, toes, and feet, the amount of SQ tissue is too small to warrant layered closure; in fact, SQ stitches may leave tender nodules in these sensitive locations. In the sebaceous skin of the nasal tip, SQ sutures should be avoided, because they provoke inflammation and increase the risk of infection. However, deep sutures do not increase the risk of infection in minimally contaminated wounds. [83] Layered closure is not recommended in wounds without tension, those with poor vascularity, and those with moderate infection potential. With single-layer closure, the surface stitch should be placed more deeply. [64] Suture Placement
Before suturing, the clinician should ensure adequate exposure and illumination of the wound. The clinician should assume a comfortable standing or sitting position, with the patient placed at an appropriate height. The best position for
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Figure 36-18a Variation in the structure of skin. A, Section of the skin of the scalp, ×15. B, Skin of the human fingertip, illustrating a very thick stratum corneum. Hematoxylin and eosin, ×65.
the clinician is at one end of the long axis of the wound. Knot construction using the instrument tie technique is described in other references.
[ 84]
SQ layer closure.
Once fascial structures have been reapproximated, the SQ layer is sutured. Although histologically the fatty and fibrous SQ tissue (hypodermis) is an extension of (and is continuous with) the reticular layer of the dermis, [85] suturing of these layers is traditionally referred to as an "SQ closure." One approach is to close this layer in segments, placing the first stitch in the middle of the wound and bisecting each subsequent segment until the closure of the layer has been completed. [48] This technique is useful in the closure of wounds that are long or sinuous and is particularly effective in wounds with one elliptic and one linear side. The needle is grasped by the needle holder close to the suture end. Greater speed in suturing is possible if the fingers are placed
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Figure 36-18b C, Section of human sole perpendicular to the free surface, ×100. D, Section through human thigh perpendicular to the surface of the skin. Blood vessels are injected and appear black. Low magnification. (A Courtesy of H Mizoguchi. C and D after AA Maximow. From Bloom W, Fawcett DW: A Textbook of Histology, 10th ed. Philadelphia, WB Saunders, 1975. Reproduced by permission.)
on the midshaft of the needle holder rather than in the rings of the instrument ( Fig. 36-19 ). The suture enters the SQ layer at the bottom of the wound ( Fig. 36-20A ) or, if the wound has been undermined, at the base of the flap ( Fig. 36-20B ), and exits in the dermis. Once the suture has been placed on one side of the wound, it can be pulled across the wound to the opposite side (or the wound edges pushed together) to determine the matching point on the opposite side. It is at this matching point along the opposite side of the wound that the needle is inserted. The needle should enter the dermis at the same depth as it exited from the opposite side, pass through the tissue, and exit at the bottom of the wound (or the base of the flap). The edges of the wound can be closely apposed by pulling the two tails of the suture in the same direction along the axis of the wound ( Fig. 36-21 ). Some clinicians place their SQ suture obliquely rather than vertically to facilitate knot tying. When the knot in this SQ stitch is tied, it will remain inverted, or "buried," at the bottom of the wound. Burying the knot of the SQ stitch avoids a painful, palpable nodule beneath the epidermis and keeps the bulk of this foreign material away from the skin surface. The techniques of tying knots by hand and by instrument are well described and illustrated in wound care texts. [86] [87] Once the knot has been secured, the tails of the suture should be pulled taut for cutting. The scissors are held with the index finger on the junction of the two blades. The blade of the scissors is slid down the tail of the suture until the knot is reached. With the cutting edge of the blade tilted away from the knot, the tails are cut. This technique prevents the scissors from cutting the knot itself and leaves a tail of 3 mm, which protects the knot from unraveling ( Fig. 36-22 ). [88] The entire SQ layer is sutured in this manner.
Figure 36-19 The thenar grip technique of handling the needle holder. The index finger is placed on the side of the needle holder, where it guides the placement of the needle. Neither the index nor the middle finger is placed in the ringlet hole. An alternate method (the thumb-ring finger grip) is shown in Figure 36-27 .
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Figure 36-20 A and B, Inverted subcutaneous stitches.
After the SQ layer has been closed, the distance between the skin edges indicates the approximate width of the scar in its final form. If this width is acceptable, percutaneous sutures can be inserted. [89] Despite undermining and placement of a sufficient number of SQ sutures, on rare occasions a large gap between the wound edges may persist. In such cases a horizontal dermal stitch may be used to bridge this gap ( Fig. 36-23 ).
Figure 36-21 The two tails of the subcutaneous suture are pulled in the same direction, tightly opposing the edges of the wound.
Figure 36-22 Cutting the tails of the subcutaneous suture. Note that the cutting blade is tilted away from the knot to avoid cutting it. (Modified from Anderson CB: Basic surgical techniques. In Klippel AP, Anderson CB (eds): Manual of Outpatient and Emergency Surgical Techniques. Boston, Little, Brown, 1979. Reproduced by permission.)
Skin closure.
The epidermis and the superficial layer of dermis are sutured with nonabsorbable synthetic sutures. The choice of suture size, the number of sutures used, and the depth of suture placement depend on the amount of skin tension remaining after SQ closure. If the edges of the wound are apposed following closure of deeper layers, small 5-0 or 6-0 sutures can be used simply to match the epithelium of each side. If the wound edges remain retracted or if SQ stitches were not used, a larger size suture may be required. Skin closure may be accomplished with sutures placed in segments ( Fig. 36-24 ) or from end to end. Either technique is acceptable. Unless the wound edges are uneven, sutures should be placed in a mirror-image fashion such that the depth and width are the same on both sides of the wound .[52] In general, the distance between each suture should be approximately equal to the distance from the exit of the stitch to the wound edge. [48] [86] Grabb suggests that "the number of sutures used in closing any wound will vary with the case, location of the repair, and degree of accuracy required by the clinician and patient. In an area such as the face, sutures would probably be placed between 1 and 3 mm apart and 1 to 2 mm from the wound edge." [68]
Figure 36-23 Horizontal dermal stitch. (A vertical suture also closes the deep tissue.)
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Figure 36-24 Closure of the surface of the wound in segments.
Sutures act as foreign bodies in a wound, and any stitch may damage a blood vessel or strangulate tissue. Therefore, the clinician should strive to use the smallest size and the least number of sutures that will adequately close the wound ( Fig. 36-25 ). [63] Wounds with greater tension should have skin stitches placed closer to each other and closer to the wound edge; layered closure is important in such wounds. If sutures are tied too tightly around wound edges or if individual stitches are under excessive tension, blood supply to the wound may be impeded, increasing the chance of infection, and suture marks may form even after 24 hours. [52] [86A] When suturing the skin, right-handed operators should pass the needle from the right side of the wound to the left. The needle should enter the skin at an oblique angle to produce an everting, bottle-shaped stitch that is deeper than it is wide ( Fig. 36-26 ). If the skin stitch is intended to produce some eversion of the wound edges, the stitch must include a sufficient amount of SQ tissue. However, encompassing too much tissue with a small needle is a common error. Forcefully pushing or twisting the needle in an effort to bring the point out of the tissue may bend or break the body of the needle. Using a needle of improper size will defeat the best suturing technique. The needle should be driven through tissue by flexing the wrist and supinating the forearm; the course taken by the needle should result in a curve identical to the curvature of the needle itself ( Fig. 36-27 ). The angle of exit for the needle should be the same as its angle of entrance so that an identical volume of tissue is contained within the stitch on each side of the wound. Once the needle exits the skin on the opposite side of the wound, it is regrasped by the needle holder and is advanced through the tissue; care should be taken to avoid crushing the
Figure 36-25 A, Too few stitches used. Note gaping between sutures. B, Too many stitches used. C, Correct number of stitches used for a wound under an average amount of tension.
point of the needle with the instrument. Forceps are designed for handling tissue and thus should not be used to grasp the needle. The forceps can stabilize the needle by holding the needle within the tissue through which the needle has just passed. An assistant can keep excess thread clear of the area being sutured, or the excess can be looped around the clinician's fingers. If the point of the needle becomes dulled before all of the attached thread has been used, the suture should be discarded. If these techniques are applied to most wounds, the edges of the wound will be matched precisely in all three dimensions. Eversion techniques.
If the edges of a wound invert or if one edge rolls under the opposite side, a poorly formed, deep, noticeable scar will result. Excessive eversion that exposes the dermis of both sides also will result in a larger scar than if the skin edges are perfectly apposed, but inversion produces a more visible scar than does eversion. Because most scars undergo some flattening with contraction, optimal results are achieved when the epidermis is slightly everted without excessive suture tension ( Fig. 36-28 ). Wounds over mobile surfaces, such as the extensor surfaces of joints, should be everted; in time, the scar will be flattened by the dynamic forces acting in the area. Numerous techniques can be used to avoid inversion of the edges of the wound. If the clinician angles the needle away from the laceration, percutaneous stitches can be placed so that their depth is greater than their width. [80] Converse described this method as follows: "The needle penetrates the skin close to the incision line, diverging from the edge of the wound in order to encircle a larger amount of tissue in the lower depths of the skin than at the periphery." [90] The edge of the wound can be lifted and everted with a skin hook or fine-tooth forceps before insertion of the needle on each side ( Fig. 36-29 ). Eversion can also be obtained simply by slight retraction of the wound with the thumb ( Fig. 36-30 ). This technique puts the operator at risk for a needle stick; eversion may be done more safely by applying slight pressure on the wound edge with a closed forceps. Each of these methods also serves to steady the skin against the force of the needle. [86] [90] Vertical mattress sutures are particularly effective in everting the wound edges and can be used exclusively or alternated with simple interrupted sutures ( Fig. 36-31 ). [90] In wounds that have been undermined, an SQ stitch placed at the base of the flap on each side can in itself evert the wound (Fig. 36-32 (Figure Not Available) ). Interrupted stitch.
The simple interrupted stitch is the most frequently used technique in the closure of skin. It consists of separate loops of suture individually tied. Although the tying and cutting of each stitch are time consuming, the advantage of this method is that if one stitch in the closure fails, the remaining stitches continue to hold the wound together ( Fig. 36-33 ). Continuous stitch.
In a continuous, or "running," stitch, the loops are the exposed portions of a helical coil tied at each end of the wound. A continuous suture line can be placed more rapidly than a series of interrupted stitches. The continuous stitch has the additional advantages of strength (with tension being evenly distributed along its entire length), fewer knots (which are the weak points of stitches), and more effective hemostasis. This stitch will accommodate mild wound swelling. The continuous technique is useful as an epithelial or "surface" stitch in cosmetic closures; however, if the underlying SQ layer is not stabilized in a separate closure, the continuous surface stitch tends to invert the wound edges.
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Figure 36-26 The simple suture. A, Hold the needle pointing down by excessively pronating the wrist so that the needle tip initially moves farther from the laceration as the needle penetrates deeper into the skin. Thus, there is more dermis in the depth of the wound than at the surface. Drive the needle tip downward and away from the cut edge, into the fat. B, Advance the needle into the laceration. The needle tip can be advanced directly into the opposite side. This can be achieved by rolling the needle holder as the needle enters the opposite side at the same level, and the arc pathway of the needle is controlled by retracting the skin edge. This causes more dermis to be incorporated into the depths than at the surface. As an alternative, if a small needle is used in thick skin or the distance across the wound is great, the needle can be removed from the first side, remounted on the needle holder, and advanced to the opposite side. C, Advance the needle upward toward the surface so that it exits at the same distance from the wound edge as on the contralateral side of the wound. Grasp the needle behind the tip and roll it out in the arc of the needle. D, The final position, with more tissue in the depth than the surface. The distance from each suture exit to the laceration is one half the depth of the dermis. (Redrawn from Kaplan EN, Hentz VR: Emergency Management of Skin and Soft Tissue Wounds: An Illustrated Guide. Boston, Little, Brown, 1984, p 86. Reproduced by permission.)
The continuous suture technique has other disadvantages. This technique cannot be used to close wounds overlying joints. If a loop breaks at one point, the entire stitch may unravel. Likewise, if infection develops and the incision must be opened at one point, cutting a single loop may allow the entire wound to fall open. There is also the theoretical problem of impeded blood supply to the wound edges, particularly if the suture is interlocked. [52] Speer found that wounds closed with an interrupted stitch had 30% to 50% greater tensile strength, less edema and induration, and less impairment in the microcirculation at the wound margin than did wounds closed with a continuous stitch. [91] The simple continuous stitch has a tendency to produce suture marks if used in large wound closures and if left in place for more than 5 days.[78] However, if all tension on the wound can be removed by SQ sutures, stitch marks are seldom a problem. Among the variations of the continuous technique, the simple continuous stitch is the most useful to emergency clinicians ( Fig. 36-34 ). An interrupted stitch is placed at one end of the wound, and only the free tail of the suture is cut. As suturing proceeds, the stitch encircles tissue in a spiral pattern. After each passage of the needle, the loop is tightened slightly, and the thread is held taut in the clinician's nondominant hand. The needle should travel perpendicularly across the wound on each pass. The last loop is placed just beyond the end of the wound, and the suture is tied, with the last loop used as a "tail" in the process of tying the knot ( Fig. 36-35 ). A locking loop may be used in continuous suturing to prevent slippage of loops as the suturing proceeds ( Fig. 36-36 ). The interlocking technique allows the use of the continuous stitch along an irregular laceration. [80] A continuous stitch is an effective method for closing relatively clean wounds that are under little or no tension and are on flat, immobile skin surfaces in patients who have no medical conditions that would impair healing.
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Figure 36-27 Motion of the needle holder. (From Anderson CB: Basic surgical techniques. In Klippel AP, Anderson CB (eds): Manual of Outpatient and Emergency Surgical Techniques. Boston, Little, Brown, 1979. Reproduced by permission.) Continuous subcuticular stitch.
Nonabsorbable sutures used in percutaneous skin closure outlast their usefulness and must be removed. On occasion, wounds require an extended period of support, longer than that provided by surface stitches. Some patients with wounds that require skin closure are unlikely or unwilling to return for suture removal. Some sutured wounds are covered by plaster casts. On occasion, the patient (child or adult) is likely to be as frightened and uncooperative for suture removal as for suture placement. The continuous subcuticular (or "dermal") suture technique is ideal for these situations; the wound can be closed with an absorbable subcuticular stitch, obviating the need for later suture removal. In patients prone to keloid formation, the subcuticular technique can be used in lieu of percutaneous stitches, and disfiguring stitch marks can thereby be avoided. (Because children's skin is under greater tension than that of adults, percutaneous sutures are more likely to produce stitch marks in children.) Because stitch marks are avoided, a nonabsorbable subcuticular suture can be left in place for a longer period than a percutaneous suture.[90]
Figure 36-28 Skin edges that are everted will gradually flatten to produce a level wound surface. (From Grabb WC: Basic technique of plastic surgery. In Grabb WC, Smith JW: Plastic Surgery: A Concise Guide to Clinical Practice. Boston, Little, Brown, 1979. Reproduced by permission.)
Figure 36-29 The use of a skin hook to evert the wound edge. This technique allows the operator to see the needle path, ensuring that the proper depth has been reached, and promotes eversion of the skin edges.
Although this technique is commonly used in cosmetic closures, some researchers believe that closure of the subcuticular layer alone does not alter the scar width. [92] This technique does not allow for perfect approximation of the vertical heights of the two edges of a wound [93] and in cosmetic closures it is often followed by a percutaneous stitch. Although theoretically the large amount of suture material left in the wound might increase the risk of infection, some investigators report a lower infection rate with the subcuticular technique. [92] [94] Buried, absorbable subcuticular stitches do not appear to provoke more inflammation than percutaneous running stitches with monofilament nylon. [83] The subcuticular stitch requires a 4-0 or 5-0 suture made of either absorbable material or nonabsorbable synthetic monofilament. An absorbable suture can be "buried" within
Figure 36-30 Eversion can often be obtained by slight thumb pressure. Care should be taken to avoid a needle stick, a common complication of this technique. (From Converse JM: Introduction to plastic surgery. In Converse JM: Reconstructive Plastic Surgery: Principles and Procedures in Correction, Reconstruction, and Transplantation, vol 1, 2nd ed. Philadelphia, WB Saunders, 1977. Reproduced by permission.)
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Figure 36-31 The vertical mattress suture is the best technique for producing skin edge eversion. A, Usual type of mattress suture for approximating and everting wound edges. B, "Tacking" type of vertical mattress suture, extending into deep fascia to obliterate dead space under wound. Note that only a small bite of skin is included on the inner suture. (Modified from Converse JM: Introduction to plastic surgery. In Converse JM: Reconstructive Plastic Surgery: Principles and Procedures in Correction, Reconstruction, and Transplantation, vol 1, 2nd ed. Philadelphia, WB Saunders, 1977. Reproduced by permission.) Figure 36-32 (Figure Not Available) Deep dermis suturing technique. The suture enters the base of the flap, is brought up into the dermis, and exits just proximal to the wound edge along the base of the flap to be tied and cut. (From Stuzin J, Engrav LH, Buehler PK: Emergency treatment of facial lacerations. Postgrad Med 71:81, 1982. Reproduced by permission.)
Figure 36-33 Simple interrupted stitch. Additional throws in a partially tied knot are not shown. (From Grabb WC: Basic techniques of plastic surgery. In Grabb WC, Smith JW (eds): Plastic Surgery: A Concise Guide to Clinical Practice. Boston, Little, Brown, 1979. Reproduced by permission.)
the wound, whereas a nonabsorbable suture is used for a "pullout" stitch. The absorbable synthetic monofilament suture polydioxanone (PDS, Ethicon) is designed for subcuticular closure. It passes through tissues as easily as nonabsorbable monofilament sutures and is absorbed if left in the wound. Before the subcuticular stitch is placed, the SQ layer should be approximated with interrupted sutures to minimize tension on the wound. The pullout subcuticular stitch is started at the skin surface approximately 1 to 2 cm away from 1 end of the wound. The needle enters and exits the dermis at the apices of the wound ( Fig. 36-37 ). Bites through tissue are taken in a horizontal direction, with the needle penetrating the dermis 1 to 2 mm from the skin surface. These intradermal bites should be small, of equal proportion, and at the same level on each side of the wound. [74] [90] Accidental interlocking of the stitch should be avoided. Each successive bite should be placed 1 to 2 mm behind the exit point on the opposite side of the wound so that when the wound is closed, the entrance and exit points on either side are not directly apposed (see
Figure 36-34 Simple continuous stitch. (From Grabb WC: Basic techniques of plastic surgery. In Grabb WC, Smith JW (eds): Plastic Surgery: A Concise Guide to Clinical Practice. Boston, Little, Brown, 1979. Reproduced by permission.)
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Figure 36-35 Completing the simple continuous stitch. A series of square knots is tied, with the loop as one of the ties.
Fig. 36-37 ). Small bites should be taken to avoid puckering of the skin surface. Some clinicians prefer to place a fine (6-0) running skin suture in addition to the subcuticular suture for meticulous skin approximation. The skin suture is removed in 3 to 4 days to avoid suture marks.
Figure 36-36 Continuous interlocking stitch. (Modified from Suture Use Manual: Use and Handling of Sutures and Needles. Somerville, NJ, Ethicon, Inc, 1977. Reproduced by permission.)
Figure 36-37 A, Pullout subcuticular stitch. The suture is introduced into the skin in line with the incision, approximately 1 to 2 cm away. (From Grimes DW, Garner RW: "Reliefs" in intracuticular sutures. Surgical Rounds 1:46, 1978. Reproduced by permission.) B, By backtracking each stitch slightly, one can produce a straight scar. (From Grabb WC: Basic techniques
of plastic surgery. In Grabb WC, Smith JW (eds): Plastic Surgery: A Concise Guide to Clinical Practice. Boston, Little, Brown, 1979. Reproduced by permission.)
If the subcuticular stitch is used on lengthy lacerations, it is difficult to remove the suture. The placement of "reliefs" consisting of periodic loops through the skin during the length of the stitch facilitates later removal ( Fig. 36-38 ). Reliefs should be placed every 4 to 5 cm. The suture is crossed to the opposite side, and the needle is passed from SQ tissue to the skin surface. The suture is carried over the surface for approximately 2 cm before reentering the skin and SQ tissue. The subcuticular stitch is then continued at approximately the point at which the next bite would have been placed had the relief not been used. At the completion of the stitch, the needle is placed through the apex to exit the skin 1 to 2 cm away from the end of the wound. One should tighten the stitch by pulling each end taut. If reliefs have been used, one can take up any slack in the stitch by pulling on the reliefs. The clinician can secure the two ends of the stitch by taping them to the skin surface with wound closure tape, by placing a cluster of knots on each tail close to the skin surface, or by tying the two ends of the suture to each other over a dressing. Laxity of the subcuticular stitch is often noted with a decrease in tissue swelling 48 hours after wound closure. Some clinicians tighten the stitch when they reexamine the wound after 48 hours. Subcuticular closure using absorbable sutures that do not penetrate the skin is possible. The closure is begun with a dermal or SQ suture placed at one end of the wound and secured with a knot. After placement of the continuous subcuticular stitch from apex to apex, the suture is pulled taut, and a knot is tied using a tail and a loop of suture ( Fig. 36-39 ). The final knot can be buried by inserting the needle into deeper tissue; the needle exits several millimeters from the wound edge. If one pulls on the needle end, the knot disappears into the wound. [73] The obvious advantage of this technique is that there are no suture marks in the skin. Another method that avoids penetrating the skin is the interrupted subcuticular
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Figure 36-38 In constructing the relief to facilitate suture removal, the suture is crossed to the opposite side, going into the subcuticular area beneath the skin for approximately 2 cm before exiting (A). The suture is then carried over the epidermis for approximately 2 cm (B) and then back under the dermis again (C). Reentry is made into the wound area (D) at approximately the same location where the next "bite" would have been placed had the relief not been used. (From Grimes DW, Garner RW: "Reliefs" in intracuticular sutures. Surgical Rounds 1:47, 1978. Reproduced by permission.)
stitch ( Fig. 36-40 ). [90] Wounds with strong static skin tension may benefit from a few interrupted dermal stitches placed horizontal to the skin surface instead of a continuous subcuticular stitch. Nonabsorbable sutures can be left in place for 2 to 3 weeks, thus providing a longer period of support than percutaneous sutures, without the problem of stitch marks.[78] If skin sutures are used in conjunction with the subcuticular stitch, they are removed in 3 to 4 days. A subcuticular closure in itself is stronger than a tape closure. If the subcuticular technique is used exclusively to approximate the skin surface, it is advisable to apply skin tape to correct surface unevenness and to provide a more accurate apposition of the epidermis. Mattress stitch.
The various types of mattress stitches are all interrupted stitches. The vertical mattress stitch is an effective method of everting skin edges ( Fig. 36-41 and see Fig. 36-31 ). The vertical mattress stitch may be used to take a deep bite of skin in lieu of a layered closure in areas where excessive tension does not result. If the superficial loop is placed first, the tails can be pulled upward while the deep loop is placed, ensuring wound eversion in less time than with the traditional technique. [95] Unfortunately, this stitch causes more ischemia and necrosis inside its loop than either simple or continuous stitches. [96] The horizontal mattress stitch approximates skin edges closely while providing some degree of eversion ( Fig. 36-42 ). [78] The horizontal mattress suture may be ideal for areas where eversion is desirable but there is little SQ tissue. The half-buried horizontal mattress stitch, also called a mattress stitch with a dermal component, combines an interrupted skin stitch with a buried intradermal stitch ( Fig. 36-43 ). It is effective in joining the edges of a skin flap to the edges of the "recipient site"; the dermal component is placed through the dermis of the flap. [90] The half-buried horizontal mattress stitch is also useful at the scalp-forehead junction when there is tension on the wound edges. This technique halves the number of suture marks in the skin and avoids necrosis of the edge of a skin flap. The half-buried horizontal mattress stitch is particularly useful in suturing the easily damaged apex of a V-shaped flap ( Fig. 36-44 ). In the execution of the "corner stitch," the suture needle penetrates the skin at a point beyond the apex of the wound and exits through the dermis. The corner of the flap is elevated, and the suture is passed through the dermis of the flap. The needle is then placed in the dermis of the base of the wound and returned to the surface of the skin. All dermal bites should be placed at the same level. The suture is tied with sufficient tension to pull the flap snugly into the corner without blanching the flap. [78] [97] If the tip of a large flap with questionable viability may be further jeopardized by postoperative swelling, a cotton stent can be placed underneath the knot of the corner stitch. The cotton absorbs the tension produced by swelling. Figure-of-eight stitch.
The figure-of-eight stitch is useful in wounds with friable tissue, on the eyelids where the skin is too thin for buried sutures, or in areas in which buried sutures are undesirable ( Fig. 36-45 ). [98] This stitch reduces the amount of tension placed on the tissue by the suture, allowing the stitch to hold in place when a simple stitch would tear through the tissue. One disadvantage of this technique is that more suture material is left in the wound. A vertical variation of the figure-of-eight stitch is sometimes used to approximate close, parallel lacerations ( Fig. 36-46 ). [99] Another technique involves a vertical mattress stitch. The central "island" of tissue is secured by passing the superficial portion of the stitch through the island at the subcuticular level ( Fig. 36-47 ). [100] If the viability of the central island is questionable and the surrounding tissue is loose, it can be excised. Correction of dog-ears.
When wound edges are not precisely aligned horizontally, there will be excess tissue on one or both ends. This small flap of excess skin that bunches up at the end of a sutured wound is commonly called a dog-ear. This effect also occurs when one side of the wound is more elliptical than the opposite side or when an excision of a wound is not sufficiently elliptical—that is, when it is either too straight or too nearly circular. [48] [90] If a dog-ear is present, it can be eliminated on one side of the wound in the following manner: The flap of excess skin is elevated with a skin hook, and an incision is carried at an oblique angle from the apex of the wound toward the side with the excess skin. The flap is then undermined and laid flat. The resulting triangle of skin is trimmed, and the closure is completed ( Fig. 36-48A ). [89] [97] An alternative method consists of carrying the incision directly from the apex, in line with the wound. The flap of excess tissue is pulled over the incision while skin hooks are used to retract the extended apex of the wound. Excess tissue is excised, and the remainder of the wound is sutured. [90] If dog-ears are present on both sides of one end of the wound, the bulge of excess tissue can be excised in an elliptical fashion, and the wound can be closed ( Fig. 36-48B ). [97]
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Figure 36-39 Subcuticular closure without epidermal penetration. A, The initial knot is secured in the dermal or subcutaneous tissue. B, The short strand is cut, and the needle is inserted into the dermis at the apex of the wound. C, The needle in the dermis, close to the corner of the wound and exiting the wound at the same horizontal level. D, After the subcuticular stitch has been completed, a knot is tied with the tail and the loop of the suture. (Modified from Stillman RM: Wound closure: Choosing optimal materials and methods. ER Reports 2:43, 1981.) V-Y advancement flap.
If a corner stitch produces excessive tension on the tip of the flap, a V-Y closure can be used to approximate the edges without undue tension. An incision carried away from the apex of the wound converts it from a V to a Y configuration ( Fig. 36-49 ). The newly formed wound edges are undermined, and the repair is completed. A half-buried mattress stitch is placed at the fork of the Y. [97]
Figure 36-40 Interrupted subcuticular stitch (also called a horizontal dermal stitch). Absorbable sutures are used. A deep vertical suture is also shown. Stellate lacerations.
The repair of a stellate laceration is a challenging problem. Usually a result of compression and shear forces, these injuries contain large amounts of partially devitalized tissue. The surrounding soft tissue is often swollen and contused. Much of this contused tissue cannot be
Figure 36-41 Vertical mattress stitch. The key to a tight closure is to place the inner sutures very close to the suture line (wound edge). (From Grabb WC: Basic techniques of plastic surgery. In Grabb WC, Smith JW (eds): Plastic Surgery: A Concise Guide to Clinical Practice. Boston, Little, Brown, 1979. Reproduced by permission.) See also Fig. 36-31 .
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Figure 36-42 A, Horizontal mattress stitch. B, The dorsum of the hand, foot, or finger is an ideal place for a horizontal mattress suture to evert the wound edges. The relatively thin skin in these areas precludes the use of vertical mattress sutures. (A from Grabb WC: Basic techniques of plastic surgery. Grabb WC, Smith JW (eds): Plastic Surgery: A Concise Guide to Clinical Practice. Boston, Little, Brown, 1979. Reproduced by permission.)
Figure 36-43 Half-buried horizontal mattress stitch. (From Grabb WC: Basic techniques of plastic surgery. In Grabb WC, Smith JW: Plastic Surgery: A Concise Guide to Clinical Practice. Boston, Little, Brown, 1979. Reproduced by permission.)
Figure 36-44 A and B, Approximation of a corner flap with a half-buried horizontal mattress stitch. Because of its applicability to this closure, the stitch is often called a corner stitch.
Figure 36-45 Figure-of-eight stitch-two methods. (Modified from Dushoff IM: About face. Emerg Med 6:11:1974. Reproduced by permission.)
Figure 36-46 Vertical figure-of-eight suture technique. This can be used to close parallel lacerations. (From Mitchell GC: Repair of parallel lacerations [letter]. Ann Emerg Med 16:924, 1987.)
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Figure 36-47 Techniques for closure of parallel lacerations. A, Central tissue island with intact base. B, Central tissue island shaved from base. (Redrawn from Samo DG: A technique for parallel lacerations. Ann Emerg Med 17:297, 1988.)
Figure 36-48 A, Correction of a dog-ear. B, Excision of bilateral dog-ears. (A from Dushoff IM: A stitch in time. Emerg Med 5:1, 1973. Reproduced by permission.)
Figure 36-49 A and B, V-Y advancement flap. (From Rosen P, Sternbach G: Atlas of Emergency Medicine. Baltimore, Williams & Wilkins, 1979, p 132. Reproduced by permission.)
debrided without creating a large tissue defect. Sometimes tissue is lost, yet the amount is not apparent until key sutures are placed. In repairing what often resembles a jigsaw puzzle, the clinician can remove small flaps of necrotic tissue with an iris scissors; large, viable flaps can be repositioned in their beds and carefully secured with half-buried mattress stitches. If interrupted stitches are used to approximate a thin flap, small bites should be taken in the flap and larger, deeper bites in the base of the wound. A modification of the corner stitch can be used to approximate multiple flaps to a base ( Fig. 36-50 ). The V-Y advancement flap technique is also useful. Thin flaps of tissue in a stellate laceration with beveled
Figure 36-50 View from above stellate laceration, showing closure with half-buried mattress stitches.
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edges are often most easily repositioned and stabilized with a firm dressing. [78] Closure of stellate lacerations cannot always be accomplished immediately, especially if there is considerable soft tissue swelling. It may be best in some instances to consider delayed closure or revision of the scar at a later date. In complicated lacerations, inexact tissue approximation may be all that is possible initially. Repair of Special Structures Facial Wounds (General Features)
The ideal result in the repair of a facial laceration is an extremely narrow, flat, and unapparent scar. In addition to basic wound management, a few additional techniques can be used to achieve this result. One factor that contributes to wide scars is necrosis of partially devitalized wound edges. However, skin with apparently marginal circulation may survive because of the excellent vascularity of the face. SQ fat, which in other locations may be debrided thoroughly, should be preserved if possible in facial wounds to prevent eventual sinking of the scar and to preserve normal facial contours. Therefore, debridement of most facial wounds should be conservative.[81] Facial and forehead lacerations that follow natural skin creases or lines will heal with a less noticeable scar than those that are oblique or perpendicular to the natural wrinkles of the skin ( Fig. 36-51 ). Converse pointed out that "precise approximation of skin edges without undue tension ensures primary healing with minimal scarring." [90] A layered closure is essential in the cosmetic repair of many facial wounds. Approximation of the dermis with an SQ stitch or a combination of SQ and subcuticular stitches should bring the epithelial edges together or within 1 to 2 mm of apposition—close enough that the use of additional sutures seems almost unnecessary. [89] If an SQ stitch is the only stitch used to close the deeper layers, it should pass
Figure 36-51 Lacerations following natural skin lines (shown here) heal with a less noticeable scar than those that are oblique or perpendicular to natural lines (or wrinkles).
through the dermal-epidermal junction or within 1 to 2 mm of the skin surface without causing a dimpling effect. The clinician must tie this stitch snugly, pulling the two ends of the suture in the same direction (see Fig. 36-21 ). Should the first SQ stitch placed at the midpoint of a wound perfectly appose the skin edges, one can "protect" that stitch from disruption during further suturing by immediately placing a percutaneous stitch in the same location. If there is a slight gap in the wound edges after SQ closure, the skin can be partially approximated with a few guide stitches. The first is placed at the midpoint of the wound, and subsequent stitches bisect the intervening spaces. Guide stitches allow the definitive epithelial sutures to be placed with little tension on each individual stitch, and they protect the SQ stitches from disruption. Once the definitive stitches have been placed, the guide stitches, if slack, can be removed. Because a needle damages tissue with each passage through the skin, guide stitches should be used only when necessary. The epithelial stitch should never be used to relieve the wound of tension; it serves only to match the epidermal surfaces precisely along the length of the wound. If there is significant separation of the wound edges after closure of the SQ layer, a 5-0 or 6-0 subcuticular suture can be used to eliminate the tension produced by this separation and to provide prolonged stability. Once the skin edges are apposed, the epithelial stitch can be used to correct discrepancies in vertical alignment. A 6-0 synthetic nonabsorbable suture is an excellent material for this stitch. A continuous stitch is preferable because it can be placed quickly, but interrupted stitches are acceptable. In a straight laceration, better apposition is achieved if the wound is stretched lengthwise by finger traction or by the use of skin hooks. When the needle is placed on one side of the wound, if that side is higher than the opposite side, a shallow bite is taken. The needle is used to depress the wound edge to the proper height, after which the needle "follows through" to the other side, pinning the two sides together. If the first side entered is lower, the needle is elevated when entering the second side to match the epithelial edges.
Grabb pointed out that "the closer the needle lies to the skin edge, the greater will be its effect in controlling the ultimate position of that edge." [68] Epithelial stitches should be spaced no more than 2 to 3 mm apart and should encompass no more than 2 to 4 mm of tissue. [80] If widely spaced, the sutures will leave marks. [89] Once skin closure is complete, final adjustments in the tension on any continuous suture line are made before the end of the stitch is tied. If any level discrepancies persist, interrupted sutures or tape can be used to flatten these few irregularities. Surgical tape is useful as a secondary support, protecting the epithelial stitch from stresses produced by normal skin movements ( Fig. 36-52 ). Facial wounds have a tendency to swell and place excessive stretch on an epithelial stitch. This can be minimized by applying a pressure dressing and cold compresses to the wound following closure. Surgical tape can serve to a limited extent as a pressure dressing. Forehead
Although the forehead is actually a part of the scalp, lacerations in this region are treated as facial wounds. Vertical lacerations across the forehead are oriented 90° to skin tension lines, and the resulting scars are more noticeable than those
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Figure 36-52 Wound closure tape can be used to provide additional support while sutures are in place and after they are removed. This may be especially useful in cosmetic areas, such as the face.
from horizontal lacerations. Midline vertical forehead lacerations may result in cosmetically acceptable scars with standard closure techniques; uncentered lacerations may benefit from S-plasty or Z-plasty techniques during the initial repair or during later revision of the scar. Superficial lacerations may be closed with skin stitches alone, but deep forehead lacerations must be closed in layers. The periosteum should be approximated before the closure of more superficial layers. If skin is directly exposed to bone,
Figure 36-53 A, Elevation of a forehead flap. The "trap-door effect" is a natural healing process of elliptical or round lacerations. Patients should be advised of this phenomenon. B, This flap-type laceration of the knee will heal with a puffed-up center (trap door), even under the best of circumstances. (A from Grabb WC, Kleinert HE: Technics in Surgery: Facial and Hand Injuries. Somerville, NJ, Ethicon, Inc., 1980. Reproduced by permission.)
adhesions may develop that in time may limit the movement of skin during facial expressions. The frontalis muscle fascia and adjacent fibrous tissue should be approximated as a distinct layer; if left unsutured, the retracted ends of this muscle will bulge beneath the skin. If the gap in a muscle belly is later filled with scar tissue, movement of the muscle pulls on the entire scar and makes it more apparent. [81] A U-shaped flap laceration with a superiorly oriented base poses a difficult problem. Immediate vascular congestion and later scar contraction within the flap produce the "trap-door effect," with the flap becoming prominently elevated ( Fig. 36-53 ). This effect can be minimized by approximation of the bulk of SQ tissue of the flap to a deeper level on the base side of the wound; the skin surfaces of the two sides are apposed at the same level ( Fig. 36-54A ). A firm compression dressing helps eliminate "dead space" and hematoma formation within the wound. Despite these efforts, secondary revision is sometimes necessary. [78] Often, swelling of the flap resolves over a 6- to 12-month period. Because flap elevation can be quite disconcerting, the clinician should forewarn the patient and family about a possible trap-door effect. When a forehead laceration borders the scalp and the thick scalp tissue must be sutured to thinner forehead skin, a horizontal or vertical mattress stitch with an intradermal component can be used ( Fig. 36-54B ). [90] Eyebrow and Eyelid Lacerations
Jagged lacerations through eyebrows should be managed with little, if any, debridement of untidy but viable edges. The hair shafts of the eyebrow grow at an oblique angle, and vertical excision may produce a linear alopecia in the eyebrow,
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Figure 36-54 A, Repair of a U-shaped flap laceration with a superiorly oriented base to minimize the trap door effect. A, Excision of edges. B, undermining. C, Approximation of SQ tissue on the flap to SQ tissue at a deeper level on the base; D, skin closure. B and C, When a laceration in the thin skin of the forehead borders the thicker skin of the scalp, a horizontal mattress suture with an intradermal component can enhance healing by bringing tissues to the same plane. These figures show eversion of thinner skin to obtain adequate approximation with thicker scalp tissue. (B from Converse JM: Introduction to plastic surgery. In Converse JM (ed): Reconstructive Plastic Surgery: Principles and Procedures in Correction, Reconstruction, and Transplantation, vol 1, 2nd ed. Philadelphia, WB Saunders, 1977. Reproduced by permission.)
whereas with simple closure, the scar remains hidden within the hair. If partial excision is unavoidable, the scalpel blade should be angled in a direction parallel to the axis of the hair shaft to minimize damage to hair follicles. Points on each side of the lacerated eyebrow should be aligned precisely; a single percutaneous stitch on each margin of the eyebrow should precede SQ closure. The edges of the eyebrow serve as landmarks for reapproximation; therefore, the eyebrow must not be shaved, as these landmarks will be lost. Shaved eyebrows grow back slowly and sometimes incompletely, and shaving them often results in more deformity than the injury itself. Care must be taken not to invert hair-bearing skin into the wound. [93] The thin, flexible skin of the upper eyelid is relatively easy to suture. A soft 6-0 suture (or smaller) is recommended for closure of simple lacerations. Traumatized eyelids are susceptible to massive swelling; compression dressings and cool compresses can be used to minimize this problem. It is essential that the emergency clinician recognize complicated eyelid lacerations that require the expertise of an ophthalmologist. Lacerations that traverse the lid margin require exact realignment to avoid entropion or ectropion ( Fig. 36-55A ). Injuries penetrating the tarsal plate frequently cause damage to the globe. A deep horizontal laceration through the upper lid that divides the thin levator palpebrae muscle or its tendinous attachment to the tarsal plate produces ptosis. If this muscle
cannot be identified and repaired by the emergency clinician, a consultant should repair the injury primarily. A laceration through the portion of the upper or lower lid medial to the punctum frequently damages the lacrimal duct or the medial canthal ligament and requires specialized techniques for repair ( Fig. 36-55B ). If adipose tissue is seen within any periorbital laceration, one must assume that the orbital septum has been penetrated and that retrobulbar fat is herniating through the wound ( Fig. 36-55C ). The repair of lid avulsions, extensive lid lacerations with loss of tissue, and any of the other complex types of lid lacerations mentioned earlier should be left to ophthalmologists. Ear Lacerations
The primary goals in the management of lacerations of the pinna are expedient coverage of exposed cartilage and minimization of wound hematoma ( Fig. 36-55D ). Cartilage is an avascular tissue, and when ear cartilage is denuded of its protective, nutrient-providing skin, progressive erosive chondritis ensues. The initial step in the repair of an ear injury involves trimming away jagged or devitalized cartilage and skin. If the skin cannot be stretched to cover the defect, additional cartilage along the wound margin can be removed. Depending on the location, as much as 5 mm of cartilage can be removed without significant deformity. Cartilage should be approximated with 4-0 or 5-0 absorbable sutures initially placed at folds or ridges in the pinna representing major landmarks. Sutures tear through cartilage; therefore, the anterior and posterior perichondrium should be included in the stitch. No more tension should be applied than is needed to touch the edges together. In through-and-through ear lacerations, the posterior skin surface should be approximated next, using 5-0 nonabsorbable synthetic sutures. Once closure of the posterior surface is completed, the convoluted anterior surface of the ear can be approximated with 5-0 or 6-0 nonabsorbable synthetic sutures, with landmarks joined point by point. On the free rim, the skin should be everted if later notching is to be avoided. Care should be taken to cover all exposed cartilage. In heavily contaminated wounds of the ear (e.g., bite wounds) that already show evidence of inflammation, the necrotic tissue should be debrided, the cartilage covered by a loose approximation of skin, and the patient placed on antibiotics. [78] [101] After a lacerated ear has been sutured, it should be enclosed in a compression dressing (see Fig. 65-29 ). Lacerations of the Nose
In the repair of lacerations of the nose, reapproximation of the wound edges is difficult because the skin is inflexible, and even deeply placed stitches will slice through the epidermis and pull out. When the wound edges cannot be coapted easily,
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Figure 36-55 A, Repair of a simple lid laceration. The first sutures are placed at the lid margin so that the lid can be extended by traction with a hemostat. Interrupted absorbable sutures are used to close the tarsus (1), followed by separate closure of the muscle layer with absorbable sutures (2), and finally by closure of the skin with interrupted 8-0 black silk or synthetic sutures (3). Such a repair should not be performed by the novice. B, A method of identifying and repairing the canaliculus. This repair is best left to the ophthalmologist, but recognizing the potential for a canaliculus injury is the task at hand in the emergency department. C, Deep laceration of the left upper lid with herniation of orbital fat. For fat to prolapse, the orbital septum (and potentially the globe itself) must have been perforated. This is a wound requiring operating room exploration and repair. D, Lacerations of the ear require a special repair aimed at covering cartilage and preventing hematoma formation. With this through-and-through laceration of the margin of the pinna, the cartilage is trimmed just enough to allow the skin to be approximated to cover all exposed cartilage. The repair is easiest if the posterior pinna is sutured first.
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6-0 absorbable sutures can be placed in the fibrofatty junction in an SQ stitch before skin closure. Because it is difficult to approximate gaping wounds in this location, debridement must be kept to a minimum. Nasal cartilage is frequently involved in wounds of the nose, but it is seldom necessary to suture the cartilage itself. The free rim of the nostril must be aligned precisely to avoid unsightly notching. Many clinicians recommend early removal of stitches to avoid stitch marks, yet the oily nature of skin in this area makes it difficult to keep the wound closed with tape. A subcuticular stitch is recommended if the wound is gaping before closure, as this will provide support for a prolonged period. [102] Lip and Intraoral Lacerations
Lip lacerations are cosmetically deforming injuries, but if the clinician follows a few guidelines, these lacerations usually heal satisfactorily. The contamination of all intraoral and lip wounds is considerable; they must be thoroughly irrigated. Regional nerve blocks are preferred to local injection, because the latter method distends tissue, distorts the anatomy of the lip, and obscures the vermilion border. Losses of 25% require a reconstructive procedure. Extensive lacerations directly through the commissure of the mouth also require surgical consultation in most cases.[101] Deep scars in the vermilion of the upper lip may produce a redundancy of tissue that requires later revision. [101] Large through-and-through lacerations of the lip should be closed in three layers. With a multilayer closure, the muscle layer is approximated with a 4-0 or 5-0 absorbable suture securely anchored in the fibrous tissue located anterior and posterior to the muscle. The vermilion-cutaneous junction of the lip is a critical landmark that, if divided, must be repositioned with precision; a 1-mm "step-off" is apparent and cosmetically unacceptable. The vermilion border should be approximated with a 5-0 or 6-0 nonabsorbable stay suture before any further closure to ensure proper alignment throughout the remainder of the repair ( Fig. 36-56 ). The
Figure 36-56 A, In the repair of lip lacerations, the first stitch should be placed at the vermilion-cutaneous border to obtain proper alignment. (A from Grabb WC, Kleinert HE: Technics in Surgery: Facial and Hand Injuries. Somerville, NJ, Ethicon, Inc., 1980. Reproduced by permission.)
vermilion surface of the lip and the buccal mucosa are then closed with interrupted stitches using an absorbable 4-0 or 5-0 suture. Finally, the skin is closed with 6-0 nonabsorbable sutures. [103] Small puncture-type lacerations heal well only if the skin is closed and the small intraoral laceration is left open. Such injuries are common from a punch in the face when the victim's tooth lacerates the lip. In general, small lacerations of the oral mucosa heal well without sutures. If a mucosal laceration creates a flap of tissue that falls between the occlusal surfaces of the teeth or if a laceration is extensive enough to trap food particles (e.g., 2 to 3 cm or greater in length), it should be closed. Small flaps may be excised. Closure is easily accomplished with 4-0 Dexon or Vicryl using a simple interrupted suturing technique. These materials are soft and less abrasive than gut sutures, which become hard and traumatize adjacent mucosa. Similarly, nylon sutures whose sharp ends are annoying and painful should be avoided inside the mouth. Muscle and mucosal layers should be closed separately. Sutures in the oral cavity easily become untied by the constant motion of the tongue. Each suture should be tied with at least four square knots. These sutures need not be removed; they either loosen and fall out within 1 week or are rapidly
absorbed. [81] [103] [104] All lacerations that penetrate the oral mucosa should be evaluated for the presence of a tooth fragment. A retained tooth fragment should be searched for in the depths of the wound if a tooth is missing or chipped. The search should be intensified if the patient returns with an infection of a sutured wound. Probing the wound with forceps may identify fragments not seen directly in the wound. In the setting of marked facial swelling, a radiograph of the soft tissue may help identify an embedded tooth fragment. Tongue Lacerations
There is some controversy regarding when to suture tongue lacerations. Simple, linear lacerations, especially those in the central portion of the tongue, heal quickly with minimal risk of infection. Most tongue lacerations that occur from falls or seizures do not require sutures. Most tongue lacerations in children heal well without sutures. Snyder suggests that only those lacerations that involve the edge or pass completely through the tongue, flap lacerations, and lacerations that continue to bleed excessively need to be sutured ( Fig. 36-57 ). All lacerations bisecting the tongue require repair. [102] Small flaps on the edge of the tongue may be excised, but large flaps should be sutured. When dilute peroxide mouth rinses and a soft diet are used for a few days, healing is rapid. Persistent bleeding from minor lacerations brings most patients to the hospital, and closure may be necessary to prevent further bleeding. The repair of a tongue laceration in any patient is somewhat difficult, but in an uncooperative child, the procedure may prove impossible under anything other than general anesthesia. A Denhardt-Dingman side mouth gag aids in keeping the patient's mouth open. A localized area of the tongue may be anesthetized topically by covering the area with 4% lidocaine-soaked gauze for 5 minutes; the maximum safe dose of local anesthesia should be determined and exposure to greater doses avoided. Large lacerations require infiltration anesthesia (1% lidocaine with buffered epinephrine) or a lingual nerve block. If the tip of the tongue has been anesthetized, a towel clip or suture can be used to
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Figure 36-57 Through-and-through injuries and lacerations of the tongue margins require sutures to achieve anatomic healing. Dexon, Vicryl, or silk sutures are ideal for suturing the tongue surface. Bleeding is usually controlled with direct pressure and local infiltration of lidocaine with epinephrine. For through-and-through lacerations, the muscle layer should be closed separately (with absorbable sutures) to prevent hematoma formation. In general, buried sutures are better tolerated by the patient.
maintain protrusion of the tongue. Further anesthesia and subsequent wound cleansing and closure are possible while an assistant applies gentle traction to the tongue. Size 4-0 absorbable sutures should be used to close all 3 layers—inferior mucosa, muscle, and superior mucosa—in a single stitch, or the stitch should include one half of the thickness of the tongue, with sutures placed on the superior and inferior surfaces as well as on the edge of the tongue. [102] Sutures on the tongue frequently become untied. This problem can be avoided if the stitches are buried. Do not use nylon sutures in the tongue, because the sharp edges are quite uncomfortable. [81] Closure of the lingual muscle layer is usually sufficient to control bleeding and return motor function to the lacerated tongue. Mucosal healing is rapid, and closure of the muscle layer with only a deep absorbable suture may be sufficient. Scalp
The scalp extends from the supraorbital ridges anteriorly to the external occipital protuberances posteriorly and blends with temporalis fascia laterally. There are five anatomic layers of the scalp: skin, superficial fascia, galea aponeurotica, subaponeurotic areolar connective tissue, and periosteum (see Fig. 36-18A ). Surgically, the scalp may be divided into three distinct layers. The outer layer consists of the skin, superficial fascia, and galea (the aponeurosis of the frontalis and occipitalis muscles), which are firmly adherent and surgically are considered as one layer. The integrity of the outer layer is maintained by inelastic, tough, fibrous septa, which keep wounds from gaping open unless all three portions have been traversed. Wounds that gape open signify a laceration extending beneath the galea layer. The galea itself is loosely adherent to the periosteum by means of the slack areolar tissue of the subaponeurotic layer. The periosteum covers the skull. The periosteum is often mistakenly identified as the galea, and vain attempts are made to suture the flimsy periosteum in the hope of "closing the galea" ( Fig. 36-58 ). [105] Several unique problems are associated with wounds of the scalp. The presence of a rich vascular network in the superficial fascia results in profuse bleeding from scalp wounds. Severed scalp vessels tend to remain patent, because the fibrous SQ fascia hinders the normal retraction of blood vessels that have been cut, allowing persistent or massive hemorrhage in simple lacerations. The subgaleal layer of loose connective tissue contains "emissary veins" that drain through diploic vessels of the skull into the venous sinuses of the cranial hemispheres. In scalp wounds that penetrate this layer, bacteria may be carried by these vessels to the meninges and the intracranial sinuses. Thus, a scalp wound infection can result in osteomyelitis, meningitis, or brain abscess. [102] Careful approximation of galeal lacerations not only ensures control of bleeding, but also protects against the spread of infection. Shear-type injuries can cause extensive separation of the superficial layers from the galeal layer ( Fig. 36-59 ). Debris and other contaminants can be deposited several centimeters from the visible laceration. Careful exploration and cleaning of scalp wounds are important. Because the scalp is vulnerable to blunt trauma and because its superficial fascial layer is inelastic and firmly adherent to the skin, stellate lacerations are common in this region. Stellate lacerations not only pose additional technical problems in closure, but also have a greater propensity for infection. Multiple scalp wounds that are hidden by a mat of hair are easily overlooked. When scalp wounds are debrided, obviously devitalized tissue should be removed, but debridement should be conservative, because closure of large defects is difficult on the scalp. When facing profuse bleeding, especially from extensive lacerations, the clinician should instruct an assistant to maintain compression around the wound during the closure rather than try to tie off bleeding vessels. Unless the vessels are large or few, ligation of individual scalp vessels seldom provides effective hemostasis, and considerable blood loss can occur during the attempt. Bleeding from scalp lacerations is best controlled by expeditious suturing. [97] A simple procedure that often provides hemostasis of scalp wounds is placing a wide, tight rubber band or Penrose drain around the scalp, from forehead to occiput ( Fig. 36-60A ). Sterile rubber bands may be kept on the suture cart for this purpose. The clinician also may control bleeding temporarily in some cases by grasping the galea and the dermis with a hemostat and everting the instrument over the skin edge. The disadvantage of this technique is that tissue grasped by the hemostat may be crushed and devitalized [97] and if the SQ tissue also is everted for a prolonged period, necrosis can occur. If an assistant is not available to apply direct pressure, local anesthetics containing epinephrine are sometimes effective in controlling the persistent bleeding from small vessels in scalp wounds. If bleeding from the edge of the scalp wound is vigorous, and definitive repair must be postponed while the patient is resuscitated, Raney scalp clips can be applied quickly to the edge of the scalp wound to control the hemorrhage. The applicator is loaded by inserting the tip of the instrument into the back of the clip and then locking the handles. The clip is slid onto the bleeding wound edge and released from the applicator. When the wound is repaired at a later time, the clip is removed by reversing the procedure. The plastic clips are radiolucent and do not interfere with plain radiography or computed tomography scanning ( Fig. 36-60B ). [106] [107]
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Figure 36-58 A, Anatomy of the scalp. Note that the skin, superficial fascia, and galea are adherent and constitute the outer layer. Blood vessels in the fascia are the major source of the blood loss noted in scalp lacerations. B, To temporarily control bleeding from vessels in the fascia, the galea can be everted to compress the fascia. C, The galea has been transected in wounds that gape open like this one, and to achieve hemostasis and obtain the best closure, the galea should be sutured. This is most easily accomplished with the use of a long needle, forceps, and 3-0 sutures that incorporate the skin, SQ tissue, and galea in a single bite (D). In this figure, the needle is passing through the galea from the underside, having traversed all three layers on the other side of the laceration. If this technique is used, individual buried sutures in the galea are not required, and hemostasis is ensured. At the base of this wound is the periosteum, a tissue-like covering of the skull. In C, the galea is actually adherent to the avulsed flap; the anesthetic needle is touching the underside of the galea. A simple laceration that does not gape open (E) means the galea is intact. It can be easily closed with superficial sutures or staples.
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Figure 36-59 Large partial scalp avulsion.
Before wound closure, the underlying skull should be visually examined and palpated in an attempt to detect fractures. More small skull fractures are detected with the clinician's eyes and gloved finger than with radiographs. A common error is to mistake a rent in the galea or the periosteum for a fracture during palpation inside the wound. Direct visualization of the area should resolve the issue. In wounds that expose bone but do not penetrate the skull, prolonged exposure may leave a nidus of dead bone that may develop osteomyelitis. Exposed bone that is visibly necrosed should be removed with rongeurs until active bleeding appears. [97] Hair surrounding the scalp wound usually must be clipped far enough from the wound edge so that suturing can proceed without entangling the hair in knots or embedding hair within the wound. If hairs along the wound
Figure 36-60 A, To achieve hemostasis of a scalp laceration, a wide, tight, sterilized rubber band or Penrose drain may be placed around the forehead and occiput. This compresses the arterial supply to the scalp. B, Alternatively the wound margins can be temporarily clamped to control hemorrhage. Raney scalp clips and accompanying instrument for application to scalp wound edges are shown.
edges become embedded in the wound, they will stimulate excessive granulation tissue and delay healing. [108] Vaseline or tape may be placed on stubborn hairs that persistently fall into the wound. Although clipping scalp hair is not popular with some patients, failure to expose an area adequately is a common cause of improper cleaning and closure of scalp wounds. Unlike most wounds involving multiple layers of tissue, scalp wounds can be closed with a single layer of sutures that incorporate skin, SQ fascia, and the galea ( Fig. 36-58D ). The periosteum need not be sutured. To minimize the chance of infection, SQ deep sutures generally are avoided. The galea is firmly attached to the underside of the SQ fascia and is rarely identified as a distinct layer in the depths of a wound. In superficial wounds, skin and SQ tissue should be approximated with simple interrupted or vertical mattress stitches using a nonabsorbable 3-0 nylon or polypropylene suture on a large needle. Smaller suture material tends to break while firm knots are being tied and should not be used. The ends of the tied scalp sutures should be left at least 2 cm long to facilitate subsequent suture removal. The use of blue nylon, as opposed to black, may make suture removal easier. If the galea is also torn, it should be included in the skin stitch. [109] Some investigators recommend a separate closure of the galea with an absorbable 3-0 or 4-0 suture, using an inverted stitch that "buries" the knot beneath the galea. [97] Separate closure of the galea introduces additional suture material into the wound, but in extremely large wounds provides a more secure approximation of the galea than obtained with large needle single layer closure. With microvascular techniques, large sections of skin avulsed from the scalp can be reimplanted. The emergency clinician should use the same techniques in salvaging avulsed scalp as are used for amputated extremities [109] (see Chapter 48 for further discussion).
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Figure 36-61 Anatomy of the fingernail. The fingernail rests on the nailbed, also termed the matrix. The distal nail covers the sterile matrix; the proximal nail arises from and covers the germinal matrix. The tissue adherent to the proximal dorsal nail is the eponychium (also termed the cuticle), and the potential space between the nail and the eponychium is the nail fold.
There may be no absolute time interval between injury and closure that automatically precludes primary suturing of scalp lacerations. Because of the extensive collateral blood supply of the scalp, most lacerations in this area heal without problems. Nonetheless, wound care must be thorough to avoid the devastating complication of scalp infection. Sutured scalp lacerations need not be bandaged, and patients can rinse their hair in 24 hours. If bleeding is persistent, an elastic bandage can be used as a compression dressing. Gauze sponges are placed over the laceration to provide direct local pressure beneath the elastic bandage.
Figure 36-62 This subungual hematoma occupies about two thirds of the nail and should be drained by simple nail trephination. The injury does not require nailbed repair, because the nail is still firmly attached to the matrix. Even though there must be a nail matrix laceration (the source of the bleeding), the cosmetic result will be excellent. The presence of an underlying digital tuft fracture does not change management (see also description of nail trephination in Chapter 38 ). Nail Lacerations
Injuries to the nail and nailbed (also called the nail matrix) are common problems in emergency medicine, yet controversy exists over proper management ( Fig. 36-61 ). Sixty percent of patients with subungual hematomas that are greater than one half the size of the nailbed and with associated fractures of the distal phalanx have a nailbed laceration. [110] [111] In the case of a simple subungual hematoma (even in the presence of a tuft fracture) in which the nail is firmly adherent and the disruption of the surrounding tissue is minimal, the nail need not be routinely removed to search for nailbed lacerations ( Fig. 36-62 ). [112] Despite the presence of a nailbed laceration, a good result can be
expected as long as the tissue is held in anatomic approximation by the intact fingernail. Nail trephination is discussed in Chapter 38 . If the nail is partly avulsed (especially at the base) or loose, or if there are deep lacerations that involve the nailbed, the nail should be lifted to assess and potentially repair the nailbed ( Fig. 36-63 ). When the integrity of the fingernail is disrupted a rippled nail may develop ( Fig. 36-34 ). Anatomic repair of the nailbed theoretically should minimize subsequent nail deformity. If the nailbed is exposed and has been extensively lacerated or partially avulsed, it may be necessary to refer the patient to a hand surgeon who can raise a flap of tissue extending from the proximal nail fold, explore the wound for foreign bodies, and clean under the nailbed. A simple nailbed laceration should be approximated with 6-0 or 7-0 absorbable sutures (to obviate the need for suture removal), generally using loupe magnification and a finger tourniquet to maintain a bloodless field ( Fig. 36-65 ). The exposed nailbed should be protected by reapplying the avulsed nail (best choice) or by applying a nonadherent dressing or Silastic sheet for approximately 3 weeks. Reinsertion of the nail may occasionally result in infection, so cleaning the nail is recommended. After cleaning, the avulsed nail may be sutured in place or secured with wound closure tape. The replaced nail serves three purposes: (1) it acts as a splint or mold to maintain the normal anatomy of the nailbed, (2) it covers a sensitive area and facilitates dressing changes,
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Figure 36-63 This fingernail was avulsed at the base (A), a common result of having a door slam on the digit. Since the nail is mobile (B) and there is subungual bleeding, the nail can be removed and the nailbed inspected. Any large laceration should be meticulously repaired. Absorbable sutures size 6-0 or smaller should be used. After repair, the nail is replaced under the eponychium (cuticle). See Figure 36-68 for a simple technique for removal of the fingernail.
and (3) it maintains the fold for new nail growth. Splinting should be maintained for 2 to 3 weeks. If longitudinal scar bands are formed between the proximal nail fold and the matrix, a permanently split or deformed nail may result. A nail that is partially avulsed distally can be used as a temporary splint or "dressing" that protects and maintains the integrity of the underlying nailbed. When the base of the nail is avulsed from the germinal matrix, some authors advocate trimming the proximal portion of the traumatized nail so that it can be placed more easily in the nail fold. [113] If the germinal matrix of the nail is avulsed intact, the nail should be reimplanted using a 5-0 or 6-0 absorbable suture in a mattress stitch ( Fig. 36-66 ). [81] [114] If the root is not replaced, the space between the proximal nail fold and the nailbed is obliterated within a few days. [115] [116] If an open fracture exists, the matrix must not be allowed to remain trapped in the fracture line. [117] A replaced nail may grow normally, acting as a free graft,
Figure 36-64 This nail is permanently deformed with ridges. Although crush injury to the nailbed is likely responsible for this deformity, nailbed repair is believed to minimize the resultant deformity.
but often it is dislodged by a new nail. Nails grow at a rate of 0.1 mm/day, and it requires approximately 6 months for a new nail to reach to the fingertip. If part of the nailbed has been lost, the patient should be referred to a surgical consultant for a matrix graft. [81] [113] [118] Conservative therapy that allows large portions of an avulsed nailbed to granulate is inadvisable, although this is quite acceptable therapy for a fingertip avulsion that does not involve the nailbed. If the exposed nailbed is left open to granulate, it will heal with scar tissue and could produce a distorted and sensitive digit. Wounds should be rechecked in 3 to 5 days following repair. At that time the nail fold may be repacked if nonadherent material was used, and the wound is assessed for infection. The use of absorbable suture for nailbed repair makes suture removal unnecessary. Tape or sutures are removed from any replaced nail in 2 weeks, and the old nail is allowed to fall off as the new nail grows. The value of antibiotics is unproven. All patients with nail injuries should be advised of a possible cosmetic defect in the new nail. When repairing distal digit lacerations involving a nail, the clinician should first approximate the onychial fold ( Fig. 36-67 ). A sturdy needle attached to a 4-0 thread is recommended for suturing lacerated nails. Needles seem to penetrate nails with the least difficulty when they enter at 90°. The point of the needle carves a rigid path through the nail. Unless the entire length of the needle is allowed to follow this path as it passes through the nail, the needle is likely to bend or break. Alternatively, an electrical cautery instrument or a heated paper clip can be used to perforate the nail, thus permitting easy passage of the needle. The method for atraumatically removing a nail is demonstrated in Fig. 36-68 . Drains in Sutured Wounds Drains do not prevent infection; they primarily keep wounds open to encourage drainage of purulence or blood that may
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Figure 36-65 A laceration involving the nailbed, germinal matrix, and skinfold must be carefully approximated. First the nail is completely removed. (see Fig. 36-68 ). Fine, absorbable sutures are used to repair the nailbed under a bloodless field provided by a finger tourniquet. The avulsed nail (trimmed at the base) or a gauze pack is gently placed between the matrix and eponychium for 2 to 3 weeks to prevent scar formation (A). If the original nail is replaced (the best option), it may be sutured or taped in place (B). A large hole in the nail will allow drainage. The old nail is gradually pushed out by a new one. If the nail matrix is replaced quickly and atraumatically, the nail may act as a free graft and grow normally. Note: Only absorbable sutures are used to repair the nailbed.
otherwise collect in the wound. When no infection exists and drains are used in soft tissue wounds "prophylactically," they are more harmful than beneficial. Edlich and coworkers state that "drains act as retrograde conduits through which skin contaminants gain entrance into the wound. Furthermore, the presence of a drain impairs the resistance of the tissue to infection." [72] Magee and colleagues found that drains placed in experimental wounds contaminated with subinfective doses of bacteria greatly enhanced the rate of infection, whether the drain was placed entirely within the wound or was brought out through the wound. [119] Drains behave as foreign bodies, provoking rather than preventing infection. If the wound is considered at high risk for infection, instead of suturing the
Figure 36-66 Avulsion of the nail, leaving the matrix intact, requires only a nonadherent dressing to separate the skinfold from the nailbed. If the germinal matrix is avulsed, as shown in this figure, it should be replaced to its original position under the eponychium with 6-0 plain absorbable sutures. (From Grabb WC, Kleinert HE: Technics in Surgery: Facial and Hand Injuries. Somerville, NJ, Ethicon, Inc., 1980. Reproduced by permission.)
Figure 36-67 Repair of a distal finger laceration involving the nail and the onychial fold. In this case the nail is still adherent to the nail matrix and acts as a natural splint. If the nail is loose or completely transected, it is prudent to remove the entire nail and then carefully suture the nailbed under direct vision. (From Dushoff IM: Handling the hand. Emerg Med 1976, p 111. Reproduced by permission.)
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Figure 36-68 To remove a fingernail or toenail atraumatically, the blades of iris scissors are held parallel to the nailbed to avoid lacerating the matrix. A digital block is usually performed to make the procedure painless. The closed blades are slowly advanced in the plane between the nail and the nailbed (A) and then gently spread (B) to loosen the nail. The scissors are advanced and spread in stages until the base of the nail is reached and the entire nail is loose. The nail is grasped with a hemostat and pulled from the base (C), exposing the nail matrix (D). The nail can be replaced, if desired, once the nailbed laceration has been repaired.
wound with a drain in place (in anticipation of disaster), the clinician should leave the wound open and consider delayed primary closure later when the risk of infection is minimal. Furthermore, drains should not serve as substitutes for other methods of achieving hemostasis in traumatic wounds.
SUMMARY Various techniques are available for reapproximating wound edges. Stapling is fast, but this technique does not allow meticulous control of wound edges, as may be necessary for a cosmetically appealing repair. Tape and tissue adhesive are the quickest and least painful methods of wound closure. Both eliminate the risk of self-injury with suture needles. These techniques can be used only on small superficial wounds or after approximation of the SQ layer. The traditional and most commonly used method of closure is suturing. Stitches provide the most secure closure initially, but placement of sutures is time consuming and technically more difficult than other methods. All suture materials provoke inflammation and increase the risk of infection. Suture repair is the most appropriate method for wounds with complex configurations, those that extend into SQ tissue, and those in mobile areas. At the conclusion of any wound repair, dried blood on the skin surface should be wiped away gently with moistened gauze, and the wound should be covered with a dressing. Dressing techniques, wound care instructions, and suture removal skills are discussed in Chapter 35 .
References 1. Officer
C: Scalp lacerations in children. Aust Fam Physician 10:970, 1981.
2. Davies
MJ: Scalp wounds: An alternative to suture. Injury 19:375, 1988.
3. Efron
G, Ger R: Use of adhesive tape (Steri-Strips) to secure skin grafts. Am J Surg 116:474, 1968.
4. Weisman 5. Connolly 6. Edlich
PA: Microporous surgical tape in wound closure and skin grafting. Br J Plast Surg 16:379, 1963. WB, Hunt TK, Zederfeldt B, et al: Clinical comparison of surgical wounds closed by suture and adhesive tape. Am J Surg 117:318, 1969.
RF, Rodeheaver GT, Kuphal J, et al: Technique of closure: Contaminated wounds. JACEP 3:375, 1974.
7. Emmett
AJJ, Barron JN: Adhesive suture strip closure of wounds in plastic surgery. Br J Plast Surg 17:175, 1964.
8. Golden
T: Nonirritating, multipurpose surgical adhesive tape. Am J Surg 100:789, 1960.
9. Koehn 10.
GG: A comparison of the duration of adhesion of Steri-Strips and Clearon. Cutis 26:620, 1980.
Rodeheaver GT, Halverson JM, Edlich RF: Mechanical performance of wound closure tapes. Ann Emerg Med 12:203, 1983.
692
11.
Rodeheaver GT, Spengler MD, Edlich RF: Performance of new wound closure tapes. J Emerg Med 5:451, 1987B.
12.
Sutton R, Pritty P: Use of sutures or adhesive tapes for primary closure of pretibial lacerations. Br Med J 290:1627, 1985.
13.
Panek PH, Prusak MP, Bolt D, et al: Potentiation of wound infection by adhesive adjuncts. Am Surg 38:343, 1972.
14.
Ellenberg AH: Surgical tape wound closure: A disenchantment. J Plast Reconstr Surg 39:625, 1967.
15.
Noordzij JP, Foresman PA, Rodeheaver GT, et al: Tissue adhesive wound repair revisited. J Emerg Med 12:645, 1994.
16.
Bresnahan KA, Howell JM, Wizorek J: Comparison of tensile strength of cyanoacrylate tissue adhesive closure of lacerations versus suture closure. Acad Emerg Med 26:575, 1995.
17.
Quinn JV, Wells GA, Sutcliffe T, et al: A randomized trial comparing octylcyanoacrylate tissue adhesive and sutures in the management of traumatic lacerations. JAMA 277:1527, 1997B.
18.
Yaron M, Halperin M, Huffer W, et al: Efficacy of tissue glue for laceration repair in an animal model. Acad Emerg Med 2:259, 1995.
19.
Quinn JV, Drzewiecki A, Li MM, et al: A randomized, controlled trial comparing a tissue adhesive with suturing in the repair of pediatric facial lacerations. Ann Emerg Med 22:1130, 1993.
20.
Bruns TB, McLario DJ, Simon HK, et al: Laceration repair using a tissue adhesive in a children's emergency department [abstract]. Acad Emerg Med 2:427, 1995.
21.
Simon HK, McLario DJ, Bruns TB, et al: Long term appearance of lacerations repaired using tissue adhesive. Pediatrics 99:193, 1997.
22.
Maw JL, Quinn JV, Wells GA, et al: A prospective comparison of octylcyanoacrylate tissue adhesive and suture for the closure of head and neck incisions. J Otolaryngol 26:26, 1997.
23.
Simon HK, Zempsky WT, Bruns TB, Sullivan KM: Lacerations against Langer's lines: To glue or suture? J Emerg Med 16:185, 1998.
Singer AJ, Hollander JE, Valentine SM, et al: Prospective randomized controlled trial of tissue adhesive (2-octylcyanoacrylate) vs standard wound closure techniques for laceration repair. Acad Emerg Med 5:94, 1998. 24.
25.
Hollander JE, Singer AJ: Laceration management. Ann Emerg Med 34:356, 1999.
26.
Quinn JV, Osmond MH, Yrack JA, et al: N-2-Butylcyanoacrylate: Risk of bacterial contamination with an appraisal of its antimicrobial effects. J Emerg Med 13:581, 1995.
27.
Quinn JV, Maw JL, Ramotar K, et al: Octylcyanoacrylate tissue adhesive wound repair versus suture wound repair in a contaminated wound model. Surgery 122:69, 1997A.
27A. Singer
AJ, Hollander JE: Tissue adhesives for laceration closure. JAMA 278:703, 1997.
27B. Quinn
JV, Wells GA, Sutcliffe T, et al: Tissue adhesive vs. suture wound repair at one year: Randomized clinical trial correlating early, three-month, and one year cosmetic outcome. Ann Emerg Med 32:645–649, 1998. 28.
Cooper P, Christie S: Development of the surgical stapler with emphasis on vascular anastomosis. Trans NY Acad Sci 25:365, 1963.
29.
Steichen FM, Ravitch MM: Mechanical sutures in surgery. Br J Surg 60:191, 1973.
30.
Meiring L, Cilliers K, Barry R, et al: A comparison of a disposable skin stapler and nylon sutures for wound closure. South Afr Med J 62:371, 1982.
31.
Lennihan R, Macereth M: A comparison of staples and nylon closure in varicose vein surgery. Vasc Surg 9:200, 1975.
32.
Steele RJC, Chetty V, Forrest APM: Staples or sutures for mastectomy wounds? A randomized trial. J R Coll Surg Edinb 28:17, 1983.
33.
Nilsson T, FrimÀdt-Moller C, Jeppensen N: Long-term cosmetic results comparing Proximate with Dermalon skin closure. Ann Chir Gynaecol 74:30, 1985.
34.
Harvey CF, Hume CJ: A prospective trial of skin staples and sutures in skin closure. Ir J Med Sci 155:194, 1986.
35.
Shuster M: Comparing skin staples to sutures in an emergency department. Can Fam Physician 35:505, 1989.
36.
Dunmire SM, Yealy DM, Karasic R, et al: Staples for wound closure in the pediatric population. Ann Emerg Med 18:448, 1989.
37.
George TK, Simpson DC: Skin wound closure with staples in the accident and emergency department. J R Coll Surg Edinb 30:54, 1985.
38.
Windle BH, Roth JH: Comparison of staple-closed and sutured skin incisions in a pig model. Surg Forum 35:546, 1984.
39.
Johnson A, Rodeheaver GT, Durand LS, et al: Automatic disposable stapling devices for wound closure. Ann Emerg Med 10:631, 1981.
40.
Stillman RM, Marino CA, Seligman SJ: Skin staples in potentially contaminated wounds. Arch Surg 119:821, 1984.
41.
Roth JH, Windle BH: Staple versus suture closure of skin incisions in a pig model. Can J Surg 31:19, 1988.
Kanegaye JT, Vance CW, Chan L, et al: Comparison of skin stapling devices and standard sutures for pediatric scalp lacerations: A randomized study of cost and time benefits. J Pediatr 130:808, 1997. 42.
43.
Brickman KR, Lambert RW: Evaluation of skin stapling for wound closure in the emergency department. Ann Emerg Med 18:1122, 1989.
44.
MacGregor FB, McCombe AW, King PM, et al: Skin stapling of wounds in the accident department. Injury 20:347, 1989.
45.
Ritchie AJ, Rocke LG: Staples versus sutures in the closure of scalp wounds: A prospective, double-blind, randomized trial. Injury 20:217, 1989.
46.
Orlinsky M, Goldberg RM, Chan L, et al: Cost analysis of stapling versus suturing for skin closure. Am J Emerg Med 13:77, 1995.
47.
Francis EH, Towler MA, Moody FP, et al: Mechanical performance of disposable surgical needle holders. J Emerg Med 10:63, 1992.
48.
Grossman JA: The repair of surface trauma. Emerg Med 14:220, 1982.
49.
Laufman H, Rubel T: Synthetic absorbable sutures. Surg Gynecol Obstet 145:597, 1977.
50.
Herrmann JB: Tensile strength and knot security of surgical suture materials. Am Surg 37:209, 1971.
51.
Conn J, Beal JM: Coated Vicryl synthetic absorbable sutures. Surg Gynecol Obstet 150:843, 1980.
52.
Macht SD, Krizek TJ: Sutures and suturing-Current concepts. J Oral Surg 36:710, 1978.
53.
Thacker JG, Rodeheaver G, Moore JW, et al: Mechanical performance of surgical sutures. Am J Surg 130:374, 1975.
54.
Westreich M, Kapetansky DI: Avoiding the slippery knot syndrome [letter]. JAMA 236:2487, 1976.
55.
Postlethwait RW, Willigan DA, Ulin AW: Human tissue reaction to sutures. Ann Surg 181:144, 1975.
56.
Webster RC, McCollough G, Giandello PR, et al: Skin wound approximation with new absorbable suture material. Arch Otolaryngol 111:517, 1985.
57.
Craig PH, Williams JA, Davis KW, et al: A biologic comparison of polyglactin 910 and polyglycolic acid synthetic absorbable sutures. Surg Gynecol Obstet 141:1, 1975.
58.
Katz AR, Mukherjee DP, Kaganov AL, et al: A new synthetic monofilament absorbable suture made from polytrimethylene carbonate. Surg Gynecol Obstet 161:213, 1985.
59.
Wallace WR, Maxwell GR, Cavalaris CJ: Comparison of polyglycolic acid suture to black silk, chromic, and plain catgut in human oral tissues. J Oral Surg 28:739, 1970.
60.
Rodeheaver GT, Powell TA, Thacker JG, et al: Mechanical performance of monofilament synthetic absorbable sutures. Am J Surg 154:544, 1987A.
61.
Bourne RB: In-vivo comparison of four absorbable sutures: Vicryl, Dexon Plus, Maxon and PDS. Can J Surg 31:43, 1988.
62.
Howes EL: Strength studies of polyglycolic acid versus catgut sutures of the same size. Surg Gynecol Obstet 137:15, 1973.
63.
Edlich RF, Panek PH, Rodeheaver GT, et al: Physical and chemical configuration of sutures in the development of surgical infection. Ann Surg 177:679, 1973.
64.
Kaplan EN, Hentz VR: Emergency Management of Skin and Soft Tissue Wounds: An Illustrated Guide. Boston, Little, Brown, 1984.
65.
Postlethwait RW: Further study of polyglycolic acid suture. Am J Surg 127:617, 1974.
66.
Stone IK, Von Fraunhofer JA, Masterson BJ: Mechanical properties of coated absorbable multifilament suture materials. Obstet Gynecol 67:737, 1986.
67.
Adams IW: A comparative trial of polyglycolic acid and silk as suture materials for accidental wounds. Lancet 2:1216, 1977.
68.
Grabb WC: Basic techniques of plastic surgery. In Grabb WC, Smith JW (eds): Plastic Surgery: A Concise Guide to Clinical Practice. Boston, Little, Brown, 1979, p 3.
69.
Sharp WV, Belden TA, King PH, et al: Suture resistance to infection. Surgery 91:61, 1982.
70.
Gristina AG, Price JL, Hobgood CD, et al: Bacterial colonization of percutaneous sutures. Surgery 98:12, 1985.
71.
Pham S, Rodeheaver GT, Dang MC, et al: Ease of continuous dermal suture removal. J Emerg Med 8:539, 1990.
72.
Edlich RF, Thacker JG, Buchanan L, Rodeheaver GT: Modern concepts of treatment of traumatic wounds. Adv Surg 13:169, 1979.
73.
Stillman RM: Wound closure: Choosing optimal materials and methods. ER Reports 2:41, 1981.
74.
Laufman H: Is catgut obsolete? Surg Gynecol Obstet 145:587, 1977.
75.
Edlich RF, Rodeheaver GT, Morgan RF, et al: Principles of emergency wound management. Ann Emerg Med 17:1284, 1988.
693
76.
Towler MA, McGregor W, Rodeheaver GT, et al: Influence of cutting edge configuration on surgical needle penetration forces. J Emerg Med 6:475, 1988.
77.
Bernstein G: Needle basics. J Dermatol Surg Oncol 11:1177, 1985A.
78.
Osterberg B, Blomstedt B: Effect of suture materials on bacterial survival in infected wounds: An experimental study. Acta Chir Scand 145:431, 1979.
79.
Wray RC: Force required for wound closure and scar appearance. Plast Reconstr Surg 72:380, 1983.
80.
Walike JW: Suturing technique in facial soft tissue injuries. Otolaryngol Clin North Am 12:425, 1979.
81.
Grabb WC, Klainert HE: Techniques in Surgery: Facial and Hand Injuries. Somerville, NJ, Ethicon, Inc, 1980.
82.
DeHoll D, Rodeheaver G, Edgerton MT, et al: Potentiation of infection by suture closure of dead space. Am J Surg 127:716, 1974.
83.
Austin PE, Dunn KA, Eily-Cofield K, et al: Subcuticular sutures and the rate of inflammation in noncontaminated wounds. Ann Emerg Med 25:328, 1995.
84.
Martin J, Herfel R: Methods for wound closure. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide. New York, McGraw-Hill, 2000.
85.
Bloom W, Fawcett DW: A Textbook of Histology, 10th ed. Philadelphia, WB Saunders, 1975, p 564.
86.
Kirk RM: Basic Surgical Techniques. Edinburgh, Churchill Livingstone, 1978.
86A. Edlich
RF, Rodeheaver GT, Thacker JG, et al: Technical factors in wound management. In Hunt TK, Dunphy JE (eds): Fundamentals of Wound Management. New York, Appleton-Century-Crofts, 1979, p 364. 87.
Trott AL: Wounds and Lacerations: Emergency Care and Closure, 2nd ed. St. Louis, Mosby-Year Book, 1991.
88.
Gant TD: Suturing techniques for everyday use. Patient Care 13(14):45, 1979.
89.
Peacock EE, Van Winkle W: Surgery and Biology of Wound Repair. Philadelphia, WB Saunders, 1970.
Converse JM: Introduction to plastic surgery. In Converse JM (ed): Reconstructive Plastic Surgery: Principles and Procedures in Correction, Reconstruction, and Transplantation, vol 1, 2nd ed. Philadelphia, WB Saunders, 1977, p 3. 90.
91.
Speer DP: The influence of suture technique on early wound healing. J Surg Res 27:385, 1979.
92.
Winn HR, Jane JA, Rodeheaver G: Influence of subcuticular sutures on scar formation. Am J Surg 133:257, 1977.
93.
Rodeheaver GT, Rye DG, Rust R, et al: Mechanisms by which proteolytic enzymes prolong the golden period of antibiotic action. Am J Surg 136:379, 1978.
94.
Stillman RM, Bella FJ, Seligman SJ, et al: Skin wound closure: The effect of various wound closure methods on susceptibility to infection. Arch Surg 115:674, 1980.
95.
Jones JS, Gartner M, Drew G, et al: The shorthand vertical mattress stitch: Evaluation of a new suture technique. Am J Emerg Med 11:483, 1993.
96.
Myers MB, Cherry G: Functional and angiographic vasculature in healing wounds. Am Surg 36:750, 1970.
97.
Rosen P, Sternbach G: Atlas of Emergency Medicine. Baltimore, Williams & Wilkins, 1979, p 125.
98.
Bernstein G: The far-near/near-far suture. J Dermatol Surg Oncol 11:470, 1985B.
99.
Mitchell GC: Repair of parallel lacerations [letter]. Ann Emerg Med 16:924, 1987.
100. Samo
DG: A technique for parallel lacerations. Ann Emerg Med 17:297, 1988.
101. Weatherley-White 102. Snyder
RCA, Lesavoy MA: The integument. In Hill GJ II (ed): Outpatient Surgery. Philadelphia, WB Saunders, 1980, p 334.
CC: Scalp, face and salivary glands. In Wolcott MW (ed): Ferguson's Surgery of the Ambulatory Patient, 5th ed. Philadelphia, JB Lippincott, 1974, p 153.
103. Heintz
WD: Traumatic injuries: Dealing with dental injuries. Postgrad Med 61:261, 1977.
104. Horton
CE, Adamson JE, Mladick RA, et al: Vicryl synthetic absorbable sutures. Am Surg 40:729, 1974.
105. Roberts
JR: Pathophysiology, diagnosis and treatment of head trauma. Top Emerg Med 1:41, 1979.
106. Lemos
MJ, Clark DE: Scalp lacerations resulting in hemorrhagic shock: Case reports and recommended management. J Emerg Med 6:377, 1988.
107. Kauder
DR, Schwab CW: Immediate emergency room control of hemorrhage from severe scalp lacerations. Curr Concepts Wound Care 10:17, 1987.
108. Zitelli
JA: Secondary intention healing: An alternative to surgical repair. Clin Dermatol 2:92, 1984.
109. Weinstein 110. Simon
PR, Wilson CB: The skull and nervous system. In Hill GJ II (ed): Outpatient Surgery. Philadelphia, WB Saunders, 1980, p 298.
RR, Wolgin M: Subungual hematoma: Association with occult laceration requiring repair. Am J Emerg Med 5:302, 1987.
111. Seaburg
DC, Paris PM, Angelos WJ: Treatment of subungual hematomas with nail trephination: A prospective study. Am J Emerg Med 9:206, 1991.
112. Roser
SE, Gellman H: Comparison of nail bed repair versus nail trephination for subungual hematomas in children. J Hand Surg 24A:1166, 1999.
113. Brown
PW: The hand. In Hill GJ II (ed): Outpatient Surgery. Philadelphia, WB Saunders, 1980, p 643.
114. Wolcott
MW: Hands and fingers: Part I—Soft tissues. In Wolcott MW (ed): Ferguson's Surgery of the Ambulatory Patient, 5th ed. Philadelphia, JB Lippincott, 1974, p 396.
115. Kleinert
HE, Putcha SM, Ashbell TS, et al: The deformed finger nail, a frequent result of failure to repair nail bed injuries. J Trauma 7:177, 1967.
116. Coyle
MP, Leddy JP: Injuries of the distal finger. Primary Care 7:245, 1980.
117. Matthews 118. Shepard 119. Magee
P: A simple method for the treatment of finger tip injuries involving the nail bed. The Hand 14:30, 1982.
GH: Treatment of nail bed avulsions with split-thickness nail bed grafts. J Hand Surg 8:49, 1983.
C, Rodeheaver GT, Golden GT, et al: Potentiation of wound infection by surgical drains. Am J Surg 131:547, 1976.
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Chapter 37 - Foreign Body Removal Daniel B. Stone Theodore K. Koutouzis
Soft tissue foreign bodies (FBs) are a common occurrence in emergency departments (EDs). FB identification and removal is rewarding to both the patient and clinician. However, it is not possible, or considered standard of care, that all soft tissues or wound FBs be identified or removed on the initial encounter. Although the history or physical examination may suggest the presence of an FB, and a reasonable attempt should be made to find or remove it, some foreign material simply defies suspicion, identification, or removal on the first clinician examination. Missed FBs are, however, among the leading causes of malpractice claims made against emergency clinicians, usually because of simple errors in documentation or communication. Often litigation arises merely because the clinician does not pay attention to details of the mechanism of injury or nuances of the examination, or fails to inform the patient that not all foreign material is immediately accessible to diagnosis or removal. Many times known, suspected, or identified FBs can be removed at a later date without a significant increase in morbidity if the patient is properly informed and prepared. This chapter will provide guidelines for the identification, evaluation, and removal of a variety of FBs.
GUIDELINES FOR APPROACHING FOREIGN BODIES A thorough history and physical examination must initially be performed. It is important to determine the exact mechanism of injury and to determine if the specific characteristics of the foreign material are known. For instance, did the patient step on a rusty nail or piece of broken glass? Was an FB initially present but removed before arrival by the patient? Under many circumstances, a simple direct question to the patient, asking if he or she suspects the presence of a retained FB, will initiate the proper clinical scenario. The history, physical examination, and localization techniques available will determine the best time and place for FB removal. Some material, such as wood, should be removed immediately when accessible. Retained wood will invariably lead to inflammation and infection. Other material, such as glass or plastic, may be removed on an elective basis, whereas innocuous metallic FBs may often be permanently left embedded in soft tissue. If localization is certain and if removal can be produced under local anesthesia within a manageable period of time (1 hour is usually the upper limit of operative time using local anesthesia), and without unacceptable worsening of the injury, an attempt at removal is generally indicated on the initial visit (given clinician and support staff availability). Before the procedure, it is prudent to inform the patient that the FB may not be located in the time allotted and that subsequent referral or additional procedures may be necessary. With deeply embedded, small, and inert materials (such as a BB) that are not located near any vital structures, the time, effort, and trauma involved with removal may be excessive compared with the possible adverse effects of the foreign material remaining in place. An ill-conceived extended search for an elusive but otherwise harmless FB often results in frustration for the clinician and discomfort and dissatisfaction for the patient. When reviewing the decision of when and how to remove the FB, the possibility of the FB migrating to involve vital structures, while quite remote, should be discussed with the patient. Cases of reported missile embolization in the vascular system are influenced by missile caliber, impact velocity, physical wound characteristics, point of vessel entrance, body position and movement, and velocity of blood flow. [1] Retained bullets usually remain in soft tissues, but rarely make their way into the vascular system. This usually occurs at the time of injury. Schurr and colleagues [2] reported a paradoxical bullet embolization from the left external iliac vein to the left iliac artery via a patent foramen ovale. When clinicians first examined the patient, a bullet was noted on the chest radiograph, and an isolated chest wound was suspected. However, the bullet had apparently entered the chest, traversed the abdomen to the iliac vein, and then embolized back to the chest and arterial system. All clinical decisions require an evaluation for the possibility of infection. Some FBs may produce an inflammatory reaction or infection in a few days and other objects may not cause such problems for weeks or months, often flaring up for no apparent reason. FBs such as wood will always produce inflammation eventually, while others, such as bullets, rarely do. Some inert FBs may carry dirt particles, pieces of clothing, or other sources of bacterial contamination. Expeditious removal may be necessary, even though the FB itself is relatively small and unlikely to cause a reaction. In old injuries, a thorough history of the type of foreign material and method of introduction is warranted. However, a hasty or extensive exploration for the foreign material that may or may not still exist is not recommended. The initial history should also include any unusual medical problems that would preclude use of adequate local anesthesia, such as allergy to local anesthetics, bleeding diathesis, and medical problems (including diabetes mellitus, vascular disease, uremia, or a compromised immune status) that might lead to unusual or more difficult wound management. Finally, a cooperative and willing patient is essential. Attempting to remove an FB in an intoxicated, drugged, mentally retarded, or overtly uncooperative patient is obviously self-defeating. It is not uncommon to serendipitously encounter soft tissue FBs, even though their presence was not suggested by history. Anderson and associates reported that clinicians who initially treated a series of hand injuries did not suspect FBs in 75 of 200 consecutive cases. [3] A patient who experiences a sharp, sudden pain in the foot while walking barefoot across a carpet may have a sewing needle or toothpick embedded, rather than a "sprained foot" ( Fig. 37-1 ). An abscess or cellulitis that recurs or wounds that do not heal as expected should always be investigated for retained FBs. [4] [5] Finally, it should be determined if metallic or other FBs that are captured on radiograph are extrinsic to the patient (located in clothes or on the table) or actually embedded within soft tissue ( Fig. 37-2 ). If a FB is left in place, remember to inform the patient as to why it was not removed. If the patient is referred for delayed removal, this should also be carefully explained and documented. Regardless of whether the FB is removed, all wounds should be cleaned appropriately and tetanus prophylaxis updated if indicated (see Chapter 36 ).
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Figure 37-1 A common foreign body (FB) of the foot is a splinter, toothpick, pin, or needle that is impaled while walking barefoot on a carpet. This sewing needle was obvious, but some FBs may be mistaken for a heel spur, contusion, or tendinitis. Preoperative (A) and postoperative (B) radiographs demonstrate complete removal.
Rarely do retained lead FBs, such as bullets or shotgun pellets, leach out lead into the general circulation and produce systemic lead poisoning ( Fig. 37-3 ). If this process occurs, it may take years to develop and can cause vague or nondescript symptoms (e.g., fatigue, arthralgia, headache, or abdominal pain) many years after the initial injury. Elevated blood lead levels are more likely to occur if bodily fluids such as joint, pleural, peritoneal, or cerebrospinal fluids bathe the lead. Bullets retained in muscle or other soft tissues are not likely to produce any sequelae related to their lead content. However, Farrell and coworkers reported unsuspected elevated lead levels in patients with retained lead fragments who presented to the ED with a variety of complaints. [6] Lead levels of up to 50 µg/dL were reported. Levels >45 µg/dL are generally considered an indication for chelation therapy. The relation between the retained lead and presenting symptoms was unclear, but this report verifies the observations of others that retained lead FBs in selected areas can significantly elevate blood lead levels and may produce symptomatic plumbism. Finally, the patient should be clearly informed that there is no absolute guarantee that all foreign material has been identified or extracted, regardless if some or any FB was removed during initial exploration. The prudent clinician always leaves open the option that an occult FB may still remain in any wound and informs the patient of signs and symptoms of problems related to any retained material. Some centers routinely add this caveat on all discharge instructions for patients treated
Figure 37-2 This patient fell, landed on a metal pipe, and suffered a laceration to the thigh. A radiograph was taken to rule out a fracture, and the key was seen but thought to be an artifact (i.e., an item left on the backboard). During the examination the key was found embedded in the wound. It had been in the patient's pants pocket and was forced into the wound by the pipe during the injury.
for lacerations or soft tissue defects. Patients should be assured that additional steps may be undertaken should the presence of foreign material be subsequently suspected.
IMAGING TECHNIQUES A variety of imaging techniques are available to emergency clinicians to help detect and localize FBs. Many emergency clinicians mistakenly believe that, in the absence of adipose tissue, if the base of the wound can be clearly visualized and explored, an FB can always be ruled out. While this is commonly true, Avner and Baker detected glass by routine radiographs in 11 of 160 wounds (6.9%) that were inspected and believed by the clinician to be free of glass. [7] Whenever there is an index of suspicion for a retained FB as a result of the history, mechanism of injury, patient complaint, or examination, attempts should be made to visualize it. Modalities available include plain radiographs, fluoroscopy, computed tomography (CT), magnetic resonance imaging (MRI), and ultrasound (US) ( Fig. 37-4 ). Fluoroscopy is not a standard technique in the ED but is helpful for localizing FBs that are
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Figure 37-3 Most lead foreign bodies are well tolerated, but if a bullet is bathed in synovial, pleural, peritoneal, or cerebrospinal fluid, the lead may leach out over time and produce a significant elevation in blood lead levels. Symptoms are often vague, and the relation between the retained lead and the patient's clinical scenario may be difficult to sort out. (From Schwartz DT, Goldfrank LR: Toxicologic imaging. In Goldfrank LR, Flomenbaum NE, Lewin NA, et al [eds]: Goldfrank's Toxicologic Emergencies. 5th ed. Norwalk, CT, Appleton & Lange, 1994, p 116. Reproduced with permission.)
visualized on routine plain films. Yet even fluoroscopy under magnification may not identify plastic or wooden FBs.
[8]
Plain Radiography Plain radiographs are readily available, easily interpreted, and cost significantly less than CT, US, or MRI.
[ 9]
The ability
Figure 37-4 Comparison of plain radiography, computed tomography, and ultrasonography in imaging wooden, glass, and plastic foreign bodies (FBs) in an in vitro preparation. Computer manipulation of a digitized radiograph may aid in FB assessment. (From Ginsburg MJ, Ellis GL, Flom LL: Detection of soft-tissue FBs by plain radiography, xerography, computed tomography, and ultrasonography. Ann Emerg Med 19:701, 1990. Reproduced with permission.).
of plain films to detect FBs in soft tissues depends on the object's composition (relative density), configuration, size, and orientation. Multiple views should always be obtained when attempting to visualize an FB since many clearly radiopaque objects are obscured by superimposed bone on one view, but are quite obvious when viewed from another angle. However, certain FBs that are radiolucent may still not be visualized with this approach. Metallic objects, such as pins, bullets, and BBs, are readily visualized. Aluminum, which has traditionally been deemed radiolucent, can occasionally be visualized on plain films if the object is projected away from underlying bone. Ellis demonstrated that pure aluminum fragments as small as 0.5 mm × 0.5 mm × 1 mm could be identified in a chicken wing model simulating a human hand or foot. Ellis cautioned that other aluminum FBs, such as pull tabs from cans, may not be visualized in other parts of the body such as the esophagus or stomach.[10] It is a common misconception that glass must contain lead to be visualized on a plain radiograph. Almost all types of glass objects in soft tissue (bottles, windshield glass, light bulbs, microscope cover slips, laboratory capillary tubes) can be detected by plain radiographs, unless they are obscured by bone ( Fig. 37-5 ). [9] [11] Very small glass fragments (5 cm in diameter) intact blisters and all blisters that have ruptured. Large, firm blisters of the palms and soles may be left intact longer. Do not aspirate blisters. 2. Do not debride small or spotty blisters until they break, or until 5 to 7 days after the burn. Five to 7 days after the burn: 1. Debride all blisters completely Note: Intact blisters provide significant pain relief. Be prepared for an exacerbation of pain immediately after debridement. Prophylactic analgesia is recommended. *All blisters and burned skin are debrided in the presence of infection.
compartments. Third, edema has been associated with the inactivation of streptococcicidal skin fatty acids, thus predisposing the patient to burn cellulites.
[20]
The successful management of burn edema hinges on immobilization and elevation. Most patients are unfamiliar with the medical definition of elevation and are not aware of or convinced of its value. Patient education in this regard is critical; however, certain burns (e.g., burns in dependent body areas) are prone to edema, despite everyone's best intentions. It is for this reason that lower extremity burns in general, and foot burns in particular, are prone to problems. Major burns of the hand should be elevated while the patient is still in the ED. This is most readily accomplished by hanging the injured hand from an IV pole, with stockinette used to support the bandaged hand ( Fig. 39-7 ). Use of Topical Preparations/Antimicrobials
Minor burns result in insignificant impairment of normal host immunologic defenses, and burn wound infection is usually not a significant problem. Topical antimicrobials are often used; however, some believe these agents may actually impair wound healing. [21] Although the procedure is of unproven value, many clinicians routinely use antibiotic creams or ointments on even the most minor of burns. Most patients expect some type of topical concoction, so a discussion of their use, or nonuse, is prudent. Topical antimicrobials were designed for the prevention and care of burn wound sepsis or wound infection, primarily in hospitalized patients with major burns, and there is no convincing evidence that their use alters the course of first-degree burns and superficial partial-thickness injuries. As noted, the burn dressing is the key factor in minimizing complications in all burns. Nonetheless, topical antimicrobials are often soothing to minor burns, and their daily use prompts the patient to look at the wound, assess healing, perform prescribed dressing changes, or otherwise become personally involved in his or her care. Keep in mind that if a topical antimicrobial is used, its effectiveness is decreased in the presence of proteinaceous exudate, necessitating regular dressing changes if the antimicrobial benefit of topical therapy is to be realized. In reality, once-daily dressing changes are most practical and are commonly prescribed, and there are no data to indicate that this regimen is inferior to more frequent dressing changes.
