Pediatric Trauma

Pediatric Trauma
Pathophysiology, Diagnosis, and Treatment
edited by

DAVID E. WESSON
Baylor College of Medicine Houston, Texas, U.S.A. Associate Editors

ARTHUR COOPER
Columbia University College of Physicians and Surgeons New York, New York, U.S.A.

L. R. TRES SCHERER III

KiwanisRiley Regional Pediatric Trauma Center Indianapolis, Indiana, U.S.A.

STEVEN STYLIANOS
Columbia University College of Physicians and Surgeons Morgan Stanley Childrens Hospital of New York-Presbyterian New York, New York, U.S.A.

DAVID W. TUGGLE
University of Oklahoma College of Medicine Oklahoma City, Oklahoma, U.S.A.

Published in 2006 by Taylor & Francis Group 270 Madison Avenue New York, NY 10016 2006 by Taylor & Francis Group, LLC No claim to original U.S. Government works Printed in the United States of America on acid-free paper 10 9 8 7 6 5 4 3 2 1 International Standard Book Number-10: 0-8247-4117-X (Hardcover) International Standard Book Number-13: 978-0-8247-4117-4 (Hardcover) This book contains information obtained from authentic and highly regarded sources. Reprinted material is quoted with permission, and sources are indicated. A wide variety of references are listed. Reasonable efforts have been made to publish reliable data and information, but the author and the publisher cannot assume responsibility for the validity of all materials or for the consequences of their use. No part of this book may be reprinted, reproduced, transmitted, or utilized in any form by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying, microfilming, and recording, or in any information storage or retrieval system, without written permission from the publishers. For permission to photocopy or use material electronically from this work, please access [Link] ([Link] or contact the Copyright Clearance Center, Inc. (CCC) 222 Rosewood Drive, Danvers, MA 01923, 978-750-8400. CCC is a not-for-profit organization that provides licenses and registration for a variety of users. For organizations that have been granted a photocopy license by the CCC, a separate system of payment has been arranged. Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without intent to infringe. Library of Congress Cataloging-in-Publication Data Catalog record is available from the Library of Congress

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Preface

Injuries cause more than half of all deaths among children in the United States. The spectrum of causes varies with age, but blunt forces cause the overwhelming majority of injuries. Children are not just small adults. They differ in many ways from adults. Many of the differences in behavior, risk exposure, anatomy, and physiology have a direct bearing on trauma care. In recent years, this reality has been widely accepted in the eld. The Committee on Trauma of the American College of Surgeons has specically addressed the needs of injured children in its resources document and in the curriculum of its Advanced Trauma Life Support course. The Committee on Trauma recommends at least six hours of pediatric traumarelated continuing medical education for all surgeons providing pediatric trauma care, and many states have established specic requirements for hospitals receiving injured children. Across the United States, childrens hospitals, pediatric surgeons, and pediatric emergency physicians have focused on the needs of injured children and established pediatricspecic benchmarks in the management of solid organ injuries, neurotrauma, fractures, and numerous other types of trauma. But there is a problem. There are just not enough childrens hospitals or pediatric trauma specialists to meet the needs of all injured children in the United States. Much, if not most, pediatric trauma care is provided in general hospitals by nonpediatric specialists. This book is intended for all physicians and surgeons who treat children with life- and limb-threatening injuries. The primary target audience includes general surgeons, trauma surgeons, and emergency physicians experienced in trauma care who want to expand their knowledge of pediatric trauma. The content relates primarily to direct patient care, excluding such topics as prevention, organ procurement, and medical legal and legislative issues. The emphasis is on injuries caused by blunt and penetrating mechanical forces to the exclusion of burns and scald injuries and drowning. The book is divided into four sections. The rst deals with trauma systems for children, including epidemiology and preparations for pediatric trauma care. Section two covers general principles of resuscitation and supportive care relevant to all pediatric trauma patients. Section three covers the management of specic injuries. Section four deals with rehabilitation and long-term outcomes and how to effectively communicate with families, particularly when the outcome is not good. I would like to thank Geoff Greenwood and Taylor & Francis for encouraging and supporting us in this project. I would also like to thank the authors, who were selected because of their expertise, for their efforts, and my administrative assistant
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Laura Barrera for her help in editing the book. I would also like to thank my coeditors, Steven Stylianos, David Tuggle, Arthur Cooper, and Tres Scherer, for their efforts, particularly in recruiting expert authors for each of the chapters. David E. Wesson, M.D.

Contents

Preface iii Contributors

xiii

PART I: TRAUMA SYSTEMS FOR CHILDREN 1. Epidemiology of Pediatric Trauma . . . . . . . . . . . . . . . . . . . . . . . . . 1 David E. Wesson Introduction . . . . 1 Historical Perspective . . . . 1 Injury Facts . . . . 2 Risk Factors . . . . 3 Costs . . . . 3 Trends . . . . 4 Comparisons with Other Countries . . . . 4 Common Clinical Scenarios and Patterns of Injury . . . . 5 Role of the Trauma Center . . . . 5 Summary . . . . 6 References . . . . 6 2. Organizing the Community for Pediatric Trauma . . . . . . . . . . . . . . . 9 Arthur Cooper Introduction . . . . 9 Trauma and Emergency Medical Services for Children . . . . 10 The Public Health Approach to Pediatric Trauma . . . . 11 Evidence in Support of Specialized Hospital Care for Pediatric Trauma . . . . 15 Elements of Contemporary Pediatric Trauma System Design . . . . 18 Evidence in Support of Specialized Pre-Hospital Care for Pediatric Trauma . . . . 19 Elements of Contemporary Pediatric Pre-Hospital Trauma Care . . . . 23 Summary . . . . 27 References . . . . 27

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3. Organizing the Hospital for Pediatric Trauma Care . . . . . . . . . . . . 33 Max L. Ramenofsky History of Trauma Centers . . . . 33 Pediatric Trauma Centers . . . . 34 Preplanning . . . . 34 Education . . . . 37 Severity Predictors and the Tiered Response . . . . 38 Emergency Medical Services . . . . 40 Summary . . . . 40 References . . . . 41 PART II: GENERAL PRINCIPLES OF RESUSCITATION AND SUPPORTIVE CARE 4. The ABCs of Pediatric Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . 43 Robert W. Letton Introduction . . . . 43 Anatomic and Physiologic Considerations . . . . 44 Airway . . . . 44 Breathing . . . . 48 Circulation . . . . 53 Conclusion . . . . 57 References . . . . 58 5. Clearance of the Cervical Spine in Children . . . . . . . . . . . . . . . . . . 61 Brian D. Kenney References . . . . 70 6. Trauma from Child Abuse . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73 Charles S. Cox, Jr. Introduction . . . . 73 Literature-Based Guidelines . . . . 73 Epidemiology . . . . 73 Initial Evaluation and Treatment . . . . 74 CNS Injury . . . . 76 Abdominal Injury . . . . 77 Fractures and Fracture Patterns . . . . 79 Stairway Injuries and Low-Level Falls . . . . 80 Physician Responsibilities . . . . 80 References . . . . 81 7. Fetal Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 83 Amir Kaviani, Dario Fauza, Moritz Ziegler, and Russell Jennings Introduction and Background . . . . 83 Anatomic and Physiologic Changes Associated with Pregnancy . . . . 84 Initial Evaluation and Management . . . . 86

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Diagnostic Studies . . . . 89 Management Strategies . . . . 90 References . . . . 94 8. Imaging the Injured Child . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97 David Tuggle and Michele A. Markley Introduction . . . . 97 Literature-Based Guidelines . . . . 97 Types of Studies . . . . 98 References . . . . 104 9. Transfusion Therapy in Injured Children . . . . . . . . . . . . . . . . . . . 107 Denis D. Bensard Introduction . . . . 107 Literature-Based Guidelines . . . . 108 Epidemiology . . . . 108 Pathophysiology . . . . 109 Component Therapy . . . . 111 Emergency Management . . . . 113 Denitive Management . . . . 116 Complications of Transfusion . . . . 117 Red Blood Cell Substitutes . . . . 119 References . . . . 120 10. Pediatric ICU Management . . . . . . . . . . . . . . . . . . . . . . . . . . . 123 Cameron Mantor, Nikola Pufnbarger, and David Tuggle ICU Care . . . . 123 Monitoring . . . . 123 Management of PICU Transfusions . . . . 125 Nutrition . . . . 126 Commonly Used Medications . . . . 126 Acute Respiratory Failure . . . . 126 References . . . . 133 11. Nutritional Support for the Pediatric Trauma Patient Tom Jaksic and Biren P. Modi Introduction . . . . 135 The Metabolic Response to Trauma . . . . 135 Metabolic Reserves . . . . 137 Nutritional Needs . . . . 137 Routes of Nutrient Provision . . . . 143 Summary . . . . 143 References . . . . 143 . . . . . . . . . 135

12. Anesthesia for Pediatric Trauma . . . . . . . . . . . . . . . . . . . . . . . . 147 J. Thomas and J. Lerman Introduction . . . . 147

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Airway Management . . . . 147 Pharmacological Agents for Induction and Maintenance of Anesthesia . . . . 160 Assessment and Management of Shock . . . . 165 Anesthesia for Neurotrauma . . . . 169 Anesthesia for Thoracic Trauma . . . . 171 References . . . . 174 13. Prevention and Treatment of Trauma-Related Infection in Children . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 181 Randall S. Burd, Roshni Shukla, and Michael S. Cooperstock Introduction . . . . 181 Statement of the Problem . . . . 181 Trauma-Related Infections . . . . 183 Nosocomial Infections . . . . 189 Recommendations for Evaluation and Treatment of Infectious Complications . . . . 195 Conclusion . . . . 195 References . . . . 195 14. Pediatric Organ Failure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 197 Anthony Dilley and David E. Wesson Introduction . . . . 197 Denitions . . . . 198 MODS/SIRS/Sepsis . . . . 198 Hypothermia . . . . 199 Abdominal Compartment Syndrome . . . . 201 Severe Extremity and Crush Injuries . . . . 202 Child Abuse . . . . 202 CNS Dysfunction and Failure . . . . 202 Acute Respiratory Distress Syndrome . . . . 203 Renal Failure . . . . 204 Liver Failure . . . . 205 Gastrointestinal Failure . . . . 205 Pancreatic Failure . . . . 206 Derangement of Blood . . . . 206 Summary . . . . 206 References . . . . 206 PART III: SPECIFIC INJURIES 15. Treatment of Severe Pediatric Head Injury: Evidence-Based Practice . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211 Jodi L. Smith Introduction . . . . 211 Pathophysiology of Head Injury . . . . 213

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Evidence-Based Treatment StrategiesPre-Hospital Care . . . . 213 Evidence-Based Treatment StrategiesIntensive Management . . . . 216 Conclusion . . . . 225 References . . . . 225 16. Pediatric Facial Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 231 Barry L. Eppley Introduction . . . . 231 Epidemiology . . . . 231 Anatomy and Pathophysiology . . . . 232 Diagnostic Tests . . . . 232 Emergency Management . . . . 233 Denitive Treatment . . . . 233 References . . . . 243 17. Pediatric Thoracic Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . 245 Anthony Dilley Introduction . . . . 245 Blunt Injuries . . . . 246 Penetrating Injuries . . . . 246 Traumatic Asphyxia . . . . 247 Pre-Hospital Management . . . . 247 Initial Evaluation . . . . 247 Adjunctive Investigations During the Resuscitative and Diagnostic Phase . . . . 248 Emergency Room Resuscitative Thoracotomy . . . . 248 Rib Fractures . . . . 249 Pulmonary Contusion . . . . 250 Pneumothorax . . . . 251 Traumatic Pleural EffusionHemothorax . . . . 252 Traumatic Pneumatocele . . . . 252 Lung Parenchymal and Hilar Vessel Laceration . . . . 253 Tracheobronchial Injuries . . . . 253 Injuries of the Thoracic Aorta and Its Branches . . . . 254 Cardiac Injury . . . . 256 Diaphragmatic Injuries . . . . 257 Esophageal Injury . . . . 258 References . . . . 259 18. Abdominal Trauma in Children . . . . . . . . . . . . . . . . . . . . . . . . . 267 Steven Stylianos, Richard Pearl, and Paul Babyn Introduction . . . . 267 Solid Organ Injury . . . . 268 Injuries to the Duodenum and Pancreas . . . . 281 Injuries to the Stomach, Small Intestine, and Colon . . . . 289

Contents

Injuries to the Perineum, Anus, and Genitalia . . . . 294 Diagnostic Peritoneal Lavage and Laparoscopy . . . . 295 References . . . . 297 19. Pediatric Genitourinary Trauma . . . . . . . . . . . . . . . . . . . . . . . . 303 James R. Colvert, Bradley P. Kropp, and Earl Y. Cheng Introduction . . . . 303 Renal Trauma . . . . 303 Ureteral Injuries . . . . 312 Bladder Injuries . . . . 313 Urethral Injuries . . . . 316 Testicular Injuries . . . . 319 References . . . . 320 20. Pediatric Orthopedic Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . 325 Angus J. Gray Introduction . . . . 325 Incidence of Skeletal Trauma . . . . 325 Pathophysiology . . . . 326 Multiple Trauma . . . . 329 Open Fractures . . . . 330 Amputations . . . . 332 Compartment Syndrome . . . . 334 Spinal Fractures . . . . 335 Upper Limb Fractures . . . . 337 Lower Limb and Pelvic Fractures . . . . 342 Non-Accidental Injury . . . . 345 An Approach to Orthopedic Trauma . . . . 348 References . . . . 351 21. Pediatric Hand Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 357 Ann Licht, John Potochny, and Larry Hollier Introduction . . . . 357 History . . . . 357 Recent Literature . . . . 357 Diagnosis of Hand Injuries . . . . 358 Treatment of Hand Injuries . . . . 364 References . . . . 369 PART IV: OUTCOMES 22. Rehabilitation of the Child with Injuries . . . . . . . . . . . . . . . . . . . 371 James R. Christensen and Charles N. Paidas Introduction . . . . 371 Efcacy of Rehabilitation . . . . 371 Denitions . . . . 373 Rehabilitation as a Member of the Acute Trauma Team . . . . 375