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Figure 39-7 Elevation of a burned hand should begin in the ED. After a properly applied hand dressing is applied, the arm is suspended from an IV pole with stockinette.
All full-thickness burns should receive topical antimicrobial therapy, because the eschar and burn exudate are potentially good bacterial culture media, and deep escharotic or subescharotic infections may not be easily detected until further damage is done. All deep partial-thickness injuries likewise benefit from the application of a topical antimicrobial. In deep partial-thickness injuries, re-epithelialization occurs from a few remaining deep epidermal appendages whose protection is important. Clinical studies and culture results support the hypothesis that surface destruction of dermal islands by bacterial enzymes and catabolic processes has the potential to convert a deep partial-thickness injury to a full-thickness injury. [22] Initial topical therapy is prophylactic. [23] A burn wound infection that develops despite this therapy mandates a change to a different agent. Topical therapy, if chosen, should cover the usual bacteria responsible for burn wound infections (see later discussion of minor burn infections). Although topical agents are an important part of a burn treatment program, they are not substitutes for good local wound care or a careful program of management. Their successful use may prevent the conversion of deep thermal burns to deeper injury and allow better wound healing for earlier (and more successful) skin grafting. Criteria for choosing a specific topical agent include in vitro and clinical efficacy, toxicity (absorption), superinfection rate, ease and flexibility of use, cost, patient acceptance, and side effects. Note that there are no firm scientific data that convincingly support the use of any specific topical antimicrobial in minor outpatient burns. Specific Topical Agents
Silver sulfadiazine (Silvadene).
This poorly soluble compound is synthesized by reacting silver nitrate with sodium sulfadiazine. It is the most commonly used topical agent for outpatients, and it is well tolerated by most patients. It has virtually no systemic effects and moderate eschar penetration, and it is painless on application. Although Silvadene is commonly used, many burn specialists prefer plain bacitracin ointment as the topical of choice because of its cost, equal efficacy, and good patient acceptance. Silver sulfadiazine is available as a "micronized" mixture with a water-soluble white cream base in a 1% concentration that provides 30 milliequivalent (mEq)/L of elemental silver. It does not stain clothes, is nonirritating to mucous membranes, and washes off easily with water. It may be used on the face, but such use may be cosmetically undesirable for open treatment. Its broad gram-positive and gram-negative antimicrobial spectrum includes ß-hemolytic streptococci, Staphylococcus aureus and Staphylococcus epidermidis, Pseudomonas spp., Proteus spp., Klebsiella spp., Enterobacteriaceae spp., Escherichia coli, Candida albicans, and possibly Herpesvirus hominis. Silver sulfadiazine often interacts with wound exudate to form a pseudomembrane over partial-thickness injuries. The pseudomembrane is often difficult and painful to remove. Except for term pregnancy and in newborns (i.e., due to possible induction of kernicterus), there are no absolute contraindications to the use of silver
sulfadiazine. Allergy and irritation are unusual, although there is a potential cross-sensitivity between silver sulfadiazine and other sulfonamides. Other topical preparations.
Mafenide acetate (Sulfamylon), gentamicin, chlorhexidine, povidone-iodine, and silver nitrate are products that have been replaced with newer topicals, but they are mentioned for historical interest. These products are not used in modern burn therapy, although they are generally acceptable alternatives. Broad-spectrum antibiotic ointments.
Many nonprescription topical antimicrobials are used for minor burn therapy. Included are bacitracin zinc ointment, polymyxin B-bacitracin (Polysporin), triple-antibiotic ointments such as polymyxin B-neomycin-bacitracin (Neosporin), and nitrofurazone (Furacin). These are all soothing, cosmetically acceptable for open treatment (such as on the face), and are effective antiseptics under burn dressings. Some researchers caution against agents containing neomycin because of a potential for sensitization ( Fig. 39-8 ). The editors suggest plain bacitracin ointment as the routine topical agent, although Silvadene is a very acceptable alternative. Aloe vera cream.
Aloe vera cream is commercially available in a greater than or equal to 50% concentration with a preservative. It exhibits antibacterial activity against at least four common burn wound pathogens: Pseudomonas aeruginosa, Enterobacter aerogenes, S. aureus, and Klebsiella pneumoniae. Heck and colleagues compared a commercial aloe vera cream with silver sulfadiazine in 18 patients with minor burns. [24] Healing times were found to be similar, and there was no increase in wound colonization in the aloe vera group as compared with the patients treated with silver sulfadiazine. Other authors have promulgated the use of aloe gel preparations for minor burns. [25] Aloe vera cream is an acceptable inexpensive option for open or dressed outpatient care of minor burns. Honey.
Honey has long been advocated as an inexpensive and effective topical for minor outpatient burns. The
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Figure 39-8 A, The most popular topical burn preparation is Silvadene cream. While commonly used on minor burns, it likely has little beneficial effect on healing, and minor burns rarely become infected. Nonetheless, Silvadene is a standard intervention that at least causes the patient to look at the burn and become involved in dressing changes. B, Many burn specialists suggest inexpensive topical antibiotic ointments (such as bacitracin and neosporin) for all outpatient burns. They are commonly used on face and neck burns. Bacitracin is preferred since a contact dermatitis, such as noted in this abrasion, can occur from the neomycin portion of some topicals.
physicochemical properties of honey (osmotic effect, pH) give this product antibacterial and anti-inflammatory properties that support its use. It may be superior to Silvadene with regard to minor burn wound healing. Honey is not widely used, but it has been promulgated as a safe, effective, and inexpensive dressing for the management of outpatient burn wounds.[26] [27] [28] Corticosteroids.
High-potency topical steroid preparations have no beneficial effects on the rate of healing, or limitation of scarring, of thermal burns. Although likely not harmful, their use is not supported. [29]
FOLLOW-UP CARE OF MINOR BURNS The specifics of outpatient follow-up of minor burns are controversial and often based on clinician preference and personal bias rather than on firm scientific data. Follow-up should be individualized for each patient and should be based on the reliability of the patient, the extent of the injury, the frequency and complexity of the dressing changes, and the amount of discomfort anticipated during a dressing change. Often fast-track sections of the ED are used for burn checks. The physical therapy departments of most hospitals have excellent facilities to follow outpatient burns with periodic clinician oversight. If a topical antibiotic agent is used, the dressing should be changed daily with removal and reapplication of the topical preparation. The wound should be rechecked by a clinician after 2 to 3 days and periodically thereafter, depending on compliance, healing, and other social issues. If a dry dressing is opted for, follow-up every 3 to 5 days is usually adequate. The purpose of any burn dressing changes or home care regimen is defeated if the patient cannot afford the material or is not instructed in the specifics of burn care. Many EDs supply burn dressing material on patient release. (A complete pack includes antibiotic ointment/cream, gauze pads [fluffs], an absorbent gauze roll, a sterile tongue blade to apply cream, and tape.) Providing limited supplies of the items necessary for dressing changes may enhance compliance to follow-up if the patient has to return for additional supplies. Writing a prescription and merely stating that the dressing should be changed daily is often futile. Daily home care can be performed by the patient with help from a family member or visiting nurse ( Table 39-5 ). The dressing may be removed each day and gently washed with a clean cloth or a gauze pad, tap water, and a bland soap. Sterile saline and expensive prescription soaps are not required. A tub or shower is an ideal place to gently wash off burn cream. The affected area may be put through a gentle range of motion during dressing changes. After the burn is cleaned, it is inspected by the patient. The patient is instructed to return if signs or symptoms of infection, significant blistering, or skin slough develop. Following complete removal of the old cream, a new layer is applied with a sterile tongue blade and covered with absorbent gauze. If the undermost fine mesh gauze of a dry dressing is dry and the coagulum is sealed to the gauze, the patient should simply reapply the overlying gauze dressing. If the wound is macerated, the fine mesh gauze should be removed and the wound cleaned and redressed. The patient is instructed not to remove a dry adherent fine mesh gauze from the underlying crust. When epithelialization is complete, the crust will separate, and the gauze can be removed at that time. Dryness in healing skin may be treated with mild emollients such as Nivea (Beiersdorf, Inc., Norwalk, CT) or Vaseline Intensive Care lotion (Chesebrough Ponds, Inc., Greenwich, CT). Natural skin lubrication mechanisms usually return by 6 to 8 weeks. [14] Excessive sun exposure should be avoided during wound maturation, as this may lead to hyperpigmentation. When the patient is outdoors, a commercially available sun block should be used. Exposure of the recently healed burned area to an otherwise minor trauma (chemicals, heat, sun) may result in an exaggerated skin response. Pruritus is common, and may be treated with oral antihistamines or a topical moisturizing cream. Deep partial-thickness burns, along with small third-degree burns, may be initially managed in the outpatient setting with proper follow-up. Topical antimicrobials are recommended.
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TABLE 39-5 -- How to Change a Burn Dressing at Home: Patient Instructions 1. Take pain medicine ½ hour before dressing change if you find dressing changes to be painful. 2. If the burn is on the hand, foot, or other area that is difficult to reach, have someone help you. 3. Have all material available. Gloves may be worn. 4. Remove the dressing and rinse off all burn cream or ointment with tap water, under a shower, or in the bathtub. The area can be gently washed with mild soap and a clean cloth or gauze pads. 5. Look at the burn and assess the healing, blistering, and amount of swelling. Note any signs of infection. 6. Gently exercise the area through range of motion. 7. Apply the burn ointment with a sterile tongue blade. 8. Cover the cream with fluffed-up gauze. 9. Wrap the area in bulky gauze. 10. Repeat this dressing change daily.
Outpatient Physical Therapy for Burn Care When the hospital's outpatient physical therapy department is equipped to treat minor burns, it is prudent to consider this option. Many centers make available daily or periodic burn treatment, consisting of dressing changes, whirlpool debridement, and range-of-motion exercises. When patients are unable to handle their own burns at home, this can be an invaluable adjunct. An additional advantage is that medically trained personnel evaluate the burn daily, thereby decreasing clinician visits and enabling identification of problems prior to the development of serious complications. Generally all that is required from the clinician is to write a prescription for "burn care and dressing changes" and set up the appointment. The physical therapy department, or wound care center, can receive clinician input as needed during subsequent visits. Burn Healing Follow-up care will in part be guided by expectations of burn healing and observed healing. The following discussion is intended to serve as a general guide. However, burn healing is different from that of other wounds. [2] The timing is often variable, but it is proportional to burn depth. The inflammatory phase lasts 3 to 7 days (at times longer) and, if the burn is severe enough, is accompanied by the release of histamine and bradykinins, along with complement degradation. This degradation of complement may lead to immunologic, coagulation, and metabolic aberrations. Within 1 to 3 weeks, neovascularization of the burn occurs, accompanied by fibroblast migration. Macrophages begin to replace the tissue neutrophils. Collagen production begins, but the molecules are often laid down in random fashion, leading to a scar. Re-epithelialization follows, but the presence of necrotic tissue and eschar impedes all aspects of wound healing. The amount of scar tissue produced is directly related to healing time. Burns requiring fewer than 16 days to heal generally do not scar excessively. [2] Healing in superficial partial-thickness burns occurs within 10 to 14 days. After healing, the new epithelial layer tends to dry easily and crack. Using bland, lanolin-containing creams for 4 to 8 weeks following healing alleviates this problem. Deep partial-thickness burns heal by re-epithelialization from the wound edge and from residual dermal elements. Healing is slow and often unsatisfactory, frequently taking longer than 3 weeks, producing an unstable epithelium that is prone to hypertrophic scarring and contractures. This is a particular problem in burns that extend across joints. Burns that take longer than 2 to 3 weeks to heal are prone to infection; hence, topical antimicrobials should be used. Because these burns often heal in complicated fashion, they should be considered for referral to expedite early excision, grafting, and physical therapy.
Full-thickness burns can heal only by contraction and epithelialization at the wound edge. Burns larger than 2 to 3 cm must be excised and grafted. Cosmetic and functional recovery follows complete epithelialization of a partial-thickness injury or successful skin grafting of a full-thickness burn. The ultimate goal is to prevent scar thickening; achieve and maintain optimal range of motion; and prevent secondary environmental damage to the skin, particularly from sun exposure. [15] Nonscented skin lotions may be used after epithelialization to keep the burn scar soft. Compression dressings are especially helpful in preventing scar thickening. Repeated evaluations are important, because burn contractures can occur up to 12 months after the injury. Nighttime splinting is useful in maintaining full extension of joints.
SPECIAL MINOR BURN CARE CIRCUMSTANCES Blisters The management of blisters in minor burns is controversial. In reality, there is little one can do wrong when it comes to a clinical approach to blisters in minor burns. Management arguments are generally theoretic or emotional; the ultimate outcome of a minor burn is rarely determined by how one deals with blisters. Intact blisters do offer a physiologic dressing that rarely becomes infected; however, most large blisters spontaneously rupture after 3 to 5 days and eventually require debridement. When the integrity of the blister is breached, the fluid becomes a potential culture medium. Clinical choices include debridement, aspiration, or simply leaving the blister intact. Some studies suggest that intact burn blisters may allow for reversal of capillary stasis and less tissue necrosis. exudate (as contained within intact blisters) is beneficial for the stimulation of epidermal cell proliferation. [30]
[ 2]
Madden and colleagues have shown that burn
Swain and colleagues demonstrated that the density of wound colonization with microorganisms was much lower in minor burns with blisters left intact. [31] They also found that 37% of patients with aspirated blisters experienced a reduction in pain versus none of those whose blisters were unroofed. Other investigators believe that undressed wounds with debrided blisters have additional necrosis secondary to desiccation, which can convert a partial-thickness burn to a full-thickness injury. [3] Finally, intact blisters clearly provide some pain relief, as evidenced by a sudden increase in pain immediately following debridement. Increased pain should be anticipated and analgesia offered as appropriate when debridement is necessary. We suggest the guidelines in Table 39-4 as a general approach to burn blisters. Minor Burn Infections
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Prophylactic systemic antibiotics are not warranted in the routine treatment of outpatient burns.
It may be difficult to separate the erythema of the injury or healing process from cellulitis, but minor burns rarely become infected, with infection rates well under 5%. There are bacteria on the skin at all times—normal skin usually harbors nonvirulent pathogens such as S. epidermidis and diphtheroids. Therefore, all burns are contaminated but not necessarily infected. Thermal trauma results in a coagulative necrosis. Burn wounds therefore contain a variable amount of necrotic tissue, which, if infected, acts much as an undrained abscess, preventing access of antibiotics and host defensive factors.
[32]
The microbial flora of outpatient burns varies with time after the burn. Shortly after injury, the burn becomes colonized with gram-positive bacteria such as S. aureus and S. epidermidis. After this period of time there is a gradual shift toward inclusion of gram-negative organisms, 80% of which originate from the patient's own gastrointestinal tract. [4] Common organisms seen on days 1 to 3 include S. epidermidis, ß-hemolytic streptococci, Bacillus subtilis, S. aureus, enterococci, Mima polymorpha, Enterobacter spp., Acinetobacter spp., and C. albicans. One week after the burn, these organisms may be seen along with E. coli, P. aeruginosa, Serratia marcescens, K. pneumoniae, and Proteus vulgaris. Anaerobic colonization of burn wounds is rare unless there is excessive devitalized tissue, as occurs in a high-voltage electrical injury. anaerobic cultures are generally unnecessary in an assessment of infective organisms that produce minor infections.
[33]
For this reason, routine
The vast majority of superficial burns that have been treated properly do not get infected. Infection rates are well below 5%. [32] However, it is sometimes difficult to differentiate wound infection from the normal healing process, as both involve pain, edema, and erythema. A healing burn may produce a leukocytosis and a mild fever in the absence of infection, especially in children. Early (days 1 to 5) burn infections are generally caused by gram-positive cocci, especially ß-hemolytic streptococci. Streptococcal cellulitis is characterized by marked, spreading erythema extending outward from the wound margins. Despite the plethora of organisms and the presence of some gram-negative pathogens noted in superficial burn cultures, first-line treatment in the normal host is oral penicillin, 1 to 2 g/day. Alternatives include erythromycin, cephalosporins, and dicloxacillin. Effective topical treatment at the time of initial burn care and subsequent dressing changes is meant to delay bacterial colonization, maintain the wound bacterial density at low levels, and produce a less diverse wound flora. Because outpatient management of burns should be attempted only when the risk of infection is minimal, the use of systemic antibiotics is unnecessary for minor burns, even in the setting of delayed treatment, diabetes, and steroid use. [34] Unnecessary antibiotic use may select out resistant organisms. Antibiotics in the management of minor burns have been recommended for patients undergoing an autograft procedure. [35] There are no data on the use of antibiotics as prophylaxis for patients with burns in the setting of valvular heart disease, although their use seems logical. In minor burn care, wound cultures are not required or recommended. It is useless, for example, to culture blister fluid in the patient who presents for emergency care immediately after a thermal injury. Cultures are necessary only when overt infection develops, especially when this occurs while a topical or systemic antibiotic is being used. Cultures may also be of benefit when the infected wound is old, when hygiene is poor, or when there are old abrasions nearby. [36] Swab surface cultures are generally eschewed. Although they may adequately reflect wound flora, falsely sterile cultures are relatively frequent. These cultures do not reflect deep burn flora and give no quantitative information. Sterile wound biopsy for culture is most satisfactory for the assessment of intraescharotic, subescharotic, or invasive infections and allows for quantification of bacterial flora. If a wound culture is taken, it should be obtained from the deepest or worst-appearing area of the burn. Surface bacterial densities greater than 10 5 /cm2 or tissue bacterial densities greater than 10 5 /g correlate with invasive infection. Surface colonization may be treated with an alternative topical agent, but truly invasive infection warrants the administration of systemic antibiotics. Generally, the infectious process resolves in 24 to 48 hours. Foot Burns Despite their relatively small surface area, foot burns tend to heal poorly, usually due to excessive edema; therefore, they are formally categorized as major burns. Foot burns are the most common burn category to fail outpatient therapy and subsequently require admission and inpatient care ( Fig. 39-9 ). Zachary and coworkers reported on a series of 104 patients with foot burns. [37] No patient admitted on the day of injury developed burn cellulitis; in contrast, 27% of delayed admission patients had cellulitis. Their study also noted a higher incidence of hypertrophic scarring and need for skin grafting in the delayed admission group. Overall, fewer days of hospitalization were required for the initially admitted group. Specific problems in the care of foot burns include pain, wound drainage, difficulty in changing dressings without help, inability of even motivated patients to comply with requirements for elevation, and prolonged convalescence. Hospital admission allows for splinting, intensive local burn care, physical therapy, and bed rest with elevation, which minimizes edema. For these reasons, initial admission for all but the most minor of foot burns is advised. Hand Burns Because of their functional importance, hand burns can be a devastating injury, despite involvement of a relatively small TBSA. Hand function is critical, regardless of whether the patient is dealing with loss of use during healing, later limitation by scar contractures, a long-term appearance change, or loss due to amputation. [38] As with other burns, the depth and extent of the burn determine the severity of the injury. The entire surface of one hand represents only 2.5% TBSA, yet even small
burns can cause a disproportionate functional loss. Deep partial- or full-thickness hand burns, even if quite small, often warrant referral for early excision and grafting in order to limit scarring and maintain function. The skin on the dorsum of the hand is thinner than that on the palm and is more susceptible to burn injury, but must remain flexible to allow for finger motion. Any exposed tendon or bone, such as may be seen with an electrical burn, constitutes a true fourth-degree injury, which
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Figure 39-9 Burns of the feet are specialized burns that require a careful evaluation and an individualized treatment plan, even if the burn surface area is relatively small. It is difficult for most patients to provide ideal burn care at home when the feet are involved. A, It is tempting to initially treat this seemingly minor superficial second-degree foot burn in an outpatient setting, but the patient's compliance and social situation must be ideal for a successful outcome. Hospitalization until home health care can be established is prudent. B, An example of a foot burn that is a potential disaster, in this case due to a late presentation in a diabetic.
requires either flap closure or amputation in order to heal the wound. Many of the issues complicating outpatient management of foot burns are relevant to the care of hand burns. After initial burn cooling, the wound should be gently cleansed with mild soap. Any loose skin or ruptured blisters should be gently debrided, rinsed, patted dry, and covered with a topical antimicrobial agent and a nonadherent, bulky gauze dressing. The fingers should be carefully separated and bandaged individually. Small, intact blisters that do not interfere with hand function should be left intact to serve as a biologic dressing. Elevation of the hand is very important in the first few days after a burn injury in order to minimize edema. Deep partial-or full-thickness burns to the dorsum of the hand should be splinted after bandaging to avoid the development of contractures or a boutonniere deformity. Hospital admission should be considered for all hand burns, particularly full-thickness injuries and circumferential burns involving the digits ( Fig. 39-10 ). If outpatient treatment is attempted, the patient must be given comprehensive instructions and should have the resources available to perform daily dressing changes and range-of-motion exercises of the fingers and wrist during these dressing changes. An initial follow-up visit should be arranged in 48 to 72 hours, but the patient should be encouraged to return if there is development of a burn cellulitis, worsening pain, fever, or lymphangitis. Ideally, the patient should be seen twice in the first week after injury and once a week after that until the burn is healed. Facial Burns Facial burns commonly result from unexpected ignition flash burns (e.g., from a stove, oven, or charcoal grill) or from car radiator accidents ( Fig. 39-11 ). [39] [40] Facial burns from these sources usually do well, but often result in singeing of facial hair, significant edema, and pain. However, facial burns from these etiologies may rarely produce airway problems and require skin grafting. Concurrent globe or corneal injury is quite rare due to protective blinking reflexes. If the eye is burned, it is usually in the setting of a life-threatening concomitant burn injury. [41] Burns to the eyelids can cause significant scarring. Fluorescein staining and slit-lamp examination should be used to confirm the diagnosis of suspected corneal injury. The treatment of a corneal injury involves irrigation, topical ophthalmic antibiotic ointment, and consideration of eye patching versus protective soft contact lens (see Chapter 64 ). Referral to an ophthalmologist is usually prudent. Facial burns are otherwise treated in the usual fashion, and with an open (no dressing) technique. Patients are instructed to wash the face two to three times a day with a mild soap and then apply a thin layer of antibiotic ointment,
Figure 39-10 This badly burned hand requires referral to a burn center and should not be handled as an outpatient.
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Figure 39-11 A, Flash burns to the face from lighting a gas stove. These burns are painful and may cause edema, but usually they do well. Note the singed facial hair. The eyes are usually protected by rapid reflex blinking and carbon monoxide poisoning and pulmonary burns are not an issue. Most can be handled in the outpatient setting with bacitracin ointment and no dressing. Pain control may be problematic unless opioids are prescribed. B, Facial and neck burns when a radiator cap was removed and the victim was sprayed with steam and hot antifreeze.
such as bacitracin zinc. There are no compelling reasons to avoid Silvadene on the face, but by tradition bacitracin ointment has become the preferred topical. Car radiator burns result from the combination of a hot liquid and steam burn. Antifreeze does not produce a caustic injury, nor is it systemically absorbed. Neck burns are treated similarly. All patients presenting with head or neck burns should be carefully evaluated for a concomitant inhalation injury. Such patients may present with direct evidence of injury, such as oral burns, blisters, soot, or hyperemia, a history of being in an enclosed space, or with indirect evidence, such as dyspnea, wheezing, arterial hypoxemia, or an elevated carboxyhemoglobin level. The definitive diagnostic test for inhalation injury is fiberoptic bronchoscopy. [42] Flash ignition burns to the face do not pose a problem with carbon monoxide poisoning and inhalation injuries are generally not a consideration Inpatient care should be considered for all patients with significant facial burns. Outpatient pain control may be difficult in facial burns, the degree of edema may be difficult to predict, and home care can be problematic. There are no universally agreed-upon standards for admission versus outpatient treatment of facial burns, but a liberal admission policy is suggested. Corneal contact burns, as from accidental contact with a curling iron, often present rather dramatically, with opacified, "heaped-up" corneal epithelium. Despite their appearance, the end result is usually excellent. Treatment is the same as for a corneal abrasion. [43] Abuse of Children and Elderly Individuals Recognition of the possibility of deliberate abuse by burning in the pediatric and geriatric populations is essential. In addition, children younger than 2 years old have a thinner dermis and a less well-developed immune system than do adults. Elderly patients (older than 65 years) likewise tolerate burns poorly. These two populations are the most prone to abuse, often by family members ( Fig. 39-12 ). For these reasons, both groups of patients often require inpatient care. [9] The majority of abused children are 18 to 36 months old, and for unknown reasons the majority are male. [21] Immersion burns are a common type of abuse. These are characterized by circumferential, sharply demarcated burns of the hands, feet, buttocks, and perineum. Cigarette burns and burns from hot objects such as irons should be obvious. Contact burns on "nonexploring" parts of the child also warrant suspicion. A delay in seeking treatment may be a tip-off that a burn results from abuse. Burns in Pregnancy There is little information in the literature concerning the special problems of the pregnant burn victim. Ying-bei and Ying-jie reported on 24 pregnant burn patients representing a wide range of burn severity. [44] Complications of the burn injuries included abortion and premature labor, although all patients in this series with burns covering less than 20% TBSA did well and delivered living full-term babies.
As the resistance of pregnant women to infection is lower than that of nonpregnant women, control of burn wound infection is paramount. Gestational age appears to have no direct bearing on prognosis. Silver sulfadiazine cream should be avoided near term because of the potential for kernicterus.
SPECIFIC BURNING AGENTS Hot Tar Burns Asphalts are products of the residues of coal tar commonly used in roofing and road repair. These products are kept heated to approximately 450°F. When spilled onto the skin, the tar cools rapidly, but the retained heat is sufficient to produce a partial-thickness burn. Fortunately, full-thickness burns are unusual. Cooled tar is nonirritating and does not promote infection. When cooled tar is physically removed, the adherent skin is usually avulsed ( Fig. 39-13 ). Careless removal of the tar may inflict further damage on burned tissues. Agents such as alcohol, acetone, kerosene, or gasoline have been used to remove the tar, but these are flammable and may cause additional skin damage or toxic response secondary to absorption. There is no great need to meticulously remove all tar at the first visit.
Obviously devitalized skin can be debrided, but adherent tar should be emulsified or dissolved rather than
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Figure 39-12 Burns can be a manifestation of child abuse, spouse abuse, or abuse of the elderly. A, Abuse burns from contact with a hot metal grate, from a child allegedly falling. B, This burn was the result of spouse abuse, caused by throwing hot soup during an argument. The delayed presentation to the hospital was a clue. C, Burns of the face and neck are common when a toddler pulls hot liquid from a stove. This case was never proven to be child abuse, but burns in young children often are due to abuse, especially if they are in atypical places. Although the body surface area of this burn is relatively small, the patient's age and the burn's location, coupled with the possibility of child abuse, require that this child be hospitalized.
manually removed ( Fig. 39-14 ). Polyoxyethylene sorbitan (Tween 80 or polysorbate 80) is the water-soluble, nontoxic emulsifying agent found in neosporin and several other topical antibiotic creams. Note that the cream formulations, not the ointments, contain the most useful tar dissolvers. The creams contain a complex mixture of ethers, esters, and sorbitol anhydrides that possess excellent hydrophilic and lyophilic characteristics when used as nonionic, surface-active emulsifying agents. With persistence, most tar may be removed (emulsified) on the initial visit. Another household product (De-Solv-It multi-use solvent) also appears logical for topical ED use. [45] The De-Solv-It product has a surface-active moiety that wets the chemical's surface and emulsifies tar and asphalt. Since the latter product is itself a petroleum-based solvent, it should be applied only briefly, and the operator should wear gloves and protective eyewear during application. It should be used only for external exposure to tar or asphalt. Many clinicians prefer instead to emulsify the majority of tar on an outpatient basis. A generous layer of polysorbate-based ointment can be applied under a bulky absorbent gauze dressing. The patient is then released home, and the residual is easily washed off after 24 to 36 hours ( Fig. 39-15 ). A number of dressing changes may be required. Once the residual tar is removed, the wound is treated like any other burn. Shur-Clens, a nontoxic, nonionic detergent, also works well for tar burn wound cleansing, as do mineral oil; petrolatum; and Medisol (Orange-Sol, Inc, Chandler, AZ), a petroleum-citrus product. Butter-soaked gauze has been suggested as an emulsifier of tar. Chemical Burns Chemical burns usually occur in the workplace, and the offending substance is usually well-known. More than 25,000 chemicals currently in use are capable of burning the skin or mucous membranes. Commonly used chemical agents capable of producing skin burns are shown in Table 39-6 . Injury is caused by a chemical reaction, rather than a thermal burn. [46] Reactions are classified as oxidizing, reducing, corrosive, desiccant, or vesicant or as protoplasmic poisoning. The injury to skin continues until the chemical agent is physically removed or exhausts its inherent destructive capacity. The degree of injury is based on chemical strength, concentration, and quantity; duration of contact; location of contact; extent of tissue penetration; and mechanism of action. Immediate flushing with water is recommended for all chemical burns, with the exception of those caused by alkali metals. Flushing serves to cleanse the wound of unreacted surface chemical, dilute the chemical already in contact with tissue, and restore lost tissue water. Leonard and colleagues clearly demonstrated that patients receiving immediate copious water irrigation for chemical burns showed less
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Figure 39-13 There is no compelling reason to remove all tar on the first visit. Physical removal of cooled tar usually results in avulsion of the underlying skin. Skin that is obviously loose should be debrided, but adherent tar is best liquefied with an emulsifying agent. Neomycin cream, not ointment, is a suggested emulsifier, but others are acceptable (see text). Final removal may be delayed for several days to permit loosening of the tar. Frequent dressing changes using an emulsifying agent can be performed by the patient, removing the tar over a few days.
full-thickness burn injury and a greater than or equal to 50% reduction in time of hospital stay.
[47]
Acid and Alkali Burns
Alkalis cause saponification and liquefactive necrosis of body fats. Alkaline burns are penetrating and cause much tissue destruction. With acid burns, tissue coagulation produces a thick eschar that limits the penetration of the agent. Desiccant acids, such as sulfuric acid, create an exothermic reaction with tissue water and can cause both chemical and thermal injury. With extensive immersion injuries, acids may be systemically absorbed, leading to systemic acidosis and coagulation abnormalities. Chemical burns may be excruciatingly painful for long periods of time. Discomfort can be out of proportion to what one might expect from the depth or extent of the burn.
The emergency care team should remove all potentially contaminated clothing. Any dry (anhydrous) chemical should be brushed off the patient's skin. The involved skin should be irrigated with large amounts of water under low pressure. Any remaining particulate matter should be carefully debrided during irrigation. Strong alkali burns may require irrigation for 1 to 2 hours before the tissue pH returns to normal. Some recommend that after extensive irrigation, if the burn continues to feel "slippery" or tissue pH has not returned to normal, chemical neutralization may be helpful. [48] [49] Given that any heat of neutralization will be carried away with the irrigation solution, [50] prompt irrigation with a dilute acid (e.g., vinegar; 2% acetic acid) may hasten neutralization and patient comfort. Wet Cement Burns
The major constituent of Portland cement, an alkaline substance, is calcium oxide (64%), combined with oxides of
Figure 39-14 Tar stuck to the face (A) can be emulsified with various agents and a lot of patience and persistence (B). Fortunately, tar burns are usually not full-thickness burns.
silicon, aluminum, magnesium, sulfur, iron, and potassium. There is considerable variability in the calcium oxide content of different grades of cement, with concrete having less and fine-textured masonry cement having more. [47] The addition of water exothermically converts the calcium oxide to calcium hydroxide, a strongly corrosive alkali with a pH of 11 to 13. As the cement hardens, the calcium hydroxide reacts with ambient carbon dioxide and becomes inactive. Both the heat and the Ca(OH) 2 produced in this exothermic reaction can result in significant burns. Because of its low solubility and consequent low ionic strength, a long exposure to calcium hydroxide is required to produce injury. This usually occurs when a worker spills concrete into his or her boots or kneels in it for a prolonged period. The burn wound and the resultant protein denaturation of tissues produce a thick, tenacious, ulcerated eschar. Concrete burns are insidious and progressive. What may appear initially as a patchy, superficial burn may in several days become a full-thickness injury requiring excision and skin grafting. [51] The pain of these burns is often severe and more intense than the appearance of the wound might suggest ( Fig. 39-16 ). Interestingly, many workers are not warned of the dangers of prolonged contact with cement, and because initial contact with cement is
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Figure 39-15 There is no need to remove all the tar on the first visit (A). This extremity was covered with an emulsifying agent and with gauze, and the residual tar was washed off easily 36 hours later (B).
usually painless, exposure may not be realized until the damage is done. Treatment is as follows: Any loose particulate cement or lime is brushed off, contaminated clothing is removed, the wound is copiously irrigated with tap water (the pH of the effluent is tested and irrigation continued if the effluent is still alkaline). Compresses of dilute acetic acid (vinegar) may be applied to neutralize the remaining alkali and provide pain relief after irrigation, and antibiotic ointment is applied to the eschar during the early postburn period. Sutilains ointment (Travase, Flint Pharmaceuticals, Deerfield, IL) is often recommended because it contains proteolytic enzymes and helps speed eschar separation, but any common topical burn preparation is acceptable. The depth of burns from wet cement can be difficult to assess in TABLE 39-6 -- Commonly Used Acids and Alkalis Acids
Alkalis
Picric
Sodium hydroxide
Tungstic
Ammonium hydroxide
Sulfosalicylic
Lithium hydroxide
Tannic
Barium hydroxide
Trichloroacetic Calcium hydroxide Cresylic
Sodium hypochlorite
Acetic Formic Sulfuric Hydrochloric Hydrofluoric Chromic the first several days. If it becomes apparent that the burns are full-thickness burns, early excision and skin grafting are recommended. Cement burns should be differentiated from cement dermatitis, which is far more common. The latter is a contact sensitivity reaction, probably due to the chromates present in cement. The contact dermatitis can initially be treated as a superficial partial-thickness burn. Air Bag Keratitis/Thermal Burns
Safety legislation has mandated increased use of air bags to protect automobile occupants in the event of collision. Burns from air bags can be thermal, friction, or chemical. The automobile air bag is a rubberized nylon bag that inflates on spark ignition of sodium azide, yielding nitrogen gas, ash, and a small amount of sodium hydroxide. Within seconds the superheated air is vented, and this can produce a thermal burn if it contacts an extremity, face, or upper torso. [52] [53] If the air bag ruptures, the alkaline contents of the bag are dispersed as a fine, black powder that usually causes no problems unless the eyes are exposed. Patients present with clinical evidence of a chemical keratoconjunctivitis, including photophobia, tearing, redness, and decreased visual acuity. The tear pH is usually elevated, and there may be a small amount of particulate material in the fornices. [54]
The severity of an ocular alkaline burn is related to the duration of exposure and the concentration and pH of the chemical. For this reason, prompt, copious irrigation of the eyes with frequent assessment of tear pH is essential to prevent or minimize the injury (see Chapter 64 ). A rising pH suggests that trapped particulate matter is releasing additional chemical. Corneal edema and conjunctival blanching are signs of serious injury and necessitate immediate ophthalmologic consultation. Hydrocarbon Burns
Hydrocarbons are capable of causing severe contact injuries by virtue of their irritant, fat-dissolving, and dehydrating properties. Cutaneous absorption may cause even more dangerous systemic effects. Gasoline, the usual agent involved, is a complex mixture of C 4 to C11 alkane hydrocarbons and benzene; the hydrocarbons appear to be the major toxic agent. Lead poisoning caused either by absorption through intact skin or burns from "leaded" gasoline exposure have been previously reported but are currently quite rare, as unleaded gasoline has virtually replaced the leaded version for most purposes. [55] Depth of injury is related to the duration of exposure and concentration of the chemical agent. Gasoline immersion injuries resemble scald burns and are usually partial thickness. [56] Occasionally, gasoline-injured skin exhibits a pinkish brown discoloration, possibly related to dye additives. A common source of exposure is a comatose patient from a motor vehicle crash who had been lying in a pool of gasoline. The lungs are the usual site of systemic absorption and are often the only major route of excretion. The resultant high pulmonary concentrations may lead to pulmonary hemorrhages, atelectasis, and adult respiratory distress syndrome (ARDS). Treatment of hydrocarbon burns includes the following: removal of contaminated clothing, prolonged irrigation or soaking of the contaminated skin, early debridement in significant burns caused by lead-containing gasolines (to reduce systemic lead absorption), and use of topical antibiotic ointments.
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Figure 39-16 Alkali burns from wet cement develop insidiously, are extremely painful, and are frequently full-thickness injuries. They are most common on the feet when cement leaks over the top of the boots (A) or from kneeling in wet cement while working (B). The alkali can penetrate clothing. Phenol Injury
Phenol is a highly reactive aromatic acid alcohol that acts as a corrosive. Carbolic acid, an earlier term for phenol, was noted to have antiseptic properties and was used as such by Joseph Lister in performing the first antiseptic surgery. Hexylresorcinol, a phenol derivative, is in current use as a bactericidal agent. Phenols, in strong concentrations, cause considerable eschar formation, but skin absorption also occurs and can cause systemic effects such as central nervous system depression, hypotension, hemolysis, pulmonary edema, and death. Interestingly, phenol acts differently from other acids in that it penetrates deeper when in a dilute solution than when in a more concentrated form. [46] Therefore, irrigation with water is suboptimal for phenol burns, but because water commonly is readily available, it is frequently used for irrigation. Full-strength polyethylene glycol (PG 300 or 400) is more effective than water alone in removing phenolic compounds and should be obtained and used after water irrigation has begun. Polyethylene glycol is nontoxic and nonirritating and may be used anywhere on the body. When immediately available, polyethylene glycol can be used to remove the surface chemical before water irrigation (and chemical dilution) is begun. Hydrofluoric Acid Injury
Hydrofluoric acid (HFA) is one of the strongest inorganic acids known; it has been widely used since its ability to dissolve silica was discovered in the late 17th century.[57] Currently, HFA is used in masonry restoration, glass etching, and semiconductor manufacturing; for control of fermentation in breweries; and in the production of plastics and fluorocarbons. It is also used as a catalyst in petroleum alkylating units. It is available in industry as a liquid in varying concentrations up to 70%. It is also readily sold in home improvement and hardware stores. Significant concentrations of HFA are present in many home rust-removal products, and in aluminum brighteners, automobile wheel cleaners, and heavy-duty cleaners in concentrations of less than 10%. Despite its ability to cause serious burns, unregulated and poorly labeled HFA products are recklessly used on a regular basis in the home and in small businesses. The public and many clinicians are generally unaware of the potential problems with this acid ( Fig. 39-17 ). Although HFA is quite corrosive, the hydrogen ion plays a relatively insignificant role in the pathophysiology of the burn injury. The accompanying fluoride ion is a protoplasmic poison that causes liquefaction necrosis and is notorious for its ability to penetrate tissues and cause delayed pain and deep tissue injury. This acid can penetrate through fingernails and cause nailbed injury. With home products, the unwary user does not realize that the substance is caustic until the skin (usually the hands and fingers) is exposed for a few minutes to hours, at which time the burning begins and becomes progressively worse. At this point the damage is done, and the absorbed HFA cannot be washed off. With higher-strength industrial products, symptoms are almost immediate. The initial corrosive burn is due to free hydrogen ions; secondary chemical burning is due to the tissue penetration of fluoride ions. Fluoride is capable of binding cellular calcium, resulting in cell death and liquefaction necrosis. The ionic shifts that result, particularly shifts of potassium, are believed to be responsible for the severe pain associated with HFA burns. In high concentrations, the fluoride ions may penetrate to the bone and produce demineralization. Skin exposure to concentrated HFA involving as little as 2.5% TBSA can lead to systemic hypocalcemia and death from intractable cardiac arrhythmias; it has been calculated that exposure to 7 mL of anhydrous HFA (HFA gas) is capable of binding all of the free calcium in a 70-kg adult. [58] [59] If the hands are exposed, the acid characteristically penetrates the fingernails and injures the nailbed and cuticle area. As with most caustics, the pain is generally out of proportion to the evident external physical injury. HFA burns produce variable areas of blanching and erythema, but rarely are blisters or skin sloughing seen initially. Skin necrosis and cutaneous hemorrhage may be noted in a few days.
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Figure 39-17 A, Initially this very painful hydrofluoric acid burn of the thenar and hypothenar emminence appeared minimal. B, Despite infiltration with calcium gluconate, a deep burn developed 3 days later.
Immediate treatment should begin with copious irrigation with water. Another approach is to wash the area with a solution of iced magnesium sulfate (Epsom salts) or a 1:500 solution of a quaternary ammonium compound such as benzalkonium chloride (Zephiran) or benzethonium chloride (Hyamine 1622). Magnesium and calcium salts form an insoluble complex with fluoride ions, preventing further tissue diffusion. While frequently recommended, topical preparations are often ineffective in limiting injury or controlling pain. If there is no or only minimal visible evidence of skin injury and minimal pain, the burn may be dressed with topical calcium gluconate paste. This is not commercially available in the United States but is easily compounded in the pharmacy by mixing 3.5 to 7 g of pulverized calcium gluconate with 5 oz of a water-soluble lubricant such as K–Y Jelly. This will form a thick paste with a calcium gluconate concentration of 2.5% to 5.0%. Some have suggested dimethyl sulfoxide (DMSO) as a vehicle to aid in skin penetration of the calcium. Plastic wrap (e.g., Saran wrap) is used over a standard dry burn dressing to cover the calcium paste on the limbs; a vinyl or rubber glove is used over the paste when used on the hands. The wound should be completely redressed and the paste reapplied every 6 hours for the first 24 hours.
As with most topical treatments of HFA burns, calcium gluconate is only minimally effective in relieving pain, and its value is likely overestimated in the literature. A digital or regional nerve block with long-acting bupivacaine is an excellent way to provide prolonged pain relief if the hands are involved, but this does nothing to ameliorate the injury. In most cases oral opioids are required. If bullae or vesicles have formed, these should be debrided to decrease the amount of fluoride present, and the wound should then be treated as any partial-thickness burn. Burns with HFA of less than 10% strength will heal spontaneously, usually without significant tissue loss, but pain and sensitivity of the fingertips may persist for 7 to 10 days. In addition, the fingernails may become loose. The presence of significant skin injury or intense pain implies penetration of the skin by fluoride ions. This scenario is particularly common with exposure to HFA solutions in concentrations of greater than or equal to 20%, but tissue injury can occur with prolonged exposure to less concentrated products. Initial treatment of a more concentrated exposure begins as described earlier and includes immediate debridement of necrotic tissue to remove as much fluoride ion as possible. Following this, a 10% solution of calcium gluconate (note: avoid calcium chloride for tissue injections) is injected intradermally and subcuticularly with a 30-ga needle about the exposed area, using about 0.5 mL/cm 2 of burn. Pain relief should be almost immediate if this therapy is adequate. Since the degree of pain is a measure of the effectiveness of treatment, the use of anesthetics, especially by local infiltration, may be deleted if the burn is on the arm or leg. HFA can penetrate fingernails without damaging them. Soft tissue can be injected without prior anesthesia, but if the fingertips or nailbeds are involved, they may be injected after a digital nerve block has been performed ( Fig. 39-18 ). Before anesthesia and prior to injecting calcium, the patient can outline the affected areas with a pen to ensure accurate injection of the antidote (see Fig. 39-18B ). Although some investigators recommend that the fingernails be removed routinely, we strongly advise against this unless the nails are very loose or there is obvious necrosis of the nailbed. Fingers are best injected with a 25- or 27-ga needle (a tuberculin syringe works well). [60] Nails frequently become loose in a few days, but often they return to normal and do not require removal, particularly when lower concentration nonindustrial products are involved. Although calcium gluconate infiltration is somewhat effective, the technique has certain limitations. Injections are painful, and the calcium gluconate solution itself causes a burning sensation. Because of the volume restrictions, not enough calcium may be delivered to bind all the free fluoride ions present. For example, 0.5 mL of 10% calcium gluconate contains 4.2 mg (0.235 mEq) of elemental calcium, which will neutralize only 0.025 mL of 20% HFA. Several authorities have advocated intra-arterial calcium infusions in the treatment of serious HFA burns of the extremities. [58] [61] Although very effective, this technique is not recommended for burns secondary to dilute HFA (i.e., concentrations 24 hours [2] [25] and when they are sharp. [26] An estimated 1500 deaths occur annually from esophageal FBs, primarily from complications of esophageal perforation. [9] Presentation An esophageal foreign body impaction usually presents acutely, particularly in adults who will have a clear history of ingestion. Children commonly remember an ingestion also, but some will have a vague presentation or history. As many as one-third of children with proven esophageal FBs are asymptomatic on presentation [27] [28] [ 29] ; therefore, a high index of suspicion is indicated, especially in a child who was seen with an object in his or her mouth that disappeared. This is especially true if there was transient coughing or gagging, even though actual ingestion was not witnessed. Poor feeding, irritability, fever, stridor, cough, and aspiration can all be caused by an underlying esophageal foreign body in a child, usually young infants. [12] [30] [31] Dysphagia is a common presenting complaint in esophageal FBs. Drooling is suggestive of a high-grade obstruction, and the complete inability to handle oral secretions is a sign of complete obstruction. The esophagus is well-innervated proximally, and patients typically can accurately localize foreign objects in
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TABLE 40-1 -- Complications of Esophageal Foreign Bodies Airway compromise due to tracheal compression Aspiration pneumonia Esophageal necrosis Esophageal perforation Esophageal stricture Failure to thrive Mediastinitis Mucosal abrasion Paraesophageal abscess Pericarditis/pericardial tamponade Pneumothorax
[24]
Pneumomediastinum Retropharyngeal abscess Tracheoesophageal fistula Vascular injury including aortic perforation Vocal cord paralysis the oropharynx or upper one-third of the esophagus. However, scratches or abrasions of the esophagus can create a foreign body sensation. Upper esophageal foreign objects often cause gagging or vomiting. In rare cases, an upper esophageal foreign body can impinge upon the trachea, especially in children, creating stridor or frank respiratory distress. The lower two-thirds of the esophagus is not as well-innervated, and FBs in this location typically cause vague symptoms of discomfort, fullness, or non-localizing pain. The location of retained esophageal FBs is age-related ( Table 40-2 ). Children more typically have entrapped objects in the upper esophagus at the level of the cricopharyngeus muscle, while adults more commonly have entrapments at the lower esophageal sphincter. [31] [32] [33] [34] [35] With regard to esophageal coins in children, one report noted the frequency of impacted coins at various levels of the esophagus as: proximal esophagus 64%, middle third 8%, and distal third 26%. [35] Evaluation The most useful aspect of the evaluation is the history. The time of the ingestion, size and shape of the ingested object, and any current symptoms should be ascertained. The physical examination is frequently normal in patients with esophageal FBs, unless they present with a complete obstruction. In this case they will be drooling and unable to handle oral secretions. Even though asymptomatic on presentation, transient coughing or gagging should raise the index of suspicion for an esophageal FB. An examination of the oropharynx, neck, respiratory system, cardiac system, and abdomen are essential in the evaluation of possible complications. After attending to life-threatening conditions such as airway compromise, the goal of the ED evaluation is to localize the foreign body to determine what, if any, interventions need to be undertaken to remove it or assist its transit into the stomach. Once a foreign body passes into the stomach, it TABLE 40-2 -- Level of Entrapment of Esophageal Foreign Bodies Level
Pediatric Adult
Cricopharyngeus muscle
74%
24%
Aortic crossover
14%
8%
Lower esophageal sphincter
12%
68%
has a greater than 90% likelihood of passing through the entire gastrointestinal tract without any further problems. FBs will often target the entire gastrointestinal tract with relative ease.
[ 26]
Even large, irregular, and seemingly dangerous
RADIOLOGY OF ESOPHAGEAL FOREIGN BODIES Background Radiographic imaging of a patient with a suspected esophageal foreign body is common, and is particularly useful for the detection of radiopaque foreign objects. Traditionally, the inability to quickly identify the object by physical examination encouraged the use of plain radiography in attempts to verify and localize the retained foreign body. Plain radiography limitations require that other diagnostic approaches be considered as well. Indications Interactive, verbal patients can provide valuable information about the ingested culprit and can typically localize the retained body with reliable accuracy. [36] In these cases, the diagnostic workup should be tailored to the localization of symptoms and the ingested material. However, non-verbal patients including preschool children and those who are senile or debilitated warrant a low-threshold for screening radiography in cases with a suspicious history. Examples include a child seen with an object in the mouth that "disappeared" or a patient with symptomatology suggestive of an esophageal foreign body such as drooling, gagging, or unexplained respiratory symptoms. Plain Radiographs Plain radiographs reliably verify and localize radiopaque FBs such as glass and metal and are indicated as the main method of radiologic evaluation for these objects. As previously mentioned, FBs are most frequently entrapped at one of three locations in the esophagus: the cricopharyngeus muscle ( Fig. 40-2 ), the aortic cross-over ( Fig. 40-3 ), and the lower esophageal sphincter ( Fig. 40-4 ). Unfortunately, many ingested FBs are non-opaque including non-bony foods, plastic, wood, and aluminum such as the pull-tab from beverage cans. A magnetic metal detector has been reported to help localize radiolucent aluminum pull-tabs. [37] [38] Calcification of fish and chicken bones is often incomplete, making them radiolucent on plain films. The degree of bony calcification varies with fish species and varies between different samples of the same species, thus preventing useful guidelines. [39] [40] [41] [42] For these reasons, plain films provide little substantive evidence in the majority of cases of fish or chicken bone dysphagia. They detect only 25 to 55% of endoscopically proven bones and carry a high rate of false-negative and false-positive interpretations. [36] [42] [43] [44] [45] [46] Because of the lack of diagnostic value for detecting bones, many clinicians do not routinely order plain radiographs, opting for a computed tomography (CT) scan if radiographic evaluation is required. When considered, a complete oropharyngeal radiograph series includes the nasopharynx to the lower cervical vertebra in both lateral and anteroposterior views. Optimum quality radiographs are mandatory. Patients should be positioned
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Figure 40-2 PA radiograph of an esophageal foreign body (coin) lodged at the level of the cricopharyngeus muscle. This is the most common area of the esophagus to harbor a coin in children.
upright with the neck extended and the shoulders held low. Soft tissue technique enhances the discrimination of weak radiopaque FBs. Phonation of "eeeee" during radiography prevents motion artifact from swallowing, distends the hypopharynx, and enhances soft tissue landmarks.
Figure 40-3 Posteroanterior radiograph of an esophageal foreign body (coin) lodged at the level of the aortic cross-over.
Figure 40-4 A posteroanterior radiograph of an esophageal foreign body (coin) lodged at the level of the lower esophageal sphincter (LES).
Plain radiography of the neck is limited by the radiographic properties of ingested materials and the complicated anatomy of the upper aerodigestive tract. The tongue base, palatine and lingual tonsils, vallecula, and pyriform recesses are common regions of entrapment for small, sharp objects and deserve careful interpretive attention ( Fig. 40-5 ). Superimposition of the mandible contributes to suboptimal resolution of this region on lateral neck films. [47] Calcified
Figure 40-5 A lateral neck radiograph showing a chicken bone lodged in the pharynx with associated soft tissue swelling. The arrow points to the bone. Plain radiographs have poor diagnostic accuracy for detecting bones in the esophagus and they are often eschewed in favor of a CT scan if radiographic evaluation is deemed necessary.
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airway cartilages often masquerade as FBs and contribute to false-positive rates as high as 25%. [36] [41] [43] [45] [48] [49] [50] Normal ossification of airway cartilages begins in
the third decade and progresses with age. [51] The typical curvilinear contour and well-defined margins of bony FB fragments may help distinguish them from normal laryngeal calcifications. Orientation of bony FBs is variable. The C6 vertebra approximates the level of the cricopharyngeus, a common site of FB impaction. Increased prevertebral soft tissue width, air within the cervical esophagus, and soft tissue emphysema are rare indirect findings that may help identify radiolucent objects.[42] [52] Posteroanterior and lateral views of the chest evaluate the remainder of the esophagus. Both projections are indicated to identify multiple objects and those FBs visible in only one plane. Esophageal FBs typically lie in the vertical plane and are differentiated from airway bodies or calcifications by their location posterior to the tracheal air column on lateral radiographs. As a rule, flat objects such as coins perch in the coronal plane in the esophagus and in the sagittal orientation in the trachea. Intra-esophageal air and air-fluid levels represent indirect evidence of esophageal obstruction and may aid in verification of radiopaque FBs. Soft tissue swelling, extraluminal air, and aspiration pnuemonitis can occasionally help identify complicated impactions radiographically. Xeroradiography provides no additive benefit over plain films. [53] In children, a "mouth-to-anus" film is frequently obtained, allowing visualization of the entire esophagus as well as the abdomen in case the foreign body has passed into the stomach or beyond. Swallowed coins or other FBs have become lodged in the nasopharynx, usually after gagging or vomiting, and could be missed if this area is not included on the radiograph. In adults, if neck or chest films are negative, abdominal films are sometimes obtained for reassurance of the presence of the foreign body in the stomach. Contrast Esophagrams Background
The contrast esophagram is another somewhat controversial method to evaluate for esophageal foreign body but may be considered when plain radiographs are negative. In clinical practice, however, they are seldom used since CT scanning has become widely available. This technique uses swallowed contrast to help identify the presence and location of an impacted radiolucent foreign body, the degree of obstruction, underlying anatomical abnormalities, and the presence of perforation. A variation of this technique is to have the patient swallow contrast-soaked cotton pledgets. This technique uses smaller contrast loads and may identify impacted FBs by impeding progression of the cotton or by tagging sharp irregular objects with radiopaque cotton as the bolus passes. Theoretically this variation might interfere less with follow-up endoscopy due to attenuated contrast loads. Unfortunately, liquid contrast ingestion yields overall results no better than plain film radiography. Two series document 19% to 26% false-positive and 40% to 55% false-negative interpretations using this technique, and the authors legitimately question the utility of this test. [43] [54] More importantly, contrast may interfere with the detection and extraction of FBs at endoscopy and may increase the risk of aspiration. [42] [55] [56] Routine, serial contrast esophagrams following negative plain radiography for patients with known or suspected FBs are unnecessary for diagnostic purposes in most cases. Selective use in complicated cases is reasonable but may be substituted by CT or endoscopy in many institutions. Procedure
Esophagrams couple voluntary ingestion of enteric contrast and plain radiography. Immediately after ingestion, erect and horizontal radiographs are performed at right-angle projections (posteroanterior [PA] and lateral or right and left anterior oblique). In addition to anatomic abnormalities, radiolucent FBs may be identified by contrast delineation or filling defects within the contrast column ( Fig. 40-6 ). The initial choice of contrast agent is debated and should be individualized depending on the threat of aspiration and perforation. Water-soluble Gastrografin is indicated first in most cases of suspected perforation as it causes less mediastinal inflammation when extravasated; however, it can cause a severe chemical pneumonitis if aspirated and is relatively contraindicated in patients with a complete esophageal obstruction. [10] Patients without evidence of complete esophageal obstruction are instructed to swallow progressively larger aliquots of contrast agent up to approximately 50 mL. If these films are normal, the procedure is repeated with half-strength and then full-strength barium to delineate small esophageal injuries. Note that water-soluble contrast causes more pulmonary reaction than barium when inadvertently aspirated and should be used in small aliquots if aspiration or complete esophageal obstruction is a concern. Contrast esophagrams coupled with fluoroscopy are seldom used in acute esophageal FB impactions, although slowed progression or abnormal peristalsis may suggest a retained FB or anatomic abnormality. Barium interferes with endoscopy and should not be used when endoscopy is anticipated.
Figure 40-6 A barium swallow demonstrating a complete esophageal obstruction in the proximal to mid-esophagus.
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Computed Tomography Non-contrast CT of the neck and mediastinum is an easy, rapid, and non-invasive means of detecting (and ruling out) upper gastrointestinal FBs ( Fig. 40-7 ).[41] [42] [44] First reported in 1983, CT has garnered increasing support in the clinical setting of suspected FB entrapment. [57] [58] [59] One series of 45 patients revealed 100% sensitivity with one false-positive CT interpretation yielding 93% specificity and 96% positive predictive value, [44] while another yielded equally impressive results in patient and cadaver models, respectively. [41] [42] CT further excels at localization and characterization of the impacted FB and identification of associated complications such as perforation. [42] [57] [60] [61] [62] The exact role of CT for symptomatic stable patients with cervical aero-digestive FB sensation remains to be delineated. It clearly provides improved diagnostic utility for fish bone FB compared to plain radiography with and without barium. [41] [42] [44] Application to every patient with acute bone dysphagia is probably unwarranted. Use in cases with high clinical suspicion of a retained FB has the potential to reduce the number of unnecessary endoscopies. [44] Cost analysis data for this practice have not yet been published. Optimum non-contrast CT scans of the neck and mediastinum use axial 2- to 2.5-mm cuts with bone and soft-tissue windows. Conclusions Diagnostic radiography for esophageal FB requires case individualization. Plain radiographs clearly assist the clinician in two situations: (1) screening of children, senile adults, and nonverbal patients with a history or symptoms suspicious for purposeful or inadvertent FB ingestion, and (2) localization of known radiopaque ingestants to clarify the necessity and means of FB extraction. Conversely, attempts to verify radiolucent bodies, including bones, are often misleading. Contrast esophagrams may be used in special situations but
Figure 40-7 Computed tomography demonstrating an esophageal foreign body.
have largely been replaced by CT and direct endoscopy. The utility of CT to exclude fish bone FB is promising but requires discriminatory application to achieve cost efficiency.
VISUALIZATION OF ESOPHAGEAL/PHARYNGEAL FOREIGN BODIES Direct Pharyngoscopy Background
Direct visualization of the oropharynx is simply a physical examination using a light source and aided by a tongue blade. This examination is limited to visualizing only the upper oropharynx, tonsils, tonsillar pillars, and in some cases, the tip of the epiglottis. In many cases, a foreign body such as a fish bone can be visualized and then removed with forceps. Indications
Direct visualization is indicated in most patients who have a foreign body sensation in the oropharynx or upper neck. The only contraindication is a patient with potential airway obstruction. Procedure
The supplies needed for a direct visualization are a light source and a tongue depressor. Although penlights are traditionally used for this purpose, a fiberoptic headlight or a head mirror reflecting a bright light source are superior for a thorough examination. When using a headlamp, the lamp should be positioned on the forehead between the eyes, with the beam focused at a distance of approximately 2 feet. This can be tested by focusing the beam on the examiner's thumbs held together at a comfortable working distance. A head mirror is positioned with the central hole over the examiner's dominant eye. Normally the light source is positioned behind one shoulder of the patient and reflected by the head mirror into the oropharynx. For the best direct visualization, the patient is placed in a sitting position, with the examiner standing. The entire visible oropharynx is examined using a tongue depressor to carefully depress the base of the tongue for better visualization of the pharyngeal wall, tonsils, and tonsillar pillars. Having the patient apply gentle but firm traction to their own tongue can aid exposure. The patient should generally assume a "sniffing" position with the neck slightly flexed and the head extended. Using a preprocedural topical anesthetic on the pharyngeal mucosa will minimize discomfort and gagging when using the tongue blade. In some patients, especially children, the tip of the epiglottis can be seen. If a foreign body is visible, forceps can be used to grasp and remove the object. Indirect Laryngoscopy Background
Indirect laryngoscopy is an examination of the middle and lower oropharynx using a mirror. This technique allows evaluation of the epiglottis, vallecula, arytenoids, arytenoid folds, and the vocal cords. Indirect visualization requires experience with the procedure and a cooperative patient. Indications
Indirect visualization is indicated in patients who have a FB sensation in the oropharynx or upper neck, with the exception of those with airway compromise.
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Procedure
Indirect visualization requires a light source (head lamp or head mirror), a gauze pad to hold the patient's tongue, a laryngeal mirror, and frequently, a topical anesthetic agent. Place the patient in a sitting position leaning slightly forward as discussed for direct pharyngoscopy. Standing in front of the patient, grasp the tongue with the gauze pad and pull lightly while having the patient open his or her mouth widely. Warm the laryngeal mirror either in warm water or a mirror warmer, check the temperature of the mirror with the back of the hand, and insert the mirror without touching the tongue (see Chapter 65 , Fig. 65-2 ). The mirror can elevate the uvula and soft palate slightly, but should avoid the pharyngeal wall. If the patient cannot tolerate this maneuver without gagging, instill some topical anesthetic and reattempt. Evaluate the base of the tongue, the epiglottis, vallecula, arytenoids, arytenoid folds, and the vocal cords. Use forceps to attempt to remove a visible FB. Failure to extract a visible FB with forceps is an indication for otorhinolaryngology referral for removal. Nasopharyngoscopy Background
Careful visualization of the oropharynx and hypopharynx is vital in the evaluation of patients presenting with complaints of FB sensation of the neck. Although a significant proportion of complete evaluations will not discover any abnormalities, the combination of direct, indirect, and flexible endoscopic nasopharyngoscopy is simple, fast, and curative in those with an identifiable FB. [36] [47] [63] One series of 168 oral, pharyngeal, and esophageal retained fish bones demonstrated the efficacy of thorough examination. Clinicians removed 73% of the bones via direct or indirect laryngoscopy. [47] Flexible nasopharyngoscopy with topical analgesia was successful in an additional 15% of cases, thereby reducing by half the need for rigid esophagoscopy and general anesthesia in this series of patients. Indications and Contraindications
Indications for this procedure span the scope of clinical situations necessitating thorough visual examination of the pharynx and proximal esophagus, including patients with foreign body sensation and acute pill and postprandial food dysphagia. Croup is quoted as the sole absolute contraindication to flexible nasopharyngoscopy. [64] The risk-to-benefit ratio of endoscopy should be considered in patients with coagulopathy or severe bleeding diathesis, although the risk of initiating significant hemorrhage is low. Medication allergy precludes the use of some topical agents. Equipment
All equipment should be assembled and checked before initiation of endoscopy ( Table 40-3 ). Nasopharyngoscopy is best accomplished via a 3- to 6-mm external diameter flexible fiberoptic nasopharyngoscope (see Chapter 65 , Fig. 65-4 ). Scope side ports enable suction, anesthetic injection, and FB extraction via forceps, but are not mandatory. Traditional scopes require an external light source while some newer generation fiberoptic scopes include battery-powered, self-contained light sources. Inexpensive adapters enable a laryngoscope handle to double as an endoscopy light source. The endoscope eyepiece should be adjusted to accommodate the operator's visual acuity. Yankauer suction and angled McGill forceps or a Kelly clamp should be available to retrieve TABLE 40-3 -- Equipment for Nasopharyngoscopy Flexible fiberoptic nasopharyngoscope External light source (necessary for scopes without self-contained light source)
Suction and foreign body forceps (for applicable scope with channels) McGill forceps or Kelly clamp Topical anesthetic and decongestant Water-soluble surgical lubricant identified FBs orally. Topical cocaine, phenylephrine (Neo-synephrine), oxymetazoline (Afrin) and liquid or viscous lidocaine may be used for anesthesia and vasoconstriction, but are not a necessity. Procedure
Nasopharyngoscopy is generally well-tolerated, but patients should have a clear understanding of the examination procedure prior to initiation. Discussion of the procedure with the patient should include potential complications and alternatives. Topical anesthesia is recommended for patient comfort but is not mandatory. [36] [47] Examine the nares and choose the one with the least anatomical resistance for endoscopy. Cotton balls or pledgets soaked with 10% cocaine or a combination of 0.05% oxymetazoline (Afrin) and 2% lidocaine (Xylocaine) provide nasal mucosal anesthesia and vasoconstriction within minutes. Viscous 2% to 4% lidocaine applied by a cotton-tipped applicator is an alternative anesthetic. Atomized 2% lidocaine (Xylocaine) or topical benzocaine spray (20% Hurricane spray, Cetacaine) can be used to further anesthetize the hypopharynx. Patients may complain of discomfort or globus sensation following anesthesia and may require explanation and reassurance. Patients only rarely need an anti-sialogogue, such as glycopyrrolate. Others may need mild sedation with a short-acting benzodiazepine. The patient is seated erect in a chair with posterior headrest support to prevent movement during examination. The examiner stands upright in front of the patient, holding the body of the scope in the non-dominant hand (see Chapter 65 , Fig. 65-5 ). Scope maneuvers are controlled solely with the hands. The dominant hand controls the depth of scope insertion at the naris and directs the scope along the horizontal plane at the floor of the nose. This hand should rest lightly on the patient's face for comfort and to prevent abrupt changes in scope position in case of movement during examination. Flexion in the sagittal plane is achieved with the thumb lever on the scope handle. Rotation clockwise and counterclockwise is performed via simple rotation of the wrist, not the entire upper body. It is important to maintain mild tension on the two ends of the scope for wrist action to be translated to motion at the tip of the scope. Warming the tip of the scope in water and applying silicone drops helps prevent scope fogging. Manipulation against the patient's mucosa will clear the scope during endoscopy. Water-soluble lubricant aids in passing the scope but should not be applied to the distal 2 cm of the scope. Effective examination of the oropharynx requires some practice and reference to normal anatomy. Although many patients can localize the FB, systematic examination in a caudal direction is vital. [36] Direct the patient to focus on slow, steady mouth breathing to attenuate discomfort and gagging during the procedure. Insert the scope horizontally along
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the floor of the nose and pass it below the inferior turbinate. Upon reaching the soft palate, deflect the scope tip inferiorly (via directing the thumb lever toward the eyepiece) and advance it into the oropharynx. Examine the laterally located palatine tonsils and palatopharyngeal arches, along with the proximal tongue and lingual tonsil. Advance the scope caudally to allow further visualization of the tongue base, epiglottis, and the interposed spaces, known as the epiglottic vallecula. Voluntary or manual protrusion of the tongue helps reveal this anatomy. Scan posteriorly to reveal the vocal cords, aryepiglottic folds, and pyriform recesses. Patients can gently exhale against a closed mouth and nose to distend the lower pharyngeal structures and improve visualization of these areas. Avoid contact with the epiglottis and vocal cords. Explore all pharyngeal walls fully and compare the structures bilaterally, even when patients localize symptoms to one side. Signs of trauma, including bleeding, mucosal hyperemia, and edema require close investigation to differentiate retained FBs from mucosal irritation. If a FB is visualized ( Fig. 40-8 ), the method of extraction depends on the location and size of the retained object. Small FBs may be extracted transnasally via forceps passed through the scope side port. Large or irregular bodies may be withdrawn orally with angled forceps. [47] Alternatively, endoscopy may be used primarily for FB confirmation. Extraction can then be performed via handheld forceps under endoscopy guidance, subsequent direct laryngoscopy, or under general anesthesia. Careful attention to prevent FB dislodgment into the airway is critical with any extraction attempt. Complications
Complications of nasopharyngoscopy are rare and typically mild. Reflex tearing, sneezing, and coughing are the most common and are self-limited. Some patients experience a residual FB sensation for several hours after manipulation. Mild bleeding, including epistaxis, is common secondary to mucosal abrasion. Extraction of an embedded FB may result in bleeding but is also generally self-limited. Vasovagal syncope has been reported in up to 3% of patients undergoing this procedure. [64] Inadvertent dislodgement of the FB farther into the esophagus or into the airway may occur with manipulation or attempted extraction.
Figure 40-8 Esophageal foreign body seen on nasopharyngoscopy.
Esophagoscopy Esophagoscopy is the definitive diagnostic and therapeutic procedure for impacted esophageal FBs. [9] [33] Although esophagoscopy is not a procedure performed by the emergency clinician, its proper role in the ED evaluation of FBs must be understood. With esophagoscopy the clinician can document the presence and location of the FB along with any underlying lesion. The clinician can then remove the object and reevaluate the esophagus after FB removal to rule out perforation or underlying pathology. Esophagoscopy may be necessary even if a radiologic contrast study does not reveal complete obstruction, because x-ray studies are not always conclusive. [8] [65] Esophagoscopy may be necessary to rule out predisposing pathology or resultant perforation, even when symptoms presumed to be due to an esophageal FB have resolved. Esophagoscopy is the preferred method for removal of sharp or pointed objects such as bones, open safety pins, and razors. In the case of sharp objects prone to causing esophageal perforation, IV antibiotics should be administered before the procedure. Esophagoscopy is also indicated for a FB retained for more than 24 to 48 hours both to remove it and to examine for esophageal wall erosion or perforation. Esophagoscopy is the only appropriate removal technique for multiple or large esophageal FBs. This technique is also indicated in the patient with a FB proven to have passed into the stomach and who has persistent symptoms possibly caused by esophageal wall injury. The flexible endoscope is more commonly used than the rigid esophagoscope. Flexible endoscopic procedures can usually be performed without general anesthesia, even in most children.[66] The success rate of flexible endoscopy in patients with retained esophageal FBs exceeds 96%. [33] [67] Traditionally, esophagoscopy is more expensive than other maneuvers such as Foley catheter removal or esophageal bougienage (described later), [3] [7] [68] largely due to charges for the surgical suite, but it has a higher success rate than the other two techniques. Recently, the ED removal of esophageal FBs in children by experienced endoscopists, while the child is under ketamine sedation administered by the emergency clinician, has been reviewed. [69] In select cases, this approach can shorten the interval to procedural completion and expense.
ESOPHAGEAL PHARMACOLOGIC MANEUVERS Background Because the lower esophageal sphincter (LES) is the narrowest portion of the entire gastrointestinal tract, most FBs that reach the stomach eventually move through the gastrointestinal tract without further problems. As a large number of entrapped esophageal FBs are lodged at the LES, especially in adults, several therapeutic maneuvers have been developed to assist transit into the stomach including pharmacologic relaxation of the LES. In theory, agents that promote smooth muscle relaxation should improve mobility through the LES. Although many clinicians use pharmacologic adjuncts for all esophageal FBs, objects lodged at the LES will probably benefit most from such interventions. Nonspecific pain relief, anxiolysis, and spontaneous passage
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may account for the success of many pharmacologic manipulations of esophageal FBs. Several pharmacologic agents have been shown to be unsuccessful for removing or resolving esophageal FB impactions, including diazepam, meperidine, and atropine.[11] These agents, alone or in combination, have success rates below 10%, which is no better than observation alone. [2] Glucagon, nitroglycerin, nifedipine, and gas-forming agents ( Table 40-4 ) are described later and are the most effective pharmacologic agents for treatment of distal esophageal food impactions. Indications and Contraindications The indication for pharmacologic relaxation of the LES is the presence of a smooth or blunt FB such as a coin or food bolus. Angulated, abrasive, or sharp FBs should not be treated with pharmacologic modalities but instead should be removed by esophagoscopy. Analgesics and sedatives are routinely indicated if pain is present or if the patient is excessively anxious. Glucagon Pharmacology
Glucagon has been a prototype for the spasmolytic agents. [70] [71] [72] Its use has been advocated for enhancing the passage of esophageal FBs since 1977, and there have been several isolated reports of dramatic relief. [70] [73] [74] [75] Glucagon theoretically relaxes esophageal smooth muscle and decreases the LES resting pressure. One study of normal subjects found that glucagon significantly lowers the mean LES resting pressure, but causes no significant difference in the mean amplitude of contraction in the distal esophagus. [76] Glucagon has no effect on the upper third of the esophagus, a common site of coin impaction in children, where striated muscle is present and some voluntary control is operative. It only minimally affects the middle third of the esophagus, although the successful use of glucagon to dislodge food in the middle third of the esophagus has been reported. [70] [73] Peristalsis is not affected by glucagon. Glucagon was successful in approximately 30 to 69% of lower esophageal obstructions in several studies [70] [72] [73] [74] [75] ; however, in two studies glucagon was not
Class and Agents
TABLE 40-4 -- Recommended Pharmacologic Therapies for Esophageal Foreign Bodies Site of Action Dose and Route Adverse Effects
Spasmolytics Glucagon
LES
1–2 mg IV*
Nausea, vomiting, hyperglycemia, hypersensitivity
Nitroglycerin
Body and LES
0.4–0.8 mg SL†
Hypotension, tachycardia, or bradycardia
Nifedipine
LES
10 mg SL‡
Hypotension, tachycardia (use with caution)
Distal and proximal
15 mL tartaric acid
Vomiting, increased intraesophageal pressure
Gass-forming agents Tartaric acid
(18–20 g/100 mL)§ 15 mL sodium bicarbonate (10 g/100 mL) §
Sodium bicarbonate Carbonated beverage
Distal and proximal
100 mL PO
Vomiting, increased intraesophageal pressure
IV, intravenously; LES, lower esophageal sphincter; PO, per os; SL, sublingually. * May be repeated once or used in conjunction with nitroglycerin. † 1–2 inches of nitroglycerin paste applied under an occlusive dressing may be an alternative. ‡ A capsule is punctured, chewed, held in the mouth for 3 minutes, and then swallowed. Do not use if the patient has cardiovascular disease, is hypotensive, or has also been recently given nitroglycerin. § Alternatively, dissolve 2–3 g tartaric acid and 2–3 g sodium bicarbonate in 30 mL water.
significantly different from treatment with a placebo. [76A] [77] Its use, however, is still advocated by some authorities and has little downside. Glucagon may cause vomiting, and this action may be responsible for some of the drug's success. [78] Indications and Contraindications
Glucagon is most useful for smooth FBs or food impactions at the LES that are suspected because of the patient's complaint of pain or "something stuck" in the lower chest or epigastrium. The clinical diagnosis is usually straightforward, especially if there is a complete esophageal obstruction and the patient is unable to tolerate oral secretions. Nevertheless, some clinicians recommend that the FB be localized first with radiographs (with or without contrast) to establish that the impaction is indeed there. The radiographs can then serve as the baseline study for comparison following glucagon administration. However, with a classic history and physical examination, most investigators agree that an initial contrast study can be omitted. Glucagon is not effective in upper and middle esophageal obstructions, and it is not widely recommended for use in children. Also, glucagon is usually not effective in patients with fixed fibrotic strictures or rings at the gastroesophageal (GE) junction. [71] Glucagon is contraindicated if the patient has an insulinoma, a pheochromocytoma, Zollinger-Ellison syndrome, a hypersensitivity to glucagon, or a sharp esophageal FB. Administration of Glucagon
Some reports recommend a small test dose to check for hypersensitivity to glucagon. In practice, this is rarely done. The therapeutic dose is 0.25 to 2 mg administered intravenously over 1 to 2 minutes in the sitting patient, although one study found that in normal subjects, 1 mg provides no significant additive benefit over 0.5 mg glucagon.[76] The patient is given water orally within 1 minute after the injection of glucagon to stimulate normal esophageal peristalsis; this helps push the food through the relaxed LES into the stomach. Glucagon has a rapid onset and short duration of action. The gastrointestinal smooth muscle relaxes within 45 seconds, and the duration of action is about 25 minutes. If there are no results within 10 to 20 minutes, a second administration of 0.25 to 2 mg may be tried. Success
rates are higher when combining glucagon with gas-forming agents or even carbonated beverages. [79] [80] It is recommended that a small volume of
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some oral fluid be routinely given to enhance the activity of glucagon. Complications
Glucagon is associated with a few minor side effects. If administered too rapidly, it causes nausea and vomiting. Therefore, the adult patient must be alert and mobile enough to avoid aspiration. Occasionally vomiting dislodges the impacted food bolus. Theoretically, there is a risk of rupture of the obstructed esophagus during induced emesis, so slow injection is preferred to minimize this side effect. The administration of glucagon is also associated with dizziness. Mild elevation of blood glucose levels is also common but is not of clinical concern and blood glucose levels do not need to be monitored. No fatalities have been reported. Although theoretically glucagon can stimulate catecholamine release with a pheochromocytoma and induce hypoglycemia from reflex insulin release with insulinoma, these endocrine tumors are rare. Nonetheless, precipitation of either profound catecholamine or insulin reactions with glucagon use should direct a workup for these underlying tumors. Further Evaluation and Therapy
If the patient experiences symptomatic relief following glucagon administration, a post-procedure radiograph or contrast study may be obtained to confirm passage of a radiopaque object, but this is not mandatory. Adult patients with successful passage into the stomach may also be discharged home, but careful follow-up should be obtained to rule out coexistent esophageal pathology. This is because a significant number of patients (65% to 80%) will have underlying esophageal disorders. [9] If glucagon fails to produce symptomatic relief or resolve radiograph findings, its use does not preclude other methods from being used. Nitroglycerin and Nifedipine Pharmacology
Both sublingual nitroglycerin and nifedipine have been used in a manner similar to that of glucagon to relieve LES tone and allow the passage of a distal esophageal FB.[81] [82] [83] Although these two agents have been used less than glucagon for the treatment of esophageal FBs, both agents are useful for the relief of chest pain associated with esophageal smooth muscle spasm[57] and may be administered concurrently with glucagon. Manometric and radiographic studies after the administration of nitroglycerin reveal abolition of repetitive high-pressure wave contractions characteristic of esophageal spasm. Nifedipine, on the other hand, significantly reduces LES pressure without changing contraction amplitudes in the body of the esophagus. Thus, nitroglycerin may relieve partial or complete obstruction of the middle or lower esophagus secondary either to intrinsic esophageal disease or to simple FB impaction, and nifedipine, like glucagon, is most likely to succeed when the bolus is lodged at the GE junction. Indications and Contraindications
Similar to the clinical indications for the use of glucagon, any patient presenting with an impacted smooth esophageal FB, especially a food bolus, may be a candidate for nitroglycerin and/or nifedipine. Also, similar to the mode of action of glucagon, neither of these agents is expected to relax a fixed fibrotic stricture or ring at the GE junction. [71] Nevertheless, because both agents have a relatively benign side effect profile, if the patient has no contraindication to their use, they may be tried with or without previous documentation of the distal esophageal obstruction by contrast study. Contraindications to their use include a history of allergic reactions, a sharp esophageal FB, hypovolemia, and hypotension. Use and Complications
Doses of 1 to 2 (0.4 mg) sublingual nitroglycerin tablets, 1 to 2 inches of nitroglycerin paste, or 10 mg of nifedipine have been reported. [81] [82] [83] Remember that some patients with esophageal FBs may present with some degree of dehydration due to the inability to swallow liquids or their own saliva. These patients may be prone to hypotension from the vasodilation associated with the use of either agent. Ideally, rehydration should precede therapy with these agents. Sublingual niphedipine has been rarely implicated in cerebral or coronary insufficiency in patients with cardiovascular disease, so caution is warranted. Further Evaluation and Therapy
As with the use of glucagon, if nitrate therapy fails to produce symptomatic relief or resolve radiographic findings, its use does not preclude trying another method. If a patient experiences symptomatic relief, a post-procedure radiograph may be obtained to confirm passage of a radiopaque object, but this is not mandatory. The adult patient may be discharged home, but careful follow-up should be obtained to rule out coexistent esophageal pathology, as a significant number of patients will have underlying esophageal disorders. Gas-Forming Agents Pharmacology
The use of gas-forming agents for the treatment of distal esophageal food impactions, especially meat boluses, was first described in 1983. [84] The combination of tartaric acid solution followed immediately by a solution of sodium bicarbonate or even carbonated beverages was reported. In theory, the use of this acid-base mixture or of a carbonated beverage (e.g., Coca-Cola) may produce sufficient carbon dioxide to distend the esophagus, relax the LES, and push impacted food through the GE junction into the stomach. [85] [86] Indications and Contraindications
Gas-forming agents are indicated for the relief of smooth distal esophageal FB impactions, with or without prior FB confirmation by a radiographic study. They are often given to patients with food impaction or retained coins. Although gas-forming agents are more likely to succeed with distal esophageal impactions, they have also been successful in relieving obstructions in the proximal esophagus. Concurrent administration of spasmolytic agents may improve the effectiveness of gas-forming agents.[80] Use and Complications
A solution of 15 mL of tartaric acid (18.7 g/100 mL), followed by 15 mL of a sodium bicarbonate solution (10 g/100 mL), or 1.5 to 3 g of tartaric acid and 2 to 3 g of sodium bicarbonate dissolved in 15 mL of water can be used. [84] [85] Carbonated beverages (100 mL) have also been successful in the transit of FBs into the stomach. [84] [86] Many patients with esophageal FB impactions have been noted to retch after receiving gas-forming agents, which theoretically puts
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patients at risk for esophageal trauma. The only reported complication with the use of gas-forming agents for this indication was a mucosal tear of the esophagus (requiring surgical exploration to rule out mediastinitis) in a 66-year-old patient with an 18-hour-old esophageal impaction. [85] For this reason, gas-forming agents should not be given to patients with impactions of more than 6 hours duration or to patients with chest pain that might be indicative of an esophageal injury.
Further Evaluation and Therapy
As with the use of glucagon, nitroglycerin, or nifedipine, even if administration of the gas-forming agent is successful, as judged by relief of symptoms, follow-up evaluation is necessary to determine the underlying esophageal abnormality that potentially led to the FB impaction. Papain Papain is not recommended for treatment of an esophageal FB. It is a proteolytic enzyme that has been touted for dissolving meat impactions. [87] Papain is available commercially in a variety of meat tenderizers. This therapy has never been tested in a clinical trial. In vitro studies suggest that the commercial preparation may have no intrinsic proteolytic activity. [88] Although it is harmless when in brief contact with the normal esophagus, if it is left too long in the obstructed esophagus, papain may begin to dissolve the esophageal mucosa underlying a foreign body. [88] [89] This is likely to occur when the esophageal wall is ischemic owing to FB impaction and resultant wall pressure, when esophageal injury results from small bony spicules in the FB, or when an underlying lesion is responsible for the obstruction. The subsequent rupture and leakage of the proteolytic enzymes result in a self-perpetuating mediastinitis. Patients with esophageal FBs are at increased risk for aspiration, and pulmonary aspiration of papain results in acute hemorrhagic pulmonary edema. In general, papain is not currently recommended because of the unacceptable complication risk and the availability of safer, more effective interventions.
FOLEY CATHETER REMOVAL OF ESOPHAGEAL FOREIGN BODIES Introduction Foley catheter removal of esophageal FBs was first described in 1966 [90] and in the emergency medicine literature in 1981. [91] The technique is essentially unchanged since the first reports, and is now used by emergency clinicians, radiologists, otolaryngologists, and general surgeons. [92] [93] [94] [95] [96] The classic patient for this technique is a small child who is brought to the hospital shortly after swallowing a coin that is documented by radiograph, but the procedure may be used for a wide variety of smooth FBs in all ages of patients. Success rates for Foley catheter removal of FBs have been cited from 85% to 100%, with complication rates of 0 to 2%. [7] [67] [97] [ 98] [99] [ 100] Many of the reported complications were due to the nasal insertion of the catheter, and complication rates are lower when the catheter is inserted orally and at centers that perform the procedure frequently. Foley catheter extraction costs significantly less than endoscopy. [7] [101] Fluoroscopic assistance may be preferable, but it is not essential. Whether the procedure is performed in the ED or the radiology department, equipment and personnel capable of emergency pediatric airway management must be present. Indications and Contraindications Recently ingested smooth, blunt objects that are radiographically opaque are most suitable for balloon catheter extraction. Recently ingested FBs carry little likelihood of causing pressure necrosis, perforation, or other significant injury; however, 24 to 48 hours duration of impaction should be the upper limit for consideration of this technique. [7] [26] [102] Coins are particularily amenable to Foley manipulation, but food boluses and button batteries have also been extracted successfully. [93] Radiographically opaque objects are most easily located by plain radiographs. Radiolucent objects can be manipulated, but uncertainties about location mandate contrast esophagrams. Contraindications to catheter removal of esophageal FBs include total esophageal obstruction, as manifested by an air-fluid level on plain radiograph or contrast esophagram, or when patients are unable to handle oral secretions. The presence of a total obstruction prevents passage of the catheter tip distal to the FB. Esophageal perforation, as recognized by the typical symptoms and signs, requires immediate surgical consultation and precludes blind esophageal manipulation, as does airway distress. The presence of multiple esophageal FBs also precludes Foley catheter use. Sharp, irregularly shaped FBs should not be removed with this technique because esophageal perforation or laceration can result, and the balloon may burst during the procedure. Finally, lack of expertise or equipment to handle an airway problem arising during the procedure is a contraindication. Equipment The necessary equipment is basic and present in most EDs ( Table 40-5 ). Although never reported, airway obstruction during the procedure is the most feared potential complication. Thus, the proper equipment and personnel capable of managing airway obstruction must also be present, including suction devices. Forceps (bayonet and Magill) of various sizes should be available to extract the FB from the pharynx. Foley catheters ranging in size from No. 8 Fr with 3-mL balloons to No. 26 Fr with 30-mL balloons have been used. In settings in which both children and adults are treated, sizes ranging from 10 Fr to 16 Fr with 5- to 10-mL balloons should suffice. Child restraint devices (e.g., papoose board), topical anesthetics, or moderate sedation may be used.
TABLE 40-5 -- Equipment for Foley Catheter Extraction of Esophageal Foreign Bodies Standard resuscitation equipment for advanced airway management of children and adults Foley catheters (10 to 16 Fr) Topical anesthetics * Parenteral sedatives * Child restraint device * Fluoroscope* *Optional equipment.
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Procedure Every patient should be appropriately coached concerning the procedure. Young children should be restrained. Moderate sedation and nasopharyngeal topical anesthesia may be used; however, this may increase the risk of aspiration due to decreased airway protective reflexes. The patient is then placed in a head-down Trendelenburg, lateral decubitus, supine, or prone position. The procedure is often done under fluoroscopic guidance, although this is not mandatory if the FB has been localized on plain radiographs. Assuming the procedure is being performed on a young child, a 12 Fr to 16 Fr Foley catheter is used. After checking for symmetric balloon inflation, the balloon is inflated and the catheter is inserted orally ( Fig. 40-9 ). When using fluoroscopy, the catheter is visually passed distal to the FB. Intermittent inflation with 1 to 2 mL of contrast may be needed to verify the catheter tip location. If performed without fluoroscopy, the distance from nose or mouth to FB is estimated, and the catheter is inserted accordingly. On occasion, the operator feels the catheter tip passing the object. The balloon is slowly filled with 3 to 5 mL of saline or contrast agent (if fluoroscopy is used). Balloon inflation should be stopped if the patient complains of increased pain and the catheter should be repositioned before an attempt at reinflation. Fluid is preferable to air, as it is less compressible. Overdistention of the balloon is undesirable, and in children no more than 5 mL of fluid should be used.
Figure 40-9 Technique of Foley catheter extraction. In children, this procedure is best done with the patient restrained on a papoose board, or consciously sedated, with the head lowered. Some operators place the patient in a prone position or roll the patient to the prone position after catheter insertion to enhance oral expulsion of the foreign body. A, A catheter is inserted orally into the esophagus distal to the coin. A bite block may be used to assist oral passage. B, The balloon is inflated. Gentle traction moves the coin proximally through the esophagus. C, The coin is moved steadily past the glottis. D, The coin is present in the mouth to be expectorated or grasped. (Adapted from McSwain N: Esophageal foreign body. Emerg Med 21:85, 1989.)
The catheter with its balloon inflated beyond the FB is then withdrawn with steady, gentle traction. Contact with the object can be sensed as the friction of withdrawal increases. Significant impedance to traction requires termination of the attempt. If the catheter slides past the object without dislodging it, the balloon can be deflated and repositioned. An additional 2 to 3 mL can be used to enlarge the balloon and another attempt made. Often when the object reaches the hypopharynx, the balloon and gravity act in concert to fully externalize the FB. The patient can be instructed to spit it out or the operator can grasp the object with the fingers, forceps, or a
clamp. A follow-up radiograph may be necessary to exclude the possibility of multiple objects. If fluoroscopy is not used and no FB is retrieved, another radiograph should be obtained, because 10% to 20% of the time, the FB will pass distally into the stomach. [103] Multiple attempts should not be required if catheter size, placement, and balloon inflation are correct. Failed attempts are best followed by a change in one of the aforementioned parameters or repeat x-ray studies to confirm the continued presence of the esophageal FB before esophagoscopy. Complications Complication rates of 0% to 2% have been reported. [7] [67] [97] [98] [99] [100] Many complications (nosebleeds or displacement of the foreign object into the nose) have been related to the nasal
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insertion of the catheter. Complication rates are lower when the catheter is inserted orally and generally lower at centers that perform the procedure frequently. No deaths have been reported. One esophageal rupture has occurred. [100] Laryngospasm and aspiration are rare complications. Failure to either remove the object or displace it into the stomach occurs in approximately 2 to 10% of carefully selected patients, [98] [99] [100] but success rates are lower in adults or patients with underlying esophageal disorders. [100] Disposition Children who have a FB successfully removed by the Foley catheter need no further follow-up if they remain asymptomatic. If the FB was moved into the stomach, clinical follow-up should be adequate to verify movement of gastric FBs through the alimentary tract. Discharge instructions should include warnings about potential symptoms of gastrointestinal obstruction, perforation, and hemorrhage. Parents of children who swallow coins can be instructed to watch for coins in the stool. Adults with esophageal FBs that have been removed successfully must be referred for evaluation of possible esophageal pathology. Should a FB remain lodged in the esophagus, immediate referral for endoscopy is necessary.
ESOPHAGEAL BOUGIENAGE Background Displacement of esophageal FBs into the stomach can be done using naso- or orogastric tubes or esophageal bougienage. Esophageal bougienage is a technique for dislodging impacted esophageal coins by blind mechanical advancement of the coin into the stomach, a procedure first described in 1965. [104] The technique has a greater than 95% success rate with essentially no reported complications. [7] [68] [105] [106] Rates as successful as endoscopy have been reported. [102] Furthermore, bougienage is unrivaled in overall cost-effectiveness, approximating 10% of the cost of endoscopic removal. [7] [68] [102] [107] There have traditionally been warnings against forceful advancement of esophageal FBs, but growing evidence verifies the efficacy and safety of blind esophageal bougienage as first line therapy for coin ingestions in properly selected patients. Although early articles suggested that esophageal bougienage should be performed exclusively by pediatric surgeons, the technique is easily mastered and used by emergency clinicians and junior surgical residents. [68] [106] Indications and Contraindications Strict patient selection is paramount for successful and uncomplicated bougienage. The criteria have changed little since initially proposed and define a group in whom a round, smooth object can be forcibly passed into the stomach with little risk. [105] [108] While many swallowed objects meet this description, only coins hold clear supportive evidence in the literature. Selection criteria are the following: a single, smooth FB, lodged 3 g) bolus weights on some feeding tubes may be inconvenient to pass through the ostomy. Tubes that are approximately 90 cm (3 feet) long are appropriate for gastric feeding; tubes that are longer—108 to 112 cm (43 or 45 in)—are used for duodenal feeding. The feeding tube replacement technique is the same for pharyngostomy and esophagostomy. The outside of the tube tip can be lubricated with a small amount of water-soluble lubricant jelly. Mineral oil, which irritates the airways if aspirated, should never be used. The tip of the tube is inserted into the ostomy and directed caudally to ensure that it enters the esophagus and does not pass upward into the nasopharynx or mouth ( Fig. 41-16 ). The patient may be able to assist by attempting to swallow. The length of feeding tube required varies depending on the position of the ostomy and is several centimeters longer than the distance from ostomy to xiphoid. For duodenal feeding, the tube should be advanced about 20 cm beyond the distance from ostomy to xyphoid. If the feeding tube persistently exits the mouth during attempts at passage instead of passing down the esophagus, the following two techniques may prove useful. After insertion of the feeding tube a short distance into the ostomy, a flashlight is used to visualize the tube in the pharynx. The feeding tube is grasped slightly proximal to the end bulb using Magill forceps, and the end bulb is directed toward the esophagus in the posterior inferior pharynx. Once the tube is properly directed, it may be possible to advance the
Figure 41-16 Proper path for an esophagostomy or a pharyngostomy tube.
remainder of the tube through the external ostomy. Sometimes it is necessary to use the forceps to advance the entire length of the feeding tube. An alternative method is to allow the feeding tube placed through the ostomy to exit the mouth for the entire distance that must be passed down the esophagus. The end bulb of the tube is then directed into the posterior pharynx, and the patient is directed to swallow as for an orogastric tube. Toward the end of tube passage, it may be necessary to use a Magill forceps or to pull back the tube slightly at the ostomy to eliminate a short loop of extra tubing in the oropharynx. Tube replacement is more difficult in the first week after the creation of a pharyngostomy or an esophagostomy. A tract forms after the first week and helps prevent tissue dissection by the tube. The angle of a well-formed tract also encourages appropriate esophageal passage. A well-formed tract closes more slowly than a new ostomy, although in some people even a long-term ostomy may begin sealing within a few hours. If an ostomy is too narrow for the replacement tube, the ostomy should be stented with a narrower tube and the patient's surgeon contacted. Complications Complications of pharyngostomy and esophagostomy include local soft tissue irritation, accidental extubation because of excess length of the external tube, pulmonary aspiration from vomiting, arterial erosion with exsanguination, and esophagitis or stricture of the esophagus from reflux. Accidental pulmonary intubation is less common with cervical ostomy tubes than with NG tubes, at least partially because patients with cervical ostomies are more likely to be alert and have functioning cough reflexes. Auscultation and aspiration are still advisable techniques to check tube placement. Radiographic evaluation may also be necessary and is essential to confirm duodenal feeding.
GASTROSTOMY, GASTROENTEROSTOMY, DUODENOSTOMY, AND JEJUNOSTOMY TUBES The mid-19th century clinician Sedillot described the first functioning gastrostomy, which formed as a complication of a war wound. The gastrostomies performed by Sedillot on two patients resulted in peritonitis and death. [73] [74] The jejunostomy procedure was first performed by Surmay in 1879. It was not until the 1890s that further innovations in surgical technique allowed the gastrostomy to be popularized. The Witzel serosal-lined gastric tunnel technique ( Fig. 41-17 ) and the Stamm procedure of concentric pursestring sutures placed around the gastrostomy tube were developed in the 1890s. These two techniques prevent significant intraperitoneal gastric fluid leakage, a complication that had frequently resulted in the deaths of gastrostomy patients. Both Witzel and Stamm gastrostomies tend to close rapidly without a stenting gastrostomy tube. In the early 1900s, the tubular (Depage-Janeway) gastrostomy was developed. The Depage-Janeway gastrostomy results in the creation of a permanent mucocutaneous ostomy. Since the turn of the century, more than 30 different operative techniques have been described for tube gastrostomy. [49]
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Figure 41-17 A, Formation of the Witzel tunnel. B, Final catheter placement. (From Wiedeman JE, Smith VC: Use of the Hickman catheter for jejunal feedings in children. Surg Gynecol Obstet 162:69, 1986.)
Operative Indications and Contraindications Neurologic diseases constitute the most frequent indication for a gastrostomy tube. [52] Facial fractures, oropharyngeal trauma, and tracheal and laryngeal injuries may be indications for placement of a temporary feeding gastrostomy. Rare indications for gastrostomy include enhancement of nutrition by continuous feeding in severely debilitated patients who still are capable of oral intake, provision of a route for bile replacement in patients with an external biliary fistula, and the need for long-term gastric decompression. Indications for gastrostomy tube placement in children include neurologic diseases, facial reconstructive surgery for congenital deformities, and maxillofacial trauma. Young children who require long-term administration of unpalatable medications or dietary components may also require a gastrostomy. Tube duodenostomies are created almost exclusively for duodenal decompression after partial gastrectomy with Billroth II anastomoses. [73] Permanent jejunostomies are rarely used. Tube jejunostomy is indicated when the proximal bowel has a fistula or is obstructed, when recovery of small bowel motility is anticipated long before recovery of gastric motility, and after a gastrectomy. [49] [73] Contraindications for gastrostomy feeding include severe gastroesophageal reflux, upper gastrointestinal fistulas, repeated aspiration of gastric contents, and intestinal or gastric outlet obstruction. [49] Jejunal feeding is contraindicated if the highly osmolar feeding solutions required for jejunal feeding are poorly tolerated and cause copious diarrhea. Indications and Contraindications for Tube Replacement The nursing home patient with a nonfunctioning or dis-placed feeding tube represents a common ED presentation. The clinician cannot always determine the location of the original feeding tube by simply looking at the patient who arrives in the ED for tube replacement. Nevertheless, the emergency clinician should attempt to ensure that the terminal end of a replaced tube is in the same viscus as the original. External inspection may or may not reveal where a feeding tube should terminate. A de Pezzer (mushroom) or Foley gastrostomy tube is designed only for intragastric termination. Some tubes have two lumina, one terminating in the stomach for decompression and the other in the small bowel for feeding. These can be confused with tubes that have two entrances to one lumen (one for continuous feeding and the other for medications) and tubes that have a second lumen leading to an inflatable balloon. The clinician has a few options when faced with the task of replacing a feeding tube. Unfortunately, old records or nursing home personnel rarely give specific information that is helpful to the emergency clinician. If the tube is blocked, yet still present, a contrast study may demonstrate the final position of the tube. If only a stoma exists, one may request that the nursing home describe or send the prior tube to the ED. If a blocked tube is removed, it can be replaced with a similar device. If no surgical scar is seen at the stoma site, the tube is almost certainly a G tube, or a G tube that terminated in the jejunum. Placing a new tube followed by a contrast study usually settles the issue and allows the clinician to make decisions on balloon inflation, or possibly substitute a new device. When in doubt there is no downside of passing a Foley catheter without balloon inflation, taping it to the skin, and referring the patient to a consultant or the original referring clinician. It is unwise to avoid placement of some type of tube since the stoma will quickly close and may necessitate a more complicated procedure later. The only real concern of placing a gastric tube into the jejunum is that the balloon will produce intestinal obstruction if it is fully inflated. If the tube is nonfunctioning yet still in place, the clinician must make a judgment as to the risk versus benefit of removal and replacement versus an attempt at unclogging the tube (see subsequent section on unclogging). The major concern is that a new tube may be misplaced (i.e., into the peritoneal cavity) . If it appears that a skin incision was used to place the tube, it is unlikely that the patient has an easily removable tube. If the patient has signs of a complication (e.g., infection, ileus, intestinal obstruction), surgical consultation is warranted. Ease and safety of transabdominal feeding tube replacement depend on the surgical procedure performed and the length of time since placement of the feeding tube. For a simple gastrostomy, the insertion site of the tube through the gastrointestinal wall is sealed by either annular or plication sutures. The gastrointestinal wall is approximated to the peritoneum around the site of penetration to provide a further leakage barrier. The tube is then secured outside the abdominal wall. A Witzel tunnel is a serosal tunnel created when the feeding tube is placed alongside the viscus for a distance after exiting the viscus, and the bowel is pulled up over it along this distance and secured with sutures (see Fig. 41-17 ). [75] [76] In one type of Hickman catheter jejunostomy, the tube passes
807
through a Dacron cuff and a Witzel tunnel. [76] Reinsertion of a Hickman catheter through a tortuous, rough Witzel tunnel is unlikely to be simple. gastrostomy may have been placed without any attempt to affix the stomach to the abdominal wall.