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Model Systems . . . . 375 Criteria for Rehabilitation Services . . . . 380 Rehabilitation . . . . 381 Rehabilitation of Traumatic Brain Injury . . . . 382 Rehabilitation of Spinal Cord Injury . . . . 384 Summary . . . . 385 References . . . . 386 23. Long-Term Outcomes in Injured Children . . . . . . . . . . . . . . . . . . 389 Michael Vitale and David P. Mooney Pediatric Trauma: Scope of the Problem . . . . 389 The Challenge of Assessing Pediatric Outcomes . . . . 389 Volume Outcome Relationships . . . . 390 Functional Status and Quality-of-Life Assessment in a Pediatric Population . . . . 391 Pediatric Polytrauma: Outcomes . . . . 391 Outcomes of Traumatic Brain Injury (TBI) . . . . 392 Outcomes of Trauma to the Extremity in Children . . . . 394 Outcomes of Pediatric Pelvic Fractures . . . . 395 Outcomes of Spinal Cord Injuries . . . . 396 References . . . . 399 24. Communication with Families of Injured Children . . . . . . . . . . . . 405 Mary E. Fallat, Monica Hall, and Maria Trozzi Introduction . . . . 405 When a Child Dies . . . . 407 Family Presence During Resuscitation . . . . 407 Understanding Brain Death . . . . 408 Organ Donation Issues . . . . 409 Bereavement . . . . 409 The FamilyCoping with Unpredictability . . . . 409 The Familys Acute Grief Reaction . . . . 410 The Grieving Parents Defense Mechanisms . . . . 410 Next Steps: Surgery or The Impossible Outcome . . . . 411 Long-Term Bereavement . . . . 411 Coping Skills: Personal, Professional . . . . 412 Summary . . . . 415 References . . . . 416 Additional Reading . . . . 417 Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 419

Contributors

Paul Babyn Department of Radiology, University of Toronto Faculty of Medicine, and Radiologist-in-Chief, Department of Diagnostic Imaging, The Hospital for Sick Children, Toronto, Ontario, Canada Denis D. Bensard The Childrens Hospital, The University of Colorado, Denver, Colorado, U.S.A. Randall S. Burd Department of Surgery, Robert Wood Johnson University Hospital, New Brunswick, New Jersey, U.S.A. Earl Y. Cheng Department of Urology, Childrens Hospital of Oklahoma, University of Oklahoma, Health Sciences Center, Oklahoma City, Oklahoma, U.S.A. James R. Christensen Physical Medicine, Rehabilitation, and Pediatrics, The Kennedy Krieger Institute and The Johns Hopkins University School of Medicine, Baltimore, Maryland, U.S.A. James R. Colvert Urology Resident, University of Oklahoma, Health Sciences Center, Oklahoma City, Oklahoma, U.S.A. Arthur Cooper Department of Clinical Surgery, Columbia University College of Physicians and Surgeons, New York, New York, U.S.A. Michael S. Cooperstock Department of Child Health, University of MissouriColumbia Medical School, Columbia, Missouri, U.S.A. Charles S. Cox, Jr. Department of Surgery, Division of Pediatric Surgery, University of Texas-Houston Medical School, Houston, Texas, U.S.A. Anthony Dilley Department of Trauma, Sydney Childrens Hospital, New South Wales, Australia Barry L. Eppley U.S.A. Indiana University School of Medicine, Indianapolis, Indiana,

Mary E. Fallat Department of Surgery, University of Louisville and Kosair Childrens Hospital, Louisville, Kentucky, U.S.A.
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Contributors

Dario Fauza Department of Surgery, The Childrens Hospital and Harvard Medical School, Boston, Massachusetts, U.S.A. Angus J. Gray Sydney Childrens Hospital, University of New South Wales, Randwick, New South Wales, Australia Monica Hall Three Rivers Medical Center, Louisa, Kentucky, U.S.A.

Larry Hollier Division of Plastic and Reconstructive Surgery, Baylor College of Medicine, Houston, Texas, U.S.A. Tom Jaksic Department of Surgery, Childrens Hospital Boston, Boston, Massachusetts, U.S.A. Russell Jennings Department of Surgery, The Childrens Hospital and Harvard Medical School, Boston, Massachusetts, U.S.A. Amir Kaviani Department of Surgery, The Childrens Hospital and Harvard Medical School, Boston, Massachusetts, U.S.A. Brian D. Kenney Ohio, U.S.A. Department of Surgery, The Ohio State University, Columbus,

Bradley P. Kropp Department of Urology, Childrens Hospital of Oklahoma, University of Oklahoma, Health Sciences Center, Oklahoma City, Oklahoma, U.S.A. J. Lerman Department of Anesthesia, Women and Childrens Hospital of Buffalo, SUNY at Buffalo, Buffalo, New York, U.S.A. Robert W. Letton Pediatric Trauma and Burns, Brenner Childrens Hospital, Wake Forest University School of Medicine, Winston-Salem, North Carolina, U.S.A. Ann Licht Division of Plastic and Reconstructive Surgery, Baylor College of Medicine, Houston, Texas, U.S.A. Cameron Mantor The Section of Pediatric Surgery, Department of Surgery, University of Oklahoma College of Medicine, Oklahoma City, Oklahoma, U.S.A. Michele A. Markley U.S.A. Chris Everts Childrens Hospital, Fort Lauderdale, Florida,

Biren P. Modi Department of Surgery, Childrens Hospital Boston, Boston, Massachusetts, U.S.A. David P. Mooney Childrens Hospital, Harvard Medical School, Boston, Massachusetts, U.S.A.

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Charles N. Paidas Surgery, Pediatrics, Oncology, and Anesthesia, and Critical Care Medicine, The Johns Hopkins University School of Medicine, The Johns Hopkins Hospital, Baltimore, Maryland, U.S.A. Richard Pearl Departments of Surgery and Pediatrics at the University of Illinois College of Medicine-Peoria and Director of Pediatric Trauma and Surgeon-in-Chief, Childrens Hospital of Illinois, Peoria, Illinois, U.S.A. John Potochny Division of Plastic and Reconstructive Surgery, Baylor College of Medicine, Houston, Texas, U.S.A. Nikola Pufnbarger The Section of Pediatric Surgery, Department of Surgery, University of Oklahoma College of Medicine, Oklahoma City, Oklahoma, U.S.A. Max L. Ramenofsky Geisinger Medical Center, St. Christophers Hospital for Children, Danville, Pennsylvania, U.S.A. Roshni Shukla Department of Surgery, University of Missouri-Columbia Medical School, Columbia, Missouri, U.S.A. Jodi L. Smith Pediatric Neurosurgery, James Whitcomb Riley Hospital for Children, Indiana University School of Medicine, Indianapolis, Indiana, U.S.A. Steven Stylianos Departments of Surgery and Pediatrics, Columbia University College of Physicians and Surgeons, and Director, Regional Pediatric Trauma Program, Morgan Stanley Childrens Hospital of New York-Presbyterian, New York, New York, U.S.A. J. Thomas Department of Anesthesia, Women and Childrens Hospital of Buffalo, SUNY at Buffalo, Buffalo, New York, U.S.A. Maria Trozzi Department of Pediatrics, Boston University School of Medicine, Boston, Massachusetts, U.S.A. David Tuggle The Section of Pediatric Surgery, Department of Surgery, University of Oklahoma College of Medicine, Oklahoma City, Oklahoma, U.S.A. Michael Vitale Childrens Hospital, Presbyterian Hospital, New York, New York, U.S.A. David E. Wesson Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, Texas, U.S.A. Moritz Ziegler Department of Surgery, The Childrens Hospital and Harvard Medical School, Boston, Massachusetts, U.S.A.

PART I: TRAUMA SYSTEMS FOR CHILDREN

1
Epidemiology of Pediatric Trauma
David E. Wesson
Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, Texas, U.S.A.

INTRODUCTION Epidemiology is the study of the distribution of diseases in groups or populations. One of its aims is to dene the occurrence of disease by place and time in the general population and in specic subpopulations. The overarching goal is to reduce the incidence and severity of specic diseases. Injury epidemiology involves the collection of data on the time, place, mechanism, and victim of injury. Over the past 25 years, injury epidemiology has had a major impact on our understanding of pediatric trauma. It has allowed us to identify and quantify specic injury risks, develop prevention and treatment strategies, and monitor their effectiveness. The study of injury epidemiology has produced one fundamental fact: Injuries are the leading threat to the health and well-being of young people in our society today (1). This is of major importance to public health ofcials and health care providers alike. Epidemiology can help clinicians by identifying common causes, mechanisms, and patterns of injury. It tells us that motor vehicle crashes and falls from a great height cause more life-threatening injuries than sports and recreational activities. We know that blunt injuries far outnumber penetrating injuries and that children are prone to develop intracranial hypertension from cerebral edema after a closed head injury. The astute trauma surgeon will learn to suspect and recognize these patterns based on the age of the child and the mechanism of injury. As in most areas of surgical practice, the history of events before presentation aids signicantly in diagnosis and treatment.

HISTORICAL PERSPECTIVE One hundred years ago, infections were the great scourge of children in our society. Today the problem is injury or trauma. Changing social conditions, better housing and nutrition, immunization, and quarantine of infectious cases all helped reduce the threat from infectious diseases. Over the same time period, new environmental factors, notably the introduction of the automobile, increased the risk of injury.
1

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Our present understanding of the epidemiology of trauma in our society began in the 1960s with the publication of a monograph entitled Accidental Death and Disability: The Neglected Disease of Modern Society by the Committees on Trauma and Shock of the National Academy of Sciences (2). This report pointed out that accidental injuries were the nations most important environmental health problem. This was followed by another important publication Injury in America, which documented in much greater detail the impact of injuries on American society and suggested a broad approach to the problem encompassing epidemiology, prevention, biomechanics, acute treatment, and rehabilitation (3). Since these two important publications appeared, much progress has been made both in prevention and treatment of injuries. During the 1980s and 1990s, the mortality rate from pediatric trauma in the United States fell by about 50%. No doubt this resulted from improvements in both prevention and treatment. But, there are many reasons why we will have to increase our prevention efforts if we hope to see another 50% reduction in the next 20 years.  The cost of treating trauma victims and the pain and suffering they endure are very high, even when the nal outcome is excellent. Prevention would eliminate these effects.  About 50% of pediatric trauma deaths occur in the eld before the victim even reaches a trauma center. Here, too, prevention is the answer.  Most trauma systems now have very low preventable death rates. There is always room for improvement, but the curve is attening out. It is unlikely that substantial reductions in the overall trauma mortality rate in the United States can be achieved by better trauma care.  We lack effective treatments for primary brain injuries, the most common cause of death in pediatric trauma. Here, too, prevention is the solution. A report from the National Pediatric Trauma Registry showed that about 70% of the deaths were caused by central nervous system (CNS) injury (4). Only prevention can signicantly reduce these deaths.

INJURY FACTS More than half of all childhood deaths in the United States result from preventable injuries. For children 1 to 19 years old, unintentional injuries (accidents) and homicide (assault) were the rst and second leading causes of death, respectively (1). Together they account for >50% of all childhood deaths among children 1 to 19 years of age. Unintentional injuries are the number one childhood killer in all age brackets, 1 to 4, 5 to 9, 10 to 14, and 15 to 19 years of age accounting for 34%, 42%, 39%, and 49% of all deaths in each of these age groups, respectively (1). In 2001, unintentional injuries of all types, including suffocation, drowning, burns, and scalds, as well as blunt and penetrating trauma, caused more than 11,196 deaths among children 1 to 19 years of age in the United States. This represents 44% of all pediatric deaths. Homicide, the second leading cause, resulted in 2640 more deaths or 10% overall. In Harris County, Texas, which includes the City of Houston, injuries are the leading cause of death among children, even when neonates with birth weights >500 g and infants less than one year old are included (5). In 2000, injuries were the leading cause of death in all pediatric age groups in Houston and Harris County except infants <1 year of age. The mortality rate for injuries among children, from

Epidemiology of Pediatric Trauma

birth to 17 years of age, in Houston and Harris County actually rose from 14.9 to 16.8 per 100,000 from 2000 to 2001. In 2000, injuries caused 147 deaths from birth to 17 years of age, compared to 93 for congenital anomalies and 86 for perinatal conditions. About 50% of the fatal injuries were sustained in motor vehicle crashes. Most were passengers, followed by pedestrians struck by a motor vehicle and drivers. The external causes of injury death were unintentional in 59%, homicide in 24%, suicide in 8%, and undetermined in 9%. In Houston, almost half of pediatric homicides are committed with a rearm, usually a handgun. Gunshot wounds are also the most common mechanism of child suicide.

RISK FACTORS The risk of most types of injury varies with age. Homicide is the leading cause of injury death for infants from one month to one year of age in the United States. Plotted by age, homicide rates produce a U-shaped curve. In Harris County, Texas, in 2001, the homicide rates were 12.5/100,000 infants, 5.3/100,000 1 to 4 year olds, 1.1/100,000 5 to 9 year olds, 1.3/100,000 10 to 14 year olds, and 9.0/100,000 15 to 19 year olds (5). The homicide rate for boys is almost three times that for girls. It is also much higher among African Americans than Caucasians. Child abuse causes the majority of homicides in the rst year of life; gunshot wounds predominate among teenagers. A person known to the victim, most commonly a parent, perpetrates the vast majority of homicides. Suffocation is the number one cause of unintentional injury death in infants, but is rare in other groups. Drowning and submersion are the leading cause of death for children one to four years of age. Toddlers have a much higher death rate for burns and scalds than older children do. The risk of injury for school-aged boys is far greater than for girls. Motor vehicle occupant injuries predominate among teenagers 15 to 19 years old. The likelihood of a child being fatally injured is associated with single parentage, low maternal education, young maternal age at birth, poor housing, large family size, and parental abuse of alcohol and other drugs. A study from Newcastle, England, of fatal head injuries revealed that children from poorer neighborhoods were at greater risk than were those from more afuent areas (6). The authors concluded that the lack of proper playgrounds, which forced poor children to play in the streets, accounted for the difference. Children living in trailer homes in the United States have twice the risk of dying in house res than children living in other types of housing. Children who live in rural counties have a higher incidence of motor vehicle related injury and a higher risk of dying compared to urban children. There is also a strong correlation between per capita income and mortality from motor vehicle crashes among all the counties in the lower 48 states. Racial and ethnic factors correlate with other socioeconomic determinants, but even when these are controlled for, American Indians have the highest rates of injury mortality in the country.