[ 77]
A percutaneous
Nonoperative tube replacement techniques are safe only through an established tract between the skin and the bowel. Catheter replacement should not be attempted in the immediate postoperative period. A simple gastrostomy takes about a week to form a tract. [72] A Witzel tunnel may take up to 3 weeks after the operation to mature sufficiently for safe nonoperative tube replacement. A nonfunctional tube can still serve as the stent for the gastrostomy tract and should not be removed if it cannot be promptly and safely replaced. Equipment Gastrostomy tubes come in an unusually varied selection of styles and materials. Rubber, silicone, and polyurethane tubes are all in common use. Many gastrostomy tubes are designed with a flange or a crossbar (bumper) to anchor them in the stomach and prevent migration into the small bowel. A Foley catheter may be used as a replacement tube but it is more temporary, difficult to secure to the skin, and the latex balloon may be weakened by stomach acid. When possible, a dedicated feeding
tube should be used instead of a Foley catheter ( Fig. 41-18 ). Equipment for feeding tube insertion includes gloves, stethoscope, feeding tube, external bolster, lubricant, basin, and a syringe that fits the tube. Tincture of benzoin, tape, and absorbent dressing material may be used to dress the wound, although many are better left undressed. [78] Some feeding tubes require special plugs or connectors. Others need to be pinched with a clamp when not in use to prevent leakage. Some tubes are placed with the aid of accompanying guidewires or stents. For still others, it is necessary to use a clamp or hemostat, endotracheal tube stylet, urinary or uterine sound, laryngeal dilator (no. 14), guidewire, or other appropriate rod or support as an aid to tube passage ( Fig. 41-19A, B ). A stylet to assist introduction of de Pezzer catheters can be fashioned by cutting half the stylet from a 9 Fr pediatric chest tube inserter. The tip can be filed smooth. The device will be 10 to 12 cm long and can be inserted alongside the de Pezzer catheter and into its tip to distend and flatten the mushroom ( Fig. 41-20 ). Transabdominal Feeding Tube Removal A feeding tube may have to be removed because it is irreversibly clogged, leaking, or broken; persistently developing kinks; too large or too small; causing a hypersensitivity reaction; associated with an abscess; or not the appropriate length for feeding into the desired viscus. Before a new transabdominal feeding tube is inserted, the old tube must be removed. Most, but not all, tubes can be removed without endoscopy. It is imperative to know whether the tube in place is safe to remove before attempting to remove it. Standard de Pezzer or mushroom catheters that have been modified with bolsters or rings at the time of endoscopic or surgical insertion may no longer be safe to remove with traction. Tubes are occasionally secured with sutures or rigid internal bumpers or stays. It is rare, however, to encounter a tube that cannot be removed with traction. Recently placed feeding tubes may need to be left in until a tract has formed (1 to 2 weeks depending on the procedure) even if the tube is nonfunctional. The externally visible tube does not always reveal the internal stabilization (see Fig. 41-18 ). A simple Foley catheter gastrostomy is easiest to remove. Once the Foley balloon is deflated, the tube should slide right out. If the Foley balloon cannot be deflated, cutting the tube may allow the balloon to deflate. The catheter must not be cut so close to the abdomen that it will be impossible to maintain a grip on it for a traction removal if the balloon still does not deflate. The balloon also may be punctured to cause it to deflate. To puncture a Foley balloon, traction is applied to the catheter to draw the balloon up against the ostomy. Using the taut feeding tube as a guide, a 20- or 21-ga needle is passed along the tube to puncture the balloon. It may be necessary to try again on the other side of the catheter, because the balloon may be asymmetrically inflated, and contact with the needle may be established on one side and not the other. The clinician should be careful not to track away from the ostomy into the patient's abdominal wall or to cause separate punctures of the stomach. The balloon is allowed a minute to deflate before another attempt is made at traction removal. Large nondeflating balloons should probably be punctured, whereas small balloons may be removed with traction. Traction is an acceptable removal technique for feeding tubes that are secured by a small mushroom. A towel is placed over the orifice, and the clinician applies counterpressure with the flat part of the hand against the abdominal wall as the tube is placed under tension ( Fig. 41-21 ). This causes the tube and end mushroom to narrow, and the tube should come out easily. The inner crossbar, if present, may remain in the stomach when the rest of the feeding tube complex is removed by traction. Obstruction from the crossbar, which will pass in the stool, has yet to be reported for adults. In small children, obstruction is a possibility, and the crossbar should be removed by endoscopy.[77] [79] A local anesthetic may be useful in selected cases of feeding tube removal, especially when the tube is in some way secured subcutaneously—for example, by a Dacron cuff.[76] It may be difficult to remove a catheter accidentally caught by a fascial suture during operative closure. [80] Removal of gastrostomy tubes with moderate to large mushrooms may be easier if the mushroom is distended with a sound or stylet. The length of the gastrostomy tube should be known so that the sound may be inserted to the correct depth. Firm resistance should be noted at that point. Firm resistance at deeper depths represents pressure on the viscus wall and can result in viscus puncture. [59] The premeasured stylets that come with feeding devices are useful instruments for assisting in removal. This is particularly true of gastrostomy "buttons," whose ends resemble de Pezzer catheters. Because buttons come in a variety of lengths, it is important to have the proper stylet. Following elective permanent removal of a gastrostomy tube, a pressure dressing should aid in closure of the fistula. [59] If it is not possible to pull the inner bolster or mushroom out through the ostomy, it may be acceptable to cut the tube at the skin, push the remaining short stump into the stomach, and rely on later rectal passage. Although obstruction or impaction is infrequent, it can occur, and this alternative has the potential to be problematic with children or patients who have had previous impaction, potential for bowel obstruction,
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Figure 41-18 A, Various types of gastrostomy tubes. 1, Polyurethane catheter with collapsible foam flange (CORPAK MedSystems of Kentec Medical Inc, Irvine, CA). 2, Silicone catheter (American Endoscopy [Bard Interventional Products, Billerica, MA]). 3, Latex catheter with a movable external bolster and an internal mushroom or de Pezzer-type flange on the end (American Endoscopy [Bard Interventional Products, Billerica, MA]). 4, Balloon (Foley) catheter (Wilson-Cook Co., Winston-Salem, NC). B, A user-friendly gastrostomy tube is supplied by CORPAK MedSystems (Wheeling, IL). The tube is packaged with lubricant, a prefilled syringe for inflating the balloon, and an extension set. The color-coded inflation valve indicates tube size (12–24 Fr). The silicone tube uses a retention balloon and a movable bolster, similar in design to a Foley catheter. Note that the retention bolster is designed to prevent inward migration of the tube and is not to be an anchoring device sutured to the skin. C, Placement of the CORPACK feeding tube and inflation of the balloon. Note that the bolster on the external tube is advanced to the skin to secure the tube. D, A standard Foley catheter may serve as a more specialized feeding tube replacement. The latex balloon may deflate or be weakened by gastric acid; so, this catheter is not ideal for long-term use. In addition, unless the Foley catheter is secured to the skin, it may migrate and the balloon may cause a pseudo obstruction.
or stool-passing problems. Rigid or large internal mushrooms and bolsters, the very kind that cause the most difficulty with percutaneous removal, also are more likely to cause difficulty with rectal passage. In no case should a device be released into the gut with a long length of tubing attached. Remember that double-part tubes may have an additional length of tubing for duodenal or jejunal feeding that extends far past the inner bolster. Korula and Harma [81] reported the successful intestinal elimination of 63 of 64 gastrostomy tubes that were cut at the skin entrance and advanced into the stomach through the stoma. These cases included tubes with internal bumpers, and success occurred regardless of the nature of the patient's underlying medical disorder, age, or method of original tube placement. However, no patient had suspected obstruction or potential for obstruction (e.g., no prior radiotherapy, inflammatory bowel disease). The one lodged tube required endoscopic removal from the pylorus. In most cases, tube passage was documented by sequential radiographs, with a mean interval to passage of 24 days (range, 4 to 181 days). Some clinicians and surgeons may strongly condemn cutting off the tube at the skin, even when the risks posed by the procedure are very low. It is always advisable to contact
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Figure 41-19 A, An endotracheal tube stylet used to distend the flange of the de Pezzer catheter. B, A lubricated wooden cotton-tipped swab can also be used as a makeshift stylet.
the patient's private clinician before cutting the tube. In some cases endoscopic retrieval of the tube remnant will be preferred to allowing rectal passage, and the tube should not be cut until just before or during endoscopy to ensure that migration does not occur before endoscopy. Transabdominal Feeding Tube Replacement Dislodged tubes should be replaced as soon as possible. If a similar sized tube will not easily pass, it is preferable to replace
Figure 41-20 A modified pediatric chest tube inserter used to distend the flange of the de Pezzer catheter. The sharpened end of the inserter (trocar) has been rounded.
a dislodged tube with a smaller or temporary tube to maintain the patency of the tract, rather than wait for an ideal situation. The tract may close or narrow in a matter of hours, and it is very difficult to easily replace tubes that have been out for more than a day. Some clinicians will first gently explore the tract with a blunt probe, such as a cotton swab, to ascertain the patency and course of the tract ( Fig. 41-22A ). Gently dilating the ostium and carefully probing and dilating the tract with a hemostat may facilitate passage ( Fig. 41-22B ). It is emphasized that a false tract may be created with vigorous exploration or manipulation. Ideally the new tube slips into position with minimal force, but a number of attempts may be required to negotiate tissue planes and manipulate the tube into the proper position. A relaxed patient aids in placement. Injecting a local anesthetic into the opening of the tract may ameliorate pain. Systemic sedation/analgesia is seldom required but should be considered in the combative or extremely uncooperative patient. The clinician should not use excessive force to pass a tube since misplacement may result. It is not uncommon to precipitate some bleeding, and although this may be distressing to the patient or family, it is not a significant clinical issue. A Foley catheter is a simple gastrostomy tube to replace. After the tract opening and distal Foley catheter are lubricated, the Foley balloon's integrity is checked by inflation. The catheter is then inserted into the tract. Good placement can be recognized by easy passage, prompt borborygmi with 20 mL of air insufflation, and rapid return of stomach juices with aspiration. The balloon is then inflated with saline (30-mL balloons are best), and gentle traction is applied to draw the balloon against the stomach wall. Always inflate the Foley balloon with saline, because balloons inflated with air deflate more easily. Tube replacement is usually successful if the tube has not been dislodged for more than 4 to 6 hours. If passage is impossible, a radiologist may be consulted to advance the tube over a guidewire that has been passed through the tract using fluoroscopy.
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Figure 41-21 Gentle, firm traction (A), using the flat part of the opposite hand for countertraction, may remove most percutaneous endoscopic gastrostomy tubes, even those with internal mushroom bumpers (B).
An external bolster may be threaded onto the catheter. The external bolster is a ring or bar of material threaded onto a tube that creates a large bulge on the tube and prevents inappropriate ingress of the tube into the ostomy. The anchor must adhere strongly to the tube so that mild stress on the tube does not cause the bolster to migrate up the tube. The bolster can be salvaged from the old tube or constructed in a number of ways. An anchor may be made from the end nipple of a de Pezzer catheter. The ring from a 24 Fr catheter, taken off at its junction with the end nipple, fits snugly over a 22 Fr Foley catheter when the balloon is distended slightly. The nipple can be pushed forward to an anchoring position near the stoma. The nipple can be fixed in this position by fully distending the Foley balloon and applying a circle of adhesive tape just adjacent to the nipple on the stem on the
Figure 41-22 The tract of a feeding tube may close or become narrowed within a few hours after removal. When replacing a tube that has been removed, gentle probing of the tract of the previously placed feeding tube gives the clinician an idea of the patency and direction of the tract. In this case, a sterile cotton swab is gently advanced, being careful not to produce a false tract.
side away from the body. [82] Adhesive tape sticks better if the lubricant is removed and the stem is prepared with tincture of benzoin. An external anchor may be made from a segment of tube from a large rubber catheter ( Fig. 41-23 ). A segment approximately 3 cm in length is cut to form the bolster. Two diamond-shaped openings can be formed on both sides of the segment by bending the segment and clipping it with scissors on either side of the bend. The diameter of the holes should be slightly smaller than the catheter. A hemostat or a Kelly clamp can be inserted through both holes to grasp the external end of the gastrostomy tube, which can be bent in half—with some difficulty—to narrow its diameter ( Fig. 41-24 ). The hemostat can then pull the tube through the bolster, which can be threaded down the tube and anchored with tape as described previously ( Fig. 41-25 ). The outer crossbar should be located 1 cm away from the skin. [83] Contact between the crossbar and the skin promotes moisture entrapment and maceration. Too much tension on the gastrostomy tube can result in necrosis of the gastric wall where it abuts the inner mushroom or balloon. Proper placement of the external bolster helps avoid this complication ( Fig. 41-26 ). Many clinicians prefer mushroom or de Pezzer gastrostomy tubes, which are more difficult to replace than Foley catheters. The advantage of these catheters over Foley catheters is that the mushroom nipple keeps its shape more reliably than the Foley balloon, which tends to deflate. [67] Foley catheters also have a greater tendency to migrate internally and block the pylorus. [49] A Kelly clamp or other stylet can be placed through a side hole into the tip of a gastrostomy mushroom and used to elongate the end for easy passage through the gastrostomy (see Fig. 41-19 and Fig. 41-20 ). Lubrication of the mushroom may make it more difficult to maintain the stylet's position in the mushroom. Some stylets are suitable for passage down the catheter lumen to elongate the end. Tubes should never be forced through a stoma for replacement, because this can cause separation of the viscus from the external stoma and lead to viscus leak or tube misplacement. [59] The replacement tube provided in the ED does not have to be—and in a few cases should not be—the same type placed at surgery. The tube must be compatible with the feeding system, terminate in the same viscus, and fit through the ostomy. When a Witzel tunnel jejunostomy is created, the catheter most frequently used is a Broviac catheter.
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Figure 41-23 A, A 3-cm segment of thick latex tubing is cut from the proximal segment of a catheter. This segment is used to make an external bolster for a feeding tube and anchors the feeding tube, preventing unwanted ingress of the tube into the patient. B, A 3-cm segment of latex tubing is bent in half and cut to create a hole on each side of the segment.
An appropriate replacement is a lubricated polyurethane tube shortened to a total tube length of 30 to 40 cm. Although the polyurethane tube is strong enough to be used for tube replacement through the Witzel tunnel without a guidewire, Broviac (silicone) catheters are too pliant to be coaxed
Figure 41-24 A hemostat is inserted through the holes in the completed bolster and grasps the feeding tube. The end of the feeding tube has been folded to reduce its external diameter.
through the resistive tunnel. [76] Jejunal feeding tubes are generally advanced 20 to 30 cm into the jejunum. Jejunal feeding tubes may be placed through or alongside a decompressing gastrostomy. Original placement of the jejunal feeding tube is endoscopic. Replacement of these tubes also
Figure 41-25 The feeding tube is pulled through the bolster. The bolster is advanced to 1 cm above the skin of the external abdomen.
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Figure 41-26 A Foley catheter can always be used as a temporary feeding tube replacement (A). The thin-walled Foley balloon usually only remains inflated for a month or so, and a specialized feeding tube, such as the CORPAK (see Fig. 41-18 ) is preferred for long-term use. A bolster can be made to prevent inward migration of the tube. In this case the previously removed Foley catheter was used to make the bolster for the new one (B).
generally requires endoscopic assistance. [84] [85] [86] Fluoroscopic techniques can be used to help guide these tubes; however, these techniques are out of the realm of emergency practice. [48] Occasionally, feeding tubes are placed in the jejunum because of gastric ileus. [49] [87] If gastric ileus is no longer present, a gastrostomy tube may suffice. The rationale for jejunal feeding, risk of aspiration, and acceptability of gastric feeding to the primary clinician should be established before changing from a jejunal feeding tube to a feeding gastrostomy tube. Techniques discussed in the nasoenteric feeding section of this chapter (metoclopramide and right decubitus position) may in selected cases coax gastrostomy-placed feeding tubes into the small bowel. Gastric decompression tubes are either clamped or put at continuous drainage. [85] Verification of tube placement can be made radiographically using a fluoroscope or with a small amount of contrast material passed into the tube ( Fig. 41-27 and Fig. 41-28 ). In the latter scenario, a catheter-tip syringe is used to introduce water-soluble contrast solution (e.g., diatrizoate meglumine-diatrizoate sodium [Gastrografin]) into the tube. Barium is contraindicated. Generally 20 to 30 mL of water-soluble solution is adequate for documenting the intraluminal tube position. A supine abdominal film should be taken within 1 to 2 minutes of dye instillation to optimize gut visualization. Since the film must be quickly obtained, it is easiest to perform the injection in the radiology suite, followed by an x-ray. If the contrast material does not flow freely into the tube, the procedure should be terminated immediately and the position of the tube questioned. With proper positioning, contrast will outline the gut containing the tube (e.g., stomach with gastrostomy tube). An irregular or rounded blotch with wispy edges or streamers suggests peritoneal leakage. In questionable cases, dye injection can be performed under fluoroscopy. It should be noted that there is no universally agreed upon standard of care with regard to performing a confirmatory contrast study for all easily replaced feeding tubes. Some clinicians verify position routinely with a contrast radiograph while others use the clinical criteria outlined earlier. The editors advocate a cautious and conservative approach. The routine use of post placement contrast radiography to confirm proper placement should be considered when the tube tract is immature (i.e., 30 mm Hg) on the esophagus for long periods of time can result in mucosal ischemia and may induce esophageal necrosis. [15] Therefore, it is recommended that periodic deflation of the esophageal balloon be undertaken for approximately 5 minutes every 6 hours. If bleeding can be controlled with an intraesophageal balloon pressure of 25 mm Hg, this pressure is generally maintained for the next 12 to 24 hours. [15] [20] The pressure in the esophageal balloon can transiently vary with respiration and esophageal spasm. This may result in intermittent increases in the measured pressure of 30 mm Hg above baseline, although this should only be for transient periods. If it remains high, air must be removed until the pressures are acceptable. If a 3-lumen GEBT tube has been used, it will not have an esophageal aspiration port. Because the amount of oropharyngeal and esophageal secretions can exceed 1500 mL/day, additional suction proximal to the esophageal balloon must be provided. [15] This can be done with a standard 14 to 16 Fr NG tube passed to a position measured or calculated to be just above the esophageal balloon. This should be placed even if the esophageal balloon is not maintained in an inflated position, because an inflated gastric balloon will also interfere with the ability to swallow or pass secretions. Once satisfactory positioning of the GEBT tube has been confirmed, the tube is generally then not disturbed for some 24 hours, unless necessary due to complications.[15] During this time, adjunctive therapy is ongoing and additional evaluation instituted. [20] These tubes are very uncomfortable, and patients should be provided with analgesics and sedation. In addition, soft restraints are needed on the arms to prevent the patient from dislodging the tube. If the bleeding does not remain controlled, other therapeutic interventions must be considered. These include endoscopic interventions with sclerotherapy, as well as emergency surgery. If these are not available, patient transfer may be necessary. [12]
COMPLICATIONS Complications associated with the use of GEBT tubes are frequent and often very serious. [22] Mortality rates are high with patients in need of these devices. Table 42-1 lists both major and minor complications. Major complications have been reported to occur in 8% to 16% of patients. [2] Mortality directly related to use of these tubes is generally reported to be 3%. [15] [22] However, one study reported the GEBT tube directly caused death in 22% of the patients in which it was used. [7] This must be considered in the context that variceal hemorrhage itself carries a 20% to 80% overall mortality. [20] Therefore, use of a GEBT tube is sometimes viewed as a desperate measure for a desperate disease process. GEBT tubes can be temporizing or even life-saving, but the high associated complication rate requires an individual risk-benefit analysis for each patient in whom it is being considered. Aspiration pneumonitis is probably the most frequent major complication. [22] This can result from aspiration of oral secretions, gastric contents, or, most commonly, blood. [2] The volume of aspiration can be substantial, and associated deaths
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Complications Common Major
TABLE 42-1 -- Complications of Esophageal Balloon Tamponade Therapy Uncommon
Aspiration pneumonia
Esophageal perforation
Asphyxiation
Duodenal rupture
Esophageal necrosis
Tracheobronchial rupture Periesophageal abscess Mediastinitis
Minor
Gastroesophageal ulceration
Epistaxis Pharyngeal erosions
Regurgitation
Pressure necrosis of tongue
Chest discomfort Back pain
Hiccups
Pressure necrosis of nose or lip have been reported. [2] [7] The likelihood of this complication can be decreased by evacuating the stomach prior to placement of the GEBT tube and having a low threshold for tracheal intubation to protect the airway. [19] Asphyxia owing to airway obstruction has been reported to occur with dislodgment of the tube such that the esophageal balloon migrates into the oropharynx. [2] [5] This is more likely when the tube is passed through the nares such that the inflated esophageal balloon cannot pass through the nasopharynx, and it is one of the reasons that oral placement is preferred. Tube migration can be prevented by maintaining full inflation of the gastric balloon through periodic monitoring of pressures and radiographic reconfirmation. Of course, airway obstruction can be completely prevented by prophylactic tracheal intubation. If the tube suddenly migrates, resulting in an airway obstruction in a nontracheally intubated patient, the balloons must be immediately deflated and the tube extracted. This can be achieved most quickly by cutting across all of the tube lumens just distal to the bifurcation points. This will immediately vent all of the balloons, and the entire tube can be extracted. For this reason, it is recommended that surgical scissors be kept available at the patient's bedside whenever a GEBT tube is in place. The other relatively common major complication is esophageal perforation or rupture. [7] [8] This occurs with overinflation of a misplaced gastric balloon and can be prevented through careful employment of the placement steps already outlined. However, this can also occur as a result of esophageal mucosal necrosis caused by excessive or prolonged pressure in the esophageal balloon. Crerar-Gilbert reported a case of massive esophageal rupture with the use of balloon tamponade and associated sclerotherapy. [9] The treatment is immediate removal of the GEBT and initiation of diagnostic studies (e.g., contrast swallow) and broad-spectrum antibiotics (for potential mediastinitis). Again, risk for this complication can be decreased by periodic deflation of the balloons at 6-hour intervals and limiting the amount of pressure in the esophageal balloon to the minimum amount necessary to control bleeding. This problem is also more common when the balloons are left inflated for more than 24 hours. [15] Common minor complications include pain, discomfort, and local pressure effects of gastric or esophageal erosions or mucosal ulcers. [6] [22] These latter can be minimized by frequently checking and optimizing tube position to minimize pressure on the nasal or oral mucosa, the tongue, and other structures. Although less common, other complications can occur; these are also listed in Table 42-1 .[1] [13] [16] [17] [22]
INTERPRETATION GEBT tubes are used to temporarily control bleeding varices. This is assessed by monitoring the rate of blood aspirated from the gastric and esophageal ports after tube placement. It is not uncommon for the GEBT tube to fail to control the hemorrhage. [14] [15] [20] When significant bleeding continues, consider correctable causes, which include malpositioned balloons, inadequate balloon pressures, and misdiagnosis of the site of bleeding (e.g., a duodenal ulcer instead of variceal source). [7] [15] When these have been addressed but bleeding continues, other therapeutic options must be considered, including sclerotherapy, angiographic embolization, and surgery (see Fig. 42-3 ). [12] [20]
CONCLUSION Gastroesophageal balloon tamponade is an uncommon procedure in general, and particularly for emergency clinicians. Some emergency clinicians may not have performed this procedure previously. However, the procedure can temporarily control an exsanguinating hemorrhage from gastric or esophageal varices in about 80% of patients when other options are unsuccessful or unavailable. As such, the emergency clinician may periodically be called upon to place a balloon tamponade tube. Because of the high incidence of associated serious complications, the procedure should be used in carefully selected patients in whom the potential benefit is favorable, given the risk of exsanguination. Each hospital is unlikely to stock more than one tube type, and this may not be the type most familiar to the clinician. However, currently most balloon tamponade tubes are fairly similar and are packaged with a complete set of instructions. These instructions must be carefully reviewed before tube placement. There can be great difficulty locating these tubes within the hospital when they are suddenly needed, so advance planning is recommended, when possible. The most serious common complications are those of aspiration and airway occlusion. [22] A low threshold for prophylactic tracheal intubation is recommended. The most serious iatrogenic complication is due to balloon inflation of a misplaced tube, with resultant esophageal rupture. This is avoidable by carefully following the instructions and insisting on radiographic confirmation of tube position before fully inflating the balloons.
Acknowledgment
The author and editors acknowledge the contributions made to this chapter by Jonathan M. Glauser, MD, in earlier editions of this textbook.
References 1. Akgun
S, Lee DW, Weissman PS, et al: Hemoptysis and tracheoesophageal fistula in a patient with esophageal varices and Sengstaken-Blakemore tube. Am J Med 85:450, 1988.
2. Bauer
JJ, Kreel I, Kark AE: The use of the Sengstaken-Blakemore tube for immediate control of bleeding esophageal varices. Ann Surg 179:273, 1974.
823
3. Boyce
HW Jr: Modification of the Sengstaken-Blakemore balloon tube. N Engl J Med 267:195, 1962.
4. Burcharth 5. Butler
F, Malstrom J: Experiences with the Linton-Nachlas and the Sengstaken-Blakemore tubes for bleeding esophageal varices. Surg Gynecol Obstet 142:529, 1976.
ML: Variceal hemorrhage: A review. Milit Med 145:766, 1980.
6. Chojkier
M, Conn HO: Esophageal tamponade in the treatment of bleeding varices: A decade's progress report. Dig Dis Sci 25:267, 1980.
7. Conn
HO: Hazards attending the use of esophageal tamponade. N Engl J Med 259:701, 1958.
8. Conn
HO, Simpson JA: Excessive mortality associated with balloon tamponade of bleeding varices: A critical reappraisal. JAMA 202:587, 1967.
9. Crerar-Gilbert
A: Oesophageal rupture in the course of conservative treatment of bleeding oesophageal varices. J Accid Emerg Med 13:225, 1996.
10.
Dave P, Romeu J, Messer J: Upper gastrointestinal bleeding in patients with portal hypertension: A reappraisal. J Clin Gastroenterol 5:113, 1983.
11.
Edlich RF, Lande AJ, Goodale RL, et al: Prevention of aspiration pneumonia by continuous esophageal aspiration during esophagogastric tamponade and gastric cooling. Surgery 64:405, 1968.
12.
Feneyrou B, Hanana J, Daures JP, et al: Initial control of bleeding from esophageal varices with the Sengstaken-Blakemore tube. Am J Surg 155:509, 1988.
13.
Goff JS, Thompson JS, Pratt CF, et al: Jejunal rupture caused by a Sengstaken-Blakemore tube. Gastroenterology 82:573, 1982.
14.
Gostout CJ: Acute gastrointestinal bleeding: A common problem revisited. Mayo Clin Proc 63:596, 1988.
15.
Hermann RE, Traul D: Experience with the Sengstaken-Blakemore tube for bleeding esophageal varices. Surg Gynecol Obstet 130:879, 1970.
16.
Juffe A, Tellez G, Eguaras MG, et al: Unusual complication of the Sengstaken-Blakemore tube. Gastroenterology 72:724, 1977.
17.
Kandel G, Gray R, Mackenzie RL, et al: Duodenal perforation by a Linton-Nachlas balloon tube. Am J Gastroenterol 83:492, 1988.
18.
Kline JJ: Modification of the adult Blakemore tube for use in children with bleeding esophageal varices. J Pediatr Gastroenterol Nutr 5:153, 1986.
19.
Mandelstam P, Zeppa R: Endotracheal intubation should precede esophagogastric balloon tamponade for control of variceal bleeding. J Clin Gastroenterol 5:493, 1983.
20.
Matloff DS: Treatment of acute variceal bleeding. Gastroenterol Clin North Am 21:103, 1992.
21.
Meeroff JC: Management of massive gastrointestinal bleeding. Hosp Pract 21:154, 1986.
22.
Panes J, Teres J, Bosch J, et al: Efficacy of balloon tamponade in treatment of bleeding gastric and esophageal varices. Dig Dis Sci 33:454, 1988.
Paquet KJ, Feussner H: Endoscopic sclerosis and esophageal balloon tamponade in acute hemorrhage from esophagogastric varices: A prospective, controlled randomized trial. Hepatology 5:580, 1985. 23.
24.
Sengstaken RW, Blakemore AH: Balloon tamponade for the control of hemorrhage from esophageal varices. Ann Surg 131:781, 1950.
25.
Smith JL, Graham DY: Variceal hemorrhage: A critical evaluation of survival analysis. Gastroenterology 82:968, 1982.
26.
Stump DI, Hardin TC: The use of vasopressin in the treatment of upper gastrointestinal hemorrhage. Drugs 39:38, 1990.
27.
Teres J: Balloon tamponade versus endoscopic sclerotherapy in the management of acute variceal hemorrhage. Hepatology 10:393, 1989.
28.
Trudeau W, Prindiville T: Endoscopic injection sclerosis in bleeding gastric varices. Gastrointest Endosc 32:264, 1986.
29.
Weissberg J, Stein DT, Fogel M, et al: Variceal bleeding: Does it matter to the patient whether his gastric or esophageal varices bleed? Gastroenterology 86:1296, 1984.
30.
Westphal K: Uber eine Kompressionsbehandlung der Blutungen aus Osophagusvarizen. Dtsch Med Wochenschr 56:1135, 1930.
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Chapter 43 - Decontamination of the Poisoned Patient Christopher P. Holstege Alexander B. Baer
The presentation of poisoned patients to the emergency department (ED) is a common occurrence. In 2000, the Toxic Exposure Surveillance System of the American Association of Poison Control Centers reported 2,168,248 toxic exposures and 920 resultant fatalities. [72] Of these total exposures, 264,526 (12.2%) were managed in a health care facility. A massive exposure to some very toxic agents (such as cyclic antidepressants, cardiovascular preparations, colchicine, cocaine, carbon monoxide, chloroquine, iron, cyanide, amanita mushrooms, paraquat, and many others) will likely result in severe morbidity or a fatality regardless of even the most sophisticated and timely medical intervention. With general supportive care and the use of a few specific antidotes, however, the mortality rate of unselected overdose patients is only 1% to 2% if the patient arrives at the hospital in time for the clinician to intervene. The management of poisoned patients presenting to health care facilities initially focuses on confirming the diagnosis of a possible toxin exposure, providing standard cardiovascular and respiratory supportive care, and the use of a small cadre of specific antidotes. In selected instances, the prevention of further toxin absorption by various decontamination procedures may theoretically ameliorate morbidity or reduce mortality. Although a better final outcome from gastric decontamination may seem intuitively reasonable, there is no definitive evidence from prospective clinical trials proving that the use of various decontamination techniques positively alters the morbidity or mortality of the poisoned patient. Before the availability of objective, experimental evidence addressing gastric emptying procedures, most clinicians instituted such procedures in the ED as a reflex response for the majority of patients suspected of drug overdose, often without much forethought, and certainly without confirming data. Significant controversy exists concerning the need for routine gastric emptying in the poisoned patient, and mounting evidence relegates any form of gastric decontamination to selected cases and individual specific scenarios. At this time, it is the editors' opinion that there is no universally accepted standard of care that mandates any form of gastric decontamination as a routine medical intervention in the patient suspected or proved to have been exposed to a toxic substance. (Note: This statement does not apply to ocular or dermal decontamination issues.) Nonetheless, there may a selective role for gastric decontamination, and there will always be a role for clinical judgment. Since compelling circumstances may call for gastric decontamination, this chapter will discuss specific clinical procedures. These techniques include syrup of ipecac-induced emesis, gastric lavage, oral activated charcoal administration, and whole-bowel irrigation (WBI). Before performing these techniques, the clinician responsible for the care of the poisoned patient must clearly understand that these procedures are not without hazards, and any decision on their use must consider whether the benefit of decontamination outweighs any procedure-related harm.
GASTRIC DECONTAMINATION Ipecac-Induced Emesis Background
Syrup of ipecac is available as a nonprescription product in many countries, including the United States. It is prepared from the dried rhizome and roots of the Cephaelis ipecacuanha or Cephaelis acuminata plant, both of which contain the alkaloids emetine and cephaeline. These alkaloids are potent emetics inducing vomiting by both direct local gastrointestinal effects and central nervous system actions. Emesis following syrup of ipecac ingestion typically occurs within 20 minutes of ingestion and persists for 30 to 120 minutes. [91] There have been numerous animal and human volunteer studies examining both the efficacy of syrup of ipecac to expel specific ingested agents from the stomach and its ability to decrease serum drug levels. [1] [20] [33] [35] [37] [47] [65] [84] [126] [129] [132] [137] [140] [146] In these studies, the amount of marker removed by syrup of ipecac was highly variable. Syrup of ipecac's efficacy at expelling experimental markers decreased as the administration time postingestion increased. Syrup of ipecac is of very limited benefit if more than 60 to 90 minutes have elapsed since the time of ingestion. Although syrup of ipecac may be effective in reducing the quantity of a drug absorbed, no studies have demonstrated that its use improves patient outcome. [65] [69] [87] [106] Saetta et al suggested in their study that syrup of ipecac may actually enhance gastric emptying and potentially facilitate drug absorption. [116] Ipecac use may delay the use of, or reduce the effectiveness of, other methods of decontamination. Indications
The administration of ipecac in the ED is rarely indicated. Although theoretically some indications may arise in the ED, there is no standard of care that mandates its use in the management of the poisoned patient in the hospital. Even the historical use of ipecac-induced emesis in the home, prior to definitive medical intervention, has been questioned. The position statement written by the American Academy of Clinical Toxicologists and the European Association of Poisons Centres and Clinical Toxicologists ( Fig. 43-1 ) declared that the routine administration of ipecac in the ED should be abandoned. [67] Bateman's review stated that "ipecac is effectively obsolete" in the management of the poisoned patient. [13] Whether specific subsets of poisoned (e.g., iron, lithium, mushroom) patients may benefit from syrup of ipecac has not been clearly delineated. If syrup of ipecac is administered to a patient, it should be given only to an alert, conscious patient who has ingested a potentially toxic amount of a poison no more than 60 minutes before administration. Contraindications
The administration of syrup of ipecac is contraindicated in any person who demonstrates compromised airway protective reflexes or has the potential to lose such protective reflexes.[66] Its use should be avoided in persons who have ingested substances that could result in coma, seizures, cardiovascular collapse, or paralysis. Syrup of ipecac is also contraindicated in persons who have ingested corrosive substances (acids or
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Figure 43-1 Position statement: ipecac syrup. (From the American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. Published in Clin Toxicol 35:699, 1997.)
alkalis), hydrocarbons, or foreign bodies that could potentially result in airway obstruction. Caution should be exercised in using syrup of ipecac in patients who have medical conditions that could be further compromised by the induction of emesis, such as patients with bleeding diatheses. Technique
Syrup of ipecac is sold in packages of 15 mL and 30 mL. It is administered orally in the following dosages: • 0 to 6 months: No ipecac. • 6 to 12 months: 10 mL ipecac plus 120 to 240 mL clear liquids. • 1 year to 12 years: 15 mL ipecac plus 120 to 240 mL of clear liquids and repeat 15 mL ipecac if no vomiting occurs within 20 minutes of the first dose. • Older than 12 years: 30 mL ipecac plus 240 mL of clear liquids and repeat 30 mL ipecac if no vomiting occurs within 20 minutes of the first dose. Complications
The most commonly reported complications of ipecac administration include diarrhea, lethargy, and prolonged vomiting. [28] [36] [73] Other reported complications include pulmonary aspiration of gastric contents, bradycardia, cerebral hemorrhage, gastric rupture, gastric diaphragmatic herniation, Mallory-Weiss tear, and pneumomediastinum.[62] [63] [68] [115] [127] [135] [145] Prolonged emesis may result in the inability to subsequently administer charcoal. Gastric Lavage Background
Reports of the use of gastric lavage in the poisoned patient dates as far back as the early 19th century. [26] [58] Numerous animal and human volunteer studies have been conducted examining the effectiveness of gastric lavage in removing toxins from the stomach, especially in comparison to other gastrointestinal decontamination methods.[7] [10] [21] [25] [32] [33] [126] [129] [137] [143] [146] The reported efficacy of gastric lavage in removing markers from the stomach varies significantly in these studies. The difference in these study results is due in part to the variability of the methods used (different fluid instilled markers, animal models, positioning, amount of lavage and lavage tube sizes) and the time that elapsed from the instillation of the marker in the stomach until gastric lavage was performed. Even within individual studies, the range of effectiveness of gastric lavage to remove the marker varied considerably. For example, Tandberg et al performed gastric lavage 10 minutes after ingestion of the marker and reported its effectiveness to remove the marker varied from 18.9% to 67.7%. [126] There is a possible theoretical benefit of gastric lavage for the evacuation of a toxic liquid from the stomach. Grierson et al, however, were unable to demonstrate a significant benefit of an optimal lavage 1 hour after the ingestion of liquid acetaminophen, further casting doubt on the benefit of the procedure in the clinical scenario. [50] Many of these studies do not replicate the typical clinical scenario encountered in emergency medicine. [79] The efficiency of gastric lavage to remove a marker significantly decreases with increasing time following ingestion. This is due to the fact that as time increases after ingestion, the more time there is for the marker to be absorbed and for the marker to pass out of the stomach. For example, Shrestha et al reported that greater than 70% of the marker used in their study passed out of the stomach by 60 minutes.[123] It is rare that gastric lavage can be performed within the first hour after toxic ingestion. Not only does it take time for these patients to present to the ED, but it also takes time for evaluation, stabilization, and for the gastric lavage to take place. For example, Watson et al reported that the mean time required by experienced emergency medicine nurses to perform lavage was 1.3 hours. [143] Gastric lavage may also propel the marker from the stomach into the small
intestine, decreasing the effectiveness of removing the toxin from the stomach and enhancing the rate of absorption. [116] Gastric lavage is still considered as a potentially advantageous procedure because, to date, there have been no controlled studies that have included enough patients with confirmed life-threatening ingestions to adequately evaluate lavage versus no lavage. Only three major studies have been performed examining whether gastric lavage positively influences the outcome of poisoned patients. [69] [87] [106] In a study performed by Kulig et al, there was no difference in outcome among patients who received gastric lavage followed by charcoal vs charcoal alone when these were performed >1 hour after ingestion. [69] In patients who were treated within 1 hour of ingestion, gastric lavage followed by charcoal provided a small but statistically significant advantage over activated charcoal alone. Merigian et al, demonstrated that for symptomatic patients, the rate of intensive care admission and the need for intubation was significantly higher for those patients who received gastric lavage followed by charcoal than for those who received charcoal alone. [87] This increased admission and intubation rate was directly attributed to the aspiration of gastric contents owing to gastric lavage. Pond et al replicated the Kulig study. They found no difference in outcome between those who received gastric lavage followed by charcoal versus charcoal alone, regardless of time of performance of gastric lavage. [106] They concluded that "gastric emptying procedures can be omitted from the treatment regimen for adults after acute overdose, including those who present within 1 hour of overdose and those that manifest severe toxicity."
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Indications
Based on the available literature, gastric lavage should not be routinely used in the management of poisoned patients [138] ( Fig. 43-2 ). There is no universally accepted standard of care that can be applied to the use of gastric lavage in the unselected poisoned patient in the ED. Because there may be a theoretical benefit from gastric emptying, usually by lavage, under certain circumstances, a listing of circumstances that may increase the appropriateness of gastric emptying appears in Table 43-1 (Table Not Available) . It is stressed that these indications are theoretical, not evidenced based, and are the opinion of one toxicology textbook. Whether specific subsets of overdose patients may benefit from gastric lavage has not been clearly defined. Only patients who have ingested a potentially life-threatening amount of poison where the procedure can be performed within 60 minutes should be considered candidates for gastric lavage. Oral charcoal alone is considered superior to gastric lavage if a drug is adsorbed by charcoal. Contraindications
Although generally safe, gastric lavage is not an innocuous procedure. The performance of gastric lavage is contraindicated in any person who demonstrates compromised airway protective reflexes unless they are intubated. Many clinicians opt for lavage in a seriously ill patient who is intubated, because airway protection is already accomplished. Tracheal intubation, however, does not ensure a totally protected airway. Paralyzing and intubating a patient merely to initiate gastric lavage is generally eschewed. Gastric lavage is contraindicated in persons who have ingested corrosive substances (acids or alkalis), hydrocarbons (unless containing highly toxic substances such as paraquat, pesticides, heavy metals, halogenated and aromatic compounds), known esophageal strictures, or history of gastric bypass surgery. Caution should be exercised in performing gastric lavage in patients who have medical conditions that could be compromised by performing this procedure, such as patients with bleeding diatheses, and in combative patients.
Figure 43-2 Position statement: gastric lavage. (From the American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. Published in Clin Toxicol 35:711, 1997.)
TABLE 43-1 -- Factors that Cumulatively Increase the Appropriateness of Gastric Emptying (Not Available) From Smilkstein MJ: Techniques used to prevent gastrointestinal absorption of toxic compounds. Goldfrank's Toxicologic Emergencies, 7th ed., New York, NY. McGraw Hill, 2002.
Equipment and Preparation
If the decision is made to perform gastric lavage, careful attention to the details of the procedure results in increased safety for the patient and more effective removal of the ingested poison. Before lavage, the patient should have IV access secured and should have continuous cardiac monitoring and pulse oximetry. A large, rigid suction tip should be immediately available. If the level of consciousness is significantly depressed or the patient's airway-protective reflexes are diminished, the airway should be protected with a cuffed endotracheal tube before initiation of gastric lavage. If the patient is highly anxious or agitated, small doses of a benzodiazepine (e.g., 1 to 2 mg midazolam IV) may be given. If the airway status is questionable, or has the potential to be compromised during the procedure, rapid-sequence induction and intubation should be considered. If patients are fully alert and awake, lavage may be done without tracheal intubation. The procedure should proceed deliberately without significant patient resistance. The procedure is intended to be therapeutic, not punitive. Antiquated arguments promulgating that a noxious lavage will keep patients from overdosing again should be abandoned. The position of the patient during gastric lavage is important. All patients should be placed in the left lateral decubitus position with the head down (approximately 20° tilt on the table) ( Fig. 43-3 ). This position diminishes the passage of gastric contents into the duodenum during lavage and decreases the risk of pulmonary aspiration of gastric contents
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Figure 43-3 The effect of patient positioning on lavage. The left lateral decubitus position is preferred.
should vomiting or retching occur. The uncooperative patient's hands should be restrained to prevent removal of the gastric or endotracheal tube. Intubated patients on a ventilator may be lavaged in the supine position because of logistical reasons. Under no circumstances should the nonintubated patient undergo lavage in the restrained supine position. Such positioning invites aspiration and diminishes the patient's natural protective maneuvers, such as coughing and sitting up. Most clinicians prefer the oral route for gastric lavage, but in selected circumstances, a standard large-bore nasogastric (NG) tube (Salem sump pump) may be used. Large-diameter gastric hoses with extra holes cut near the tip have been traditionally recommended for gastric lavage ( Fig. 43-4 ). There are no convincing data on humans to refute or support this recommendation, and one study of a small number of dogs failed to show any difference in efficacy with lavage through a 32 Fr tube
compared with a 16 Fr lavage tube. [41] It is generally held that large-diameter NG or orogastric tubes (>1 cm) are more likely to retrieve particulate matter successfully. Smaller, more flexible tubes may kink and are significantly more difficult to pass. An NG tube may be passed through the mouth or nose, but orogastric hoses should not be passed through the nose. Because most pills disintegrate in the stomach in a few minutes, significant amounts of particulate matter may be retrieved with a large-bore NG tube, such as an 18 Fr Salem sump tube. Nasogastric tubes are considerably easier to pass, and are less traumatic for the patient (see Chapter 41 ). Nasogastric tubes are preferred for liquid ingestions.
Figure 43-4 A large-diameter gastric tube. Note the extra side holes that have been cut near the tip. This is a theoretical advantage over a standard tube or a nasogastric tube. For small pill particles and liquids, a large-bore nasogastric tube may suffice.
In most cases a 36 to 40 Fr or 30 English gauge tube (external diameter 12 to 13.3 mm) should be used in adults and a 24 to 28 Fr gauge (diameter 7.8 to 9.3 mm) tube in children. [138] (See discussion of pediatric issues in Fig. 43-5 .) Before passage, the length of the tube required to enter the
Figure 43-5 Gastric lavage in a child is always problematic. Obviously, an adult-sized large-bore oral gastric tube cannot be used, but a nasogastric (NG) tube may suffice. Some pediatric textbooks recommend a 24 Fr oral gastric tube for toddlers, and a 36 Fr tube for adolescents. In this case, a child was found with an open bottle of digoxin, and it could not be determined if ingestion had occurred. She would not drink charcoal. The 18 Fr NG tube was used to attempt to aspirate digoxin from the stomach (none was recovered) and to instill charcoal. Some would suggest the oral route for this tube, but it was passed rather easily through the nose. An NG tube is not ideal for some ingestants (iron, sustained-release products), but most pills quickly dissolve in the stomach and the small particles can easily be removed with an NG tube. Although lavage may have been reasonable in this scenario, a potent and safe antidote for digoxin does exist. The common routine practice of passing an NG tube in a child who is unwilling to drink charcoal is controversial and likely done far too often for benign ingestions. (Reprinted with permission from Elsevier [The Lancet, vol 338 (8778), 1991, pp 1313–1315].)
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stomach should be estimated by approximating the distance from the corner of the mouth to the mid-epigastrium; premeasurement avoids the curling and kinking of excess hose in the stomach ( Fig. 43-6 ). Passage of an excessive length of hose may cause gastric distention, bruising, and perforation, whereas passage of an insufficient length of hose may result in lavage of the esophagus and the increased risk for emesis and aspiration. Commercial lavage systems are available and often use either a gravity fill-and-empty system with a Y connector (e.g., Travenol, Ethox) or a closed irrigation syringe system. Alternatively, an irrigation syringe can be used for intermittent lavage fluid input and withdrawal. Technique
In most cases gastric lavage should be performed through an orogastric tube. Use of a standard NG tube may be adequate if only small pill fragments are present, but an NG tube is associated with two problems: It is of insufficient bore to produce satisfactory lavage of large particulate matter, and the larger bore tubes may cause epistaxis or damage to the turbinates. The latter problem may be obviated by oral passage. The gastric tube should be lubricated and passed gently to avoid damage to the posterior pharynx. A bite block or an oral airway should be used to avoid chewing of the orogastric tube and biting of the fingers of the inserter. If the patient is obtunded or paralyzed, the clinician may extend the jaw to facilitate passage. Force should never be used to pass the tube. Putting the patient's chin on the chest can facilitate passage of the tube into the esophagus once the pharynx has been entered ( Fig. 43-7 ). Cough, stridor, or cyanosis indicates that the tube has entered the trachea; the tube should be withdrawn immediately and passage reattempted. Once the tube is passed, its intragastric location should be confirmed. Intragastric placement is usually evident on clinical grounds, and confirmed by auscultation of the stomach during injection of air with a 50-mL syringe and aspiration of gastric contents. In
Figure 43-6 Failure to premeasure a lavage tube before passage is a common error. Here a piece of tape marks the depth of proper passage to ensure that the tip is in the stomach without excess tubing that may hinder fluid egress.
Figure 43-7 Positioning the patient's chin on the chest can facilitate passage of the tube into the esophagus once the pharynx has been entered. Once the tube is positioned, lavage is performed in the left lateral decubitus position. If the patient begins to vomit, the tube is immediately withdrawn.
the intubated or obtunded patient or the young child, some clinicians consider confirming tube position radiographically before lavaging, although this is not routinely performed. A misplaced tube may irrigate the esophagus with a tube that has doubled back on itself during passage. The most serious complication is inadvertent passage of the tube into the lungs. Tracheal passage of a lavage tube should be readily obvious in the awake patient prior to lavage, and obtunded patients are intubated, obviating this problem. If an awake patient begins to vomit during the lavage, immediately remove the tube to allow the patient to protect the airway. Before gastric irrigation, the gastric contents should be removed by careful gastric aspiration with repeated repositioning of the tube tip. With the Y connector closed system, lavage is performed by clamping the drainage arm of the Y adapter and infusing aliquots of fluid into the stomach from a reservoir ( Fig. 43-8 ). The reservoir arm of the Y is then clamped, and the drainage arm is opened to permit gravity drainage of the stomach contents. The procedure is then repeated. Some resistance is produced by the Y connector and tubing. Suction can be applied intermittently to the drainage tubing to enhance stomach emptying. Lavage can be performed adequately with tap water in adults. Because electrolyte disturbance has occurred in children who were lavaged with tap water, prewarmed (45°C) normal saline is generally recommended for children. [11] [27] [104] Warmed lavage fluid increases the solubility of most substances, delays gastric emptying, and theoretically should increase the effectiveness of the procedure. [83] [113] Small aliquots of lavage solution (200 to 300 mL in adults and 10 mL/kg body weight in children up to a maximum of 300 mL) should be repeatedly introduced into the stomach and removed. If larger amounts of fluids are used, there is a potential for an increased risk of washing gastric contents into the duodenum or the lungs, and much smaller amounts are not clinically practical because of the dead space in the tubing (approximately 50 mL in the 36 Fr
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Figure 43-8 An example of the Y connector closed system with the patient in a left lateral decubitus position. Patients on a ventilator, or those who are intubated may be lavaged in the supine position due to logistic issues, but an awake nonintubated patient is never lavaged in the restrained supine position.
hose) and the increase in time that is required. The amount of fluid that is returned should approximate the amount that is introduced. Manual agitation of the patient's stomach by gently "kneading" the stomach with a hand placed on the abdomen may increase recovery. [83] Lavage should be continued until the lavage fluid becomes clear. After gastric aspiration and lavage have been completed, a slurry of activated charcoal should be administered through the gastric tube. When no longer needed, the gastric tube should be pinched or clamped during its removal to avoid "dribbling" fluid into the airway. With the increasing use of repetitive doses of activated charcoal, the gastric tube is often left in place after the lavage procedure is completed. Because this large tube is irritating and may predispose the patient to gagging, drooling, or aspiration, it should be removed. The alert patient should take subsequent doses orally as necessary. The patient who remains obtunded may receive additional doses via a standard NG tube, although the high viscosity of the charcoal makes this route challenging. If endotracheal intubation was required prior to lavage tube placement, the endotracheal tube should not be removed until the patient is clearly awake and able to control his or her airway, because emesis is common after an overdose and in association with the procedure. Complications
A correctly performed procedure is generally safe but there have been numerous complications associated with gastric lavage. The complications can be divided into those caused by mechanical trauma and those resulting from the lavage fluid. Depending on the route selected for tube insertion, damage to the nasal mucosa, turbinates, pharynx, esophagus, and stomach have all been reported. [8] [34] [80] [142] After tube insertion, it is imperative to confirm correct placement. Scalzo et al found radiographically that 7 of 14 children had improper tube placement (too high or too low) despite positive gastric auscultation in all cases. [117] Although not a routine standard, radiographic confirmation of tube placement should be considered in young children and intubated patients. Instillation of lavage fluid and charcoal into the lungs through tubes inadvertently misplaced within the airways has been reported. [57] During lavage, changes in cardiorespiratory function have been noted. Thompson et al, reported that during lavage, 36% of patients had atrial or ventricular ectopy, 4.8% had transient ST elevation, and 29% had a fall in oxygen tension to 60 torr or less. [134] Patients at greatest risk for these findings included the elderly, smokers, those with lung disease, or cyclic antidepressant overdose. Laryngospasm may also occur during gastric lavage. [138] The lavage fluid itself is a potential source of complications. The large amount of fluid administered during lavage has been reported to cause patient fluid and electrolyte disturbances. These disturbances have been seen with both the use of hypertonic and hypotonic lavage fluids in the pediatric population. [11] [27] [104] Hypothermia is a possible complication if the lavage fluid is not pre-warmed. Pulmonary aspiration of gastric contents or lavage fluid is the primary potential risk during gastric lavage, especially in patients with compromised airway protective reflexes.[81] Merigian et al, reported a 10% incidence of aspiration pneumonia in patients who received gastric lavage. [87] This risk is reduced by using small aliquots of lavage fluid, by adequately positioning the patient, and by intubating patients with compromised airway protective reflexes. Excessive force should be avoided if the lavage tube cannot be easily removed. Kinking or knotting of the tube can occur, but occasionally a tube may become stuck because of lower esophageal spasm. If fluoroscopy demonstrates no deformation to the lavage tube, 1 to 2 mg of IV glucagon can be infused in an attempt to relieve lower esophageal spasm.[133] Surgical removal may be necessary if the gastric tube is deformed by kinking or knotting. Activated Charcoal Background
Activated charcoal is a carbon product that is subjected to heat and oxidized to increase the surface area and its capacity to adsorb substances onto the surface of the charcoal. A high surface charcoal, termed superactivated charcoal, is intermittently available to the clinician. Superactivated charcoal adsorbs more toxin per gram of charcoal and is recommended if available. Activated charcoal acts both by adsorbing a wide range of toxins present in the gastrointestinal tract and by enhancing toxin elimination, if systemic absorption has already occurred. It enhances elimination by creating a concentration gradient between the contents of the bowel and the circulation, but it also has the potential of interrupting enterohepatic circulation if the particular toxin is secreted in the bile and enters the gastrointestinal tract prior to reabsorption. [103] Oral activated charcoal is given as a single-dose or in multiple doses. The adsorptive capacity of charcoal depends on inherent properties of the toxin, and the local milieu, such as pH. Adsorption begins within minutes of contact with a toxin, but may not reach equilibrium for 20 to 30 minutes. Desorption of toxins from charcoal occurs over time, although this has little clinical significance for most patients and can be overcome by administering additional charcoal. Indications
For years the administration of oral activated charcoal for essentially all overdoses has been routine. Clearly charcoal
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binds many toxins in the gut, thereby decreasing some systemic absorption. Despite a lack of scientific data demonstrating a decrease in morbidity and mortality, and without firm evidence to support its widespread use, charcoal is a reasonable intervention for most poisoned patients presenting to the ED; if it can be easily and safely administered. The exact indications are not established, and no universally accepted standard of care has been promulgated. In the opinion of the editors, single-dose activated charcoal is indicated if the clinician estimates that a clinically significant fraction of the ingested substance remains in the GI tract, the toxin is adsorbed by charcoal, and further absorption may result in clinical deterioration. This will essentially always be a clinical decision, since adequated historical data may often be lacking. It may also be administered by multiple dosing, if the clinician anticipates that the charcoal will result in increased clearance of an already absorbed drug. In 1997, the American Academy of Clinical Toxicology released a position statement advising that activated charcoal should not be routinely administered but should be reserved for cases in which serious toxicity is anticipated [31] ( Fig. 43-9 ). It is most effective within the first 60 minutes after oral overdose and decreases in effectiveness over time. Charcoal is generally considered to provide superior gut decontamination when compared to gastric lavage. Combining lavage and charcoal, although intuitively attractive, has no proven additional benefit. Contraindications
The administration of charcoal is contraindicated in any person who demonstrates compromised airway protective reflexes, unless they are intubated. [31] It is contraindicated in persons who have ingested corrosive substances (acids or alkalis). Charcoal not only provides no benefit in a corrosive ingestion, but its administration could precipitate vomiting, obscure endoscopic visualization, and lead to complications if a perforation developed and charcoal entered the mediastinum, peritoneum, or pleural space. Charcoal should be avoided in cases of a pure aliphatic petroleum distillate ingestion. Hydrocarbons are not well adsorbed by activated charcoal and its administration
Figure 43-9 Position statement: single-dose activated charcoal. (From the American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. Published in Clin Toxicol 35:721, 1997.)
could lead to further aspiration risk. Many hydrocarbons are potential systemic toxins (e.g., carbon tetrachloride and benzene) or are mixed with other potentially significant toxins such as pesticides. In these cases, data are lacking, but charcoal administration can be considered. Caution should be exercised in using charcoal in patients who have medical conditions that could be further compromised by charcoal ingestion, such as those with gastrointestinal perforation or bleeding. Charcoal is not indicated for isolated ingestions of ethanol, iron, or lithium because these substances are not adsorbed. If the airway is not secure, charcoal should be given with caution, to minimally symptomatic patients who have ingested a toxin that may suddenly induce seizures. Such as cyclic antidepressants and theophylline. Charcoal will adsorb cyanide, strychnine, and mercuric chloride. Because it is often impossible to determine the exact nature of an ingestion, a liberal use policy is advocated for potentially mixed overdoses. The use of activated charcoal in the treatment of acetaminophen ingestion presents a special issue because the antidote, N-acetylcysteine, is approved only for oral use in the United States. Although activated charcoal could potentially prevent acetaminophen from reaching toxic concentrations in the blood, there are concerns that charcoal may also adsorb significant amounts of the antidote as well. Pharmacokinetic studies evaluating the effect of activated charcoal on N-acetylcysteine absorption have produced conflicting results. [39] [62] [97] The standard N-acetylcysteine dosing currently in use is much larger than needed to treat the vast majority of acetaminophen overdoses, and therefore no adjustment is required in this scenario. This issue is totally circumvented by the use of IV N-acetylcysteine. Although not FDA approved, the oral N-acetylcysteine preparations are universally used as an IV antidote, a technique recommended by the authors. Charcoal administration by paramedics and other emergency response personnel should be performed with caution. The same indications and contraindications apply as for those patients who are in the hospital. The motion of the ambulance during transport may make the patient more prone to emesis. Either the spilling of charcoal or the vomiting of charcoal may result in significant contamination of the transport vehicle and subsequently place that vehicle out of commission until it can be cleaned. Technique
There is no universally accurate dose for charcoal. A 10:1 ratio (charcoal:toxin) is recommended if the amount of ingestion is known. Charcoal dosing should be considered in light of the specific ingestion, but the recommended empiric doses of single-dose activated charcoal (standard aqueous products, such as Liqui-Char) are as follows [31] : • Up to 1 year: 1 g/kg of body weight • 1 year to 12 years: 25 to 50 g • Older than 12 years: 25 to 100 g If the ingestion were, for example, clonidine (0.1-mg tablets) or digoxin (0.25-mg tablets), this regimen would be more than adequate for even a massive overdose to achieve the desired 10:1 ratio. If the ingestion consisted of a large number of 325-mg aspirin tablets, or 240-mg verapamil tablets, the dosing regimen could be insufficient. If toxic medications with a high milligram dosage are ingested, it would be prudent to administer more charcoal than indicated by these guidelines. We recommend superactivated charcoal if it is commercially available. There is no known benefit of
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mixing charcoal with a cathartic, and the combination is not suggested. Sorbitol increases the incidence of vomiting. In many formulations the contents settle with time and vigorous shaking before administration is recommended. This should be followed by rinsing the container with a small amount of tap water prior to administering it to the patient, which will allow ingestion of the full dose. [66] Aqueous activated charcoal has a gritty texture that most patients find unpleasant and attempts have been made to improve the taste and texture. Mixing activated charcoal with chocolate milk, chocolate- or cherry-flavored syrup, or ice cream may increase palatability, but mixing with these additives has been suggested, though not proved, to cause a decrease in the adsorptive capacity of activated charcoal. [71] Rangan et al have recently reported no decrease in adsorption after mixing superactivated charcoal with a non-caffeinated cola. [111] Scharman et al demonstrated that a regular, sugared cola was favored by children over a diet cola, but it was very difficult to cajole even nonpoisoned children under age 3 years to drink a therapeutic amount of flavored charcoal. [119] It is very difficult to convince a toddler to drink a therapeutic dose of charcoal under the best of circumstances, questioning the long-held practice of keeping charcoal in the home to hasten the use of the antidote. The patient should be given a brief (5- to 10-minute) period of time to drink the dose. If the dose is not consumed by that time, the clinician should consider giving the dose by NG tube to maximize charcoal efficacy. If a nasogatric tube is inserted, correct placement must be verified. Radiographic confirmation of tube placement should be considered in obtunded or intubated patients if doubts about placement exist ( Fig. 43-10 ). Instillation of charcoal into the lungs through tubes inadvertently misplaced within the airways has been reported. [57] Activated charcoal may be given orally if the patient is awake and cooperative or by NG tube if the patient is unconscious ( Fig. 43-11 ). It may also be given through the lavage tube after gastric lavage ( Fig. 43-12 ). The common tactic of passing an NG tube in the awake but uncooperative patient, merely to administer charcoal, is controversial. Such a scenario is more likely to result in trauma from the tube, a misplaced tube, or subsequent emesis from the rapid administration of charcoal. Given the unproven efficacy of charcoal, the editors advise against the routine insertion of an NG tube to simply administer charcoal in the awake and minimally symptomatic patient. Such a decision is, however, a clinical one that must be made based on the entire clinical milieu. Complications
Charcoal is generally very safe and few adverse effects from the use of single-dose activated charcoal have been reported, despite its widespread use. There are no reports of gastrointestinal obstruction associated with single-dose activated charcoal. The most common complications of charcoal administration include constipation, diarrhea, and vomiting. [96] Pulmonary aspiration of activated charcoal is a dreaded complication that can result in pneumonitis, obstruction of the respiratory tree, and bronchiolitis obliterans. [14] [44] [80] [105] Aspiration of large amounts of charcoal can be fatal. [86] Risk factors for serious aspiration are large amounts of charcoal instilled over a short period of time, multiple dose charcoal in the setting of an ileus, charcoal administration in a patient who becomes obtunded, or the forced administration of charcoal via an NG tube, especially in a restrained supine
Figure 43-10 Radiographic confirmation of nasogastric tube placement before lavage or instillation of charcoal. Tracheal placement of a lavage tube is usually readily evident. Vomiting during lavage suggests that the tube has curved back into the esophagus. A confirmatory radiograph is suggested in the obtunded patient if gastric placement is questioned. Tracheal intubation precludes passage of a tube into the lungs, but it does not ensure proper gastric placement.
patient. Trivial aspirations of charcoal are common, even if the patient is intubated, and are usually innocuous.
Multiple Doses of Activated Charcoal Indications
The use of multidose activated charcoal (MDAC) may be indicated in select cases. [30] Its use has been advocated for two purposes: first, to prevent continued absorption of a drug that may still be present within the gastrointestinal tract; second, to increase the clearance of a drug that has already been absorbed. The recommendations of various toxicology organizations for MDAC are presented in Figure 43-13 . MDAC prevents continued absorption by either binding a drug that may be present throughout the gastrointestinal tract or binding a drug that exists as extended-release or enteric-coated preparations. MDAC enhances elimination of a drug by interrupting enterobiliary recirculation or augmenting enterocapillary exsorption.[96] By interrupting enterobiliary recirculation, charcoal binds to an active drug that is secreted by the biliary system, subsequently preventing reabsorption. By augmentation of enterocapillary exsorption, charcoal produces sink conditions that drive diffusion of drug from the capillaries into the entraluminal space, where it is subsequently eliminated. This process is called "intestinal dialysis". [70] Drug characteristics that are associated with enhanced systemic clearance with MDAC include a low intrinsic clearance, a prolonged distributive phase, low protein binding, and a small volume of distribution. [29]
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Figure 43-11 If the overdose patient will voluntarily drink charcoal, there are few reasons to withhold it, even though a definite clinical benefit in the routine case cannot be proved. If a patient will not drink charcoal, patient management becomes controversial. Passing a nasogastric tube in a struggling patient or in a recalcitrant child merely to instill the unproven, but theoretically useful, antidote is not supported by scientific data. Nonetheless, it remains a common procedure. Although not always easy or pleasant, such an intervention is usually safe. Pulmonary aspiration, even in the awake patient, is the major downside. Restrained supine patients are at greatest risk for aspiration, and that position should be avoided, even in the initially awake patient.
MDAC has been shown to increase total body clearance of multiple drugs, including carbamazepine, [18] [90] [93] dapsone,[94] [95] phenobarbital, [15] [16] [19] [42] [47] [93] [107] [141] quinine, [74] [109] and theophylline. [5] [17] [30] [38] [43] [55] [76] [99] [101] [103] [110] [121] [122] [136] MDAC may be beneficial in the management of overdoses of the drugs listed in Table 43-2 . Despite the reported increase in drug clearance associated with the use of MDAC, improved clinical outcomes have not been definitively demonstrated. For example, Pond et al described 10 comatose patients following phenobarbital overdose who were randomized to receive either single-dose activated charcoal or MDAC.[107] Despite the fact that the MDAC group had a significantly shorter phenobarbital serum half-life, there was no difference between the groups in regard to the duration of intubation or hospitalization. Contraindications
MDAC is contraindicated if there is evidence of bowel obstruction. An ileus is a relative contraindication. Many ill patients who develop an ileus may be selected candidates for MDAC if the airway is protected. The administration of MDAC is contraindicated in any patient who does not
Figure 43-12 Charcoal that is voluntarily swallowed or instilled via an oral-gastric lavage tube or nasogastric tube can induce emesis. This occurs in both the obtunded and awake patient. In this instance, the patient was unconscious from the overdose and the airway was protected with prior tracheal intubation. Although the intubation procedure does not totally exclude pulmonary aspiration, and it carries some morbidity in its own right, it is recommended prior to charcoal use in the patient who is not able to fully protect the airway. Patients who initially are asymptomatic or minimally affected but have ingested drugs that have the potential to produce rapid deterioration, seizures, or loss of airway protection make decisions on the use of charcoal difficult for the clinician. In borderline cases, some experienced clinicians avoid the use of charcoal altogether.
have an intact or protected airway. MDAC should be avoided in patients who have repetitive emesis, especially when associated with decreased mental status or a decreased gag reflex. The concurrent use of cathartics with MDAC remains unproved and is not recommended. [108] MDAC with cathartics should not be administered to young children because of the propensity for laxatives to cause fluid and electrolyte imbalance. For example, MDAC with sorbitol has been associated with hypernatremia and dehydration [2] [82] and MDAC with magnesium cathartics has been associated with hypermagnesemia, neuromuscular weakness, and coma. [56] [124] Technique
The first dose of activated charcoal should be 1 g/kg (maximum of 100 g). If a cathartic is used, it should be administered only with the first dose of charcoal to decrease the risk of cathartic-induced electrolyte abnormalities that can potentially develop, especially in children. [2] [56] [82] [124] The initial dose of charcoal is followed by 0.5 g/kg (up to 50 g) of activated charcoal every 4 hours. If repeat examination reveals an absence of bowel sounds or reveals a distended abdomen, then MDAC should be terminated and the clinician should consider placement of a NG tube on low intermittent suction. Patients receiving MDAC may be at increased risk for emesis because of the larger total dose of activated charcoal received. The use of antiemetics may help decrease the incidence of vomiting associated with MDAC. [5] [22] [114] Charcoal therapy should be continued until
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Figure 43-13 Position statement and practice guidelines on the use of multi-dose activated charcoal in the treatment of acute poisoning. (From the American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. Published in Clin Toxicol 37:731, 1999.)
there is clinical improvement and plasma drug levels have fallen to acceptable levels. Complications
The complications encountered in single-dose activated charcoal are also encountered in multiple dose activated charcoal. In addition, there have been reports of gastrointestinal obstruction and perforation from MDAC therapy, especially in conjunction with the ingestion of drugs with anticholinergic properties. [9] [48] [49] [112] [144]
TABLE 43-2 -- Drugs Whose Serum Clearance May Be Enhanced by Multiple Doses of Activated Charcoal Aspirin Caffeine Carbamazepine Cyclosporine Dapsone Digoxin Disopyramide Nadolol Phenobarbital Phenytoin Quinine Sotalol Sustained-release thallium Theophylline Valproate Vancomycin
Cathartic Use Background
The use of cathartics is intended to decrease the absorption of substances by accelerating the expulsion of the poison from the gastrointestinal tract. Theoretically, this would also minimize the possibility of desorption of drug bound to activated charcoal. The majority of data suggest negligible clinical benefit from cathartic use. [3] [89] There is little evidence that a single dose of aqueous activated charcoal is significantly constipating; however, cathartics are often given for this potential problem. Indications
The routine administration of a cathartic in combination with activated charcoal is not endorsed by the American Academy of Clinical Toxicology or the European Association of Poison Centres and Clinical Toxicologists. [12] Figure 43-14 gives a consensus recommendation on the use of cathartics. In addition, the administration of a cathartic alone has no role in the management of the poisoned patient. Contraindications
Cathartics are contraindicated if there is volume depletion, hypotension, significant electrolyte imbalance, corrosive ingestion, ileus, recent bowel surgery, intestinal obstruction or perforation. The administration of cathartics is also
Figure 43-14 Position statement: cathartics. (From the American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. Published in Clin Toxicol 35:743, 1999.)
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contraindicated with patients who do not have an intact or protected airway. They should be avoided in patients who have repetitive emesis, especially when associated with decreased mental status or a decreased gag reflex. Cathartics should be used cautiously in young children and the elderly because of the propensity for laxatives to cause fluid and electrolyte imbalance. Technique
There are two types of osmotic cathartics: saccharide cathartics (sorbitol) and saline cathartics (magnesium citrate, magnesium sulfate, and sodium sulfate). The optimal dose of sorbitol or magnesium citrate remains to be determined. The recommended dose of sorbitol is approximately 1 to 2 g/kg of body weight or 1 to 2 mL/kg of 70% sorbitol in adults and 4.3 mL/kg of 35% sorbitol in children (single administration only). [12] Many charcoal formulations come premixed with sorbitol, but there is considerable variation in sorbitol content: Liqui-Char with sorbitol contains 50 g of activated charcoal in 54 g of sorbitol; Actidose with sorbitol contains 50 g of activated charcoal in 96 g of sorbitol; activated charcoal USP with sorbitol contains 25 g of activated charcoal in 27 g of sorbitol; CharcoAid contains 30 g of activated charcoal in 110 g of sorbitol. The recommended dose of magnesium citrate is 250 mL of 10% solution in an adult and 4 mL/kg body weight of 10% solution in a child. Multiple doses of cathartics should be avoided. Complications
The administration of sorbitol has been associated with vomiting, abdominal cramps, nausea, diaphoresis, and transient hypotension. content varies between different charcoal/sorbitol combination products,
[46] [59] [88]
Because the sorbitol
Figure 43-15 This "body packer" (A) attempted to smuggle more than 50 packets of heroin. All packets were passed intact after 12 hours of whole-bowel irrigation. Note the integrity of the carefully wrapped packets that were passed (B).
attention should be paid to the sorbitol content in each brand to avoid excessive sorbitol administration. Multiple doses of sorbitol have been associated with volume depletion. [2] Multiple doses of magnesium-containing cathartics have been associated with severe hypermagnesemia. [56] [124] Children are particularly susceptible to the adverse affects of cathartics, and therefore cathartics should be used with caution, or totally avoided, in children. Whole-Bowel Irrigation
Background
Whole-bowel irrigation (WBI) has emerged as the newest technique in gastrointestinal decontamination. It involves the enteral administration of an osmotically balanced polyethylene glycol-electrolyte solution (PEG-ES) in a sufficient amount and rate to physically flush ingested substances through the gastrointestinal tract, purging the toxin before absorption can occur ( Fig. 43-15 ). [129] PEG-ES (CoLyte, GoLYTELY) is isosmotic, is not systemically absorbed, and will not cause electrolyte or fluid shifts. Available data suggest that the large volumes of this solution needed to mechanically propel pills, drug packets, or other substances through the gastrointestinal tract are safe, including in pregnancy and in young children. [128] [139] Indications
WBI may be considered for ingestions of exceedingly large quantities of potentially toxic substances, ingestions of toxins that are poorly adsorbed to activated charcoal (e.g., iron, lithium), ingestions of delayed-release formulations, late presentation after ingestion of a toxin, pharmacobezoars,
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Figure 43-16 Position statement: whole-bowel irrigation. (From the American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. Published in Clin Toxicol 35:753, 1997.)
and body stuffers or packers. [53] [60] [125] [129] WBI remains a theoretical option for these ingestions. There is no definitive evidence that WBI improves the outcome of the poisoned patient [131] ( Fig. 43-16 ). Although not a proven procedure, WBI is often suggested by toxicologists. Its use is intuitively reasonable and supported by the editors. The most common indication for WBI in the ED is for the treatment of toxic sustained-release medications (such as calcium channel blockers, theophylline, and lithium) and iron tablets ( Fig. 43-17 ).
Figure 43-17 Whole-bowel irrigation is commonly recommended for the treatment of iron ingestion. These radiographs depict the effect of 5 hours of whole-bowel irrigation. Note the marked decrease of radiopaque pills in the gastrointestinal tract. Intact pills were recovered in the rectal effluent. Contraindications
WBI is contraindicated in patients with gastrointestinal obstruction, perforation, ileus, and corrosive ingestion. It should also be avoided in patients with hemodynamic instability or an unprotected airway. [130] WBI should be avoided with patients who have repetitive emesis, especially when associated with decreased mental status or a decreased gag reflex. WBI should be used cautiously in debilitated patients. Technique
PEG-ES is marketed in a powder form. Tap water is added to make a total volume of 4 L. The recommended rate of administration is as follows. [129] • 9 months to 6 years: 500 mL/hour • 6 years to 12 years: 1000 mL/hour • Older than 12 years: 1500 to 2000 mL/hour Cooperative patients with intact airway protective reflexes may drink the solution. The large volume and taste often limit even the most motivated patient's ability to comply. If the patient is unable or unwilling to drink this solution, it should be administered through a small-bore NG tube after placement is confirmed. Because it is common for WBI to be delayed while the patient and medical personnel attempt to administer the large volumes of WBI solution required to be effective, it is suggested that NG instillation be instituted early in the ED course ( Fig. 43-18 ). Unconscious patients with protected airways may receive WBI. Pre-warming the irrigant to a temperature of approximately 37°C avoids the potential complication of hypothermia. To collect the waste products, the awake patient may need to be seated on a commode; a rectal tube will need to be placed in the obtunded patient. Many toxicologists recommend adding two to three bottles of activated charcoal to each liter of WBI solution. The benefit is unproved but there is little theoretical downside to this technique, and it is supported by the editors. The binding capacity of charcoal is decreased when combined with PEG-ES, but the clinical consequences of this observation are unknown. Empirically, metoclopramide may be coadministered to decrease nausea and facilitate GI passage. The endpoint of WBI is until the arrival of clear rectal effluent and/or resolution of toxic effect. parts, and tablets
[130]
There are rare case reports of late purging of drug packets, plant
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Figure 43-18 It is very difficult for even the most motivated patient to drink an effective volume of whole-bowel irrigation solution. To enhance compliance and to decrease vomiting, PEG-ES may be slowly and continuously administered via a nasogastric tube. An empty bag of saline is hung on an IV pole, the corner of the bag is removed, and the PEG-ES is poured into the bag. Standard IV tubing is connected to the proximal end of a nasogastric tube and the solution is infused continuously. In this picture, charcoal has been added to the whole-bowel irrigation solution. Metoclopramide was coadministered to reduce nausea.
after the arrival of clear effluent. [53] [118] Radiographic studies may also be beneficial to determine the endpoint in body packers or in patients who have ingested radiopaque medications. Complications
There have been few reported complications from WBI therapy, especially pertaining to acute poisonings. Nausea, vomiting, abdominal cramps, and bloating have been described. [40] Nausea and vomiting may make administration of WBI difficult. Antiemetics and a 15- to 30-minute break followed by a slower rate may allow readministration. As discussed with the other methods of decontamination, attention should be directed to the airway and the potential for aspiration. Administration of a large amount of chilled or room temperature WBI fluid to pediatric patients could potentially cause hypothermia. Warmed fluid should be considered in these
patients. If activated charcoal is administered concurrently with WBI, there may be a desorption of toxin from charcoal.
[ 52] [61] [ 77]
DERMAL DECONTAMINATION Background Numerous hazardous material (HAZMAT) incidents occur each year in the United States. The National Response Center Database, which tracks comparatively large incidents such as train derailments and industrial accidents, reported 34,360 HAZMAT incidents in 2001. [92] In 1996, 5502 HAZMAT events in 14 states involving 5887 substances were reported to the Hazardous Substances Emergency Events Surveillance System (HSEESS). [51] HAZMAT events frequently result in injuries, and the ED treatment of contaminated HAZMAT patients is not a rare event. Many of these patients transport themselves to the ED, including those involved in past terrorist events. For example, in the Tokyo sarin gas attack, 93% of 498 patients reporting to St. Luke's Hospital arrived by means other than ambulance. [100] The risk of injury to medical personnel incurred while treating contaminated patients is significant. Of the patients reported to HSEESS, emergency responders accounted for 10% of injuries and hospital personnel for 4.1% of injuries. [51] After the Tokyo attack, 13 of 15 clinicians (87%) reported symptoms while treating patients in the ED and 23% of involved hospital staff complained of acute poisoning symptoms. [98] Burgess et al reported that 13% of Washington state emergency care facilities had evacuated their ED or another part of the hospital for contamination during a 5-year period. [23] Ghilarducci et al (2000) surveyed Level 1 trauma centers in the United States and reported that only 6% had the necessary equipment required for safe decontamination, less than 36% of emergency medicine staff had received appropriate training in handling the contaminated patient, and 5.6% had experienced injuries to their staff due to contact with contaminated patients during a 1-year period. It is imperative that EDs have plans in place to handle patients who are exposed to potential toxins, provide adequate decontamination facilities, and ensure the safety of the treating medical staff. Technique There are a number of key components in the management of a hazardous materials incident and the care of the contaminated patients who present to the ED. These components should include early recognition of a HAZMAT event, rapid activation of a plan to manage contaminated patients, initiation of primary triage, appropriate patient registration, patient decontamination, secondary triage, and final treatment.
[75]
First, the ED must be able to recognize that an event has occurred before contaminated patients gain entrance into the health care facility. Communication with local fire, police, and paramedics provides early detection of such events and allows preparation before patients arrive. Security should be arranged to prevent contaminated patients from entering the hospital, and a "lockdown" of the facility should be considered. Second, the ED should have the authority to activate a plan expeditiously to prepare the decontamination facility and allow appropriate personnel to don personal protective equipment (PPE). If necessary, the hospital disaster plan should be activated quickly at the discretion of the ED attending clinician who is in contact with scene operations and incoming patients. Specific data to determine the appropriate level PPE to maintain hospital worker protection remains limited. Most chemical exposures do not pose a risk of secondary exposure. With unknown chemical and biologic exposures, level B and level A PPE, respectively, is recommended by OSHA. Fortunately, most chemical exposures are known. For those that occur in the workplace, Material Safety Data Sheets can be obtained and either the local poison center or the Agency for Toxic Substances and Disease Registry (ATSDR) can be contacted to obtain advice on what level of protection is appropriate. Third, appropriate primary triage should occur. Contaminated patients should not enter the ED until proper decontamination has occurred to assure that the hospital staff will not get secondary contamination. Appropriate triage should then occur with experienced personnel performing an initial brief assessment of each patient. Fourth, a brief sign-in process should capture the patient's name and date of birth with full registration to occur following decontamination. Contaminated clothing and valuables should be placed in an impervious bag to avoid potential off gassing. [54] [120]
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Fifth, decontamination should be performed. The hospital ED should have preexisting hazardous materials incident protocols that designate the decontamination area and the triage and decontamination team. The decontamination area should meet several qualifications: (1) it should be secured to prevent spread to other areas of the hospital, (2) the ventilation system should be separate from the rest of the hospital or it should be shut off to prevent airborne spread of contaminants, and (3) provisions must be made to collect the rinsate from contaminated patients to prevent contamination of the facility and water supply. Some hospitals may have designated decontamination rooms. At most facilities, the best place to begin initial treatment and evaluation is outdoors ( Fig. 43-19 ). Portable decontamination facilities are available, but their cost may be prohibitive for many institutions. A practical alternative is to have a warm shower nozzle, soap, and a wading pool available outside the entrance to the ED. A tent or screen can provide privacy. Decontamination should proceed by using soap and copious warm water irrigation. Starting from head to toe, irrigate the exposed skin and hair for 10 to 15 minutes and scrub with a soft surgical sponge with careful attention not to abrade the skin. Irrigate wounds for an additional 5 to 10 minutes with water or saline. Irrigate the eyes for 10 to 15 minutes with saline, directed away from the medial canthus to avoid forcing contaminants into the lacrimal duct. Longer irrigation times may be needed with strongly alkaline substances. Irrigate the nares and the ear canals with frequent suctioning if contamination is suspected. Clean underneath the nails with a brush. Stiff brushes and abrasives should be avoided as they may enhance dermal absorption of the toxin and can produce skin lesions that may be mistaken for chemical injuries. Sponges and disposable towels are effective alternatives. Secondary triage should occur after decontamination. Patients with major or moderate casualties can then be transferred to areas designated for such cases. Those with minor or no injuries should be sent to appropriate holding areas for further evaluation. Medical care at this stage would then depend on the toxin to which the patient has been exposed and the potential toxicity of that agent.
Figure 43-19 Decontamination of personnel using copious water irrigation.
In order for the ED to care for the contaminated patient, protocols should be in place and regularly rehearsed by the facility. There are template protocols in both peer-reviewed literature and in the government literature. [24] [64] For example, guidelines for managing hazardous materials incidents are available from the Emergency Response and Consultation Branch (E57), Division of Health Assessment and Consultation, Agency for Toxic Substances and Disease Registry, 1600 Clifton Road NE, Atlanta, Georgia 30333. [78]
CONCLUSION Gastric emptying techniques such as gastric lavage and ipecac-induced emesis are rarely being used to decontaminate the poisoned patient who presents to the ED. There may be future indications for these procedures with specific toxins. At this time the documented risks associated with these procedures should be carefully weighed in light of the rare indications. Activated charcoal as the sole means of gastric decontamination is increasing in popularity, but its efficacy has specific limitations. Protocols for the evaluation and treatment of asymptomatic or minimally symptomatic patients, who have not ingested significantly toxic substances, continue to evolve, and it has been suggested that these patients will do well regardless of therapy. The major issue currently facing the clinician is the choice of gastrointestinal decontamination in the significantly poisoned patient. The choice of decontamination method for these patients must be individualized using both evidence-based medicine and clinical acumen. No patient should undergo any of the available procedures unless it is anticipated that decontamination will provide clinical benefit.
Acknowledgment
The authors acknowledge the contributions of Dr. Patrick E. McKinney to the previous editions of this text.
References 1. Abdallah 2. Allerton
A, Tye A: A comparison of the efficacy of emetic drugs and stomach lavage. Am J Dis Child 113:571, 1967.
J, Strom J: Hypernatremia due to repeated doses of charcoal and sorbitol. Am J Kidney Dis 17:581, 1991.
3. Al-Shareef
A, Buss D, Allen E, et al: The effects of charcoal and sorbitol (alone and in combination) on plasma theophylline concentrations after a sustained-release formulation. Hum Exp Toxicol
9:179, 1990. 4. Amitai
Y, Mitchell AA, McGuigan MA, et al: Ipecac-induced emesis and reduction of plasma concentrations of drugs following accidental overdose in children. Pediatrics 80:364, 1987.
5. Amitai
Y, Yeung AC, Moye J, et al: Repetitive oral activated charcoal and control of emesis in severe theophylline toxicity. Ann Intern Med 105:386, 1986.
6. Arimori
K, Nakano M: Accelerated clearance of intravenously administered theophylline and phenobarbital by oral doses of activated charcoal in rats. A possibility of the intestinal dialysis. J Pharmacobiodyn 9:437, 1986. 7. Arnold
F, Hodges J, Barta R, et al: Evaluation of the efficacy of lavage and induced emesis in treatment of salicylate poisoning. Pediatrics 23:286, 1959.
8. Askenasi
R, Abramowicz M, Jeanmart J, et al: Esophageal perforation: An unusual complication of gastric lavage (letter). Ann Emerg Med 13:146, 1984.
9. Atkinson
SW, Young Y, Trotter GA: Treatment with activated charcoal complicated by gastrointestinal obstruction requiring surgery. Br Med J 305:563, 1992.
10.
Auerbach P, Osterloh J, Braun O, et al: Efficacy of gastric emptying: Gastric lavage versus emesis induced with ipecac. Ann Emerg Med 15:692, 1986.
838
11.
Bachrach L, Correa A, Levin R, Grossman M: Iron poisoning: Complications of hypertonic phosphate lavage therapy. J Pediatr 94:147, 1979.
Barceloux D, McGuigan M, Hartigan-Go K: Position statement: Cathartics. American Acadamy of clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. Clin Toxicol 35:743, 1997. 12.
13.
Bateman D: Gastric decontamination—A view for the millennium. J Accid Emerg Med 16:84, 1999.
14.
Benson B, VanAntwerp M, Hergott T: A fatality resulting from multiple dose activated charcoal therapy (abstract). Vet Hum Toxicol 31:335, 1989.
15.
Berg MJ, Berlinger WG, Goldberg MJ, et al: Acceleration of the body clearance of phenobarbital by oral activated charcoal. N Engl J Med 307:642, 1982.
16.
Berg MJ, Rose JQ, Wurster DE, et al: Effect of charcoal and sorbitol-charcoal suspension on the elimination of intravenous phenobarbital. Ther Drug Monit 9:41, 1987.
17.
Berlinger WG, Spector R, Goldberg MJ, et al: Enhancement of theophylline clearance by oral activated charcoal. Clin Pharmacol Ther 33:351, 1983.
18.
Boldy DA, Heath A, Ruddock S, et al: Activated charcoal for carbamazepine poisoning. Lancet 1:1027, 1987.
19.
Boldy DA, Vale JA, Prescott LF: Treatment of phenobarbitone poisoning with repeated oral administration of activated charcoal. Q J Med 61:997, 1986.
Bond GR, Requa RK, Krenzelok EP, et al: Influence of time until emesis on the efficacy of decontamination using acetaminophen as a marker in a pediatric population. Ann Emerg Med 22:1403, 1993. 20.
21.
Boxer L, Anderson FP, Rowe DS: Comparison of ipecac-induced emesis and lavage in the treatment of acute salicylate ingestion. J Pediatr 74:800, 1969.
22.
Brown SG, Prentice DA: Ondansetron in the treatment of theophylline overdose. Med J Aust 156:512, 1992.
23.
Burgess J, Blackmon G, Brodkin C, et al: Hospital preparedness for hazardous materials incidents and treatment of contaminated patients. West J Med 167:387, 1997.
24.
Burgess JL, Kirk M, Borron SW, et al: Emergency department hazardous materials protocol for contaminated patients. Ann Emerg Med 34:205, 1999.
25.
Burton B, Bayer M, Barron L, et al: Comparison of activated charcoal and gastric lavage in the prevention of aspirin absorption. J Emerg Med 1:411, 1984.
26.
Bush F: On the common syringe with a flexible tube, as applicable to the removal of opium and other poisons from the stomach. London Med Phys Jo 48:218, 1822.
27.
Carter RF, Fotheringham FJ: Fatal salt poisoning due to gastric lavage with hypertonic saline. Med J Aust 1:539, 1971.
28.
Chafee-Bahamon C, Lacouture PG, Lovejoy FH Jr: Risk assessment of ipecac in the home. Pediatrics 75:1105, 1985.
29.
Chyka P: Multi-dose activated charcoal and enhancement of systemic drug clearance: Summary of studies in animals and human volunteers. Clin Toxicol 33:399, 1995.
30.
Chyka PA, Holley JE, Mandrell TD, Sugathan P: Correlation of drug pharmacokinetics and effectiveness of multiple-dose activated charcoal therapy. Ann Emerg Med 25:356, 1995.
Chyka PA, Seger D: Position statement: Single-dose activated charcoal. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol 35:721, 1997. 31.
32.
Comstock EG, Boisaubin EV, Comstock BS, et al: Assessment of the efficacy of activated charcoal following gastric lavage in acute drug emergencies. J Toxicol Clin Toxicol 19:149, 1982.
33.
Corby D, Lisciandro R, Lehman R, et al: The efficiency of methods used to evacuate the stomach after acute ingestions. Pediatrics 40:871, 1967.
34.
Coutselinis A, Poulos L, Boukis D, et al: A lethal complication to gastric lavage leading to malpractice suit: A case report. Forensic Sci Int 11:47, 1978.
35.
Curtis R, Barone J, Giacona N: Efficacy of ipecac and activated charcoal/cathartic. Arch Intern Med 144:48, 1984.
36.
Czajka PA, Russell SL: Nonemetic effects of ipecac syrup. Pediatrics 75:1101, 1985.
37.
Danel V, Henry J, Glucksman E: Activated charcoal, emesis, and gastric lavage in aspirin overdose. Br Med J 296:1507, 1988.
38.
Davis R, Ellsworth A, Justus RE, et al: Reversal of theophylline toxicity using oral activated charcoal. J Fam Pract 20:73, 1985.
39.
Ekins BR, Ford DC, Thompson MI et al: The effect of activated charcoal on N-acetylcysteine absorption in normal subjects. Am J Emerg Med 5:483, 1987.
Ernstoff J, Howard D, Marshall J, et al: A randomized blinded clinical trial of a rapid colonic lavage solution (GoLYTELY) compared with standard preparation for colonoscopy and barium enema. Gastroenterology 84:1512, 1983. 40.
41.
Fane L, Comba H, Decker W, et al: Physical parameters in gastric lavage. Clin Toxicol 4:389, 1971.
Frenia ML, Schauben JL, Wears RL, et al: Multiple-dose activated charcoal compared to urinary alkalinization for the enhancement of phenobarbital elimination. J Toxicol Clin Toxicol 34:169, 1996. 42.
43.
Gal P, Miller A, McCue JD: Oral activated charcoal to enhance theophylline elimination in an acute overdose. JAMA 251:3130, 1984.
44.
Geller RJ: Death complicating gastrointestinal decontamination—Time to rethink "routine therapy"? (abstract). Vet Hum Toxicol 35:335, 1993.
45.
Ghilarducci DP, Pirrallo RG, Hegmann KT: Hazardous materials readiness of United States level 1 trauma centers. J Occup Environ Med 42:683, 2000.
46.
Goldberg M, Spector R, Park G, et al: The effect of sorbitol and activated charcoal in prevention of salicylate absorption. Clin Pharmacol Ther 41:108, 1987.
47.
Goldberg MJ, Berlinger WG: Treatment of phenobarbital overdose with activated charcoal. JAMA 247:2400, 1982.
48.
Gomez HF, Brent JA, Munoz DC, et al: Charcoal stercolith with intestinal perforation in a patient treated for amitriptyline ingestion. J Emerg Med 12:57, 1994.
49.
Goulbourne KB, Cisek JE: Small-bowel obstruction secondary to activated charcoal and adhesions. Ann Emerg Med 24:108, 1994.
50.
Grierson R, Green R, Sitar DS, Tenenbein M: Gastric lavage for liquid poisons. Ann Emerg Med 35:435, 2000.
51.
Hazardous Substances Emergency Events Surveillance (HSEES) Annual Report 1996. Registry ATSDR. Atlanta, U.S. Department of Health and Human Services, 1996.
52.
Hoffman RS, Chiang WK, Howland MA, et al: Theophylline desorption from activated charcoal caused by whole bowel irrigation solution. J Toxicol Clin Toxicol 29:191, 1991.
53.
Hoffman RS, Smilkstein MJ, Goldfrank LR: Whole bowel irrigation and the cocaine body-packer: A new approach to a common problem. Am J Emerg Med 8:523, 1990.
54.
Huff JS: Lessons learned from hazardous materials incidents. Emergency Care Q 7:17, 1991.
55.
Ilkhanipour K, Yealy DM, Krenzelok EP: The comparative efficacy of various multiple-dose activated charcoal regimens. Am J Emerg Med 10:298, 1992.
56.
Jones J, Heiselman D, Dougherty J: Cathartic-induced magnesium toxicity during overdose management. Ann Emerg Med 15:1214, 1986.
57.
Justiniani F, Hippalgaonkar R, Martinez L: Charcoal-containing empyema complicating treatment for overdose. Chest 87:404, 1985.
58.
Jukes E: New means of extracting opium and cocaine from the stomach. London Med Phys J 48:384, 1822.
59.
Keller R, Schwab R, Krenselok E: Contribution of sorbitol combined with activated charcoal in prevention of salicylate absorption. Ann Emerg Med 19:654, 1990.
Kirshenbaum LA, Mathews SC, Sitar DS, et al: Whole-bowel irrigation versus activated charcoal in sorbitol for the ingestion of modified-release pharmaceuticals. Clin Pharmacol Ther 46:264, 1989. 60.
Kirshenbaum LA, Sitar DS, Tenenbein M: Interaction between whole-bowel irrigation solution and activated charcoal: Implications for the treatment of toxic ingestions. Ann Emerg Med 19:1129, 1990. 61.
62.
Klein-Schwartz W, Gorman RL, Oderda GM, et al: Ipecac use in the elderly: The unanswered question. Ann Emerg Med 13:1152, 1984.
63.
Knight KM, Doucet HJ: Gastric rupture and death caused by ipecac syrup. South Med J 80:786, 1987.
Koplan JP, Falk H, DeRosa CT: Managing Hazardous Materials Incidents in Hospital Emergency Departments. A Planning Guide for the Management of Contaminated Patients. Atlanta, U.S. Department of Health and Human Services, Public Health Service Agency for Toxic Substances and Disease Registry, 2000. 64.
65.
Kornberg AE, Dolgin J: Pediatric ingestions: Charcoal alone versus ipecac and charcoal. Ann Emerg Med 20:648, 1991.
66.
Krenzelok E, Lush R: Container residue after the administration of aqueous activated charcoal products. Am J Emerg Med 9:144, 1991.
Krenzelok E, McGuigan M, Lheur P: Position statement: Ipecac syrup. American Academy of Clinical Toxicology; European Association of Poison Centres and Clinical Toxicologists. J Toxicol Clin Toxicol 35:699, 1997. 67.
68.
Kruse J, Carlson R: Fatal rodenticide poisoning with brodifacoum. Ann Emerg Med 21:331, 1992.
839
69.
Kulig K, Bar-Or D, Cantrill SV, et al: Management of acutely poisoned patients without gastric emptying. Ann Emerg Med 14:562, 1985.
70.
Levy G: Gastrointestinal clearance of drugs with activated charcoal. N Engl J Med 307:676, 1982.
71.
Levy G, Soda DM, Lampman TA: Inhibition by ice cream of the antidotal efficacy of activated charcoal. Am J Hosp Pharm 32:289, 1975.
72.
Litovitz TL: 2000 Annual Report of the American Association of Poison Control Centers Toxic Exposure Surveillance System, American Association of Poison Control Centers, 2000.
73.
Litovitz TL, Klein-Schwartz W, Oderda GM, et al: Ipecac administration in children younger than 1 year of age. Pediatrics 76:761, 1985.
74.
Lockey D, Bateman DN: Effect of oral activated charcoal on quinine elimination. Br J Clin Pharmacol 27:92, 1989.
75.
Macintyre AG, Christopher GW, Eitzen E Jr, et al: Weapons of mass destruction events with contaminated casualties: Effective planning for health care facilities. JAMA 283:242, 2000.
76.
Mahutte CK, True RJ, Michiels TM, et al: Increased serum theophylline clearance with orally administered activated charcoal. Am Rev Respir Dis 128:820, 1983.
Makosiej FJ, Hoffman RS, Howland MA, et al: An in vitro evaluation of cocaine hydrochloride adsorption by activated charcoal and desorption upon addition of polyethylene glycol electrolyte lavage solution. J Toxicol Clin Toxicol 31:381, 1993. 77.
78.
Managing Hazardous Materials Incidents, vols. 1 & 2. Agency for Toxic Substances and Disease Registry. Atlanta, U.S. Government Printing Office, 1992.
79.
Manoguerra A: Gastrointestinal decontamiation after poisoning. Where is the science? Crit Care Clin 13:709, 1997.