COSTS It is difcult to accurately determine all of the costs of pediatric trauma. But most estimates suggest that the costs are enormous. Hospital costs represent only one slice

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of the pie. Other costs include medical services, lost productivity, indirect costs to families for lost income, etc. Rice and Mackenzie estimate that the cost of injury to children from birth to 14 years of age in the United States in 1985 was $13.8 billion (7). A recent report entitled Unintentional Injuries in Childhood in the Future of Children series published this year by the David and Lucille Packard Foundation provides a lot of data on this subject (8).  In 1996, 13,000 children and adolescents died of unintentional injuries in the United States.  For school-aged children and teenagers, injuries are almost as frequent as the common cold.  In 1996, injuriesmostly to the brain, spinal cord, and limbsand burns left an estimated 150,000 children permanently disabled.  Injuries to children resulted in the loss of 2.7 million quality adjusted life years (QALYs). This publication also attempted to express the impact of childhood injuries in nancial terms. It estimated the total nancial burden of childhood injury in America for 1996 at $81 billion.  Direct spending for medical services over the lifetime of the victim amounted to $14 billion.  Other resource costs including emergency medical services totaled $1 billion.  Lifetime productivity losses amounted to $66 billion. TRENDS We have made substantial progress in the ght against childhood injury. The death rate has declined signicantly in one generation. Unintentional injury mortality fell by 50% from 1970 to 1995 in the Organization for Economic Co-operation and Development (OECD) nations (the 26 richest nations in the world) (9). During the same period, the proportion of all childhood deaths caused by injuries rose from 25% to 37%. Improved highway and vehicle design, smoke detectors and alarms, car seats, and seat belts have all played a part in reducing childhood injury mortality. Even the homicide rate has declined. This trend continues: The injury death rate in the United States decreased by 3.3% in 2001 (1). In the province of Ontario, the number of children seriously injured while bicycling has fallen sharply over the past ve years (10). This is due to legislation making helmets mandatory for children riding on public roads. Across Canada, there is a clear association between bike helmet legislation and the risk of head injury. Provinces with helmet laws had 25% lower head injury risk.

COMPARISONS WITH OTHER COUNTRIES Injuries are the principal cause of death for children 1 to 14 years of age in all nations in the OECD (9). Injuries account for 40% of all deaths in children 1 to 14 years of age. Together they take the lives of more than 20,000 children each year in the OECD nations. Trafc accidents account for 41% of the deaths. For every death,

Epidemiology of Pediatric Trauma

there are 160 hospital admissions and 2000 emergency department visits. Injuries account for almost 30% of the total burden of childhood disease measured by disability adjusted life years (DALYs). The Swedish, British, Italian, and Dutch child injury death rates are among the lowest; the United States rate is among the highest along with Poland, New Zealand, Portugal, and Mexico. The United States accounts for almost one-third of all child injury deaths in the developed nations. More than 12,000 child injury deaths a year could be prevented if all countries had the same child injury death rate as Sweden. Bringing the United States rate down to that of Sweden would save 4700 American children each year.

COMMON CLINICAL SCENARIOS AND PATTERNS OF INJURY Astute clinicians learn to recognize common clinical scenarios and patterns of injury. Thus, knowledge of the circumstances can help identify patients with certain types of injury. For example, restrained children in side impact crashes are much more likely to sustain injuries from compartment intrusion than children in frontal crashes. Side impact crashes also cause more severe injuries (ISS > 15; GCS < 9) and more injuries to the head, cervical spine, and chest to restrained children (11). In contrast to this, restrained children in frontal crashes are more likely to suffer injuries to the abdomen and lumbar spine. The following is a partial list of common pediatric trauma clinical scenarios:  The infant brought in with a vague history (e.g., a fall at home), altered mental status, and severe neuro-trauma from child abuse  The properly restrained toddler involved in a high-speed motor vehicle crash brought in by ambulance who proves to have no signicant injury  The school-aged child struck by a motor vehicle who presents with a lower limb fracture, intra-abdominal or thoracic visceral trauma, and a closed head injury  The pre-teen who suffers a high-grade hepatic or splenic injury from an offroad all-terrain vehicle (ATV) crash  The child with an acute epidural hematoma following a seemingly minor direct blow to the head  The rear seat passenger with a transverse abdominal bruise and occult small bowel and lumbar spine and/or spinal cord injuries from a lap belt  The child with a duodenal hematoma or pancreatic laceration from a direct blow to the abdomen from a hockey stick or bike handle bar Emergency physicians and trauma surgeons should be on the alert for children with these typical clinical presentations.

ROLE OF THE TRAUMA CENTER The primary role of the trauma center is, of course, to care for patients with life- and limb-threatening injuries. Trauma centers can also make important contributions to injury control through education and prevention. Education efforts can target health care providers and the greater community. Education is a necessary component of all injury prevention programs and is usually

Wesson

a necessary rst step before new legislation mandating injury prevention measures such as seat belts, child restraints, bike helmets, etc. Trauma centers can also help to identify specic causes of injury and associations or patterns of injury. Data from the trauma registry showing a signicant number of fatal bicycling injuries motivated the trauma program staff at the Hospital for Sick Children, Toronto, to start a bike helmet campaign. The rst phase of the campaign was intended to educate the public, health care workers, government ofcials, and politicians of the risk of bike-related head trauma and of the benets of bike helmets. This eventually lead to a bike helmet law in the province of Ontario, which contributed signicantly to a 26% reduction in bicycling-related head injuries among children 1 to 19 years of age. A national population-based study across Canada conrmed that parts of the country with helmet laws had lower head injury rates (12).

SUMMARY Injuries are the leading risk to the lives and limbs of children from infancy through adolescence in our modern world. The mechanisms and the numbers vary with age, gender, race, parental education, social class, and economic status. Awareness of these variations can assist clinicians in the management of pediatric trauma victims. Analysis of these variations can also help us to develop ways of preventing childhood injuries from occurring in the rst place.

REFERENCES
1. Arias E, MacDorman MF, Strobino DM, Guyer B. Annual summary of vital statistics. Pediatrics 2003; 112:12151230. 2. Committee on Trauma and Committee on Shock. Division of Medical Sciences. National Academy of Sciences. National Research Council. Accidental Death and Disability: The Neglected Disease of Modern Society. Public Health Service Publication Number 1071A-13. Sixth Printing September 1970. 3. Committee on Trauma Research, Commission on Life Sciences, National Research Council and the Institute of Medicine. Injury in America: A Continuing Public Health Problem. Washington: National Academy Press, 1985. 4. The National Pediatric Trauma Registry. [Link] 5. Houston/Harris County Child Fatality Review Team 20002001. Child Fatality Report. Harris County Public Health and Environmental Services. April 2003. 6. Sharples PM, Storey A, Aynsley-Green A, Eyre JA. Causes of fatal childhood accidents involving head injury in northern region, 197986. BMJ 1990; 301:11931197. 7. Rice DP, Mackenzie EJ. Cost of Injury in the United States. A Report to Congress, 1989. San Francisco: Institute for Health & Aging, University of California and Injury Prevention Center, The Johns Hopkins University, 1989. 8. The David and Lucille Packard Foundation. Unintentional Injuries in Childhood. The Future of Children. Vol. 10. 2000:1188. [Link] 9. A League Table of Child Deaths by Injury in Rich Nations. Innocenti Report Card Number 2. UNICEF. Florence: Innocenti Research Centre. February 2001. 10. Wesson DE, Spence L, Hu X, Parkin P. Trends in bicycling-related head injuries in children after implementation of a community-based bike helmet campaign. J Pediatr Surg 2000; 35:688689.