80.
Mariani PJ, Pook N: Gastrointestinal tract perforation with charcoal peritoneum complicating orogastric intubation and lavage. Ann Emerg Med 22:606, 1993.
81.
Matthew H, Mackintosh TF, Thompsett SL, et al: Gastric aspiration and lavage in acute poisoning. Br Med J 1:1333, 1966.
82.
McCord M: Toxicity of sorbitol-charcoal suspension. J Pediatr 110:307, 1987.
83.
McDougal C, MacClean MA: Modifications in the technique of gastric lavage. Ann Emerg Med 10:514, 1981.
84.
McNamara RM, Aaron CK, Gemborys M, et al: Efficacy of charcoal cathartic versus ipecac in reducing serum acetaminophen in a simulated overdose. Ann Emerg Med 18:934, 1989.
85.
Meester W: Emesis and lavage. Vet Hum Toxicol 22:225, 1989.
86.
Menzies DG, Busuttel A, Prescott LF: Fatal pulmonary aspiration of oral activated charcoal. Br Med J 297:459, 1988.
87.
Merigian KS, Woodard M, Hedges Jr, et al: Prospective evaluation of gastric emptying in the self-poisoned patient. Am J Emerg Med 8:479, 1990.
88.
Minocha A, Herold D, Bruns D, et al: Effect of activated charcoal in 70% sorbitol in healthy individuals. J Toxicol Clin Toxicol 22:529, 1984.
89.
Minton N, Henry J: Prevention of drug absorption in simulated theophylline overdose. J Toxicol Clin Toxicol 33:43, 1995.
Montoya-Cabrera MA, Sauceda-Garcia JM, Escalante-Galindo P, et al: Carbamazepine poisoning in adolescent suicide attempters. Effectiveness of multiple-dose activated charcoal in enhancing carbamazepine elimination. Arch Med Res 27:485, 1996. 90.
91.
Moran D, Crouch D, Findle B: Absorption of ipecac alkaloids in emergency patients. Ann Emerg Med 13:1100, 1984.
92.
National Response Center Database, 2001. http://www.nrc.uscg.
93.
Neuvonen PJ, Elonen E: Effect of activated charcoal on absorption and elimination of phenobarbitone, carbamazepine and phenylbutazone in man. Eur J Clin Pharmacol 17:51, 1980.
94.
Neuvonen PJ, Elonen E, Mattila MJ: Oral activated charcoal and dapsone elimination. Clin Pharmacol Ther 27:823, 1980.
95.
Neuvonen PJ, Elonen E, Haapanen EJ: Acute dapsone intoxication: Clinical findings and effect of oral charcoal and haemodialysis on dapsone elimination. Acta Med Scand 214:215, 1983.
96.
Neuvonen PJ, Olkkola KT: Oral activated charcoal in the treatment of intoxications. Role of single and repeated doses. Med Toxicol Adverse Drug Exp 3:33, 1988.
97.
North DS, Peterson RG, Krenzelok EP: Effect of activated charcoal administration on acetylcysteine serum levels in humans. Am J Hosp Pharm 38:1022, 1981.
98.
Nozaki H, Hori S, Shinozawa Y, et al: Secondary exposure of medical staff to sarin vapor in the emergency room (abstract). Intensive Care Med 21:1032, 1995.
99.
Ohning BL, Reed MD, Blumer JL: Continuous nasogastric administration of activated charcoal for the treatment of theophylline intoxication. Pediatr Pharmacol 5:241, 1986.
100. Okumura
T, Suzuki K, Fukuda A, et al: The Tokyo subway sarin attack: Disaster management, part 2: Hospital response. Acad Emerg Med 5:625, 1998.
101. Park
GD, Radomski L, Goldberg MJ, et al: Effects of size and frequency of oral doses of charcoal on theophylline clearance. Clin Pharmacol Ther 34:663, 1983.
102. Park
GD, Spector R, Goldberg MJ, Johnson GF: Expanded role of charcoal therapy in the poisoned and overdosed patient. Arch Intern Med 146:969, 1986.
103. Park
GD, Spector R, Goldberg MJ, et al: Effect of the surface area of activated charcoal on theophylline clearance. J Clin Pharmacol 24:289, 1984.
104. Peterson 105. Pollack
C: Electrolyte depletion following emergency stomach evacuation. Am J Hosp Pharm 36:1366, 1979.
MM, Dunbar BS, Holbrook PR, et al: Aspiration of activated charcoal and gastric contents. Ann Emerg Med 10:528, 1981.
106. Pond
SM, Lewis-Driver DJ, Williams GM, et al: Gastric emptying in acute overdose: A prospective randomised controlled trial. Med J Aust 163:345, 1995.
107. Pond
SM, Olson KR, Osterloh JD, et al: Randomized study of the treatment of phenobarbital overdose with repeated doses of activated charcoal. JAMA 251:3104, 1984.
108. Position
statement and practice guidelines on the use of multi-dose activated charcoal in the treatment of acute poisoning. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol 37:731, 1999. 109. Prescott
LF, Hamilton AR, Heyworth R: Treatment of quinine overdosage with repeated oral charcoal. Br J Clin Pharmacol 27:95, 1989.
110. Radomski 111. Rangan 112. Ray
L, Park GD, Goldberg MJ, et al: Model for theophylline overdose treatment with oral activated charcoal. Clin Pharmacol Ther 35:402, 1984.
C, Nordt SP, Hamilton R, et al: Treatment of acetaminophen ingestion with a superactivated charcoal-cola mixture. Ann Emerg Med 37:55, 2001.
MJ, Radin DR, Condie JD, et al: Charcoal bezoar. Small-bowel obstruction secondary to amitriptyline overdose therapy. Dig Dis Sci 33:106, 1988.
113. Ritschell 114. Roberts
W, Erni W: The influence of temperature of ingested fluid on stomach emptying time. Int J Clin Pharmacol 15:172, 1977. JR, Carney S, Boyle SM, et al: Ondansetron quells drug-resistant emesis in theophylline poisoning. Am J Emerg Med 11:609, 1993.
115. Robertson
W: Syrup of ipecac associated fatality: A case report. Vet Hum Toxicol 21:87, 1979.
116. Saetta
JP, March S, Gaunt ME, et al: Gastric emptying procedures in the self-poisoned patient: Are we forcing gastric content beyond the pylorus? J R Soc Med 84:274, 1991.
117. Scalzo
J, Tominack R, Thompson M: Malposition of pediatric gastric lavage tubes demonstrated radiographically. J Emerg Med 10:581, 1992.
118. Scharman
EJ, Lembersky R, Krenzelok EP: Efficiency of whole bowel irrigation with and without metoclopramide pretreatment. Am J Emerg Med 12:302, 1994.
119. Scharman
EJ, Cloonan HA, Durback-Morris LF: Home administration of charcoal: Can mothers administer a therapeutic dose? J Emerg Med 21:357, 2001.
120. Schultz
M, Cisek J, Wabeke R: Simulated exposure of hospital emergency personnel to solvent vapors and respirable dust during decontamination of chemically exposed patients. Ann Emerg Med 26:324, 1995. 121. Sessler
CN, Glauser FL, Cooper KR: Treatment of theophylline toxicity with oral activated charcoal. Chest 87:325, 1985.
122. Shannon
M, Amitai Y, Lovejoy FH, Jr: Multiple dose activated charcoal for theophylline poisoning in young infants. Pediatrics 80:368, 1987.
123. Shrestha
M, George J, Chiu M: A comparison of three gastric lavage methods using radionuclide gastric emptying study. J Emerg Med 14:413, 1996.
124. Smilkstein
M, Steedle D, Kulig K, et al: Magnesium levels after magnesium containing cathartics. J Toxicol Clin Toxicol 26:51, 1988.
125. Smith
SW, Ling LJ, Halstenson CE: Whole-bowel irrigation as a treatment for acute lithium overdose. Ann Emerg Med 20:536, 1991.
126. Tandberg
D, Diven BG, McLeod JW: Ipecac-induced emesis versus gastric lavage: A controlled study in normal adults. Am J Emerg Med 4:205, 1986.
127. Tandberg
D, Liechty EJ, Fishbein D: Mallory-Weiss syndrome: An unusual complication of ipecac-induced emesis. Ann Emerg Med 10:521, 1981.
840
128. Tenenbein
M: Whole bowel irrigation for toxic ingestions. J Toxicol Clin Toxicol 23:177, 1985.
129. Tenenbein
M: Whole bowel irrigation as a gastrointestinal decontamination procedure after acute poisoning. Med Toxicol Adverse Drug Exp 3:77, 1988.
130. Tenenbein
M: Position statement: Whole bowel irrigation. American Academy of Clinical Toxicology; European Association of Poison Centres and Clinical Toxicologists. J Toxicol Clin Toxicol
35:753, 1997. 131. Tenenbein 132. Teshima 133. Thoma
M, Cohen S, Sitar DS: Efficacy of ipecac-induced emesis, orogastric lavage, and activated charcoal for acute drug overdose. Ann Emerg Med 16:838, 1987.
D, Suziki A, Otsubo K: Efficacy of emetic and United States Pharmacopeia ipecac syrup in prevention of drug absorption. Chem Pharm Bull 38:2242, 1990.
ME, Glauser JM: Use of glucagon for removal of an orogastric lavage tube. Am J Emerg Med 13:219, 1995.
134. Thompson
AM, Robins JB, Prescott LF: Changes in cardiorespiratory function during gastric lavage for drug overdose. Hum Toxicol 6:215, 1987.
135. Timberlake
GA: Ipecac as a cause of the Mallory-Weiss syndrome. South Med J 77:804, 1984.
136. True
RJ, Berman JM, Mahutte CK: Treatment of theophylline toxicity with oral activated charcoal. Crit Care Med 12:113, 1984.
137. Underhill
T, Greene M, Dove A: A comparison of the efficacy of a gastric lavage, ipecacuanha and activated charcoal in the emergency management of paracetamol overdose. Arch Emerg Med
7:148, 1990. 138. Vale
JA: Position statement: Gastric lavage. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. J Toxicol Clin Toxicol 35:711, 1997.
139. Van
Ameyde KJ, Tenenbein M: Whole bowel irrigation during pregnancy. Am J Obstet Gynecol 160:646, 1989.
140. Vasquez
T, Evans D, Ashburn W: Efficacy of syrup of ipecac-induced emesis for emptying gastric contents. Clin Nucl Med 13:638, 1988.
141. Veerman
M, Espejo MG, Christopher MA, et al: Use of activated charcoal to reduce elevated serum phenobarbital concentration in a neonate. J Toxicol Clin Toxicol 29:53, 1991.
142. Wald
P, Stern J, Weine B, et al: Esophageal tear following forceful removal of an impacted oral gastric lavage tube. Ann Emerg Med 15:80, 1986.
143. Watson
W, Leighton J, Guy J: Recovery of cyclic antidepressants with gastric lavage. J Emerg Med 7:373, 1989.
144. Watson
WA, Cremer KF, Chapman JA: Gastrointestinal obstruction associated with multiple-dose activated charcoal. J Emerg Med 4:401, 1986.
145. Wolowodiuk 146. Young
OJ, McMicken DB, O'Brien P: Pneumomediastinum and retropneumoperitoneum: An unusual complication of syrup-of-ipecac-induced emesis. Ann Emerg Med 13:1148, 1984.
WF Jr, Bivins HG: Evaluation of gastric emptying using radionuclides: Gastric lavage versus ipecac-induced emesis. Ann Emerg Med 22:1423, 1993.
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Chapter 44 - Peritoneal Procedures John A. Marx
Paracentesis and diagnostic peritoneal lavage constitute the two primary intraperitoneal procedures. They are fundamentally similar in purpose and design. However, the former is generally reserved for medical concerns and the latter for traumatic pathology.
DIAGNOSTIC PERITONEAL LAVAGE Root and colleagues introduced diagnostic peritoneal lavage in 1964. [1] It has withstood the passage of more than 3 decades and remains a mainstay in the management of penetrating torso trauma. Following a blunt mechanism of injury, its greatest utility is as a triage tool in the hemodynamically unstable multiply injured patient. Otherwise, it serves with computed tomography (CT) and with the intent of rapidly discovering or excluding the presence of intraperitoneal hemorrhage, a purpose identical with that of ultrasound (US) in the diagnostic armamentarium of blunt trauma. [2] While commonly referred to as diagnostic peritoneal lavage (DPL), this procedure comprises two distinct components: peritoneal aspiration and peritoneal lavage. Peritoneal aspiration, in which an attempt is made to retrieve free intraperitoneal blood, precedes lavage. A finding of intraperitoneal blood presages intraperitoneal organ injury and precludes the need for subsequent lavage. In the lavage portion, normal saline is introduced by catheter into the peritoneal cavity, recovered by gravity, and analyzed. Peritoneal lavage can be used as a therapeutic tool in hypothermia and as a means of removing toxins. [3] It has also been used as a diagnostic instrument for suspected intra-abdominal infection and nontraumatic sources of hemorrhage. [4] [5] However, its primary use is as a determinant for the need for laparotomy following trauma, and this chapter focuses on that use. Indications Blunt Trauma
Prior to the advent of CT and US, DPL was the sole diagnostic option to physical examination for predicting the need for operative intervention ( Table 44-1 ). It was integral both to the reduction of unnecessary laparotomies and to the discovery of unsuspected and life-threatening intra-abdominal hemorrhage in patients with significant closed head injury. [6] [7] In a number of respected centers in the United States, DPL continues to be a focal diagnostic instrument. It serves two primary functions. [8] First, it can rapidly determine or exclude the presence of intraperitoneal hemorrhage ( Table 44-2 ). Thus, the patient with a critical closed head injury, the unstable motor vehicle crash victim with multiple potential sources of blood loss, or the patient with pelvic fracture and retroperitoneal hemorrhage can be appropriately routed to life-saving laparotomy. [9] [10] Furthermore, given its exquisite sensitivity, a negative peritoneal aspiration allows the clinician to proceed to alternative management steps and the patient to forego unnecessary laparotomy. Second, DPL can be used in less exigent circumstances as a means of predicting solid or hollow visceral injury requiring laparotomy. [11] [12] In this venue, its sensitivity to the presence of hemorrhage may prompt unnecessary laparotomy in a small percentage of patients with self-limited lacerations of the liver or spleen. [13] [14] [15] [16] CT scan specifically evaluates all intraperitoneal structures as well as the retroperitoneum, a region inaccessible to DPL. Because resolution and the speed with which it can be undertaken have vastly improved, CT has become an invaluable adjunct in the management of blunt trauma. [17] [18] It is most useful in the identification of injury to solid organs with accompanying intraperitoneal hemorrhage and greatly assists nonoperative management of those injuries. Using DPL and CT in a complementary fashion can mitigate the number of unnecessary laparotomies while prompting therapeutic operations in other cases. The ability of CT to discern hollow viscus and pancreatic pathology has improved but remains inconsistent. [19] [20] With regard to hollow viscus injury, it is when serial clinical evaluations cannot be performed that gut perforation leads to preventable mortality. It is for this express scenario that certain authorities recommend the performance of DPL: following a negative CT or particularly one demonstrating free fluid without evidence of solid organ damage. [21] [22] Experience with US in North America is meager in comparison with that in Western Europe (notably Germany) and Asia (notably Japan). In the past, US in the United States had been used exclusively for the detection and serial examination of traumatic pancreatic pseudocysts. There are two paradigms that have brought US to the forefront. First, this modality has been adopted as the primary triage instrument, in lieu of DPL, for the detection of intraperitoneal hemorrhage on the basis of identifying which pouches and gutters are fluid-filled. [23] [24] [25] [26] Clinical success in this role has been mixed with reported sensitivities for intraperitoneal hemorrhage of 65 to 95%.[27] [28] [29] [30] [31] [32] [33] Additionally, to be useful in this role, a competent technician, interpreter, and equipment must be present in real-time. It has been demonstrated that emergency clinicians and surgeons can be trained in this technique to a level of competence sufficient for this need. [34] In centers that rely upon US, DPL should serve as a reliable study when US equipment is unavailable, the US is technically difficult, or when the results
Manifestation
TABLE 44-1 -- Clinical Indications for Laparotomy after Blunt Trauma Pitfall
Unstable vital signs with strongly suspected abdominal injury
Alternate sources of shock
Unequivocal peritoneal irritation
Unreliable
Pneumoperitoneum
Insensitive; may be due to pulmonary source or invasive procedures (diagnostic peritoneal lavage, laparoscopy)
Evidence of diaphragmatic injury
Nonspecific
Significant gastrointestinal bleeding
Uncommon, unknown accuracy
From Marx J: Abdominal trauma. In Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen's Emergency Medicine Concepts and Clinical Practice, 5th ed. Philadelphia, Mosby, 2002, p 433.
842
Purpose
TABLE 44-2 -- Indications for Diagnostic Peritoneal Lavage Following Blunt Mechanism Circumstance Alternate or Complementary Diagnostic
Rapidly determine presence of IPH
Hemodynamically unstable multiple blunt trauma
US
Determine presence of organ injury
Suspected or known blunt trauma with unreliable examination:
CT
• Head injury with altered mental status • Alcohol intoxication • Drug intoxication • Spinal cord injury Determine presence of IPH or injury
Multiple trauma patients who require general anesthesia for other injuries
CT, US
CT, computed tomography; IPH, intraperitoneal hemorrhage; US, ultrasound. of the US are indeterminate, especially when the patient demonstrates hemodynamic compromise. Second, US can determine injury to solid viscera such as the liver, spleen, kidneys, and pancreas. This requires considerably greater expertise, and in most centers
US has not supplanted CT for this purpose. [35] DPL is a readily available procedure that can be conducted rapidly in the safe confines of the emergency department (ED). The ability to undertake CT, in particular, or to a lesser extent, US in a similar manner requires careful consideration of clinical circumstances, equipment location, and the capabilities of available personnel ( Table 44-3 ) ( Fig. 44-1 ). [36] [37] Penetrating Trauma
The advent of DPL was seminal in the promotion of selective management for penetrating abdominal injury. Here its role is more dominant than for blunt trauma due to the far greater likelihood of occult injury to hollow viscera and the diaphragm following a penetrating mechanism. [38] [39] Instruments and missiles may penetrate the abdominal cavity via the anterior abdominal wall, flank, back, or low chest. [40] The intraperitoneal space is vulnerable if penetration occurs as high as the fourth intercostal space anteriorly and the sixth or seventh laterally and posteriorly, as the diaphragm may rise to these levels in the expiratory phase of respiration. [41] Coincident thoracic penetration has occurred in up to 46% of abdominal injuries. [42] [43] [44] The likelihood of retroperitoneal
Scenario
TABLE 44-3 -- Diagnostic Studies in Blunt Abdominal Trauma Study Purpose Primary Study
Alternate/Compensatory
Hemodynamically unstable General
IPH
DPL, US
—
Pelvic fracture
IPH
DPL,* US
—
General
OI†
CT
DPL, US‡
Nonoperative management§
OI
CT?
DPL¶ , US‡
CHI
OI, HVI
DPL¶ , CT?
US‡
BAD
IPH
DPL, US
CT£
Hemodynamically stable
BAD, blunt aortic disruption; CHI, closed head injury; CT, computed tomography; DPL, diagnostic peritoneal lavage; HVI, hollow viscus injury; IPH, intraperitoneal hemorrhage; OI, organ injury; US, ultrasound. From Marx J: Abdominal trauma. In Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen's Emergency Medicine Concepts and Clinical Practice, 5th ed. St. Louis, Mosby, 2002, p 431. *+ peritoneal aspirate mandates laparotomy, + red blood cell count only, warrants attention to pelvic fracture. †Specific organ damage or fluid/blood suggesting injury. ‡US for OI much less reliable than for IPH. §Institutional capability should be carefully considered. ?CT less reliable for HVI than for solid visceral injury. ¶Complementary to CT if HVI suspected. £May be more appropriate if can be rapidly acquired or if CT primary study for BAD.
injury increases when the entry site is over the flank or back, but the prospect of intraperitoneal pathology remains considerable with cited incidences of 21 to 44% for the flank and 7 to 14% for the back ( Table 44-4 ). [45] [46] [47] Stab wounds.
Because only one fourth to one third of patients who sustain stab wounds to the anterior abdomen require laparotomy, diagnostic algorithms are used to decrease the rate of unnecessary operation. [38] [43] [48] [49] An optimal approach would not sacrifice sensitivity for morbid intraperitoneal injury. A pathway using a combination of clinical mandates, local wound exploration, and DPL is well established ( Fig. 44-2 ). [50] These clinical mandates are reasonably accurate predictors of significant intraperitoneal injury ( Table 44-5 ). Thus, the presence of one or more mandates suggests the need for urgent laparotomy and precludes the undertaking of other diagnostic studies. DPL fills three roles in the evaluation of patients with abdominal stab wounds ( Table 44-6 ): (1) rapid determination of the presence of hemoperitoneum, (2) discovery of intraperitoneal injury requiring operation in stable patients, and (3) the establishment of diaphragmatic violation. As is the case in blunt trauma patients, DPL can be invaluable as a rapid triage tool when the source of hemodynamic instability is not known. Pericardial tamponade, intrathoracic hemorrhage, and intraperitoneal hemorrhage may be contributory to hemodynamic instability or wholly causal. Again, as for blunt trauma evaluation, US is the only diagnostic modality for
843
Figure 44-1 Blunt abdominal trauma algorithm. BAT, blunt abdominal trauma; CT, computed tomography; D/C, discharge; DPA, diagnostic peritoneal aspiration; DPL, diagnostic peritoneal lavage; IP, intraperitoneal; IPH, intraperitoneal hemorrhage; LAP, laparotomy; SPE, serial physical examinations; US, ultrasound. *Determined by unequivocal free intraperitoneal fluid on ultrasound or positive peritoneal aspiration on diagnostic peritoneal lavage. †Can be unreliable because of closed head injury, intoxicants, distracting injury, or spinal cord injury. ‡One or more studies may be indicated. §Need for laparotomy is based on clinical scenario, diagnostic studies, and institutional resources. (From Marx J: Abdominal Trauma. In Marx JA, Hockberger RS, Walls RM, et al. [eds]: Rosen's Emergency Medicine Concepts and Clinical Practice, 5th ed. St. Louis, CV Mosby, 2002, p 432.)
intraperitoneal hemorrhage that is competitive for this role and carries the added advantage of scanning for intrapericardial and intrathoracic hemorrhage as well. [44] In the determination of injury following stab wounds, DPL carries 90% accuracy. [51] [52] [53] Serial examinations, [54] [55] [56] CT, and laparoscopy [57] [58] [59] [60] are alternative modalities in specific circumstances and centers. [61] Diaphragmatic rents created by stab wounds are generally small; thus, at the outset, they do not create apparent clinical or radiologic abnormalities. [62] [63] However, TABLE 44-4 -- Injury Likelihood by Entry Site Intraperitoneal Retroperitoneal Diaphragm Anterior abdomen
++
+
+
Flank
+
++
+
Back
+
++
+
Low chest
+
+
++
From Marx JA: Diagnostic peritoneal lavage. In Ivatury RR, Cayten CG (eds): The Textbook of Penetrating Trauma. Baltimore, Williams & Wilkins, 1996, p 336. morbidity due to delayed herniation of bowel is common and substantive. [64] DPL is currently the most sensitive means of discerning this injury in the immediate
post-trauma phase. [51] Physical examination and CT are notoriously insensitive. Laparoscopy has demonstrated promise in experienced hands. [57] [58] For these small diaphragmatic wounds, the advanced radiologic tool called magnetic resonance imaging (MRI) may be diagnostic, but due to safety and accessibility concerns, it should be reserved for the non-acute phase of management. Gunshot wounds.
Multiple organ injury is the rule following gunshot wounds, and mortality is significantly greater when compared with that for stab wounds. [65] The diagnostic approach is more conservative for gunshot wounds because the likelihood of intraperitoneal injury requiring operative intervention exceeds 95% when the projectile has entered the intraperitoneal cavity ( Fig. 44-3 ). [66] [67] [68] If clinical mandates are met (see Table 44-5 ) or if peritoneal violation has occurred, most centers proceed to laparotomy. [50] One series,
844
Figure 44-2 Anterior abdomen stab wound algorithm. *Plain films, ultrasound, laparoscopy, and computed tomography (CT) can assess peritoneal entry. †Laparoscopy or CT can complement or replace diagnostic peritoneal lavage. ‡Expectant management of injuries is infrequently attempted. D/C, discharge; DPL, diagnostic peritoneal lavage; LAP, laparotomy; LWE, local wound exploration; PEx, physical examination. (From Marx J: Abdominal Trauma. In Marx JA, Hockberger RS, Walls RM, et al. [eds]: Rosen's Emergency Medicine Concepts and Clinical Practice, 5th ed. St. Louis, CV Mosby, 2002, p 427.)
however, cited intra-abdominal injury in 70% to 80% of cases, supporting the contention that nonoperative management could be applied to a substantial percentage of patients. [69] DPL is reserved for two circumstances: (1) the wound tract is neither obviously superficial nor intraperitoneal, and (2) penetration is to the low chest, where diaphragmatic injury is more likely, yet the possibility of intraperitoneal injury exists. Contraindications Diagnostic peritoneal lavage can be undertaken in virtually any patient irrespective of age, pregnant state, or comorbid illness. Adjustment of the technique and site of performance allows relative contraindications to be overcome. Relative contraindications include prior abdominal surgery or infections,
Manifestation
TABLE 44-5 -- Clinical Indications for Laparotomy Following Penetrating Trauma Premise Pitfall
Hemodynamic instability
Major solid visceral or vascular injury
Thorax, mediastinum
Peritoneal signs
Intraperitoneal injury
Unreliable, especially immediately postinjury
Evisceration
Additional bowel, other injury
No injury in ¼ to ? of stab wound cases
Diaphragmatic injury
Diaphragmatic herniation
Rare clinical, radiographic findings
Gastrointestinal and vaginal hemorrhage
Proximal gut or uterine injury
Uncommon, unknown accuracy
Impalement in situ
Vascular impalement
High operative risk, pregnancy
Intraperitoneal air
Hollow viscus perforation
Insensitive; may be caused by intraperitoneal entry only or be due to cardiopulmonary source
Modified from Marx JA: Diagnostic peritoneal lavage. In Ivatury RR, Cayten CG (eds): The Textbook of Penetrating Trauma. Baltimore, Williams & Wilkins, 1996. obesity, coagulopathy, and second- or third-trimester pregnancy. The sole absolute contraindication is when clinical mandates for urgent laparotomy already exist. Technique Preliminary Steps
The stomach and bladder should preferably be decompressed to prevent inadvertent injury. The patient is kept supine and administered sedation and analgesia as appropriate (see Chapter 34 ). This is most relevant when the semi-open technique is used and a trocar is passed through the peritoneum. DPL should be performed according to compliance with standards for body fluid precautions (see Chapter 71 ). Prior to making the skin incisions described later, the site of placement should be prepped with standard skin antiseptics (e.g., povidone-iodine) and appropriately draped. The operator should observe sterile precautions throughout the procedure. Prophylactic antibiotics are not indicated for routine DPL because local and systemic infections are rare. [52] [70] Local anesthesia (1% lidocaine with epinephrine) should be infiltrated liberally into the area for incision and dissection ( Fig. 44-4 ). It is best to delay the incision for more than 30 seconds following local anesthetic infiltration to permit local vasospasm, which minimizes wound bleeding during the procedure. Standard equipment for an open peritoneal lavage catheter placement is shown in Figure 44-5 . Catheter Placement
DPL is performed via two basic methods: open and closed. The two open techniques are semi-open and fully open, and they typically require an assistant. DPL is clearly within the diagnostic armamentarium of the emergency clinician and surgeon. It may be undertaken by either or both in keeping with clinical policies established at the particular trauma center. Open technique.
In the semi-open method, sharp then blunt dissection using a No. 11 scalpel and Army-Navy retractors, respectively, proceeds to the rectus fascia ( Fig. 44-6A and B ). The skin incision should be 4 to 6 cm in length. When the selected site is infraumbilical in the midline, the operator should reach the linea alba; its crossing bands of crural fibers may be apparent. [71] A small 2- to 3-mm opening is then made in the linea alba, preferably with a No. 15 scalpel blade ( Fig. 44-6C ). (The operator will notice a tough, gritty sensation when cutting the linea alba with the scalpel.) Towel clips can be placed through this opening to grasp each side of the rectus fascia ( Fig. 44-6D ). These two towel clips are then lifted to allow safe advancement of the catheter via trocar in a 45° to 60° caudad orientation through the peritoneum and into the peritoneal cavity ( Fig. 44-6E and F ). [72] [73]
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TABLE 44-6 -- Indications for DPL Following Penetrating Mechanism
Purpose
Circumstance
Alternate or Complementary Diagnostic
Rapidly determine presence of IPH
Hemodynamically unstable SW or GSW to low chest, abdomen, flank, back
Ultrasound
Determine presence of organ injury
SW or GSW to low chest, abdomen, flank, back
Serial clinical examinations, CT, laparoscopy
Determine diaphragmatic violation
SW or GSW to low chest, upper abdomen
Laparoscopy
CT, computed tomography; GSW, gunshot wound; IPH, intraperitoneal hemorrhage; SW, stab wound.
To decrease the likelihood of penetrating underlying viscera, some operators advocate holding the fingers low on the catheter-trocar instrument such that on entering the abdominal peritoneum, the fingers will prevent deep penetration. Excessive pressure during trocar penetration is a common error. Steady "one-finger pressure" applied to the handle is sufficient to "pop" through the fascia and peritoneum. After controlled peritoneal penetration of 0.5 to 1.0 cm in the midline, the trocar is retracted 1.0 to 2.0 cm within the catheter, and the catheter is carefully advanced toward the pelvis. Some operators prefer to advance the catheter toward the right or left side of the pelvis. Use of a
Figure 44-3 Gunshot wound algorithm. D/C, discharge; DPL, diagnostic peritoneal lavage; LAP, laparotomy. *Can be assessed by missile path, plain films, local wound exploration, ultrasound, and laparoscopy. †Most centers proceed to laparotomy if peritoneal entry is suspected. ‡Patients with documented superficial and low-velocity injuries can be discharged; unknown depth or high-velocity injuries require further tests or observation. §Serial examinations, laparoscopy, or a computed tomography scan can complement or replace diagnostic peritoneal lavage. ¶Expectant management of injuries caused by gunshot wounds is rarely attempted. (From Marx J: Abdominal Trauma. In Marx JA, Hockberger RS, Walls RM, et al. [eds]: Rosen's Emergency Medicine Concepts and Clinical Practice, 5th ed. St. Louis, CV Mosby, 2002, p 430.)
slight twisting motion during advancement may minimize visceral or omental injury. The fully open technique extends the semi-open technique by one step. The opening in the linea alba is lengthened, and the peritoneum is opened to allow direct visualization during catheter placement into the peritoneal cavity. The two open techniques can be accomplished with a single technician, but an additional pair of hands is advised in order to assist in retraction and handling of instruments. The fully open method is the more technically demanding and time-consuming. It is reserved for clinical circumstances in which the closed or even semi-open technique is not deemed safe or has been attempted and failed. These include pelvic fracture, pregnancy, prior abdominal surgery or infections, and obesity. Closed technique.
With closed techniques, the catheter is introduced into the peritoneal space in a blind percutaneous fashion. [74] Formerly, this was accomplished via trocar. This has been abandoned in favor of the much safer but equally simple Seldinger (guide wire) method, in which a small-gauge guide needle is inserted into the peritoneal cavity in the infraumbilical midline ( Fig. 44-7A ). A flexible wire is then passed through the needle ( Fig. 44-7B ), and the needle is removed, allowing the over-the-wire placement of a soft catheter into the peritoneal cavity. A stab with a No. 11 scalpel at the entry site of the wire allows easier passage of the catheter through the abdominal wall ( Fig. 44-7C and D ). Rotating the catheter while pushing it over the guide wire is recommended to facilitate entry into the peritoneal cavity. The catheter is placed into the right or left pelvic gutter.
Figure 44-4 Local anesthesia is introduced at incision or puncture site. The patient is supine with the head of the bed elevated slightly.
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Figure 44-5 Standard equipment used for open lavage technique.
The wire is then withdrawn, and aspiration conducted, followed by lavage when necessary. The guide wire should always be controlled to avert intra-abdominal migration of the wire. Proponents of the guide wire technique promote its ease and rapidity. [75] [76] [77] [78] [79] Those who prefer the semi-open method argue that the time to peritoneal aspiration, the more critical interval, is minimally different, and that this method may have fewer complications and thus be more accurate than the guide wire technique. [80] [81] [82] [83] Note that time to aspiration for semi-open or closed approaches should entail no more than 2 to 5 minutes. Site
The optimum location for DPL is at the infraumbilical ring, at the inferior border of the umbilicus ( Table 44-7 ). Here, between the rectus abdominis muscles, there is adherence of the peritoneum and relative lack of vascularity and preperitoneal fat. [71] Closed DPL should always be conducted here. In the event of second- or third-trimester pregnancy, a suprauterine approach is used. If there is midline scarring, a fully open technique at the lateral border of the rectus abdominis in the left lower quadrant may be necessary. The left is preferred to avoid later confusion about whether an appendectomy has been performed. It is interesting to note that Moore and colleagues found no increase in complications or misclassified lavages when the closed technique was used in a small series of patients with prior abdominal surgery. [84] In the presence of a pelvic fracture, a fully open supraumbilical approach is recommended. This greatly decreases the likelihood of passing the catheter through retroperitoneal hematoma that has dissected from the fracture anteriorly and across the abdominal wall. [85] In penetrating trauma, DPL should not be conducted through the stab or missile entry site. Such an approach may contaminate the intraperitoneal cavity and potentially exacerbate abdominal wall bleeding, which could in turn lead to a false-positive result. Aspiration and Lavage
Once the catheter has been placed successfully into the peritoneal cavity and the right-angle adapter, extension tubing, and a non-Luer-Lok syringe have been attached, aspiration is attempted ( Fig. 44-8 ). The recovery of 10 mL of blood is considered positive, and the procedure terminated. In penetrating trauma, the acquisition of lesser amounts may be meaningful because of the tendency for the diaphragm and bowel to hemorrhage minimally when injured. However, there are no
established rules in this regard. If little to no blood is aspirated, the peritoneal cavity is lavaged with either normal saline or lactated Ringer's solution ( Fig. 44-9 ). A blood pressure cuff or blood infusion pump can be applied to the plastic intravenous (IV) bag to speed the influx (i.e., decrease lavage time), but they are rarely needed. Large-bore infusion tubing (e.g., urologic irrigation tubing sets, such as the Abbott No. 6544 cystoscopy/irrigation set) also shortens fluid influx time. The normal amount is 1 L in adults or 15 mL/kg in children. When possible, the patient is rolled or shifted from side to side after infusion to increase mixing. The IV bag or bottle is placed on the floor
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(or below abdominal level), and the fluid is allowed to return by gravity. The fluid may not continue to return because of several factors. Some IV tubing contains a one-way valve; if tubing with a valve was used in error, valveless tubing must be reinserted into the IV bag. Another reason for poor return is inadequate suction. This problem can be corrected by insertion of a needle into the second opening at the bottom of the IV bag or into the head of the IV bottle for aspiration of 10 mL of air. Alternatively, the catheter may be adherent to the peritoneum. If so, relieving some of the pressure in the IV bottle or gently wiggling and twisting the catheter as well as applying abdominal pressure may aid flow return. It is generally accepted that the return of greater than or equal to 700 mL in the adult is adequate for interpretation of findings. However, as little as 10 to 20% of the infusate may give a representative sample for both gross and microscopic determinations. Only 10 mL of fluid from the return need be sent to the laboratory for cell count analysis; another 10 mL can be sent for enzyme analysis (see interpretation later in this chapter). Some operators prefer to leave the dialysis catheter in place until the returned fluid is analyzed. The clinician may wish to re-lavage when the initial results are borderline or an occult bowel perforation is suspected. Complications Local and Systemic
Local wound complications, including infection, hematoma, and dehiscence, have occurred in only 0.3% of patients in 2 large series. evisceration is likely an even more rare condition. [88] Systemic infection has been described rarely ( Table 44-8 ).
[ 51] [86] [87]
Dehiscence with
Intraperitoneal
Iatrogenic intraperitoneal injury can be inflicted by the trocar, wire, and, rarely, the catheter. Virtually any structure in the peritoneal cavity can be breached, including the small and large bowel, the bladder, and major vessels. Typically, if the needle is the culprit, and even if the trocar is responsible, injury to these structures is minimal and self-limiting, and observation of the patient is sufficient. Technical Failure
Inability to recover peritoneal aspirate or lavage fluid can result in a false-negative interpretation. This can occur in several circumstances. It follows unwitting placement of the catheter into the preperitoneal space, which is less likely to occur with either open technique. Compartmentalization of fluid by adhesions or obstructing omentum can impede egress of fluid. When a fully open supraumbilical or suprauterine technique is used, the catheter may be too short to access the depths of the intraperitoneal cavity. Finally, large diaphragmatic tears typical of blunt pathophysiology allow flow of lavage fluid from the intraperitoneal to the thoracic cavity. Saunders and colleagues compared percutaneous DPL versus the open technique in a prospective randomized trial. [89] Fluid obtained by the two techniques had similar test performance for intra-abdominal pathology. The open technique took on average more than 4 minutes longer to perform, but the percutaneous approach had an 11.2% (versus 3.8% with the open approach) technical failure rate. False-positive findings can occur in two ways. First, iatrogenic misadventure can be responsible. Second, in penetrating trauma, particularly stab wounds, bleeding from the abdominal wall injury site into the peritoneal cavity can lead to positive findings when no injury to intraperitoneal structures has occurred. [52] Interpretation Gross Blood
The recovery of =10 mL blood via aspiration is considered a positive finding. Lesser-volume aspirates are generally discarded and are not factored into lavage analysis. Grossly bloody aspirates are typically indicative of solid visceral or vascular injury, with a positive predictive value >90%. [86] [90] Aspiration of blood is responsible for approximately 80% of true-positive DPL findings in blunt trauma and for 50% of those following stab wounds. [51] A positive aspiration in the blunt trauma patient who is hemodynamically stable or has been resuscitated to apparent stability need not mandate urgent operation. Unnecessary laparotomy will occur if there has been minimal and self-limited damage to the liver, spleen, bowel serosa, or mesentery. [17] [91] In this situation, CT and clinical indicators should be used in concert with the DPL findings. Red Blood Cell (RBC) Count
The recommended RBC threshold varies according to mechanism and, in the case of stab wounds, the external site of injury ( Table 44-9 ). The optimum criterion will deliver excellent sensitivity, a high positive-predictive value, and, therefore, a minimum incidence of unnecessary laparotomy. Negative laparotomy incurs a prolongation of hospitalization and increases the cost of care, in addition to creating the potential for procedural complications. [92] [93] RBC counts greater than 10 5 /mm3 (i.e., >10 5 /µL) are generally considered positive with a blunt mechanism or following stab wounds to the anterior abdomen, flank, or back. Counts of 20,000 to 100,000/mm3 should be considered indeterminate. [51] [53] [94] [95] For stab wounds to the low chest, where the diaphragm is at increased risk of injury, the RBC criterion should be lowered to 5000/mm3 to maximize sensitivity for isolated injury to this structure. [43] [51] [96] [97] With gunshot wounds to the abdomen or low chest, the same criterion is applied. This is intended to increase the sensitivity of the test, because intraperitoneal entry by a missile carries a likelihood of intraperitoneal injury of greater than or equal to 95%. [43] [69] [98] [99] An uncomplicated DPL should not create more than several hundred to several thousand RBCs in the peritoneal lavage fluid. The incidence of false-positive RBC interpretation in the setting of pelvic fracture is considerable. However, aspiration of free blood in the critical pelvic fracture patient predicts active intraperitoneal hemorrhage in greater than 80% of cases. [100] A positive RBC count should generally prompt corroboration or refutation of intraperitoneal injury by CT. In this fashion, needed pelvic angiography and embolization will not be delayed unnecessarily should active intraperitoneal bleeding not be found ( Fig. 44-10 ). White Blood Cell (WBC) Count
An inflammatory peritoneal response occurs to a multitude of stimuli, including stool, blood, and enzymes. predict small
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[101]
The WBC count in lavage effluent was formerly touted to
Figure 44-6 A, After bladder decompression (generally by Foley catheter placement), a 4- to 6-cm long vertical infraumbilical incision is made with a No. 11 scalpel. B, Blunt dissection using Army-Navy retractors is carried down to the rectus fascia. Crossing bands of crural fibers may be seen. C, A 2- to 3-mm incision is made through the rectus fascia in the midline ( linea alba) with a No. 15 scalpel. D, Towel clips grasp each side of the rectus fascia, which is lifted prior to insertion of the trocar and diagnostic peritoneal lavage (DPL) catheter. E, The trocar with DPL catheter is passed at a 45° caudad angle into the fascial opening and through the peritoneum. Note that in the fully open method, the incision in the rectus fascia is extended, the peritoneum is directly visualized and incised, and the catheter alone is placed into the peritoneal cavity. F, As soon as the peritoneum has been entered, only the catheter is gently advanced into the peritoneal cavity while the trocar is withdrawn. It is often helpful to advance the catheter with a slight twisting motion and to direct it toward either the right or left pelvic gutter.
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Figure 44-7 A, For the closed diagnostic peritoneal lavage (DPL) method using a guide wire (Seldinger technique), the needle is inserted into the peritoneal cavity in the midline just below the umbilicus and aimed slightly caudad. B, The flexible guide wire is passed through the needle and into the peritoneal cavity. Ideally, the wire should be directed toward the right or left pelvic gutter. The needle is withdrawn while the wire is stabilized with the operator's free hand at all times. C, A stab incision is made with a No. 11 scalpel immediately below the wire to permit easier passage of the DPL catheter. D, The DPL catheter is directed over the wire and into the peritoneal cavity using a slight twisting motion. The wire is stabilized by the operator at all times and removed after catheter placement. The catheter should be directed toward the right or left pelvic gutter when advanced.
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Clinical Circumstance
TABLE 44-7 -- Preferred Site of Diagnostic Peritoneal Lavage Site
Method
Standard adult
Infraumbilical midline
C or SO
Standard pediatric
Infraumbilical midline
C or SO
Second- and third-trimester pregnancy
Suprauterine
FO
Midline scarring
Left lower quadrant
FO
Pelvic fracture
Supraumbilical
FO
Penetrating trauma
Infraumbilical midline *
C or SO
C, Closed; FO, fully open; SO, semiopen. *The stab wound or gunshot wound site should be avoided.
bowel injury but has since been proven unreliable. [102] It is insensitive in the immediate postinjury period, as 3 to 5 hours are necessary before the test becomes positive ( Table 44-10 ). [103] [104] Moreover, a positive finding is likely to be falsely so. [103] [105] Therefore, the WBC level in and of itself should not determine the need for laparotomy. Enzymes
Alkaline phosphatase is contained in intramural small bowel as well as in hepatobiliary secretions released into the proximal intestine. Amylase is contained in the latter only. Perforation of small bowel allows access of these two markers into the peritoneal cavity, where they can be recovered by peritoneal lavage. [106] [107] [108] While levels of the two markers usually rise in tandem, lavage amylase has been shown to be a more accurate marker than lavage alkaline phosphatase (see Table 44-10 ). In contradistinction to the WBC count, these tests will be positive in the immediate postinjury period. However, they may not be economical if used on a mandatory rather than a selective basis. Neither is helpful in discerning the presence of pancreatic pathology. Miscellaneous
Routine bile staining, Gram stain, and microscopy to identify vegetable fibers are rarely productive and are of untested accuracy. Deck and Porter have reported that finding urine in the lavage fluid as evidenced by a straw color and creatinine in the peritoneal fluid should suggest an intraperitoneal bladder or collecting system injury.[109]
Figure 44-8 After attachment of the right angle connector and extension tubing, aspiration of the peritoneum is attempted.
Figure 44-9 If the aspiration is negative, normal saline or Ringer's lactate solution is instilled through the catheter. The IV tubing should have no valves in place. After infusion, the fluid bag is placed on the floor and allowed to fill with peritoneal effluent via gravity.
Conclusion DPL remains an invaluable diagnostic instrument in trauma. It should be used in common-sense fashion. Laboratory parameters are guidelines and should not be embraced to
Category
TABLE 44-8 -- Diagnostic Peritoneal Lavaage Complications Comments
Local and systemic Hematoma-incision site
Local wound care
Dehiscence-incision site
Local wound care
Local wound infection
As indicated
Systemic infection
As indicated
Intraperitoneal injury Bowel
Observe, usually self-limited
Bladder
Observe, usually self-limited
Vascular
Observe, usually self-limited
Technical failure INABILITY TO RECOVER FLUID* Preperitoneal catheter placement
Repeat DPL
Compartmentalization of fluid
US, CT
Obstructed catheter
Gentle catheter manipulation
Diaphragm injury
Reverse Trendelenburg; consider US, CT
"Short" catheter (supraumbilical or suprauterine approach)
Trendelenburg
INTRAPERITONEAL HEMORRHAGE† Iatrogenic injury
As indicated by clinical markers
Stab wound abdominal wall bleed
As indicated by clinical markers
Pelvic fracture (RBC count)
Complementary CT
CT, computed tomography; DPL, diagnostic peritoneal lavage; RBC, red blood cell; US, ultrasound. *May lead to false-negative DPL †May lead to false-positive DPL
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TABLE 44-9 -- Diagnostic Peritoneal Lavage Red Blood Cell Criteria (per mm 3 ) Positive Indeterminate 100,000* 20–100,000
Blunt trauma Stab wound Anterior abdomen
100,000 20,000–100,000
Flank
100,000 20,000–100,000
Back
100,000 20,000–100,000
Low chest
5000
1000–5000
5000
1000–5000
Gunshot wound
From Marx J: Abdominal trauma. In Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen's Emergency Medicine Concepts and Clinical Practice, 5th ed. St. Louis, Mosby, 2002, p 425. *In a hemodynamically stable patient with pelvic fracture and positive or equivocal red blood cell count, computed tomography should be obtained to corroborate or refute intraperitoneal injury.
the exclusion of pertinent clinical features. CT, US, or both can serve in lieu of or in addition to DPL in its various roles. capability of an institution's resources and personnel in each clinical scenario.
[110]
Optimal strategies depend largely on the
Figure 44-10 Pelvic fracture algorithm. CT, computed tomography; D/C, discharge; DPA, diagnostic peritoneal aspiration; DPL, diagnostic peritoneal lavage; IP, intraperitoneal; IPH, intraperitoneal hemorrhage; LAP, laparotomy; Pelvic Fx, pelvic fracture; US, ultrasound. *Determined by unequivocal free intraperitoneal fluid on ultrasound or positive peritoneal aspiration on diagnostic peritoneal lavage. †One or more studies may be indicated. ‡Need for laparotomy is based on clinical scenario, diagnostic studies, and institutional resources. (From Marx J: Abdominal Trauma. In Marx JA, Hockberger RS, Walls RM, et al [eds]: Rosen's Emergency Medicine Concepts and Clinical Practice, 5th ed. St. Louis, CV Mosby, 2002, p 434.
PARACENTESIS Ascites connotes an abnormal accumulation of fluid within the peritoneal cavity. The word derives from the Greek askos, which means bag or sack. It is a symptom with important diagnostic, therapeutic, and prognostic implications. Therapeutic abdominal paracentesis is one of the oldest medical procedures, dating to approximately 20 BC. Paracentesis was first described in modern medical literature by Saloman at the beginning of this century, and it became a valued decompressive therapy. [111] With the advent of diuretics in the early 1950s, paracentesis fell out of favor as a treatment option. Controlled clinical trials in the late 1980s up to the present have restored its reputation by demonstrating the safety and efficacy of large-volume paracentesis in adults and children. [112] [113] [114] [115] [116] [117] [118] Because this mode is invasive and consumes clinician hours, it is generally reserved for the treatment of patients with chronic ascites who have tense ascites or whose condition is refractory to diuretic therapy. [115] [119] However, paracentesis remains an important diagnostic agent for patients with new-onset ascites or to determine the presence
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TABLE 44-10 -- Diagnostic Peritoneal Lavage Non-Red Blood Cell Criteria Positive Indeterminate LAM (IU/L)
=20
10–19
LAP (IU/L)
=3
NA
WBCs (per mm3 )
>500
250–500
LAM, lavage amylase; LAP, lavage alkaline phosphatase; NA, not applicable; WBCs, white blood cells. From Marx JA: Diagnostic peritoneal lavage. In Ivatury RR, Cayten CG (eds): The Textbook of Penetrating Trauma. Baltimore, Williams & Wilkins, 1996, p 337. of worrisome conditions, notably infection, in those with preexistent ascites. [120] [121] Clinical Features Determination of Ascites
Small amounts of ascites may be asymptomatic. Larger collections typically cause a sense of abdominal fullness, anorexia, early satiety, and perhaps nausea and abdominal pain. Considerable accumulations create symptoms of respiratory distress by virtue of restricting lung capacity. [122] The most predictive history and physical findings for excluding the diagnosis of ascites are the absence of ankle swelling and increased abdominal girth and the inability to demonstrate bulging flanks, flank dullness, or shifting dullness. [123] [124] Positive predictors for the diagnosis are a positive fluid wave, shifting dullness, or peripheral edema. [125] [126] Patients who lack obvious clinical markers may benefit from the performance of ultrasonography, which can discern the presence of as little as 100 mL fluid. [127] Endoscopic-guided ultrasound may discover just 10 mL. It is more sensitive than computed tomography in this respect and can assist in the identification of malignancy.[128] Additionally, it is a useful adjunct to determine the location of fluid that may be compartmentalized by preexistent infection or surgical adhesions. Differential Diagnosis
The etiologies of ascites can be categorized in several ways. On a structural basis, these are divided into diseases of the peritoneum and diseases not involving the peritoneum. The former group includes infections, neoplasms, collagen vascular diseases, and idiopathic causes. The latter includes cirrhosis, congestive heart failure, nephrotic syndrome, protein-losing enteropathy, malnutrition, myxedema, pancreatic disease, ovarian disease, chylous effusion, Budd-Chiari syndrome, and hepatic venous occlusive disease. [121] [129] [130] Pathophysiologic categories are found in Table 44-11 . In this country, parenchymal liver pathology is overwhelmingly the most likely cause. Within this group, alcoholic liver disease is responsible for approximately 80% of cases ( Table 44-12 ). [131] [132] Finally, ascites can be classified on the basis of a serum-ascites albumin gradient, that is, the difference between albumin values obtained simultaneously from serum and ascites samples ( Table 44-13 ). [133] Indications and Contraindications Therapeutic paracentesis may be undertaken in the emergency setting to relieve the cardiorespiratory and gastrointestinal TABLE 44-11 -- Pathophysiologic Classification of Ascites I. Elevated hydrostatic pressure A. Cirrhosis B. Congestive heart failure C. Constrictive pericarditis D. Inferior vena cava obstruction E. Hepatic vein obstruction (Budd-Chiari syndrome) II. Decreased osmotic pressure A. Nephrotic syndrome B. Protein-losing enteropathy C. Malnutrition D. Cirrhosis or hepatic insufficiency III. Fluid production exceeding resorptive capacity A. Infections 1. Bacterial 2. Tuberculosis 3. Parasitic B. Neoplasms
From Runyon BA: Diseases of the peritoneum. In Wyngaarden JB, Smith LH (eds): Cecil Textbook of Medicine, 18th ed. Philadelphia, WB Saunders, 1988, pp 790–793. manifestations of tense ascites. [134] [135] [136] Diagnostic paracentesis is indicated in any patient whose ascites is of new onset or to disclose the presence of infection in patients with known or suspected ascites, particularly in the context of alcohol-related cirrhotic liver disease. [137] [138] Diagnostic paracentesis is also useful in the management of the AIDS patient, in whom the etiology of ascites will be non-AIDS related in three-quarters of cases. [139] There are few relative contraindications to abdominal paracentesis. Certain systemic and anatomic risks should be considered. Systemic
Given the predominance of alcohol-related cirrhotic liver disease as the cause for ascites, as many as two-thirds to three-quarters of patients subjected to paracentesis will have a coagulopathy. However, the only prospective study to evaluate the complications of paracentesis determined that transfusion-requiring abdominal hematomas occurred in less than 1% of cases despite the fact that 71% of patients had an abnormal prothrombin time. [140] Because transfusion-requiring hematoma is so unlikely, even in this population, prophylactic administration of fresh frozen plasma or platelets imposes TABLE 44-12 -- Causes of Ascites* Cause
% of Patients
Parenchymal liver disease
80
"Mixed"
5
Malignancy
10
Heart failure
5
Tuberculosis
2
Pancreatic
1
Nephrogenous ("dialysis ascites")
70% lymphocytes
Peritoneal biopsy, stain and culture for acid-fast bacilli
Pyogenic peritonitis
Turbid or purulent
If purulent, >1.016
Unusual
>250; mainly polymorphonuclear leukocytes
Positive Gram stain, culture
Congestive heart failure
Straw-colored
Variable, Variable, 4 RBCs per high-power field (HPF) attributable to the procedure. [54] They suggest that >4 RBCs per HPF following catheterization is unlikely to be due to the procedure and is, in fact, evidence of preexisting hematuria, which must be explained. Undesirably retained urethral catheters are an uncommon but frustrating problem. Catheters may be retained because of balloons that do not deflate (see following section) or very rarely because of a knot that has spontaneously developed in the catheter (very rare). Catheter knotting has been associated with the insertion of a highly flexible catheter far into the bladder. [55] A guide wire passed up the catheter may be successful to manipulate some knots free, but urethral dilation with progressively larger catheters adjacent to the retained catheter may be needed to permit urethral passage of the knot.
REMOVING THE NON-DEFLATING CATHETER The self-retaining Foley balloon-type catheter obviates the need for cumbersome taping or suturing of the catheter to keep it in place. Occasionally, however, an indwelling catheter balloon does not deflate. Needless to say, this problem has challenged and frustrated many clinicians and has produced a number of solutions. The usual cause of the nondeflating catheter balloon is the malfunction of the flap-type valve in the balloon lumen of the catheter, which normally allows fluid to enter the balloon of the catheter but prevents passive egress ( Fig. 56-23 ). [56] The ideal solution is one that resolves the problem—deflating the balloon—without creating another problem (i.e., unnecessary bladder irritation or balloon fragmentation). Of the methods recommended to decompress nondeflating catheter balloons, the only technique that approaches the ideal directly attacks this flap valve deformity. Other methods of deflation are effective but require more creativity and dexterity on the part of the catheterist. Techniques One method of balloon deflation consists of simply overstretching the balloon with air or water to the point of rupture. Up to 200 mL of fluid can be injected before a 5-mL balloon will rupture. [56] [57] Adding volume to the empty bladder may not be a problem. Unfortunately, this technique may produce unacceptably painful bladder distention for the patient whose catheter is blocked and whose bladder is either secondarily
Figure 56-23 A flap-like defect in the inflating channel of a balloon catheter that is being raised by a wire stylet passed down the inflating channel to deflate the balloon. (From Eichenberg HA, Amin M, Clark J: Nondeflating Foley catheters. Int Urol Nephrol 8:171, 1976. Reproduced by permission.)
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contracted due to chronic infection or neurogenic bladder dysfunction or distended to the point of maximum filling. An even more compelling reason not to use this technique is the disconcerting frequency of balloon fragmentation and subsequent foreign-body bladder stone formation. In an experimental study of 100 catheters (50 of which were overdistended with water and 50 of which were overdistended with air), all 100 catheter balloons ruptured into fragments. [56] Cystoscopic inspection of the bladder and removal of any fragments will be required to prevent bladder stone formation if this method of balloon deflation is selected. A second method of balloon deflation involves injecting an erosive substance into the balloon port. This causes the balloon to deflate after part of the balloon wall has been eroded. Organic compounds that attack the latex polymers are often used. Ether, acetone, mineral oil, and even petrolatum ointment have been used. In general, the more volatile the substance, the more rapidly it ruptures the balloon. Rupture of the balloon may be partly a result of the rapid expansion that some of these volatile substances—especially ether—undergo at body temperature. Ether was reported to rupture 58 of 60 catheter balloons within 2 minutes of injection into the balloon port. Unfortunately, in 56 of the catheters, a free fragment of the balloon was created. Mineral oil, which works more slowly, was associated with fragment production in 95 of 100 catheters tested. [56] When released into the bladder, organic substances often produce a symptomatic chemical cystitis. Use of these substances is discouraged. A third method of deflating the balloon is to puncture it with a needle. With gentle traction, the balloon is located in the urethra or drawn against the bladder neck and is punctured with a thin 25- or 27-ga spinal needle. This needle may be directed suprapubically (transvesically), transvaginally, transperineally, or transrectally. The procedure may be done either blindly [58] or with the aid of ultrasound. In women, a spinal needle may be gently introduced transurethrally alongside the catheter. Fragmentation during puncture can occur, but it is much rarer than in the two techniques described previously. The easiest way to deflate a nondeflating balloon is to attack the inflate-deflate channel that normally prevents the passive egress of inflating fluid. Patients may be sent to the ED in the late evening or early morning hours after their catheters have been progressively shortened by ingenious health care providers during the day. Cutting the catheter may result in rapid deflation if the valve-flap defect happens to be present in the part of the catheter that is cut off. This is an uncommon occurrence. A shorter catheter with a more proximal valve-flap defect can often be left for 24 hours with ongoing slow balloon deflation, but this maneuver leaves the problem of managing an unconnected catheter and an incontinent patient. Devising a waterproof and aseptic method of collecting urine from the shortened Foley catheter may require use of a ureteral catheter drainage bag or other ingenious approaches. When presented with this situation, it is often best to insert a thin, rigid wire into the balloon-port lumen in an effort to deflate the valve-flap defect sufficiently and promote the escape of fluid from the balloon. A stainless steel wire suture of 3-0 or 4-0 gauge is the thinnest suitable material. The wire stylet from an angiographic catheter, guide wires from ureteral catheters, and very small, well-lubricated ureteral catheters themselves have all been reported to be successful. When a ureteral catheter guide wire was used in one series, 34 of 39 balloons were deflated without fragmentation. In the five unsuccessful cases, needle puncture of the balloon was required and was successful. [58] One approach is to use a stepwise series of maneuvers. If the balloon does not deflate, remove the syringe adapter plug from the balloon-inflating channel. This rules out a malfunction of the adapter. If the balloon water does not escape, next insert an angiographic catheter stylet into the balloon-inflating channel and rotate it. Usually, the water from the balloon flows out along the wire. If it does not, place the catheter on traction and attempt to locate the balloon by palpation either perineally, transvaginally, or transrectally. If this is successful, a 25- to 27-ga spinal needle under local anesthesia is used to blindly puncture the balloon and then remove the catheter. If localization is unsuccessful, multiple blind passes with the 27-ga needle can be attempted; this is usually successful in decompressing the balloon and removing the catheter. [59] If the patient requires a permanent indwelling catheter, one may be replaced immediately. Concomitant inadvertent needle punctures of the rectum are usually of no clinical significance. Once a malfunctioning balloon has been deflated, it is mandatory to carefully inspect the balloon itself for missing fragments. If a piece of the balloon is missing, it is necessary to arrange for subsequent cystoscopy to look for and remove the fragment. Unfortunately, pretesting Foley catheter balloons by trial inflation and deflation before insertion does not eliminate the potential for a nondeflating Foley catheter balloon.
SUPRAPUBIC ASPIRATION OF THE BLADDER One problem of interpreting voided urine samples is that the urine from the bladder passes through a progressively more contaminated urethral conduit. In the female, the perineum is a culture medium where bacteria are seemingly eager to be swept along into the sterile collection cup and onto the agar plate. To avoid the dilemma of interpretation, clinicians have devised maneuvers to minimize the presence of contaminating organisms. Male patients are instructed to retract the foreskin, cleanse the meatus, discard the first portion of urine, and catch the midstream part of the voided specimen. Female patients are asked to perform even more difficult maneuvers to avoid bacterial contamination: sit backward on the commode facing the wall, hold the labia apart with one hand, cleanse the periurethral skin blindly with the other, then reach for the cup, initiate voiding, and catch the midstream urine—all while holding the labia apart and maintaining the precarious position on the commode. Some experts[60] have women void in the lithotomy position after an assistant retracts the labia, cleanses the perineum, and then catches the midstream urine. In standard transurethral bladder catheterization, even under ideal circumstances, the procedure is often uncomfortable. The catheter must traverse the distal contaminated urethra and may infrequently introduce contaminating bacteria into the specimen and into the bladder of the patient, resulting in infection, primarily in patients who don't empty their bladder with normal voiding. Suprapubic aspiration of the bladder, first reported as a method of collecting urine for bacteriologic study in 1956, [61] offers the clinician a relatively simple means of obtaining uncontaminated bladder urine. Urethral contamination is successfully avoided, and positive results always represent
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true bacteriuria. The one caveat is that the bladder must be full to avoid multiple painful needle sticks, a clinical situation that may be difficult to discern in a sick child. Indications In the neonate or the young child, suprapubic aspiration or urethral catheterization can provide the clinician with a sample that is reliable for bacteriologic interpretation. [61] [62] [63] Although disconcerting to some parents (they may wish to leave the room or look away during the procedure), suprapubic aspiration is not a dangerous procedure, and the sensitivity of urinalysis of this urine for bacteriuria approaches 100%. However, for children 2 years or older, urine can generally be more easily collected by urethral catheterization. For adult patients, the indications for suprapubic aspiration are more limited, because these patients usually can cooperate with the clinician. Men with condom catheters or phimosis, however, may require suprapubic aspiration to minimize urethral contamination. Aspirated cultures, rather than catheterized specimens, may help rule out contamination in patients with asymptomatic bacteriuria on routine urine collection. In infections caused by organisms that in other circumstances are often discounted as contaminants (e.g., Staphylococcus epidermidis or Candida albicans), suprapubic aspiration or a catheterized specimen is required to confirm the presence of such pathogens. In patients in whom the possibility of infravesical infection is a concern (e.g., patients with chronic infections of the urethra or the periurethral glands), suprapubic aspiration may help localize a bladder from a urethral source.
Figure 56-24 A, For a suprapubic bladder tap, the infant is restrained and placed in a frog-legged position. B, A 22-ga needle punctures the abdominal wall in the midline approximately 1 to 2 cm cephalad to the superior border of the pubic bone. The syringe is perpendicular to the plane of the abdominal wall (usually 10°–20° from the true vertical). The bladder is an abdominal organ in infants, and placing the needle too close to the pubic bone or angling toward the feet may cause the needle to miss the bladder. Localizing the bladder with bedside ultrasound facilitates this procedure.
Procedure The clinician must first locate the bladder. A full, palpable, or percussible bladder should be readily apparent, but this can be difficult to discern in all but the thinnest patients. If there is any question about the location or the amount of bladder urine, a quick ultrasound examination is informative. The point of entry in the skin should be 1 to 2 cm above the superior edge of the symphysis pubis. The syringe and needle are passed perpendicular to the abdominal wall toward the bladder, usually a 10° to 20° angle from the true vertical, somewhat cephalad in children ( Fig. 56-24 ) and somewhat caudad in adults ( Fig. 56-25 ). Note that the bladder of a newborn is an abdominal organ and that it will be missed if the needle is inserted too close to the pubis or is angled toward the feet. The child is placed supine and is restrained with the legs in a frog-legged position. Once the prepared skin has been draped and the point of entry has been chosen, a skin wheal of local anesthesia is raised to reduce discomfort. When the skin has been anesthetized, a longer, larger-caliber needle (usually 22-ga, 3.75 to 8.75 cm in length) is advanced in the midline through the skin and quickly into the bladder. The editors prefer to advance the needle attached to a syringe, with active aspiration during advancement. As soon as the bladder is entered, urine appears in the syringe. A short needle is adequate for virtually all pediatric patients. After the urine is collected, the syringe and needle are withdrawn. Microscopic hematuria always follows the procedure but gross hematuria is uncommon. A bandage may be placed over the puncture site. If urine is not obtained, the needle is not removed but withdrawn to a subcutaneous position and redirected at a
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Figure 56-25 The peritoneum is pushed cephalad by the filled bladder during suprapubic aspiration in an adult. The needle is directed slightly caudad.
different angle. Often a child may spontaneously start to void following any type of invasive stimulus (e.g., bladder irritation by a probing needle, venipuncture, or lumbar puncture). Hence, preparation to collect a spontaneously voided specimen is recommended, should that option arise. This should be anticipated before beginning blood or spinal fluid collection during the bacteremic workup of the febrile neonate. In most patients, an acceptable urine sample can be obtained with the first needle pass. If the needle points too caudad in an effort to avoid entering the peritoneum, it is possible to enter the retropubic space, skimming the bladder muscle and never penetrating the bladder mucosa. Complications
Stamey has performed several thousand aspirations without complications. [60] Bacteremia does not result from this procedure. [64] Bowel penetration has occurred in children with distended abdomens from gastrointestinal disturbances. [65] The combination of gaseous bowel distention and relative hypovolemia may displace and flatten the relatively empty bladder against the pelvic floor. Even when the large bowel has been penetrated, patients recover uneventfully. Simple penetration of the bowel with a needle is considered an innocuous event and requires no specific treatment.
PERCUTANEOUS SUPRAPUBIC CYSTOSTOMY Background Although suprapubic cystostomy was described as early as 4 centuries ago, the safety of the procedure was first demonstrated by Garson and Peterson in 1888. The first modern method was the Campbell trocar set, described in 1951. [66] [67] Campbell used a sharp trocar passing through a sheath. The sheath had one longitudinal portion of its wall missing to permit a balloon-type Foley catheter to be passed into the bladder. The Campbell trocar is a large-diameter instrument, accepting up to a 20 Fr catheter. Newer technologies have made its use obsolete in the ED. The development of punch thoracostomy tube sets suggested their use as modified cystostomy tubes. This led to the invention of medium-caliber cystostomy tubes, which were easier to insert than the Campbell trocar but provided more satisfactory drainage than adaptations of IV infusion sets. [68] [69] [70] Ingram's trocar catheter is perhaps the best known of these tubes. It has three lumina: one for inflating the retention balloon and the other two for drainage or irrigation. The Ingram catheter is available in a 12 or 16 Fr size. The Stamey suprapubic catheter is another variation of this type, but it uses a four-wing Malecot-type retention device rather than a preferred user-friendly inflatable balloon. Perhaps the most widely known and frequently used trocar-type cystostomy tube is the Cystocath. [71] It is available in 8 and 12 Fr sizes. The latter is more commonly used for adult patients. The Cystocath is packaged as a self-contained set supplying virtually everything needed for insertion. The device is easy to insert and may be satisfactory for relatively long periods of trouble-free use if the patient is given conscientious nursing care. The major difficulty with cystostomy tubes of all designs has been securing them to the patient's skin. Those with retention balloons, such as the regular Foley urethral catheter or the Ingram catheter, are most secure and only need tape to secure them to the anterior abdominal wall. Virtually all other systems depend on tape or skin adhesive to hold either the tube or the appliance in place. They become an annoyance to both the patient and the care provider. The most user-friendly device for suprapubic bladder access is the Cook peel-away sheath unit. [38] It uses the Seldinger (guide wire) technique to gain bladder access and allows suprapubic placement of a Foley balloon catheter for definitive bladder drainage. This device is recommended for ED use over other suprapubic bladder access approaches and is discussed in this section. Indications In general, any patient who would require a urethral catheter but in whom a catheter cannot be passed is a candidate for a suprapubic cystostomy tube. In emergency situations, the majority of these patients are men with urethral stricture or complex prostatic disease and trauma patients with urethral disruption. Depending on the experience of the catheterist, dilation can usually be performed in patients with urethral strictures using filiforms and followers. If there is any difficulty with urethral instrumentation, a suprapubic cystostomy tube is prudent and prevents further urethral injury. Complete urethral transection associated with a pelvic fracture is an absolute indication for emergent suprapubic cystostomy. Many affected patients need laparotomy because of associated injuries, and a large suprapubic catheter can be placed intraoperatively. However, if the patient does not require laparotomy, a percutaneously placed Foley catheter allows urologic surgery to be done electively after the patient's condition has stabilized clinically. Patients with lower genitourinary infection deserve special care before instituting any type of urethral instrumentation. The risk of inciting an episode of gram-negative bacteremia with urethral dilation must be considered, and
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appropriate IV gram-negative antibiotic coverage started before the patient is instrumented. Foley catheter drainage is the first choice and suprapubic drainage is an option in patients with acute prostatitis or epididymitis who require bladder drainage. Ideally, a suprapubic catheter allows both bladder drainage and unobstructed drainage of prostatic, seminal vesicle, and urethral secretions but requires an invasive procedure with its associated risks. Neurologically disabled patients (e.g., quadriplegics or paraplegics) or patients with any type of neurogenic bladder dysfunction who have been successfully maintained on a program of intermittent self-catheterization occasionally have difficulty with urethral catheterization. In these patients, especially those with high spinal cord lesions, suprapubic needle aspiration or suprapubic cystostomy can be a rapidly effective method of relieving autonomic hyperreflexia associated with acute bladder distention. Bladder decompression in the dysreflexic, profusely perspiring, hypertensive quadriplegic in sympathetic crisis provides dramatic symptom resolution, whether by suprapubic bladder decompression or Foley catheter placement. Suprapubic catheterization is not recommended as first-line treatment for the patient who is voiding poorly from lower urinary tract prostatic obstruction. Such patients, although symptomatic, are better off with intermittent self-catheterization or an indwelling Foley catheter if they are in retention or have chronically infected urine. Young women with psychosocial or emotional neurogenic bladder dysfunction are best managed by intermittent self-catheterization. In all such cases, clinical judgment will dictate the most appropriate form of treatment and whether concomitant antibiotic therapy is required. Contraindications Because placement of a suprapubic tube involves some risk, patient selection is important. The procedure should not be performed in a patient whose bladder is not definable. Although no absolute reported minimum bladder volume has ever been established, there must be enough urine in the bladder to allow the needle to fully penetrate the bladder dome without immediately exiting through the base. There must also be enough urine in the bladder to displace the bowel away from the anterosuperior surface of the bladder and the entrance of the needle. Ultrasound may be helpful in defining bladder anatomy. Individuals who have a history of previous lower abdominal surgery, intraperitoneal surgery, or irradiation may have developed adhesions or adherence of the bowel to the anterior bladder wall. They are potentially at greater risk for bowel injury during percutaneous suprapubic cystostomy tube placement than those without previous abdominal surgery. Blind suprapubic cystostomy tube placement in these patients should be avoided. The absence of any of these risk factors does not totally exclude the risks of bowel or intraperitoneal injury, but it reduces them significantly. Patients with bleeding diatheses are at greater risk for postinsertion bleeding, either into the bladder or into the retropubic space, than their normal counterparts. Equipment The items of equipment needed for Cook's peel-away sheath placement are listed in Table 56-6 . Procedure The following comments describe the placement of the Cook peel-away sheath. With modifications, these guidelines are adaptable for any type of suprapubic catheter placement. Preparing the Patient
If necessary, the lower abdomen is shaved. Povidone-iodine skin preparation or another suitable bactericide is used to cleanse the area. The extra liquid is removed, and the skin is allowed to dry. A 6-mL syringe is filled with 1% lidocaine, and a 22-ga, 7.75-cm spinal needle is attached. A skin wheal is raised in the proposed site (approximately 2 to 3 cm above the pubic symphysis), and the subcutaneous tissue and rectus abdominis muscle fascia is infiltrated at a 10°–20° angle toward the pelvis. The bladder is located by advancing the needle in the prescribed direction while aspirating the syringe. Urine is easily aspirated when the bladder is entered ( 56-26A ).
Fig.
Placing the Tube
Once the bladder has been located, the syringe is removed from the needle and a guide wire is advanced through the needle into the bladder ( Fig. 56-26B ). The needle is withdrawn, leaving only the guide wire traversing the anterior abdominal wall and positioned inside the bladder. A No. 15 scalpel blade is used to make a stab incision directly posterior to the wire through the skin, subcutaneous tissue, and superficial anterior abdominal wall fascia. The peel-away sheath and indwelling fascial dilator are then passed together over the wire into the bladder ( Fig. 56-26C ). The guide wire and fascial dilator are removed, leaving only the peel-away sheath inside the bladder ( Fig. 56-26D ). A preselected Foley balloon catheter is then passed through the indwelling intravesical sheath into the bladder ( Fig. 56-26E ). Urine is aspirated to confirm proper placement. The Foley balloon is inflated with a minimum of 10 mL of air, water, or saline ( Fig. 56-26F ). The peel-away sheath is withdrawn from the bladder and anterior abdominal wall and is literally peeled away from the catheter, leaving only the indwelling suprapubic Foley catheter ( Fig. 56-26G ). The catheter is withdrawn slowly until the inflated balloon approximates the cystostomy site ( Fig. 56-26H ). The catheter is connected to a drainage bag, and the wound is dressed with 4 × 4 gauze pads to complete the procedure. Complications A wide variety of complications specific to each procedure have been reported, which serve as reminders that suprapubic cystostomy is not innocuous. Occasionally, despite the best intentions, the suprapubic tube or catheter cannot be positioned or maintained successfully without untoward sequelae ( Table 56-8 ). The most serious complications involve perforation of the peritoneum or the intraperitoneal contents. Any condition that might fix the anterior peritoneum so that the filled bladder cannot lift the peritoneum cephalad may result in either transperitoneal bladder puncture or possible perforation of small or large bowel. [73] [74] [75] Although finding the bladder using a small-gauge scout needle may help reduce bowel injury, even in the most apparently successful of bladder punctures, a complication may result.
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Figure 56-26 Suprapubic cystostomy with the Cook peel-away sheath introducer. A, Bladder is entered with a syringe and needle. Location is confirmed by the aspiration of urine. B, Syringe is removed and the guide wire is passed through the needle into the bladder. C, The needle is removed, then the dilator and peel-away sheath are passed over the wire into the bladder. A small stab wound in the anterior abdominal fascia may be required to accommodate the dilator and sheath. D, The dilator and wire are removed, leaving only the sheath inside the bladder. E, The preselected Foley balloon catheter is passed through the sheath into the bladder. Urine is aspirated to confirm location. F, The balloon is inflated with a minimum of 10 mL of air, saline, or water. A 5-mL balloon will accommodate 10 mL easily and make accidental catheter distraction less likely. G, The sheath is removed from the bladder, anterior abdominal wall, and cutaneous entry site, and is then literally peeled away from the indwelling catheter. H, The catheter is withdrawn until a snug fit is ensured at the cystostomy site.
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TABLE 56-8 -- Reported Complications of Suprapubic Cystostomy Bowel perforation Intraperitoneal extravasation (without a prior history of surgery) Extraperitoneal extravasation Infection of space of Retzius Ureteral catheterization Obstruction of tubing by blood, mucus, or kinking Tubing comes out Hematuria
The cystostomy tube or catheter that merely traverses the peritoneum may produce a mild ileus, serve as a route for peritoneal infection, or drain the bladder contents into the peritoneal cavity. The last situation would be expected if a Cystocath, rather than a peel-away sheath, were used, and one of the extra holes of the Cystocath tubing opened into the peritoneal cavity. Through-and-through bladder penetration with associated rectal, vaginal, or uterine injury has been reported, although the consistent use of small-gauge bladder locator needles and the judicious advancement of fascial dilators should reduce the incidence. Occasionally the clinician is tempted to proceed with suprapubic cystostomy when the bladder is not palpable and has not been located with a syringe and needle. Injury of adjacent organs is much more frequent in these circumstances. If clinicians remind themselves that the bladder eventually refills, they will find waiting much more tolerable. If faced with an emergency, ultrasound guidance may be helpful for determining bladder size and location. Infection may occur at the suprapubic cystostomy skin site or anywhere along the course of the catheter. [76] Use of antimicrobial ointment daily after cleaning the catheter entry site may reduce purulence around the tube. However, topical care does not prevent eventual deep space or bladder infection from the presence of a foreign body. Deeper tissue infections may result from extravasated infected urine or from a superficial infection spreading along the tube to a hematoma at the bladder or fascial level. Parenteral antibiotics may be required. Open drainage is rarely needed unless a loculated abscess has formed. Hematuria is rarely more than a transient problem. [77] After suprapubic Foley catheter insertion, bladder irrigation may occasionally be required to clear the hematuria. Transient Toomey syringe aspiration may be needed to evacuate clots.
EMERGENCY LOWER GENITOURINARY RADIOLOGIC PROCEDURES Trauma to the urinary tract accounts for about 10% of all injuries seen in EDs. Although the signs of genitourinary trauma in general can be quite subtle, lower urinary tract injury can often be quickly identified and thoroughly evaluated radiographically in the ED. Radiologic imaging of the upper urinary tract is generally a less urgent matter and can usually be done in the radiology suite or, when important for emergency operative decision-making, as a single shot intravenous pyelogram (IVP) in the operating room. Hence, this section does not discuss the role or technique of IVP in detail. Note that the timing of any radiologic evaluation can be challenging to the emergency clinician, especially when faced with a critically ill multiple trauma patient. The priority and extent of such an evaluation, of course, must be determined by the trauma team of clinicians involved in each resuscitation. Indications for Evaluation The urinary tract includes the kidneys, ureters, bladder, urethra, and external genitalia. Approximately 8% to 10% of blunt abdominal trauma is associated with injuries to the urinary tract. [78] In one large series, [79] 7% of gunshot wounds and 6% of stab wounds to the abdomen resulted in penetrating wounds to the kidney. For injury identification purposes, the genitourinary system is best divided into lower urinary tract (i.e., urethra and bladder), upper urinary tract (i.e., kidneys and ureter), and external genitalia (i.e., penis, scrotum, and testes or vagina, labia majora, and labia minora). Each of these subdivisions has its own markers for potential injury. These markers are addressed during the resuscitation phase of trauma care and during secondary injury survey when the abdomen, pelvis, external genitalia, vaginal vault, and rectum are systematically examined. The markers for lower urinary tract injury are blood at the urethral meatus, abnormal position of the prostate on rectal examination (in men), and gross hematuria. [80] Perineal ecchymosis and scrotal hematoma also represent potential lower urinary tract injury, but these findings are usually seen later in the patient's course rather than acutely in the ED. Gross hematuria or microscopic hematuria (=3 to 5 RBCs per HPF-spun specimen) in conjunction with any history of shock (systolic blood pressure =90 mm Hg) in the field or in the ED following blunt trauma are markers of potential upper urinary tract injury in any adult. [81] In children, a meta analysis has defined 50 RBC/hpf as the quantity below which imaging may be omitted and no significant injuries missed. [82] In genitourinary trauma, the lower urinary tract is always evaluated before the upper urinary tract. Retrograde urethrography and retrograde cystography are the diagnostic procedures of choice to evaluate potential injury to the lower urinary tract. These studies must be carried out in the proper sequence and in a retrograde fashion to avoid missing potential injuries. Retrograde refers to the technique of instilling contrast retrograde through the urethra or by gravity filling of the bladder. It must be distinguished from antegrade filling, in which IV contrast for IVP or abdominal computed tomography (CT) is excreted from the kidneys and allowed to fill the bladder passively over time. Contrast-enhanced CT is the diagnostic examination of choice for suspected renal trauma. It provides greater resolution and sensitivity than bolus infusion IVP with nephrotomography and has the advantage of evaluating other intra-abdominal structures as well. [83] However, it is expensive, and in some hospitals it is not readily available on a 24-hour basis. A reasonable course of action under these circumstances would be to initiate the upper urinary tract investigation with bolus-infusion IVP with nephrotomography and to investigate further with contrast-enhanced CT if an ill-defined or poorly visualizing kidney is the result of the initial study. Contrast-enhanced CT should be performed initially if thoracic or intra-abdominal injuries are present or suspected, or if there is concern about renal pedicle injury.
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Gross Hematuria
Gross hematuria is indicated by any color of urine other than clear or yellow. It is an absolute marker for urinary tract injury and an indication for diagnostic evaluation. The resuscitating clinician must be responsible for observing the initial bladder effluent following Foley catheter insertion. Vigorous fluid resuscitation may quickly clear initial gross hematuria and eliminate the only marker for potential injury. When gross hematuria is encountered as an injury marker, the bladder and kidneys are thought of as potential sources for the hematuria. In most cases, gross hematuria in association with a pelvic fracture will implicate the bladder as the most likely source of injury. In the absence of a pelvic fracture and with a history of upper abdominal or chest trauma, the kidneys are the most likely source of the hematuria. In urologic trauma, the lower urinary tract must always be studied before the upper urinary tract (i.e., study the urethra before the bladder, study the bladder before the kidneys). The specific diagnostic studies must always be done in a retrograde fashion. This allows the responsible clinician to directly control the amount of contrast used to investigate potential urethral or bladder injuries. Whenever any doubt exists about the mechanism of injury, the patient's physical examination, or the source of gross hematuria, the resuscitating clinician is always advised to begin with an evaluation of the lower urinary tract before evaluating the upper urinary tract. Evidence of Lower Urinary Tract Injury
In the resuscitation of any trauma patient, placement of a Foley catheter has become the standard method of monitoring urinary output. Blood at the urethral meatus, however, indicates a potential partial or complete urethral disruption and dictates the need for a retrograde urethrogram to delineate urethral integrity. This study can be done by the resuscitating clinician in the ED or on the operating room table by the trauma surgeon or urologist if the patient requires immediate surgical intervention for life-threatening injuries. The male posterior urethra, which includes the membranous and prostatic urethra, is injured more frequently than the anterior urethra. The urogenital diaphragm encloses and fixes the membranous urethra; the prostate and prostatic
Figure 56-27 A common posterior urethral injury is a disruption of the membranous urethra. In this case, a distended bladder and attached prostate gland are sheared from the fixed membranous urethra. Note the development of a perivesical hematoma and the presence of a "high-riding" prostate gland.
urethra are firmly attached to the posterior surface of the symphysis pubis by the puboprostatic ligaments. Blunt trauma and pelvic fractures, especially in the presence of a full bladder, may result in shearing forces that partially or completely avulse portions of the firmly attached posterior urethra. Usually the bladder and prostate gland are sheared from the membranous urethra, resulting in a complete urethral disruption ( Fig. 56-27 ). The female urethra, in contrast, is short and relatively mobile and generally escapes injury in blunt trauma. Occasionally, a significant pelvic fracture will result in a laceration or avulsion of the female urethra at the bladder neck. Direct injuries to the female urethra may also occur secondary to penetrating trauma to the vagina or perineum. These injuries often are disclosed by blood at the introitus or an abnormal vaginal examination in the female pelvic fracture patient. [84] Contusions or lacerations of the male anterior urethra occur when the bulbous urethra is compressed against the inferior surface of the symphysis pubis. This happens most commonly as a result of straddle injuries in males but may result from any blunt perineal trauma. Significant trauma to the penile urethra is rare without penetrating injuries or urethral instrumentation. Anterior urethral injuries may result in extravasation of blood or urine into the penis, scrotum, or perineum, or along the anterior abdominal wall, depending on whether or not Buck fascia has been violated ( Fig. 56-28 ).[37] This is in contrast to posterior urethral injuries, in which blood and urine extravasate into the pelvis. The rectal examination is highly specific in the evaluation of a posterior urethral disruption. If the prostate is not clearly defined (it should have the consistency of the examiner's thenar eminence), is high-riding rather than in its normal anatomic location, or if a pelvic hematoma can be palpated (see Fig. 56-27 ), one should be
suspicious of a posterior urethral injury, and a retrograde urethrogram should be performed before attempting urethral catheterization. However, a normal rectal examination, by itself, should not be considered definitive evidence of an intact urethra if other clinical signs raise suspicion for urethral injury. Retrograde urethrography is a quick, technically easy study to perform and should be part of every emergency clinician's armamentarium.
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Figure 56-28 A, Disruption of the anterior urethra (bulbous urethra) occurs with straddle-type injuries in the male. Extravasation of urine and blood may occur in the perineum or scrotum, or along the anterior abdominal wall. Note that in this diagram, Buck fascia has been penetrated. B, Anterior urethral injury in which Buck fascia remains intact. In this situation, extravasation is confirmed and results in a swollen and ecchymotic penis. Such an injury usually results from instrumentation of the anterior urethra. Pelvic Fracture
Pelvic fractures occur commonly in patients with urethral or bladder injury. The incidence of lower tract injuries in males with pelvic fractures ranges from 7% to 25%. Conversely, approximately 80% of all posterior urethral and bladder injuries are associated with pelvic fractures. [80] Because of the severity of late complications, especially urethral strictures, which most often require difficult surgical repair, it is paramount that these injuries not be missed. Again, in any female patient with a pelvic fracture, it is most important to examine the introitus and vaginal vault for blood, which may be indicative of urethral, bladder neck, or vaginal wall lacerations. In male patients, rectal examination of the prostate to assess its position will be most helpful in assessing the posterior urethra. A pelvic fracture in association with gross hematuria is an absolute indication for retrograde cystography. In a review of 234 patients with traumatic pelvic fractures, no major lower urinary tract injuries were found in the absence of gross hematuria. [80] Radiographic Contrast Material Radiographic contrast material is used to fill vessels and other structures to render them diagnostically radiopaque. To evaluate the urethra and bladder, contrast is injected or instilled into these structures in a retrograde manner. To evaluate the kidneys and ureters, a bolus of contrast material is injected into the venous system, opacifying the renal parenchyma and collecting system as it is excreted unchanged in the urine. Three types of contrast material are currently available ( Table 56-9 ). All contain iodine, and all are hyperosmolar with respect to blood. Conventional agents, such as Hypaque and Renografin (diatrizoate), are triiodinated water-soluble agents (ionic monoacetic monomers) that completely dissociate into anion and cation moieties on intravascular injection. Osmolality is quite high, ranging from 1200 to 2000 mOsm/kg. Many of the side effects of contrast agents have been attributed to their osmolarity. Although iodine concentrations do determine the quality of the radiographic image, iodine itself is not thought to play a major role in the typical anaphylactoid side effects. [85] Two new classes of contrast agents are ioxaglate (Hexabrix), an ionic monoacetic dimer, and nonionic (nondissociating) agents, such as iopamidol (Isovue) and iohexol (Omnipaque). The newer agents have twice as many iodine atoms per particle in solution as conventional agents and therefore provide significantly higher urinary iodine concentration, offering better diagnostic imaging. The osmolality of the newer agents is markedly lower, ranging from 600 to 700 mOsm/kg. The lower osmolality and improved chemical structure may be associated with fewer adverse side effects. [86] [87] Although these new agents are promising for intravascular use, there is still some skepticism that they will truly limit major or clinically significant contrast reactions. [88] The lower-osmolarity nonionic agents have not been associated with a lower incidence of contrast-induced nephropathy. Furthermore, there is no indication for using these more expensive products in the retrograde evaluation of the injured lower urinary tract. Radiographic Techniques Kidneys, Ureters, and Bladder
The plain film, scout film, or KUB (for kidneys, ureters, and bladder) film of the abdomen, as this view is variously referenced, includes the kidneys, ureters, bladder, and full pelvis. It is essential as the initial diagnostic film because it serves as a reference for all subsequent films after injection or instillation of contrast material. Incidental nondiagnostic findings on initial KUB that may alert the clinician to the possibility of
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TABLE 56-9 -- Clinical Use of Radiographic Contrast Material (RCM) for Intravenous Pyelogram (IVP) and Retrograde Studies Use of RCM for IVP Iodine Content (mg/mL of Solution) Osmolality (mOsm/kg) (H 2 O) Average Volume for IVP Conventional ionic RMC
288
1511
Child: 1.5 mL/kg †
Renografin-60 (diatrizoate sodium) Hypaque (50%) (diatrizoate sodium)
Adult: 100 mL over 30–60 sec *
300
1500
Adult: 100 mL over 30–60 sec * Child: 1.5 mL/kg †
Conray (methyl glucamine iothalamate)
282
1217
Adult: 100 mL over 30–60 sec * Child: 1.5 mL/kg †
New nonionic RMC
300
616
Adult: 50 mL over 30–60 sec‡ Child: 1–1.5 mL/kg†
Isovue (iopamidol) Omnipaque 300 (iohexol)
300
672
Adult: 50 mL over 30–60 sec‡ Child: 1–1.5 mL/kg†
Use of RCM for Retrograde Studies
Use
Procedure
Renografin-60 or Hypaque (50%)
Dilute stock solutions with Urethrogram: 10–15 mL of dilute solution injected slowly through urethral meatus. Children: 0.2 mL/kg saline 1:10 (10% solution) Cystogram: after plain film and with Foley catheter in place, fill bladder of adult with 400 mL of dilute contrast material, introduced under gravity. Children: 5 mL/kg
*Average dose of iodine for IVP with ionic RCM: 350–400 mg/kg or 1.5 mL/kg Adult: Low dose: 10 g Intermediate dose: 30 g High dose: 60 g †Do not exceed 3 mL/kg total dose. ‡Because the ratio of iodine atoms to dissolved particles is 1.5 with conventional ionic agents and 3.0 with the nonionic agents, less volume is required with the new agents. Average dose is 200–350 mg/kg.
Figure 56-29 Retrograde urethrogram. The foreskin is fully retracted and an unwrapped 4 × 4 gauze sponge is folded in half longitudinally and wrapped around the penis proximal to the coronal sulcus, to prevent foreskin reduction. A, The penis is held between the long and ring fingers of the nondominant hand. The thumb and index finger ensure a snug fit of the syringe in the urethra. B, Equipment needed for retrograde urethrography and cystography. C, Alternative technique for securing the "irrigation-tip" syringe in the urethra.
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urinary tract injury include the following: 1. 2. 3. 4.
Loss of one or both psoas shadows secondary to blood in the retroperitoneum. Spinal curvature secondary to splinting—usually concave to the side of the injury. Lower rib or transverse process fractures, both of which may be associated with upper urinary tract injury. Pelvic fracture.
The KUB must always precede the injection or instillation of contrast material, because radiopaque shadows seen on the plain film must be differentiated from extravasation on the postevacuation film. Retrograde Urethrogram
Retrograde urethrography is indicated whenever there is uncertainty about the integrity of the urethra. In cases associated with pelvic fracture, the patient should remain supine throughout the entire radiographic examination. This is important to ensure stability of any possible retropubic hematoma that may result from extensive venous bleeding associated with the initial pelvic fracture. In cases of suspected urethral injury not associated with pelvic fracture, it is acceptable to obtain oblique films during the study that may complement the examination findings. Perpendicular stretching of the penis across the thigh or oblique films may be needed to ensure urethral unfolding and a high-quality urethrogram. Although several techniques have been promoted for retrograde urethrography, one is emphasized in this section. The choice of technique is not as important as attention to detail. Solutions of either full-strength Hypaque (50%), Cystografin or Renografin-60, or the same agents diluted to a less than 10% solution using sterile saline as the diluent, are frequently used (see Table 56-9 ). First, a plain film (KUB) of reference must be taken before injection of any contrast material. [81] The penile foreskin must be retracted and secured with a folded 4 × 4 gauze sponge. Second, the penis should be held between the long and ring fingers of the nondominant hand to allow the thumb and index finger of the nondominant
Figure 56-30 Normal retrograde urethrogram. The patient is supine on the examination table. The penis is stretched perpendicularly across the patient's right thigh to allow urethral unfolding and complete urethral visualization.
hand (see Fig. 56-18 ) a snug fit of the contrast-filled syringe inside the urethra ( Fig. 56-29A ). After sterile penile preparation, a catheter-tipped Toomey irrigating syringe or a regular 60-mL syringe with an attached Christmas-tree adapter ( Fig. 56-29B ) is gently advanced inside the urethral meatus until a snug fit is ensured ( Fig. 56-29C ). Third, approximately 50 to 60 mL of full- or half-strength contrast material is then injected slowly under constant pressure into the urethra. Prior to the injection of contrast, the penis should be stretched perpendicularly across the patient's thigh to prevent urethral folding (i.e., the double image of the proximal penile and bulbous urethra superimposed on one another) ( Fig. 56-30 ). Overly forceful injection of contrast material may cause intravasation of contrast material into the venous plexus of the urethra ( Fig. 56-31 ). Finally, during the injection of the last 10 mL of contrast, a film (the urethrogram) is taken.
Figure 56-31 Venous intravasation (arrows) during a forceful retrograde urethrogram. This may mimic urethral extravasation, but it clears immediately, as opposed to actual extravasation, which remains indefinitely. The presence of intravasation is benign. (From Richter MW, Lytton B, Myerson D, Grnja V: Radiology of genitourinary trauma. Radiol Clin North Am 11(3):626, 1973.)
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The alternative to this technique, which is discussed in most standard textbooks, is to insert a Foley catheter just inside the urethral meatus, inflate the balloon to ensure a snug fit in the fossa navicularis, and then inject contrast through the catheter ( Fig. 56-32 ). If not done carefully, this technique often results in the spillage and deposition of contrast outside the urethra and onto the patient and the examination table, thus yielding a spurious result. The extravasation of contrast material from a urethral disruption usually appears as a flame-like density outside the urethral contour ( Fig. 56-33A–C ). If any contrast material is seen within the bladder in conjunction with urethral extravasation, a partial rather than complete urethral disruption is more likely. In a complete urethral disruption, urethral extravasation will be present without evidence of contrast within the bladder. The examiner needs to be certain that the lack of bladder contrast is not secondary to voluntary contraction of the external sphincter. Occasionally, as mentioned previously, intravasated contrast material is seen in the periurethral penile venous
Figure 56-32 Retrograde urethrogram using a Foley catheter (8 Fr). Slowly inflate the balloon with 2 mL of air, tap water, or sterile saline to create a snug fit; then slowly inject 60 mL of a 10% solution of contrast material through the catheter lumen (see text).
Figure 56-33 A, Retrograde urethrogram. Urethrogram in case of supramembranous urethral rupture. Contrast extravasation is typical of that seen with this type of injury. B, A
rupture at the proximal bulbous urethra into the scrotum ( arrows). C, Residual contrast material within perineum and scrotum. (A from Morehouse DD, MacKinnon KJ: Posterior urethral injury: Etiology, diagnosis, initial management. Urol Clin North Am 4:74, 1977. C from Richter MW, Lytton B, Myerson D, Grnja V: Radiology of genitourinary trauma. Radiol Clin North Am 11:627, 1973.)
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plexus (see Fig. 56-31 ). It is of no clinical significance and should not be mistaken for urethral extravasation. As expected, penile venous intravasation (venous plexus opacification) is seen to clear spontaneously on any post-void films, as compared with urethral extravasation, which remains indefinitely. If a Foley catheter has been successfully placed into the bladder and a partial urethral injury is suspected later, such an injury can be easily demonstrated without removing the catheter. The lubricated end of a pediatric feeding tube is placed into the penile urethra alongside the existing Foley catheter ( Fig. 56-34 ). A seal can be obtained by compressing the glans penis with the nondominant thumb and index finger and gently injecting contrast material via a Luer-Lock syringe with the dominant hand. In this way, extravasation can be demonstrated. It should be noted, however, that successful placement of the Foley catheter obviates the need for further treatment of a partial urethral tear in the emergency setting, because an indwelling catheter alone is appropriate initial management for this type of injury. The finding of an associated urethral injury must be conveyed to a urologist, as it will dictate the duration of definitive Foley catheter drainage. Retrograde Cystogram
A retrograde cystogram is performed any time a bladder injury is suspected. It assumes the urethra is normal prior to passing the Foley catheter. A preliminary KUB is obtained that will serve as the reference film for the entire examination. Next, the bladder is filled under direct operator supervision by gravity instillation of contrast material. After the central piston is removed from a 60-mL catheter-tip syringe, the catheter-tipped end of the syringe is attached to the Foley catheter and held above the level of the patient's bladder. The contrast material is poured into the syringe
Figure 56-34 Evaluation of a urethral injury with a Foley catheter in place. A lubricated pediatric feeding tube has been advanced into the urethra beside the indwelling Foley catheter.
and allowed to fill the bladder by gravity instillation to 1 of 3 end points: (1) 100 mL with evidence of gross extravasation on fluoroscopy or on plain film, (if the examiner elects to check at this point); (2) 400 mL in an adult or any child 11 years or older. In children younger than 11 years, bladder capacity, and therefore appropriate contrast volumes, are estimated based on the formula "(age in years + 2) × 30"; or (3) to the point of initiating a bladder contraction (see later), then adding an additional 50 mL by hand injection under pressure. Anteroposterior (AP) and complementary oblique projections are obtained so long as there is no evidence of a
Figure 56-35 Retrograde cystogram. A, In patients with pelvic fracture, retrograde cystography should be done with the patient supine throughout the examination. Here, gross extravasation is evident, but its superior extent is not well defined. B, A lateral film may help define the extent of any extravasation. This film shows no intraperitoneal extension, so the extravasation must be totally extraperitoneal.
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Figure 56-36 Retrograde cystogram. A, Anteroposterior (AP) filled-bladder film. B, AP postevacuation film of same patient showing extensive extravasation not seen on the AP filled-bladder film. Balloon of catheter is identified by arrows. C, "KUB" (kidneys, ureters, and bladder) showing bullet in the area of pelvis. D, AP filled-bladder film of same patient showing bladder displacement to right, presumably from a pelvic hematoma. No extravasation is visible with the bladder full of contrast. E, AP postevacuation film of same patient, showing subtle contrast extravasation in area of bullet that could easily be missed without a high-quality preliminary KUB and post-evacuation film.
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Figure 56-37 Examples of extraperitoneal bladder rupture. A, Note the amorphous extravasation of contrast material within the perivesical space ( arrows) in a patient with a right pelvic fracture (arrowheads). B, A second patient with a pelvic fracture ( arrowhead) and perivesical hematoma shows the teardrop shape of a deformed bladder and extraperitoneal extravasation ( arrows). (From Richter MW, Lytton B, Myerson D, Grnja V: Radiology of genitourinary trauma. Radiol Clin North Am 11:623, 1973.)
pelvic fracture. In the presence of a pelvic fracture, all films are obtained with the patient in the supine position for the same reasons that were elucidated for retrograde urethrography. A lateral film may be informative when oblique films are not possible ( Fig. 56-35 ). An AP postevacuation film must be obtained in all cases following bladder drainage. This will disclose posterior perforation in select cases, especially those associated with penetrating trauma ( Fig. 56-36A–E ). Again, a dilute solution of contrast material (see Table 56-9 ) may be used, rather than full-strength contrast. Some authors recommend a dilute solution of contrast material (=10%) because extravasation into periurethral or perivesical tissues may cause considerable inflammatory reaction at higher concentrations. The dilute solutions do not appear to compromise the quality of the study, but this must be a consideration. Retrograde cystography done by any technique other than hand-poured gravity instillation is subject to inadequate bladder filling or connector tubing-catheter disconnection. Both conditions will result in spurious examination results, which may adversely impact important patient management decisions. It must be stressed that in the absence of initial gross extravasation, the bladder must be filled to 400 mL in an
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Figure 56-38 Intraperitoneal bladder rupture. A, A 22-year-old pedestrian hit by an automobile. Note extravasation of contrast material beginning at the dome and tracking up the left paracolic gutter (arrows). B, This 57-year-old man had fulguration of a bladder tumor at the bladder dome and sustained perforation. A cystogram dramatically demonstrates the extravasation of contrast material that outlines the bowel loops ( arrows) and the paracolic gutters. (Courtesy of Morton A, Bosniak MD, New York.) (From Richter MW, Lytton B, Myerson D, Grnja V: Radiology of genitourinary trauma. Radiol Clin North Am 11:623, 1973.)
adult, and to an appropriate capacity in a child, and the catheter clamped with a Kelly clamp. Volumes less than 400 mL have been associated with false-negative findings, especially in penetrating bladder injuries. [89] At times, the patient may have difficulty cooperating with bladder filling because of a head injury or associated pain; and in the case of severe injury, the patient may have involuntary bladder contractions, causing contrast material to back up into the Toomey syringe. If this occurs, refill the bladder to the point of initiating a bladder contraction, clamp the Foley, remove the initial syringe, and replace it with a 60-mL contrast-filled syringe, unclamp the catheter, hand-inject the additional 50 mL under pressure, and reclamp the catheter. The goal is to overdistend the bladder. Once the filled-bladder films have been obtained and reviewed, the Foley catheter is unclamped and the contrast material is allowed to drain into a bedside drainage bag. The AP postevacuation film is then obtained to visualize any posterior extravasation that may have been hidden by the distended bladder during the AP filled-bladder film. Once again, care must be taken to ensure that contrast material is not spilled onto the patient or the examination table during the procedure. Spilled contrast can lead to spurious examination results. Extravasation from an injured bladder may be intraperitoneal, extraperitoneal, or both. Extraperitoneal extravasation is usually seen as flame-like areas of contrast material confined to the pelvis and projecting lateral to the bladder ( Fig. 56-37 ). If the contrast material extravasates intraperitoneally, it tends to fill the paracolic gutters and outline intraperitoneal structures, particularly the bowel, spleen, or liver ( Fig. 56-38 ). It is important to distinguish extraperitoneal from intraperitoneal injury, as the treatment options are totally different (i.e., surgical repair for all intraperitoneal injuries and for extraperitoneal injuries that extend into or primarily involve the bladder neck, especially in women). Most other extraperitoneal injuries can be managed confidently by Foley catheter drainage alone. Retrograde cystography may be done in conjunction with contrast-enhanced abdominal CT scanning. The bladder must be filled just as if a conventional retrograde cystogram were being obtained. The catheter is clamped, and evidence for contrast ascites is sought on the CT scan ( Fig. 56-39 ). When this is encountered, bladder injury with extravasation must be looked for with selective images of the pelvis.
Figure 56-39 Retrograde cystogram and abdominal computed tomography (CT) scan. These two procedures can be done concomitantly. The bladder is filled in the standard retrograde fashion and the catheter is clamped. Intravenous and oral contrast can then be administered and CT scanning performed. This film demonstrates contrast ascites, which is consistent with intraperitoneal bladder rupture and extravasation.
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Contrast Medium Reactions and Toxic Effects In the lower genitourinary tract radiologic procedures that are described in this section, the contrast material is administered within the urinary collecting and drainage system. Hence, the patient is at low risk for systemic absorption and allergic reaction. Even with IV infusion, contrast medium reactions are rare; the incidence of significant reactions (i.e., of sufficient severity to require medical intervention) with IV administration is between 1 in 1000 and 1 in 10,000 uses. Although IV use of contrast medium is outside the scope of this text, volumes and administration information are outlined in Table 56-9 . The ED use of contrast agents is often necessary and justified despite the small possibility of untoward reactions. At times, the patient's past history may not be known, underlying renal function cannot be rapidly assessed, or alternative imaging techniques (e.g., ultrasonography) are unavailable. In such circumstances, the risks vs the benefits of emergent imaging using IV contrast must be carefully weighed. Often the potential information gain of contrast-enhanced imaging in the unstable patient far outweighs the small associated additional risk.
Acknowledgments
The authors and editors acknowledge the contributions made to previous editions by Ivan Zabaraschuk, MD, Richard E. Berger, MD, Jerris R. Hedges, MD, Martin Schiff, Jr., MD, Morton G. Glickman, MD, and Geoffrey E. Herter, MD.
References 1. Chapra
R, Fisher RD, French F: Phimosis and diabetes mellitus. J Urol 127:1101, 1982.
2. Goulding 3. Soliman
FJ: Penile block for postoperative pain relief in penile surgery. J Urol 126:337, 1981.
MG, Trumble NA: Nerve block of the penis for postoperative pain relief in children. Anesth Analg 57:495, 1978.
4. Campbell 5. Schenck 6. Ganti
M, Harrison JH (eds): Urology, vol 3. 6th ed. Philadelphia, WB Saunders, 1992.
GF: The treatment of paraphimosis. Am J Surg 8:329, 1930.
SU, Sayegh N, Addonizio JC: Simple method for reduction of paraphimosis. Urology 25:77, 1985.
7. Ratcliff
RK: Hyaluronidase in treatment of paraphimosis. JAMA 156:746, 1954.
8. Houghton
GR: The "iced-gloved" method of treatment of paraphimosis. Br J Surg 60:876, 1973.
9. Skoglund
RW, Chapman WH: Reduction of paraphimosis. J Urol 104:137, 1970.
10.
Cletsoway RW, Lewis EL: Treatment of paraphimosis. US Armed Forces J 8:361, 1957.
11.
Cumston CG: The correct operation for paraphimosis. Int Clin 2:47, 1920.
12.
Barry CN: A simple method for reduction of paraphimosis. J Urol 71:450, 1954.
13.
Green J, Hakim L: Cocaine-induced veno-occlusive priapism: Importance of urine toxicology screening in the emergency room setting. Clin Urol 161(4S):180, 1999.
14.
Volkmer BG, Nesslauer T, Kraemer SC, et al: Prepubertal high flow priapism: Incidence, diagnosis and treatment. J Urol 166:1018, 2001.
15.
Fernandez JA, Basha MA, Wilson GC: Emergency treatment of papaverine priapism. J Emerg Med 5:289, 1987.
16.
Winter CC, McDowell G: Experience with 105 patients with priapism: Update review of all aspects. J Urol 140:980, 1988.
17.
Shantha TR, Finnerty DP, Rodriguez AP: Treatment of persistent penile erection and priapism using terbutaline. J Urol 141:1427, 1989.
18.
Mulhall JP, Honig SC: Priapism: Etiology and management. Acad Emerg Med 3:810, 1996.
19.
Lue TF, Helstrom WJ, McAninch JW, et al: Priapism: A refined approach to diagnosis and treatment. J Urol 136:104, 1986.
20.
O'Brien WM, O'Connor KP, Lynch JH: Priapism: Current concepts. Ann Emerg Med 18:980, 1989.
22.
Boyarsky S, Steinhardt GF, Onder R: Medico-legal aspects of testicular torsion. Mo Med 87:359, 1990.
23.
Melekos MD, Asbach HW, Markou SA: Etiology of acute scrotum in 100 boys with regard to age distribution. J Urol 139:1023, 1988.
24.
Witherington R, Jarrell TS: Torsion of the spermatic cord in adults. J Urol 143:62, 1990.
25.
Berger RE, Kessler D, Holmes KK: The etiology and manifestations of epididymitis in young men: Correlations with sexual orientation. J Infect Dis 155:1341, 1987.
26.
Eisner DJ, Goldman SM, Petronis J, Millmond SH: Bilateral testicular infarction caused by epididymitis. AJR Am J Roentgenol 157:517, 1991.
27.
Lindsey D, Stanisic D: Diagnosis and management of testicular torsion: Pitfalls and perils. Am J Emerg Med 6:42, 1988.
28.
Middleton WD, Siegel BA, Nelson GL, et al: Acute scrotal disorders: Prospective comparison of color Doppler US and testicular scintigraphy. Radiology 177:177, 1990.
29.
Blackshear WM, Phillips DJ, Strandness DE: Pulsed Doppler assessment of normal human femoral artery velocity patterns. J Surg Res 27:73, 1979.
30.
Brereton RJ: Limitation of the Doppler flow meter in the diagnosis of the "acute scrotum" in boys. Br J Urol 53:380, 1981.
31.
Smith DP: Treatment of epididymitis by infiltration at spermatic cord with procaine hydrochloride. J Urol 46:74, 1941.
32.
Lee LM, Wright JE, McLoughlin MG: Testicular torsion in the adult. J Urol 130:93, 1983.
33.
Kresling V, Schroeder D, Panljev P, et al: Spermatic cord block and manual reduction: Primary treatment for spermatic cord torsion. J Urol 132:921, 1984.
34.
Amir J, Ginzburg M, Straussberg R, Varsano I: The reliability of midstream urine culture from uncircumcised male infants. Am J Dis Child 147:969, 1993.
35.
Lipsky BA, Inui TS, Plorde JJ, Berger RE: Is the clean catch midstream void procedure necessary for obtaining urine culture specimens from men? Am J Med 76:257, 1984.
36.
Walter FG, Knopp RK: Urine sampling in ambulatory women: Midstream clean-catch versus catheterization. Ann Emerg Med 18:166, 1989.
37.
Spirnak JP: Pelvic fracture and injury to the lower urinary tract. Surg Clin North Am 68:1057, 1988.
38.
O'Brien WM: Percutaneous placement of a suprapubic tube with peel away sheath introducer. J Urol 145:1015, 1991.
39.
Warwick R, William PL: Gray's Anatomy, 35th British ed. Philadelphia, WB Saunders, 1973, p 1336.
40.
Blandy JP: Acute retention of urine. Br J Hosp Med 19:109, 1978.
41.
Turck M, Goffe B, Petersdorf RG: The urethral catheter and urinary tract infections. J Urol 88:834, 1962.
42.
Kaplan GW: Complications of circumcision. Urol Clin North Am 10:543, 1983.
43.
Pfaff G, Bokenius M: Hands off the prepuce. Lancet 2:874, 1984.
44.
Walden TB: Urethral catheterization in anasarca. Urology 13:82, 1979.
45.
Blandy JP: Urethral stricture. Postgrad Med J 56:383, 1980.
46.
Platt R, Polk BF, Murdock BS, Rosner B: Mortality associated with nosocomial urinary tract infection. N Engl J Med 357:637, 1982.
47.
Gulhan PD, Bayley BC, Metzger W, et al: The case against the Foley catheter: Initial report. J Urol 101:909, 1969.
48.
Cohen A: A microbiological comparison of a povidone-iodine lubricating gel and a control as catheter lubricants. J Hosp Infect 6(suppl):155, 1985.
49.
Warren JW, Damron D, Tenney JH, et al: Fever, bacteremia, and death as complications of bacteriuria in women with long-term urethral catheters. J Infect Dis 155:1151, 1987.
50.
Johnson DE, O'Reilly JL, Warren JW: Clinical evaluation of an external urine collection device for nonambulatory incontinent women. J Urol 141:535, 1989.
51.
Farraye MJ, Seaberg D: Indwelling Foley catheter causing extraperitoneal bladder perforation. Am J Emer Med 18:497, 2000.
52.
Steidle CP, Mulcahy JJ: Erosion of penile prostheses: A complication of urethral catheterization. J Urol 142:737, 1989.
53.
Ferrie BG, Groome J, Kirk D: Comparison of silicone and latex catheters in the development of urethral stricture after cardiac surgery. J Urol 58:549, 1986.
1114
54.
Sklar DP, Diven B, Jones J: Incidence and magnitude of catheter-induced hematuria. Am J Emerg Med 4:14, 1986.
55.
Klein EA, Wood DP, Kay R: Retained straight catheter: Complication of clean intermittent catheterization. J Urol 135:780, 1986.
56.
Eichenberg HA, Amin M, Clark J: Non-deflating Foley catheters. Int Urol Nephrol 8:171, 1976.
57.
Moisey CA, Williams LA: Self-retained balloon catheter: A safe method for removal. Br J Urol 52:67, 1980.
58.
Sood SC, Sahota H: Removing obstructed balloon catheter. Br Med J 4:735, 1972.
59.
Browning GG, Barr L, Horsburg AG: Management of obstructed balloon catheters. Br Med J 289:89, 1984.
60.
Stamey TA: Pathogenesis and Treatment of Urinary Tract Infections. Baltimore, Williams & Wilkins, 1980.
61.
Huze LB, Beeson PB: Observations on the reliability and safety of bladder catheterization for bacteriologic study of the urine. N Engl J Med 255:474, 1956.
62.
Pryles PV: Percutaneous bladder aspiration and other methods of urine collection for bacteriologic study. Pediatrics 36:128, 1965.
63.
Nelson JD, Peters PC: Suprapubic aspiration of urine in term infants. Pediatrics 36:132, 1965.
64.
Mustonen A, Uhari M: Is there bacteremia after suprapubic aspiration in children with urinary tract infection? J Urol 119:822, 1978.
65.
Weuthers WT, Wenzl JE: Suprapubic aspiration: Perforation of the viscus other than the bladder. Am J Dis Child 117:590, 1969.
66.
Campbell M: A new fenestrated trocar for introduction of balloon catheter in cystostomy, nephrostomy and pyelostomy. J Urol 65:160, 1951.
67.
Hodgkinson CP, Hodari H: Trocar suprapubic cystostomy for postoperative bladder drainage in the female. Am J Obstet Gynecol 96:773, 1966.
68.
Ingram JM: Suprapubic cystostomy by trocar catheter. Am J Obstet Gynecol 113:1108, 1972.
69.
Tinckler LF: Intracath in suprapubic cystostomy. Lancet 2:206, 1971.
70.
Mitchell JP, Gingell JC: Intracath in suprapubic cystostomy. Lancet 1:206, 1972.
71.
Greene WR, McLeod DG, Mittemeyer BR: Nonoperative suprapubic urinary drainage. Am Fam Physician 16:136, 1977.
72.
McClain WA, Shields CP, Sixsmith DM: Autonomic dysreflexia presenting as a severe headache. Am J Emerg Med 17:238, 1999.
73.
Moody TE, Howards SS, Schneider JA, et al: Intestinal obstruction: A complication of percutaneous cystotomy: A case report. J Urol 118:680, 1977.
74.
Herbert DB, Mitchell GW Jr: Perforation of the ileum as a complication of suprapubic catheterization. Obstet Gynecol 62:663, 1983.
75.
Noller KL, Pratt JH, Symonds RE: Bowel perforation with suprapubic cystostomy. Obstet Gynecol 48(suppl 1):67s, 1976.
76.
Langley II: Suprapubic cystostomy. Postgrad Med 50:171, 1972.
77.
Wolf H, Olsen S, Madsen PO: Suprapubic trocar cystostomy with balloon catheter. Scand J Urol Nephrol 1:66, 1967.
78.
McAninch JW: The injured kidney. Monogr Urol 4:46, 1983.
79.
Carlton CE, Scott R Jr, Goldman M: The management of penetrating injuries of the kidney. J Trauma 8:1071, 1968.
80.
Antoci JP, Schiff M Jr: Bladder and urethral injuries with pelvic fractures. J Urol 128:25, 1982.
81.
Nicolaisen GS, McAninch JW, Marshall GA, et al: Renal trauma: Re-evaluation of the indications for radiographic assessment. J Urol 133:183, 1985.
82.
Morey AF, Bruce JE, McAninch JW: Efficacy of radiographic imaging in pediatric blunt renal trauma. J Urol 156:2014, 1996.
83.
McAninch JW, Federle MP: Evaluation of renal injuries with computerized tomography. J Urol 128:456, 1982.
84.
Perry MO, Husmann DA: Urethral injuries in female subjects following pelvic fractures. J Urol 147:139, 1992.
85.
Lasser EC, Berry CC, Talner LB, et al: Pretreatment with corticosteroids to alleviate reactions to intravenous contrast material. N Engl J Med 317:849, 1987.
86.
Spartaro RF: New and old contrast agents: Pharmacology, tissue opacification, and excretory urography. Urol Radiol 10:2, 1988.
87.
Katzberg RW: New and old contrast agents: Physiology and nephrotoxicity. Urol Radiol 10:6, 1988.
88.
Schwab SJ, Hlatky MA, Pieper KS, et al: Contrast nephrotoxicity: A randomized controlled trial of a nonionic and an ionic radiographic contrast agent. N Engl J Med 320:149, 1989.
89.
Cass AS: False-negative retrograde cystography with bladder rupture owing to external trauma. J Trauma 24:168, 1984.
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Section X - Obstetric and Gynecologic Procedures
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Chapter 57 - Emergency Childbirth Lynnette Doan-Wiggins
The past century has witnessed a marked improvement in prenatal and obstetric care in the United States and with that a marked reduction in infant and maternal mortality. At the beginning of the 20th century, for every 1000 live births in the United States, six to nine women died of pregnancy-related complications and approximately 100 infants died before 1 year of age. [2] From 1900 through 1997, the maternal mortality rate declined almost 99% to less than 0.1 reported deaths per 1000 live births. Similarly from 1915 to 1997 the infant mortality rate declined 93%, to 7.2 per 1000 live births. [2] Environmental interventions, improvements in nutrition, access to health care, and medical advances (such as better management of pregnancy-related hypertension) and an increase in the number of in-hospital deliveries have all contributed to this remarkable decline. [2] [36] The degree to which the emergency clinician interacts in the process of labor and delivery varies among institutions, depending on the availability and readiness of inpatient obstetric services. The role of the emergency clinician may be only to determine that the patient is indeed in active labor and to order transport directly to the labor and delivery area. In a hospital with little or no obstetric services, the emergency clinician may alternatively be called on to manage a complicated delivery and neonatal resuscitation until transfer to another hospital is possible. To this end, the emergency clinician should be able to assess the stage and timing of labor, aid the mother in delivery of the infant, and provide initial stabilization of the newborn.
LABOR Labor is defined as the coordinated sequence of involuntary uterine contractions that result in progressive effacement and dilation of the cervix. This, coupled with the voluntary bearing-down efforts of the mother, terminates in delivery, the actual expulsion of the products of conception. Labor is normally divided into three stages. The first stage begins when uterine contractions reach sufficient force to cause cervical effacement and dilation and ends when the cervix is completely dilated. Although the average duration of the first stage of labor is about 4 hours in parous patients and 7 hours in nulliparous patients, there is marked individual variation. [22] The second stage of labor begins when dilation of the cervix is complete and ends with delivery of the infant. The duration of this stage is also highly variable, with a median of 50 minutes in nulliparas and 20 minutes in multiparas. [22] In general, if the second stage lasts more than 2 hours, abnormal labor has developed. [22] The third stage of labor begins after delivery of the infant and ends after delivery of the placenta. Infrequently, a fourth stage of labor is described as the hour immediately following delivery and is the period in which postpartum hemorrhage due to uterine atony is most likely to occur. [22]
IDENTIFICATION OF LABOR True versus False Labor
Before the establishment of true or effective labor, women may experience so-called false labor. Quite common in late pregnancy, false labor is characterized by irregular, brief contractions of the uterus, usually with discomfort confined to the lower abdomen and groin. These contractions, commonly referred to as Braxton-Hicks contractions, are typically irregular in timing and strength, and there is no change in the cervix and no descent of the fetus. True labor is characterized by a regular sequence of uterine contractions, with progressively increasing intensity and decreasing intervals between contractions. The discomfort produced by the uterine contractions of true labor begins in the fundal region and radiates over the uterus into the lower back. The uterine contractions of true labor are accompanied by effacement and dilation of the cervix, with descent of the presenting part of the fetus. False labor is most common in late pregnancy and in parous women. Although false labor usually stops spontaneously, it may convert rapidly to the effective contractions of true labor. Therefore, a period of observation may be necessary. The interval between true labor contractions gradually diminishes from 10 minutes at the onset of the first stage of labor to as short as 1 minute or less in the second stage. [22] Show
A rather common and dependable sign of the approach of labor is the "show" or "bloody show." A rather late sign of labor, show consists of a small amount of blood-tinged mucus discharged from the vagina and indicates that labor is already in progress or will likely occur during the next several hours to few days. Show represents extrusion of the mucus plug that filled the cervical canal during pregnancy and is evidence of cervical effacement and dilation. Normally, only a few drops of blood escape with the mucus plug. [22] More substantial bleeding during labor suggests an abnormal cause such as abruption of placenta or placenta previa, and vaginal examination is generally contraindicated. [22] Rupture of the Membranes
Spontaneous rupture of the membranes usually occurs during the course of active labor. Typically, rupture is evident by a sudden gush of a variable amount of clear or slightly turbid fluid. Rupture of the membranes before the onset of labor at any stage of gestation is referred to as premature rupture of the membranes (PROM). Rupture occurring at term, but before the onset of labor, is called term premature rupture of the membranes and complicates approximately 8% of pregnancies. [7] Term PROM is followed by the onset of labor and delivery within 5 hours in approximately 95% of cases. [7] The most significant maternal risk of term PROM is intrauterine infection. Fetal risks associated with PROM include umbilical cord compression and ascending infection. [7] Membrane rupture occurring before 37 weeks of gestation is called preterm premature rupture of the membranes (pPROM). Delivery within 1 week of pPROM occurs in approximately 75% of patients regardless of management or clinical presentation. [7] The most significant maternal risk of pPROM is intrauterine infection, although with appropriate management, serious maternal sequelae are uncommon. [7] The most significant risks to the fetus are complications of prematurity such as respiratory distress, necrotizing enterocolitis, and intraventricular hemorrhage. [7] Definitive treatment of
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PROM at any stage of gestation is left to the clinician and is dependent on multiple factors including the presentation, status and gestational age of the fetus, and maternal factors, such as suspected infection and placental location. Treatment options include the induction of labor, operative delivery, the use of prophylactic antibiotics, and the use of antenatal corticosteroids to promote fetal lung maturity. [7] [48] [52] Although membrane rupture during labor is typically manifested by a sudden gush of fluid, presentation, particularly that of PROM, may be more subtle. Because accurate diagnosis is crucial to management, symptoms suggestive of PROM should be confirmed. Examination should be performed in a manner that minimizes the risk of introducing infection. Therefore digital cervical examinations, which increase this risk, should be avoided unless prompt labor and delivery is anticipated. When obstetric facilities are not immediately available, a sterile speculum examination can be performed. Rupture of the membranes is verified if amniotic fluid is seen extruding from the cervical os or pooling in the posterior fornix. [7] [22] Differentiation of amniotic fluid from vaginal fluid may be made by testing the pH of a drop of the fluid with Nitrazine paper. Amniotic fluid has a pH of 7.0 to 7.5 and turns the paper blue-green to deep blue. In the presence of vaginal secretions only, with a pH of 4.5 to 5.5, Nitrazine paper remains yellow. [2] [7] [12] [22] Abe[2] found the Nitrazine test to be positive in 98.9% of women with known rupture of the membranes and negative in 96.2% of women with intact membranes. In clinical practice, however, the test is less reliable because it is frequently used in cases of questionable rupture in which the amount of amniotic fluid is small and, therefore, more subject to pH changes from admixed blood and vaginal secretions. False positive tests may occur with blood, semen, or bacterial vaginosis and false-negative tests with minimal fluid.[2] [7] [12] [22] A less frequently used method to test for amniotic fluid is ferning. A drop of fluid from the cervical os or vaginal fornix is placed on a clean glass slide. Owing to the high sodium chloride content of amniotic fluid, a fern pattern is seen through the microscope as amniotic fluid dries. [7] [29] When the clinical history or physical examination is unclear, ultrasound examination may be useful to document oligohydramnios that, in the absence of fetal abnormalities, is suggestive of membrane rupture. Although outside the scope of the emergency clinician, membrane rupture can be diagnosed unequivocally with ultrasonographically guided transabdominal instillation of indigo carmine dye with subsequent passage of blue fluid from the vagina. [7] If rupture of the membranes is documented in the emergency department (ED), the patient's clinician should be notified and hospital admission of the patient considered. Evaluation of Labor When a woman presents in labor, the general condition of the fetus and mother must be quickly ascertained by means of the patient history and physical examination. Inquiry is made as to the onset and frequency of contractions, the presence or absence of bleeding, the possible loss of amniotic fluid, and the prenatal care and condition of the mother and fetus. In the absence of active vaginal bleeding, the position, presentation, and lie of the fetus may be determined by abdominal palpation and sterile vaginal examination. Staging of labor is assessed by vaginal examination. Fetal well-being is monitored by auscultation of fetal heart tones, particularly immediately after a uterine contraction. Lie, Presentation, and Position
In the latter months of pregnancy, the fetus assumes a characteristic posture within the uterus, usually forming an ovoid mass that corresponds roughly to the shape of the uterine cavity. Typically, the fetus becomes folded or bent on itself in such a way that the back becomes markedly convex, with the head, thighs, and knees sharply flexed. Usually the arms are crossed over the thorax and are parallel to the sides of the body. The umbilical cord lies in the space between the arms and the lower extremities. This characteristic posture is due in part to the mode of growth of the fetus and is also a result of accommodation to the uterine cavity. Lie refers to the relation of the long axis of the fetus to that of the mother. Lie is either longitudinal or transverse (Fig. 57-1 (Figure Not Available) ). Longitudinal lies occur in greater than 99% of pregnancies at term. [22] The presentation, or presenting part, refers to that portion of the body of the fetus that is nearest to, or foremost in, the birth canal. The presenting part is felt through
the cervix on sterile vaginal examination. In longitudinal lies, the presenting part is either the fetal head, the buttocks, or the feet. In transverse lie, the shoulder is the presenting part. Cephalic presentations are classified by the relation of the fetal head to the body of the fetus (Fig. 57-2 (Figure Not Available) ). Ordinarily, the head is sharply flexed so that the occipital fontanel is the presenting part. This is referred to as the vertex or occiput presentation. Less commonly, the neck is fully extended and the face is foremost in the birth canal; this is termed face presentation. Occasionally, the fetal head assumes a partially flexed or partially extended position, resulting in sinciput and brow presentations, respectively. Sinciput and brow presentations, associated with preterm infants, are almost always unstable and convert to either the occiput or face presentation as labor progresses. Breech presentations are classified as frank, complete, and footling or incomplete (Fig. 57-3 (Figure Not Available) ). When the fetus presents with the hips flexed and the legs extended over the anterior surfaces of the body, this is termed frank breech. Flexion of the fetal hips and knees results in complete breech presentation. When one or both of the feet or knees are lowermost in the canal, an incomplete or footling breech results. Figure 57-1 (Figure Not Available) A, Transverse lie with shoulder presentation. B, Longitudinal lie with vertex presentation. (From Romney S, Gray MK, Little AB, et al [eds]: Gynecology and Obstetrics: The Health Care of Women. New York, McGraw-Hill, 1975.)
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Figure 57-2 (Figure Not Available) Cephalic presentations-deflexion attitude of fetal head. A, Vertex. B, Sinciput. C, Brow. D, Face. Diameter of the presenting fetal head is shown for each of the attitudes. (From Romney S, Gray MK, Little AB, et al [eds]: Gynecology and Obstetrics: The Health Care of Women. New York, McGraw-Hill, 1975.)
At or near term, the incidence of the various presentations is approximately 96% for vertex, 3.5% for breech, 0.3% for face, and 0.4% for shoulder.
[ 22]
Position refers to the relation of the presenting part to the birth canal and may be either left or right. The occiput, chin, and sacrum are the determining parts in vertex, face, and breech presentations, respectively. The presentation and position of the fetus are initially determined by abdominal palpation using Leopold maneuvers. Abdominal palpation (Leopold maneuvers).
Although abdominal ultrasonography has largely replaced abdominal palpation for determination of fetal lie, these maneuvers may be helpful when ultrasound evaluation is unavailable. They can be performed throughout the latter months of pregnancy and during labor in the intervals between contractions. The findings from abdominal palpation provide information about the presentation and position of the fetus and the extent to which the presenting part has descended into the pelvis (Fig. 57-4 (Figure Not Available) ). The mother should be placed on a firm bed or examining table with her abdomen bared. For the first three of the four maneuvers, the examiner stands at the side of the bed facing the patient. During the first maneuver (see Fig. 57-4 A (Figure Not Available) ), the upper abdomen is gently palpated with the fingertips of both hands to determine which fetal pole is present in the uterine fundus. The fetal breech gives the sensation of a large, nodular body, whereas the fetal head is hard, round, and freely movable. During the second maneuver, the examiner places his or her hands on either side of the abdomen, exerting deep, gentle pressure (see Fig. 57-4 B (Figure Not Available) ). On one side, the hard, resistant back is felt; on the other side, the fetal extremities or small parts are felt. By noting whether the back is directed anteriorly, Figure 57-3 (Figure Not Available) Fetal attitude in breech presentations. A, Frank. B, Complete. C, Single footling—incomplete. D, Double footling—incomplete. (From Romney S, Gray MK, Little AB, et al [eds]: Gynecology and Obstetrics: The Health Care of Women. New York, McGraw-Hill, 1975.)
posteriorly, or transversely, fetal orientation or lie is determined. The third maneuver is performed by grasping the lower portion of the maternal abdomen just above the symphysis pubis with the thumb and forefinger of one hand (see Fig. 57-4C (Figure Not Available) ). If the presenting part is not engaged, the position of the head in relation to the back and extremities is ascertained. If the cephalic prominence is palpated on the same side as the small parts, the head must be flexed and therefore a vertex or occiput presentation exists. If the cephalic prominence is on the same side as the back, the head must be extended. If the presenting part is deeply engaged in the pelvis, the findings from this maneuver indicate that the lower pole of the fetus is fixed in the pelvis. The details of presentation and position are then defined by the fourth maneuver. To perform the fourth maneuver, the examiner changes position and faces the mother's feet. With the tips of the first three fingers of each hand, the examiner exerts deep, gentle pressure in the direction of the axis of the pelvic inlet (see Fig. 57-4 D (Figure Not Available) ). When the head is the presenting part, one examining hand will be stopped sooner than the other by a rounded body, the cephalic prominence, while the other hand continues more deeply into the pelvis. The cephalic prominence is felt on the same side as the small parts in vertex presentations and on the same side as the back in face presentations. In breech presentations, the information obtained from this maneuver is less precise. [22] Vaginal examination.
Unless there has been bleeding in excess of a bloody show, a manual (not speculum) vaginal examination should be performed to identify fetal presentation and position and to assess the progress of labor.
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Figure 57-4 (Figure Not Available) Abdominal palpation (four maneuvers of Leopold). A, Determination of the fetal part occupying the uterine fundus. B, Palpation of fetal small parts and back. C, Determination of the part occupying the lower uterine segment. D, Determination of the cephalic prominence. (From Romney S, Gray MK, Little AB, et al [eds]: Gynecology and Obstetrics: The Health Care of Women. New York, McGraw-Hill, 1975.)
The vulva and perineal area are prepared with an antiseptic solution such as povidone-iodine. The woman is placed on a bedpan with her legs widely separated. Scrubbing is directed from anterior to posterior and away from the vaginal introitus; each sponge should be discarded after it passes over the anal region. A dry sponge placed on the introitus prevents contaminated solution from running into the vagina. After preparation of the vulvar and perineal regions, the examiner uses the thumb and forefinger of a sterile-gloved hand to widely separate the labia to expose the vaginal opening; this prevents the examining fingers from coming into contact with the inner surfaces of the labia. The index and second fingers of the other hand are then introduced into the vagina to perform the examination. Cervical effacement, dilation, and fetal station are assessed. Fetal presentation and position are confirmed.[22] Cervical effacement refers to the process of cervical thinning that occurs before and during the first stage of labor as the cervical canal shortens from a length of about 2 cm to a circular opening with almost paper-thin edges (Fig. 57-5 (Figure Not Available) ). The degree of cervical effacement is assessed by palpation and is determined by the palpated length of the cervical canal compared with that of the uneffaced, or normal, cervical canal. Effacement is expressed as a percentage from 0%, or totally uneffaced, to 100%, or completely effaced. Cervical dilation is determined by estimating the average diameter of the cervical os. The examining finger is swept Figure 57-5 (Figure Not Available) Effacement of the cervix. A, None. B, Partial. C, Complete. (From Romney S, Gray MK, Little AB, et al [eds]: Gynecology and Obstetrics: The Health Care of Women. New York, McGraw-Hill, 1975.)
from the cervical margin on one side across the cervical os to the opposite margin. The transverse diameter is expressed in centimeters. Ten centimeters constitutes full cervical dilation. A diameter of 6 cm, it is frequently easier to determine the width of the remaining cervical rim
and subtract twice that measurement from 10 cm. For example, if a 1 cm rim is felt, dilation is 8 cm. Station refers to the level of the presenting fetal part in the birth canal relative to the ischial spines which lie halfway between the pelvic inlet and the pelvic outlet ( Fig. 57-6 ). Zero station is used to denote that the presenting part is at the level of the ischial spines. The birth canal above and below the spines is divided into fifths. When the presenting part lies above the spines the distances are stated in negative figures (-5, -4, -3, -2, and -1). Below the ischial spines the presenting fetal part passes +1, +2, +3, +4, and +5 stations to delivery. Determination is made by simple palpation. [22] Position and presentation of the fetus may be inconclusive before labor, because the presenting parts must be palpated through the lower uterine segment. After dilation and effacement of the cervix, however, further delineation of presentation and position of the fetus may be made by vaginal examination. After the perineal area has been appropriately prepared, as described previously, 3 maneuvers are used to determine fetal presentation and position. In the first maneuver, 2 fingers of the examiner's gloved hand are introduced into the vagina and advanced to the presenting part, differentiating face, vertex, and breech presentations. In vertex presentations, the examiner's
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Figure 57-6 Station of the fetal head. As a reference point, the level of the ischial spines is zero station. (From Benson RC [ed]: Current Obstetric and Gynecologic Diagnosis and Treatment, 3rd ed. Los Altos, Calif., Lange Medical Publications, 1980.)
fingers are carried up behind the symphysis pubis and then swept posteriorly over the fetal head toward the maternal sacrum, identifying the course of the sagittal suture. The positions of the two fontanels, located at opposite ends of the sagittal sutures, are then defined by palpation. The anterior fontanel is diamond shaped; the posterior fontanel is triangular. In face and breech presentations, the various parts are more readily distinguished. In breech presentations, the fetal sacrum is the point of reference; in face presentations, the easily identifiable fetal chin is used. Fetal Well-Being Auscultation.
Auscultation of fetal heart tones is necessary to determine fetal well-being. The heart rate of the fetus can be identified with a stethoscope, a fetoscope, or preferably a Doppler ultrasound device placed firmly on the maternal abdominal wall overlying the fetal thorax and repositioned until fetal heart tones are heard. When a Doppler device is used, a conducting gel should be applied to the abdominal wall, interfacing with the Doppler receiver. The region of the abdomen in which fetal heart sounds are heard most clearly varies with fetal presentation and the degree to which the presenting part has descended. In cephalic presentations, fetal heart sounds are heard best midway between the maternal umbilicus and the anterior superior spine of the maternal ilium. [22] To avoid confusion of maternal and fetal heart sounds, the maternal pulse should be palpated as the fetal heart rate is auscultated. Normal baseline fetal heart rate is 120 to 160 bpm with heart rate varying considerably from beat to beat. [5] [22] Rates above or below this range may indicate fetal distress. Fetal tachycardia occurs when fetal heart rate is >160 beats/min. [22] Brief accelerations in fetal heart rate (i.e., those lasting 24 hours. When repatching is required, a clean patch should be applied within each 24 hours. Repatching prevents a patch from becoming moist and serving as a nidus for the development of infection. The Donaldson Eyepatch (Keeler Instruments, Inc, Broomall, PA) is a commercial product used for enforced eyelid closure that avoids the bulkiness of pressure patching ( Fig. 64-28 ). The device has two components: one adheres to the upper lid, and the other is a circle that adheres to the
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Figure 64-26 Final appearance of pressure eye patch.
ipsilateral cheek. A tab on the upper component connects by Velcro to the lower component. This patch may be advantageous in some settings, but its design may encourage some individuals to release the lid closure prematurely. Because of conjugate eye movement, patching only one eye does not totally immobilize the globe. When all movement must be stopped, bilateral eye patches should be applied. The use of bilateral patches may not be accepted by all patients, and one must seek both patient understanding and family support for patient home activities if dual eye patching is to be successful. Complications There are few complications involved in patching. It is possible to patch the patient's lashes in between the lids so that they abrade the cornea. This can occur if the patient partially
Figure 64-27 Use of the adjustable elastic strap pressure patch, Presspatch II. The clinician should ensure that the elastic straps for the patch are adjusted to avoid excessive globe pressure. (Courtesy of Precision Therapeutics, Inc, Las Vegas, NV.)
Figure 64-28 Donaldson eye patch (Keeler Instruments, Inc, Broomall, PA). Inset shows the means by which the patch can be released for eye inspection or medication administration.
opens the eye during the procedure. This can be avoided by insisting that both eyes stay closed during the entire patching. Most problems develop when the eye is not securely patched and excessive lid motion occurs. In this situation the corneal epithelial cells are not permitted to migrate over and close the epithelial defect. This leads to increased pain and delayed healing. Some corneal defects are extensive and may require 3 to 5 days for healing. Patients with extensive injuries should be observed frequently and treated with cycloplegic agents, pain medication, and (if clinically indicated) sedatives for sleep. The practitioner should document the size of the corneal defect at each visit. If healing does not occur in a progressive fashion, ophthalmologic consultation should be obtained. As mentioned earlier, patching is contraindicated when a corneal ulcer is present, the possibility of infection is high, or there has been soft contact use. A corneal "abrasion" that does not heal could very well be a herpetic ulcer. Recurrent Corneal Erosions Patients whose eyes have been patched for a corneal abrasion may experience recurrent corneal erosions in the future as a complication of the original injury. The original abrasion may appear to have healed perfectly, but days, weeks, or even months later a small area of corneal epithelium can come off, re-creating the symptoms of the original abrasion in the absence of new trauma. This usually occurs in the mornings as the patient opens the eyes, presumably due to adherence of the weaker, recently healed corneal epithelium to the upper lid during sleep. These erosions may heal before the patient is reexamined and can be very puzzling. The cause is
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a failure of bonding of the corneal epithelium to its basement membrane. [71] Patients who develop this syndrome are given 5% sodium chloride ointment to use nightly to prevent the erosions; some require bandage soft (collagen) contact lenses. [72] Summary Patching is generally not necessary in the treatment of corneal epithelial defects, but if performed, should be an easy, straightforward procedure. A common problem is the lack of follow-up instructions given to the patient after the patching. Too often, the patient is given a bottle of antibiotic drops to be used every 4 hours and only vague recommendations for a follow-up check. When patients remove the patch to put in an antibiotic drop, they are never able to replace the patch properly again and may actually deter any healing that has already taken place. Instead, they should be told to keep the patch on for 24 hours and to return to have their abrasion checked by a clinician after that time. Generally a large abrasion will take several days to heal. Serial assessment is valuable for patient reassurance and assuring that complications do not develop. The patient with an eye patch should be instructed to rest the uninjured eye. Reading should be discouraged, because involuntary movement of the patched eye will result. Watching television from a distance of 10 feet or more promotes eye fixation and is acceptable. Distant vision is unaffected by patching, although a small degree of peripheral vision is lost on the patched side. Although the visual field is minimally affected, driving after a patch is placed is not advisable. Preferably, the patient should be driven home from the hospital to minimize the potential for patient injury. An elderly patient may require assistance with routine ambulation after eye patching. Use of collagen shields applied directly to the cornea may offer an attractive alternative to eye patches. [72] These devices have yet to be introduced into ED practice.
CONTACT LENS PROCEDURES An estimated 24 million Americans wear a form of contact lenses. [73] Removal of these lenses in the ED may be required to permit further evaluation of the eye or to prevent injury from prolonged wear. Emergency clinicians also evaluate patients for "lost" contact lenses, which may be trapped under the upper lid. At times, the patient may request that the clinician remove a lens that he or she has failed to extract from the cornea. Corneal ulcers may occur in patients who wear contact lenses and may require prompt treatment. This section on contact lens procedures addresses these concerns and discusses injuries associated with removal attempts, the mechanism of injury from prolonged wear, and instructions to be given to patients at discharge. The first contact lenses were scleral lenses made of glass. These lenses, covering the cornea as well as much of the surrounding sclera, are reported to have been in use from 1888 to 1948. [74] Glass corneal lenses (sitting entirely on the cornea) made by the Carl Zeiss Optical Works of Jena were first described in 1912. A practical synthetic scleral lens using methyl methacrylate rather than glass was discussed by Obrig and Mullen in 1938. [75] [76] In 1947, Tuohy redeveloped the corneal lens using methyl methacrylate. This was the forerunner of the current hard contact lens. [77] The development in Czechoslovakia of lenses made of soft gas-permeable polymers was reported in 1960. [78] These hydrogel (hydrophilic gelatinous-like) lenses have evolved into today's soft contact lenses. Soft contact lenses now come in a variety of types including extended and daily wear. Some extended-wear lenses are disposable. All lenses should be removed at least once a week. Mechanism of Corneal Injury from Contact Lens Wear Hard Contact Lenses
The oxygenation of the cornea is dependent on movement of oxygen-rich tears under the hard contact lens during blinking. During the "adaptation" phase of early wear, the wearer of hard contact lenses produces hypotonic tears as a result of mechanical irritation from the lens. [74] This results in corneal edema, which reduces subsequent tear flow under the lens during blinking. Overwearing a lens at this time leads to corneal ischemia, with superficial epithelial defects predominantly in the central corneal area (see Fig. 64-10D ), where the least tear flow occurs. With adaptation, the tears become isotonic and the blinking rate normalizes, permitting increased wear time. During early adaptation blinking is more rapid than normal and then slows to a subnormal rate during late adaptation. Mucus delivery to the cornea in the tear film may also play an important role in maintaining corneal lubrication. Tight-fitting contact lenses may never permit good tear flow despite an adaptation phase; individuals with tightly fitted lenses may never be able to wear their original contact lenses for longer than 6 to 8 hours. Lenses that are excessively loose can also cause irritation by moving during blinking. Rough or cracked edges can cause corneal abrasions. In the ED, the patient who presents with irritation caused by prolonged wear may be either a new or an adapted wearer. The adapted wearer may have been exposed to chemical irritants (e.g., smoke), which reduce the tonicity of tears and lead to corneal edema and decreased tear flow. Alternatively, the adapted wearer with irritation may have ingested sedatives (e.g., alcohol) or may have fallen asleep wearing the contact lenses, thus decreasing blinking and tear flow. Another possibility is that the patient may actually be wearing tight-fitting contact lenses that have never allowed true adaptation despite many months of wear. The patient with the overwear syndrome usually awakens a few hours after removing the lenses. The patient experiences intense pain and tearing similar to that caused by an FB. The delay in the onset of symptoms until after removal of the lenses is caused by a temporary corneal anesthesia produced by the anoxic metabolic by-products that build up during extended lens wear. [79] A second factor is the slow passage of microcysts of edema, which are pushed up to the corneal surface by mitosis of the underlying cells. When the cysts break open on the surface, the corneal nerve endings are exposed. [80] Most patients with the overwear syndrome can be managed with reassurance, frequent administration of artificial tears, oral analgesics, and advice to "wait it out" in a darkened room. Some patients require patching for comfort. A patient who has experienced no problems with contact lenses before an overwear episode can return to using the lenses after 2 or 3 days of wearing glasses but should be
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advised to build up wearing time gradually. A patient who was having chronic problems with lens comfort before the episode should check with an ophthalmologist before using the contact lenses again. Soft Contact Lenses
Although there is also oxygenation of the cornea by way of the tear film with soft contact lenses, only approximately one tenth of the flow behind the lens that occurs with a hard lens is present during soft contact wear. [74] The high degree of lens gas permeability permits the majority of oxygenation to occur directly through the lens. The hydrogel lens is more comfortable than the hard contact lens because lid motion over the lens is smooth. The minimization of lid and corneal irritation allows a more rapid adaptation phase because the initial reflex-induced tearing and blinking changes are reduced. Nonetheless, the lenses may still lead to corneal edema and secondary hypoxic epithelial changes if worn for an excessive period when blinking is inhibited. Some individuals can tolerate the lenses for extended periods and may on occasion sleep with the contact lenses in place, although this practice is not encouraged. Newer extended-wear hydrogel lenses (e.g., Permalens) permit wear for several days without injury. These lenses are not discernible from standard soft lenses on examination. Although the acute overwear syndrome that occurs with hard contact lenses can also occur with soft lenses, it is infrequent. More commonly, ocular damage from soft contact lenses falls into one of the three following categories: 1. Corneal neovascularization. Often the patient is asymptomatic, but on slit lamp examination fine vessels are seen invading the peripheral cornea. The treatment is to have an ophthalmologist refit the patient with looser or thinner lenses or with contact lenses that are more gas permeable. 2. Giant papillary conjunctivitis.[81] The patient notes decreased lens tolerance and increased mucus production. On examination of the tarsal conjunctiva (best seen on eversion of the upper lid), large papillae are seen. These grossly appear as a cobblestoned surface. The treatment is to discontinue wearing the lenses until the process reverses and then have the lenses refitted. 3. A sensitivity reaction to the contact lens solutions (usually thimerosol or chlorhexidine). [82] [83] There is diffuse conjunctival injection and sometimes a superficial keratitis. The treatment is to switch to preservative-free saline with the use of heat sterilization. Often, the contact lenses will need to be replaced before lens wear can be resumed. All of these problems with soft lenses have bilateral, subacute onsets and do not require emergency treatment. The only form of ocular damage associated with soft contact lenses that is a true emergency is a bacterial (often Pseudomonas or Acanthamoeba with soft contact lenses) or fungal corneal ulcer. [84] [85] [86] Because the nature of soft contact lenses is to absorb water, they can also absorb pathogens, which then can invade the cornea. This is especially true if the soft lens is worn continuously for extended periods of time. The patient presents with a painful, red eye with associated discharge and a white infiltrate on the cornea. Immediate ophthalmologic consultation is required for appropriate culturing and antimicrobial treatment. These infections can permanently affect the patient's visual acuity. Indications for Removal Removal of a contact lens is recommended in the following situations: 1. Contact lens wearer with an altered state of consciousness. The emergency clinician should always be aware that the patient with a depressed or acutely agitated sensorium may be unable to express the need to have his or her contact lenses removed. Furthermore, it is likely that patients with a depressed sensorium will have decreased lid motion. During the secondary survey of these patients, the emergency clinician should identify the presence of the lenses and should arrange for their removal and storage to prevent harm from excessive wear or possible accidental dislodgment at a later time. Without magnification, soft
contact lenses may be difficult to see. Examination with an obliquely directed penlight should reveal the edge of the soft lens 1 to 2 mm from the limbus on the bulbar conjunctiva. 2. Eye trauma with lens in place. After measurement of visual acuity with the patient's lenses in place, the lenses should be removed to permit more detailed examination of the cornea. Fluorescein may discolor hydrogel lenses; when possible, extended-wear lenses should be removed before the use of this chemical. After the dye is instilled, the eyes should be flushed with normal saline; at least 1 hour should pass before reinsertion. [74] The availability of single-use droppers of 0.35% fluorexon (Fluresoft) has permitted the safe staining of eyes when soft lenses are to be worn immediately after the examination. A limited eye irrigation after the use of fluorexon drops is still recommended before the reinsertion of soft contact lenses. 3. Inability of the patient to remove the contact lens. A patient may present with a hard contact lens that cannot be removed because of corneal edema from prolonged wear. Alternatively, the patient may present with a "lost" contact lens that is believed to be behind the upper lid. There is no urgency for contact removal in the out-of-hospital setting; hence, removal can wait until the patient has been evaluated by a clinician. Contraindication to Removal The only major problem with contact lens removal occurs when the cornea may have been perforated. In this case, the suction cup technique of removal described later is preferred. Procedure Hard Contact Lens Removal
A number of maneuvers have been devised for removal of the corneal lens. One technique is to first lean the patient's face over a table or a collecting cloth. The clinician pulls the lids temporally from the lateral palpebral margin to lock the lids against the contact lens edges. The patient should look toward the nose and then downward toward the chin. This movement works the lower eyelid under the lower lens edge and flips the lens off the eye. The technique requires a cooperative patient because the clinician must pull the patient's lids tightly against the edge of the contact lens. The movement of the patient's eye then flips the contact free. In the unresponsive patient, a modification of the technique can be used while the patient is supine. The clinician
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takes a more active role in lid movement using the following procedure: one thumb is placed on the upper eyelid and the other on the lower eyelid near the margin of each lid. With the lens centered over the cornea, the eyelids are opened until the lid margins are beyond the edges of the lens ( Fig. 64-29A ). The clinician then presses both eyelids gently but firmly on the globe of the eye and moves the lids so that they are barely touching the edges of the lens ( Fig. 64-29B ). One presses slightly harder on the lower lid to move it under the bottom edge of the lens. As the lower edge of the lens begins to tip away from the eye, the lids are moved together, allowing the lens to slide out to where it can be grasped ( Fig. 64-29C ). The clinician should remember to use clean hands (and preferably wear examination gloves that have been rinsed in tap water or saline) when removing the lens. Alternatively, one can move the lens gently off the cornea using a cotton-tipped applicator to guide the lens onto the sclera, where the applicator tip can be forced under an edge of the lens to flip the contact loose. Topical anesthesia is indicated when using an applicator and the patient is awake. Care must be taken with this technique to avoid contact of the applicator with the cornea when the lens is moved off the eye. Perhaps the easiest technique is to use a moistened suction-tipped device and simply lift the lens off the cornea ( Fig. 64-30 ). Several lenses (those hard contact lenses that cover both the cornea and an amount of the sclera) can be removed by an exaggeration of the manual technique described earlier ( Fig. 64-31 ). Elevation of the lens with a cotton-tipped applicator or a suction-tipped device is also an effective technique. Soft
Figure 64-29 Manual technique for removing a hard contact lens. A, Separation of lids. B, Entrapment of lens edges with lids. C, Expulsion of lens by forcing of lower lid under inferior edge of lens. (From Grant HD, Murray RH, Bergeron JF: Brady Emergency Care, 5th ed. Englewood Cliffs, NJ, Prentice Hall, 1990, p 338. Reproduced by permission.)
Figure 64-30 Use of a moistened suction cup to remove a hard contact lens. (From Grant HD, Murray RH, Bergeron JF: Brady Emergency Care, 5th ed. Englewood Cliffs, NJ, Prentice Hall, 1990, p 338. Reproduced by permission.)
contact lenses should not be removed with a suction-tipped device because tearing or splitting of the lens may occur. Soft Contact Lens Removal
With clean hands (preferably using gloves rinsed in saline or tap water), the clinician pulls down the lower eyelid using the middle finger. The tip of the index finger is placed on the lower edge of the lens. The lens is slid down onto the sclera and is compressed slightly between the thumb and the index finger. This pinching motion folds the lens and allows its removal from the eye ( Fig. 64-32 ).
Figure 64-31 Removal of a hard scleral lens. A, Separation of lids. B, Forcing of lower lid beneath edge of scleral lens by temporal traction on lower lid. C, Lifting of lens off eye. (From Grant HD, Murray RH, Bergeron JF: Brady Emergency Care, 5th ed. Englewood Cliffs, NJ, Prentice Hall, 1990, p 338. Reproduced by permission.)
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Figure 64-32 Removal of a soft contact lens. A, Separation of lids and movement of contact onto sclera using index finger. B, Pinching of lens between thumb and index finger. (From Grant HD, Murray RH, Bergeron JF: Brady Emergency Care, 5th ed. Englewood Cliffs, NJ, Prentice Hall, 1990, p 338. Reproduced by permission.)
Lens Storage After a contact lens is removed, it should be stored in sterile normal saline solution. It is best to use the patient's own storage container and, if available, the patient's lens solution. A variety of alternative sterile containers are available for use in the ED. One should be certain that right and left lenses are kept separate and in appropriately labeled containers. The containers should be kept with the patient until a friend or family member can procure them, or they should be locked with the patient's valuables. Evaluation of the "Lost Contact" A patient may present with a request to be examined for a "lost" contact lens. The patient may be unsure if the lens is hidden under a lid, remains on the cornea, or is truly outside the eye. The evaluation of the patient with a "lost" contact should begin, as should all eye examinations, with the measurement of visual acuity. Visual acuity is preferably measured using a 20-foot eye chart. A diminished visual acuity in the eye in which a patient just cannot seem to "take out" a soft contact lens may be the most convincing evidence that the lens is missing. Although transparent, soft contact lenses in proper position are usually seen easily when viewed closely with loupes or on slit lamp examination. The lens forms a fine line where it ends on the sclera several millimeters peripherally to the limbus. Hard contact lenses are even more evident as they change in position on the cornea. If the contact is not evident on initial inspection, the lids are everted as discussed in the section on FB removal (double eversion of the upper lid). If the lens is still not visible, a drop of topical anesthetic is placed in the eye. The upper fornix is gently swept with a moistened cotton-tipped applicator while the patient looks toward the chin. If the lens is still not evident even though the patient remains insistent that it is in the eye, one may perform a fluorescein examination after explaining that the dye will color the lens (permanently). The upper lid should again be doubly everted and visualized using an ultraviolet light source. If the lens remains elusive, the patient should be reassured that a thorough examination was performed and that no object was located under the eyelids or on the cornea. The cornea should then be examined for defects that warrant antibiotic ointment and a pressure patch placed over the eye (as discussed in the section on patching). Follow-up with the patient's eye specialist for a replacement lens and further reassurance is encouraged. One also should ask the patient to retrace movements at the time the contact began to give trouble or was missed and to check the clothing being worn for the presence of the lens. A final possibility is that the patient may have accidentally placed the two lenses together in the same side of the carrying case, causing them to stick together. In fact, patients have inadvertently placed one contact lens over the other—both in the same eye. One should note that hard contact lenses have been found embedded in conjunctival tissue under the upper lid ( Fig. 64-33 ) after more than a year. [87] [88] Hence, a methodical approach, as outlined earlier, should be taken to ensure that no lens remains hidden in the eye. Complications of Lens Removal Unless care is used during lens removal, a corneal abrasion can occur. It is difficult at times to determine whether the injury was produced by the patient or was a result of the clinician's technique. Fortunately, the corneal injury is usually of a superficial nature and responds well to eye patching, or other symptomatic care. Summary Contact lens removal is seldom a difficult task. More challenging situations are the identification of emergency patients at risk for corneal injury due to overuse, the evaluation of patients who cannot locate a soft lens, and the instruction of patients with contact lens-related problems concerning aftercare.
Figure 64-33 Hard contact lens embedded in conjunctival tissue of upper lid. (From Mandell RB: Contact Lens Practice, 3rd ed. Springfield, IL, Charles C Thomas, 1981. Reproduced by permission.)
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INFECTIOUS KERATITIS Infectious keratitis with corneal ulceration can have a variety of causes, including the overwear of contact lenses. Diagnosis of a corneal ulcer requires the use of a slit lamp and an accurate determination of the patient's history. Infectious keratitis is a frequent problem in ophthalmic practice. Herpes simplex is a common corneal pathogen. Acanthamoeba is another pathogen that is particularly associated with contact lens use and exposure to organism-tainted environments. Patients presenting with a corneal ulcer require prompt referral to an ophthalmologist. When immediate referral to an ophthalmologist is not possible, telephone guidance from the ophthalmologist and therapy needs to be initiated with ophthalmology follow-up in 24 hours or less. Patients with herpes simplex keratitis often give a history of prior episodes of the disease. Patients who undergo almost any form of corneal stress may sustain an activation of preexisting corneal disease. Herpes simplex keratitis is classically recognized by its dendritic pattern on fluorescein staining. Acanthamoeba keratitis is a disease with potentially devastating consequence. Its frequency seems to be increasing, particularly in contact lens wearers, and its pathophysiology is not completely understood. Patients often present with a red eye in which initial bacterial culture results are negative. Bacterial keratitis occurs in a variety of settings. Organisms range from the relatively common Staphylococcus or Streptococcus to Mycobacterium, which can be difficult to identify. A variety of antibiotics are used against bacterial agents. Ciprofloxacin is a quinolone that has demonstrated efficacy against most of the common causative agents. Bacterial organisms in the cornea can develop resistance to any antibiotic and resistance to fluoroquinolones has been observed. [89] Ideally, treatment follows culturing of the ulcer. In instances in which a cellular infiltrate is seen on slit lamp examination and in which there will be a delay of hours before an ophthalmologic consultant can culture the patient, it is prudent to initiate therapy with topical ciprofloxacin. In such circumstances, the emergency clinician may consider corneal cultures if suggested under the telephone guidance of the consultant before administering the antibiotic. One approach is to lightly touch a culture-moistened cotton-tipped swab against the ulcer and then streak standard culture media. If the ulcer is chronic or the patient is immunocompromised, fungal organisms may be culprit. Finally, a saline-moistened cotton-tipped swab may be used to obtain a Gram stain of the ulcer. Initiation of therapy before obtaining specimens for culture makes the subsequent identification of an organism difficult. For this reason the immediate initiation of treatment depends on the circumstances of the individual case.
TONOMETRY Tonometry is the estimation of IOP obtained by measurement of the resistance of the eyeball to indentation of an applied force. Prolonged elevated IOP is associated with visual field loss and blindness. Sudden elevation of IOP can follow trauma or occur with primary angle-closure glaucoma. Often, patients with primary angle-closure glaucoma come to the ED with systemic complaints that include nausea, vomiting, and headache. The emergency clinician must determine the IOP and its relationship to the systemic symptoms. Occasionally, such patients are surprisingly free of pain in or about the eye. Ophthalmologists depended on tactile estimation of eye pressure until the 1860s when von Graefe developed the first mechanical tonometer. [3] [22] Applanation tonometry was introduced in 1885 by Maklakoff [90] but was not popularized until Goldmann [91] improved the instrument in the 1930s. Schiotz developed an impression tonometer in 1905 and modified it in the 1920s; this form is still in use today. [92] Aside from modifications in configuration, current tonometers closely resemble the devices popularized by Schiotz and Goldmann. The most dramatic variations are the Mackay-Marg tonometer, [93] which permits a continuous tonographic recording, and the noncontact tonometer, which is a pneumatic applanation tonometer. [94] Pocket-sized tonometers using the MacKay-Marg tonometer principle are available. One such device is the Tono-Pen XL (Mentor O & O, Inc, Norwell, MA). [95] These devices are portable, lightweight, and relatively accurate, with built-in provisions for calibration. They have the advantage of a one-time-use replaceable cover that eliminates concern about the possible transmission of an infectious agent. While numerous devices are available, the Schiotz tonometer is the standard way for emergency clinicians to measure IOP. Tonometric Techniques Three tonometric techniques are reliable and clinically useful for estimating IOP: 1. The impression method uses a plunger (3 mm in diameter) to deform the cornea and the "indentation" is then measured. This technique was popularized by Schiotz and commonly bears his name. 2. The MacKay-Marg method is a refined version of the impression technique in which smaller amounts of cornea are indented. 3. In the applanation method a planar surface is pressed against the cornea. One can either measure the pressure necessary to flatten a defined area or measure the size of a flattened area produced by the defined pressure. These tonometric techniques are based on the Imbert-Fick law, which states that if a plane surface is applied with force (F) to a thin, spheric membrane within which a pressure (P t ) exists, at equilibrium the expression P t = F/A is valid if A is the area of the applied surface ( Fig. 64-34 ). The Schiotz tonometer ( Fig. 64-35 ) actually measures the total IOP (initial pressure plus the pressure added by the weight of the tonometer and the plunger). Friedenwald empirically found that a "rigidity coefficient" could be introduced to allow an estimation of the true intraocular eye pressure. [96] One must be aware, however, that calculated conversion tables for Schiotz tonometers use an average estimate of the rigidity coefficient and hence are not accurate when eye rigidity is altered (e.g., after scleral buckle procedures for retinal detachment or with extreme myopia). Although the applanation tonometer ( Fig. 64-36 ) also increases the IOP during measurement, the applied pressure is much smaller and is partially countered by the surface tension of the eye tear film. Emergency clinicians usually do not have experience or availability of this technique, but studies have shown applanation tonometer measurements to be within 2% of the true IOP. [97]
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Figure 64-34 Principle of tonometry. At equilibrium: P t = F/A. (From Draeger J, Jessen K: Tonometry and tonography. In Bellows JG (ed): Glaucoma: Contemporary International Concepts. New York, Masson Publishing USA, 1979. Reproduced by permission.)
The noncontact tonometer is a pneumatic applanation tonometer that permits IOP measurement without eye contact. A pulsed air jet is used to deform the cornea. The technique is also dependent on ocular rigidity. Although readings taken by different examiners correlate well, the measurements are altered by the use of local anesthetics and show a wide standard deviation of measurement in patients with pathologic elevation of ocular pressure (when standard applanation tonometry is used as a reference). [98] Furthermore, the technique is not useful with corneal surface irregularities (e.g., corneal edema, keratoconus, corneal perforation) or when medications in viscous preparations have been used. The use of this type of tonometer is not recommended when accurate determination of the IOP is required. This type of device is primarily useful for glaucoma screening. Indications for Tonometry Measurement of IOP in the ED by tonometry is a technique available to most emergency clinicians. Tonometry is not a standard procedure for many eye-related complaints, but special situations in which tonometry may be particularly helpful are as follows: Confirmation of a clinical diagnosis of acute angle-closure glaucoma. The middle-aged or elderly patient who presents with acute aching pain in one eye, blurred vision (including "halos" around lights), and a red eye with a smoky cornea and a fixed midposition pupil obviously needs a pressure reading. Sometimes the findings are less dramatic, and
Figure 64-35 Principle of impression tonometry. In reality, P t is increased slightly by the weight of the instrument. (From Draeger J, Jessen K: Tonometry and tonography. In Bellows JG (ed): Glaucoma: Contemporary International Concepts. New York, Masson Publishing USA, 1979. Reproduced by permission.)
Figure 64-36 Principle of applanation tonometry. The effect of surface tension counters the pressure rise produced by application of the instrument. (From Draeger J, Jessen K: Tonometry and tonography. In Bellows JG (ed): Glaucoma: Contemporary International Concepts. New York, Masson Publishing USA, 1979. Reproduced by permission.)
sometimes the patient complains mostly of nausea and vomiting that suggest a "flu" rather than an eye disorder. Determination of a baseline ocular pressure after blunt ocular injury. Patients with hyphema often have acute rises in IOP because of blood obstructing the trabecular meshwork. [99] Later, angle recession can cause a permanent form of open-angle glaucoma. Arts and coworkers suggest that an IOP >22 mm Hg or a
difference of 3 mm Hg or greater between eyes is a good marker for "ocular injury" in the setting of an orbital fracture.
[100]
Tonometry may also be considered under the following scenarios: Determination of a baseline ocular pressure in a patient with iritis. Patients with iritis can develop both open- and closed-angle glaucoma as well as corticosteroid-induced glaucoma. Since most cases of iritis are referred, tonometry may also be deferred unless there are signs of increased IOP. Documentation of ocular pressure in the patient at risk for open-angle glaucoma. All patients older than 40 years with a familial history of open-angle glaucoma, optic disc changes, visual field defects, and pressures =21 mm Hg should be referred to an ophthalmologist for further work-up. Referral should also be made for those patients with suspiciously cupped discs who have normal pressures; some of these patients may have "low pressure" glaucoma associated with visual field defects. This is usually part of an ophthalmologist's examination. Contraindications to Tonometry Tonometry is relatively contraindicated in eyes that are infected unless one is using a device such as the Tono-Pen XL, which uses a sterilized cover. [2] One should sterilize a tonometer before and after applying it to a potentially infected eye. Infected eyes are preferably measured with either a noncontact tonometer or a device with a covered tip (e.g., Tono-Pen). The contact portions of any device should be swabbed with alcohol and allowed to dry before use on another eye. Not all viruses are destroyed by alcohol cleansing. Hydrogen peroxide is effective for deactivating the human immunodeficiency virus responsible for the acquired immunodeficiency syndrome (AIDS). Ultraviolet sterilization, cold-sterilizer
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bathing of the footplate and plunger, and ethylene oxide sterilization have been advocated as alternatives to sterilize the Schiötz tonometer tip. The Schiötz tonometer is also used with sterile disposable coverings (marketed as Tonofilm). Nonetheless, measurement of IOP in an obviously infected eye can be deferred until a subsequent visit to the ED or private clinician unless the red eye demands an immediate determination of IOP. Examples of indications for immediate tonometry in the setting of a red eye are suspected angle-closure glaucoma (acute onset of redness and pain in the eye with smoky vision, a cloudy cornea, and a fixed pupil in mid-dilation) and iritis (ciliary injection with photophobia), in which secondary angle-closure or corticosteroid-induced pressure changes may occur. Reported cases of conjunctivitis spread by tonometry predominantly tend to be viral infections. Particular efforts should be made to avoid use of the instrument on patients with active facial or ocular herpetic lesions or on patients who may have AIDS. The presence of corneal defects also represents a relative contraindication to tonometry. [3] [22] The use of a tonometer on an abraded cornea may lead to further injury and is commonly deferred until a subsequent visit. Patients who cannot maintain a relaxed position (e.g., because of significant apprehension, blepharospasm, uncontrolled coughing, nystagmus, or uncontrolled singultus) are unlikely to permit an adequate examination and can receive corneal injury when sudden movements occur during an examination. Furthermore, tonometric examination, with the exception of the palpation technique (through the lids) and the noncontact method, should not be performed on a cornea without complete anesthesia. Tonometry should not be performed with a suspected penetrating ocular injury. [2] Globe perforation may be exacerbated by pressure on the globe with resultant extrusion of intraocular contents. Slit lamp examination can be used for detection of a possible perforation. Procedure Palpation Technique
All forms of tonometry are essentially ways of determining the ease of deforming the eye; an eye that is easily deformed has a low pressure. The most direct way to do this is simply to press on the sclera through the lids and grossly compare one eye with the other. One can easily distinguish the rock-hard eye of acute glaucoma from the normal opposite eye by this method. The patient is directed to look down but without closing the lids. The examiner rests both hands upon the patient's forehead and alternately applies just enough digital pressure on the globe to indent it slightly with one index finger while feeling the compliance of the globe with the other ( Fig. 64-37 ). [101] An experienced examiner is able to estimate the IOP within 3 to 5 mm Hg of the actual IOP with the palpation technique, but most emergency clinicians do not have enough experience to trust this method. [39] Another method is to anesthetize the eyes topically and press a wetted applicator on the sclera of each eye. Again, eye deformation is inversely related to ocular pressure. Rigidity of the globe also is a factor in this crude method of tonometry. Impression (Schiötz) Technique
Use of the Schiotz tonometer requires relaxation on the part of the patient and steadiness on the part of the clinician. The
Figure 64-37 The relatively unskilled examiner can detect very high intraocular pressure of acute angle closure glaucoma with tactile tonometry. The examiner rests both hands upon the patient's forehead and alternately applies just enough digital pressure on the globe to indent it slightly with one index finger while feeling the compliance of the globe with the other.
patient is placed in either a supine or a semirecumbent position and is instructed to gaze at a spot directly above the eyes. A spot on the ceiling should suffice; alternatively, the patient can stretch the arm up over the head and gaze at the thumb. A drop of topical anesthetic is placed in each eye. After the irritation of the drop passes, the patient is allowed to blink while the clinician blots the tears away with a tissue. Rubbing the eyes lowers IOP. The patient is reassured that further discomfort during the procedure will not occur. The patient keeps both eyes wide open and fixed on an object, and the clinician separates the eyelids on the side to which he or she is standing. Care must be taken to direct pressure onto the orbital rims rather than into the orbit, because pressure directed into the orbit falsely raises the reading ( Fig. 64-38 ). The tonometer is momentarily held over the open eye, and the patient is informed that the instrument will block vision in the one eye. The patient is instructed to continue to gaze at the fixation point as though the instrument were not there. After the patient relaxes the involuntary muscle contraction that occurs when the instrument is first placed in the line of sight, the instrument is gently lowered onto the middle portion of the cornea. This is a painless experience for the patient with an anesthetized cornea. The instrument is vertically aligned with the footplate resting on the cornea; the reading should be in mid-scale. Should the reading be on the low end of the scale ( 20% reflects an unreliable measurement, which should be repeated). If four dashes ("----") appear on the LCD after the final beep, too few valid readings were obtained. In such a case, the probe can be reactivated (without recalibration) and the
Figure 64-40 After topical anesthesia, the Tono-Pen XL is touched lightly and briefly to the cornea with a tapping motion, then withdrawn. Disposable tip covers are used to minimize any cross contamination.
measurement procedure repeated. If the probe is not reactivated within 20 seconds, the LCD will clear, but the device can be activated as noted previously without recalibration. The values are interpreted as outlined earlier for the Schiötz device. Readings may be affected by the same features noted as causes of errors with impression tonometry via the Schiötz device. The device should be stored with an unused Ocu-Film cover protecting the probe tip. Applanation Technique
One can perform this technique using a slit lamp attachment for an applanation tonometer with the patient's head stabilized in the headrest of the slit lamp (see the following section on the slit lamp examination) ( Fig. 64-41 ). [107] [108] A portable device also is available and is similar in principle. The portable device is not discussed specifically. The patient must be comfortable and relaxed. The clinician should anesthetize the eye as discussed previously, avoiding ocular pressure, which can lower the subsequent measurements. Fluorescein should be applied to each eye. Excess fluorescein should be blotted from the eye. The patient's head should be in the slit lamp with the forehead firmly against the headrest, and the clinician should direct the patient to gaze straight ahead. One can use a light for fixation or can ask the patient to focus on the clinician's ear on the side opposite the eye being examined. The cobalt blue light filter is placed in the light beam, and the slit diaphragm is opened fully. The light arm is angulated to shine on the applanation prism in the region of the encircling black line near the anterior prism tip at an angle of 45°–60° to the line of observation. The voltage is turned to the maximum setting, and the low-power microscopic system is focused through the plastic prism so that the front face is
Figure 64-41 Goldmann applanation tonometer with the biprism aligned with the patient's right cornea.
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clearly seen through the chosen eyepiece. The pressure knob of the tonometer is turned to 1 g (10 mm Hg), bringing the prism arm to its forward stop. Thus, when corneal contact is made, the prism will be exerting only light pressure. The room lights are dimmed. The patient's eye that is being examined and the applanation prism are watched from the side (or with the operator's eye not sighting through the microscope) as the instrument is brought forward by the joystick control until gentle contact is made between the prism face and the corneal center. Contact is evidenced by an immediate bluish glow throughout the limbus. The patient's lids must be wide open and unblinking. Contact with the lid margins produces reflex blinking, and the lids may require separation by the clinician's fingers. Pressure during lid separation must be exerted only against the orbital rims. Through the microscope, the clinician sees two blue semicircles (surrounding the flattened area of cornea). Each semicircle is bordered by an arc of green light and pulses synchronously with the cardiac rate ( Fig. 64-42 ). The semicircles should be of equal size; their width should be approximately one tenth the diameter of the flattened surface contained within each arc. If the semicircles are grossly widened, either excessive tears are present or the prism was probably wet before contact. A wet prism must be withdrawn, dried, and reapplied. If the semicircles are grossly narrowed, the tear film has dried excessively. In this case, the prism must be withdrawn and the patient instructed to blink several times before contact with the cornea is attempted again. If the semicircles are so broad that they extend beyond the illuminate field, there is excessive flattening and the slit lamp must be drawn back. If the semicircles suddenly shrink, either the patient has moved back or the instrument has been backed away from the eye. The semicircles should be of equal extent above and below a horizontal dividing line. If the dividing line is not horizontal, the applanation prism assembly should be rotated on its holder until the line is horizontal. If the semicircles are not equally divided above and below the line, vertical adjustments of the slit lamp should be made. Readings should be taken at approximately the midpoint between systole and diastole, when the inner (concave) boundaries of each semicircle rhythmically glide past each
Figure 64-42 Schematic representation of semicircles seen through the contact applanation prism of the Goldmann tonometer. A, Semicircles are too wide, suggesting excessive moistening of the prism or cornea. The prism must be withdrawn and dried. B, Semicircles are too narrow, suggesting that the lacrimal fluid has dried out, as during a prolonged measurement. The prism must be withdrawn so that the patient may blink a few times. The measurement is then repeated. C, Semicircles are of appropriate width, and their inner borders just touch. Cardiac pulsations transmitted through the globe cause rhythmic or pulsating movement of the semicircles over each other through a small amplitude. D, Semicircles are slightly separated, indicating applied pressure below that of the eye. The measuring drum must be turned to increase applanation pressure until the end point is reached. (From Keeney AH: Ocular Examination, 2nd ed. St Louis, CV Mosby, 1976. Reproduced by permission.)
Figure 64-43 Appearance of the semicircles in applanation tonometry. Rotate the pressure knob to align the innermost concave margins of the two semicircles. IOP = intraocular pressure. (1) Pressure on the tonometer head is too high—rotate the knob to decrease reading. (2) Pressure on the tonometer head is too low—rotate the knob to increase reading. (3) Pressure on the tonometer head is equal to IOP—the dial reading equals IOP. (From Knoop K, Trott A: Ophthalmologic procedures in the emergency department—Part III: Slit lamp use and foreign bodies. Acad Emerg Med 2:224, 1995. Reproduced by permission.)
other through excursions of equal distance (see Fig. 64-42C ). One finalizes adjustments to the end point of properly located and sized semicircles by rotating the pressure knob back and forth. When applanation pressure exceeds IOP, the semicircles are too small to intersect ( Fig. 64-43 ). At the end point is a flattened disc area 3.06 mm in diameter within the 7-mm diameter of the prism face. Here the attractive surface tension of the tears toward the prism is counterbalanced by the elasticity, or springiness, of the cornea; at this point the grams of force applied through the prism (indicated on the pressure knob) are directly convertible (when multiplied by 10 into mmHg) to express IOP. With an
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applanation tonometer, the average IOP in a seated adult is 14 to 17 mm Hg. After use, the tonometer should be wiped dry and removed for storage if used infrequently in the ED. One should verify the pressure adjustment periodically using the test weight or metal balance bar supplied with the instrument. Potential sources of error with the applanation tonometer are similar to those mentioned for the impression tonometer, with the exception that ocular rigidity is not a factor. Inaccuracies primarily result from ocular motion or tensing of the lids. Complications When tonometric instruments are used properly and reasonable precautions are taken, complications are unusual. The eye with preexisting corneal injury should be spared the additional trauma of tonometer placement. Corneal abrasions can be produced by ocular movement during testing. In particular, patients with uncontrollable nystagmus, singultus, or coughing or those who are extremely apprehensive should not be subjected to tonometry. Infection can be transmitted by the use of the instrument. Careful cleansing of the device and avoidance of tonometry in patients with obvious conjunctivitis, corneal ulcers, or active herpetic lesions should minimize the risk of spreading the infection to the unaffected eye or to subsequent patients. Although protective coverings can be placed over the tonometer contact, tonometry can usually be postponed in the aforementioned individuals until the risk of infection is minimal. Extrusion of ocular contents with penetrating injuries is a potential but rare complication. Summary Tonometry is an easily learned technique that should be used by the emergency clinician for the detection of elevated IOP. An elevated IOP in conjunction with physical findings suggestive of acute angle-closure glaucoma is an indication for therapy and consultation with an ophthalmologist. The baseline measurement of IOP will aid the ophthalmologist in subsequent evaluation of a referred patient. In addition, the emergency clinician can serve as a referral source for patients with elevated IOP who are suspected of having open-angle glaucoma. In particular, future drug therapy for systemic hypertension may be altered by the presence of concomitant intraocular hypertension. The emergency clinician who aggressively manages patients with hypertensive crises must also be aware of potential visual field defects when systemic blood pressure is vigorously lowered without concurrent lowering of IOP.
SLIT LAMP EXAMINATION The slit lamp is an extremely useful instrument; it makes the examination of the anterior segment of the eye a pleasure. The instrument can reveal pathologic conditions that would otherwise be invisible. The slit lamp permits detailed evaluation of external eye injury and is the definitive tool for diagnosing anterior chamber hemorrhage and inflammation. Since the 1800s, clinicians have searched for a better way both to magnify and to illuminate the anterior segment of the eye. In 1891, Aubert developed the first true binocular stereoscopic microscope. Then, in 1911, Gullstrand introduced a slit illuminator device. The microscope and the illuminator were combined by Henker in 1916; the result was the first true slit lamp. Goldmann improved the mechanical supports for the microscope and the illuminator and in 1937 marketed a slit lamp that closely resembles the device used today. [109] Indications and Contraindications The slit lamp can be used in the majority of eye examinations. It is especially useful in the ED for the diagnosis of corneal abrasions, FBs, and iritis. [39] The slit lamp facilitates FB removal and is also used in conjunction with most applanation tonometers. Although portable slit lamp instruments exist, emergency clinicians generally have access only to a stationary, upright device. Therefore, in the absence of a portable device, a slit lamp examination is contraindicated in patients who cannot tolerate an upright sitting position (e.g., those with orthostatic syncope). Equipment The slit lamp has three essential components: a binocular microscope mounted horizontally, a light source that can create a beam of variable width, and a mechanical assembly to immobilize the patient's head and to manipulate the microscope and the light source. The location and arrangement of the knobs that control these components vary in devices made by different manufacturers. Usually, by simply turning each knob and watching the results, one can quickly master a new machine. Figure 64-44 illustrates the location of the functional controls on one particular instrument. The first knob that one should locate is the on/off switch for the entire machine. Often this switch incorporates or is adjacent to a rheostat that provides two or three different power settings. The lowest setting is adequate for routine examination and will preserve bulb life. One can use a high-intensity setting when examining the anterior chamber with a narrow slit beam. Often, these controls are located on a transformer placed beneath the table to which the slit lamp has been attached. The second knob that one should find is the locking nut for the mechanical assembly. This must be loosened for the assembly to be moved. The patient should be comfortable while sitting with the head in the device. The patient's forehead should be firmly against the headrest, and the chin should be in the chinrest. By varying the table height and height of the chinrest, one should be able to maximize the comfort of the patient's neck and back. The chinrest should be adjusted to align the patient's eye level with the mark on the headrest support rods. The binocular microscope has a control for varying the magnification. Usually low powers, such as 10× or 16×, are the most useful. A higher power is helpful when the anterior chamber is examined for cells and flare and when the cornea is examined in minute detail. The binocular interpupillary distance should be adjusted to match that of the examiner. One can focus the eyepieces by moving the instrument forward and backward until the narrowed vertical beam is sharpest on the patient's cornea when viewed with the unaided eye. Then, while viewing through each eyepiece individually, the clinician adjusts the focus of each to produce a sharp image of the anterior cornea.
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Figure 64-44 Slit lamp controls. (From Operating Instructions for Slit Lamp Microscopes. Marco Equipment, Inc., Jacksonville, FL.)
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The light source is mounted on a swinging arm. There are knobs to vary the width and the height of the light beam. There are also filters that can be "clicked" in; only white and blue filters are usually needed. The angle of the slit beam can be varied from vertical to horizontal. The vertical alignment is preferred for routine examinations in the ED. Both the microscope and the light source are mounted on swivel arms, linked at their base to a movable table. One can change the position of this table by pushing on any part of it. For finer movements, the clinician uses a joystick. One can vary the height of the microscope and the light source by twisting either the joystick or a separate knob at the base, depending on the design of the instrument. Procedure There are 3 setups that every slit lamp operator must know. [107] [110] The first is for an overall screening of the anterior segment of the eye. For examination of the patient's right eye, the light source is swung to the examiner's left at a 45° angle while the microscope is directly in front of the eye. The slit beam is set at the maximum height and the minimum width using the white light. To scan across the patient's cornea, one first focuses the beam on the cornea by moving the entire base of the slit lamp forward and backward. One then moves the whole base left and right to scan across. The 45° angle between the microscope and the light source should be the default position. The most common mistake is to try to scan by swinging the arm of the light source in an arc; this does not work because the light beam will remain centered on the same point of the patient's eye. The examiner scans across at the level of the conjunctiva and the cornea and then pushes slightly forward on the base or joystick and scans at the level of the iris. The depth of the anterior chamber is easily appreciated with this low magnification setup ( Fig. 64-45 ). When the depth of the anterior chamber is reduced, one should suspect a corneal perforation or a predisposition to angle-closure glaucoma.
Figure 64-45 Slit lamp photograph of a normal right eye under low power. The curved slit of light on the left is reflected off the cornea while the slit on the right is reflected off the iris. The depth of the anterior chamber can easily be appreciated under this low magnification setup. (Courtesy of D. Price.)
This basic setup can also be used to examine the conjunctiva for traumatic lesions, inflammation, and FBs. The lids can be examined for hordeolum, blepharitis, or trichiasis. Complete lid eversion (as described earlier in the section on FB removal) can be performed in conjunction with the slit lamp examination to permit evaluation of the undersurface of the upper lid for FB retention. Corneal FB removal can be enhanced by use of the slit lamp. In particular, the instrument allows stabilization of the patient's head. Magnification also minimizes corneal injury during FB or rust ring removal. The upper eyelid may be immobilized by a cotton-tipped applicator, as discussed previously. The clinician's hand can be steadied against the patient's nose, cheek, or forehead or against the support rods of the headrest. The patient should be instructed to stare straight ahead at a fixed light or at the clinician's ear during removal of the FB. The second setup is essentially the same as the first but uses the blue filter. The purpose is to identify any areas of fluorescein staining. After fluorescein is applied, the blue filter is "clicked" into position, and the beam is widened to 3 or 4 mm. A patient can tolerate a wider beam without photophobia if it is blue. Corneal defects (as discussed earlier in the section on the fluorescein examination) are sought with this setup. The blue filter is also used with applanation tonometry, as discussed earlier in the section on tonometry. The purpose of the third setup is to search for cells in the anterior chamber—either the white cells of iritis or the red cells of a microscopic hyphema. The height of the beam should be shortened to 3 or 4 mm and should be as narrow as possible. The microscope should be switched to high power. The beam is first focused on the center of the cornea and is then pushed forward slightly so that it is focused on the anterior surface of the lens. When the joystick is again pulled back to a focus point midway between the cornea and the lens, it will be focused on the anterior chamber ( Fig. 64-46 ). One should keep the beam centered over the pupil so that there is a black background. Normally, the aqueous humor of the anterior chamber is totally clear. If small particles are visible floating up or down through the beam, these are usually circulating cells. If the beam lights up the aqueous like a searchlight in the fog, then the examiner has found the protein flare that accompanies iritis. Note should be made of the fact that
Figure 64-46 Appearance of the left eye during anterior chamber examination under low power: a, corneal epithelium; b, corneal stroma; c, corneal endothelium; d, anterior chamber (potential location of cells or flare); e, iris; f, lens reflection. The slit of light shines in the temporal to nasal direction at 45° to the anterior surface of the cornea. The depth of the cornea and anterior chamber examination are best done under high power in a dark room.
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fluorescein can penetrate an abraded cornea, producing a fluorescein flare on slit-lamp evaluation. To avoid confusion, some clinicians prefer to examine for anterior chamber flare before the stain is used. Summary In practice, the 3 setups described here take only 1 minute per eye. Experience with the instrument enhances the ability of the user. The device is helpful for the evaluation of ocular infections and corneal lesions, the removal of corneal FBs, the measurement of IOP by applanation tonometry, and the diagnosis of iritis.
UNILATERAL LOSS OF VISION There are a variety of reasons that an individual may sustain a complete loss of vision in one eye, but most commonly such loss may be related to occlusion of the central retinal vein or the central retinal artery or to optic nerve damage. Less commonly, pressure in the orbit from a retro-orbital hemorrhage may compromise the ophthalmic artery. Although discussion of all the potential causes of unilateral loss of vision is beyond the scope of this text, amaurosis fugax deserves special mention. Amaurosis fugax is a transient loss of vision that is most commonly due to cholesterol or platelet emboli from atherosclerotic carotid occlusive disease. When plaques are visualized in the retinal vasculature, it is prudent to auscultate for carotid bruits and to refer the patient for ultrasound examination of the carotid artery. [111] [112] Central Retinal Artery Occlusion The patient with central retinal artery occlusion generally presents with a recent sudden (complete or nearly complete) unilateral vision loss. On examination there is an afferent pupillary defect (i.e., sluggish or nonreactive pupil in the affected eye with direct illumination with a normal consensual response) and reduced visual acuity. Immediately after the event, the fundus may appear nearly normal; however, it soon becomes pale and a classic "cherry-red spot" in the macula may be evident as a result of patent choroidal vessels showing through the transparent fovea. Therapy
Visual recovery has been noted to occur up to 3 days after central retinal arterial obstruction. It has been recommended that treatment be started if the patient is seen within 24 hours after onset of symptoms. [113] Ophthalmologic consultation should be made while initiating therapy. Most of the emergency techniques suggested to treat vascular insults to the eye in the ED are theoretically sound but are not supported or refuted by rigorous scientific data. No specific standard of care has been promulgated for these interventions by emergency clinicians. Techniques discussed below are likely safe and possibly useful, and may be attempted in an emergency situation. It is unknown whether or not these interventions will be vision saving. Although of unknown value, slow rebreathing into a paper bag is believed to increase the arterial CO 2 level, thus aiding vasodilation and permitting the occlusion to move more peripherally, possibly reducing the ischemic area. The clinician should concurrently initiate digital globe
Figure 64-47 Digital globe massage is performed by applying firm steady pressure on the globe with the examiner's thumb for approximately 5 seconds, followed by abruptly releasing the pressure for 5 to 10 seconds. The process is repeated for up to 20 minutes or until improvement of vision is observed.
massage. With the patient lying supine, firm steady pressure is applied to the affected globe through the patient's closed lids using the clinician's thumb. The pressure is applied for 5 seconds and then abruptly released ( Fig. 64-47 ). The procedure is immediately repeated several more times for up to 20 minutes. The technique is intended to help break up the occlusion and to encourage its movement more peripherally. A more aggressive therapy, generally performed only by ophthalmologists, is anterior chamber paracentesis. In the absence of available consultation, this technique may be considered when central retinal occlusion is recent and unresponsive to the previously described therapeutic approaches. For this procedure, the patient is kept supine with the head and eyelids secured. The cornea is anesthetized with topical anesthetic drops (e.g., 0.5% proparacaine drops) and the conjunctiva is anesthetized. The conjunctiva is injected adjacent to the limbus using a 27- or 30-ga needle until the entire perilimbal area is infiltrated, giving the appearance of chemosis in all quadrants. During the remainder of the procedure, an assistant must firmly grasp the conjunctiva with toothless forceps at the 3 and 9 o'clock positions to stabilize the eye. A 30-ga needle on a tuberculin syringe is then inserted obliquely just adjacent to the limbus, at either the 4:30 or 7:30 o'clock position and directed toward the 6 o'clock position to avoid the lens ( Fig. 64-48 ). After 1 to 2 drops of aqueous are expressed with gentle pressure on the globe, the needle is withdrawn.[114] [115] One study describes a systematic approach in which ocular massage, sublingual isosorbide dinitrate 10 mg, acetazolamide 500 mg intravenously (IV), mannitol 20% (1 mg/kg) or oral glycerol 50% (1 mg/kg), anterior chamber paracentesis, methylprednisolone 500 mg IV, streptokinase 750 kIU, and retrobulbar tolazoline 50 mg were given until visual symptoms improved or until all steps were complete. [116] Of the 11 patients in this arm of the study, 8 had improved visual acuity. In those who improved, all had symptoms =12 hours. The presumed cause was either platelet-derived or cholesterol embolus from atheroma, or glaucoma. [115] Although this study is small, it supports emergent ophthalmology consultation and aggressive treatment of patients who present within 12 to 24 hours of symptom onset.
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Figure 64-48 Anterior chamber paracentesis. After topical and subconjunctival anesthesia (see text), a 30-ga needle is directed obliquely from the 4:30 or 7:30 o'clock position toward the 6 o'clock position to avoid the lens. An assistant stabilizes the globe with forceps, grasping the conjunctiva (see text). Top, Anteroposterior projection. Bottom, Tangential projection. (From Knoop K, Trott A: Ophthalmologic procedures in the emergency department: I. Immediate sight-saving procedures. Acad Emerg Med 1:408, 1994.) Complications
Overzealous globe massage has the potential to produce intraocular trauma including retinal detachment and intraocular hemorrhage. Anterior chamber paracentesis may produce hemorrhage, infection, or mechanical injury to the cornea, iris, or lens. [117] Although these complications are rare, ophthalmologic consultation for assistance with the underlying central retinal artery occlusion and surveillance for these potential complications should be initiated on an emergent basis. Orbital Compartment Syndrome Acute facial trauma or recent retrobulbar anesthesia may produce retrobulbar hemorrhage with sufficient pressure to compromise the ophthalmic artery, resulting in an orbital compartment syndrome. A form of post-traumatic glaucoma may also occur when the retrobulbar hematoma forces the globe against the eyelids. In this case IOP rises precipitously because the globe is in a relatively closed space due to the firm attachment of the eyelids to the orbital rim by the medial and lateral canthal ligaments. The optic nerve and its vascular supply, and the central retinal artery are compressed, resulting in ischemia and subsequent visual loss. In this situation an emergency canthotomy may be considered for relief of the pressure on the eye. It would not be considered a standard of care for most emergency
clinicians to possess the skills for this procedure, but under the proper scenario, it may be a prudent intervention. Ophthalmoscopic evaluation reveals a blanched ophthalmic artery in the presence of obvious retrobulbar pressure and ecchymosis around the eye. The patient exhibits decreased visual acuity, and an afferent pupil defect is often seen. The IOP is markedly elevated but may be relieved by an emergency lateral canthotomy and cantholysis. Such a procedure needs to be performed quickly because the ischemic retina will not retain function if it is deprived of blood for a long period of time. Technique: Lateral Canthotomy and Cantholysis
The goals of the procedure are to release pressure on the globe and to decrease IOP enough to reinstitute retinal artery blood flow. Because retinal recovery is unlikely to occur if rapid relief of ischemia is not accomplished, taking time to clean the eye beyond simple saline cleansing of the lids and lateral canthus is ill-advised. While the patient's head and lids are stabilized, the lateral canthus is first anesthetized with injectable 1% to 2% lidocaine with epinephrine. A small hemostat is used to crush the lateral canthus for 1 to 2 minutes to minimize bleeding before incising the lateral canthus. The canthus is incised using iris or Steven's scissors, with precautions taken to avoid injury to the protruding globe ( Fig. 64-49 ). The incision begins at the lateral canthus and extends toward the orbital rim. The superior and inferior crus of the lateral canthal tendon are found and released from the orbital rim. Some operators prefer to release the inferior crus and reassess the IOP before considering release of the superior crus. An instructional video of the procedure can be found on the World Wide Web at www.brown.edu/Administration/Emergency_Medicine/eye.htm. [118] Complications
Although hemorrhage, infection, and mechanical injury may result from the procedure, these complications generally respond to therapy better than retinal injury from prolonged ischemia. Emergent ophthalmologic consultation should be obtained, although when the procedure is indicated, it may be considered by the emergency clinician. Lateral canthotomy incisions generally heal without suturing or significant scarring.
REDUCTION OF GLOBE LUXATION Although luxation of the globe is uncommon, the emergency clinician should be aware of the condition and its mechanisms, know how to reduce the globe, and know when to prioritize ophthalmologic consultation. With luxation of the globe there is extreme proptosis, which permits the lids to slip behind the globe equator ( Fig. 64-50 ). Subsequent spasm of the orbicularis oculi muscles sustains the luxation and limits extraocular movements. Traction on the optic nerve and retinal vessels may produce direct or indirect injury to the optic nerve and retina. Luxation may be spontaneous, voluntary, or traumatic. A variety of conditions (e.g., orbital neoplasms, Graves disease, histiocytosis X, cerebral gumma, and craniofacial dysostoses) may predispose the patient to luxation. Triggering events include maneuvers increasing intraorbital pressure (e.g., the Valsalva maneuver), trauma to the orbit or forehead, or eyelid manipulation. Indications and Contraindications Early globe reduction is indicated to relieve symptoms and to minimize visual impairment. Attempts at reduction in the ED
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Figure 64-49 A, Severe proptosis secondary to acute traumatic retrobulbar hemorrhage. B, Anatomy of orbital structures demonstrating the inferior and superior crura of the lateral canthal tendon beneath the lateral canthus. The crura join and as a common tendon are attached to the inner aspect of the lateral orbital wall, forming Whitnall's tubercle. The lateral canthus, formed by the upper and lower eyelid, has been removed. C, D, A clamp crushes the lateral canthus to reduce bleeding when it is incised. The canthotomy allows the inferior crus to be exposed and cut to decompress the eyeball. E, A 1 centimeter horizontal incision is made in the lateral canthus, through the tissue that was compressed. F, The lower lid is pulled down and away from the lateral orbital rim, separating the skin and conjunctiva. If bleeding hinders identification of the inferior crus, it may be palpated. G, Only the inferior crus need be lysed initially. If intraocular pressure is not reduced, the superior crus is lysed. (From S. Vassallo et al: Traumatic retrotubular hemorrhage: Emergent decompression by lateral canthotomy and cantholysis. J Emerg Med 22:21, 2002.)
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Figure 64-50 Appearance of bilateral luxated globe; superior ( top) and lateral (bottom) projections. (From Love JN, Bertram-Love JE: Luxation of the globe. Am J Emerg Med 11:61, 1993; original photographs courtesy of WR Green, MD, Wilmer Eye Institute, Baltimore.)
are relatively contraindicated when there is obvious rupture of the globe. Technique Before globe reduction, it is valuable to perform a rapid eye examination to document visual acuity, range of eye motion, pupillary reactivity, and any evidence of globe rupture (see earlier discussion). [119] The patient is made comfortable in a recumbent position, and a topical ocular anesthetic agent (e.g., 0.5% proparacaine) is administered. When the lashes are visible, an assistant should apply steady outward and upward traction while the globe is gently pushed behind the lids. The globe is manipulated back into the orbit using gloved fingers to apply steady scleral pressure. When the lashes cannot be grasped, a lid retractor may be introduced behind the lid to provide countertraction. Others recommend placement of a suture through the anesthetized skin of each lid to provide countertraction. After the procedure, a repeat eye examination documenting visual acuity and extraocular movement is warranted. It is not uncommon for return of full visual function to be delayed for several days, occasionally longer. Complications It is common with this procedure for lashes to be retained in the conjunctival fornices. It is important to evaluate for and remove any free lashes to prevent corneal injury. Edema, retrobulbar hemorrhage, or orbital deformity may prevent outpatient reduction. When reduction is not possible in the ED, saline drops should be applied to the globe and a noncontact eye shield applied. Aftercare Patients with spontaneous luxation and no visual impairment in whom the globe is easily reduced warrant follow-up within 24 to 48 hours. Instructions to avoid potential triggering maneuvers should be given. Recurrent luxation may warrant lateral tarsorrhaphy. Further evaluation of potential precipitating illness can be pursued on an outpatient basis. Patients with traumatic luxation are at greater risk for underlying ophthalmic injury and warrant emergent consultation. A computed tomographic scan of the orbit is helpful for
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evaluating both the soft tissue and bony structures about the globe.
Acknowledgment
The authors recognize the many contributions by John R. Samples, MD, and David Barr, MD, to this chapter through the previous three editions of the textbook.
References 1. Knoop
K, Trott A: Ophthalmologic procedures in the emergency department: II. Routine evaluation procedures. Acad Emerg Med 2:144, 1995.