Epidemiology of Pediatric Trauma

11. Orzechowski KM, Edgerton EA, Bulas DI, McLaughlin PM, Eichelberger MR. Patterns of injury to restrained children in side impact motor vehicle crashes: the side impact syndrome. J Trauma 2003; 54:10941101. 12. Macpherson AK, To TM, Macarthur C, Chipman ML, Wright JG, Parkin PC. Impact of mandatory helmet legislation on bicycle-related head injuries in children: a population-based study. Pediatrics 2002; 110:e60.

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Organizing the Community for Pediatric Trauma
Arthur Cooper
Department of Clinical Surgery, Columbia University College of Physicians and Surgeons, New York, New York, U.S.A.

INTRODUCTION Modern pediatric trauma care, like adult trauma care, has undergone constant evolution during the past generation, since the care of injured children rst emerged as a distinct discipline. In part, this was driven by the growing recognition among pediatric surgeonsled by Dr. Jacob Alexander Haller, Junior, of the Johns Hopkins University in Baltimore, Marylandthat pediatric trauma care constituted a key component of the subspecialty of pediatric surgery, and in part by the growing recognition of the federal government that emergency medical services (EMS) for children had been neglected during the development of EMS systems nationwide (1,2). Since their inception, pediatric trauma programs have stressed the need for full integration with their afliated adult trauma programs and their regional EMS systems, to ensure seamless care, and cost-effective use of scarce human and nancial resources (3). They have also recognized the need for all who care for pediatric patients to ensure that the special needs of injured children are met at every level of trauma and EMS system organization (4). To this end, this chapter will describe the current state of the art with respect to pediatric trauma system design. Consistent with this purpose, the public health approach to trauma and EMS systems will be emphasized. Additionally, the literature supporting the need for and components of pediatric-capable trauma and EMS systems will be reviewed. Finally, critical elements of pre-hospital care for the pediatric trauma patient will be delineated. The objective is to arm the adult trauma surgeonthe physician who provides most pediatric trauma care nationwidewith a working knowledge of pediatric trauma system design and function to ensure, insofar as is possible, that every child in every community has the benet of stateof-the-art pediatric trauma care and, accordingly, the greatest possible chance for recovery and rehabilitation.

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TRAUMA AND EMERGENCY MEDICAL SERVICES FOR CHILDREN Modern EMS systems evolved because of the recognition that trauma and sudden cardiac emergencies were the leading causes of death in the United States, and that the largely volunteer, re companybased rescue squads that historically comprised most EMS were not optimally prepared to meet this challenge. The physicians who rst created the EMS systems were trained chiey in the adult-oriented specialties of surgery, internal medicine, cardiology, and anesthesiology (5). Infants and children were cared for in these EMS systems, but their needs were not specically addressed, and deciencies in their care were not recognized, based on the false notion that children could be treated as little adults. Hence, none of the key legislative initiatives that resulted in the creation of modern EMSthe Highway Safety Act of 1966, the Emergency Medical Service Systems Act of 1973, and the Preventive Health and Health Services Block Grant Program of 1982, which ultimately replaced the EMS Systems Actmade special mention of the unique needs of infants and children in the emergency care system, even though neonatal care was regionalized under the EMS Systems Act. The development of pediatric surgery and pediatric emergency medicine as distinct disciplines, each with approved residency and fellowship training programs and recognized board certication, fostered the development of EMS for children (EMSC) in many parts of this country. It was recognized that pediatric patients comprised some 5% to 10% of pre-hospital transports, 30% of emergency department visits, 21% of all pre-hospital trauma care, and 12% of all in-hospital trauma care (6,7). Seminal reports described the unique epidemiology of pediatric pre-hospital care documented deciencies in the way trauma systems provided access for children and in the way they educated, equipped, and provided medical control of pre-hospital personnel (6,810). These led, in turn, to major federal initiatives in EMSC, including legislation and funding, systematic analysis of the nations strengths and weaknesses in EMSC by the Institute of Medicine (IOM), and development of specic plans to remedy the weaknesses it identied, which have continued to be updated on a regular basis (11,12). The current federal EMSC program is administered by the Maternal and Child Health Bureau (MCHB) of the Health Resources and Services Administration (HRSA) in collaboration with its Division of Trauma and EMS (DTEMS) and the EMS Division of the National Highway Trafc Safety Administration (NHTSA), with the assistance of the EMSC National Resource Center (NRC) at the Childrens National Medical Center in Washington, DC, and the National EMSC Data Analysis and Research Center (NEDARC) at the Primary Childrens Hospital in Salt Lake City, Utah. EMSC consists of six phases of care and contains several of the elements addressed in the EMS Systems Act of 1973. It encompasses the entire spectrum of care for the child requiring emergency services and exists within the established EMS system. These phases of care may reside in one or more of the multiple independent agencies that comprise the EMS system. The program has long enjoyed generous congressional support and has been progressively expanded over the years to embrace a wide variety of projects designed and selected through competition to enhance the efcacy of each of these six phases of emergency care, as delineated in Tables 1 and 2. Numerous professional organizations have also contributed to the development of EMSC. These efforts have led to the promulgation of national guidelines dening minimum standards of pediatric equipment and protocols for ambulances,

Organizing the Community for Pediatric Trauma Table 1 EMS System Components and EMSC System Phases EMS component Manpower Training Communications Transportation Facilities Critical care units Public safety agencies Consumer participation Access to care Patient transfer Coordinated patient record-keeping Public information and education Review and evaluation Disaster plan Mutual aid EMSC phase

11

Prevention System access Field treatment Emergency department treatment Inpatient treatment Rehabilitation

pediatric equipment and care for hospital emergency departments and trauma centers, and postgraduate training and continuing education requirements in pediatric emergency and trauma care (1320). Experiments with voluntary consensus standards for pediatric emergency and trauma care have also been successful in many locales, particularly southern Californias Emergency Departments Approved for Pediatrics (EDAP) program and New York Citys 911 Receiving Hospital System (21,22). The depth and breadth of resources now provided by regional and national EMSC programs are truly expansivean EMSC program now exists in virtually every state and territory. They provide both the foundation and the framework on which and within which to build a pediatric trauma system for every region with the United States.