2. Keeney
AH. Ocular Examination: Basis and Technique. St. Louis, CV Mosby, 1970, pp 26, 120.
3. Duke-Elder 4. Adler
S: System of Ophthalmology, vol III. St Louis, CV Mosby, 1962a, pp 542 and 571.
AG, McElwain GE, Merli GJ, et al: Systemic effects of eye drops. Arch Intern Med 142:2293, 1982.
5. Barker
DB, Solomon DA: The potential for mental status changes associated with systemic absorption of anticholinergic ophthalmic medications: Concerns in the elderly. Ann Pharmacother 24:847,
1990. 6. Solosko
D, Smith RB: Hypertension following 10% phenylephrine ophthalmic. Anesthesiology 36:187, 1972.
7. McReynolds 8. Kim
WV, Havener WH, Henderson JW: Hazards of the use of sympathomimetic drugs in ophthalmology. Arch Ophthalmol 56:176, 1956.
MK, Stevenson CE, Mathewson MD: Hypertensive reactions to phenylephrine eye drops in patients with sympathetic denervation. Am J Ophthalmol 85:862, 1978.
9. Adler
AG, McElwain GE, Martin JH, et al: Coronary artery spasm induced by phenylephrine eye drops. Arch Intern Med 141:1384, 1981.
10.
Fraunfelder FT: Interim report: National registry of possible drug induced ocular side effects. Ophthalmology 86:126, 1979.
11.
Hoefnagel D: Toxic effects of atropine and homatropine eye drops in children. N Engl J Med 264:168, 1961.
12.
Heath WE: Death from atropine poisoning. BMJ 2:608, 1950.
13.
Freund M, Meun S: Toxic effects of scopolamine eye drops. Am J Ophthalmol 70:637, 1970.
14.
Beswick JA: Psychosis from cyclopentolate. Am J Ophthalmol 53:879, 1962.
15.
Binkharst RD, Weinstein GW, Borety RM, et al: Psychotic reaction induced by cyclopentolate: Results of pilot study and double-blind study. Am J Ophthalmol 55:1243, 1963.
16.
Carpenter WT Jr: Precipitous mental deterioration following cycloplegia with 0.2% cyclopentolate HC1. Arch Ophthalmol 78:445, 1967.
17.
Lanscke RK: Systemic reactions to topical epinephrine and phenylephrine. Am J Ophthalmol 61:95, 1966.
18.
Fraunfelder FT, Scafidi AF: Possible adverse effects from topical ocular 10% phenylephrine. Am J Ophthalmol 85:447, 1978.
19.
Bresler MJ, Hoffman TLS: Prevention of iatrogenic acute narrow-angle glaucoma. Ann Emerg Med 10:535, 1981.
20.
Hovding G, Sjursen H: Bacterial contamination of drops and dropper tips of in-use multidose bottles. Acta Ophthalmol 60:213, 1982.
21.
Havener WA: Ocular Pharmacology. St Louis, CV Mosby, 1978, pp 70, 413, 419.
22.
Duke-Elder S: System of Ophthalmology, vol VII. St Louis, CV Mosby, 1962b, pp 243, 349.
23.
Vaughn DG: The contamination of fluorescein solutions. Am J Ophthalmol 39:55, 1955.
24.
Deutsch TA, Feller DB: Paton and Goldberg's Management of Ocular Injuries, 2nd ed. Philadelphia, WB Saunders, 1985, pp 61, 93, 124.
25.
Brown L, Takeuchi D, Challoner K: Corneal abrasions associated with pepper spray exposure. Am J Emerg Med 18:271, 2000.
26.
Grant MW: Toxicology of the Eye. Springfield, IL, Charles C Thomas, 1974, p 495.
27.
National Registry of Drug-Induced Ocular Side Effects, Case Reports 404a, 404b, 421. Portland, OR, University of Oregon Health Sciences Center, 1979.
28.
Cohn HC, Jocson VL: A unique case of grand mal seizures after Fluress. Ann Ophthalmol 13:1379, 1981.
29.
Cain W Jr, Sinskey RM: Detection of anterior chamber leakage with Seidel's test. Arch Ophthalmol 99:2013, 1981.
30.
Sexton RR: Herpes simplex keratitis. In Wilson LA (ed): External Diseases of the Eye. Hagerstown, MD, Harper & Row, 1979, p 235.
31.
Sexton RR: Superficial keratitis. In Wilson LA (ed): External Diseases of the Eye. Hagerstown, MD, Harper & Row, 1979, p 203.
32.
Wilson LA: Bacterial corneal ulcers. In Wilson LA (ed): External Diseases of the Eye. Hagerstown, MD, Harper & Row, 1979, p 215.
33.
Jones DB: Fungal keratitis. In Wilson LA (ed): External Diseases of the Eye. Hagerstown, MD, Harper & Row, 1979, p 265.
34.
Weiss JN, Kreter JK, Dalton HP, et al: Detection of Pseudomonas aeruginosa eye infections by ultraviolet light. Ann Ophthalmol 14:242, 1982.
35.
Vesserill FR, O'Connor RE: Corneal abrasion during eyelid retraction [letter]. Ann Emerg Med 26:756, 1995.
36.
American Academy of Orthopedic Surgeons: Emergency Care and Transportation of the Sick and Injured, 3rd ed. Menasha, WI, George Banta, 1981, p 298.
37.
Grant HD, Murray RH, Bergeron JF: Emergency Care, 3rd ed. Bowie, MD, RJ Brady, 1982, p 166.
38A. Herr
RD, White GL, Bernhisel K, et al. Clinical comparison of ocular irrigation fluids following chemical injury. Am J Emerg Med 9:228, 1991.
38B. Jones
JB, Schoenleber DB, Gillen JP. The tolerability of lactated Ringer's solution and BS plus for ocular irrigation with and without the Morgan therapeutic lens. Acad Emerg Med 5:1150, 1998.
39.
Ernst AA, Thomson T, Haynes M, et al: Warmed versus room temperature saline solution for ocular irrigation. Ann Emerg Med 32:676, 1998.
40.
Harris LS, Cohn K, Galin MA: Alkali injury from fireworks. Ann Ophthalmol 3:849, 1971.
41.
Smith RS, Shear G: Corneal alkali burns arising from accidental instillation of a hair straightener. Am J Ophthalmol 79:602, 1975.
42.
Scharpf LG Jr, Hill ID, Kelly RE: Relative eye-injury potential of heavyduty phosphate and non-phosphate laundry detergents. Food Chem Toxicol 10:829, 1972.
43.
Smally AJ, Binzer A, Dolin S, Viano D: Alkaline chemical keratitis: Eye injury from airbags. Ann Emerg Med 21:1400, 1992.
44.
Lippas J: Continuous irrigation in the treatment of external ocular diseases. Am J Ophthalmol 57:298, 1964.
45.
Vaughn D, Asbury J: General Ophthalmology, 8th ed. Los Altos, CA, Lange, 1977, p 40.
46.
Bentur Y, Tannenbaum S, Yaffe Y, Halpert M: The role of calcium gluconate in the treatment of hydrofluoric acid eye burn. Ann Emerg Med 22:1488, 1993.
47.
Rost KM, Jaeger RW, deCastro FJ: Eye contamination: A poison center protocol for management. Clin Toxicol 14:295, 1979.
48.
Levinson RA: Ascorbic acid prevents corneal ulceration and perforation following experimental alkali burns. Invest Ophthalmol 15:986, 1976.
49.
Grove AS, New PFJ, Momose KJ: Computerized tomographic (CT) scanning for orbital evaluation. Trans Am Acad Ophthalmol Otolaryngol 79:137, 1975.
50.
Lobes LA Jr, Grand MG, Reece J, et al: Computerized axial tomography in the detection of intraocular foreign bodies. Ophthalmology 88:26, 1981.
51.
Newman DK: Eyelid foreign body mimics an intraocular foreign body on plain orbital radiography. Am J Emerg Med 17:283, 1999.
52.
Newell FW: Ophthalmology Principles and Concepts. St Louis, CV Mosby, 1978, p 186.
53.
Hulbert MF: Efficacy of eye pad in corneal healing after corneal foreign body removal. Lancet 337:643, 1991.
54.
Benson WH, Snyder IS, Granus V, et al: Tetanus prophylaxis following ocular injuries. J Emerg Med 11:677, 1993.
55.
Bartfield JM, Holmes TJ, Raccio-Robak N: A comparison of proparacaine and tetracaine eye anesthetics. Acad Emerg Med 1:364, 1994.
56.
Zagelbaum BM, Tostanoski JR, Hochman MA, Hersh PS: Topical lidocaine and proparacaine abuse. Am J Emerg Med 12:96, 1994.
57.
Brahma AK, Shah S, Hillier VF et al: J Accid Emerg Med 13:186, 1996.
58.
Szucs PA, Nashed AH, Allegra FR, Eskin B: Safety and efficacy of diclofenac ophthalmic solution in the treatment of corneal abrasions. Ann Emerg Med 35:131, 2000.
59.
Salz JJ, Reader AL III, Schwartz LJ, Van Le K: Treatment of corneal abrasions with soft contact lenses and topical diclofenac. J Refract Corneal Surg 10:640, 1994.
Kaiser PK, Pineda R, and the Corneal Abrasion Patching Study Group: A study of topical nonsteroidal anti-inflammatory drops and no pressure patching in the treatment of corneal abrasions. Ophthalmology 104:1353, 1997. 60.
1279
61.
Le Sage N, Verreault R, Rochette L: Efficacy of eye patching for traumatic corneal abrasions: A controlled clinical trial. Ann Emerg Med 38:129, 2001.
62.
Campanile TM, St Clair DA, Benaim M: The evaluation of eye patching in the treatment of traumatic corneal epithelial defects. J Emerg Med 15:769, 1997.
63.
Flynn CA, D'Amico F, Smith G: Should we patch corneal abrasions? A meta-analysis. J Fam Pract 47:264, 1998.
64.
Miles KA, Hayball M, Dixon AK: Colour perfusion imaging: A new application of computed tomography. Lancet 337:643, 1991.
65.
Kirkpatrick JNP, Hoh HB, Cook SD: No eye pad for corneal abrasion. Eye 7:468, 1993.
66.
Rao GP, Scott JA, King A, et al: No eye pad for corneal abrasion [letter]. Eye 8:371, 1994.
67.
Schein OD: Contact lens abrasions and the nonophthalmologist. Am J Emerg Med 11:606, 1993.
68.
King JWR, Brison RJ: Emergency department management of traumatic corneal epithelial injuries without topical antibiotic prophylaxis [abstract]. J Emerg Med 8:373, 1990.
69.
Hanna C, Fraunfelder FT, Cable M, et al: The effect of ophthalmic ointment on corneal wound healing. Am J Ophthalmol 76:193, 1973.
70.
Fraunfelder FT, Hanna C, Cable M, et al: Entrapment of ophthalmic ointment in the cornea. Am J Ophthalmol 76:475, 1973.
71.
Laibson PR: Epithelial basement membrane dystrophy and recurrent corneal erosion. In Fraunfelder FT, Roy FH (eds): Current Ocular Therapy. Philadelphia, WB Saunders, 1980, p 362.
72.
Wedge CI, Rootman DS: Collagen shields: Efficacy, safety and comfort in the treatment of human traumatic corneal abrasion and effect on vision in healthy eyes. Can J Ophthalmol 27:295, 1992.
73.
Forstot SL, Ellis PP: Identifying and managing contact lens emergencies. ER Rep 3:35, 1982.
74.
Mandell RB: Contact Lens Practice. Springfield, IL, Charles C Thomas, 1981, pp 11, 142, 496, 574.
75.
Obrig T, Salvatori P: Contact Lenses, 3rd ed. New York, Obrig Laboratories, 1957, p 188.
76.
Mullen JE: Contact Lens. U.S. patent No. 2,237,744.
77.
Nugent MW: The corneal lens, a preliminary report. Ann West Med Surg 2:241, 1948.
78.
Dreifus M, Wichtenle O, Lim D: Intercameral lenses of hydrocolloid acrylates. Cesk Oftalmol 16:154, 1960.
79.
Krezanoski JZ: Physiology and biochemistry of contact lens wearing. In Encyclopedia of Contact Lens Practice, vol 4. South Bend, IN, International Optic, 1959, p 18.
80.
Cogger TJ: Correction with hard contact lenses. In Duane TD (ed): Clinical Ophthalmology. New York, Harper & Row, 1982, p 17.
81.
Fowler SA, Allansmith MR: Evolution of soft contact lens coatings. Arch Ophthalmol 98:95, 1980.
82.
Mondino BJ, Gorden LR: Conjunctival hyperemia and corneal infiltrates with chemically disinfected soft contact lenses. Arch Ophthalmol 98:1767, 1980.
83.
Shaw EL: Allergies induced by contact lens solutions. Contact Intraocular Lens Med J 6:273, 1980.
84.
Krachmer JH, Purcell JJ Jr: Bacterial corneal ulcers in cosmetic soft contact lens wearers. Arch Ophthalmol 96:57, 1978.
85.
Bohigian GM: Management of infections associated with soft contact lenses. Ophthalmology 86:1138, 1979.
86.
Binder PS: Complications associated with extended wear of soft contact lenses. Ophthalmology 86:1093, 1979.
87.
Long JC: Retention of contact lens in upper fornix. Am J Ophthalmol 56:309, 1963.
88.
Michaels DD, Zugsmith GS: An unusual contact lens complication. Am J Ophthalmol 55:1057, 1963.
89.
Snyder ME, Katz HR: Ciprofloxacin-resistant bacterial keratitis. Am J Ophthalmol 114:336, 1992.
90.
Maklakoff C: L'ophthalmotonometrie. Arch Ophthalmol (Paris) 5:159, 1885.
91.
Goldmann H: Un nouveau tonometre a .. applanation. Bull Soc Fr Ophthalmol 67:474, 1955.
92.
Schiotz H: Tonometry. Br J Ophthalmol 4:201, 1920.
93.
Mackay RS, Marg E: Fast automatic electronic tonometers based on an exact theory. Acta Ophthalmol 37:495, 1959.
94.
Grolman B: A new tonometer system. Am J Ophthalmol 49:646, 1972.
95.
Boothe WA, Lee DA, Panek WC, et al: The Tono-Pen: A manometric and clinical study. Arch Ophthalmol 106:1214, 1988.
96.
Friedenwald JS: Tonometer calibration: An attempt to remove discrepancies found in the 1954 calibration used for the Schiotz tonometers. Trans Am Acad Ophthalmol Otolaryngol 61:108, 1957.
97.
Goldmann H, Schmidt TH: Über Applanation stonometrie. Ophthalmologica 134:221, 1957.
98.
Longham ME, McCarthy E: A rapid pneumatic applanation tonometer. Arch Ophthalmol 79:389, 1968.
99.
Wilensky JT: Blood induced secondary glaucomas. Ann Ophthalmol 11:1659, 1979.
100. Arts
HA, Eisele DW, Duckert LG: Intraocular pressure as an index of ocular injury in orbital fractures. Arch Otolaryngol Head Neck Surg 115:213, 1989.
101. Bedford
MA. Color Atlas of Ophthalmological Diagnosis, 2nd ed. London, Year Book Medical Publishers, 1986, p 17.
102. Hillman
JS: Acute closed-angle glaucoma: An investigation into the effect of delay in treatment. Br J Ophthalmol 63:817, 1979.
103. Gorin
G: Clinical Glaucoma. New York, Marcel Dekker, 1977, p 76.
104. Wilke
K: Effects of repeated tonometry: Genuine and sham measurements. Acta Ophthalmol 50:574, 1972.
105. Harbin
TS, Laikam SE, Lipsitt K, et al: Applanation-Schiotz disparity after retinal detachment surgery utilizing cryopexy. Ophth AAO 86:1609, 1979.
106. Lichter
PR, Bergstrom TJ: Premature ventricular systole detection by applanation tonometry. Am J Ophthalmol 81:797, 1976.
107. Keeney
AH: Ocular Examination: Basis and Technique. St Louis, CV Mosby, 1976, pp 85, 141.
108. Chandler 109. Tate
PA, Grant WM: Glaucoma, 2nd ed. Philadelphia, Lea & Febiger, 1979, p 11.
GW, Safir A: The slit lamp: History, principles, and practice. In Duane TD (ed): Clinical Ophthalmology, vol I. New York, Harper & Row, 1981.
110. Cogger 111. Muller
TJ: Correction with hard contact lenses. In Duane TD (ed): Clinical Ophthalmology, vol I. New York, Harper & Row, 1981.
M, Wessel K, Mehdorn E, et al: Carotid artery disease in vascular ocular syndromes. J Clin Neuro ophthalmol 13:175, 1993.
112. O'Farrell 113. Sharma 114. Knoop
CM, Fitzgerald DE: Prognostic value of carotid ultrasound lesion morphology in retinal ischemia: Result of a long-term follow-up. Br J Ophthalmol 77:781, 1983.
S, Brown M, Brown GC: Retinal artery occlusions. Ophth Clinics North Am 11:591, 1998.
K, Trott A: Ophthalmologic procedures in the emergency department: I. Immediate sight-saving procedures. Acad Emerg Med 1:408, 1994.
115. Vaughn 116. Rumelt
D, Asbury T, Tabbara K (eds): General Ophthalmology, 12th ed. East Norwalk, CT, Appleton & Lange, 1989, p 166.
S: Aggressive systematic treatment for central retinal artery occlusion. Am J Ophthal 128:733, 1999.
117. Joondeph 118. Suner 119. Love
BC, Joondeph HC: Purulent anterior segment endophthalmitis following paracentesis. Ophthalmic Surg 17:91, 1986.
S, Simmons W, Savitt DL: A porcine model for instruction of lateral canthotomy. Acad Emerg Med 7:837, 2000.
JN, Bertram-Love JE: Luxation of the globe. Am J Emerg Med 11:61, 1993.
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Chapter 65 - Otolaryngologic Procedures Ralph J. Riviello
Examination of the oropharynx, larynx, ear canals, and nasal passages and the management of related acute disorders are most effectively performed using special equipment and techniques. This chapter addresses these techniques from the perspective of the emergency clinician, who often must assess injuries or illnesses of potential compromise to the airway and to auditory function. Decisions related to definitive treatment in the emergency department (ED) vs timely referral are addressed. Related topics, including airway management, esophageal and laryngeal foreign bodies (FBs), and assessment of caloric testing, are discussed elsewhere in the book.
PHARYNX/LARYNX Examination of the Larynx Several techniques to visualize the larynx are discussed. The clinician should become adept at examining the hypopharynx and larynx with more than one method ( Fig. 65-1 ). Laryngoscopy is indicated for the evaluation of unexplained hoarseness, dysphagia, odynophagia, or FB sensation. The majority of patients will require a repeat examination by an otolaryngologist for verification, but laryngoscopy in the ED may identify pathologic conditions requiring more urgent consultation. Clinicians should follow guidelines for "universal precautions" (as described in Chapter 71 ) to protect themselves and their patients from infection transmitted by blood and body fluids. Laryngoscopy has traditionally been discouraged in the patient with a high potential for epiglottitis, as oropharyngeal manipulation may in rare cases precipitate laryngospasm and acute respiratory arrest. However, some authors report that careful laryngoscopy may be performed in stridulous patients with the presumed diagnosis of croup to rule out epiglottitis when the suspicion for the latter condition is low. [1] When impending airway obstruction from epiglottitis is suspected, the first priority is to quickly assemble a predesignated team (usually consisting of an anesthesiologist and an otolaryngologist) in the operating room. Any attempt at laryngoscopy should follow full preparation for rigid bronchoscopy or a surgical airway. Patients with severe laryngeal trauma or partially obstructing hypopharyngeal FBs should be approached in a similar manner. Illumination
The reflected light from a head mirror or direct illumination from a head lamp can be used not only for indirect laryngoscopy, but also for inspection of, and procedures in, the oropharynx, nares, and auditory canal. For example, a peritonsillar abscess is afforded excellent illumination for drainage with such devices. The advantages of a head mirror are the high degree of brightness it provides into deep recesses and its simplicity of design. Generally, the beam of light from an electric head lamp is easier to focus than is the head mirror. Procedure Head mirror/Light source.
The head mirror is convex with a central hole that allows the examiner to see directly along the reflected light beam. Begin by swinging the mirror down over the dominant eye just touching the skin or glasses. Position the light source (a 150-watt bulb works well) over the patient's shoulder on the same side as the head mirror. Keeping your eyes open, adjust the focus of light by adjusting your distance from the patient. Change the direction of the beam by tilting the mirror or turning your head slightly. Head lamp.
The electric head lamp also attaches by a forehead strap, and the light should be placed nearly between the examiner's eyes to be maximally effective. The intensity of light in this position is nearly as bright as the head mirror. After securing the head lamp, hold your hands in front of you at a distance that is comfortable for working. Focus the beam of light at this point by adjusting the head lamp into position without moving your head or eyes. This allows for the beam to shine on and follow the area on which your eyes are focused. Indirect Laryngoscopy
This traditional method is most commonly used by the otolaryngologist, but it has some application in the emergency setting if the necessary equipment is readily available.
Figure 65-1 Anatomy of the oropharynx. Sagittal section of the neck. Also depicted is the use of the nasopharyngeal scope through the nasopharynx and the oropharynx.
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The clinician who is unfamiliar with this method should practice frequently, as it requires significant eye-to-hand coordination to reflect the light beam off the angulated mirror onto the larynx. When this procedure is properly performed, most patients are able to tolerate it without anesthesia of the oropharynx. Fiberoptic nasopharyngoscopy has largely replaced indirect laryngoscopy in the ED when the equipment is available. Begin by establishing rapport with the patient by explaining how the examination will be performed. Have the patient sit erect in the "sniffing position," with the feet flat on the floor and leaning slightly forward. Warm the mirror with warm water or in a flame to prevent fogging, but check the temperature of the mirror with your hand before placing it into the oropharynx so as not to burn the patient. Alternatively, anti-fogging solutions can be applied to the mirrored side. Wrap the patient's tongue with gauze to prevent it from slipping or being injured by the lower incisors and then grasp it with the nondominant hand ( Fig. 65-2 ). Apply gentle traction to the tongue with your thumb and index finger while lifting the patient's upper lip with your middle finger. Slide the mirror into the oropharynx with the glass surface parallel to the tongue but not touching it. Place the back of the mirror against the uvula and soft palate, smoothly lifting until the larynx is visualized. While this should not induce gagging, try to make only slight changes in mirror position to inspect the appropriate structures. In patients who cannot tolerate this procedure without gagging, apply topical anesthetic to aid in the examination. Benzocaine (Hurricaine spray or Cetacaine gargle) or aerosolized tetracaine or lidocaine may be used. One or two quick sprays of benzocaine into the posterior oropharynx are sufficient. Prolonged or repeated spraying may rarely result in methemoglobinemia. Reassure the patient beforehand that although this may make the throat feel as if it is swelling or paralyzed, in actuality it is just the numbness that accounts for
Figure 65-2 Indirect mirror evaluation of oropharynx. Grasp the patient's tongue between the thumb and first finger, using a gauze pad to provide traction. Elevate the upper lip with the middle finger. Advance the warmed laryngeal mirror into the posterior oropharynx, taking care not to stimulate the posterior tongue or pharynx. Remember that the structures in the mirror will
be reversed. Always use universal precautions.
the sensation. The tendency to gag also can be minimized by having the patient concentrate on his or her breathing efforts and keep the eyes open, with vision fixed on an object in the distance. Once the patient is anesthetized, repeat the steps described earlier and position the mirror against the soft palate. Rotate the angle of the mirror and systematically inspect the base of the tongue, valleculae, epiglottis, pyriform recess, arytenoids, false and true vocal cords, and, if possible, the superior aspect of the trachea ( Fig. 65-3 ). Observe for masses, evidence of infection, asymmetry, or FBs. Further evaluate the anterior structure of the larynx and function of the vocal cords by having the patient say "eeee" in a high-pitched voice. This should move the epiglottis away from blocking the view of the larynx and bring the true cords together at the midline. Laryngoscopy by Angled Telescopes
A less frequently used method of examining the larynx in the emergency setting is by rigid angled laryngoscopy (e.g., LarynxVue II, Astralite Corp., Anaheim, CA). This provides a clear and more continuous view of the larynx during respiration, but its use is limited in patients whose epiglottis blocks the view. The light source is powered by batteries or a wall outlet. The degree of mirror angulation is fixed, but it may vary between instruments (usually 70° to 90°). At 70° of mirror angulation, the scope does not need to be placed as far posteriorly into the oropharynx to visualize the structures. Position the patient as for indirect laryngoscopy and anesthetize the soft palate if necessary, as previously described. Gently grasp the tongue and slide the scope into the oropharynx. Stabilize the scope on the fingers that are holding the tongue, taking care not to touch the sensitive base of the tongue. Once the scope is touching the soft palate and is near proper position, look into the eyepiece and make final adjustments to bring the laryngeal structures into focus. Observe the anatomy and function as previously described in a systematic fashion. Flexible Fiberoptic Laryngoscopy
Fiberoptic examination of the nasopharynx and larynx can be accomplished with either a flexible nasopharyngoscope or a bronchoscope. The nasopharyngoscope is thinner, shorter, and easier to manipulate ( Fig. 65-4 ). Fiberoptic visualization is especially useful in patients who are difficult to examine because of persistent gagging or unusual anatomy.
Figure 65-3 View of the larynx from above. The true and false vocal cords are sketched, with the arytenoid eminences behind them on each side. The epiglottis, piriform fossae, and valleculae are also labeled.
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Figure 65-4 Fiberoptic scope with light source.
Attach the endoscope to its light source, attach the suction to its port (if available), and ensure that both are functioning properly before beginning. Before inserting the scope, adjust the eyepiece to the operator's visual acuity; it is helpful to check the scope focus on newsprint or a small object at this time. Review of the scope's directional controls is also recommended. Examine the nares and choose the more patent one to enter. Anesthetize and vasoconstrict the naris with lidocaine and epinephrine (as described in Epistaxis, later in the chapter). Some clinicians also anesthetize the pharynx to minimize gagging. Warm the end of the scope in warm water to help prevent fogging. The patient should be seated, with the head placed against a headrest, in the "sniffing" position. Insert the tip of the lubricated scope just inside the naris. A series of soft nasal trumpets may be used to dilate the nasal cavity, allowing easier passage of the scope. The movement of the scope against the inside of the nasal passage may be irritating; this discomfort can be minimized by resting the fourth and fifth fingers on the bridge of the patient's nose while stabilizing and guiding the passage of the scope between the thumb and index finger ( Fig. 65-5 ). While looking through the eyepiece, slowly advance the endoscope past the inferior turbinate into the nasopharynx or through the lumen of the trumpet. To clear fogging or mucus off the lens, have the patient swallow, wipe the lens against the pharyngeal mucosa, or use the suction. Once it is in the nasopharynx, direct the tip inferiorly, using the thumb control near the eyepiece. Up-and-down movements of the scope may be accomplished with the thumb control, whereas rotating the scope about its axis and then applying the thumb control provides for lateral movement and visualization. At this point, the base of the tongue and tonsils will come into view. Slide the scope further caudad to bring the larynx into focus. Once again, systematically view the anatomy and function during both respiration and phonation. If the nasopharyngeal scope will not pass through either naris, pass it through the oropharynx. Properly anesthetize the oropharynx and avoid the posterior tongue to prevent gagging. Cut a 10-mL syringe (without the plunger) in half. Have the patient hold this in the mouth between the incisors. Pass the fragile endoscope through this tube to prevent accidental biting of the scope. Complications include traumatic abrasions and bleeding anywhere along the path of the laryngoscope. In patients with
Figure 65-5 Fiberoptic nasopharyngoscope in use. Prepare the patient's throat and nares with topical anesthetic. Topical vasoconstrictors may also be used in the nares. The use of a nasal trumpet is optional. Advance the scope slowly into the naris with the hand stabilized on the patient's nose; guide the scope using the thumb and index finger. Visualize the passage of the scope through the naris into the posterior nasopharynx. Always use universal precautions.
head injury, there is always the slight risk of passing the scope intracranially if a basilar skull fracture exists, but use of a soft nasal trumpet significantly reduces this risk. The induction of laryngospasm and acute airway compromise is possible in patients with paraglottic infections. Peritonsillar Abscess Anatomy
Peritonsillar abscess (PTA), also known as quinsy, is most common during the second and third decades. It is rarely seen in children younger than 6 years of age, making it diagnostically challenging in younger children and infants. It remains the most common head and neck abscess in children and adults. The incidence for PTA is about 45,000 cases annually in the United States. The relative anatomy must be understood to treat peritonsillar abscesses ( Fig. 65-6 ). The palatine tonsils are located between the anterior and posterior pillars of the throat, bound in a capsule and covered by mucosa. The lateral wall of the tonsil is defined by the superior pharyngeal constrictor muscle. Of great importance is the internal carotid artery, which lies approximately 2.5 cm posterolateral to the tonsil. Pathophysiology and Presentation
Peritonsillar abscesses occur in patients with inadequately treated tonsillitis and in recurrent tonsillitis. The abscess is usually unilateral and is defined as a collection of pus between the tonsillar capsule, the superior constrictor muscle, and the palatopharyngeus muscle. It is believed to arise from the spread of infection from the tonsil or from the mucous glands of Weber, located in the superior tonsillar pole. [2] The abscess is most commonly initiated from the upper pole of the tonsil. However, it can also spread from the middle or inferior poles. Complications may include pharyngeal obstruction or extension into the closely approximated neurovascular bundles and parapharyngeal space.
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Figure 65-6 Anatomy of a peritonsillar abscess. The palatine tonsil and peritonsillar space are identified on the patient's right. A peritonsillar abscess is shown on the patient's left. Note that the abscess can extend medially, displacing the uvula. The carotid artery and jugular vein are posterior and lateral to the abscess. Avoid lateral angulation of the aspirating needle and use a needle guard to prevent injury.
Most patients present primarily with a peritonsillar abscess, but some have been previously treated for tonsillitis. There are no data proving that antibiotics, even the correct ones in proper doses, invariably prevent the progression of tonsillitis to abscess formation. Inadequately treated tonsillitis can progress to abscess when a patient fails to follow the prescribed regimen or when the regimen is inadequate. The latter may occur as the result of an improperly chosen antibiotic or because of increasing antibiotic resistance. Although penicillin still remains the best initial treatment for tonsillitis, anecdotal cases of failure after intramuscular long-acting penicillin have also been noted. Although Group A Streptococcus remains the leading cause of peritonsillar abscess, Staphylococcus aureus, Haemophilus influenzae, Bacteroides, Peptostreptococcus, and mixed anaerobic infections are common. ß-lactamase-producing organisms are present in about 50% of cases. [3] Fine-needle aspiration of peritonsillar abscesses may allow identification of organisms and appropriate modification in antibiotic therapy, thus avoiding the need for tonsillectomy. Patients with peritonsillar abscesses present with sore throat, odynophagia, low-grade fever, and a variable degree of trismus. The trismus develops secondary to pterygoid muscle irritation. The patient may also complain of ipsilateral otalgia. As the abscess expands, the patient may experience dysphagia with drooling. Patients are often dehydrated secondary to poor oral intake. Voice changes are common (hot potato voice) and are caused by transient velopharyngeal insufficiency and muffled oral resonance. Rancid breath is also common. Tender ipsilateral anterior cervical lymphadenopathy is frequently present. Fever >39.4°C has been associated with parapharyngeal extension and sepsis. [4] Examination of the oropharynx may be difficult because of associated trismus. Have the patient sit with the head in the "sniffing" position. Encourage the patient to open the mouth as wide as possible, and depress the tongue to obtain a better view of the oropharynx. Use a head lamp or head mirror/light source to ensure adequate illumination. Digital palpation for a fluctuant site can be useful, and may be the best way to differential abscess from cellulitis. The clinician places the gloved index finger into the mouth and feels for hardness or fluctuance in the peritonsillar region ( Fig. 65-7 ). If no abscess can be appreciated, the diagnosis is unlikely. This technique is usually well tolerated but the patient may gag or bite the examiner by reflex. Physical findings are often diagnostic of a peritonsillar abscess, but in about 20% of cases the diagnosis is in doubt until needle aspiration is performed. Inferior and medial displacement of the tonsil and uvula are noted along with a fluctuant mass involving the tonsillar pillar. Swelling obliterates the normally sharply delineated pillar-like
Figure 65-7 Clinical symptoms and visual inspection may not be sufficient to differentiate peritonsillar abscess from cellulitis. The clinician's gloved index finger is used to palpate the peritonsillar area to search for fluctuance and localized swelling.
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structure. The tonsil looks edematous and erythematous, and may be covered with a whitish exudate. The differential diagnosis for this acute process includes unilateral tonsillitis, peritonsillar cellulitis, retropharyngeal abscess, infectious mononucleosis, Herpes simplex tonsillitis, retromolar abscess, neoplasm, FB, and, possibly, internal carotid artery aneurysm. Chronic conditions include leukemia, carcinoma, and parapharyngeal space tumor. Differentiation of a peritonsillar abscess from peritonsillar cellulitis may be difficult, especially in the early stages of an abscess. The history and time course for the two disease processes are quite similar. Trismus and uvular deviation are uncommon in peritonsillar cellulitis. [5] Needle aspiration will be diagnostic if purulent material is removed. However, a negative test does not rule out an abscess. The abscess may be located posteriorly, and not accessible by the aspiration needle. Intraoral sonography has a sensitivity and specificity of 91% and 80%, respectively, in detecting peritonsillar abscesses [6] and may therefore augment diagnostic accuracy. Also, if there is any question as to the diagnosis or actual location of the abscess, CT scanning may be utilized. General Treatment
The treatment of peritonsillar abscess has undergone significant change in the past 100 years and continues to do so at this writing. A myriad of opinions exists on the appropriate treatment method, although most agree that some form of drainage procedure should be performed in conjunction with antibiotics and pain control. Three options for surgical drainage include: needle aspiration, incision and drainage, and immediate (quinsy) tonsillectomy. Each method will be discussed. Needle aspiration is relatively simple, can be performed by clinicians who are not head and neck specialists, does not require special equipment, and is relatively inexpensive. Other benefits of needle aspiration over incision and drainage include decreased pain and trauma. Many feel that this should be the initial surgical drainage procedure for adults and children. The recurrence rate following needle aspiration is 10% [7] and its cure rate is about 94%. [2] About 4% to 10% of patients require repeat aspiration. [2] [7] One drawback is that needle aspiration may miss the peritonsillar abscess and therefore allow misdiagnosis as peritonsillar cellulitis. Up to 12% to 24% of abscesses have been missed on initial aspiration. [8] [9] Therefore, some authors propose admission of patients with negative aspirations with the presumed diagnosis of peritonsillar cellulitis for intravenous (IV) antibiotics and observation to prevent further morbidity. [10] Although most studies were performed with hospitalization and IV antibiotics, selected outpatient treatment with oral antibiotics has been successful. [10] [11] Most patients with a successfully drained peritonsillar abscess can be safely and effectively managed with needle aspiration and outpatient antibiotics. [12] Incision and drainage is commonly done as an outpatient procedure under local anesthesia. This procedure is usually performed after pus is obtained by needle aspiration, but occasionally it is the primary procedure. It seems most logical to first attempt aspiration and only follow with incision and drainage if additional pus is suspected or there are other extenuating circumstances. The recurrence rate following incision and drainage is 5.9% to 22.7%. [13] Despite these shortcomings, incision and drainage is the initial surgical treatment used by an estimated 54% of U.S. otolaryngologists. [2] Immediate (quinsy) tonsillectomy is thought by some to be the only way to completely drain the abscess and completely eliminate the risk of recurrence. They also feel that hospital time and the patient's disability are shortened. Arguments against this rationale include: 1. An initial PTA is no longer an indication for tonsillectomy. 2. Needle aspiration/incision and drainage have high success rates.
3. Studies have shown longer recovery times for patients following immediate tonsillectomy compared to the other drainage procedures. 4. There is a time delay (6 to 70 hours) in assembling equipment and personnel for the tonsillectomy. Patients successfully treated with needle aspiration are often well on the way to recovery in that amount of time. [7] Treatment guidelines based on a review of the literature [2] [7] suggest that pediatric patients with peritonsillar abscess and adults without history of recurrent tonsillitis be initially treated with needle aspiration. Incision and drainage and immediate tonsillectomy should be reserved for treatment failures or recurrences. Adult patients with recurrent tonsillitis/peritonsillar abscess should be treated with either needle aspiration followed by delayed tonsillectomy or with abscess tonsillectomy alone. These procedures can be done in combination with hospital admission and administration of IV antibiotics or as an outpatient with oral antibiotics. The approach depends on the patient's clinical status and medical history. Decisions about the treatment of a peritonsillar abscess in the ED are often made by the emergency clinician, but as local protocols dictate, consultation with an otolaryngologist is often appropriate. Needle Aspiration/Incision and Drainage
The two procedures described here include needle aspiration and incision and drainage. They should only be performed in the cooperative patient without severe trismus. With the carotid artery located 2.5 cm behind and lateral to the tonsil, there is minimal room for error, patient movement, or poor anesthesia. Have the patient sit upright, with a support behind the head. This is best done as a two-person procedure. An assistant can retract the cheek laterally to maximize visibility. A head lamp provides optimal lighting; a double tongue-blade setup aids visualization of the operative area ( Fig. 65-8 ). It is
Figure 65-8 Needle aspiration of a peritonsillar abscess. The patient sits upright with the head supported by the back of the stretcher (or a dental chair head rest). A head lamp provides light and an assistant retracts the cheek laterally to maximize visibility.
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Figure 65-9 A, As a safeguard to prevent deep penetration of a needle used to drain a peritonsillar abscess, select a long 18- to 20-gauge needle. Remove the plastic needle guard and cut off the distal 1 cm. B, Replace the guard on the needle and tape it to the hub.
suggested that parenteral narcotic analgesia or mild sedation, or both, be administered before attempts at aspiration. Fentanly, 2 to 3 mcg/kg IV a few minutes before the procedure, is often ideal. Midazolam may be judiciously used, but the patient should not be overly sedated. The combination of midazolam, ketamine, and glycopyrrolate has been reported as being safe and effective for the outpatient peritonsillar drainage in children. [14] Anesthetize the area topically with Cetacaine spray, or 4% to 10% lidocaine. Determine the fluctuant area of the abscess by manual palpation. Additionally anesthetize this area with local infiltration of 1 to 2 mL of 1% lidocaine with 1:100,000 epinephrine via a 27-gauge (ga) needle. Using a 5-mL syringe with a long needle allows visualization of the area to be injected, while a small syringe often causes the clinician's hand to block the view. Infiltrate the lidocaine intramucosally for the best results, and seek a blanching area
Figure 65-10 A, Needle aspiration of a peritonsillar abscess. Anesthetize the posterior pharynx with topical lidocaine spray. Blanch the mucosa with lidocaine/epinephrine with a 27-gauge (ga) needle on a long syringe (to allow visualization of the site) in the area to be aspirated. Advance an 18- or 20-ga needle with needle guard into the area of greatest fluctuance, usually the superior pole. Aspirate as you advance the needle. Advance the needle in the sagittal plane. Do not direct the needle laterally toward the carotid artery or jugular vein. B, The superior pole is aspirated first, but the middle and inferior poles should be aspirated if pus is not obtained initially. Note that the tonsil itself is not aspirated. The peritonsillar space contains the abscess.
on the mucosal surface. During the injection, be careful not to increase the abscess size by direct injection into the abscess cavity. With proper local infiltration the patient will not feel the penetration of the aspirating needle. If the trismus is so pronounced as to prevent adequate anesthesia administration, it will probably be too difficult to aspirate or incise the abscess properly. For aspiration, prepare a long 18- to 20-ga needle on a 10- to 20-mL syringe. Fashion a needle guard by cutting off the distal 1 cm of the plastic needle cover, replace the cover on the needle, and securely attach this guard to the needle and syringe with tape to prevent inadvertent displacement ( Figs. 65-9 A & B ). Ensure that the needle protrudes only 1 cm beyond the cover. This procedure will limit the depth of needle penetration and lessen the risk of entering any major vascular structure. If pus is not obtained at a 1-cm depth, deeper penetration is discouraged. Insert the needle into the
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most fluctuant (or prominent) area as previously determined, which is most commonly the superior pole of the tonsil. Note that the tonsil itself is not aspirated because the abscess develops in the peritonsillar space surrounding the tonsil. The needle is advanced only in the sagittal plane and is not directed laterally, where it may injure the carotid artery. If the aspirate is positive, remove as much purulent material as possible. If the aspirate is negative, attempt aspiration again in the middle pole of the tonsil approximately 1 cm caudal to the first aspiration. A third and final attempt should be performed at the inferior pole. Up to 30% of abscesses will be missed if only the superior pole is aspirated. It must be stressed that a negative aspirate does NOT rule out a peritonsillar abscess. Usually 2 to 6 mL of pus is obtained. It is unusual to recover more than 8 to 10 mL ( Fig. 65-11 ). There is no specific advantage of sending the aspirate to the laboratory for culture. Many clinicians forgo culturing since it has not been demonstrated that culture results influence treatment. [10] When significant amounts of pus are aspirated, the patient usually feels immediate improvement in pain and dysphagia. After the needle is removed, some bleeding will be noted. A slight ooze may be noted for a few hours, especially if warm water rinses are used. There may be continued drainage of pus, often sensed as a foul taste by the patient. If significant additional pus drains, this may be an indication for a repeat aspiration, incision and drainage or hospital admission. Some clinicians advise a formal incision and drainage (see later) if frank pus is obtained, whereas others now accept needle aspiration (with close follow-up) as the definitive initial treatment. Theoretical reasons to combine aspiration and formal drainage in the same visit are if large amounts of pus are obtained (>5 to 6 mL) or if pus continues to drain from the aspiration site. There are no agreed-upon standards regarding best practice for this issue. To incise a peritonsillar abscess, anesthetize the area as described earlier. Prepare a No. 11 or 15 scalpel blade by taping over all but the distal 0.5 cm of the blade to prevent deeper penetration ( Fig. 65-12 ). Incise the area of maximal fluctuance or where a preceding aspiration, if one was performed, located pus. Incise the mucosa in an area 0.5 cm long in a posterior to anterior direction. A stab incision with
Figure 65-11 Needle aspiration usually yields 2 to 6 mL of thick pus. Greater volumes are unusual. Removing only a small amount will produce a marked reduction in symptoms.
a No. 11 blade usually suffices. Warn the patient that the pus will flow posteriorly and he or she must expectorate this fluid. Expect bleeding, as this is a vascular
area. Suction the incised area with a No. 9 or 10 Frazier suction tip or a tonsil suction tip to aid in removal of the purulent material. Place a closed Kelly clamp into the opening and gently open it to break up the loculations. Allow the patient to rinse and gargle with a saline or dilute peroxide/saline solution. Packing is not used in the drainage of this abscess. Following aspiration or incision, it is prudent to observe the patient for about an hour to watch for complications (e.g., bleeding) and to ensure the ability to tolerate oral fluids. Most patients can be discharged with 24 hour follow-up. Toxic patients, those with excessive volumes of aspirate, those with persistent bleeding, or those unable to take oral antibiotics are candidates for admission or more prolonged observation. Frequent rinses with warm saline are quite helpful in relieving postaspiration symptoms. Following either needle aspiration or incision and drainage, antibiotics are recommended to eradicate the offending organisms. Penicillin, clindamycin, or cephalosporins are a reasonable first choice. Resistance rates to penicillin range from 0 to 56% but laboratory sensitivity testing is not always reflective of a clinical response.[7] Alternatives include ampicillin/sulbactam and amoxicillin/clavulanate. Reasonable cure rates have been obtained with oral penicillin in modest doses (500 mg per os [PO] four times a day [QID]). Many clinicians prefer to administer an IV loading dose of penicillin (5 million units) or cefazolin (1 g) before releasing the patient. While the benefit is not well established, many clinicians empirically also administer a single parenteral dose of dexamethasone (10 mg) and this may further ameliorate symptoms. Any patient who appears to have a toxic response, whose immune system is compromised, is unable to take oral antibiotics, or is dehydrated should be admitted for IV fluid hydration and antibiotic administration. Reevaluation of all patients treated with needle aspiration should be performed in 24 hours to assess the need for repeat aspirations or formal incision and drainage. At 24 hours most patients are markedly improved, and failure to see this response requires further evaluation. Warm saline gargles and mild opioid analgesics also are recommended with outpatient care. All patients should
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Figure 65-12 Aspiration is often the only procedure required to successfully treat a peritonsillar abscess, but it has a 10% failure rate. In some instances the clinician will opt for incision and drainage of a peritonsillar abscess. This procedure may used initially, or after aspiration if copious pus is aspirated, or if pus continues to drain or reaccumulates. A, Normal-appearing oropharynx. B, Peritonsillar abscess on the right side of the throat. C, Incision of the abscess at the area of greatest fluctuance. Notice that the scalpel is taped to prevent deep penetration. D, Loculations are removed by gentle probing with hemostats.
immediately return for recurrence of symptoms, fevers, or continued bleeding from the incision. Complications
Needle aspiration is an accepted, safe, and effective technique for the ED treatment of peritonsillar abscess. There is an approximate 10% failure rate or need for subsequent drainage. Aspiration or incision of the carotid artery or a misdiagnosed carotid artery aneurysm may have devastating results. The potential for penetrating a deep vascular structure is largely theoretical if proper technique is followed—there are no documented cases in recent literature. If the patient has cellulitis, the aspiration will be of no help, but it will not worsen morbidity. Failure to obtain pus should prompt highdose antibiotics and a recheck in 24 hours. Many clinicians will opt for admission in such instances. A too-large or too-small incision may lead to poor healing or inability to completely evacuate the abscess, respectively.
EAR Anatomy of the External Auditory Canal The external auditory canal (EAC) extends from the tympanic membrane to the concha and measures approximately 2.5 cm in the adult. It is relatively short and straight in early infancy but begins to take on its adult S-shape and overall anterocaudal orientation beginning at age 2 years. Initially, the EAC is almost entirely cartilaginous, but by adulthood its medial two-thirds is comprised of bony support with an overlying thin, stratified, squamous epithelium. The lateral third has a less sensitive, thicker, hairy epithelium that produces cerumen and retains its cartilage as support. The arterial supply to the EAC originates from the external carotid artery via the posterior auricular, maxillary, and superficial temporal branches. The mandibular branch of the fifth cranial nerve (V 3 ) and the vagus nerve innervate the ear. Other important anatomic considerations include the following: (1) Two natural narrowings of the EAC exist, which are important when considering FBs. One is located at the junction of bone and cartilage and the other lies just lateral to the tympanic membrane. (2) A blind spot may occur in the tympanic sulcus (inferior and anterior to the tympanic membrane) due to the oblique orientation of the tympanic membrane. An examiner using a simple otoscope may not visualize an FB in this sulcus. Anesthesia of the Ear External Ear/Auricle
Indications for local anesthesia of the auricle include closure of extensive lacerations or other painful procedures, such as
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Figure 65-13 A and B, External anatomy of the ear and innervation of the auricle.
hematoma incision and drainage. Four nerve branches supply the external ear, and knowledge of their anatomy is required to understand the location for anesthesia injection ( Fig. 65-13A and B ). The greater auricular nerve (branch of the cervical plexus) innervates most of the posteromedial, posterolateral, and inferior auricle. A few branches of the lesser occipital nerve may contribute to this area. The auricular branch of the vagus supplies the concha and most of the area around the auditory meatus. The auriculotemporal nerve (from the mandibular branch of the trigeminal nerve) supplies the anterosuperior and anteromedial aspect of the auricle. Procedure Fill a 10-mL syringe with either 1% lidocaine or 0.25% bupivacaine (both with epinephrine if a regional block is planned in an area without evidence of traumatized vascularity) and attach the syringe to a 25- or 27-ga needle (5 to 7 cm in length). One of several methods may be used to accomplish partial or complete anesthesia, depending on the area of concern. The greater auricular and lesser occipital nerve branches may be anesthetized by injecting between 3 and 4 mL of anesthetic in the posterior sulcus ( Fig. 65-14A ). Insert the needle behind the inferior pole of the auricle and gradually aspirate and inject toward the superior pole, following the crescent-shaped contour of the posterior auricle. Anteriorly, the auriculotemporal nerve may be anesthetized by placing 3 to 4 mL of anesthetic just superior and anterior to the cartilaginous tragus. Use the technique shown in Figure 65-15 and Figure 65-16 to provide anesthesia of the auricular branch of the vagus to include more central areas of the auricle. Another and possibly more effective option is the regional block shown in Figure 65-14B . Insert the needle subcutaneously (SQ) at a point approximately 1 cm above the superior pole of the auricle and direct it to a point just anterior to the tragus. Be sure to inject the skin of the scalp while avoiding the auricular cartilage. Aspirate, then slowly withdraw the needle, injecting anesthetic until the needle is almost to the puncture site. Redirect the needle posteriorly and repeat the process while aiming at the skin just behind the mid-auricle. Remove the needle and perform the same procedure, but
Figure 65-14 Field blocks of the auricle. A, One method uses approximately 3 to 4 mL of anesthetic, both in the posterior sulcus and at a point just anterior to the tragus. B, Alternative field block technique that deposits 2 to 3 mL of anesthetic for each needle pass. See text for more details.
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Figure 65-15 Four-quadrant field block anesthesia of the external auditory canal. Local anesthetic is injected subcutaneously in the four quadrants of the lateral portion of the ear canal. The largest speculum that will fit is used to guide the injections. The speculum is withdrawn slightly, tilted toward each of the four quadrants, and the needle is inserted subcutaneously (x). A very small amount of anesthetic (0.25 to 0.50 mL) is injected to produce a slight bulge in the soft tissue. A total of 1.5 to 2.0 mL of anesthetic is usually sufficient to anesthetize the ear canal and permit painless removal of a foreign body.
insert the needle just inferior to the insertion of the ear lobule and anesthetize in a superior direction. Again, block the auricular branch of the vagus as described in Figure 65-17 if additional anesthesia of the concha is required. Use caution if adding epinephrine to the anesthetic solution when placing regional blocks of the ear, especially if
Figure 65-16 Diagram of injection sites for an alternative technique to anesthetize the ear canal and central concha. Each site should be injected with approximately 0.5 mL of 1% lidocaine. Do not inject if external signs of infection are present.
Figure 65-17 Examination of ear canal. The pinna is retracted in a superior and posterior direction to straighten out the ear canal. The scope is held in the other hand and stabilized against the patient's head. This prevents inadvertent injury if the patient moves unexpectedly.
the blood supply has already been traumatically reduced. Do not include epinephrine when directly infiltrating wounds of the auricle, as restriction of blood flow through end arteries here may result in tissue necrosis. Other complications related to local anesthetics and regional blocks of the head and neck may be reviewed in Chapter 30 and Chapter 31 . External Auditory Canal and Tympanic Membrane
The EAC is innervated by the auricular branch of the vagus (inferiorly and posteriorly) and by the auriculotemporal nerve (superiorly, anteriorly, and inferiorly). The primary indication for local anesthesia of the auditory canal is for FB removal, including debridement of otitis externa or removal of significant cerumen impaction. It is very difficult to obtain adequate anesthesia of the inner ear and tympanic membrane for painful procedures. Simply stated, no easy and completely effective procedure consistently works well. If total anesthesia is required, general anesthesia, especially in children, is often the only alternative. Topical anesthetics are inadequate due to their poor absorption through the rather impermeable and keratinized epithelial surface of the EAC. Although effective for some procedures, injecting local anesthetics in and around the auditory meatus is quite painful and is often difficult to perform in a struggling and uncooperative patient. Certain instances warrant adjunctive use of conscious sedation (see later discussion under Foreign Body Removal). It is quite difficult to obtain anesthesia of the tympanic membrane. The membrane is sensitive and can be stimulated during attempts at removing a FB from the ear canal. Topical anesthetics have limited value, but Moller and Grontved demonstrated that 10% aerosolized lidocaine (first sprayed into a syringe and shaken to evaporate the propellant) and 4% lidocaine suspension, when dripped into the ear canal, provided good anesthesia of the membrane. [15] However, it required 30 minutes for this anesthesia to take effect. Both solutions were alkaline and it was noted that lidocaine
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hydrochloride, the form usually used for wound infiltration, is acidic and provided no anesthesia when applied topically. Auralgan, a combination of benzocaine and other ingredients, may provide analgesia for painful earaches due to otitis, but it has little benefit for painful procedures. Procedure
Local anesthesia is performed with a 25- or 27-ga needle (3 to 5 cm in length) attached to a syringe of 1% lidocaine with epinephrine (1:100,000). A 1:10 mixture of 8.4% sodium bicarbonate to lidocaine helps to reduce pain with injection in this sensitive area. Place a speculum just inside the auditory meatus and inject 0.3 to 0.5 mL of the anesthetic into the SQ tissue, stopping after a small bulge in the skin is raised. Inject in this manner in all four quadrants by moving the speculum after each injection (see Fig. 65-15 ). If additional anesthesia is necessary, give two more small injections. Inject the same amount slightly farther into the canal, once along the anterior wall and again at the posterior wall at the bone-cartilage junction. Another similar technique involves depositing the anesthetic just lateral or exterior to the external auditory meatus. Using the same size needle and type of anesthetic solution as just described, inject approximately 0.5 to 1.0 mL into each of 5 points around the auditory meatus and tragus (see Fig. 65-16 ). Examination Several methods are available to examine the EAC and tympanic membrane. In all methods, the superior pinna should be grasped and pulled cephalad and posterior to straighten the slightly tortuous EAC. The most common manner of examination is with a fiberoptic otoscope (see Fig. 65-17 ). The clinician may insufflate the tympanic membrane as well as examine the EAC with the diagnostic head, while the operating head allows for instruments to be passed into the EAC and maneuvered more easily. A plastic or metal speculum may be placed in the auditory meatus for examination, using a head lamp or head mirror/light bulb as a light source. Although this provides excellent illumination, magnifying loupes are generally needed for adequate visualization during procedures. The ideal setup for cerumen or FB removal consists of an operating microscope and a speculum. This provides binocular vision and frees the examiner's hands for instrumentation (unfortunately this equipment is seldom found outside of the otolaryngology clinic setting). The hand holding the otoscope is stabilized against the patient's temporal skull to prevent inadvertent canal injury due to unexpected patient movement. Cerumen Impaction The excretion of the ceruminous or apocrine and sebaceous glands together with cells exfoliated from the external auditory canal combine to form cerumen. One study[16] found that cerumen is composed of lipids, complex proteins, and simple sugars. Cerumen repels water, has documented antimicrobial activity, and forms a protective barrier against infection. Cerumen often becomes impacted, causing complaints of a "blocked" ear, hearing impairment, or dizziness. Symptomatic impaction is an indication for removal, although symptoms are rare until complete obstruction is present. The sudden loss of hearing is a common complaint in patients with totally occluding impacted cerumen. Cerumen obstructs visualization of the tympanic membrane and can be evacuated as a part of the evaluation of a febrile child or the patient complaining of ear pain. However, cerumen removal in a child is rarely indicated in the ED simply to visualize the tympanic membrane. Cerumen impacted for prolonged periods, and vigorous attempts to remove it, may precipitate otitis externa. It is reasonable to instill antiseptics (Vol Sol and others) or antibiotics for a few days post cerumen removal to prevent this. No standard exists and practices vary widely. Cerumen Removal
Irrigation is an effective approach for cerumen removal and has the advantage of being painless and simple to perform. The patient does not have to remain completely still; thus, it is ideal for the pediatric population. It is estimated that 150,000 ears are irrigated in the United States each week. [17] Although usually more time-consuming than manual extraction, irrigation is an appropriate initial method to attempt and can be performed by technicians with guidance from the clinician. One contraindication is known or suspected tympanic membrane perforation. Use irrigation judiciously in elderly and immunocompromised patients, as malignant otitis externa is frequently preceded by irrigation of the EAC. [18] Generally, the procedures used to remove cerumen are safe; however, otologic injury has resulted from this "minor" procedure and has even resulted in litigation. [17] Whichever of the following techniques are used, some tips for successful cerumen removal include: use proper lighting, pay attention to patient comfort, and never continue beyond the patient's comfort level. Ceruminolytics
These products may soften obviously hardened or impacted cerumen. They are used as adjuncts to other procedures—simply instilling ceruminolytics into the canal will not remove enough cerumen to aid the emergency clinician. If irrigation fails, the continued outpatient use of ceruminolytics is often prescribed, often combined
with home irrigation using a bulb syringe. Although many products are available as ceruminolytics, a 5% or 10% solution of sodium bicarbonate disintegrates cerumen much more quickly and efficiently compared with commercially prepared ceruminolytics and other products. Cerumenex, Cerumol, Auralgan, Buro-Sol, alcohol, and oils were all tested and took more than 18 hours to disintegrate cerumen vs ~90 minutes for the sodium bicarbonate solutions. [19] Hydrogen peroxide is another commonly used ceruminolytic, but its use has not been systemically studied. One study [20] found the liquid preparation of the stool softener docusate sodium (Colace) was much more effective as a ceruminolytic than Cerumenex. Place the patient in the supine position with the affected ear up and instill the solution at least 15 minutes before attempts at removal. Instillation can be repeated between attempts at manual extraction or irrigation. Irrigation (Ear Syringing)
This procedure is best achieved by having the patient sit upright and holding an emesis or ear irrigation basin flush against the skin just below the ear lobule ( Fig. 65-18 ). Insert the irrigation tip into the EAC only as far as the cartilage-bone junction, and direct the stream of water superiorly to wash the impacted cerumen away from the tympanic membrane. Water should be near body temperature to prevent caloric
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Figure 65-18 Irrigation is a simple, painless, and usually successful way to remove cerumen. After a wax-softening agent has been instilled for 15 to 20 minutes, an assistant applies traction on the ear to straighten the canal, and the plastic tubing of a 19-ga butterfly device (needle and wings removed) is inserted 1 cm into the canal. A basin is held by the patient, and warm water is introduced with a 20-mL syringe. A number of irrigations may be required, and the procedure may be supplemented with careful removal of large cerumen pieces with a curette.
stimulation. Multiple attempts may be necessary, and intermittent attempts at manual removal of loosened cerumen may help hasten the process. During the irrigation, the operator or an assistant should apply traction to the pinna to straighten the canal for more efficient irrigation. Irrigation techniques using manual pressure to discharge the water include metal ear syringes and bulb syringes. The metal ear syringe ( Reiner-Alexander Ear Syringe) is inexpensive and readily available. Some disadvantages include: slow operation, it is poorly balanced, the tip tends to wobble, and minor canal trauma is common.[17] [21] Improvisational irrigation systems can be assembled with equipment found in the ED. Attach a 20- or 30-mL syringe to a 19-ga or larger butterfly device, cutting off the needle and wings and leaving the resultant tubing for irrigation. A plastic or Teflon IV catheter (16- or 18-ga with the needle removed) can similarly be affixed to a syringe. Contraindications to ear syringing include [22] : Patient aversion to or history of injury from syringing History of middle ear disease History of ear surgery Perforated tympanic membrane Severe otitis externa Narrow ear canals FBs, especially sharp objects and vegetable matter Uncooperative patient Occluding aural exostoses Known inner ear disturbance, especially if patient has severe vertigo History of radiation therapy to the external or middle ear, skull base, or mastoid
The most common way to irrigate an ear is with a syringe and catheter ( Fig. 65-19 ). Although most commonly found in an otolaryngologic clinic, automated pressure devices may also be available. The DeVilbiss irrigator ( Fig. 65-20 ) uses a pressurized air source to propel the irrigating solution into the ear. It allows the clinician to control the water pressure and direction, making it pleasant for the patient. Unfortunately, it is rarely available in hospitals, requires a pressure source, and clinician training is needed. Use of oral jet irrigators (Water Pik) is another accepted method. They are fast, portable, and inexpensive. Disadvantages to the oral jet irrigator include: trauma to the stapes and cochlea, off-label use may expose the clinician to litigation, there is splash back, and many patients find it uncomfortable. The Hydro Med Ear Irrigator Tip (Hydro Med, Sherman Oaks, CA) can be combined with the Water Pik to improve safety and comfort. The tip keeps the stream of water from hitting the eardrum. The tip is smooth and convex, reducing the potential for injury. [17] Although the instances have been rare, tympanic membrane rupture has
Figure 65-19 The most readily available device for ear irrigation is an 18-gauge flexible catheter attached to a 60-mL syringe. Since multiple irrigation may be required, small syringes are counterproductive.
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Figure 65-20 This DeVilbiss irrigator uses compressed air to eject the irrigating solution, which should be near body temperature to avoid caloric stimulation of the inner ear. The more conventional metal ear syringe can be equally effective and does not require a source of compressed air to function.
been documented with these apparatuses. [23] Therefore, use the lowest-power setting and guide the stream of the water against the EAC wall, not directly toward the tympanic membrane. After irrigation of the EAC, application of several drops of isopropanol in the EAC will facilitate evaporation of residual moisture. The tympanic membrane must be intact if isopropanol is to be used. Further, topical Cortisporin Otic suspension drops may be soothing after prolonged irrigation. Since diabetics can develop severe otitis external following irrigation, some clinicians routinely prescribe antibiotic ear drops (fluoroquinolones and others) for a few days post irrigation in high-risk patients. Although more common with jet irrigators, complications may occur with any method of ear irrigation. These include otitis externa, tympanic membrane perforation, or
middle ear injury from a preexisting defect in the tympanic membrane. Irrigation should be stopped and the tympanic membrane examined in any patient experiencing sudden pain, tinnitus, hearing loss, nausea, or vertigo. If the membrane is ruptured, prophylactic antibiotics for otitis media should be given along with a referral to an otolaryngologist. Manual Instrumentation
This procedure is more advantageous as it is usually quicker, and the examiner may more easily remove hardened or larger concretions of cerumen under direct visualization. However, it is difficult to manually remove cerumen without causing significant pain. Either the diagnostic or operating head of the fiberoptic otoscope or a speculum may be placed in the auditory meatus to serve as a protective port through which instruments are passed and manipulated ( Fig. 65-21 ). An operating microscope works best in this situation, but, again, is usually not available. To prevent startling or agitating an already anxious patient, allow the patient to experience the sensation of an instrument in the canal by first placing the instrument softly against the ear canal wall. Instruments used for cerumen removal include flexible plastic or wire loops, right-angle hooks, suction-tip catheters, or plastic scoops ( Fig. 65-22 ). The spoonlike instruments and irrigation are both more effective in removing softer cerumen. Firm cerumen ordinarily is more easily withdrawn with loops or right-angle hooks. Gently tease the cerumen off of the
Figure 65-21 Technique for direct visualization and mechanical removal. Use of alligator forceps through a diagnostic otoscope. Note that the magnification device has been slid laterally and that no ear speculum has been attached. Inset, Use of ear curettage through operating otoscope. (From Fritz S, Kelen GD, Sivertson KT: Foreign bodies of the external auditory canal. Emerg Med Clin North Am 5:184, 1987.)
canal wall using loops and then pass hooks or loops around the cerumen and withdraw the cerumen slowly ( Fig. 65-23 ). Care should be taken to keep both hands in contact with the patient's head, as any sudden movement may cause trauma to the canal or the tympanic membrane. Complications most commonly occur when inadvertent contact is made with the thin, friable skin of the bony canal. Trauma may cause EAC laceration, hematomas, otitis externa, or tympanic membrane perforations. Otitis Externa Otitis externa, or "swimmer's ear," is an inflammation of the skin of the external auditory canal. This is essentially a cellulitis of the ear canal. Otitis externa can be disabling enough to cause 36% of patients to interrupt their daily activities for a median duration of 4 days. [24] Precipitants of otitis externa include water exposure and trauma. Excessive moisture in the canal raises the pH and removes the cerumen. Keratin can now absorb water, creating a medium for bacterial growth. Trauma, especially self-manipulation with FBs (cotton swabs, fingernails, etc.), causes abrasions to the ear canal and introduces infection. Removal of cerumen by water irrigation is a well-recognized risk factor for the development of otitis externa. [24] [25] The disease process involves a continuum of gradually worsening inflammatory changes. The patient may present with symptoms ranging from slight itching and discomfort to severe pain, purulent discharge, or systemic toxicity. Pain with manipulation of the pinna is the hallmark for otitis externa. Otoscopy of the external auditory canal may initially reveal minimal debris and erythema, but as the infection progresses, more edema, exudate, erythema, and possibly even a surrounding cellulitis may become apparent. In severe stages the edema may obstruct the canal, preventing instillation of eardrops.
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Figure 65-22 Instruments used for foreign body extraction. From left to right: alligator forceps, bayonet forceps, right-angle hook, wire loop, soft-tipped suction, Frazier suction.
Common bacteria cultured from patients with otitis externa include Pseudomonas aeruginosa and Staphylococcus aureus. Other bacteria include Acinetobacter, Proteus, Enterococcus, and Bacteroides. Approximately 50% of patients have polymicrobial infection and 8% have anaerobic isolates. [26] Of concern, one study [27] found that 6% of staphylococcus isolates were methicillin resistant. Fungi are identified in about 10% of otitis externa cases and are often coexistent with bacterial infections. Aspergillus is responsible for 80% to 90% of cases followed by Candida. It characteristically presents as a furry lining of the ear canal with a fluffy white discharge. Herpes zoster affecting the geniculate ganglion may appear as grouped vesicles on an erythematous base within the canal. This condition, known as Ramsay Hunt syndrome, is associated with facial nerve palsies, hearing loss, and other cranial nerve impairment.
Figure 65-23 Removal of impacted cerumen. Pass the tip of the wire loop beyond the wax and gently tease the wax off the ear canal wall. Extract the wax slowly from the canal. Under direct visualization, avoid contact with the skin of the ear canal to prevent pain and excoriation.
Diabetics and other immunocompromised patients, especially HIV-positive patients, are susceptible to malignant (necrotizing) otitis externa, a life-threatening form of otitis externa caused by Pseudomonas. Deep tissue necrosis, osteomyelitis, intracranial extension, and systemic toxicity are hallmark features. Malignant otitis externa is difficult to treat and mortality rate can be as high as 53%. [24] The diagnosis of malignant otitis externa should be considered in the diabetic or immunocompromised patient with significant symptoms who fails to respond to initial outpatient treatment. Canal Debridement/Wick Placement
It has been touted that key to successful treatment is adequate removal of canal debris. However, vigorous attempts to remove debris on the first visit are very painful, of unproven value, and often eschewed. Gentle attempts to remove debris with small swabs (e.g., urethral swab) ( Fig. 65-24 ) are reasonable, but reserving this procedure for treatment failure or at a follow-up visit is also practiced. Gentle irrigation is one initial approach, but many patients will be cured without extensive debridement. Because the inflamed canal is susceptible to trauma, debris removal may also be accomplished by suctioning under direct visualization using the open or operating otoscope head and a 5 or 7 French (Fr) Frazier tip suction. Irrigation of the canal can be performed only if the clinician is assured there is no tympanic membrane perforation, which may be difficult to confirm due to edema and patient discomfort. [24] [25] [26] For more advanced cases presenting with significant exudate and edema, debris removal remains necessary but is intensely painful. The author recommends using a local block of the auditory canal (see Fig. 65-16 ) as long as the cellulitis has not extended out to the tragus or concha. Administer parenteral analgesics if additional pain control is required. Ear wicks may be used when edema, debris, and exudate are marked enough to impede antibiotic drops from contacting the canal skin. The wick is used as a conduit to deliver the antibiotic solutions to the ear canal. After debridement, use one of several methods to accomplish this. The true benefit of wick implantation is unknown. One approach is to place a 0.25-in. strip of Nu-Gauze dressing covered with an antibiotic and steroid cream (Cortisporin Otic cream) into the external acoustic canal
in a fashion
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Figure 65-24 Debridement of external otitis. A cotton-tipped applicator is inserted into the canal and debris is gently removed from the canal. Irrigation of the ear may also be helpful if the tympanic membrane is not perforated. Inset, the edema has almost closed the canal and will not allow medication to be instilled into the inner canal. An ear wick will prove useful in this situation.
similar to the technique used for anterior nasal packing. Using an otoscope and alligator forceps, place the leading edge of the gauze deeply in the canal until it is fully packed. Withdraw the otoscope and finish by packing the lateral aspect of the canal as well. Another choice is to place commercially available ear wicks, such as the Pope Merocel ear wick. Place this wick into an edematous canal and apply antibiotic/hydrocortisone drops onto it. The wick swells and helps to reduce edema by the antimicrobial and anti-inflammatory effects of the solution and through pressure exerted against the walls as it expands. Leave wicks in place until the patient is followed up in 24 to 48 hours for removal and further debridement. Although relatively safe to use, the ear wick is designed for short-term use. Generally these wicks will fall out of the canal as edema subsides. However, the unusual retention of these wicks can harbor bacteria and cause tissue ingrowth, resulting in long-term problems for the patient. [28] Antibiotic Therapy and Follow-up
Most cases of otitis externa can be effectively treated with debridement and topical antibiotic drops. A study by Halpern [29] showed that 30°C [86°F]). Previously, it was recommended that patients should not receive a set of three countershocks until a core temperature above 30°C can be reached. However, there have been reports of successful defibrillation in patients with profound hypothermia with core temperatures of 25.6°C. [82] The decision to terminate resuscitative efforts remains a clinical decision. However, there are certain poor prognostic factors. Certainly, survival is unlikely in patients who persist in asystole or go from ventricular fibrillation to asystole as they are warmed past 32°C (89.6°F). Prognostic markers for patients with severe hypothermia and cardiac arrest have been proposed as contraindications to ED thoractomy and/or cardiac bypass by some authors. [3] These include elevated potassium levels above 10 mmol/L (meq/L) and pH levels below 6.5. Nonetheless, there are survival reports for patients with higher potassium levels and a pH as low as 6.51. [3] Therefore, the decision to continue resuscitative efforts should not be based solely on specific laboratory values or presenting core temperature. Isolated reports of survival with prolonged CPR in hypothermic patients make extended efforts to resuscitate such patients reasonable. Children may be the best candidates for heroic measures. [5] Under ideal conditions, hypothermic cardiac arrest patients may reasonably be admitted to an intensive care unit for a 4- to 5-hour trial of rewarming with CPR in progress. Manual CPR should be replaced by mechanical methods if equipment is available (see Chapter 17 ). The oxygen-powered "thumper" has been successful during prolonged hypothermic resuscitations. Absence of responsiveness to treatment in conjunction with a highly elevated potassium level is an indication for termination of resuscitative efforts. Airway Management A secure functioning airway must be maintained for the hypothermic patient, just as in any critically ill patient. In mild hypothermia, heated humidified oxygen can be delivered effectively by a face mask. The hypothermic patient can be combative and uncooperative and may require arm restraints if a mask is used. For the patient with decreased sensorium who cannot reliably maintain his or her airway or the hypothermic patient who may be hypoxic, endotracheal intubation may be performed safely without the added risk of ventricular dysrhythmias. [10] The technique for endotracheal intubation depends on the specific presenting circumstances and the expertise of the operator. Once an endotracheal tube has been placed and secured, it may be used for treatment of the patient with warm humidified oxygen. There is no evidence that tracheal intubation is detrimental in the severely hypothermic patient, and should be considered if indicated for ventilation, oxygenation, or airway protection. Acid-Base Disturbances Acid -base disturbances are variable and can lead to metabolic acidosis from carbon dioxide retention and lactic acidosis or metabolic alkalosis resulting from decreased carbon dioxide production or hyperventilation. The interpretation of arterial blood gases in the hypothermic patient has been the cause of some confusion. Previously it was suggested that all blood gases be corrected for temperature with correlation factors. With a decrease in temperature of 1°C, the pH rises 0.015, the PCO2 drops by 4.4%, and the PO 2 drops 7.2% compared to values that would be obtained on blood analyzed under normal conditions. Despite the conversion guide, optimal or normal values in hypothermia have not been well documented. [26] The most recent literature supports the use of uncorrected arterial blood gases to guide therapy with bicarbonate or hyperventilation. [24] [26] This approach appears appropriate to support optimal enzymatic function. A gradual correction of acid-base imbalance will allow for the increased efficiency of the bicarbonate buffering system as the body warms. Arterial pH did not correlate with patient death in the Multicenter Hypothermia Study [72] and should not be used as a prognostic guide to resuscitation. Coagulopathies Abnormal clotting frequently occurs in hypothermia, probably because cold inhibits the enzymatic coagulation cascade. not result from
[83]
Hypothermia-induced coagulopathy does
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excessive clot lysis, but rather from impaired clot formation. [16] Platelet function is also impaired during hypothermia because the production of thromboxane B 2 is inhibited. Hypothermia-induced platelet aggregation (HIPA) with or without neutrophil involvement has been associated with neurological dysfunction in patients undergoing surgical procedures. [12] Hypercoagulability with risks of thromboembolism may also occur, but the main importance of cold-induced coagulopathy is in patients with coincidental trauma. Such victims often have bleeding that is difficult to control. Replacement of appropriate clotting factors and use of warm blood may limit further blood loss and worsening of hypothermia. Trauma and Hypothermia Clearly, there is an increased mortality in trauma patients with temperatures below 32°C (89.6°F). It is not clear if this increased mortality is actually a result of hypothermia or whether hypothermia is merely an indicator of severe injury and response to a massive transfusion of cold fluid. [16] [84] [85] Patients with severe trauma are prone to hypothermia because their injuries often expose them to environmental heat loss. Concurrent alcohol intoxication may add to the heat loss owing to the vasodilatory effects on cutaneous vasculature and prolonged cold exposure secondary to altered mental status. Severe injury victims also lose heat because of exposure during resuscitation and rapid administration of cold fluids. The degree to which correcting the hypothermia improves outcome is unknown. Nevertheless, devices to rapidly infuse warm fluids such as the Level 1 fluid warmer (Level 1 Technologies, Rockland, MA) and the Thermostat 900 (Arrow International, Reading, PA) are frequently used to warm large volume fluid transfusions. These devices seem reasonable to prevent the hypothermia associated with massive transfusions (see Chapter 24 ). Their use in hypothermia not associated with severe trauma is limited by the relatively low fluid requirements of environmental exposure hypothermia.
PHARMACOTHERAPY AND MONITORING Hypothermia alters the pharmacodynamics of various drugs. It markedly alters drug kinetics, but not enough is known about this phenomenon to define specific therapeutic guidelines. Drug administration in the hypothermic patient must be done with caution ( Table 67-4 ). Because of the negative effects of hypothermia on both hepatic and renal metabolism, toxic levels of medications can accumulate rapidly after repeated use. Certain drugs, such as digitalis, should be avoided entirely. Sinus bradycardia and most atrial arrhythmias do not require pharmacological treatment as most resolve with rewarming. Transient ventricular dysrhythmias also do not require treatment. For those patients requiring medication for ventricular dysrhythmias, bretylium is the preferred agent, although lidocaine, magnesium, and propranolol have been used safely. [24] For severe acidosis (pH < 7.1), IV sodium bicarbonate can be used with extreme caution. Vasopressors should be used with caution, perhaps in much smaller doses than usual, because of the arrhythmogenic potential and the delayed metabolism. A review of ICU admissions for hypothermic patients found that treatment with vasoactive drugs was an independent risk factor for mortality, but this phenomenon remains poorly understood. [33] In
Clinical Situation
Medication
Hypoglycemia
D50 W
TABLE 67-4 -- Commonly Used Medications in Hypothermia Dosage 1 mg/kg IV
Alcoholic/Malnourished Thiamine
100 mg IV
Altered mental status
Naloxone
0.4 to 2 mg IV
Ventricular fibrillation
Bretylium*
5 mg/kg IV
Magnesium sulfate
100 mg/kg IV
*The role of more available antidysrhythmics such as amiodarone in hypothermia remains to be determined.
animal studies, use of epinephrine impaired myocardial efficiency in cases of moderate hypothermia. [86] There also was no advantage to repeated doses of epinephrine or high-dose epinephrine in the hypothermic cardiac arrest animal models. [87] The use of inamrinone (formerly known as amrinone) has been investigated in cases of deliberate mild hypothermia. Initial results indicate that amrinone accelerates the cooling rate of core temperature potentially limiting the usefulness in management of accidental hypothermia. [88] Intravenous fluids should be slowly administered to prevent fluid overload as a result of the decreased cardiac output. In addition, fluids should be started early because most hypothermic patients have intravascular volume depletion. Dextrose 5% with normal saline has been advocated as the ideal initial resuscitation fluid. [50] [56] Potassium should be avoided until electrolytes are measured and normal renal function is confirmed. Placement of a Swan-Ganz catheter and close monitoring of urinary output may assist in the fluid management of severely hypothermic patients. The risks of precipitating ventricular fibrillation should be weighed against the potential benefits of the Swan-Ganz catheter. Elevation of creatine phosphokinase in hypothermic patients may indicate rhabdomyolysis, and careful monitoring of renal function is essential. Aggressive fluid replacement may prevent the development of renal failure. Finally it should be emphasized that hypothermic patients exhibit a "physiologic" (and probably somewhat protective) hypotension, hypoventilation, depressed mental status, and bradycardia, the extent of which depends on the core temperature. This observation prohibits precise recommendation on the indications and use of medications, intubation, CPR, and other resuscitative interventions that are better defined in the normothermic patient. Hypothermic patients who present with a blood pressure, respiratory rate, or mental status that would prognosticate certain morbidity in normothermic patients may recover with minimal intervention to their normal pre-hypothermic state. The clinician should avoid aggressive therapies or medications that are aimed at providing the hypothermic patient with vital signs that would be desirable in the normothermic patient but which may be supraphysiologic in the hypothermic patient.
FROSTBITE Hypothermic patients frequently suffer other forms of cold-related injuries in addition to their systemic hypothermia. The mildest form of frostbite is termed frostnip, a condition that involves only the skin, sparing the subcutaneous tissues. The skin is blanched and numb, but the injury is immediately reversible with no permanent sequelae if the area is quickly
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rewarmed. Rapid rewarming should be done in a water bath at 40° to 42°C. Frostnip occurs most frequently on the distal extremities, the nose and ears. Nonfreezing temperatures also produce trenchfoot, an intermediate step in the progression to true frostbite. Trenchfoot is the result of prolonged immersion. Treatment involves rewarming followed by dry dressings. [89] [90] In frostbite, the body parts most susceptible are those farthest away from the body's core: the hands, feet, earlobes, and nose. Exposure of the fingers to severe cold leads to cold-induced vasodilation (CIVD). [91] [92] Apical structures rich with AVAs can shunt blood flow away from tissues. The pathophysiology of frostbite includes three pathways of tissue freezing: (1) through the extracellular formation of ice crystals, (2) hypoxia as a result of cold-induced local vasoconstriction, and (3) the release of inflammatory mediators. These pathways can and often do occur simultaneously, intensifying tissue damage. At the early stages of frostbite, the "hunting reaction" is observed whereby the body alternates between periods of vasoconstriction and vasodilation. As the temperature continues to decrease the reaction stops and vasoconstriction persists. [31] [90] Cold also increases blood viscosity, promotes vasospasm, and precipitates microthrombus formation. The release of inflammatory mediators prostaglandins PGF2 and thromboxane A2 that are found in blister fluid cause further vasoconstriction leading to cell death. The release of these mediators peaks during rewarming, and cycles of recurrent freezing and rewarming only increase their tissue levels. Rewarming must be avoided until refreezing can be prevented. The clinical signs and symptoms of frostbite vary according to the degree of injury. Although useful clinically, the degree classification does not predict the extent of further tissue damage. [31] [83] The appearance of the affected extremity will depend on the extent of the frostbite. In superficial frostbite, the affected extremity appears pale, waxy, and numb; has poor capillary refill; and is very painful on rewarming. In deeper frostbite, the affected extremity is hard, solid, and blanched. Hemorrhagic blisters may be present. Initially there is no pain or feeling in the frostbitten extremity. After rewarming, the affected area develops severe edema and blistering, eventually exhibiting dry gangrene and mummification, leading to tissue sloughing. Favorable prognostic signs for frostbite include intact sensation, normal color, warm tissues, early appearance of clear blisters, and edema. Unfavorable prognostic signs include no sensation, cold, cyanotic appearance, white "frozen" appearance, late appearance of hemorrhagic or dark blisters, and absence of edema. [93] Based on early bone scans and retrospective studies, researchers from France have proposed a new classification for predicting frostbite outcomes on day 0. [94] Four degrees of severity are defined. With first degree, there is complete recovery. Second degree often leads to soft tissue amputation. With third degree there is the need for bone amputation, and with fourth degree, there are systemic effects. [94] Rapid rewarming is the treatment of choice for frostbite. [89] [90] The aim is to limit the length of time the tissue remains in the frozen state. The most practical way to rewarm an extremity is to totally immerse the area in warm water at 40° to 42°C for 15 to 30 minutes. The affected area should be carefully protected to ensure that the tissue is not additionally injured through contact with the sides or rim of the container. After thawing, the area should be meticulously protected from injury. An extremity should be elevated and cotton or gauze placed between the toes/fingers to limit maceration. White or clear blisters should be debrided. Hemorrhagic or dark blisters should be left intact as disruption may cause damage to the vascular supply and viable tissue. The use of topical aloe vera (a thromboxane inhibitor) and systemic antiprostaglandins (such as ibuprofen) may be helpful. The use of semiocclusive dressings has shown promising results for management of deep frostbite injuries of the fingertips. [95] Tetanus prophylaxis should be provided. Adjuvant therapies involving the use of heparin or low-molecular-weight heparin, warfarin, vasodilators, corticosteroids, or immediate surgical sympathectomy have failed to improve outcomes. There has been mixed success with the use of hyperbaric oxygen and thrombolytics. [96] Agents that can inhibit the formation of free radicals are promising. These agents include superoxide dismutase, PGE1 analogues, and drugs containing antiplatelet activity such as pentoxifylline. [31] [90] The use of antibiotics is controversial, although some authors advocate agents with staphylococcus/streptococcus coverage (e.g., cephalosporins, pencillins). Debridement of tissue should be avoided in the ED. Patients should be given analgesics (IV opioids) as needed.
COLD WATER IMMERSION/SUBMERSION One of the leading causes of hypothermia remains cold water immersion/submersion. [97] In one retrospective review of accidental hypothermia cases in a three-year period, submersion hypothermia accounted for the greatest number of cases. [98] Unlike in cases of AH secondary to cold exposure, risk factors (both internal and external) are harder to identify secondary to the high mortality from drowning. [83] Studies have shown that at cold water temperatures (8°C), core cooling occurs at slower rates in persons with increased body mass and subcutaneous fat, and at faster rates when there is increased voluntary activity (e.g., treading water). Risk factors for submersion hypothermia include impaired performance and initial cardiorespiratory response to immersion. A study in healthy volunteers found that swimming efficiency and length of stroke decreases while rate of stroke and swim angle increases as the water temperature drops. [99] The body's response to cold-water immersion (head-out) has been previously described as occurring in three phases. [55] The initial phase involves the "cold-shock response," which typically occurs within the first 4 to 6 minutes. Signs include peripheral vasoconstriction, gasp reflex, hyperventilation, and tachycardia. At this stage, there is a higher incidence of sudden death resulting from hypocapnia, inability to breathhold, and increased cardiac output. [55] Following the initial cold shock response, the body undergoes profound cooling of the peripheral tissues. The peripheral cooling tends to be the greatest in the hands leading to incoordination and grasping difficulties. [55] In prolonged immersion in cold water, heat is lost from the body quicker than it is produced, thus predisposing to hypothermia. [100] In cases of cold-water submersion, researchers have found that rapid cooling is protective against neurological impairment and increases chances of survival. There are numerous reports in the literature of survival following cold-water submersion in children, but very few reports in adults. There are reports of survival following up to 66 minutes
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of cold water submersion.[101] Recently, there was a case report of survival in an elderly male following 22 minutes of submersion. [102] Overall, children tend to have a better prognosis because of the presence of the mammalian dive reflex, and a greater body surface area to mass ratio that allows for more rapid cooling. Orlowski identified five poor prognostic factors for near drowning in pediatric patients: (1) maximum submersion time >5 minutes, (2) comatose upon arrival to ED, (3) arterial blood gas pH 42°C), acute rhabdomyolysis, severe metabolic acidosis, disseminated intravascular coagulation, psychiatric and cognitive sequelae, renal failure, coma, seizures, and death have been described in these patients. [63] [64] [65] [66] [67] As demonstrated by Roberts and colleagues, even a patient with a core temperature of 114°F owing to acute cocaine intoxication may survive with aggressive cooling methods. [68] Treatment requires prompt recognition, maintenance of adequate hydration, rapid cooling (as outlined later), correction of metabolic acidosis, and the aggressive use of sedative or paralyzing agents, or both, to control agitation. Importantly, the longer that psychostimulant-overdosed patients remain hyperthermic, the higher their morbidity and mortality rates. Sudden unexpected death in a previously healthy individual is not uncommon if this syndrome is not aggressively treated. Agitation and seizures must be chemically controlled, as they lead to continued generation of heat and muscle injury. Physical restraint, without the use of chemical restraint, has been associated with increased mortality. Therefore, very liberal doses of benzodiazepines are recommended. [69] [70] [71] There is no maximum dose of benzodiazepines. Standard doses are generally ineffective and as much as 500 to 2000 mg of diazepam may be required to gain control of the patient. By the time such doses are required, however, muscular paralysis should have been instituted. Some have advocated the use of bromocriptine[71] and dantrolene [72] as for malignant hyperthermia and NMS, but their efficacy in the setting of drug-associated hyperthermia remains controversial. Hemorrhagic Shock and Encephalopathy Syndrome The condition of hemorrhagic shock and encephalopathy (HSE) in children (mainly infants, but some older children) resembles heatstroke in adults. The full-blown syndrome includes hyperthermia, coagulopathy, encephalopathy, and renal and hepatic dysfunction. [73] [74] [75] Although there may be an association with concurrent viral illness, the condition generally follows a temperature elevation, which may be triggered by the "bundling" of a child with a low-grade fever. Therapy is largely supportive and includes volume replacement and rapid cooling of the hyperthermic child while sources of bacterial infection are sought and treated.
COOLING TECHNIQUES The treatment of heat cramps, heat exhaustion, and other forms of hyperthermia are discussed earlier. The therapeutic
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objectives in patients with heatstroke are immediate cooling, the maintenance of adequate cardiorespiratory function, and support of all organ system functions. The basic function of all cooling measures is to transfer heat from the core, to the skin, to the environment, without compromising other physiologic functions. Cooling occurs via internal and external conduction techniques, and by convection and evaporation techniques. There have been no controlled studies comparing the effects of various commonly used techniques on cooling times or outcome in humans with heatstroke. Therefore, there are no totally agreed upon standards of care for empiric therapies that intuitively seem reasonable. Various techniques are discussed later, but the clinician should use the easiest and most logical technique as dictated by the specific clinical scenario and available logistical support. General Considerations Heatstroke mortality is proportional to the magnitude and duration of thermal stress measured in degree-minutes. [76] Delay in cooling may represent the single most important factor leading to death or residual disability in those who survive.[24] In addition, advanced age and underlying disease states are significant contributing factors. [12] [18] [19] Residual brain damage may occur in as many as 20% of survivors despite optimal treatment. The overall mortality rate may approach 50%. Many exertional heatstroke victims are volume-depleted and may present with hypotension. As a result, initial stabilization with cooled (room temperature) IV fluids and correction of electrolyte abnormalities are valuable in the hypotensive patient. Traditional sources recommend a rate of 1200 mL over the first 4 hours, [77] [78] whereas others advise a 2 L bolus over the first hour, with an additional 1 L/hour for the following 3 hours. [78] Seraj and colleagues [79] have challenged this more aggressive recommendation. In their study of pilgrims who suffered heatstroke, 65% had a normal or above normal central venous pressure (CVP) measurement on arrival. They found that an average of 1 L of saline was sufficient to normalize the CVP during the cooling period in their patients, who had a mean age of 55 years (range, 31 to 80 years). Hence, fluid resuscitation should be monitored carefully in older patients to avoid pulmonary edema. For heatstroke, there are no pharmacologic agents to accelerate cooling that are effective or that are associated with decreased morbidity or mortality. Specifically, dantrolene sodium is ineffective for heatstroke unassociated with malignant hyperthermia. Even in the latter setting, dantrolene sodium is an adjunct to direct cooling techniques. Regarding antipyretics, there is no known benefit for either salicylates or acetaminophen in the setting of heatstroke, as their efficacy depends on a normally functioning hypothalamus. In addition, overzealous use of acetaminophen could theoretically potentiate hepatic damage, and salicylates may promote bleeding tendencies. [15] [80] A study comparing acetaminophen and physical cooling methods found that in patients treated with antipyretics only, the mean body temperature increased by 0.2°C on average. [81] The role of immunomodulators, such as interleukin receptor antagonists, antibodies to endotoxin, or corticosteroids is unproven. Given that rapid cooling is accepted as the cornerstone of effective heatstroke therapy, the clinician must choose which cooling technique to use. Studies in animal models are based on the assumption that the fastest cooling technique is the best. In clinical patient care, other factors will also influence the choice of technique. Patient access, monitoring, safety, ease of use, and availability are all considerations, in addition to speed of cooling. A technique that may not be the most rapid but allows easy patient access and is readily available may be preferable to more cumbersome (albeit more rapid, once established) cooling techniques in some clinical settings. The cooling rates achieved in various human and animal studies of heatstroke are summarized in Table 68-2 . As experimental subjects and techniques vary, it is not surprising that reported cooling rates show considerable variation. The relative advantages and disadvantages of various cooling techniques are outlined in Table 68-3 . In addition to the cooling procedures outlined later, it is imperative that the clinician use judicious sedation and/or muscle paralysis to control agitation, suppress shivering, reduce energy expenditures, and to make the patient receptive to sometimes unpleasant therapies. [15] [21] [24] In general, IV benzodiazepines are the easiest and safest first-line drugs used for sedation. Indications for Rapid Cooling Rapid cooling should be instituted as soon as the diagnosis of heatstroke (rectal temperature >40°C, altered mental status, history of heat stress or exposure) is made. Rapid cooling is also indicated for the treatment of malignant hyperthermia and NMS but should be instituted concurrently with discontinuation of the triggering agent or drug and administration of dantrolene. Because studies show that the degree of organ damage correlates with the degree and duration of temperature elevation above 40°C, a reasonable clinical goal is to reduce the temperature to below 40°C within 30 minutes to an hour of the start of therapy. [12] [16] [24] There is no evidence to support a specific temperature end point at which cooling should be halted, but most series have halted aggressive cooling when the rectal temperature has dropped below 39.5°C.[25] Contraindications for Rapid Cooling Rapid cooling, per se, is never contraindicated in the presence of heatstroke. Immersion cooling is relatively contraindicated when cardiac monitoring of an unstable patient is required or when limited personnel make constant patient supervision impossible. Iced gastric lavage is contraindicated in patients with depressed airway reflexes unless the airway is protected by endotracheal intubation. Gastric lavage is also contraindicated by conditions that preclude placement of an orogastric or nasogastric tube. Cold peritoneal lavage is relatively contraindicated when multiple previous abdominal surgeries make placement of a lavage catheter risky owing to potential bowel perforation (see Chapter 44 ). Evaporative Cooling Evaporating water is thermodynamically a much more effective cooling medium than melting ice. Evaporating 1 g of water requires 540 kcal. Melting 1 g of ice requires only 80 kcal. In theory, therefore, evaporative cooling should be approximately seven times more efficient than ice packing. In practice, evaporative cooling is more efficient. [15] [82] In separate human studies, Wyndham et al. [83] and Weiner and Khogali [84]
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Technique Evaporative
TABLE 68-2 -- Cooling Rates Achieved with Various Cooling Techniques Author(s), Year
Model Rate (°C/min)
Weiner & Khogali, 1980
Human 0.31
Kielblock et al, 1986
Human 0.09
Wyndham et al, 1959
Human 0.034
Daily & Harrison, 1948
Rat
Weiner & Khogali, 1980
Human 0.14
Wyndham et al, 1959
Human 0.14
Magazanik et al, 1980
Dog
0.27
Daily & Harrison, 1948
Rat
1.86
Costrini, 1990
Human 0.15
Ice packing (whole body)
Kielblock et al, 1986
Human 0.034
Strategic ice packs
Kielblock et al, 1986
Human 0.028
Evaporative strategic ice packs
Kielblock et al, 1986
Human 0.036
Cold gastric lavage
Syverud et al, 1985
Dog
0.15
White et al, 1987
Dog
0.06
Bynum et al, 1978
Dog
0.56
White, 1993
Dog
0.14
Harris et al, 2001
Dog
0.5
Immersion (ice water)
Cold peritoneal lavage
Cyclic lung lavage
0.93
found evaporative cooling to be 1.5 to 2.2 times faster than ice water immersion. Studies in primate models demonstrated faster cooling rates using evaporative cooling as an adjunct to ice bag placement. [85] Methods using convection and evaporation were more effective than those involving conduction for the treatment of hyperthermia. [15] In clinical practice, ice water immersion or ice packing are commonly undertaken because it causes heat loss by conduction, as well as by heat consumption by the phase change of melting ice. In healthy volunteers, evaporative cooling techniques (e.g., facial fanning) were associated with decreased thermal sensation and improved thermal comfort. [86] Despite the continued enthusiasm of some clinicians for ice water immersion, evaporative cooling is the fastest noninvasive cooling technique in human studies.[13] [82] [86] To maximize evaporative cooling rates, several factors must be optimized. Air
Technique
TABLE 68-3 -- Advantages and Disadvantages of Various Cooling Techniques Advantages Disadvantages
Evaporative
Simple, readily available
Constant moistening of skin required
Noninvasive Easy monitoring and patient access Relatively fast Immersion
Noninvasive
Cumbersome
Relatively fast
Patient access and monitoring difficult
Low mortality rates reported
Shivering Poorly tolerated by conscious patients
Ice packing
Strategic ice packs
Cold gastric lavage
Noninvasive
Shivering
Readily available
Poorly tolerated by conscious patients
Noninvasive
Relatively slower cooling
Readily available
Shivering
Can be combined with other techniques
Poorly tolerated by conscious patients
Can be combined with other techniques
Relatively slower cooling Invasive Requires airway protection Human experience limited
Cold peritoneal lavage
Rapid cooling
Invasive Human experience limited
flow rates must be high (large fans are required). The air must be warm (but not humid), as evaporation is decreased at lower temperatures. The entire body surface must be exposed to airflow and continuously moistened with water (ideally the patient is suspended in a mesh sling to expose the back to airflow and moisture). Finally, the temperature of the water used to moisten the skin must be tepid (15°C). If the water is ice cold, evaporation will be slowed. Conversely, if it is hot, conductive heat gain may occur. Studies conducted in heat-stressed laying hens demonstrated superior cooling rates with ventral cooling regimes as compared to dorsal cooling. [87] Weiner and Khogali [84] have constructed a sophisticated "body cooling unit" (BCU) to maximize evaporative cooling. Patients in the BCU are suspended in a mesh net. High airflow rates (30 m/min) at temperatures of 45°C are maintained both anterior and posterior to the mesh net. Atomized water at
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15°C is continuously sprayed on all body surfaces. For emergency departments (EDs) without access to a BCU, temporary units can be set up using shower sprays and fans, providing the ambient temperature in the ED is relatively cool. [88] Dematte and colleagues recommend use of a body-cooling unit as a preferred technique for rapid cooling. [89] The realities of clinical practice make these conditions impossible to fully replicate. Half the body surface (the back) will usually be unavailable for evaporative cooling. Airflow rates and temperatures are usually limited by the ambient temperature in the treatment facility and by the size and power of the fan available. These realities are reflected in the slower cooling rates achieved with evaporative cooling in a clinical setting. Procedure
Evaporative cooling is accomplished by undressing the patient completely, positioning a fan or fans (usually at the foot of the bed or stretcher) as close to the patient as possible, and then sponging or misting the skin continuously with tepid 15°C water. A single care provider can continue the technique and monitor the patient once cooling has been initiated. It is important to keep as much body surface as possible moist and exposed to airflow. Covering sheets or clothing will impede skin evaporation and cooling. Complications
Complications of evaporative cooling are rare and more often attributed to the underlying disorder than to the cooling technique. Wet skin may interfere with electrocardiogram (ECG) monitoring, but this can usually be avoided by using electrodes on the patient's back. Shivering occurs infrequently with this technique when compared with other cooling techniques, because the water is relatively lukewarm. [88] [90] Because the rectal temperature lags behind the core (esophageal) temperature, evaporative cooling should be discontinued when the rectal temperature reaches 39°C. In cases of mild hyperthermia, tympanic temperatures also accurately reflect core temperatures and can be useful in this setting. [91] Continued cooling beyond this temperature may lead to subsequent "overshoot hypothermia" due to continued core temperature drop after active evaporative cooling is discontinued. Shivering indicates that the core temperature has decreased to 37°C or below. [20] Immersion Cooling In one of the first studies of heatstroke cooling techniques, Daily and Harrison demonstrated that rats with hyperthermia cooled faster with ice water immersion than with evaporative cooling. [92] Some contemporary sources continue to recommend ice water immersion as the cooling technique of choice for heatstroke. [89] [93] Plattner and colleagues[93] demonstrated cooling rates with ice-water immersion that were six times faster than rates seen with forced air or circulating water. Costrini and colleagues [95] reported no fatalities in 252 consecutive young marine recruits who were treated for exertional heatstroke over a 15-year period with ice water immersion within 20 minutes of diagnosis. They regard ice water immersion as superior in reducing mortality rates when compared to other conventional methods described in the literature. Overall, in clinical trials, cold water immersion remains the second fastest noninvasive cooling technique available (see Table 68-2 ). In situations where an adequate evaporative cooling system is not available, immersion may be the cooling technique of choice. Several factors are important in maximizing the rate of immersion cooling. Conductive heat loss is dependent on cutaneous blood flow to maintain a heat gradient from skin to water. Theoretically, contact with ice water causes skin and subcutaneous (SQ) vasoconstriction, blocking heat exchange and turning these structures into insulators. [96] Intense cutaneous vasoconstriction will impede conductive heat loss. Mekjavic et al. [97] reported that motion sickness actually potentiates core cooling during immersion by attenuating the vasoconstrictor response to skin and core cooling, thereby augmenting heat loss and the magnitude of the decrease in deep body temperature. Careful monitoring is required because this may predispose patients to hypothermia. Magazanik et al. [98] in a canine study, suggested that warmer water (15°C) may actually cool faster than ice water (0°C). The optimal water temperature for cooling human heatstroke patients has not been defined. Regardless of the water temperature, it is clear that increasing surface area increases conductive heat loss. Maximizing the body surface area in contact with the water will increase cooling rates with immersion cooling. In clinical practice, this means that complete immersion of the trunk and extremities will cool the patient faster than partial immersion of the trunk (back only) with the extremities extended out of the bath. Procedure
Immersion cooling is accomplished by undressing the patient completely before transfer to a tub of water of a depth sufficient to cover the torso and extremities. Various water containers have been used. A regular bathtub, if available, can be used. Most clinical reports describe tubs that can be moved to the emergency treatment area when needed. A child's plastic wading pool and a decontamination tub or stretcher with waterproof sides and drainage capability are examples of the latter approach. The patient's head must be continuously supported out of the bath. In cases where tubs are unavailable, patients can be placed on water impermeable sheets and placed in a sling apparatus while ice and water are poured into the sling. [89] Temperature and ECG leads must be securely attached to the patient if monitoring is to be continued during immersion. The patient is removed from the bath when the rectal temperature reaches 39°C, because core temperature will continue to drop for a short period, even after the patient is removed. An electronic temperature monitor with a long flexible rectal probe is useful for continuous temperature monitoring during immersion. Studies show that rates of cooling close to 1°C per minute can be achieved. [23] Complications
The common complications of immersion cooling are patient shivering, cutaneous vasoconstriction, patient discomfort, and the loss of monitoring capability. Shivering generates considerable heat through muscle metabolism. Cutaneous vasoconstriction impedes conductive heat loss. If significant shivering does occur, it can be reduced with benzodiazepine agents such as diazepam. Although the use of phenothiazines such as chlorpromazine has been advocated for shivering in the past, their use is currently discouraged because they also may impair heat loss by their anticholinergic effects on sweat glands, contribute to hypotension via a-adrenergic blockade, lower the seizure threshold, and cause dystonic reactions. In addition, they possess central dopamine-blocking effects
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that may exacerbate symptoms of NMS.[53] Benzodiazepines are also valuable if the patient is hyperthermic secondary to sympathomimetic agents such as cocaine. Magazanik et al. [98] also suggested that warmer water temperatures (15°C) minimize shivering and increase cutaneous blood flow, thereby increasing cooling rates. DeWitte and Sessler [99] reported that shivering occurs only as the body's final defense after maximal arteriovenous shunt vasoconstriction and behavior modifications have proved to be insufficient in maintaining core temperature. Shivering typically occurs after temperatures fall below 37°C. [20] Patient monitoring is a problem under water. Electrodes can be used on the nonimmersed upper shoulders. ECG artifact often becomes a major problem during vigorous shivering. Immersion cooling is not recommended for patients with unstable cardiac rhythms or patients who are at risk for developing these rhythms. A significant change in cardiac rhythm might go undetected during the labor-intensive process of immersion cooling. Patient access for resuscitative procedures is also a major problem with this technique. Should the patient develop ventricular fibrillation, he or she must be removed from the bath and dried prior to defibrillation. Invasive and diagnostic procedures (e.g., IV access, radiography) cannot be performed during the cooling period. Care must be taken to avoid displacement of IV lines during placement in and removal from the bath. As body temperature drops, mental status will improve in many heatstroke victims. When awake, most people find ice water immersion difficult to tolerate. IV sedation may be required. Finally, this technique is labor-intensive. Several caregivers must be present throughout the process. The patient's head must be maintained out of the bath. If massage is used, one or more individuals will need to immerse their own hands in water to continuously massage the patient. Medications should be given IV, and constant attention to temperature and ECG monitors is also necessary. This cooling technique should be used only if adequate personnel are available. Whole-Body Ice Packing Packing the heatstroke victim in ice may enhance conductive heat loss without the attendant logistical problems caused by water immersion ( Fig. 68-1 ). Constant attendance, as required for skin moistening with evaporative cooling and as described for immersion cooling, may not be necessary with ice packing. Kielblock et al.[100] demonstrated in a human study of mild, exercise-induced hyperthermia that whole-body ice packing cooled just as fast as evaporative cooling (see Table 68-2 ). Procedure
Whole-body ice packing is accomplished by undressing the patient completely and then covering the extremities and torso with crushed ice. As with any cooling technique, constant temperature monitoring using an electric thermometer and a long, flexible rectal probe is recommended. A large supply of crushed ice will be needed whenever this technique is used. Logistically, ice packing may be problematic. Whole-body ice packing can usually be performed on the ED stretcher without additional equipment. Ideally the patient is placed in a container that facilitates ice contact with the skin and
Figure 68-1 It is absolutely essential to rapidly lower the core temperature of a severely hyperthermic patient by instituting cooling techniques as soon as possible. Evaporative cooling (see text) is usually quite effective and technically easy. An alternative approach, albeit poorly studied, is to literally pack the patient in ice. In this case, plastic trash bags were used to hold the ice and to prevent water from dripping on the floor. A child's plastic wading pool is another option for this ice packing technique.
prevents water from dripping onto the floor. This is best accomplished by placing the patient in a child's lightweight plastic pool, which is available in toy stores. Lacking this equipment, plastic cloths or trash bags may be placed under the patient with the edges curled up to form a slinglike apparatus. As with immersion cooling, ECG monitoring can be potentially difficult owing to shivering artifact and displacement of electrodes. Alert patients usually do not tolerate ice packing well, and IV sedation or restraint is usually required. Excessive shivering can be treated with benzodiazepines if the rate of cooling is decreased. The ice is removed, and the patient dried off, when the rectal temperature reaches 39°C. Strategic Ice Packs Noakes has suggested that selective placement of ice packs over areas of the body where large blood vessels run close to the skin may be an effective cooling technique. [101] Cooling in these areas occurs despite cutaneous vasoconstriction, owing to direct conductive heat loss from the blood within the vessel, across the vessel wall, subcutaneous tissue, and skin to
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the ice. The most common areas used for strategic ice packing are the anterior neck (carotid and jugular vessels), the axilla (axillary artery and vein), and the groin (femoral vessels). There have been numerous reports of successful cooling using ice packs as primary or adjunctive therapy (see Table 68-2 ). [88] [89] [101] In addition, application of ice packs, although easier to perform than immersion or total-body ice packing, limits the conductive cooling offered by the latter two procedures. [102] However, a study in pigtail monkeys demonstrated that a combination of strategic ice packs with evaporative cooling resulted in faster cooling than either technique alone, although the relative increase achieved by adding ice packs to evaporative cooling was small. [103] In unconscious patients or in awake patients who can tolerate ice packs without excessive shivering, this technique could be added to evaporative cooling. However, the clinical value of strategic ice packs alone or in combination with other techniques remains to be determined. Anecdotally, during the Chicago heat wave of 1995, the majority of heatstroke patients who presented to EDs survived after being effectively cooled using the evaporation method accompanied by strategic placement of ice packs. Procedure
This technique is best accomplished by placing large plastic bags filled with crushed ice or an ice water mixture in both axillae and over both femoral triangles. Do not diminish the effectiveness of the ice packs by wrapping them in towels—apply them directly to the patient. If the neck is used, the packs must be placed laterally, with care taken not to compress the trachea or apply excessive weight over the carotid arteries. The neck area should probably not be packed in the presence of carotid bruits or a history of cerebrovascular disease. Some sources advocate rubbing the body surface briskly with plastic bags containing ice after the body has been wet down with water. This is effective, provided it is combined with evaporation therapy. [21] Complications
Complications of strategic ice packing are limited to shivering and patient discomfort as described previously for whole-body ice packing. The ice packs are removed when the rectal temperature reaches 39°C to avoid excessive core temperature drop. Prolonged direct contact with ice can produce cold injury. However, if the temperature is monitored and the ice packs are removed as soon as the target temperature is reached, such injury is unlikely. External vs Core Cooling All of the external cooling techniques described previously are noninvasive and use heat loss by evaporation or conduction across the skin as the primary cooling mechanism. With each of these techniques, dropping of the central temperature will continue even after the technique is discontinued and the skin is dried. This is due to a delay in the establishment of an equilibrium between the cold skin and the core. The amount of "core after-drop" can exceed 2°C. [93] For this reason, cooling is discontinued when the core temperature reaches 39°C. Because the sites of significant cell damage with heatstroke are centrally located (e.g., liver, kidney, heart), central cooling techniques theoretically are preferable to external techniques. Core cooling techniques studied in both animal and human models include iced gastric lavage, intravascular cooling, bladder lavage, and peritoneal lavage. [93] [104] [105] [106] [107] Central venous cooling is effective in rapidly decreasing core temperatures. [108] Studies conducted in healthy volunteers demonstrated reductions of core temperatures varied according to the temperature of the infused fluid. Subjects receiving 30-minute infusions of fluid at 4°C experienced decreases in core temperatures of 2.5° ± 0.4°C. Subjects receiving 30-minute infusions of fluid at 20°C experienced decreases of 1.4°C (±0.2°C). [108] Clinical trials investigating cooling via the respiratory tract had no significant impact on temperature changes when used exclusively, yet demonstrated effectiveness as an adjunctive measure to other external cooling techniques. [91] Cool air (10°C) was administered via a hood or mask. Cooling via the respiratory tract has been studied in animals but not investigated clinically. [91] Central cooling techniques are necessarily more invasive than external techniques and therefore have the potential for more significant complications. Cold Gastric Lavage The stomach lies in close proximity to the liver, great vessels, kidneys, and heart. The gastric mucosa is not subject to the intense vasoconstriction observed on skin exposure to ice water. [109] For these reasons, lavage of the stomach might be expected to be an effective central cooling method. In one human trial, lavage with ice water at a rate of 500 mL/10 minutes was associated with increased abdominal cramping and diarrhea. [93] Human heatstroke victims have been successfully cooled with gastric lavage, but only in combination with external techniques. In practice, this technique is rarely used. Cold gastric lavage seems best suited for use in patients with severe hyperthermia who are cooling at a slow rate with external techniques alone. The presence of an endotracheal tube and the passage of a large-bore gastric tube make rapid lavage without aspiration possible. This technique should be reserved for patients whose airways are protected by endotracheal intubation and who do not have contraindications to gastric tube placement (see Chapter 41 Chapter 42 Chapter 43 ). Procedure
Cold gastric lavage is best accomplished by instilling 10 mL/kg of iced tap water into the stomach as rapidly as possible (usually over 30 to 60 seconds). After a 30- to 60-second dwell time, the water is removed by suction or gravity. [107] Cooling will theoretically be faster if a high temperature gradient is maintained in the stomach. To this end, the lavage should proceed quickly. A faster lavage rate is usually maintained if suction is used to withdraw instilled fluid. A large container of ice-temperature water maintained 1 to 1.5 m above the patient's body will facilitate instillation of fluid. This container should be directly connected to the lavage tubing and should ideally allow passage of water but not ice, which may occlude the tube. Since large volumes of water are needed, it is helpful if ice can be added to the container without interrupting the lavage. A large syringe can be used as an alternative to gravity instillation, but this is usually slower. A simple system that accomplishes this procedure can be devised from readily available equipment in most EDs. A standard lavage setup (for use in drug overdoses) and a large-bore gastric tube are used. The lavage bag is cut open at
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the top to allow water and ice to be added. It is then suspended above the patient's body and connected to the orogastric tube by Y tubing with clamps. The other arm of the Y tubing is connected to suction. Using the clamps, ice water can intermittently be instilled by gravity and withdrawn by suction. Complications
A major potential complication of cold gastric lavage is pulmonary aspiration. The use of a cuffed endotracheal tube minimizes the incidence of this complication. Owing to the large volume of water used and the frequent depression of airway reflexes seen with severe heatstroke, this technique should rarely be used in a patient who is not endotracheally intubated. If tap water is used, water intoxication, hyponatremia, and other electrolyte disturbances are potential complications particularly in pediatric or geriatric patients. Water is absorbed from the stomach and, with large-volume lavage, may pass the pylorus into the small intestine. In canine studies, large-volume gastric lavage with tap water did not cause electrolyte abnormalities. [110] The actual incidence of these potential complications in human heatstroke has not been determined. The use of normal saline instead of tap water would eliminate this potential problem. Theoretically, the passage of cold water through the esophagus, located directly behind the heart, has the potential to induce cardiac dysrhythmias. Dysrhythmias have not been observed in canine studies or in case reports of human heatstroke victims cooled with this technique. [109] [110] Cold Peritoneal Lavage The surface area and blood flow of the peritoneum greatly exceed those of the stomach. Peritoneal lavage is therefore expected to exchange heat much faster than gastric lavage. Peritoneal lavage demonstrates some of the fastest cooling rates ever reported in large animal or human studies (see Table 68-2 ). A case report of cold peritoneal lavage cooling for hyperthermia following ecstasy ingestion demonstrated rapid cooling. [111] As with gastric lavage, this central cooling technique offers the advantage of directly cooling the core organs that are most susceptible to thermal damage. Unlike with gastric lavage, endotracheal intubation is not required. Peritoneal lavage is used extensively to treat hyperthermia under various conditions and typically decreases core temperatures 5°–10°C/hour. [93] [104] [111] Peritoneal lavage is a more invasive cooling technique. Surgical placement of the lavage catheter is necessary. Since heat exchange is more efficient across the peritoneum, smaller volumes of fluid can be used. This cooling technique is relatively contraindicated by conditions that preclude placement of a lavage catheter (e.g., multiple abdominal surgical scars) (see Chapter 44 ). Peritoneal lavage is the most rapid central cooling technique. It can theoretically be combined with other techniques to speed cooling of the heatstroke patient with refractory hyperthermia. Being the most invasive cooling technique, it requires time, proper equipment, and surgical expertise to institute. Although effective, it is seldom used in clinical practice. Its use is probably best suited to situations in which heatstroke patients are not responding to external cooling and adequate equipment and personnel are readily available. Procedure
To institute peritoneal lavage cooling, 2 to 8 L of sterile saline is immersed in an ice water bath to cool while the catheter is being placed. A standard peritoneal lavage catheter (as for diagnostic use in trauma patients) is placed using any of the techniques described in Chapter 44 . Standard contraindications apply. Use of a larger peritoneal dialysis catheter may speed fluid instillation and withdrawal. Actual lavage volumes and rates have not been established. One approach is to instill and withdraw 500 to 1000 mL every 10 minutes until adequate cooling is achieved. Rectal temperature may be falsely low during the lavage owing to the presence of cold water about the rectum at the level of the rectal temperature probe. [107] [112] It may be preferable to monitor tympanic membrane or esophageal temperature when using this technique. The lavage is discontinued when core temperature reaches 39°C to avoid excessive core temperature after-drop. Complications
The potential complications of peritoneal lavage cooling are primarily related to placement of the catheter and include bowel or bladder perforation and placement into the rectus sheath rather than the peritoneum. These potential problems are discussed further in Chapter 44 . Other Cooling Techniques Although high-frequency jet ventilation (HFJV) causes core cooling in critically ill patients, [114] efforts to use the respiratory tract to cool heatstroke victims have been unsuccessful. In a canine model of heatstroke, the use of HFJV is shown to be a relatively ineffective cooling technique. [115] Heat loss by convection (air transfer) is relatively inefficient compared with the conductive heat loss mechanism used by other cooling techniques. The use of dry, hot air to maximize evaporative heat loss from the lungs might cause respiratory complications. [114] In human trials, ice water lavage of the bladder (300 mL iced Ringer's solution/10 min) provided only minimal cooling with rates of 0.8°C (±0.3°C) per hour. [93] Iced water lavage of the rectum would theoretically provide faster cooling rates secondary to the increased surface area and better perfusion; however, it has not been investigated in human trials. [94] Hemodialysis or partial cardiopulmonary bypass could theoretically be used to cool heatstroke patients. Before the availability of dantrolene in 1979, partial cardiopulmonary bypass was one treatment for malignant hyperthermia. [105] Its specific use in management of heatstroke has not been studied. Drawbacks could potentially include lack of technical expertise as well as preparation time for the procedure. Cyclic lung lavage using cold perflurochemical lung lavage in animal models is currently under investigation. Benefits include rapid cooling rates of 0.5°C per minute and are minimally invasive in the already mechanically ventilated subject. [116] [117] [118] In addition to physical cooling techniques, pharmacological agents have demonstrated merit as adjunctive agents in the management of hyperthermia. There are anecdotal reports of enhanced temperature reduction using intravenous ketoralac. In a recent study, Cienki and colleagues [119] demonstrated enhanced temperature decreases using ketorolac, 30 mg IV. All patients received standard treatment for
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hyperthermia (e.g., ice packs, iced lavage, circulating air). Patients were randomized to receive ketorolac versus saline. In the group receiving ketorolac, the average rectal temperature after 90 minutes was two times lower than that of those receiving placebo saline (3.7°F vs 1.6°F).
SUMMARY Rapid cooling is the key step in the emergency management of heatstroke patients. Survival approaches 90% when elevated temperatures are lowered in a timely fashion.[19] [27] The highest documented temperature in the medical literature with survival is 48.8°C (115°F). In this case, the patient was rapidly cooled and recovered without neurologic sequelae. [34] Evaporative cooling appears to be the technique of choice. It combines the advantages of simplicity and noninvasiveness with the most rapid cooling rates achieved with any external technique. It is also logistically easier to institute, maintain, and monitor evaporative cooling than any other cooling technique. If a patient is not cooling rapidly with evaporative cooling, other techniques can be added. Ice packing or strategic ice packing is a common alternative technique that can be rapidly instituted in any ED. If the patient is endotracheally intubated, gastric lavage can be instituted. If facilities and personnel are available, peritoneal lavage cooling can be used as a rapid central cooling technique. If muscle rigidity is present or malignant hyperthermia is suspected, dantrolene sodium should be administered. In addition, the clinician should have a heightened index of suspicion for NMS and sympathomimetic drug toxicity. Regardless of the cause, a reasonable clinical goal is to reduce the rectal temperature to 40°C or below within 30 minutes of instituting therapy. [89] Immersion cooling is best limited to centers with the proper equipment and skilled medical personnel experienced in managing hyperthermic patients. This method may also be effective in conditions in which electric power for evaporative cooling is unavailable (e.g., in wilderness settings where bodies of cool water are available nearby and the victim is far from more sophisticated medical care). Central venous cooling with iced saline is a promising cooling technique for rapid cooling for severe hyperthermia. Other cooling techniques require further study before a clear recommendation as to their efficacy can be made.
Acknowledgments
The authors wish to acknowledge and thank Dwight E. Helmrich and Scott A. Syverud for their valuable contributions and authorship in previous editions.
References 1. Wolfe
MI, Kaiser R, Naughton MP, et al: Heat-related mortality in selected United States cities, summer 1999. Am J Forensic Med Pathol 22:352, 2001.
2. McGeehin
MA, Mirabelli M: The potential impacts of climate variability and change on temperature-related morbidity and mortality in the United States. Environ Health Perspect 109:185, 2001.
3. Heat-related 4. Centers
for Disease Control and Prevention. Heat-related deaths—Los Angeles County, CA, 1999–2000, and United States, 1979–1998. JAMA 286:911, 2001.
6. Heat-related 7. Taylor
mortality—Chicago, July 1995. MMWR Morb Mortal Wkly Rep 44:577, 1995.
AJ, McGwin G: Temperature-related deaths in Alabama. South Med J 93:787, 2000.
8. Hopkins 9. Khan
illnesses and deaths: 1994–1995. MMWR Morb Mortal Wkly Rep 44:465, 1995.
PM: Malignant hyperthermia: Advances in clinical management and diagnosis. Br J Anaesth 85:118, 2000.
M, Farver D: Recognition, assessment and management of neuroleptic malignant syndrome. S D J Med 53:395, 2000.
10.
Tobin JR Jason DR, Chally VR, et al: Malignant hyperthermia and apparent heatstroke. JAMA 286:168, 2001.
11.
Pham JV, Puzantian T. Ecstasy: Dangers and controversies. Pharmacotherapy 21:1561, 2001.
12.
Worfolk J: Heat waves: Their impact on the health of elders. Geriatric Nurs 21:70, 2000.
13.
McGugan EA: Hyperpyrexia in the ED. Emerg Med 13:116, 2001.
14.
Webb P: The physiology of heat regulation. Am J Physiol 268:R838, 1995.
15.
Axelrod P: External cooling in the management of fever. Clin Infect Dis 31:5224, 2000.
16.
Waters TA: Heat illness: Tips for recognition and treatment. Cleve Clin J Med 68:685, 2001.
17.
Dearing J: Exertional heat illness. Lancet 355:1993, 2000.
18.
Kalkstein LS: Saving lives during extreme weather in summer. Br Med J 7262:650, 2000.
19.
Kare J, Shneiderman A: Hyperthermia and hypothermia in the older population. Topics Emerg Med 23:39, 2001.
Noakes TD: Disturbances due to heat; heatstroke; heat Illness without evidence for internal thermoregulatory failure. In Rakel RE: Conn's Current Therapy, 53rd ed. Philadelphia, WB Saunders, 2001, p 1171. 20.
21.
Gaffin SL, Moran DS: Pathophysiology of heat-related illnesses. In Auerbach PS (ed): Wilderness Medicine, 4th ed. St. Louis, Mosby, 2001, p 240.
22.
Noakes TD: Fluid and electrolyte disturbances in heat illness. Int J Sports Med 19:S146, 1998.
23.
Hett HA, Brechtelsbauer DA: Heat-related illness. Plan ahead to protect your patients. Postgrad Med 103:107, 1998.
24.
Yoder E: Disorders due to heat and cold. In Goldman L: Cecil Textbook of Medicine, 21st ed. Philadelphia, WB Saunders, 2001, p 513.
25.
Bouchama A, Knochel JP: Heat Stroke. N Engl J Med 346:1978, 2002.
26.
Barrow MW, Clark KA: Heat-related illnesses. Am Fam Physician 58:749, 1998.
27.
Khosla R, Guntapalli KK: Heat-related illnesses. Crit Care Clin 15:251, 1999.
28.
Epstein V, Shani Y, Moran OS, et al: Exertional heat stroke—the prevention of a medical emergency. J Basic Clin Physiol Pharmocol 11:395, 2000.
29.
Samarasinghe JL: Heatstroke in young adults. Trop Doct 31:217, 2001.
Krueger-Kalinski MA, Schriger DL, Friedman L, et al: Identification of risk factors for exertional heat-related illnesses in long-distance cyclists: Experience from the California AIDS Ride. Wilderness Environ Med 12:81, 2001. 30.
31.
Cavaliere F, Di Filippo F, Botti C, et al: Peritonectomy and hyperthermic antiblastic perfusion in the treatment of peritoneal carcinomatosis. Eur J Surg Oncol 26:486, 2001.
32.
Ceelen WP, Hesse V, de Hemptinine B, et al: Hyperthermic intraperitoneal chemoperfusion in the treatment of locally advanced intra-abdominal cancer. Br J Surg 87:1006, 2000.
33.
Matsui Y, Nakagawa A, Kamiyama Y, et al: Selective thermocoagulation of unresectable pancreatic cancers by using radio frequency capacitive heating. Pancreas 20:14, 2000.
34.
Birrer RB: Heat stroke: Don't wait for the classic signs. Emerg Med 26:43, 1994.
35.
Eshel GM, Safar P, Stezoski W: The role of the gut in the pathogenesis of death due to hyperthermia. Am J Forensic Med Pathol 22:100, 2001.
36.
Bouchama A, DeVol EB: Acid-base alterations in heatstroke. Intensive Care Med 27:680, 2001.
37.
Bolster D, Tappe S, Short K, et al: Effects of cooling on thermoregulation during subsequent exercise. Med Sci Sport Exercise 31:251, 1999.
38.
Booth J, Marino F, Ward J: Improved running performance in hot humid conditions following whole body precooling. Med Sci Sport Exercise 29:943, 1997.
39.
Nelson TE. Heat production during anesthetic-induced malignant hyperthermia. Biosc Rep 21:169, 2001.
Bendahan D, Kozak-Ribbon G, Comfor-Goudy S, et al: A non-invasive investigation of muscle energetics supports similarities between exertional heat stroke and malignant hyperthermia. Anesth Analg 93:683, 2001. 40.
1369
Schneider C, Pedrosa F, Gil F, et al: Intolerance to neuroleptics and susceptibility for malignant hyperthemia in a patient with proximal myotonic myopathy(promm) and schizophrenia. Neuromuscul Disord 12:31, 2002. 41.
42.
Wappler F: Malignant hyperthermia. Eur J Anaesthesiol 18:632, 2001.
43.
Igardi T, Christensen UC, Jacobsen J, et al: How do anaesthesiologists treat malignant hyperthermia in a full-scale anaesthesia simulator? Acta Anaesthesiol Scand 45:1032, 2001.
Roberts MC, Mickelson JR, Patterson EE, et al: Autosomal dominant canine malignant hyperthermia is caused by a mutation in the gene encoding the skeletal muscle calcium release channel (RYR1). Anesthesiology 95:716, 2001. 44.
45.
Horowitz BZ: Serotonin syndrome. http://www.emedhome.com/archives.cfm.
46.
Moran D, Epistein Y, Wiener M, et al: Dantrolene and recovery for heatstroke. Aviat Space Environ Med 70:978, 1999.
47.
Zuckerman GB, Singer LP, Rubin OH, et al: Effects of dantrolene on cooling and cardiovascular parameters in an immature porcine model of heatstroke. Crit Care Med 25:135, 1997.
48.
Channa AB, Seraj MA, Saddique AA, et al: Is dantrolene effective in heat stroke patients? Crit Care Med 189:290, 1990.
49.
Bouchama A, Cafege A, Derol EB, et al: Ineffectiveness of dantrolene sodium in the treatment of heatstroke. Crit Care Med 20:1192, 1992.
50.
Orser B: Dantrolene sodium and heatstroke. Crit Care Med 20:1192, 1992.
51.
Louis CF, Balog EM, Fruen BR. Malignant hyperthermia: An inherited disorder of skeletal muscle at regulation. Biosci Rep 21:155, 2001.
52.
Ong KC, Chew El, Ong YY: Neuroleptic malignant syndrome without neuroleptics. Singapore Med J 42:85, 2001.
53.
Susman VL: Clinical management of neuroleptic malignant syndrome. Psychiatr Q 72:325, 2001.
54.
So PC, Neuroleptic malignant syndrome induced by droperidol. Hong Kong Med S7:101, 2001.
55.
Wang HC, Hsieh Y: Treatment of neuroleptic malignant syndrome with subcutaneous apormorphine monotherapy. Mov Disord 16:765, 2001.
56.
Heimann-Patterson TD: Neuroleptic malignant syndrome and malignant hyperthermia: Important issues for the medical consultant. Med Clin North Am 77:477, 1993.
57.
Russel CS, Lang C, McCambridge M, et al: Neuroleptic malignant syndrome in pregnancy. Obstet Gynecol 98:906, 2001.
58.
Nisigima K, Shigaro T: Does dantrolene influence central dopamine and serotonin metabolism in neuroleptic malignant syndrome? Biol Psychiatry 33:5, 1993.
59.
Rosenburg MR, Green M: Neuroleptic malignant syndrome—Review of response to therapy. Arch Intern Med 149:1927, 1989.
60.
Isbister GK, Dawson A, Whyte IM: Citalpram overdose, serotonin toxicity, or neuroleptic malignant syndrome? Can J Psychiatry 46:657, 2001.
61.
Demers JC, Malone M. Serotonin syndrome induced by fluvoxamine and mirtazapine. Ann Pharmacother 35:1217, 2001.
62.
Mills KC: Serotonin syndrome. Crit Care Clin 13:763, 1997.
63.
Milroy CM: Ten years of ecstasy. UR Soc Med 92:68, 1999.
64.
Dar KJ, McBrian ME: MDMA-induced hyperthermia: Report of a fatality and review of the current literature. Intensive Care Med 22:995, 1996.
65.
Teter CJ, Guthrie SK. A comprehensive review of MDMA and GHB: Two common club drugs. Pharmacotherapy 21:1486, 2001.
66.
Armstrong LE, Hubbard RW: Application of a model of exertional heat stroke pathophysiology to cocaine intoxication. Am J Emerg Med 8:178, 1990.
67.
Daras M, Kakkouras L, Tuchman AJ, et al: Rhabdomyolysis and hypothermia after cocaine abuse: A variant of the neuroleptic malignant syndrome. Acta Neurol Scand 92:161, 1995.
68.
Roberts JR, Quattrocchi E, Howland MA: Severe hyperthermia secondary to intravenous drug abuse. Am J Emerg Med 2:373, 1984.
69.
Henry JA. Metabolic consequences of drug misuse. Br J Anaesth 85:36, 2000.
70.
Tanvetyanon T, Dissin J, Selcer UM: Hyperthermia and chronic pancerebellar syndrome after cocaine abuse. Arch Intern Med 161:608, 2001.
71.
Vasallo SU: Pharmacologic effects on thermoregulation: Mechanisms of drug-related heatstroke. Clin Toxicol 27:199, 1989.
72.
Singarajah C, Lavies NG: An overdose of ectasy: A role for dantrolene. Anaesthesia 47:686, 1992.
73.
Sofer S, Phillip M, Hershkowits J, et al: Hemorrhagic shock and encephalopathy: Its association with hyperthermia. Am J Dis Child 140:1252, 1986.
74.
Weibley RE, Pimentel B, Ackerman NB: Hemorrhagic shock and encephalopathy syndrome of infants and children. Crit Care Med 17:335, 1989.
75.
Whittington LK, Roscelli JD, Parry WH: Hemorrhagic shock and encephalopathy: Further description of a new syndrome. Pediatrics 106:599, 1985.
76.
Gaffin SL, Gardner JW, Flinn S: Cooling methods for heatstroke victims. Ann Intern Med 132:678, 2000.
77.
Convertino VA, Armstrong LE, Coyle EF, et al: American college of sports medicine position stand. Exercise and fluid replacement. Med Sci Sports Exerc 28:1, 1996.
78.
Shapiro Y, Seidman DS: Field and clinical observations of exertional heat stroke patients. Med Sci Sports Excerc 22:6, 1990.
Seraj MA, Channa AB, Al Harthi SS, et al: Are heat stroke patients fluid depleted? Importance of monitoring central venous pressure as a simple guideline for fluid therapy. Resuscitation 21:33, 1991. 79.
80.
Plaisance KI: Toxicities of drugs used in the management of fever. Clin Infect Dis 31:S224, 2000.
81.
Henker R, Rogers S, Kramer DJ, et al: Comparison of fever treatments in the critically ill: A pilot study. Am J Crit Care 10:276, 2001.
82.
Graham B: Features and outcomes of classic heat stroke. Ann Intern Med 130:613, 1999.
83.
Wyndham CH, Strydom NB, Cookett M, et al: Methods of cooling subjects with hyperpyrexia. J Appl Physiol 14:771, 1959.
84.
Weiner JS, Khogali M: A physiological body-cooling unit for treatment of heat stroke. Lancet 1:507, 1980.
85.
Eshel GM, Safar P, Stezoski W: Evaporative cooling as an adjunct to ice bag use after resuscitation from heat-induced arrest in a primate model. Pediatr Res 27:264, 1990.
86.
Kato M, Sugenoya J, Matsumoto T, et al: The effects of facial fanning on thermal comfort sensation during hyperthermia. Pflugers Arch 443:175, 2001.
87.
Wolfenson D, Bachrach D, Mamam M, et al: Evaporative cooling of ventral regions of the skin in heat-stressed laying hens. Poult Sci 80:958, 2001.
88.
Ndukwu I, Dematte J, O'Mara K: Features and outcomes of classic heatstroke. Ann Intern Med 130:614, 1999.
89.
Dematte J, O'Mara K, Buescher J, et al: Near-fatal heatstroke during the 1995 heat wave in Chicago. Ann Intern Med 129:173, 1998.
90.
Bross MH, Nash BT Jr, Carlton FB Jr: Heat emergencies. Am Fam Physician 50:389, 1994.
91.
Desruelle AV, Candad V: Thermoregulatory effects of three different types of head cooling in humans during a mild hyperthermia. Eur J Appl Physiol 81:33, 2000.
92.
Daily WM, Harrison TR: A study of the mechanism and treatment of experimental heat pyrexia. Am J Med Sci 215:42, 1948.
93.
Plattner O, Kurz A, Sessler DI, et al: Efficacy of intraoperative cooling methods. Anesthesiology 87:1089, 1997.
94.
Plattner O, Kurz A, Sessler DI: Efficacy of cooling methods in malignant hyperthermia crisis. Anesthesiology 87:487, 1997.
95.
Costrini AM: Emergency treatment of exertional heatstroke and comparison of whole body cooling techniques. Med Sci Sports Exerc 22:15, 1990.
96.
Tek DA, Olshaker JS: Heat illness. Emerg Med Clin North Am 10:299, 1992.
97.
Mekjavic IB, Tipton MJ, Gennser M, et al: Motion sickness potentiates core cooling during immersion in humans. J Physiol 535:619, 2001.
98.
Magazanik A, Epstein Y, Udassin R, et al: Tap water, an efficient method for cooling heatstroke victims—A model in dogs. Aviat Space Environ Med 51:864, 1980.
99.
DeWitte J, Sessler D: Perioperative shivering: Physiology and pharmacology. Anesthesiology 96:467, 2002.
100. Kielblock 101. Noakes
AJ, Van Rensburg JP, Franz RM: Body cooling as a method for reducing hyperthermia. S Afr Med J 69:378, 1986.
TD: Heatstroke during the 1981 national cross-country running championships. S Afr Med J 61:145, 1982.
102. Yarbrough 103. Tadler 104. Khan
BE, Hubbard RW: Heat-related illness. In Auerbach PS, Geehr EC (eds): Management of Wilderness and Environmental Emergencies, 2nd ed-. St. Louis, Mosby, 1989, p 119.
SC, Callaway CW, Menegazzi JJ: Noninvasive cerebral cooling in a swine model of cardiac arrest. Acad Emerg Med 5:25, 1998.
IH, Henderson IS, Mactier RA: Hyperpyrexia due to meningococcal septicemia treated with cold peritoneal lavage. Postgrad Med J 68:129, 1992.
105. Marion
DW: Therapeutic moderate hypothermia and fever. Curr Pharm Des 7:1533, 2001.
106. Takasu
A, Ishihara S, Anada H, et al: Surface cooling, which fails to reduce the core temperature rapidly, hastens death during severe hemorrhagic shock in pigs. J Trauma 48:942, 2000.
107. White
JD: Evaporation versus iced peritoneal lavage treatment of heatstroke: Comparative efficacy in a canine model. Am J Emerg Med 11:1, 1993.
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108. Rajek
A, Greif R, Sessler DI, et al: Core cooling by central venous infusion of ice-cold (4°C and 20°C) fluid: Isolation of core and peripheral thermal compartments. Anesthesiology 93:629, 2000.
109. White
JD, Riccobene E, Nucci R, et al: Evaporation versus iced gastric lavage treatment of heatstroke: Comparative efficacy in a canine model. Crit Care Med 15:748, 1987.
110. Syverud 111. Ferrie
R, Loveland R: Bilateral gluteal compartment syndrome after "ecstasy" hyperpyrexia. J R Soc Med 93:260, 2000.
112. Horowitz 114. Kessler 115. Smith
SA, Barker WJ, Amsterdam JT, et al: Iced gastric lavage for treatment of heatstroke: Efficacy in a canine model. Ann Emerg Med 14:424, 1985.
BZ: The golden hour in heatstroke: Use of iced peritoneal lavage. Am J Emerg Med 7:616, 1989.
M, Klein R, McMlellan L, et al: Effects of conventional and high frequency jet ventilation on lung parenchyma. Crit Care Med 10:514, 1982.
RB, Cutaia F, Hoff BH, et al: Long-term transtracheal high-frequency ventilation in dogs. Crit Care Med 9:311, 1981.
116. Bussieres 117. Harris
JS: Whole lung lavage. Anesthesiol Clin North Am 19:543, 2001.
SB, Darwin MG, Russell SR, et al: Rapid (0.5 degrees C/min) minimally invasive induction of hypothermia using cold perflurochemical lung lavage in dogs. Resuscitation 50:189, 2001.
118. Kelly
KP, Stenson BJ, Drummond GB: Randomized comparison of partial liquid ventilation, nebulized perflurorocarbon, porcine surfactant, artificial surfactant, and combined treatments on oxygenation, lung mechanics, and survival in rabbits after saline lung lavage. Intensive Care Med 26:1523, 2000. 119. Cienki
JJ, Sevald J, Frisch M, et al: An evaluation of ketorolac in hyperthermia. Ann Emerg Med 36:S6, 2000.
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Chapter 69 - Ultrasound-Guided Procedures Sarah A. Stahmer Lisa Mackowiak Filippone
Sonographic guidance for invasive procedures is a logical addition to the practice of emergency medicine. As of this writing, however, it is not considered standard of care that the emergency clinician is skilled in, or has access to, bedside ultrasonography. Bedside sonography images deep tissue anatomy, thus increasing the chance of successful performance of a wide range of invasive procedures and minimizing associated complications. Consensus guidelines developed by the American College of Emergency Physicians for use of ultrasound (US) by emergency clinicians include sonographic guidance for procedures as being within the scope of practice for emergency clinicians. [1] This chapter is not meant to be a comprehensive description of the US examination, nor should it be viewed as a tutorial for emergency clinicians unskilled in the use of US. It is assumed that the emergency medicine clinician using US has had some formal training in the performance and interpretation of directed bedside US as outlined in the ACEP 2001 guidelines. The following chapter will describe those procedures within the scope of practice of emergency clinicians for which there is a role for bedside US. The procedures described here are covered in detail elsewhere in the text, and this section will focus primarily on the role of US.
PHYSICS US images are created by high-frequency sound waves, which are generated and interpreted by a transducer and then converted electronically to form an image on a screen. The transducer is a probe that contains crystals, which change shape and vibrate when an electrical current is applied, creating sound waves. This is referred to as the piezoelectric effect. The crystals emit sound for a brief moment, and then wait for the returning echo reflected from the structures in the plane of the sound beam. When the echo is received the crystals vibrate, generating an electrical voltage proportional to the strength of the returning echo. This is then converted electronically into an image on the viewing screen. Sound waves are reflected back to the transducer from tissue interfaces that have different acoustic impedances (the density of the tissue times the speed of sound in tissue). Tissues of higher density such as bone that interface with lower density substances such as muscle or fluid will reflect nearly all the sound waves, and will appear on the monitor as brightly echogenic (white) structures. Fluid transmits nearly all the sound waves, and will appear black or anechoic. Tissues will vary in their echogenicity or brightness based on their density, compliance, and adjacent structures ( Fig. 69-1 ). The purpose of using US during a procedure is to allow the clinician to "see" the area of interest below the skin surface. The area on the body surface that will provide the best images is referred to as the acoustic window. There are some general principles that help determine the suitability of an area as an acoustic window. Sound waves travel best through structures that are composed of closely packed molecules. Air, because the molecules are widely spaced, is a very poor conductor of sound. Therefore, structures that contain air, such as the lungs and bowel, cannot be imaged with US. In addition, structures that lie beneath an air-filled structure (such as the aorta, which lies beneath loops of small bowel) may not be clearly visualized. In contrast, fluids have tightly packed molecules and conduct sound well. Fluid-filled structures are readily visualized with US because the fluid/tissue interface is highly reflective, creating a clear image. Fluid-filled structures also serve as excellent acoustic windows to structures that lie beneath them. Therefore, procedures involving entry into a fluid-filled space are best suited to sonographic guidance. For each of the procedures listed in this chapter, the optimal acoustic window is described.
INDICATIONS AND CONTRAINDICATIONS US may be used to guide cannulation of vessels, aspirate fluid collections within cavities (e.g., pericardium, pleurae, bladder, or joints), and locate soft tissue foreign bodies. US may be used to mark the site for skin puncture or provide continuous real-time visualization throughout the procedure. The real and potential applications for bedside sonography continue to expand as technology improves and clinical expertise in the hands of emergency clinicians grows. It is truly an extension of the examining clinician's eyes and hands and may be used to visualize any portion of the anatomy that is amenable to sonographic imaging. US is especially helpful in answering clinical questions regarding depth, size, and nature of subcutaneous masses or collections and determination of the presence of fluid within body cavities.
Figure 69-1 Longitudinal image of the gallbladder, demonstrating variability in tissue echogenicity. A, The anechoic appearance of fluid. Water, plasma, non-clotted blood, and urine will have the same appearance. B, The highly reflective appearance of a calcified stone in the gallbladder. Foreign bodies, needles, and bone will have a similar brightly echogenic appearance. C, The relatively hypoechoic appearance of tissue. Clotted blood, particulate material within fluid (lipid or purulent material) will appear the same, with echogenicity intermediate to bone and fluid.
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The clinician choosing to use sonography must have training and experience in the use of US technology and image interpretation. Clinical errors directly related to the use of bedside US usually result from incorrect use of the technology or misinterpretation of sonographic images. Technological errors may occur when the wrong probe is used. For example, procedures requiring high resolution (central vein cannulation or foreign body detection) should be guided with a high-frequency probe. Lower frequency probes may not adequately delineate structures and hence lead to error. Imaging of the heart often requires a probe with a small "footprint" that will allow for imaging between the ribs; a larger footprint probe will include rib shadows that may affect the quality of the examination. Inadequate amounts of gel and air bubbles in the probe cover can create artifacts that adversely affect the technical quality of the images. Finally, the sonographer must be familiar with the various settings on the machine that will determine image quality. For example, inappropriate gain settings are common sources of error and image misinterpretation; too much gain may give the appearance of echogenic shadows within spaces. These shadows may then be interpreted as tissue or clot. Problems with interpretation usually arise when the clinician is attempting to interpret an image that is suboptimal, due to poor patient preparation or positioning, the presence of air-filled structures between the probe and structure of interest, or lack of appreciation of sonographic artifacts. Emergency clinicians are often required to perform procedures under suboptimal conditions, and the same is true for sonography. Bedside sonography is often performed simultaneously with other procedures on a patient who may be unable or unwilling to fully cooperate. The patient may be receiving active chest compressions or be profoundly hypotensive, leaving vessels flaccid with poor flow. There may be subcutaneous air or significant soft tissue swelling between the probe and object of interest, and veins may be filled with clot or scar from previous central lines. For these reasons, the clinician using sonography must adhere to a few important principles. First, do not attempt to interpret a sonographic image that does not clearly depict the structure or organ of interest. Second, interpret the sonographic image in the context of the clinical picture—what you see must make sense to what is happening clinically. Finally, if you are not sure of what you are seeing—obtain an alternative imaging study or expert assistance. For the remainder of this chapter, it is assumed that the clinician performing a US-guided procedure has appropriate training and experience. To avoid redundancy, this point will not be restated. That is, lack of sonographic training and experience is a contraindication for incorporating bedside sonography with any procedure.
EQUIPMENT The crystals determine transducer frequencies. Those used most commonly for medical diagnostic imaging range from 2 MHz to 10 MHz. Lower frequency probes are used for viewing deeper structures, such as the heart or the aorta, and larger patients, but produce images that are of lower resolution. Higher frequency probes provide high-resolution images of fairly superficial structures, such as veins and subcutaneous tissues, and are recommended for use in children and very
Figure 69-2 The curvilinear array probe is used for lower frequency (2.0 to 5.0 MHz) scanning of the abdomen and chest. It is best used for cardiac and abdominal imaging. The linear array probe is used for high frequency (6 to 10 MHz) scanning of superficial tissues, vessels, subcutaneous masses, and foreign bodies.
thin adults. The highest possible frequency probe should be used because it will provide superior resolution. Transducers vary also in the array of their piezoelectric elements, or crystals. The nature of the array will affect the overall field of imaging. The transducer array with the widest range of applications for emergency sonography is the curvilinear array, which has a narrow near field and pie-shaped window, allowing for a small acoustic window and large imaging area. This is ideal for imaging between ribs and curved surfaces. The linear array is used for high-frequency scanning of superficial tissues and is ideal for imaging vessels, subcutaneous masses, and fluid collections ( Fig. 69-2 ). There are several needle guidance systems available. Attached to the probe of such a system is a metal or plastic device through which the needle passes ( Fig. 69-3 ). While these systems are designed to improve the accuracy of needle insertion, the path of the needle is determined by the probe angle, which can be altered by even subtle hand movements. Needle guidance systems are most useful when the target
Figure 69-3 An ultrasound needle guide is ideally used to guide needle placement into deep or small structures. (Courtesy of Dymax Corp, a subsidiary of Bard Access Systems.)
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organ is deep or small in size, and are usually not necessary for the majority of emergency department (ED) procedures.
GENERAL APPROACH Most procedures facilitated by the use of bedside US require the use of two hands. Therefore, the clinician must make a decision whether to have an assistant hold the probe, perform the procedure with one hand while holding the probe in the other (freehand), or use the US probe to simply mark the point of entry prior to the procedure (blind approach). When the procedure requires two hands, it is best to have an assistant hold the probe. This is particularly important when one needs to visualize needle entry into the space or vessel. The freehand approach requires the operator to hold the probe in one hand while performing the procedure with the other. This is best suited for procedures that require only one hand, such as needle aspiration of large joint spaces or abscesses. The blind approach is best used for large collections of fluid, such as ascites or large pleural effusions. The optimal site is identified prior to the start of the procedure and the area marked with a sterile pen. The depth of the collection is noted by referring to the depth markers to the right of the imaging screen, which indicate the distance from the skin surface to the most anterior margin of the collection or vessel. Depending on the area of interest, it may be necessary to note the patient's position and phase of respiration when identifying the point of entry. This is particularly important when attempting thoracentesis (phase of respiration) or paracentesis (patient positioning). Catheters, wires, and needles appear as brightly reflective structures within the fluid-filled anechoic space. Keeping the needle perpendicular to the plane of the US beam will maximize the chance of visualizing the needle. Other methods that have been reported to improve visualization include placing the focal zone in the near field and bobbing the needle. The latter requires an in-and-out jiggling type of movement that moves the needle within the sonographic window. [2] When the probe is left in place during the procedure, it needs to be covered with a sterile rubber sheath (a sterile glove is usually adequate). When available, a transparent sterile drape can also be used. In either case, a layer of acoustic gel should be placed between the probe and sterile cover or drape. Another layer of sterile acoustic gel should be placed between the skin surface and the probe cover or drape. Central Venous Line Placement Obtaining vascular access is central to the care of many patients in the ED, particularly those who are critically ill or injured. Peripheral access is often difficult in these patients and central venous catheter placement is necessary. Bedside US has been shown to improve the chance of successful central vein cannulation and to reduce the number of complications. While internal jugular and femoral vein access are amenable to sonographic guidance, the subclavian vein is difficult to visualize sonographically secondary to the presence of the clavicle and will not be described here. Background
Sonographic guidance (using two-demensional echo) of central vein access was first described in 1986. [3] In 1990, Mallory et al. compared the standard landmark-guided technique to the US-guided technique for cannulation of the internal jugular vein in intensive care unit patients. They demonstrated a 100% success rate in the US-guided group versus a 65% success rate in the landmark group. [4] Another prospective study in 1991 evaluated 160 cardio-thoracic surgical patients requiring right internal jugular vein cannulation. The US group had a greater overall success rate (100% vs. 95%), a higher percentage of first-attempt cannulations (73% vs. 54%), fewer attempts per cannulation (1.4 vs. 2.8), shorter time per cannulation (61 vs. 117 seconds), and fewer carotid punctures (1 vs. 7) compared with a control group using the standard landmark technique. [5] In 1993, Denys et al. conducted the largest prospective trial to date, comparing the results of 302 US-assisted internal jugular vein cannulations with 302 cannulation attempts using the standard external landmark-guided technique. The US group had a higher success rate with fewer attempts, a decrease in the mean time to cannulation, and a reduction in complications including carotid puncture, brachial plexus injury, and hematoma. [6] Another study performed on ED patients by emergency clinicians again demonstrated more successful single-needle-pass punctures of the internal jugular vein using US guidance, particularly in patients with no visual or palpable landmarks. [7] The benefits of using US for central venous access have also been demonstrated in children. [8] [9] This is no surprise since children's vessels are smaller, cooperation is unpredictable, and tensions are often high when performed under emergent conditions. In addition, compared with older children and adults, studies have demonstrated that younger children have more failed attempts and more complications. [8] [10] [11] [12] In a study of infants under 12 months of age undergoing preoperative central line placement, one study found that cannulation of the internal jugular vein was 100% successful using US guidance (n = 43) vs 77% in infants using the standard landmark-guided technique (n = 52). [8] The time for cannulation was also significantly reduced (3.3 minutes vs 10 minutes) and the incidence of carotid punctures was lower (0% vs 25%) in the US group. [8] There have been few studies evaluating the use of US for femoral vein access, but the evidence to date is encouraging. In 1997, Kwon et al. demonstrated greater success (100%) in cannulating the femoral vein using US guidance compared with the standard landmark-guided technique (89%) in patients requiring central venous access for hemodialysis.[13] Complication rates were also lower in the US-guided group. [13] Hilty et al. compared success and complication rates of US-guided femoral line placement with that of the standard landmark-guided approach in ED patients during cardiopulmonary resuscitation. The success rate using US was 90% vs 65% in the control group. There were no arterial punctures in the US group; however, the femoral artery was punctured in 20% of blind attempts. [14] Other vessels besides the internal jugular and femoral veins can be cannulated safely using US guidance. Of particular interest is the brachial vein, which is usually not attempted due to absence of reliable landmarks, deep location, and proximity to important structures (e.g., nerves, brachial artery). A study by Keyes et al. showed that the brachial vein can be safely cannulated using sonographic guidance in patients with limited access (50 intravenous drug users and 21 obese patients). The brachial vein was successfully cannulated in 91% of patients within a mean time of
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77 seconds. Reported complications were pain, line failure due to falling out or infiltration (8%), and brachial artery cannulation (2%).
[15]
Indications and Contraindications
If sonographic equipment is readily available, the emergency clinician should have a very low threshold for using it to guide central venous cannulation. It is especially helpful when access is required on a patient with distorted anatomy, obesity, history of multiple prior central lines, and hypotension, and when blind attempts have been unsuccessful. The benefits include localization of the vein and artery and demonstration of venous patency through ease of compression and free flow (if Doppler is available). There are no reported contraindications specific to sonographic guidance of venous cannulation. Equipment
A high-frequency (7.5 MHz to 10 MHz) linear probe is highly recommended for imaging the relatively superficial internal jugular and femoral veins. A needle guide may be helpful for deep or small veins, but may make coordinating imaging and access more difficult for less experienced sonographers (see Fig. 69-3 ). If a linear probe is not available, any high-frequency probe, such as the endovaginal probe, can be used. A sterile sleeve (or glove) and sterile conductive medium are required. A sterile marking pen can be used to mark the location of the vein if the US probe is removed before puncture (see later in this section). Two persons are usually required—one to perform the US while the other obtains vascular access. Image Interpretation
The internal jugular vein and carotid artery will appear as relatively superficial structures on the monitor. When viewed in the transverse plane, the internal jugular vein is a thin-walled, circular, anechoic structure anterior and lateral to the carotid artery. However, there is some variability in the relationship between the two
vessels. [16] [17] Denys et al. studied the location of the internal jugular vein relative to the carotid artery in 200 patients. They found that 2% of patients had an internal jugular vein that was positioned medially, overlying the carotid artery. The internal jugular vein was found more laterally than expected in 1% of patients. [16] Turning the patient's head will also alter the relationship between the vein and artery, usually moving the vein medially over the artery. When patent, the internal jugular vein will increase in size with inspiration and Valsalva maneuvers. Light pressure applied with the probe directly over the vessels will easily compress the internal jugular vein and only one anechoic circular structure, the carotid artery, will be seen on the monitor. Once pressure is released, the lumen of the internal jugular vein will reappear. The external jugular vein is not usually seen on the monitor. Because of its superficial location and compressibility, it is usually flattened just by placement of the probe on the neck. The femoral artery and vein also appear as superficial anechoic circular structures when viewed in the transverse plane. The vein is located medially and the artery is located laterally. As the probe is moved toward the patient's head, this relationship changes, with the vein eventually lying behind the artery. Other sonographic findings helpful in distinguishing the femoral vein are that it is easily compressed and will increase in size by squeezing the thigh. The artery is not readily compressed and can be seen to pulsate. One exception to this may be in patients who are undergoing cardiopulmonary resuscitation, where pulsations will be seen primarily in the femoral vein and not the artery. Coletti et al. described the presence of femoral pulses in canines when cardiopulmonary resuscitation was in progress and the proximal femoral artery was clamped. These pulses disappeared when the proximal femoral vein was clamped and the artery unclamped. [18] Procedure and Technique Internal jugular vein
To access the internal jugular vein, the patient is placed in the supine position with the head turned slightly to the opposite side of the vein being cannulated. The lateral aspect of the neck is prepped and draped in the usual fashion (see Chapter 22 ). A small amount of US medium is placed on the probe. A sterile sleeve or glove is placed over the probe. It is important to remove any air bubbles between the gel on the probe and the sterile cover, as this will create artifacts. Sterile gel is then placed over the cover. A sterile towel or drape can be wrapped around the rest of the probe and cord to help maintain sterility. The US probe is placed parallel and superior to the clavicle over the groove made by the two heads of the sternocleidomastoid muscle ( Fig. 69-4 ). The beam of the US probe should intersect the carotid artery and the internal jugular vein in a transverse or cross-sectional plane. At this level, the internal jugular vein is usually anterior and lateral to the carotid artery ( Fig. 69-5A and B ). Additional maneuvers can help in differentiating the internal jugular vein from the carotid artery (e.g., the vein will markedly increase in diameter with Valsalva maneuvers). Asking the patient to blow on his or her
Figure 69-4 Imaging window for the internal jugular vein and carotid artery. The ultrasound probe should be covered with acoustic gel and then a sterile cover or glove. An additional layer of sterile gel should be placed over the cover. The probe is then placed parallel and superior to the clavicle over the groove made by the two heads of the sternocleidomastoid muscle. The probe should be pointed toward the patient's right. Care should be taken not to apply undue pressure on the probe to avoid compression of the easily collapsible internal jugular vein. Asking the patient to blow on his or her thumb or performing a Valsalva maneuver will increase the luminal diameter of the vein. (Lydia F. Roberts, Photographer)
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Figure 69-5 The internal jugular vein and carotid artery. A, Sonographic image; B, Schematic representation. The beam of the ultrasound should intersect the carotid artery and the internal jugular vein in a transverse or cross-sectional plane. The internal jugular vein is easily identified by its compressibility and response to Valsalva maneuvers (i.e., it increases in diameter).
thumb is often helpful in creating a sustained Valsalva maneuver that will readily identify a patent internal jugular vein. If one applies gentle pressure to the vein, it will collapse. On the screen, only the carotid artery lumen will remain. Either color or power Doppler can also readily distinguish a vein from an artery. Pulsatile flow within the carotid artery appears quite different from lower amplitude, phasic venous flow that augments with Valsalva maneuvers. Once visualized, the internal jugular vein should be centered on the monitor screen, allowing the center of the probe to be used as a guide for needle puncture. The needle will first indent the vein. Then the vein will appear to collapse on the monitor as it is entered ( Fig. 69-6A and B ). The needle is advanced slightly farther and the vein will re-expand once it has been entered. The needle may seen on the monitor, particularly if the US beam is perpendicular to needle ( Fig. 69-7A and B ). Once venous blood is aspirated, the US probe may be removed. A guidewire is then threaded through the needle and the catheter is placed as described in Chapter 22 . An alternative method, requiring only one operator, is to use the US to locate the underlying vein and then mark its location with a sterile pen. The internal jugular vein is usually a very superficial structure between the two heads of the
Figure 69-6 A and B, Once the vein is positioned directly under the probe, needle aspiration can be attempted. If the site of skin puncture is correct, the needle will indent the vein and the vein will appear to collapse as it is entered.
sternocleidomastoid muscle, and easily accessed once its location and patency is confirmed with US. Care must be taken not to readjust the position of the patient's head at this time. Rotating the head farther away from the vessel being cannulated will usually cause the vein to move medially over the carotid artery, and increase the risk of inadvertently puncturing it. The probe is removed after the vein has been located and needle puncture is performed. Femoral vein
The patient is placed supine with the leg extended and slightly rotated externally. The patient is prepped and draped as usual (see Chapter 22 ), and the US probe is prepared as described earlier. If the patient has a palpable pulse, the US probe is placed over the pulse in a transverse orientation inferior to the inguinal ligament. If the patient does not have a palpable pulse, the probe should be placed approximately midway between an imaginary line drawn from the anterior superior iliac spine to the ipsilateral pubic tubercle just inferior to the inguinal ligament. The vein will be the vessel located medially. Similar maneuvers as described earlier can be done to help distinguish the femoral vein from the artery. These include compression with the probe and squeezing the thigh, which is the "Valsalva equivalent" for the femoral vein and
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Figure 69-7 A and B, The needle may be visualized within the vessel lumen, and will appear as a brightly echogenic structure.
will increase the vessel caliber in a patent vein. Once located, the vein should be centered on the screen so that the middle of the probe can be used as a guide for the needle stick. Once the vein is entered the probe can be removed and a guidewire advanced through the needle. Subsequent cannulation of the vein is described in Chapter 22 .
Complications
Complication rates for the standard landmark-guided approach of internal jugular vein cannulation are between 4% and 10%. [19] [20] [21] Reported complications include vascular perforation and laceration, pneumothorax or hemothorax, tracheal perforation, brachial plexus and phrenic nerve injury, hematoma formation, thoracic duct injury, and catheter malposition. Several trials have shown that using US guidance to cannulate the internal jugular vein decreases complication rates, particularly carotid artery puncture. [5] [6] [8] [22] Troianos et al. reported a decrease in the carotid artery puncture rate from 8.43% to 1.39% using standard vs US-guided cannulation of the internal jugular vein. [5] Likewise, Denys et al. demonstrated a similar decrease in carotid artery punctures using US guidance, as well as decreases in brachial plexus irritation and hematoma formation. [6] Potential complications unique to femoral vein cannulation include retroperitoneal hematoma, bowel perforation, and bladder perforation. Two studies comparing the complication rates of US-guided vs standard femoral vein cannulation have demonstrated reduced complications using US. [13] [14] Complications unique to using US are rare and usually due to poor technique or attempts to use a low-resolution probe to image the vessels. One commonly encountered problem is in patients with proximate clot or stricture in the vein from prior central lines. In these patients, the vein will be seen and readily accessed, yet there will be little to no flow. A clue to this possibility is a vein that does not easily compress. When in doubt, comparison with the opposite side may also be helpful. In addition, Doppler can identify those vessels with proximate obstruction, but is not essential. Finally, remember that the anatomical relationships between the internal jugular vein and artery will change with head turning, and may place the artery beneath the vein. If the blind approach (i.e., marking the skin and removing the US probe prior to insertion) is used, the vessels should be imaged after final head positioning and the patient kept immobile until the line is secured. Pericardiocentesis The role of bedside sonography in the management of patients with suspected pericardial effusion is to establish the diagnosis and to visualize placement of a drainage catheter within the pericardial sac. The diagnosis of a clinically significant pericardial effusion is readily determined by bedside sonography, and is far superior to physical examination alone. Sonography is the study of choice for identification of pericardial effusions, and the availability of bedside US has the potential to shorten time to diagnosis of patients with clinically significant effusions. [23] [24] [25] [26] [27] For the subset of patients who are hemodynamically compromised by their effusion, pericardiocentesis performed under sonographic guidance is a safe and effective alternative to blind aspiration. Background
Aspiration of the pericardial sac by emergency clinicians is usually a last-ditch effort to resuscitate patients with pulseless electrical activity (PEA) and is often unsuccessful. This is because the diagnosis is usually considered only after the patient has become unstable and pericardiocentesis is performed late in the resuscitation effort. Recent studies have shown that while large pericardial effusions are a rare cause of hemodynamic instability in the ED, a low threshold for performing bedside US may increase detection of effusions before they become hemodynamically significant. [25] [28] [29] The traditional approach to the patient with a suspected clinically significant effusion has been to blindly access the pericardial sac using the subxiphoid approach. This technique is associated with a variety of complications, including puncture of the liver, lungs, myocardium, and epicardial vessels [30] [31] (see Chapter 16 ). In hemodynamically stable patients, a surgical window is usually performed in order to avoid the complications of blind aspiration. Over the past decade there has been increased enthusiasm for echocardiographically guided pericardiocentesis. The techniques first described in 1998 [30] are applicable to the ED setting and can be used for management of patients with hemodynamically significant pericardial effusions.
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Indications and Contraindications
Patients presenting with acute and subacute cardiac tamponade usually do not display the classic triad of hypotension, neck vein distention, and muffled heart tones. Waiting for their appearance to order a confirmatory test will often delay diagnosis and possibly jeopardize the safety of the patient. The heart should be imaged whenever a clinically significant pericardial effusion is suspected. Scenarios warranting consideration of a pericardial effusion include a patient with hypotension of unclear etiology, particularly those patients with known malignancies, recent myocardial infarction, and end-stage renal disease, and victims of trauma, both blunt and penetrating. [25] [26] [27] [28] [29] Early demonstration of a large pericardial effusion will guide further work-up, support early consultation from either cardiology or cardiothoracic surgery, and facilitate therapeutic drainage for those patients who remain hypotensive in spite of fluid resuscitation. For patients in extremis, the clinician most clinically experienced in both sonography and aspiration of the pericardial sac should perform pericardiocentesis without delay. For patients with large effusions who are relatively stable, management options are greater and may include a pericardial window. Consultation with either cardiology or cardiothoracic surgery is advised prior to performing aspiration on stable patients. Equipment
The optimal probe frequency is 2 to 4 MHz. It should have a small enough footprint to allow for imaging between the rib spaces, particularly if the parasternal windows are used. For the subxiphoid view, the standard 2 to 3.5 MHz curvilinear probe will provide excellent images. Acoustic Windows
The cardiac examination is dynamic. The sonographer must identify the imaging window that provides images which best demonstrate the effusion or cardiac chamber of interest. Most frequently used are the subxiphoid and parasternal windows. It is important for the sonographer to develop expertise in using a variety of imaging windows to obtain the necessary clinical information.
Figure 69-8 To obtain a subxiphoid view of the heart and pericardium, the probe should be placed beneath the xiphoid process with the probe marker pointing to the patient's right. The probe should be angled upward and slightly to the left. (Lydia F. Roberts, Photographer) Subxiphoid view
This view provides the most comprehensive information for a single view, and is therefore the most important acoustic window for the less experienced sonographer to learn. It will readily identify a circumferential pericardial effusion and allow assessment of overall cardiac wall motion. The subxiphoid view can usually be obtained within 1 minute, and may be the only view required. To obtain the subxiphoid view, the probe is placed transversely at the left costal margin at the level of the xiphoid process with the beam aimed at the left shoulder ( Fig. 69-8 ). The angle and rotation of the probe should be adjusted to obtain the appropriate views. The structures closest to the probe will appear at the top of the display and include the liver, diaphragm, pericardial space, and right ventricle ( Fig. 69-9A and B ).
Figure 69-9 A, Sonographic appearance of a normal heart and pericardium obtained through the subxiphoid window. The right ventricle will be the most anterior cardiac structure, bordered superiorly by the pericardium and diaphragm. B, Schematic representation.
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Figure 69-10 To obtain a parasternal view of the heart, the probe should be placed adjacent to the left sternal border in the left second or third intercostal space. The patient's head is at the lower edge of the photograph. (Lydia F. Roberts, Photographer) Parasternal view
The next most useful view is the parasternal long axis view. To obtain this view, the transducer is placed in the left parasternal area between the second and fourth intercostal spaces. The plane of the beam should be parallel to a line drawn from the right shoulder to the left hip with the marker pointing to the right shoulder (reverse if the image is not set for cardiac views) ( Fig. 69-10 ). The parasternal view provides excellent images of the left atrium, mitral valve, left ventricle, aortic valve, and the proximal ascending aorta. It is also the best view to identify small dependent collections within the pericardial sac ( Fig. 69-11A and B ). Image Interpretation
The normal pericardium will appear as a single, brightly echogenic stripe adjacent to the myocardium. Fluid within the pericardial space will collect between the visceral and parietal pericardium and will appear as a large, non-beating, anechoic area adjacent to the ventricular myocardium ( Fig. 69-12A and B ). A small amount of fluid in the dependent portion of the pericardial space is normal. The sonographic appearance of the clinically significant effusion is distinct. The sonogram will reveal a hyperkinetic heart within a circumferential pericardial effusion, with diastolic collapse of the right-sided chambers. This reflects pressures within the pericardial space that are greater than the right ventricular filling pressure during diastole. The inferior vena cava will be dilated and not show respiratory variation or collapse when the patient is asked to "sniff." Procedure and Technique
Tsang et al. described the technique for US-guided pericardiocentesis in 1998. [30] The ideal site of skin puncture is where the largest area of fluid accumulation is closest to the skin surface. On US, this is demonstrated by visualizing a large anechoic area at the top of the screen (which is the body area
Figure 69-11 A, Sonographic appearance of a normal heart and pericardium obtained through the parasternal long axis window. This view is an excellent imaging window for posterior effusions. B, Schematic representation.
Figure 69-12 A, Sonographic appearance of a circumferential pericardial effusion obtained through the subxiphoid window. The effusion is seen as an anechoic stripe surrounding the heart. B, Schematic representation.
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Figure 69-13 Photograph (A), sonographic image (B), and schematic representation (C) demonstrating the sonographic window that places the largest area of accumulated fluid nearest the probe (top of screen). There should be no vital structures between the probe and the pericardial space when the aspirating needle/catheter is placed over the superior border of the rib closest to the anechoic area. (Lydia F. Roberts, Photographer)
closest to the probe) and usually corresponds to the left anterior chest wall (rather than the subcostal region) ( Fig. 69-13A,B , and C ). In addition to being closer to the skin surface, this approach avoids injury to the liver. Inadvertent puncture of the lung is also prevented using this approach, because air in the lung will not conduct sound waves and will prevent visualization of the heart when located immediately beneath the probe. The clinician should avoid choosing a site that might puncture either the internal mammary artery, which lies 3 to 5 cm from the parasternal border, or the neurovascular bundle located at the inferior rib border. The best site should be marked with a sterile pen. The needle trajectory and depth should be confirmed prior to skin puncture. Repositioning the patient will alter the position of the heart and pericardial sac within the chest and requires reassessment. The skin should be prepared antiseptically and a sterile cover placed over the probe. If time permits, the selected area should be anesthetized with 1% to 2% lidocaine, using the superior border of the adjacent rib as a landmark. The needle should ideally have an "over-the-needle" sheath that allows the needle to be withdrawn after the pericardial space is entered. This helps avoid injury to the heart and other vital structures. A 16- to 18-ga needle that is 5 to 8 cm in length is ideal. A saline-filled syringe should be attached to the needle, and gentle aspiration applied while the needle is advanced. The US probe can remain on the chest wall immediately adjacent to the aspiration site or removed after the fluid is localized. Once the pericardial space is entered, agitated saline can be injected to confirm needle placement, particularly if the pericardial fluid is grossly bloody or there is any question concerning needle position. A saline echo contrast medium is prepared by using two 5 mL syringes, one with saline and the other air, connected via a three-way stopcock to the needle catheter sheath. Saline in one syringe is rapidly injected between the syringes and then injected into the sheath. Entrance of the agitated saline into the pericardial space can be monitored sonographically, appearing as a brightly echogenic stream. After confirmation of needle placement, a wire can be passed through the sheath and a dilator (6 to 8 Fr Cordis) placed over the wire. The dilator is removed and an introducer sheath-dilator (6 to 8 Fr Cordis) placed over the wire. Both the wire and the sheath can then be removed and the introducer sheath left in place. The pigtail angiocatheter is inserted through the introducer sheath, and fluid aspirated to confirm placement [30] (see Chapter 16 ). Complications
The potential complications associated with US-guided pericardiocentesis are the same as those with blind aspiration and are discussed in detail in Chapter 16 . The use of US will significantly minimize the risk of many of these complications, especially inadvertent puncture of the myocardium, epicardial vessels, and liver. [24] [30] Additional complications uniquely associated with US are due to misinterpretation of the sonographic image. For example, epicardial fat pads are common in obese patients and can be misinterpreted as clot or fluid within the pericardial space. [24] Although they have a similar echogenicity, there are a number of important findings that can aide in differentiating an epicardial fat pad from clot or fluid in the pericardial space. First, the epicardial fat pad is an anterior structure. Clot in the anterior pericardial space suggests that the effusion is circumferential, and therefore should also be seen in the dependent portion of the pericardial space. This is best
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demonstrated using the parasternal long axis view. Alternatively, the probe can be aligned longitudinally so that the inferior vena cava is visualized as it enters the right atrium. The right side of the heart can be seen adjacent to the diaphragm, and blood or fluid within the pericardial sac can be readily identified (as long as it is not loculated). [24] Second, the inferior vena cava should collapse when the patient sniffs; collapse of less than 50% indicates increased intrathoracic pressure and possibly tamponade. Third, blood clotting is a dynamic process, with clots continuously forming and being broken down. If blood is present within the pericardial sac, careful examination should reveal fronds of clot waving within an anechoic (black) pericardial space. Finally, and most importantly, an anterior fat pad should not cause collapse of the right ventricular free wall. If after careful examination doubt still exists as to the presence of an effusion, hemodynamically stable patients should have a formal echocardiogram or computed tomography scan performed. Also remember that fluid within the pericardial space is not always pathologic. A small (7000, EGA 5–6 wk TAU should show viable IUP if quant ß-hCG >6500
6–7 wk
1000–30,000
Fetal pole, cardiac activity 5.5–7 wk, quant ß-hCG >10,000
7–8 wk
3500–115,000
Yolk sac 5–6 wk or ß-hCG >7200; fetal pole/heart 5.5–7 wk or ß-hCG >11,000–17,000
8–10 wk
12,000–270,000
>10 wk
270,000–15,000
TAU: transabdominal ultrasound TVU: transvaginal ultrasound DDS: double decidual sac EGA: estimated gestational age IUP: intrauterine pregnancy
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ß-hCG level =1000 mIU/mL—is not true. Only 15% of ectopic gestational sacs examined pathologically have evidence of an embryo. This observation, combined with
a variety of pathologic characteristics and sites of implantation, leads to highly variable quantitative ß-hCG levels in ectopic pregnancies. [65] In general, an ectopic pregnancy elaborates quantitatively small amounts of ß-hCG, with 1% of ectopic pregnancies having a quantitative ß-hCG of 1 part of blood to 10 parts of medium). [282] Thus, if 30 mL of blood is obtained from one site, it should be equally divided into three of the usual 100-mL broth bottles. Volumes in Children
A blood volume of 30 mL from a 70 kg adult is equivalent to 0.5 mL of blood in a 3.5 kg neonate. Fortunately (for the validity of the blood culture), it has been shown that levels of bacteremia are typically 10-fold higher in infants than adults [64] [176] [258] ; and that the sicker the child, the greater the likelihood of a high level of bacteremia. [64] Although one study[198]
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failed to show any effect on the rate of detection of bacteremia with increasing volumes of blood specimens, many studies have suggested that small culture volumes are at increased risk of false-negative results, just as in adults. [70] [111] [264] [292] Furthermore, the studies showing high CFU/mL rates were performed on neonates. As the immune system matures during infancy, levels of bacteremia might be expected to fall toward those seen in adults. In two reviews, it was recommended to obtain a similar volume of blood with respect to body mass as would be drawn in adults: approximately 1 mL/2.5 kg, or 4 mL per 10 kg body mass. [44] [207] These recommendations are summarized in Table 70-10 . How Many Sets of Blood Cultures Should Be Tested? A set of blood cultures is the sample obtained from a single site. A one mL specimen from a neonate placed in an aerobic bottle, and a 30 mL specimen from an adult divided between fungal, aerobic, and anaerobic bottles, are both a single set of blood cultures. Two or more sets of blood cultures make up a series. [8] [49] The information derived from the blood culture sets is pooled in such a way as to make both the sensitivity and specificity of the series greater than that of the component sets. Sensitivity is enhanced because even with continuous bacteremia, an individual set is usually only 80% sensitive. [8] Specificity is improved by determining whether pathogens that are also frequently contaminants are found in more than one set of the series. While this conceptual process is applied to all blood culture series, the focus of inquiry varies depending on the infectious process being ruled in or out. For example, in an elderly patient with fever and purulent urine, it is extremely unlikely that the causative organism is a typical skin contaminant. The usual causes of "false-positive" blood cultures will therefore be easily recognized, thus lowering the false-positive rate for the series, and making for a test with intrinsically higher specificity. At the same time, with typical pathogens in this clinical context being nonfastidious organisms, sensitivity is typically around 99% with two sets of 20 mL blood per set.[287] Conversely, in a patient with a prosthetic heart valve, fever, and signs of septic emboli, many likely pathogens are also skin contaminants (this phenomenon lowers the specificity of each individual blood culture set), so at least two sets of cultures must be positive with such organisms before the overall test (i.e., of the series) is considered positive. At the same time, this clinical picture makes the pretest probability of disease very high (diminishing the negative predictive value of a negative set), so that an extremely sensitive overall test (i.e., series) will be needed to adequately rule out disease. Thus, in
Age Group/Weight (kg)
TABLE 70-10 -- Optimal Specimen Volumes to Be Drawn per Blood Culture Set in Children * Ideal Volume of Specimen per Set (mL)
Neonates
1–2
Infants (5–10)
2–4
Children (7–20)
3–8
Children > 20
10
Children > 40
20
Adults and children > 60
30
*Rule of thumb: 4 mL of blood per 10 kg weight.
No. of Sets (Minimum)
TABLE 70-11 -- Numbers of Blood Culture Sets to Be Obtained for an Adequate Series in Various Clinical Situations in Adults Clinical Context
2 sets
Etiology is likely to be easily distinguished from contaminants and pre-test probability of bacteremia is low to moderate
3 sets
Skin contaminants are possible causes of infectious process, or pre-test probability of bacteremia is high, or infectious endocarditis is a consideration, but with low to moderate pre-test probability
4 sets
Infectious endocarditis AND either moderate to high pre-test probability or the patient has recently been on antibiotics
this clinical context, most authorities would recommend four sets of blood cultures, with good volumes in each. [8] [280] Except in infants, single sets of blood cultures are of insufficient sensitivity or specificity to be of any utility, and should not be drawn. [8] [130] [202] [223] [280] [281] Recommended numbers of sets of blood cultures as they relate to the pre-test probability of disease, as well as causative organism are summarized in Table 70-11 . Aerobic versus Anaerobic (vs Other) Bottles
Anaerobic infections, by nature, tend to occur in poorly perfused tissues or locations, frequently evolving into abscesses, which further isolate them from the bloodstream, decreasing the likelihood of bacteremia, and making them intrinsically elusive to blood cultures. In addition to these pathophysiological considerations, a significant decrease in the proportion of positive blood cultures owing to anaerobic organisms has been widely reported over the past 15 years. [67] [82] [168] [194] [239] The vast majority of anaerobic bacteremias occur in clinically identifiable situations listed in Table 70-12 . In recent series, anaerobic pathogens account for only 1 to 5% of positive blood cultures. [67] [194] [239] [271] [280] Clinically significant isolates—those that could not have been predicted on the basis of the clinical picture, or that alter management—are much rarer. [168] Thus, with a typical true-positive blood culture rate of 3 to 7% and with only 3% of positive blood cultures being anaerobic, approximately 500 to 1000 series of blood cultures need to be drawn for every positive anaerobic blood culture. This is borne out by empiric observations showing positive anaerobic blood cultures in 1.4 per 1000 patients receiving blood cultures. [50] Of these, more than 90% had clinical indications of anaerobic infection, so that 10,000 blood culture series would be needed to generate a single anaerobic result to alter clinical management.[50] In addition to TABLE 70-12 -- Infectious Processes Which can Cause Anaerobic Bacteremia Odontogenic head and neck infections Aspiration pneumonia Abdominal/pelvic infections Deep soft tissue infections (e.g., myofascitis) Sepsis with decubitus ulcers or necrotic tissue
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Clinical Situation
TABLE 70-13 -- Blood Culture Bottle Types to Be Used in Various Clinical Settings Bottles to Be Obtained
Children 12 yr
If anaerobic infection is unlikely, use aerobic bottles only unless the patient is immunocompromised In the immunocompromised, consider a bottle for fungal culture (usually effective in aerobic bottles, but consult the laboratory) If anaerobic infection is possible, each set consists of 1 aerobic and 1 anaerobic bottle per set
the very limited clinical utility of anaerobic cultures, they are likely to actually diminish the sensitivity of the test to aerobic bacteremia (>95% of cultured pathogens), which increases by about 3% per additional milliliter of blood. [183] [239] The use of blood culture specimens in anaerobic bottles will also diminish the likelihood of identifying fungal infections, which are increasingly common, especially in immunocompromised patients. [197] The arguments for a selective use of anaerobic blood cultures are compelling. Based on these considerations, and analysis of a number of review articles, [207] [239] [ 271] [ 280] Table 70-13 suggests guidelines for inoculation of blood obtained for culture.
[49] [190] [197]
Identifying Contaminants The emergency clinician must be prepared for telephone calls from the laboratory with positive results of cultures obtained on previous shifts. "False-positive" blood cultures can be due to true contamination, but also may be caused by the intermittent bacteremia that occurs in normal, healthy people. This situation has been complicated by increasingly common identification of Staphylococcus epidermidis and Streptococcus viridans and fungi as pathogens in blood culture series. [63] [117] [242] [298] The expense of false-positive blood cultures has been estimated at $900 per episode for discharged patients, and more than $5,000 per episode for in-patients. These costs emphasize the importance of good technique in obtaining blood cultures. [15] [234] Distinguishing contaminants from clinically significant bacteremia is based both on microbiologic information and the patient's clinical condition. Features of false-positive blood culture results are listed in Table 70-14 .[8] [40] [287] Notwithstanding these guidelines, it would probably be prudent to contact discharged patients with positive blood cultures even when contamination is suspected on a microbiological basis, to ensure that their condition is improving. Fungal Cultures Generally, fungi are difficult to isolate in blood cultures, and it may take 4 to 6 weeks to obtain a positive yield. If a fungemia is suspected, it is best to discuss culture media and technique with the laboratory before cultures are taken. Cultures TABLE 70-14 -- Features Suggestive of Contaminant ("False Positive") Blood Culture Results 1. Coagulase-negative staphylococci (S. epidermidis) or S. viridans in a single bottle in patients not suspected of infectious endocarditis, and without chronic indwelling intravenous access catheters, are usually contaminants. 2. Corynebacteria (previously known as "diphtheroids"), propionibacterium acne, and bacillus species are usually contaminants, but can be pathogenic in the immunocompromised. 3. Multiple organisms in a series suggests contamination. 4. Species that grow out after prolonged culture have a higher likelihood of being contaminants. Conversely, early-growing bacteria have a much higher likelihood of being pathogens. [3] [145] 5. The patient's symptoms have resolved or are inconsistent with sepsis (beware with infectious endocarditis, which can have an indolent course). 6. A primary source (e.g., sputum, urine) has a different pathogen isolated. of bone marrow are occasionally positive in deep mycoses when blood cultures are negative.
BEDSIDE TESTS FOR GASTROINTESTINAL HEMORRHAGE Detection of Blood in the Stool Bedside fecal blood tests make use of the peroxidase-like activity of hemoglobin. The test card is impregnated with a compound that exhibits a blue color reaction when oxidized. The original test used guaiac, but current tests use more sensitive and more reliable dyes. The addition of hydrogen peroxide developer solution will oxidize the dye in the presence of a peroxidase (e.g., hemoglobin). Testing for occult blood in the stool is associated with false-positive and false-negative results, but in its primary role in emergency medical practice the test is usually reliable in detecting significant acute gastrointestinal (GI) hemorrhage. [114] Low pH, heat, dry stools, reducing substances (e.g., ascorbate), and antacids can cause false-negative findings. [116] [175] [220] Slow bleeding in the upper GI tract in which heme can be converted (denatured) to porphyrin during transit through the gut may not be identified by stool testing. False-positive results have been attributed to the ingestion of partly cooked or large quantities of meat (dietary sources of myoglobin and hemoglobin), and peroxidase-rich food. [87] [220] Most vegetables contain peroxidase, including (in decreasing order) broccoli, turnips, cantaloupe, red radishes, horseradish, cauliflower, parsnips, Jerusalem artichokes, bean sprouts, beans, lemon rind, mushrooms, parsley, and zucchini. [87] However, a simple in vivo study convincingly calls into question the possibility of peroxidase's passing through the stomach without being denatured. [185] False-positive tests can also be caused by the presence of povidone-iodine solution in concentrations less than 0.1% (a 1% dilution of the 10% solutions commonly available at the bedside). False-positive fecal occult blood tests are uncommon, and a positive test should be considered evidence of the presence of blood until proven otherwise. Routine iron supplementation should not be considered as a cause for a false-positive Hemoccult test, [6] [180]
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although iron does (like bismuth preparations) cause the stools to appear black on gross examination. Despite this, early in vitro studies demonstrating an artifactual false-positive effect of iron are still frequently cited. Normal GI blood loss is limited to less than 2.5 mL/day, which translates to less than 2 mg of hemoglobin per gram of stool (0.2% by weight). [2] The sensitivity of the Hemoccult test varies both with the concentration of hemoglobin present in the stool, and the extent to which hemoglobin is exposed to the proteolytic effects of the digestive tract. The Hemoccult test is 37% sensitive to stool containing 2.5 mg hemoglobin per gram of stool, but 95% sensitive when the concentration is 20 mg Hb/g of stool, indicating that low to moderate levels of blood may be missed. [99] The test is much more likely to detect lower GI hemorrhage than an identical rate of upper GI bleeding due to the 100-fold diminution of peroxidase activity of blood during transition through the GI tract. [71] Impaired detection of hemoglobin may also occur as a result of dilution due to diarrheal illness. [99] [114] [191] Method
The stool specimen is smeared onto the reagent area on the card and a drop of developer is added. Because the reaction must occur in an aqueous medium, a drop of water should be added to very dry specimens and allowed to moisten them before addition of developer. Adding water will increase the false-positive rate, however.[175] [220] Formation of a blue color on the paper anywhere around or under the specimen within 60 seconds should be considered a positive result. Testing for Gastric Blood Heme tests designed for use on stool specimens can be unreliable when applied to gastric juices, with an increasingly high false-negative rate (low sensitivity) as pH decreases.[155] Thus, while a positive test of gastric contents using a fecal Hemoccult card is likely to be accurate, a negative test with the fecal Hemoccult card does not rule out the presence of blood. The Gastroccult card uses a modified guaiac developer containing buffers to neutralize gastric acid, thereby facilitating accurate hemoglobin detection. The test works on the same basis as the fecal guaiac test using the properties of hemoglobin as a peroxidase. In product testing, the Gastroccult card was 100% sensitive in detecting specimens of =500 parts per million of blood by volume, equivalent to 0.05%, or 0.25 mL of blood in 500 mL of gastric contents. Polyethylene glycol and high concentrations of iron (in an in vitro study simulating iron overdose) prevent both fecal occult blood tests from detecting blood. [106] Method
Apply a drop of gastric aspirate to the test area. Apply two drops of developer to the sample. Look for formation of a blue dye within 1 minute. Do not use fecal blood test developer. In a specimen that is already a bilious green, the test is only considered positive if new blue color is formed. The Gastroccult card also contains a pH testing strip located close to the occult blood testing area, which might be useful in testing emesis after an acid or alkali ingestion. False-positive results might be expected to occur (although studies to investigate this have not been performed) with meats and peroxidase-rich foods. False-negative reactions are likely in the presence of reducing substances, such as ascorbic acid. The accuracy of Gastroccult should not be affected by the presence of cimetidine or sucralfate. [106]
DIAGNOSTIC AND THERAPEUTIC TOXICOLOGIC BEDSIDE PROCEDURES The management of patients who present with an altered mental status can be challenging, especially if the clinician suspects drug overdose or poisoning. These patients often present with no available history or an inaccurate history. [295] Therefore, clinicians must rely heavily on physical examination findings and other sources of information to diagnose or confirm their clinical suspicions of poisoning or overdose. [48] The hospital toxicology laboratory can be valuable in select cases. Limited screening tests for commonly ingested drugs are available, and ascertaining levels of specific drugs (e.g., acetaminophen, lithium, digoxin, phenytoin) can be helpful. However, most hospital laboratories are not equipped to perform timely analytic procedures for the thousands of possible drugs or toxins. In fact, the results obtained from the drug screening panels that most hospitals use have been shown to rarely influence medical management of adult ED patients. [127] [128] In select pediatric patients, on the other hand, the use of drug screens may have more of an impact on medical management.[18] Diagnostic bedside testing for specific poisons or toxins has the advantage of being cost-effective and timely. When applied appropriately, certain bedside tests provide immediate information to the clinician and can have a significant and timely influence on medical management. This section discusses bedside diagnostic and therapeutic toxicologic procedures. Noninvasive Diagnostic Procedures Amatoxin: Meixner Test
The ingestion of several types of mushrooms (e.g., Amanita phalloides) can be fatal. The most poisonous of these are the mushrooms containing amatoxins. Patients who have ingested these mushrooms often complain of gastrointestinal symptoms consisting of nausea, vomiting, diarrhea, and abdominal cramping beginning 6 to 8 hours after ingestion. They often bring in specimens of the mushrooms chopped, crushed, cooked, or mixed with stool or gastric contents. Standard hospital laboratories cannot confirm or exclude the diagnosis of amatoxin poisoning; therefore, treatment decisions must be made on clinical grounds. [204] [276] Meixner reported a simple colorimetric test for detecting amatoxins that can be used on gastric contents, stool, or actual mushroom samples. The basis of this test is the acid-catalyzed color reaction of amatoxins with lignin, a complex organic compound found in wood pulp. Cheaper grades of paper (e.g., newsprint or the white pages of a telephone book) contain high amounts of lignin. Although there have been no extensive reports of in vivo studies, in vitro tests have shown this method to be highly sensitive and relatively specific for amatoxins. [23] [156] Psilocybin-containing mushrooms can cause false-positive results for amatoxin. [22] The procedure for a qualitative detection of amatoxin consists of squeezing a drop of liquid from a fresh mushroom sample or squashing a piece of fresh mushroom onto a piece of newspaper. If a stool or a gastric sample is the only
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available specimen, the sample is mixed with reagent grade methanol (99.8%). The methanol will extract the amatoxin. If the samples are mixed with methanol, they should then be centrifuged and filtered. Place a drop of the liquid extract on the newspaper. Gently air dry all specimens at room temperature and avoid direct sunlight. Add two to three drops of concentrated hydrochloric acid (37%) to the dried specimen. Use an adjacent area for a control. High amounts of amatoxin in the dried samples exhibit a blue color in 1 to 2 minutes. Small amounts of amatoxin show a blue color in the sampled area in 10 to 20 minutes. Note that this procedure has not been proven effective using other bodily secretions, such as blood or urine. [23] Mothball Identification
Present day commercial mothballs are composed of either paradichlorobenzene or naphthalene. Paradichlorobenzene is nontoxic whereas naphthalene can cause a significant hemolytic reaction in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency and in neonates. [229] In the past, mothballs were also produced from camphor, which can cause central nervous system (CNS) depression and seizures in overdoses. Fortunately, these mothballs are no longer commercially available, although they may still exist in some households. A rapid differentiation between these groups of mothballs can expedite patient management and disposition. Several bedside tests that take advantage of the physical and chemical properties of these agents have been used to differentiate between them.
TABLE 70-15 -- Diagnostic Odors Characteristic Odor
Responsible Drug or Toxin
Acetone (sweet, fruity; pear-like)
Lacquer, ethanol, isopropyl alcohol, chloroform, diabetic ketoacidosis, alcoholic ketoacidosis, trichloroethane, paraldehyde, chloral hydrate, methylbromide, Pseudomonas infections
Alcohols
Ethanol, (congeners) isopropyl alcohol
Ammonia-like
Uremia
Automobile exhaust
Carbon monoxide (odorless, but associated with exhaust)
Beer (stale)
Scrofula
Bitter almond
Cyanide
Carrots
Cicutoxin (or water hemlock)
Coal gas (stove gas)
Carbon monoxide (odorless, but associated with coal gas)
Disinfectants
Phenol, creosote
Eggs (rotten)
Hydrogen sulfide, carbon disulfide, mercaptans, disulfiram, N-acetylcysteine
Feculent
Intestinal obstruction
Fish or raw liver (musty)
Hepatic failure, zinc phosphide, hypermethioninemia, trimethylaminuria
Fruit-like
Nitrites (e.g., amyl, butyl), ethanol (congeners), isopropyl alcohol
Garlic
Phosphorus, tellurium, arsenic, parathion, malathion, selenium, dimethyl sulfoxide (DMSO), thallium
Halitosis
Acute illness, poor oral hygiene
Hay
Phosgene
Mothballs
Naphthalene, p-dichlorobenzene, camphor
Peanuts
N-3-pyridyl-methyl-N-p-nitrophenyl urea (Vacor)
Pepper-like
O-chlorobenzylidene malonitrile
Putrid
Anaerobic infections, esophageal diverticulum, lung abscess, scurvy
Rope (burned)
Marijuana, opium
Shoe polish
Nitrobenzene
Sweating feet
Isovaleric acid acidemia
Tobacco
Nicotine
Vinegar
Acetic acid
Vinyl-like
Ethchlorvynol (Placidyl)
Violets
Turpentine (metabolites excreted in urine)
Wintergreen
Methyl salicylate
From Chiang WK: Otolaryngologic principles. In Goldfrank LR, Flomenbaum NE, Lewin NA, et al (eds): Goldfrank's Toxicologic Emergencies. 5th ed. East Norwalk, Conn, Appleton & Lange 1994, p 374. From 3rd edition Roberts and Hedges, p 1232, Figure 74-13.
1. Paradichlorobenzene is heavier than naphthalene, which is heavier than camphor. In lukewarm tap water, camphor will float while naphthalene and paradichlorobenzene will sink. In a solution of 3 tbsp of table salt thoroughly dissolved in 4 oz of lukewarm water, camphor and naphthalene will float and paradichlorobenzene will sink. [143] 2. Paradichlorobenzene has a lower melting point than naphthalene. Paradichlorobenzene mothballs will melt in a water bath at 53°C whereas naphthalene requires a water bath >80°C. [221] 3. Paradichlorobenzene is described as "wet and oily," whereas naphthalene is described as having a "dry" appearance. Paradichlorobenzene is familiar to many people as a cake of disinfectant used in urinals and diaper pails. Body Secretion Analysis
Careful analysis of patients' bodily secretions, odor, and urine color can help identify certain toxins. Some characteristic smells and urine colors are noted in Table 70-15 and Table 70-16 . Bedside Toxicologic Tests on Urine Ethylene glycol.
Evaluation of the urine of patients who may have been exposed to ethylene glycol can be helpful. Microscopic inspection of urine for calcium oxalate crystals (a metabolic by-product of ethylene glycol metabolism) may be helpful in the diagnosis of ethylene glycol exposure. The presence of either envelope-shaped calcium dihydrate crystals or needle-shaped calcium monohydrate indicates high oxalate
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TABLE 70-16 -- Drugs That Color Urine Yellow Yellow Quinacrine (atabrine) in acid urine Riboflavin (large doses) Yellow-green Methylene blue, see blue Yellow-orange Fluorescein sodium Yellow-pink Cascara* in alkaline urine, see yellow-brown, brown, black Senna* in alkaline urine, see yellow-brown, brown Yellow-brown Cascara* in acid urine, see yellow-pink, brown, black Nitrofurantoin* (Furadantin and others), see brown Orange Phenazopyridine * (Pyridium), see red Orange-red Rifampin (Rifadin, Rifamycin, Rimactane) Pink Phenothiazines, * see red, red-brown Phenytoin* (Dilantin), see red, red-brown Red Anthraquinone in alkaline urine Deferoxamine (Desferal) Methyldopa (Aldomet), see brown, black Phenazopyridine * (Pyridium), see orange Phenothiazines, * see pink, red-brown Phenytoin* (Dilantin), see pink, red-brown Red-purple Phenacetin,* see brown Red-brown Phenothiazines, * see pink, red Phenytoin* (Dilantin), see pink, red
Brown Cascara* in alkaline urine, see yellow-brown, yellow-pink, black Levodopa (Dopar) Methocarbamol* (Robaxin), see green, black Metronidazole (Flagyl) Methyldopa* (Aldomet), see red, black Nitrofurantoin* (Furadantin and others), see yellow-brown Phenacetin,* see red-purple Quinine, * see black Senna* in alkaline urine on standing, see yellow-brown, yellow-pink Blue Methylene blue, * see green Triamterene (Dyrenium), fluorescent Blue-green Amitryptyline (Elavil, Endep) Green Indomethacin (Indocin) from liver damage Methocarbamol* (Robaxin), see brown-black Black Cascara* in alkaline urine on standing, see yellow-brown, yellow-pink, brown Iron sorbitex* (Jectofer), see brown Methocarbamol* (Robaxin), see brown, green Methyldopa (Aldomet), see red, black Quinine, * see brown From Thoman M: Vet Hum Toxicol 1982;24:55. Used with permission. From 3rd edition Roberts and Hedges, p 1233, Figure 74-14. *Drug imparts more than one color to urine and is listed under each color it adds.
levels in the serum ( Fig. 70-3 ). Calcium monohydrate crystals can be easily confused with sodium urate crystals; therefore, the presence of the dihydrate crystal tends to be more specific for ethylene glycol ingestion. The absence of these crystals does not rule out significant ethylene glycol ingestion, because the excretion of these may occur late in the ingestion (more than 6 hours) and occasionally does not occur at all. [107] [108] [115] Visual inspection of urine under a Wood's lamp or ultraviolet light to ascertain fluorescence may also be helpful in the diagnosis of ethylene glycol exposure. Antifreeze is the most common source of ingested ethylene glycol. Fluorescein, a fluorescing material, is often placed in commercially available antifreeze to enable mechanics to detect radiator leaks with a Wood's lamp or other ultraviolet light source. Fluorescein is a nontoxic inert vegetable dye that is eliminated unchanged in the urine. Therefore, high levels of fluorescein in urine suggest significant ethylene glycol ingestion. However, a lack of fluorescein does not rule out a significant exposure, because not all antifreezes contain fluorescein or high concentrations of fluorescein in relation to ethylene glycol. False-positive findings can occur if certain plastic urine containers are used. [291] To perform the test, fill glass test tubes with (1) the test urine sample, (2) a positive control urine sample (containing fluorescein) and (3) a negative control urine sample (not containing fluorescein). Inspect all three samples for fluorescence under a Wood's lamp in a dark room. The use of positive and negative controls may increase sensitivity and specificity from 49 and 75% to a sensitivity and specificity of 100%. [278] [291] Fluorescein is readily available in most EDs since fluorescein-containing strips are commonly used in ophthalmologic procedures (see Chapter 64 ). Salicylates.
Several qualitative bedside tests have been developed to detect salicylates in urine. These include 10%
Figure 70-3 "Prism-shaped" calcium monohydrate crystals (right) resembling hippurate or urate crystals, and octagonal calcium dihydrate crystals (left). (Illustration by NJ Miller.)