THE PUBLIC HEALTH APPROACH TO PEDIATRIC TRAUMA Trauma is the leading cause of death and disability for Americans between 1 and 44 years of age (23). It kills and maims more children between 1 and 14 years of age than all other diseases combined (23). Yet despite these grim statistics, and the fact that the estimated cost to society of a single childhood injury death exceeds $300,000, trauma remains in 2005 the neglected disease of modern society as it was in 1966 when the National Academy of Sciences published its now famous white paper, Accidental Death and Disability: The Neglected Disease of Modern Society (24,25).
Table 2 Projects Supported by Federal EMSC Program EMSC National Resource Center (NRC) National EMSC Data Analysis and Resource Center (NEDARC) Partnership grants with all interested states and territories Partnership grants with stakeholder organizations in EMSC Targeted issues grants addressing specic issues in EMSC Research network grants supporting multicenter trials in EMSC

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Aficting as they do the youngest and ablest members of our society, it is self-evident that injury and trauma are the leading public health problem of our age. No doubt, much has changed over the last 30 to 40 years. In 1966, there were few trauma hospitals in America, trauma education of surgical residents was inconsistent at best, emergency medicine had yet to emerge as a distinct specialty in all but a few centers, pre-hospital care was rudimentary in most localities throughout the nation, fewif anystates had organized systems for trauma care, and injury fatalities were considered accidental events and accepted as inevitable occurrences of everyday life. In 2005, most regions have designated trauma facilities, all graduates of surgical residencies have specic education and experience in trauma care, emergency medicine is an established discipline in all but a few centers, pre-hospital care is both readily accessible and relatively sophisticated, most states have organized trauma care systems, and injuries are no longer considered accidents, but are viewed as predictable events that can be modied through the application of harm reduction strategies directed at the host, agent, and environment before, during, and after the traumatic event. Yet, despite these impressive advances in the structure and process of trauma care trauma remains the leading killer of our most productive citizens, and those who will soon become our most productive citizensour children. These facts have led the leadership of American trauma surgeryin partnership with the NHTSA EMS Division as well as the HRSA DTEMS, Injury Prevention Program, and EMS for Children Programto ask why, despite the obvious investment in trauma and EMS throughout the past generation, there remains such a gap between expectations and reality. The conclusion these experts have reached, neatly outlined in two recent documents produced by these two agencies, Trauma System Agenda for the Future, published in 2002, and Trauma Systems Planning and Evaluation: A Model Approach to a Major Public Health Problem, published in 2004, is startling in its simplicity, but imposing in its implications; it is thiswe have had the tools we need to solve this problem for nearly as long as it has been recognized, but we have failed to make use of them in a coherent and consistent manner (26,27). Specically, through lack of public education and the necessary appropriation of funds, we have failed to harness the resources required to mount a comprehensive injury control strategyone that links the expertise of our public health system in disease prevention and control with the expertise of our health care system in diagnosis and treatment. This problem is illustrated vividly in Figure 1, which depicts the disconnect between the primary and secondary prevention emphasis of the public health system and the tertiary prevention capabilities of the health care systembut in so doing, also suggests the obvious solution, namely, the formation of effective public-private partnerships in injury control between these two entities for the benet of the public. The fundamental concepts of public health are not new to trauma professionals. Indeed, the core elements of trauma system design enumerated in the Trauma System Agenda for the Future are fundamentally congruent with the 10 essential services provided by the public health system, as dened by the Public Health Functions Steering Committee of the United States Public Health Service in its 1994 report, Public Health in America, and reiterated in Trauma Systems Planning and Evaluation: A Model Approach to a Major Public Health Problem, and delineated in Table 3 (28). The three core functions of the public health system described by the IOM of the National Academy of Sciences in its 1988 and 2002 reports, The Future of Public Health and The Future of the Publics Health in the 21st Century, namely assessment, policy development, and assurance, which are the framework though which each of the 10 essential public health services are managed, are

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Figure 1 The Haddon Runyan cube of injury prevention and control. The current system maintains an articial separation between the three phases of injury control (top). The comprehensive public health approach integrates all phases of injury control into a single system (bottom).

strikingly reminiscent of the performance improvement processes well known to most health care professionals, as demonstrated in Table 4 (29,30a). Thus, there exists a natural afnity between public health professionals and trauma care professionals in their approach to problem solving. What remains is for regional leaders in public health and trauma care to form collaboratives that set goals and objectives for the public health system and the trauma care system within a given region with respect to injury control, which allow each component of these publicprivate partnerships to focus upon that which each does bestthe public health system

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Table 3 The 10 Essential Services of the Public Health System Are Fully Congruent with the Fundamental Components and Key Infrastructure Elements of the Trauma System Essential public health servicesa Monitor health Diagnose and investigate Inform, educate, and empower Mobilize community partnerships Develop policies Enforce laws Links to/provides care Assure competent workforce Evaluate Research System infrastructure
a

Trauma system components and elementsb Information management Information management Education and advocacy Education and advocacy Education and advocacy Injury prevention Pre-hospital care, acute care facilities, and posthospital care Professional resources Information management Research Leadership, information management, nances, and technology

Source: From Ref. 28. Source: From Ref. 26.

on regional data collection, processing, and analysis, as well as primary and secondary prevention efforts; the trauma care system on trauma patient care, including tertiary prevention efforts such as pre-hospital emergency care, in-hospital acute care, and posthospital and rehabilitative carewhile each keeps an eye on what the other is doing to ensure full coordination in regional injury control efforts, to the benet of both the public at large and patients as individuals. The benets of such collaboration are most obvious in primary and secondary injury prevention, but they can also accrue through tertiary prevention by improvements in EMS. For example, through a population-based study of the epidemiology of pediatric trauma care in 1992 that compared vital statistics and hospital discharge data abstracts from a single state for a single year, Cooper et al. reported that while total pediatric trauma and burn deaths occurred at a rate of 11.8/100,000 population, in-hospital pediatric trauma and burn deaths occurred at a rate of only 2.6/ 100,000 population (7). Since only 22% of trauma and burn deaths occurred after hospital admission, these authors concluded that only through effective injury prevention programs and improved EMS were pediatric injury deaths likely to decrease. Thus, to be effective, the childrens trauma surgeon must be prepared not only to operate upon the patient, but also to operate within the community, bringing the resources of the pediatric-capable trauma center to adjoining neighborhoods to keep them safe for children at play, and to neighboring EMS to ensure they
Table 4 The Three Core Functions of the Public Health System Are Fully Compatible with the Five Steps of Performance Improvement Core public health functionsa Assessment Policy development Assurance
a b

Steps in performance improvementb Plan, design, measure, and analyze Improve Cycle continues

Source: From Ref. 29. Source: From Joint Commission on Accreditation of Healthcare Organizations.

Organizing the Community for Pediatric Trauma

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have the knowledge, skills, and attitudes necessary, not only to treat pediatric injuries, but to prevent them. Effective injury prevention programs are community based and require extensive collaboration with civic leaders, governmental agencies, and neighborhood coalitions. Programs such as the Injury Free Coalition for Kids have been highly successful in creating substantial reductions in the burden of childhood injury in more than 40 communities throughout the nation (30b36). Such programs require ongoing collaboration between regional and area trauma centers and local public health entities, so the incidence of injury can be tracked by locality using population-based databases, and specic plans made can be to target injuries endemic to the community. They require major institutional commitment on the part of trauma systems and centers in prevention of injuries, including commitment of the necessary staff, equipment, and resources.