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ferric chloride solution, Trinder solution, and Phenistix reagent strips. All tests are rapid, inexpensive, and sensitive. Ferric chloride and Trinder solution both have sensitivities of 100% with serum salicylate levels of 5 mg/dL. False positives can occur with both tests in the presence of acetoacetic acid, acetone, and phenylpyruvic acid. Thus they may be falsely positive in patients with diabetic, alcoholic, or starvation ketoacidosis. Phenol-containing drugs such as diflunisal, sulfasalazine, and salicylamide may also produce false positives. A positive result, therefore, requires a confirmatory quantitative serum salicylate assay. [286] The ferric chloride test is a commonly used rapid, qualitative, urinary screening procedure. To perform this test, several drops of 10% ferric chloride are added to 1 or 2 mL of urine that has been collected in a test tube. The immediate appearance of a bluish purple color signifies that salicylates are present in urine. This test is very sensitive, and as few as two aspirin taken within 24 hours will give a positive result. It requires 90 to 120 minutes from time of ingestion for this reaction to become positive in the urine of patients with normal renal function, so when tested before this time, the results may be misleading. [33] The Trinder test uses a mixture of mercuric chloride and ferric nitrate in deionized water. To perform this test, 1 mL of urine is mixed with 1 mL of Trinder solution. A violet or purple color signifies the presence of salicylates. Acetoacetic acid and high levels of phenothiazines may give false-positive results. [136]
Phenistix reagent strips were originally developed to detect phenylketonuria. However, Phenistix strips also turn brown in the presence of salicylates. False-positive findings for salicylates can occur if phenothiazines are present. [29] Bedside Toxicologic Tests on Oral Secretions and Breath Ethyl alcohol.
There are several bedside devices to measure alcohol concentrations in bodily fluids. Measurements of alcohol concentration in expired air or saliva have been shown to correlate well with blood alcohol concentrations in the appropriate settings. Breath alcohol analyzers were developed in the 1950s and are presently used in law enforcement. These devices typically use an infrared spectral analysis to determine the concentration of alcohol in expired air. Almost all the alcohol found in expired air at the level of the mouth is secondary to alcohol diffused from the bronchial system rather than the alveolar system. [101] Minor alterations in breathing patterns can cause large variations in readings. Thus, uncooperative patients who do not exhale properly may give an inaccurate reading. Other causes of inaccurate readings include the use of alcohol-containing products including ingesting them, belching or vomiting, use of inhalers, poor technique, or restrictive pulmonary pathology. [69] [152] [159] A more recent technology for bedside measurement of alcohol concentration has been the use of a dipstick-like device to measure alcohol concentrations in saliva. These devices use an enzymatic reaction involving alcohol dehydrogenase to measure alcohol concentrations. [16] Patients who are dehydrated (a common occurrence in alcohol-intoxicated patients) are frequently unable to provide adequate saliva samples and inaccurate readings have occurred in patients with high blood alcohol concentrations. [19] [126] Bedside Toxicologic Tests on Blood Methemoglobinemia.
Patients with methemoglobinemia will often have a normal partial pressure of oxygen (pO 2 ) on routine arterial blood gas analysis, a normal calculated hemoglobin saturation, a nondiagnostic pulse oximeter reading, and cyanosis that does not clear with O 2 administration. Bedside visual inspection of venous or arterial blood may be helpful in the diagnosis of methemoglobinemia. Methemoglobinemia occurs when normal hemoglobin is exposed to an oxidant stress (Fe 2+ converted to Fe3+ ). If the erythrocytes cannot handle this stress, such as in the presence of G6PD deficiency, hemoglobin remains in an oxidized state (methemoglobin), causing a color change in the molecule. Methemoglobin levels higher than 15% are reported to cause a cyanotic appearance in a patient. [60] The evaluation procedure for methemoglobinemia is to place a drop of sample blood on a white background (a white coffee filter is appropriate) in a well-lit environment. Next to this, place a drop of normal blood as a comparison control sample. Blood with methemoglobinemia appears "darker" or "chocolate-brown."
[97]
This method relies on the ability of the examiner to distinguish color changes and therefore may have a degree of interobserver variance. Methemoglobin levels of less than 10% may only slightly alter the color of blood and thereby cause a false-negative finding. Methemoglobin levels of between 12% and 14% may cause a false-negative reading 50% of the time. However, at methemoglobin levels of 35% or higher, the identification of methemoglobinemia by visual inspection is quite accurate. [97] At this level, most patients are obviously cyanotic and significantly symptomatic. Invasive Diagnostic Procedures Several invasive diagnostic bedside procedures can be useful in the assessment of possible drug overdoses. The basic premise of these procedures is that patients who have been exposed to a certain drug or poison will respond in a particular fashion if given a diagnostic challenge dose of another particular drug or true antidote. Naloxone
Naloxone hydrochloride (Narcan) is an opioid receptor antagonist that has the ability to reverse the effects of chemical agents affecting all opioid receptor sites, particularly respiratory and CNS depression. Because of this, a trial of naloxone has been recommended for all patients with CNS depression. [68] Certain clinical findings such as miosis, decreased respiratory rate, and evidence of illicit drug use can predict many patients who will respond to a diagnostic challenge dose of naloxone.[104] If a patient's mental status improves significantly after a dose of naloxone, the patient should be considered to have been exposed to an opioid substance. This is true even if a laboratory drug screen is negative for opioids. One English study of laboratory drugs of abuse screens had false-positive rates of 4% and false-negative rates of 8%.[42] Furthermore, many of the synthetic opioid agents, such as fentanyl, propoxyphene, meperidine, methadone, and pentazocine may not be detected by the routinely used immunoassay drug screen. [78] Although cases have been reported of patients with other nonopioid overdoses (such as alcohol or phencyclidine) responding to
1410
naloxone, those single observations have not been confirmed in controlled animal or human studies. The traditional challenge dose of naloxone in an adult or child is 2 mg every 2 minutes IV until a response is achieved or 10 mg is given. [105] Some clinicians prefer to use much smaller doses (0.1 to 0.2 mg) and titrate to effect. This may partially reverse opioid overdose-related symptoms and confirm the diagnosis without precipitating the opioid withdrawal syndrome seen in patients with opioid dependency. Most patients with an opioid overdose will exhibit some response to 1 to 4 mg of naloxone, but some massive overdoses may require larger amounts. A patient who does not respond at all to 10 mg of naloxone probably does not have a pure opioid overdose. The high doses of naloxone presently recommended are needed to reverse many synthetic narcotic agents, such as propoxyphene and methadone. Lower doses can be given (0.4 to 0.8 mg in adults or 0.01 mg/kg in children) to reverse known opioid-induced respiratory depression without reversing analgesia. Because naloxone has a half-life between 30 and 60 minutes, a continuous drip of naloxone can be used to avoid resedation. A reasonable choice is to set the hourly IV dose at two-thirds of the initial bolus dose that achieved the desired reversal effect. For example, a patient who satisfactorily responded to 1.5 mg of naloxone might receive a naloxone solution of 10 mg of naloxone in 500 mL of normal saline at a rate of 1 mg (50 mL)/hour IV. [88] Nalmefene, a long-acting opioid receptor antagonist that has a terminal half-life of roughly 11 hours, can also be given to patients with suspected overdoses. Theoretically, a single dose of nalmefene will be effective longer than the effects of heroin or most abused opiate substances. The initial recommended dose is 1.0 to 1.5 mg IV. Naloxone and nalmefene have minimal significant side effects, other than precipitating withdrawal from patients addicted to opioids. Unlike alcohol withdrawal, naloxone-induced opioid withdrawal in the adult is short-lived and is usually not life-threatening. Withdrawal can be avoided if lower initial doses of naloxone or nalmefene are given and then are slowly titrated upward to the desired effect. Flumazenil
Flumazenil is a competitive benzodiazepine receptor antagonist that has the ability to reverse the CNS and respiratory depression caused by all currently commercially available benzodiazepines. The use of flumazenil as a routine diagnostic bedside challenge in all obtunded patients is discouraged, and its use in the setting of possible benzodiazepine overdose is controversial. Unlike naloxone, flumazenil can have significant side effects in certain subsets of patients. [104] These include precipitating seizures or a withdrawal syndrome in benzodiazepine-dependent patients. To minimize the chance of seizures, flumazenil should be avoided in patients who may have ingested epileptogenic drugs (e.g., cyclic antidepressants, cocaine, theophylline, lithium, carbamazepine, isoniazid). [248]
In suspected benzodiazepine overdoses where patients present with obtundation and have no history of seizures or suspicion of involvement of epileptogenic agents, flumazenil can be administered IV at a dose of 0.2 to 0.5 mg/min. Most benzodiazepine-overdosed patients show mental status improvement with 1 mg of flumazenil and almost all respond to 3 to 5 mg. It is prudent to use small, escalating doses given very slowly (maximally, 0.5 mg/min). Larger doses can be given at one time as a bolus, although this increases side effects such as anxiety, agitation, and emotional lability; it also increases the chances of precipitating withdrawal in benzodiazepine-dependent patients. [247] Fortunately, seizures that occur after flumazenil use are usually transient and can frequently be controlled with additional benzodiazepines. In rare cases, higher doses of benzodiazepines, barbiturates, and phenytoin may be required. [248] If a patient responds to flumazenil with an improvement in depressed mental status, this only suggests that the patient is under the influence of a benzodiazepine. Flumazenil can partially reverse the effects of many other agents or conditions that affect the ?-aminobutyric acid (GABA) pathway, such as zolpidem and hepatic encephalopathy [13] [92] [153] [275] ; however, it does not have any significant effect on alcohol, barbiturates, and other non-benzodiazepine sedative-hypnotics. Physostigmine
Physostigmine is an acetylcholinesterase inhibitor that can penetrate into the CNS and thus reverse both the central and peripheral effects of anticholinergic agents. In the majority of patients with anticholinergic toxicity, no laboratory tests are available to rapidly confirm the diagnosis, and testing for specific drugs is limited. A clinical picture that may consist of mydriasis, dry and flushed skin, dry mucous membranes, urinary incontinence, absent bowel sounds, tachycardia, hyperthermia, hallucinations, agitation, and seizures suggests an anticholinergic toxicologic syndrome. A rapid and dramatic response to physostigmine often confirms a diagnosis of anticholinergic toxicity. In these patients, physostigmine reduces much of the CNS toxicity of the agents and decreases the degree of agitation and confusion. [17] [43] [201] The use of physostigmine as a diagnostic challenge can be helpful in select situations, but similar to flumazenil, the routine use of physostigmine as a diagnostic bedside challenge in all obtunded patients should be discouraged. As a diagnostic challenge or therapeutic intervention, physostigmine can be administered IV under constant cardiac monitoring at a dose of 1 to 2 mg in adults and 0.02 mg/kg in children, over 5 minutes. Some clinicians empirically pretreat with a benzodiazepine to prevent seizures, but this practice has not been proven effective or necessary. Because the half-life of physostigmine is 30 to 60 minutes, a repeat dose of 2 mg can be given as clinically indicated. Similar to flumazenil, physostigmine has been reported to interact detrimentally with cyclic antidepressants, often causing life-threatening dysrhythmias. Physostigmine also can cause an excess of acetylcholine and a resultant cholinergic crisis. This syndrome includes salivation, lacrimation, urination, defecation, bradycardia, bronchorrhea, and seizures. Dysrhythmias, including asystole, have also been reported. [210] For this reason, 1 mg of atropine IV should be readily available to reverse potential cholinergic excess when using physostigmine. Deferoxamine
Deferoxamine is an organic compound derived from the bacterium Streptomyces pilosus. Deferoxamine can chelate iron and can be used as therapy or as a diagnostic challenge in patients with iron overdoses. Patients who have unstable vital signs or significant GI or CNS symptoms usually require therapeutic doses of deferoxamine. Asymptomatic patients with a
1411
history of iron overdose usually require supportive care only. Patients with persistent but mild symptoms, such as vomiting and diarrhea, may be given a diagnostic challenge dose of deferoxamine. A diagnostic challenge is preferential over ancillary laboratory testing because tests such as iron levels and total iron binding capacity in the setting of iron overdose can be inaccurate, misleading, and time-consuming. [162] [241] [268] A diagnostic challenge dose of deferoxamine is administered IM or IV over 45 minutes at doses of 40 to 90 mg/kg up to a maximum of 1 g in children and 2 g in adults. Deferoxamine can also be administered IV as a constant drip of 15 mg/kg/hour. A positive result occurs when chelated iron in the form of ferrioxamine appears in the urine. This usually causes the urine to turn a reddish orange or "vin rosé" color in 2 to 3 hours after initiation of treatment. The color change is qualitative only and has no prognostic significance. Color change caused by ferrioxamine is pH and concentration dependent, and false-negative test results occur. [181] [218] Chronically administered deferoxamine has been reported to have multiple adverse effects, such as adult respiratory distress syndrome (ARDS), visual defects, and enhancement of Yersinia enterocolitica infections. In the setting of the single challenge dose, flushing, erythema, tachycardia, urticaria, and hypotension caused by rapid administration of deferoxamine are the most serious side effects. [289] Invasive Therapeutic Procedures The indications and rationale for use of certain therapeutic procedures in toxicology are often misunderstood. Alkalinization of Urine and Blood
Alkalinization of urine consists of manipulating the pH of urine to enhance excretion of certain drugs ( Table 70-17 ). Weak acids remain in ionic form in a basic milieu. The ionic form often prevents reabsorption of that drug in the proximal tubule, and urinary alkalinization can therefore promote elimination in the urine. For certain drugs, this can play a significant role in their elimination. For example, salicylate elimination increases proportionately to the urinary flow rate, but it increases exponentially with increases in the urinary pH. [189] [216] Recommendations differ on the actual method or formula to achieve urinary alkalinization. No body of literature exists that supports one method of urinary alkalinization over another. [285] In general, this procedure should be titrated to the patient's fluid and acid-base status to achieve a urinary pH of 7.5 to 8.0. Many authors recommend the use of a constant infusion of a relatively isotonic solution consisting of 3 ampules of sodium bicarbonate (44 mmol/ ampule) added to 1 L of 5% dextrose in water (D5 W). Another reasonable formula is to begin with a bolus of two ampules of IV sodium bicarbonate, or 1 to 2 mmol/kg of body weight. The bolus is TABLE 70-17 -- Drugs That Have Increased Elimination with Urinary Alkalinization Chlorpropamide 2,4-Dichlorophenoxyacetic acid Formate Methotrexate Phenobarbital Salicylates followed with a constant infusion of three ampules of sodium bicarbonate in 1 L of D 5 W solution with 20 to 40 mmol of potassium (if the patient has normal renal function) infused at 100 to 300 mL/hour. Although repetitive boluses of sodium bicarbonate ampules also can be used, this may increase the chances of hypernatremia, hypokalemia, relative hypocalcemia, fluid overload, and alkalemia. All of these are potential adverse effects of aggressive urinary alkalinization. The actual amount of fluids and bicarbonate administered requires titration to the patient's clinical condition. Therefore careful monitoring of electrolyte, pH, and fluid status is encouraged. [267] Urinary alkalinization can sometimes be difficult to achieve or maintain. Hypovolemia is probably the leading cause of an inability to achieve alkaline urine. Other theoretical causes are hypokalemia and hypochloremia. Several authors have suggested that in patients with severe salicylate poisoning, urinary alkalinization may
be difficult if not impossible to achieve with reasonable doses of bicarbonate.
[285]
Ethanol Infusion Recently, fomepizole (4-methylpyrazole) has been approved by the FDA for the treatment of ethylene glycol poisonings. It has also been used successfully in treating methanol poisonings. [31] [182] Compared to the traditional treatment of toxic alcohol poisoning, namely ethanol, fomepizole has the advantages of ease of use, fewer side effects (specifically hypoglycemia), and ability to maintain therapeutic levels. [30] [32] However, owing to the cost and the logistics of stocking this antidote, many hospitals may not have this drug readily available. Ethanol can be used as a therapeutic intervention in patients with methanol or ethylene glycol poisoning due to ethanol's much greater affinity for alcohol dehydrogenases. These enzymes metabolize methanol and ethylene glycol to even more toxic by-products. However, with serum ethanol levels of 100 mg/dL, minimal amounts of ethylene glycol or methanol are metabolized by alcohol dehydrogenases. [31] [32] [41] Ethanol infusions are not useful in the treatment of isopropyl alcohol poisoning. Ethanol can be administered orally or IV ( Table 70-18 ). Intravenous ethanol has the advantages of obtaining therapeutic levels rapidly, ensuring complete absorption, limiting chances of aspiration, and avoiding gastritis. A 5% concentration of ethanol, which can be given in a peripheral vein, requires the use of large fluid volumes. In a 70-kg patient, a loading dose requires 1.4 L of 5% solution, with a maintenance dose of 700 mL/hr. In contrast, oral loading can be achieved using much lower volumes. However, oral loading can be difficult in the uncooperative or unconscious patient or if vomiting or GI hemorrhage is present. A therapeutic level is reached slower with oral loading. Ethanol metabolism can vary widely, and ethanol is dialyzable. Therefore, it may be difficult to maintain appropriate ethanol levels during dialysis therapy of ethylene glycol or methanol. Frequent measurements of ethanol should be obtained and the infusion adjusted accordingly. [84] When patients are given ethanol infusions, CNS depression and hypoglycemia are common adverse effects (the latter is particularly true in diabetics and children). Serial levels of ethanol and glucose should be obtained. If IV ethanol is given, careful attention to cardiopulmonary status should be maintained. [142] [249]
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TABLE 70-18 -- Ethanol in Methanol or Ethylene Glycol Poisoning * Intravenous Ethanol: Loading Dose (using a 10% ethanol solution) a (A 10% volume/volume concentration yields approximately 100 mg/mL) Volume of loading dose (given over 1–2 hr as tolerated) a
Loading dose of 1000 mg/kg of 10% ethanol (infused over 1–2 hours as tolerated); assumes a zero ethanol level to start
10 kg
15 kg
30 kg
50 kg
70 kg
100 kg
100 mL
150 mL
300 mL
500 mL
700 mL
1000 mL
Aim is to produce a serum ethanol level of 100–150 mg/dL Oral Ethanol: Loading Dose (A 20% volume/volume concentration yields approximately 200 mg/mL) Volume of loading dose 10 kg Loading dose of 1000 mg/kg of 20% ethanol, b diluted in juice; may be administered orally or via nasogastric tube; assumes a zero ethanol level to start
15 kg
30 kg
50 mL 75 mL 150 mL
50 kg
70 kg
100 kg
250 mL
350 mL
500 mL
Aim is to produce a serum ethanol level of 100–150 mg/dL Intravenous Ethanol: Maintenance Dose (using a 10% ethanol solution) c (A 10% volume/volume concentration yields approximately 100 mg/mL. Infusion to be started immediately following the loading dose. Aim is to maintain serum ethanol level of 100–150 mg/dL † ) Infusion rate (mL/hr for various weights) c Normal maintenance range
10 kg
15 kg
30 kg
50 kg
70 kg
100 kg
80 mg/kg/hr
8
12
24
40
56
80
110 mg/kg/hr
11
16
33
55
77
110
130 mg/kg/hr
13
19
39
65
91
130
15
22
45
75
105
150
250 mg/kg/hr‡
25
38
75
125
175
250
300 mg/kg/hr‡
30
45
90
150
210
300
350 mg/kg/hr‡
35
53
105
175
245
350
Approximate maintenance dose for chronic alcoholic 150 mg/kg/hr‡ Range required during hemodialysis
Oral Ethanol: Maintenance Dose (A 20% volume/volume concentration yields approximately 200 mg/mL; infusion to be given each hour immediately following a loading dose; aim is to maintain serum ethanol level of 100–150 mg/dL; † each dose may be diluted in juice and given orally or via nasogastric tube) Infusion rate (mL/hr § for various weights ¶ ) Normal maintenance range
10 kg
15 kg
30 kg
50 kg
70 kg
100 kg
80 mg/kg/hr
4
6
12
20
28
40
110 mg/kg/hr
6
8
17
27
39
55
130 mg/kg/hr
7
10
20
33
46
66
8
11
22
38
53
75
250 mg/kg/hr
13
19
38
63
88
125
300 mg/kg/hr
15
23
46
75
105
150
350 mg/kg/hr
18
26
52
88
123
175
Approximate range for chronic alcoholic or for patient receiving continuous oral activated charcoal 150 mg/kg/hr Range required during hemodialysis
*Note: Concentrations higher than 10% are not recommended for IV administration. Concentrations higher than 30% are not recommended for oral administration. The dose schedule is based on the premise that the patient initially has a zero ethanol level. The aim of therapy is to maintain a serum ethanol level of 100 to 150 mg/dL, but constant monitoring of the ethanol level is required because of wide variations in endogenous metabolic capacity. Ethanol is removed by dialysis, and the infusion rate of ethanol must be increased during dialysis. Prolonged ethanol administration may lead to hypoglycemia. Note: 10% ethanol for infusion may be difficult to find in the hospital pharmacy. To formulate 10% ethanol for infusion (1) remove 50 mL from a 1-L bottle of 5% ethanol/D 5 W and replace it with 50 ml of 100% ethanol, or (2) remove 100 mL from a 1-L bottle of D 5 W and replace it with 100 ml of 100% ethanol. a If a 5% ethanol solution is used, double the volume of the loading dose. b Equivalent to a 40 proof solution.
c
If a 5% ethanol solution is used, double the volume rate; monitor closely for potential volume overload. †Serum ethanol levels should be monitored closely. ‡At higher infusion rates, it may be necessary to administer by volume rather than by mL/hr. §For a 30% concentration, divide the amount by 1.5. ¶Rounded off to nearest milliliter.
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References 1. Adams
LJ: Evaluation of Ames multistix-SG for urine specific gravity vs. refractometer specific gravity. Am J Clin Pathol 80:871, 1983.
2. Ahlquist 3. Alpern 4. Alwall 5. Amir
DA, McGill DB, Schwartz S, et al: Fecal blood levels in health and disease. A study using Hemoquant. N Engl J Med 312:1422, 1985.
ER, Alessandrini EA, Bell LM, et al: Occult bacteremia from a pediatric emergency department: Current prevalence, time to detection, and outcome. Pediatrics 106:505, 2000.
N: Pyuria: Deposit in high-power microscopic field—WBC/HPF—versus WBC/mm
3
in counting chamber. Acta Med Scand 194:537, 1973.
J, Ginzburg M, Straussberg R, et al: The reliability of midstream urine cultures from circumcised male infants. Am J Dis Child 147:969, 1993.
6. Anderson
GD, Yuellig TR, Krone RE Jr: An investigation into the effects of oral iron supplementation on in vivo Hemoccult stool testing. Am J Gastroenterol 85:558, 1990.
7. Aronson
AS, Gustafson B, Svenningsen NW: Combined suprapubic aspiration and clean voided urine examination in infants and children. Acta Paed Scand 62:396, 1973.
8. Aronson
MD, Bor DH: Blood cultures. Ann Intern Med 106:246, 1987.
9. Arpi
M, Bentzon MW, Jenson J, et al: Importance of blood volume cultured in the detection of bacteremia. Eur J Clin Microbiol Infect Dis 8:838, 1989.
10.
Assadi FK, Fornell L: Estimation of urine specific gravity in neonates with a reagent strip. J Pediatr 108:995, 1986.
11.
Banco, VD: Ability of mothers to subjectively assess the presence of fever in their children. Am J Dis Child 138:976, 1984.
12.
Barnhart KT, Simhan H, Kamelle SA: Diagnostic accuracy of ultrasound above and below the beta-hCG discriminatory zone. Obstet Gynecol 94:583, 1999.
13.
Basile AS, Hughes RD, Harrison PM, et al: Elevated brain concentrations of 1,4-benzodiazepines in fulminant hepatic failure. N Engl J Med 325:473, 1991.
14.
Bates DW, Cook EF, Goldman L, et al: Predicting bacteremia in hospitalized patients. A prospectively validated model. Ann Intern Med 113:495, 1990.
15.
Bates DW, Goldman L, Lee TH: Contaminant blood cultures and resource utilization: The true consequences of false-positive results. JAMA 265:365, 1991.
16.
Bates ME, Martin CS: Immediate, quantitative estimation of blood alcohol concentration from saliva. J Stud Alcohol 58:531, 1997.
17.
Beaver KM, Gavin TJ: Treatment of acute anticholinergic poisoning with physostigmine. Am J Emerg Med 16:505, 1998.
18.
Belson MG, Simon HK, Sullivan K, et al: The utility of toxicologic analysis in children with suspected ingestions. Pediatr Emerg Care 15:383, 1999.
19.
Bendtsen P, Hultberg J, Carlsson M, et al: Monitoring ethanol exposure in a clinical setting by analysis of blood, breath, saliva, and urine. Alcohol Clin Exp Res 23:1446, 1999.
20.
Bennett IL, Beeson PB: Bacteremia: A consideration of some experimental bacteremias. Yale J Biol Med 226:241, 1954.
21.
Berger SA: Pseudobacteremia due to contaminated alcohol swabs. J Clin Microbiol 18:974, 1983.
22.
Beuhler M, Lee D: Psilocybin and 5-substituted tryptamines cause false-positive reactions with the Meixner test (abstract). J Toxicol-Clin Toxicol 38:504, 2000.
23.
Beutler J, Vergeer P: Amatoxins in American mushrooms: Evaluation of the Meixner test. Mycologia 72:1142, 1980.
24.
Boehm JJ, Haynes JL: Bacteriology of "midstream catch" urines. Am J Dis Child 111:366, 1966.
25.
Bonnardeaux A, Somerville P, Kaye M: A study of the reliability of dipstick urinalysis. J Clin Neph 41:167, 1994.
26.
Braude H, Forfar JO, Gould JC, et al: Cell and bacterial counts in the urine of normal infants and children. Br Med J 4:697, 1967.
27.
Bree RL, Edwards M, Bohm-Velez M, et al: Transvaginal sonography in the evaluation of normal early pregnancy: Correlation with hCG level. AJR Am J Roentgenol 153:75, 1989.
28.
Brennan DF: Ectopic pregnancy: I. Clinical and laboratory diagnosis. Acad Emerg Med 2:1081, 1995.
29.
Brenner BE, Simon RR: Management of salicylate intoxication. Drugs 24:335, 1982.
30.
Brent J: Current management of ethylene glycol poisoning. Drugs 61:979, 2001.
31.
Brent J, McMartin K, Phillips S, et al: Fomepizole for the treatment of methanol poisoning. N Engl J Med 344:424, 2001.
32.
Brent J, McMartin K, Phillips S, et al: Fomepizole for the treatment of ethylene glycol poisoning. Methylpyrazole for Toxic Alcohols Study Group. N Engl J Med 340:832, 1999.
33.
Broder, JN: The ferric chloride screening test. Ann Emerg Med 16:1188, 1987.
34.
Brown DF, Warren RE: Effect of sample volume on yield of positive blood cultures for adult patients with hematological malignancy. J Clin Pathol 43:777, 1990.
35.
Browne GJ, Ryan JM, McIntyre P. Evaluation of a protocol for selective empiric treatment of fever without localising signs. Arch Dis Child 76:129, 1997.
36.
Brumfitt W: Urinary cell counts and their value. J Clin Pathol 18:550, 1965.
37.
Bryant JK, Strand CL: Reliability of blood cultures collected from intravenous catheters versus venepuncture. Am J Clin Pathol 88:113, 1987.
38.
Buckley RG, Conine M: Reliability of subjective fever in triage of adult patients. Ann Emerg Med 27:693, 1996.
39.
Bukata WR: Treatment of urinary tract infections, part I. Emerg Med and Acute Care Essays 18:1, 1994a.
40.
Bukata WR: Blood cultures—problems and pitfalls. Emerg Med Acute Care Essays 18:7:1, 1994b.
41.
Burkhart KK, Kulig KW: The other alcohols: Methanol, ethylene glycol, and isopropanol. Emerg Med Clin North Am 8:913, 1990.
Burnett D, Lader S, Richens A, et al: A survey of drugs of abuse testing by clinical laboratories in the United Kingdom. Steering committee for the UK-external quality assessment scheme for therapeutic drug assays. Ann Clin Biochem 27:213, 1990. 42.
43.
Burns MJ, Linden CH, Graudins A, et al: A comparison of physostigmine and benzodiazepines for the treatment of anticholinergic poisoning. Ann Emerg Med 35:374, 2000.
44.
Campos JM: Detection of bloodstream infections in children. Eur J Clin Microbiol Infect Dis 8:815, 1989.
45.
Carel RS, Silverberg DS, Kaminsky R, et al: Routine urinalysis (dipstick findings in mass screening of healthy adults). Clin Chem 33:2106, 1987.
46.
Carlson KJ, Mulley AG: Management of acute dysuria. Ann Intern Med 102:244, 1985.
47.
Castle SC, Norman DC, Yeh M, et al: Fever response in elderly nursing home residents: Are the older truly colder? J Am Geriatr Soc 39:853, 1991.
48.
Chan B, Gaudry P, Grattan-Smith TM, et al: The use of Glasgow coma scale in poisoning. J Emerg Med 11:579, 1993.
49.
Chandrasekar PH, Brown WJ: Clinical issues of blood cultures. Arch Intern Med 154:841, 1994.
50.
Chandler MT, Morton ES, Byrd RP Jr, et al: Reevaluation of anaerobic blood cultures in a veteran population. South Med J 93:986, 2000.
51.
Chapnick EK, Schaffer BC, Gradon JD, et al: Technique for drawing blood for culture: Is changing needles really necessary? South Med J 84:1197, 1991.
52.
Chernow B, Zaloga GP, Soldano S, et al: Measurement of urinary leukocyte esterase activity: A screening test for urinary tract infections. Ann Emerg Med 13:150, 1984.
Christenson RH, Tucker JA, Allen E: Results of dipstick tests, visual inspection, microscopic examination of urine sediment, and microbiological cultures of urine compared for simplifying urinalysis. Clin Chem 31:448, 1985. 53.
54.
Cohen HT, Spiegel DM: Air-exposed urine dipsticks give false-positive results for glucose and false-negative results for blood. Am J Clin Path 96:398, 1991.
55.
Cole LA, Kardana A: Discordant results in human gonadotropin assays. Clin Chem 38:263, 1992.
Cole LA, Seifer DB, Kardana A, et al: Selecting human chorionic gonadotropin immunoassays: Consideration of cross-reacting molecules in first trimester pregnancy serum and urine. Am J Obstet Gynecol 168:1580, 1993. 56.
57.
Counselman FL, Shaar GS, Heller RA, et al: Quantitative ß-hCG levels less than 1000 mIU/mL in patients with ectopic pregnancy: Pelvic ultrasound still useful. J Emerg Med 16:699, 1998.
58.
Crain EF, Gershel JC: Urinary tract infections in febrile infants younger than eight weeks of age. Pediatrics 86:363, 1990.
59.
Creinin MD, Meyn L, Klimashko T: Accuracy of serum beta-human chorionic gonadotropin cutoff values at 42 and 49 days' gestation. Am J Obstet Gynecol 185:966, 2001.
60.
Curry S: Methemoglobinemia. Ann Emerg Med 11:214, 1982.
1414
61.
Dart RG, Kaplan B, Cox C: Transvaginal ultrasound in patients with low beta-human chorionic gonadotropin values: How often is the study diagnostic? Ann Emerg Med 30:135, 1997.
62.
DeCherney AH: Ectopic pregnancy. American College of Obstetricians and Gynecologists Technical Bulletin No. 150, Dec 1990, p 2.
63.
DesJardin JA, Falagas ME, Ruthazer R, et al: Clinical utility of blood cultures drawn from indwelling central venous catheters in hospitalized patients with cancer. Ann Intern Med 131:641, 1999.
64.
Dietzman DE, Fisher GW, Schoenknecht FD: Neonatal Escherichia coli septicemia—Bacterial counts in blood. J Pediatr 85:128, 1974.
65.
Dimarchi JN, Kosasa TS, Hale RW: What is the significance of human gonadotropin value in ectopic pregnancy? Obstet Gynecol 74:851, 1989.
66.
Doern GV, Saubolle MA, Sewell DL: Screening for bacteriuria with the LN strip test. Diagn Microbiol Infect Dis 4:355, 1986.
67.
Dorsher CW, Rossenblatt JE, Wilson WR, et al: Anaerobic bacteremia: Decreasing rate over a 15-year period. Rev Inf Dis 13:633, 1991.
68.
Doyon S, Roberts JR: Reappraisal of the "coma cocktail." Dextrose, flumazenil, naloxone, and thiamine. Emerg Med Clin North Am 12:301, 1994.
69.
Dubowski KM: Quality assurance in breath-alcohol analysis. J Anal Toxicol 18:306, 1994.
70.
Durbin WA, Szymczak EG, Goldman DA: Quantitative blood cultures in childhood bacteremia. J Pediatr 92:778, 1978.
71.
Ebaugh FG Jr, Clements T Jr, Rodan G: Quantitative measurement of gastrointestinal blood loss. Am J Med 25:169, 1958.
72.
Eisenberg JM, Rose JD, Weinstein AJ: Routine blood cultures from febrile outpatients: Use in detecting bacteremia. JAMA 236:2863, 1976.
73.
Epstein D, Raveh D, Schlesinger Y: Adult patients with occult bacteremia discharged from the emergency department: Epidemiological and clinical characteristics. Clin Infect Dis 32:559, 2001.
74.
Everts RJ, Vinson EN, Adholla PO, et al: Contamination of catheter-drawn blood cultures. J Clin Microbiol 39:3393, 2001.
75.
Felices FJ, Hernandez JL, Mesguer J, et al: Use of the central venous catheter to obtain blood cultures. Crit Care Med 7:78, 1979.
76.
Fitzgerald FT: Hypoglycemia and accidental hypothermia in an alcoholic population. West J Med 133:105, 1980.
77.
Fontanarosa PB, Kaeberlein FJ, Gerson LW, et al: Difficulty in predicting bacteremia in elderly emergency department patients. Ann Emerg Med 2:842, 1992.
78.
Ford M, Hoffman RS, Goldfrank LR: Opioids and designer drugs. Emerg Med Clin North Am 8:495, 1990.
79.
Fraser K, Fretter MC, Mast RL, et al: Studies with a simplified nitro-prusside test for ketone bodies in urine, serum, plasma, and milk. Clin Chim Acta 11:372, 1965.
80.
Gadeholt H: Quantitative estimation of urinary sediment, with special regard to sources of error. Br Med J 15:47, 1964.
81.
Gallagher EJ, Schwartz E, Weinstein R: Performance characteristics of urine dipsticks stored in open containers. Am J Emerg Med 8:121, 1990.
Geerdes HF, Ziegler D, Lode H, et al: Septicemia in 980 patients at a university hospital in Berlin: Prospective studies during four selected years between 1979 and 1989. Clin Infect Dis 15:991, 1992. 82.
83.
Gelbart SM, Chen WT, Reid R: Clinical trial of leukocyte test strips in routine use. Clin Chem 29:997, 1983.
84.
Gershman H, Steeper J: Rate of clearance of ethanol from the blood of intoxicated patients in the emergency department. J Emerg Med 9:307, 1991.
85.
Gillenwater JY: Detection of urinary leukocytes by Chemstrip-L. J Urol 125:383, 1981.
86.
Gleckman R, Hilbert D: Afebrile bacteremia: A phenomenon in geriatric patients. JAMA 248:1478, 1982.
87.
Gnauck R, Macrae FA, Fleisher M: How to perform the fecal occult blood test. Cancer 34:134, 1984.
88.
Goldfrank L, Weisman RS, Errick JK et al: A dosing nomogram for continuous infusion intravenous naloxone. Ann Emerg Med 15:566, 1986.
89.
Goldsmith BM, Campos JM: Comparison of urine dipstick, microscopy, and culture for the detection of bacteriuria in children. Clin Pediatr (Phila) 29:214, 1990.
90.
Grahn D, Norman DC, White ML et al: Validity of urinary catheter specimen for diagnosis of urinary tract infection in the elderly. Arch Intern Med 145:1858, 1985.
91.
Gutman SI, Solomon RR: The clinical significance of dipstick negative, culture positive urines in a veterans population. Am J Clin Pathol 88:204, 1987.
Gyr K, Meier R, Haussler J, et al: Evaluation of the efficacy and safety of flumazenil in the treatment of portal systemic encephalopathy: A double blind, randomised, placebo controlled multicentre study. Gut 39:319, 1996. 92.
93.
Haddon RA, Barnett PL, Grimwood K et al: Bacteraemia in febrile children presenting to a paediatric emergency department. Med J Aust 170:475, 1999.
94.
Hall MM, Ilstrup DM, Washington JA: Effect of volume of blood cultured on detection of bacteremia. J Clin Microbiol 3:643, 1976.
95.
Hardy JD, Furnell PM, Brumfitt W: Comparison of sterile bag, clean catch, and suprapubic aspiration in the diagnosis of urinary infection in early childhood. Br J Urol 48:279, 1976.
Harvey SC: Antiseptics and disinfectants; fungicides and ectoparasiticides. In Gilman AG, Goodman LS, Rall TW, Murad F (eds): Goodman and Gilman's The Pharmacologic Basis of Therapeutics, 7th ed. New York, Macmillan, 1980, p 959. 96.
97.
Henretig FM, Gribetz B, Kearney T, et al: Interpretation of color change in blood with varying degree of methemoglobinemia. J Toxicol Clin Toxicol 26:293, 1988.
98.
Henry NK, McLimans CA, Wright AJ, et al: Microbiological and clinical evaluation of the isolator lysis-centrifugation blood culture tube. J Clin Microbiol 17:864, 1983.
99.
Henry JB (ed): Clinical Diagnosis and Management by Laboratory Methods, 19th ed. Philadelphia, WB Saunders, 1996.
100. Hickey
RW, Bowman MJ, Smith GA: Utility of blood cultures in pediatric patients found to have pneumonia in the emergency department. Ann Emerg Med 27:721, 1996.
101. Hlastala
MP: The alcohol breath test—a review. J Appl Physiol 84:401, 1998.
102. Hoberman
A, Wald ER, Penchansky L, et al: Enhanced urinalysis as a screening test for urinary tract infection. Pediatrics 91:1196, 1993.
103. Hockberger
RS, Schwartz B, Connor J: Hematuria induced by urethral catheterization. Ann Emerg Med 16:550, 1987.
104. Hoffman
JR, Schriger DL, Luo JS: The empiric use of naloxone in patients with altered mental status: A reappraisal. Ann Emerg Med 20:246, 1991.
105. Hoffman
RS, Goldfrank LR: The poisoned patient with altered consciousness. Controversies in the use of a "coma cocktail." JAMA 274:562, 1995.
106. Holman 107. Huhn
JS, Shwed JA: Influence of sucralfate on the detection of occult blood in simulated gastric fluid by two screening tests. Clin Pharmacol Ther 11:625, 1992.
KM, Rosenberg FM: Critical clue to ethylene glycol poisoning. CMAJ 152:193, 1995.
108. Hylander 109. Ilstrup
B, Kjellstrand CM: Prognostic factors and treatment of severe ethylene glycol intoxication. Intensive Care Med 22:546, 1996.
DM, Washington JA: The importance of volume of blood cultured in the detection of bacteremia and fungemia. Diagn Microbiol Infect Dis 1:107, 1983.
110. Immergut
MA, Gilbert EC, Frensilli FJ, et al: The myth of the clean catch urine specimen. Urology 17:339, 1981.
111. Isaacman
DJ, Karasic RB: Utility of collecting blood cultures through newly inserted intravenous catheters. Pediatr Infect Dis J 9:815, 1990a.
112. Isaacman
DJ, Karasic RB: Lack of effect of changing needles on contamination of blood cultures. Pediatr Infect Dis J 9:274, 1990b.
113. Isaacman
DJ, Shults J, Gross TK et al: Predictors of bacteremia in febrile children 3 to 36 months of age. Pediatrics 106:977, 2000.
114. Jacobs
DS, DeMott WR, Finley PR, et al (eds): Laboratory Test Handbook, 3rd ed. Cleveland, OH, Lexicomp, 1994.
115. Jacobsen 116. Jaffe
D, Hewlett TP, Webb R, et al: Ethylene glycol intoxication: Evaluation of kinetics and crystaluria. Am J Med 84:145, 1988.
RM, Kasten B, Young DS, et al: False-negative stool occult blood tests caused by ingestion of ascorbic acid (vitamin C). Ann Intern Med 83:824, 1975.
117. Jarvis
WR, Martone WJ: Predominant pathogens in hospital infections. J Antimicrob Chemother 29:19, 1992.
118. Jenkins
RD, Fenn JP, Matsen JM: Review of urine microscopy for bacteriuria. JAMA 255:3397, 1986.
119. Johnson
JR, Stamm WE: Urinary tract infections in women. Ann Intern Med 111:906, 1989.
120. Kadar
N, Caldwell BU, Romero RA: A method for screening for ectopic pregnancy and its indications. Obstet Gynecol 58:162, 1981.
121. Kadar
N, Romero R: Serial human chorionic gonadotropin measurements in ectopic pregnancy. Am J Obstet Gynecol 158:1239, 1988.
122. Kaplan
BC, Dart RG, Moskos M, et al: Ectopic pregnancy: Prospective study with improved diagnostic accuracy. Ann Emerg Med 28:10, 1996.
123. Karras
DJ, Heilpern KL, Riley L, et al: Urine dipstick as a screening test for serum creatinine elevation in emergency department patients with severe hypertension. Acad Emerg Med 9:27, 2002.
1415
124. Kass
EH: Chemotherapeutic and antibiotic drugs in the management of infections of the urinary tract. Am J Med 18:764, 1955.
125. Kass
EH: Asymptomatic infections of the urinary tract. Transactions Assist Am Phys 69:56, 1956.
126. Keim
ME, Bartfield JM, Raccio-Robak N: Blood ethanol estimation: A comparison of three methods. Acad Emerg Med 3:85, 1996.
127. Kellermann
AL, Fihn SD, LoGerfo JP: Impact of drug screening in suspected overdose. Ann Emerg Med 16:1206, 1987.
128. Kellermann
AL, Fihn SD, LoGerfo JP: Utilization and yield of drug screening in the emergency department. Am J Emerg Med 6:14, 1988.
129. Kellogg
JA, Manzella JP, Shaffer S, et al: Clinical relevance of culture versus screens for the detection of pathogens in urine specimens. Am J Med 83:739, 1987.
130. Kellogg
JA: Justification and implementation of a policy requiring two blood cultures when one is ordered. Lab Med 25:323, 1994.
131. Kellogg
JA: Selection of a clinically satisfactory blood culture system: The utility of anaerobic media. Clin Micro Newslet 17:121, 1995.
132. Kellogg
JA, Manzella JP, Bankert DA: Frequency of low-level bacteremia in children from birth to fifteen years of age. J Clin Microbiol Rev 38:2181, 2000.
133. Kennedy 134. Kesson 135. Kiel
TJ, McConnell JD, Thal ER: Urine dipstick vs. microscopic urinalysis in the evaluation of abdominal trauma. J Trauma 28:615, 1988.
AM, Talbot JM, Gyory AZ: Microscopic examination of the urine. Lancet 2:809, 1978.
DP, Moskowitz MA: The urinanalysis: A critical appraisal. Med Clin North Am 71:607, 1987.
136. King
JA, Storrow AB, Finkelstein JA: Urine Trinder spot test: A rapid salicylate screen for the emergency department. Ann Emerg Med 26:330, 1995.
137. King
TC, Price PB: An evaluation of iodophors as skin antiseptics. Surg Gyn Obst 116:361, 1963.
138. Kline
MW, Lorin MI: Bacteremia in children afebrile at presentation to an emergency room. Pediatr Infect Dis J 6:197, 1987.
139. Knudsen
RP, Alden ER: Neonatal heel stick blood culture. Pediatrics 65:505, 1980.
140. Komaroff
AL: Acute dysuria in women. N Engl J Med 310:368, 1984.
141. Komaroff
AL: Urinalysis and urine culture in women with dysuria. Ann Intern Med 104:212, 1986.
142. Kowalczyk
M, Halvorsen S, Ovrebo S, et al: Ethanol treatment in ethylene glycol poisoned patients. Vet Hum Toxicol 40:225, 1998.
143. Koyama
K, Yamashita M, Ogura Y, et al: A simple test for mothball component differentiation using water and a saturated solution of table salt: Its utilization for poison information service. Vet Hum Toxicol 33:425, 1991. 144. Krumholz 145. Kumar
HM, Cummings S, York M: Blood culture phlebotomy: Switching needles does not prevent contamination. Ann Intern Med 113:290, 1990.
Y, Qunibi M, Neal TJ, et al: Time to positivity of neonatal blood cultures. Arch Dis Child Fetal Neonatal Ed 85:F182, 2001.
146. Kunin
C, Southall I, Paquin AJ: Epidemiology of urinary tract infections. N Engl J Med 263:817, 1960.
147. Kunin
CM: The quantitative significance of bacteria visualized in the unstained urinary sediment. N Engl J Med 265:589, 1961.
148. Kunin
CM, DeGroot JE: Self screening for significant bacteriuria. Evaluation of dip-strip combination nitrite/culture test. JAMA 231:1349, 1975.
149. Kunin
CM, White LV, Hua TH: A reassessment of the importance of "low-count" bacteriuria in young women with acute urinary symptoms. Ann Intern Med 119:454, 1993.
150. Kuppermann
N, Fleisher GR, Jaffe DM: Predictors of occult pneumococcal bacteremia in young febrile children. Ann Emerg Med 31:679, 1998.
REFERENCES 151. Kusumi
RK, Grover PJ, Kunin CM: Rapid detection of pyuria by leukocyte esterase activity. JAMA 245:1653, 1981.
152. Labianca
DA, Simpson G: Medicolegal alcohol determination: variability of the blood- to breath-alcohol ratio and its effect on reported breath-alcohol concentrations. Eur J Clin Chem Clin Biochem 33:919, 1995. 153. Laccetti
M, Manes G, Uomo G: Flumazenil in the treatment of acute hepatic encephalopathy in cirrhotic patients: A double-blind, randomized, placebo-controlled study. Dig Liver Dis 32:335, 2000.
154. Latham
RH, Wong ES, Larson A, et al: Laboratory diagnosis of urinary tract infection in ambulatory women. JAMA 254:3333, 1985.
155. Layne
EA, Mellow MH, Lipman TO: Insensitivity of guaiac slide tests for detection of blood in gastric juice. Ann Intern Med 94:774, 1981.
156. Lee
D, Beuhler M: An in-vitro evaluation of the Meixner test (abstract). J Toxicol Clin Toxicol 37:668, 1999.
157. Lee
S, Schoen I, Malkin A: Comparison of use of alcohol with that of iodine for skin antisepsis in obtaining blood cultures. Am J Clin Pathol 47:646, 1967.
158. Leisure 159. Lester 160. Levin
D: Breath tests for alcohol. N Engl J Med 284:1269, 1971.
K, Engström I: Inadequate hemolysis of erythrocytes at low pH causes false negative readings. Clin Chem 30:1845, 1984.
161. Levsky 162. Ling
MK, Moore DM, Schwartzman JD, et al: Changing the needle when inoculating blood cultures: A no-benefit and high-risk procedure. JAMA 264:2111, 1990.
ME, Handler JA, Suarez RD, et al: False-positive urine beta-hCG in a woman with a tubo-ovarian abscess. J Emerg Med 21:407, 2001.
LJ, Hornfeldt CS, Winter JP: Absorption of iron after experimental overdose of chewable vitamins. Am J Emerg Med 9:24, 1991.
163. Lipsky
BA, Inui TS, Plorde JJ, et al: Is the clean catch midstream void procedure necessary for obtaining urine culture specimens from men? Am J Med 76:257, 1984.
164. Lipsky
BA, Ireton RC, Fihn SD, et al: Diagnosis of bacteriuria in men: Specimen collection and culture interpretation. J Infect Dis 155:847, 1987.
165. Little
JR, Murray PR, Traynor PS, et al: A randomized trial of povidone-iodine compared with iodine tincture for venipuncture site disinfection: Effects on rates of blood culture contamination. Am J Med 107:119, 1999. 166. Lohr
JA, Donowitz LG, Dudley SM: Bacterial contamination rates for non-clean-catch and clean-catch midstream urine collection in boys. J Pediatr 109:659, 1986.
167. Lohr
JA, Portilla MG, Geuder TG, et al: Making a presumptive diagnosis of urinary tract infection by using urinalysis performed in an on-site laboratory. J Pediatr 122:22, 1993.
168. Lombardi 169. Loo
DP, Engleberg NC: Anaerobic bacteremia: Incidence, patient characteristics, and clinical significance. Am J Med 92:53, 1992.
SY, Scottolini AG, Luangphinith S, et al: Urine screening strategy employing dipstick analysis and selective culture: An evaluation. Am J Clin Pathol 81:634, 1984.
170. Lovell
DL: Preoperative skin preparation with reference to surface bacteria contaminants, and resident flora. Surg Clin North Am 26:1053, 1946.
171. Lyman
JL: Use of blood cultures in the emergency department. Ann Emerg Med 15:308, 1986.
172. Mabeck
CE: Urinary leukocyte excretion in bacteriuria. Acta Med Scand 186:193, 1969.
173. Maki
DG, Ringer M, Alvarado CJ: Prospective randomized trial of povidone-iodine, alcohol, and chlorhexidine for prevention of infection associated with central venous and arterial catheters. Lancet 338:339, 1991. 174. Males
BM, Bartholemew WR, Amsterdam D: Leukocyte esterasenitrite and bioluminescence assays as urine screens. J Clin Microbiol 22:531, 1985.
175. Mandel
JS, Bond JH, Church TR, et al: Reducing mortality from colorectal cancer by screening for fecal occult blood. Minnesota Colon Cancer Control Study. N Engl J Med 328:1365, 1993.
176. Mangurten 177. Marill
HH, LeBeau LJ: Diagnosis of neonatal bacteremia by a microblood culture technique. J Pediatr 90:990, 1977.
KA, Ingmire TE, Nelson BK: Utility of a single beta HCG measurement to evaluate for absence of ectopic pregnancy. J Emerg Med 17:419, 1999.
178. Mariani
AJ, Luangphinith S, Loo SY, et al: Dipstick chemical urinalysis: An accurate cost-effective screening test. J Urol 132:64, 1984.
179. Maymon
R, Shulman A, Maymon BB, et al: Ectopic pregnancy, the new gynecologic epidemic disease: Review of the modern work up and the non-surgical treatment option. Int J Fertil Womens Med 37:146, 1992. 180. McDonnell
WM, Ryan JA, Seeger DM, et al: Effect of iron on the guaiac reaction. Gastroenterology 96:74, 1989.
181. McGuigan
MA, Lovejoy FH Jr, Marino SK, et al: Qualitative deferoxamine color test for iron ingestion. J Pediatr 94:940, 1979.
182. Megarbane 183. Mermel
B, Borron SW, Trout H, et al: Treatment of acute methanol poisoning with fomepizole. Intensive Care Med 27:1370, 2001.
LA, Maki DG: Detection of bacteremia in adults: Consequences of culturing an inadequate volume of blood. Ann Intern Med 119:270, 1993.
184. Messing
EM, Young TB, Hunt VB, et al: The significance of asymptomatic microhematuria in men 50 or more years old: Findings of a home screening study using urinary dipsticks. J Urol 137:919,
1987.
1416
185. Meyer
GW, Komadina K, Perucca P: Vegetable peroxidase is denatured by gastric acid: Fresh vegetables do not cause false-positive stool Hemoccults in normal subjects. Gastroenterology 101:871, 1991. 186. Mimoz
O, Karim A, Mercat A, et al: Chlorhexidine compared with povidone-iodine as skin preparation before blood culture. A randomized, controlled trial. Ann Intern Med 131:834, 1999.
187. Mishalani
SH, Seliktar J, Braunstein GD: Four rapid serum-urine combination assays of choriogonadotropin compared and assessed. Clin Chem 40:1944, 1994.
188. Moore
GP, Robinson M: Do urine dipsticks reliably predict microhematuria? The bloody truth! Ann Emerg Med 17:257, 1988.
189. Morgan
AG, Polak A: The excretion of salicylate in salicylate poisoning. Clin Sci (Colch) 41:475, 1971.
190. Morris
AJ, Wilson ML, Mirrett S, et al: Rationale for the selective use of anaerobic blood cultures. J Clin Microbiol 31:2110, 1993.
191. Morris
DW, Hansell JR, Ostrow JD, et al: Reliability of chemical tests for fecal occult blood in hospitalized patients. Dig Dis 21:845, 1976.
192. Morrison 193. Mozes
MC, Lum G: Dipstick testing of urine—Can it replace urine microscopy? Am J Clin Pathol 85:590, 1986.
B, Milatiner D, Block C, et al: Inconsistency of a model aimed at predicting bacteremia in hospitalized patients. J Clin Epidemiol 46:1035, 1993.
194. Murray
PR, Traynor P, Hopson D: Critical assessment of blood culture techniques: Analysis of recovery of obligate and facultative anaerobes, strict aerobic bacteria, and fungi in aerobic and anaerobic culture bottles. J Clin Microbiol 30:142, 1992. 195. Musher
DM, Thorsteinson SB, Airola VM II: Quantitative urinalysis: Diagnosing urinary tract infection in men. JAMA 236:2069, 1976.
196. Musher
DM, Fainstein V, Young EJ, et al: Fever patterns: Their lack of clinical significance. Arch Intern Med 139:1225, 1979.
197. Mylotte
JM, Tayara A: Blood cultures: Clinical aspects and controversies. Eur J Clin Microbiol Infect Dis 19:157, 2000.
198. Neal
PR, Kleiman MB, Reynolds JK, et al: Volume of blood submitted for culture from neonates. J Clin Microbiol 24:353, 1986.
199. Nicolle 200. Niemi
LE, Bjornson J, Harding G, et al: Bacteriuria in elderly instituionalized men. N Engl J Med 309:1420, 1983.
TA, Fischer RP, Gervin AS: Povidone iodine: A cause for false-positive dipstick hematuria? Ann Emerg Med 13:984, 1984.
201. Norman
P, Gosden PE, Platt J: Pseudobacteremia associated with contaminated skin cleansing agent. Lancet 1:209, 1986.
202. Novis
DA, Dale JC, Schifman RB, et al: Solitary blood cultures: A College of American Pathologists Q-probes study of 132,778 blood culture sets in 333 small hospitals. Arch Pathol Lab Med 125:1290, 2001. 203. Oakley
P: Physostigmine versus diazepines for anticholinergic poisoning. Ann Emerg Med 37:239, 2001.
204. Olesen
LL: Amatoxin intoxication. Scand J Urol Nephrol 24:231, 1990.
205. Orlowski
JP, Porembka DT, Gallagher JM, et al: The bone marrow as a source of lab studies. Ann Emerg Med 18:1348, 1989.
206. Ouslander
JG, Greengold BA, Silverblatt FJ, et al: An accurate method to obtain urine for culture in men with external catheters. Arch Intern Med 147:286, 1987.
207. Paisley
JW, Lauer BA: Pediatric blood cultures. Clin Lab Med 14:17, 1994.
208. Pappas
PG: Laboratory in the diagnosis and management of urinary tract infections. Med Clin North Am 75:313, 1991.
209. Pels
RJ, Bor DH, Woolhandler S, et al: Dipstick urinalysis screening of asymptomatic adults for urinary tract disorders: II Bacteriuria. JAMA 262:1214, 1989.
210. Pentel 211. Perry
P, Peterson CD: Asystole complicating physostigmine treatment of tricyclic antidepressant overdose. Ann Emerg Med 9:588, 1980.
JL, Matthews JS, Weesner DE: Evaluation of leukocyte esterase activity as a rapid screening technique for bacteriuria. J Clin Microbiol 15:852, 1982.
212. Pfaller
MA, Koontz FP: Use of rapid screening tests in processing urine specimens by conventional culture and the automicrobic system. J Clin Microbiol 21:783, 1985a.
213. Pfaller
MA, Koontz FP: Laboratory evaluation of leukocyte esterase and nitrite tests for the detection of bacteriuria. J Clin Microbiol 21:840, 1985b.
214. Pfaller
M, Ringenberg B, Rames L, et al: The usefulness of screening tests for pyuria in combination with culture in the diagnosis of urinary tracy infection. Diagn Microbiol Infect Dis 6:207, 1987.
215. Pollock
HM: Laboratory techniques for detection of urinary tract infection and assessment of value. Am J Med 75:79, 1983.
216. Prescott 217. Propp
LF, Balali-Mood M, Critchley JA, et al: Diuresis or urinary alkalinisation for salicylate poisoning? Br Med J (Clin Res Ed) 285:1383, 1982.
DA, Weber D, Ciesla ML: Reliability of a urine dipstick in emergency department patients. Ann Emerg Med 18:560, 1989.
218. Propper 219. Pryles
RD, Shurin SB, Nathan DG: Reassessment of the use of desferrioxamine B in iron overload. N Engl J Med 294:1421, 1976.
CV: Percutaneous bladder aspiration and other methods of urine collection. Pediatrics 36:128, 1965.
220. Ransohoff 221. Reeves
DF, Lang CA: Screening for colorectal cancer with the fecal occult blood test: A background paper. American College of Physicians. Ann Intern Med 126:811, 1997.
RR, Pendarvis RO: Mothball melting points. Ann Emerg Med 15:1377, 1986.
222. Richardson 223. Roberts 224. Robins
JP, Hricz L: Risk factors for the development of bacteremia in nursing home patients. Arch Fam Med 4:785, 1995.
FJ: The value of the second blood culture. J Infect Dis 168:795, 1993.
DG, White RHR, Rogers KB, et al: Urine microscopy as an aid to detection of bacteriuria. Lancet 1:476, 1975.
225. Romero
RA, Kadar N, Copel JA, et al: The effect of different human chorionic gonadotropin assay sensitivity on screening for ectopic pregnancy. Am J Obstet Gynecol 153:72, 1985.
226. Saez-Llorens 227. Sandven 228. Sanford
X, Umana MA, Odio CM, et al: Bacterial contamination rates for non-clean-catch and clean-catch midstream urine collections in uncircumcised boys. J Pediatr 114:93, 1989.
P, Høiby A: The importance of blood volume cultured on the detection of bacteria. ACT Path Micr Scand 89:149, 1981.
JP, Favour CD, Mao FH: Evaluation of the "positive" urine culture: An approach to the differentiation of significant bacteria from contaminants. Am J Med 20:88, 1956.
229. Santucci
K, Shah B: Association of naphthalene with acute hemolytic anemia. Acad Emerg Med 7:42, 2000.
230. Scheer
WD: The detection of leukocyte esterase activity in urine with a new reagent strip. Am J Clin Pathol 87:86, 1987.
231. Schultz
HJ, McCaffrey LA, Keys TF, et al: Acute cystitis: A prospective study of laboratory tests and duration of therapy. Mayo Clin Proc 59:391, 1984.
232. Schifman 233. Scott
RB, Pindur A: The effect of skin disinfection materials on reducing blood culture contamination. Am J Clin Pathol 99:536, 1993.
AC: Blood-culture technique: Two needles or one? Lancet 1:1414, 1979.
234. Segal
GS, Chamberlain JM. Resource utilization and contaminated blood cultures in children at risk for occult bacteremia. Arch Pediatr Adolesc Med 154:469, 2000.
235. Selwyn 236. Sewell
S, Ellis H: Skin bacteria and skin disinfection reconsidered. Br Med J 1:136, 1972. DL, Burt SP, Gabbert NJ, et al: Evaluation of the Chemstrip 9 as a screening test for urinalysis and urine culture in men. Am J Clin Pathol 83:740, 1985.
237. Shahar
E, Wohl-Gottesman B, Shenkman L: Contamination of blood cultures during venepuncture: Fact or myth? Postgrad Med J 66:1053, 1990.
238. Shanson
DC, Thomas F, Wilson D: Effect of volume of blood cultured on detection of Streptococcus viridans bacteremia. J Clin Pathol 37:568, 1984.
239. Sharp
SE: Routine anaerobic blood cultures: Still appropriate today? Clin Micro Newsletter 13:23, 1991.
240. Shaw
ST Jr, Poon SY, Wong ET: Routine urinalysis, is the dipstick enough? JAMA 253:1596, 1985.
241. Siff
JE, Meldon SW, Tomassoni AJ: Usefulness of the total iron binding capacity in the evaluation and treatment of acute iron overdose. Ann Emerg Med 33:73, 1999.
242. Silva
HL, Strabelli TM, Cunha ER, et al: Nosocomial coagulase negative Staphylococci bacteremia: Five-year prospective data collection. Braz J Infect Dis 4:271, 2000.
243. Sinclair 244. Sklar
D, Svendsen A, Marrie T: Bacteremia in nursing home patients. Prevalence among patients presenting to an emergency department. Can Fam Physician 44:317, 1998.
DP, Rusnak R: The value of outpatient blood cultures in the emergency department. Am J Emerg Med 5:95, 1987.
245. Smart
D, Baggoley C, Head J, et al: Effect of needle changing and intravenous cannula collection on blood culture contamination rates. Ann Emerg Med 22:65, 1993.
246. Speroff
L, Glass RH, Kase NG: Clinical Gynecological Endocrinology and Infertility, 5th ed. Baltimore, Williams & Wilkins, 1994.
1417
247. Spivey
WH, Roberts JR, Derlet RW: A clinical trial of escalating doses of flumazenil for reversal of suspected benzodiazepine overdose in the emergency department. Ann Emerg Med 22:1813,
1993. 248. Spivey
WH: Flumazenil and seizures: Analysis of 43 cases. Clin Ther 14:292, 1992.
249. Sporer
KA, Ernst AA, Conte R, et al: The incidence of ethanol-induced hypoglycemia. Am J Emerg Med 10:403, 1992.
250. Stair
TO: Outpatient blood cultures: Retrospective and prospective audits in one ED. Ann Emerg Med 13:986, 1984.
251. Stalnikowicz 252. Stansfeld
R, Block C: The yield of blood cultures in a department of emergency medicine. Eur J Emerg Med 8:93, 2001.
JM: The measurement and meaning of pyuria. Arch Dis Child 37:257, 1962.
253. Stamm
WE: Measurement of pyuria and its relation to bacteriuria. Am J Med 75:53, 1983.
254. Stamm
WE, Running K, McKevitt M, et al: Treatment of the acute urethral syndrome. N Engl J Med 304:956, 1981.
255. Stamm
WE, Counts GW, Running KR, et al: Diagnosis of coliform infection in acutely dysuric women. N Engl J Med 307:463, 1982.
256. Stamm
WE, Hooton TM: Management of urinary tract infections in adults. N Engl J Med 329:1328, 1993.
257. Stamm
WE, Wagner KF, Amsel R, et al: Causes of the acute urethral syndrome in women. N Engl J Med 303:409, 1980.
258. St
Geme JW III, Bell LM, et al: Distinguishing sepsis from blood culture contamination in young infants with blood cultures growing coagulase-positive staphylococci. Pediatrics 86:157, 1990.
259. Story
P: Testing of skin disinfectants. Br Med J 2:1128, 1952.
260. Strand
CL, Wajsbort RR, Sturmann K: Effect of iodophor versus iodine tincture skin preparation on blood culture contamination rates. JAMA 269:1004, 1993.
261. Sturmann
KM, Bopp J, Molinari D, et al: Blood cultures in adult patients released from an urban emergency department: A 15-month experience. Acad Emerg Med 3:768, 1996.
262. Sullivan
NM, Sutter VL, Carter WT, et al: Bacteremia after genitourinary tract manipulation: Bacteriological aspects and evaluation of various blood culture systems. Appl Microbiol Biotechnol 23:1101, 1972. 263. Sultana
RV, Zalstein S, Cameron P, et al: Dipstick urinalysis and the accuracy of the clinical diagnosis of urinary tact infection. J Emerg Med 20:13, 2001.
264. Szymczak
EG, Barr JT, Durbin WA, Goldmann DA: Evaluation of blood culture procedures in a pediatric hospital. J Clin Microbiol 9:88, 1979.
265. Tafuro
P, Colbourn D, Gurevich I, et al: Comparison of blood culture obtained simultaneously by venepuncture and from vascular lines. J Hosp Infect 7:283, 1986.
266. Taylor
MR, Dillon M, Keane CT: Reduction of mixed growth rates in urine by using a finger tap method. Br Med J 292:990, 1986.
267. Temple
AR: Acute and chronic effects of aspirin toxicity and their treatment. Arch Intern Med 141:364, 1981.
268. Tenenbein 269. Tenney
JH, Reller LB, Mirrett S, et al: Controlled evaluation of the volume of blood cultured on detection of bacteremia. J Clin Microbiol 15:558, 1982.
270. Thanassi 271. Thomas
M: Utility of urine and blood cultures in pyelonephritis. Acad Emerg Med 4:797, 1997.
JG, Meda BA: Anaerobic cultures: Tailoring their selective use. Clin Micro Newsletter 17:16:125, 1995.
272. Tonneson 273. Väisänen 274. Vehaskari 275. Van
M, Yatscoff RW: The total iron-binding capacity in iron poisoning. Is it useful? Am J Dis Child 145:437, 1991.
A, Peuler M, Lockwood WR: Culture of blood drawn by catheter versus venepuncture. JAMA 235:1877, 1976. IY, Torsten M, Valtonen V, et al: Comparison of arterial and venous blood samples for the diagnosis of bacteremia in critically ill patients. Crit Care Med 13:664, 1985. VM, Rapola J, Koskimies O, et al: Microscopic hematuria in school children: Epidemiology and clinicopathologic evaluation. J Pediatr 95:676, 1979.
der Rijt CC, Schalm SW, Meulstee, J, et al: Flumazenil therapy for hepatic encephalopathy. A double-blind cross over study. Gastroenterol Clin Biol 19:572, 1995.
276. Vetter
J: Toxins of Amanita phalloides. Toxicon 36:13, 1998.
277. Vickers
D, Ahmad T, Coulthard MG: Diagnosis of urinary tract infection in children: Fresh urine microscopy or culture? Lancet 338:767, 1991.
278. Wallace
KL, Suchard JR, Curry SC, et al: Diagnostic use of physicians' detection of urine fluorescence in a simulated ingestion of sodium fluorescein-containing antifreeze. Ann Emerg Med 38:49,
2001. 279. Walter
FG, Knopp RK: Urine sampling in ambulatory women: Midstream clean catch versus catheterization. Ann Emerg Med 18:166, 1989.
280. Washington
JA: Evolving concepts on the laboratory diagnosis of septicemia. Inf Dis Clin Practice 1:65, 1993.
281. Washington
JA: Collection, transport, and processing of blood cultures. Clin Lab Med 14:59, 1994.
282. Washington
JA, Ilstrup DM: Blood cultures: Issues and controversies. Rev Inf Dis 8:792, 1986.
283. Waterer 284. Waters 285. Wax
GW, Wunderink RG: The influence of the severity of community-acquired pneumonia on the usefulness of blood cultures. Respir Med 95:78, 2001.
BL: Inoculating blood cultures: Recapping needles and contamination rates. JAMA 265:1685, 1991.
P, Hoffman R: Sodium bicarbonate. Contemp Manag Crit Care 1:81, 1991.
286. Weiner
AL, Ko C, McKay CA Jr: A comparison of two bedside tests for the detection of salicylates in urine. Acad Emerg Med 7:834, 2000.
287. Weinstein
MP, Reller LB, Murphy JR, et al: The clinical significance of a positive blood culture: A comprehensive analysis of 500 episodes of bacteremia and fungemia in adults: I Laboratory and epidemiological observations. Rev Inf Dis 5:35, 1983. 288. Wenz
B, Lampasso JA: Eliminating unnecessary urine microscopy. Am J Clin Pathol 92:78, 1989.
289. Westlin 290. Wing
WF: Deferoxamine in the treatment of acute iron poisoning. Clinical experiences with 172 children. Clin Pediatr (Phila) 5:531, 1966.
DA, Park AS, Debuque L, et al: Limited clinical utility of blood and urine cultures in the treatment of acute pyelonephritis during pregnancy. Am J Obstet Gynecol 182:1437, 2000.
291. Winter
ML, Ellis MD, Snodgrass WR: Urine fluorescence using a Wood's lamp to detect the antifreeze additive sodium fluorescein: A qualitative adjunctive test in suspected ethylene glycol ingestions. Ann Emerg Med 19:663, 1990. 292. Wiswell
TE, Hachey WE: Multiple site blood culture in the initial evaluation for neonatal sepsis during the first week of life. Pediatr Infect Dis J 10:365, 1991.
293. Woolhandler 294. Wormser 295. Wright
GP, Onorato IM, Preminger TJ, et al: Sensitivity and specificity of blood cultures obtained through intravenous catheters. Crit Care Med 18:152, 1990.
N: An assessment of the unreliability of the history given by self-poisoned patients. Clin Toxicol 16:381, 1980.
296. Yehezkelli 297. York
S, Pels RJ, Bor DH, et al: Dipstick urinalysis screening of asymptomatic adults for urinary tract disorders. I. Hematuria and proteinuria. JAMA 262:1214, 1989.
Y, Subah S, Elhanan G, et al: Two rules for early prediction of bacteremia: Testing in a university and a community hospital. J Gen Intern Med 11:98, 1996.
MK: Bacillus species bacteremia traced to gloves used in the collection of blood from patients with acquired immune deficiency syndrome. J Clin Microbiol 28:2114, 1990.
298. Zierdt
CH: Evidence for transient Staphylococcus epidermidis bacteremia in patients and in healthy humans. J Clin Microbiol 17:628, 1983.
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Chapter 71 - Standard Precautions and Infectious Exposure Management Peter E. Sokolove Aaron E. Bair
Body fluid contamination of health care workers is a frequent occurrence in the emergency department (ED). In a prospective study of ED health care workers, skin and clothing contamination with body fluids occurred in 1 of 35 patient visits. [30] These fluids may contain various transmissible infectious diseases, as the prevalence of HIV infection, hepatitis, and other communicable diseases can be high in certain ED patient populations. [5] [24] [27] [43] For example, investigators from an inner city ED reported a patient seroprevalence of 6% for HIV infection, 18% for hepatitis C, and 5% for hepatitis B surface antigen. [26] One in four patients tested positive for at least one of these diseases. Patient characteristics were found to be poor predictors for hepatitis positivity, making it more difficult to identify which patients pose a risk to health care workers. Unfortunately, compliance with standard precautions, formerly known as universal precautions, is far from universal. [3] [20] [25] Baraff and Talan [3] reported poor compliance, even in the setting of treating critical trauma patients. Compliance rates were 75% for gloves, 27% for gowns, 19% for eyewear, and only 2% for masks. Despite having recently received education about standard precautions, Hammond et al [20] also reported low compliance rates during invasive procedures and with high-risk patients. Compliance improved when equipment was organized and placed in trauma resuscitation rooms. In 1985, this combination of high-risk illness with low compliance barrier use prompted the Centers for Disease Control and Prevention (CDC) to recommend guidelines for the protection of health care workers. [7] In 1991, these recommendations were enacted into law by mandate of the Occupational Safety and Health Administration (OSHA).
Figure 71-1 A, Recapping a needle by holding the cap in the hand is the most common way to sustain a needle puncture. B, It is best to discard the needle/syringe without recapping, but an alternative is to partially recap without holding the guard (needle cap), so that at least 80% of the needle is covered before completing the recapping with the second hand.
The primary focus of the CDC guidelines is to reduce mucocutaneous body fluid exposures by encouraging hand washing and barrier protection. However, these measures do little to protect from percutaneous exposures, which are the most efficient exposures in the transmission of hepatitis and HIV. [31] [32] The current strategy for risk reduction in the ED includes immunization against hepatitis B virus, use of standard precautions (including re-engineered safety products), and prompt initiation of post-exposure prophylaxis (PEP) when appropriate.
STANDARD PRECAUTIONS GUIDELINES Appropriate precautions for all patient contact must be viewed as a consistent practice or "way of life" in the ED. The following guidelines, based upon the CDC recommendations, should be used when there is any possibility of body fluid contact: Barrier Precautions 1. Gloves should be used for any patient contact with the risk of body fluid exposure. Both cutaneous and percutaneous exposures can be reduced by the use of gloves. In an animal model, Mast et al. [33] reported a 46 to 86% reduction in the volume of blood transferred via needlestick injury when the needle first punctured a glove. Fisher et al [17] compared the biomechanical performance of powder-free, latex, and nitrile examination gloves. The nitrile examination gloves exhibited greater puncture resistance, despite being thinner than the latex examination gloves. 2. Mask and protective eyewear should be used when exposure to body fluid aerosols is possible (e.g., wound irrigation, traumatic chest wound). 3. Gown and shoe covers should be worn when there is the risk of large splash volumes of body fluids (e.g., chest tube, thoracotomy). Sharps Precautions Most importantly, this means no recapping, bending, or breaking of needles. If needle recapping is deemed necessary, a single-handed technique should be used ( Fig. 71-1 ). A safer alternative is immediate disposal of the needle into an approved sharps container without recapping. In an observational study
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of ED employees, the rate of needle recapping was 34%, and most practitioners used a two-handed technique. [22] There are various re-engineered products for use in the ED, including retracting scalpels, auto-capping needles, and needle-less intravenous systems. A survey of infection control professionals at Iowa and Virginia hospitals found that implementation of such devices was the most common action taken to decrease percutaneous injuries. [4] Respiratory Precautions During contact with patients with suspected or confirmed pulmonary tuberculosis, providers should wear a National Institute of Safety and Health (NIOSH)-approved N-95 particulate respirator. These masks are designed to efficiently filter 1- to 5-µm particles. A more costly and less comfortable alternative is the use of a HEPA-filtered mask. In addition, such patients should be placed into respiratory isolation in a room with negative pressure, high circulation (optimally at least 12 air changes per hour), and external exhaust. Procedures resulting in increased release of infectious droplets, such as sputum induction, should be avoided in the ED. Potentially infectious patients should wear a surgical-type mask themselves, especially during transportation outside of the respiratory isolation room (e.g., to radiology). [9] Hand washing.
Any skin surface coming into contact with body fluids should be washed immediately with soap and water. Annual education.
All workers should receive a mandatory annual review of infection control and safe practices.
OCCUPATIONAL DISEASE EXPOSURE Occupationally acquired infections cause considerable morbidity and mortality among health care workers despite OSHA requirements for precautions. Given the often occult presentation of disease in the ED patient population, emergency health care workers are at high risk for significant exposure from many pathogens. Owing to the high prevalence of particular diseases among ED patients and specific concerns for pathogens associated with high morbidity and mortality, this chapter focuses on HIV, hepatitis B and C viruses (HBV, HCV), and tuberculosis.
TABLE 71-1 -- Recommendations for Hepatitis B Prophylaxis Following Percutaneous or Permucosal Exposure Source Exposed person
HBsAg-positive
HBsAg-negative
Source unknown or not available
Unvaccinated
HBIG × 1* and HB vaccine series
Initiate HB vaccine series
Initiate HB vaccine series
Known responder
No treatment
No treatment
No treatment
Known nonresponder
HBIG × 2 or
No treatment
If known high-risk source, treat as if source were HBsAg-positive
No treatment
Test exposed person for Anti-HBs
Vaccinated
HBIG × 1 and initiate revaccination § Response unknown
Test exposed person for anti-HBs 1. If adequate,† no treatment
1. If adequate, no treatment
2. If inadequate, HBIG × 1 plus vaccine booster
2. If inadequate, HB vaccine booster and recheck titer in 1 to 2 months
Adapted from Updated U.S. public health service guidelines for the management of occupational exposures to HBV, HCV, and HIV and recommendations for postexposure prophylaxis. MMWR Recomm Rep 50:1, 2001. *HBIG dose 0.06 mL/kg IM. §§The option of giving one dose of HBIG and reinitiating the vaccine series is preferred for nonresponders who have not completed a second three-dose vaccine series. For persons who previously completed a second vaccine series but failed to respond, two doses of HBIG are preferred. †Adequate anti-HBs is = 10 mIU/mL.
Hepatitis B Virus HBV Transmission
HBV is a well-recognized occupational risk for health care providers, and multiple studies have documented the high prevalence of hepatitis among ED patients. [16] [26] [28] Despite the attention focused on transmission of HIV, the infectivity of HBV is significantly higher because of the virulence of the organism and relatively small inoculum required for disease transmission. [18] Percutaneous injuries are among the most efficient modes of HBV transmission, but many infected health care workers do not recall a specific injury. [19] [39] Many body fluids other than blood contain hepatitis B surface antigen, but the levels of infectious HBV particles in blood-free body fluids are 100 to 1000 times lower than blood itself. Because implementation of the CDC's standard precautions, along with the OSHA regulations for barrier protection and pre-exposure vaccination, the incidence of HBV transmission has sharply declined. [14] To understand the risk of HBV transmission resulting from occupational exposure, one must be familiar with a few key serologic markers for HBV. Hepatitis B surface antigen (HBsAg) is a marker of active infection in the source patient. From a practical standpoint, HBV can be transmitted when HBsAg is present, and is generally not transmissible when this marker is absent. Hepatitis B surface antibody (HBsAb) is a protective antibody against HBV. In vaccinating health care workers, the goal is to stimulate the immune system to produce a sufficient quantity of this antibody. Hepatitis Be antigen (HBeAg) can be found in the bloodstream of HBV-infected individuals during times of peak virus replication. When a source is positive for HBeAg, their bloodstream contains a much larger number of infectious HBV particles. If a non-immune individual sustains a needle stick from an HbsAg-positive patient, the risk of HBV transmission is dependent upon the HBeAg status of the source. [50] The risk of clinical hepatitis is approximately 2% (range, 1% to 6%) if HBeAg is absent, compared with a risk of 22% to 31% if HBeAg is present. [14] HBV Post-exposure Management
Post-exposure prophylaxis following exposure to an HBsAg positive source may require hepatitis B vaccine, HBIG, both, or neither ( Table 71-1 ). This is dependent upon the vaccination and antibody response status of the exposed health care worker. HBIG is derived from pooled human plasma and
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provides passive immunization for non-immune exposed individuals. This preparation is very safe and is not known to transmit disease. [14] When HBIG is used for PEP, ideally it should be given within 24 hours following exposure and it is of questionable value beyond 7 days. [8] In some cases, hepatitis B vaccine is also used for post-exposure prophylaxis. Health care workers who have any chance of exposure to infectious body fluids should be routinely vaccinated against hepatitis B. Adverse reactions to the hepatitis B vaccine are generally quite mild, and it is even safe to give during pregnancy. Primary immunization consists of an initial intramuscular (IM) injection, with subsequent IM vaccinations at 1 and 6 months. Antibody levels (HBsAb) should be checked at 4 to 6 weeks after the series is completed, and the desired titer is at least 10 mIU/mL. Vaccinated individuals who achieve this antibody level are referred to as "responders" and may be immune for life. While about 25% to 50% of vaccine responders demonstrate a decline in HBsAb antibody levels to below 10 mIU/mL within 5 to 7 years, these individuals are still protected against clinical disease. This results from a robust immune system memory or anamnestic response. [23] Post-exposure prophylaxis with these agents is not contra-indicated during pregnancy or lactation. Health care workers who have previously been infected with HBV are immune to re-infection, so PEP is not indicated in such individuals. Hepatitis C Virus HCV Transmission
Approximately 1.8% of Americans (3.9 million) are infected with hepatitis C virus, and many of these individuals are unaware they are infected. HCV is often acquired from injection drug use, and was once commonly transmitted by blood transfusion (now rare with modern screening). While HCV can be transmitted sexually, this a minor route. Percutaneous transmission is most efficient. The incidence of seroconversion following an HCV-positive needle stick is about 1.8% (estimates range from 0 to 7%).[14] Mucous membrane transmission of HCV is possible but much less common. It is useful to remember that the risk of HCV transmission following a needle stick is similar to that of HBV transmission when the source is HBeAg negative. When seroconversion does occur, 80% of patients will demonstrate antibodies at 15 weeks and 97% at 6 months following exposure. While the clinical course of hepatitis C virus is often asymptomatic or mild, approximately 85% of patients will
develop chronic hepatitis, 10% to 20% cirrhosis, and 1% to 5% hepatocellular carcinoma. [10] [11] [12] HCV Post-exposure Management
Unfortunately, post-exposure prophylaxis for HCV exposure is currently not available. HCV exhibits a high degree of genetic heterogeneity and a very rapid mutation rate, making the development of vaccine extremely difficult. The use of post-exposure immune globulin is probably not helpful, and there are currently no clinical trials of agents such as interferon or ribavirin for HCV post-exposure prophylaxis. [14] Human Immunodeficiency Virus HIV Transmission
According to the CDC, through June 2000, there were 56 cases of occupational HIV transmission to health care workers in the United States. Additionally, another 138 health care workers demonstrated HIV seroconversion, which may have been occupationally related. [13] The risk of contracting HIV from working in the ED depends upon the prevalence of HIV in the local patient population. One study reported an annual HIV seroconversion risk of 1/3800 for high-prevalence EDs and 1/55,000 for low-prevalence EDs. [32] Wears et al. [49] estimated the cumulative career risk of contracting HIV from occupational exposure in a high-prevalence ED to be as high as 1.4%. The author suggests, however, that this risk can be reduced with adequate precautionary measures. When seroconversion occurs, HIV antibodies can be detected as early as 3 weeks after exposure, and are almost always present by 6 months. Seroconversion at 6 to 12 months is rare, but has been reported with HIV and HCV virus co-infection. Acute retroviral syndrome is a clinical manifestation of HIV seroconversion that occurs in approximately 80% of newly infected individuals at a median of 25 days after exposure. The presentation of acute retroviral syndrome is similar to mononucleosis, with fever, lymphadenopathy, and rash. The overall risk of HIV seroconversion is about 1/300 (0.3%) following needlestick and less than 1/1000 for mucous membrane exposures. Cardo et al. [6] demonstrated that the risk for HIV seroconversion following needlestick injuries is not uniform. Seroconversion was found to be more likely for deep injuries (odds ratio [OR] = 15), if blood was visible on the device (OR = 6.2), if the needle had been used in a source patient's artery or vein (OR = 4.3), or if the source patient suffered from terminal AIDS (OR = 5.6). It is essential to gather information regarding the nature of the injury to "risk stratify" the exposure. HIV Post-exposure Management (CDC, 2001) Evidence supporting post-exposure prophylaxis.
In 1998, the U.S. Public Health Service recommended the use of post-exposure prophylaxis (PEP) for selected HIV exposures. [11] [12] These recommendations were based upon a number of animal and human studies suggesting that post-exposure prophylaxis may be effective. While animal studies are mixed in both methodology and outcomes, PEP with various agents has successfully prevented HIV infection. In human studies, the use of anti-retroviral agents during pregnancy decreased perinatal HIV transmission by 67%. [15] In addition, when children born to HIV-positive mothers were given HIV PEP within 48 hours of birth, HIV transmission was also decreased. [47] While perinatal exposures are different than occupational needle sticks, this evidence supports the concept of a "window of opportunity" during which PEP may prevent HIV transmission to an exposed individual. The most important human study of the efficacy of PEP is a CDC-sponsored case-control study undertaken in the United States, France, the United Kingdom, and Italy. [6] This investigation compared 33 health care workers who seroconverted following HIV exposure with 665 control health care workers who did not seroconvert following HIV exposure. About 90% of patients in this study were exposed via hollow bore needles. When post-exposure zidovudine (AZT) was used, the risk for HIV infection was reduced by 81% (95% confidence interval, 48% to 94%). While the study methodology is limited by its retrospective design and the potential for recall bias, these results strongly support the efficacy of AZT for PEP. Currently there are no published randomized controlled human trials of agents for
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HIV PEP. Given the results of the CDC case-control study, it is highly unlikely that such trials will ever be published, as the use of a control group is now considered unethical. Selecting patients for PEP.
In June 2001, the U.S. Public Health Service published updated recommendations regarding the use of HIV PEP. [14] In general, the decision to use PEP depends on the type of exposure and the source HIV status. The first step in determining if PEP is indicated is to assess the exposure severity. Percutaneous exposures can be categorized as less severe or more severe. A less severe exposure involves a solid needle, a superficial injury, and without blood visible on the device. All other percutaneous injuries are categorized as more severe. Exposure to mucus membrane and non-intact skin are categorized as either small volume (few drops of blood) or large volume (a major blood splash). There are no reported cases of HIV seroconversion following blood exposure to intact skin. Following assessment of the exposure severity, one must next determine the potential infectivity of the source. PEP should only be considered for blood and body fluid exposures from a source who is known to be or likely to be HIV-positive. Exposures from an HIV-negative source do not require PEP. Testing of sharp instruments for HIV is not recommended or reliable. HIV-positive source patients are categorized as either lower risk (class 1) or higher risk (class 2). Class 1 patients have asymptomatic HIV infection and a low viral load (less than 1500 RNA copies/mL). Higher risk patients include those with symptomatic HIV, AIDS, acute seroconversion, or a high viral load. Once exposure severity and source HIV status are determined, Table 71-2 and Table 71-3 can be used to guide the proper PEP regimen. For skin and mucous membrane exposures, the PEP regimen chosen falls into three general categories. For small volume exposures from an HIV class 1 source, the basic regimen (two drugs) should be considered. If either the exposure is of large volume or the source is HIV class 2, then the basic regimen should be recommended. In cases where there is both a large volume exposure and an HIV class 2 source, the expanded regimen (three drugs) should be recommended. For most percutaneous exposures, the expanded regimen should be recommended. However, for less severe percutaneous exposures from an HIV class 1 source, the basic regimen should be recommended. A number of special circumstances may arise when determining the need for HIV PEP. When a source is known, but his or her HIV status is pending, the use of PEP should be decided on a case-by-case basis. When the source is high-risk, PEP can be initiated and then stopped or modified once the HIV status is determined. When a source can be identified, but his or her HIV status is unknown and will not become available, PEP is generally not recommended. However, use of the basic two-drug regimen should be considered if the source has HIV risk factors. Sometimes an exposure will occur where the source is completely unknown. While PEP is generally not recommended for such exposures, the basic regimen should be considered if the exposure occurred in an HIV-likely setting (e.g., exposure to a discarded needle on an AIDS ward). Choice of PEP medications.
When HIV PEP is administered, a minimum of two drugs is recommended. While there is no direct evidence that combination PEP regimens are beneficial, concerns about antiretroviral resistance and the synergistic effects of antiviral medications when treating patients with AIDS supports such an approach. As discussed earlier, the U.S. Public Health Service recommends using a basic (two-drug) PEP regimen for lower risk HIV exposures and an expanded (three-drug) PEP regimen for higher risk exposures. The basic PEP regimen consists of two nucleoside reverse transcriptase inhibitors, usually zidovudine (AZT) plus lamivudine (3TC). Alternative basic regimens include 3TC plus d4T (stavudine) or d4T plus ddI (didanosine). When using the expanded PEP regimen, either a protease inhibitor or a non-nucleoside reverse transcriptase inhibitor is added to the basic regimen. Most commonly either nelfinavir or indinavir is preferred as the third drug. A number of second-line and alternative agents may be chosen for HIV PEP. Expert consultation is recommended if antiretroviral resistance is suspected. An important resource for emergency clinicians is the national clinicians' postexposure prophylaxis hotline at UCSF/San Francisco General Hospital. Expert consultation can be obtained by calling 888-448-4911. PEP timing, duration, and side effects.
HIV exposure should be considered a true emergency, and PEP should be initiated as soon as possible after exposure, ideally within 1 hour. Animal studies indicate
that the efficacy of PEP diminishes with delayed initiation. [42] HIV PEP regimens consist of a 4-week course of therapy. In the ED, patients can be prescribed the first 3 days of medications, as long as outpatient follow-up is arranged. Side effects are experienced by about 50% of health care workers taking PEP, causing approximately 33% of health care workers to discontinue therapy prematurely. [48] Table 71-4 lists some of the major side effects experienced when taking PEP agents. Depending upon the choice of PEP medications, patients should also be prescribed antiemetics and antidiarrheal agents when PEP is initiated. A very useful and practical resource that can be used in the ED is the UCLA needle-stick Web site, www.needlestick.mednet.ucla.edu. This Web site allows one to enter information about a specific patient exposure. It then advises the clinician of the appropriate tests to obtain, recommends a PEP regimen, and provides printable discharge instructions and prescriptions. Tuberculosis Tuberculosis Transmission
During the mid-1980s the United States experienced a resurgence in tuberculosis (TB), especially among HIV-positive patients. This disease poses a serious risk to both public health and health care workers. Tuberculosis is transmitted by infectious droplets 1 to 5 µm in size. Primary infection occurs when one to three organisms are inhaled into the alveoli, where they begin to replicate. Host defenses usually stop infection within 2 to 10 weeks, and the patient enters the latent period. During this time, patients are not contagious and are asymptomatic. Reactivation occurs when cell-mediated immunity wanes, and patients are again contagious. This can be due to advancing age, HIV infection, steroid use, malignancy, malnutrition, or other causes of immune suppression. The lifetime risk of reactivation is 10%, with about half of this risk occurring in the first 2 years after primary infection. Patients with increased infectivity include those with pulmonary or laryngeal TB, an active cough, positive sputum smears for acid-fast bacilli, cavitation on chest radiographs, and those on inadequate therapy. Children are overall less contagious than adults, but can still transmit
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TABLE 71-2 -- Recommended HIV Postexposure Prophylaxis for Percutaneous Injuries Infection Status of Source Exposure type
HIV-positive class 1*
HIV-positive class 2*
Source of unknown HIV status †
Unknown source§
Less severe¶
Recommend basic 2-drug PEP
Recommend expanded 3-drug PEP
Generally, no PEP warranted; however, Generally, no PEP warranted; however, consider consider basic 2-drug PEP ‡ for source basic 2-drug PEP‡ in settings where exposure to with HIV risk factors£ HIV-infected persons is likely
No PEP warranted
More severe¢
Recommend expanded 3-drug PEP
Recommend expanded 3-drug PEP
Generally, no PEP warranted; however, Generally, no PEP warranted; however, consider consider basic 2-drug PEP ‡ for source basic 2-drug PEP‡ in settings where exposure to with HIV risk factors£ HIV-infected persons is likely
No PEP warranted
HIV-negative
Adapted from: Updated U.S. Public Health Service Guidelines for the Management of Occupational Exposures to HBV, HCV, and HIV and Recommendations for Postexposure Prophylaxis. MMWR Recomm Rep 50:1, 2001. *HIV-Positive, Class 1—asymptomatic HIV infection or known low viral load (e.g., 2%) and suggests that ATN is the most likely the cause of his renal failure and myoglobinuria.
ACID-BASE, FLUID, AND ELECTROLYTE BALANCE Calculation of the Anion Gap The anion gap (AG) is an estimate of the amount of negatively charged (unmeasured) ions in the serum that are not bicarbonate (HCO 3 - ) and chloride (Cl - ). The AG is calculated by subtracting the sum of HCO 3 - and Cl- values from the sodium (Na+ ), which is the major positive charge in the serum. Potassium (K + ) is not used in the calculation because most of the body's potassium is intracellular and there is a relatively small amount of K + in the serum. An elevated AG usually means that there is some unmeasured anion, toxin, or organic acid in the blood. The AG is normally 8 to 12 mmol/L: AG = Na+ - (Cl- + HCO- 3 ) = 8 to 12 mmol/L
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An increase in the AG is usually associated with acidosis, referred to as an anion gap acidosis. Table A-4 lists many substances that can cause an anion gap acidosis. Example: A suicidal young male drank an unknown amount of antifreeze. His electrolyte levels are Na + 144, K+ 3.1, Cl- 108, and HCO- 3 14. The anion gap is calculated as follows: AG = [144 - (108 + 14)] = 22 mmol/L The anion gap is abnormally elevated, presumably due to ethylene glycol ingestion.
TABLE 4 -- Substances Associated with High Anion Gap * Aspirin Methanol, metformin Uremia Diabetic ketoacidosis Paraldehyde, phenformin Isoniazid, iron Lactate (multiple causes) Ethylene glycol Carbon monoxide, cyanide Alcoholic ketoacidosis Toluene *Follows the mnemonic A MUDPILE CAT.
Calculating the Osmolal Gap Serum osmolality can be measured in the laboratory by freezing point depression. The measured serum osmolality is normally higher than the calculated osmolality and the difference is termed the osmolal gap (OG). The osmolal gap is normally 5 to 10 mOsm/kg. If there is a higher gap, the osmols unaccounted for may represent methanol, ethylene glycol, isopropyl alcohol, or other solutes ( Table A-5 ). To calculate serum osmolaity (Osmcalc ) and the osmolal gap: Osmcalc = 2 × (Na+ ) + [BUN (mg/dL)/2.8] + [glucose (mg/dL)/18] = normally 280—295 OG = Osmmeas - Osmcalc
Each mg/dL of:
TABLE 5 -- The Effect of Some Solutes on Serum Osmolality Increases Serum mOsm/kg by: For Each Serum mOsm/kg Increase Due to: The Corresponding mg/dL Change is (= mol wt/10): t
Methanol
0.31
Methanol
3.2
Ethanol
0.22
Ethanol
4.6
Acetone
0.17
Acetone
5.8
Isopropyl alcohol 0.17
Isopropyl alcohol
6.0
Ethylene glycol
0.16
Ethylene glycol
6.2
Glycerol
0.11
Glycerol
9.2
Mannitol
0.05
Mannitol
18.2
Adapted from Kullig K, Duffy JP, Linden CH, et al: Toxic effects of methanol, ethylene glycol and isopropyl alcohol. Top Emerg Med 6(2):16, 1984. Table A-5 shows the effect of some solutes on serum osmolality. In general, the increase in osmolality caused by a solute can be calculated by dividing its serum concentration by the tabulated value. Example: An intoxicated patient has serum chemistry results as follows: Na + 142, K+ 4.5, Cl- 100, HCO - 3 22, Glucose 90, BUN 14. His ethanol level is 240 and his measured serum osmolality is 348. To calculate his serum osmolaity:
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To evaluate for the effect of ethanol, refer to Table A-5 , adding the alcohol level divided by 4.6:
Finally, calculate the osmolal gap: OG = Osmmeas - Osmcalc = 348 - 346 = 2
Factitious Hyponatremia Factitious hyponatremia may be due to hyperglycemia. In this hyperosmolal state, glucose tends to stay in the extracellular fluid, drawing water out of the cells and into the extracellular fluid. Serum sodium is decreased by about 1.6 mmol/L for each 100 mg/dL of excess glucose. To calculate the corrected sodium: Corrected Na + (mmol/L) = Measured Na+ (mmol/L) + [1.6 × [(measured glucose in mg/dL - 100)/100] Many labs automatically make this adjustment so it is important to check with your lab to determine the necessity of this correction. Example: An obtunded elderly man appears dehydrated. His sodium level is 126 mmol/L and his glucose is 1000 mg/dL.
His corrected Na + suggests that he has factitious hyponatremia due to hyperglycemia. Free Water Deficit in Hypernatremia Elevation of serum sodium concentration is proportionate to free water deficit when volume is depleted. Since 60% of the adult body is water, total body free water deficit is calculated using measured Na + , desired Na+ , and body weight in kg. To calculate the free water deficit: Ideal total body water (TBW) = 60% × weight in kg Current TBW = (desired serum Na + × ideal TBW)/measured Na + Free water deficit = ideal TBW - current TBW
Example: An elderly man is brought to the ED in a coma. He has signs of severe dehydration. His ideal body weight is 70 kg. His serum Na + is 165 mmol/L. To determine his free water deficit: Ideal TBW = 0.6 (70 kg) = 42 L Current TBW = 140 mmol/L × 42 L/165 mmol/L = 35.6 L Free water deficit = 42 L - 35.6 L = 6.4 L Fluid correction for hypernatremia should take place over 48 to 72 hours to avoid the potential for cerebral edema. Calculation of the Sodium Deficit In Hyponatremia The following formula may be used to calculate the Na + deficit in hyponatremia: Na+ deficit = 60% × (weight in kg) × (desired Na + - measured Na+ ) Symptoms related to hyponatremia are variable and the severity of symptoms should guide therapy. Sodium replacement is most commonly given as isotonic saline, which contains 154 mmol of Na+ per liter. Patients who are severely symptomatic may require 3% saline solution that contains 513 mmol of Na + per liter. The volume of solution needed to replace the Na + deficit (in mmol) can be calculated using the concentrations in the saline solutions listed earlier. Example: A young man is seizing on arrival to the ED. He is known to have schizophrenia and compulsive water drinking. His Na + is 116 mmol/L. He weights 65 kg. To determine his sodium deficit:
This amount of Na+ deficit can be administered as approximately 6 liters of isotonic saline or 1.8 liters of hypertonic saline. Na
+
should be replaced very slowly to
avoid the possibility of inducing central pontine myelinolysis (CPM), which results from overaggressive correction of sodium. pH and Changes in Serum Potassium Levels
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Serum potassium (K+ ) levels change with the acid-base status. In acidemic states, K + moves out of cells as H + moves in, thus raising serum K + levels. In alkalemic states, K+ moves into cells as H+ moves out, thus lowering serum K+ levels. The change in K + varies inversely with pH at the following rate: Serum K+ concentration increases 0.6 mmol/L for each 0.1 unit decrease in pH. Serum K+ concentration decreases 0.6 mmol/L for each 0.1 unit increase in pH.
Calculating the Corrected Calcium Level Approximately 50% of serum calcium is bound to serum proteins (primarily albumin), 40% is in the free ionized state (the physiologically active form), and 10% is mixed with serum anions (phosphate, bicarbonate, citrate, and lactate). For this reason, serum calcium is lowered about 0.8 mg/dL for every decrease in albumin of 1 g/dL. To correct for decreased albumin (at levels