EVIDENCE IN SUPPORT OF SPECIALIZED HOSPITAL CARE FOR PEDIATRIC TRAUMA Improved outcomes from tertiary centers of pediatric intensive care were rst noted by Pollack et al. in 1991 in a statewide comparison of tertiary and non-tertiary facilities (37). To conduct this analysis, these authors compared illness-adjusted mortality rates in pediatric intensive care units in a single state using PRISM scores to calibrate risk. They found that illness-adjusted mortality rates were signicantly higher (odds ratios 1.1, 2.3, and 8 for mortality risk groups <5%, 530%, and >30%, respectively) among patients in non-tertiary facilities, mostly for patients with severe traumatic brain injury. Thus, they concluded that critically ill children were best cared for in tertiary care pediatric intensive care units. Differences in pediatric trauma care between pediatric and non-pediatric trauma centers were reviewed by Nakayama et al. in 1992 in a comparison of outcomes between pediatric and non-pediatric trauma centers from a single state using a statewide trauma registry (38). They found that the mortality was highest in rural non-pediatric trauma centers. (Using TRISS analysis), they also found that mortality was similar in urban pediatric and non-pediatric trauma centers, although the probability of survival was slightly, but not signicantly, higher for patients with moderately severe injuries in pediatric trauma centers. They concluded that children fared better in hospitals that made special provisions for the care of injured patients, especially for the care of injured children. The question of whether pediatric trauma center designation impacts favorably upon the care of injured children was addressed by Hall et al. in 1993 (39). They reviewed medical examiner records from a large urban metropolis for a ve year period. They documented clear improvement in outcome following designation of adult trauma centers, and further improvement upon designation of pediatric trauma centers. They concluded that pediatric trauma center designation saved many lives. The efcacy of pediatric trauma care was reafrmed in a population-based study by Cooper et al. in 1993 (40). They compared the frequency and mortality of pediatric trauma hospitalizations, based upon hospital discharge data abstracts from a single state in a single year, versus those reported to the National Pediatric Trauma Registry during a similar epoch. They found evidence both of triage of more seriously injured patients to pediatric trauma hospitals and an overall tenfold increase in survival in pediatric trauma centers for patients with moderately severe

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(ISS 1519) brain, visceral, and musculoskeletal injuries. They concluded that pediatric trauma center care was efcacious for those patients who need it the most, namely, those with injuries serious enough to carry a signicant mortality risk, yet not so serious as to pose a potentially insurmountable threat. The outcome of pediatric patients with blunt injuries was also found to be best at a pediatric trauma center by Hall et al. in 1996 (41). They reviewed the fatality rates of 1797 children admitted to pediatric trauma centers using TRISS analysis to stratify risk. While the Z-scores did not differ statistically between pediatric and adult trauma centers for penetrating injuries, the Z-score was signicantly better in pediatric trauma centers for blunt injuries. They also found a lower incidence of surgical intervention for liver and spleen injuries in pediatric trauma centers compared to adult trauma centers (4% vs. 3758% and 21% vs. 4353%, respectively). The inuence of a statewide trauma system on pediatric hospitalization and outcome was studied by Hulka et al. in 1997 (42). They compared the frequency and mortality of pediatric trauma hospitalizations, based upon hospital discharge data abstracts, from two adjacent states with similar geography and demographics, one with and one without a statewide trauma system. They found the risk-adjusted mortality rate to be signicantly lower in the state with the trauma system six months after its implementation. They concluded that triage to trauma centers saved many young lives. An evidence-based review of all pediatric trauma system research reported to date was also prepared by Hulka for the Academic Symposium to Evaluate Evidence Regarding the Efcacy of Trauma Systems held in Stevenson, Washington, in 1998, also known as the Skamania Conference, and published the following year (43). Hulka found that of the studies reviewed, only two population-based studies evaluated the impact of trauma centers or trauma systems on children. One found that a trauma center did not improve the injured childs risk of death, while the other found that a statewide trauma system improved the risk of death in seriously injured children, although a third population-based study found a lower risk of death if the child was treated in an urban trauma center. It was concluded that since only two published studies had evaluated the care of injured children treated at trauma centers versus non-trauma centers, and only one had examined the impact of a trauma system on pediatric outcome, further analysis was necessary to demonstrate that trauma systems make a difference in pediatric outcome, although all three studies had found that injured children had a reduced risk of death if treated at an urban trauma center (4042). The impact of pediatric trauma centers on mortality in a statewide system was extensively studied by Potoka et al. in 2000 (44). They performed a retrospective analysis of 13,351 children reported to a statewide trauma registry over a ve year period, stratifying patients by mechanism of injury, injury severity score, specic organ injury, and type of trauma center. They found that most injured children were being treated at pediatric trauma centers or adult trauma centers with added pediatric qualications, and that this improved survival rates. Moreover, the outcome for head, liver, and spleen injuries was better, while laparotomy and splenectomy rates were lower at pediatric trauma centers versus other types of centers. Improved functional outcome for severely injured children treated at pediatric trauma centers was also documented by Potoka et al. in 2001 (45). They performed a retrospective analysis of 14,284 children reported to the same statewide trauma registry over the same ve year period, stratifying patients both by type of trauma center and functional outcome. They found an overall trend toward better functional outcome at

Organizing the Community for Pediatric Trauma

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pediatric trauma centers versus adult trauma centers with added pediatric qualications and large adult trauma centers, but not versus small adult trauma centers to which pediatric patients were rarely triaged. Moreover, signicantly improved functional outcome was documented at discharge for head injured patients treated at pediatric trauma centers versus adult trauma centers with added pediatric qualications and large adult trauma centers, but, once again, not versus small adult trauma centers to which pediatric patients were rarely triaged. The question of whether pediatric trauma centers have better survival rates than adult trauma centers was also studied by Osler et al. in 2001 (46). They performed a retrospective analysis of the experience of trauma centers participating in the National Pediatric Trauma Registry over a 10-year period from 1985 to 1996, during which 53,113 cases were enrolled. While the overall mortality was lower at pediatric trauma centers versus adult trauma centers (1.8% vs. 3.9%), there was no difference in risk-adjusted mortality rate. Overall mortality was also lower at trauma centers veried by the American College of Surgeons Committee on Trauma as appropriate for pediatric trauma care. The severity and mortality associated with pediatric blunt injuries in hospitals with pediatric intensive care units versus other hospitals was also reviewed by Farrell et al. in 2004 (47). They compared these outcomes in 8180 seriously injured (ISS  8) pediatric patients (age  12) enrolled in a population-based statewide trauma registry. They found that injury severity of patients treated in hospitals with pediatric intensive care units and regional trauma centers without pediatric intensive care units was signicantly higher than at other hospitals, and that the risk-adjusted mortality rates were lower at hospitals with pediatric intensive care units than at other hospitals, except for non-trauma hospitals without pediatric intensive care units whose patients were considerably less severely injured. They concluded that there is signicant triaging of the most seriously injured pediatric blunt trauma patients to hospitals with pediatric intensive care units, and found evidence that this policy is effective. In summary, there now exists a substantial body of scientic evidence in support of the need for specialized pediatric trauma care. As with adult trauma care, such evidence has been difcult to obtain and substantiate, and has been limited by a number of confounding variables unique to pediatric patientsthe relative infrequency of major pediatric trauma (despite the fact that it remains the leading public health problem of childhood), the sharply lower mortality rate of major pediatric trauma (about one-third the rate of major adult trauma fatalities), and the lack of statistically valid, reliable, risk-adjusted, population-based models to predict outcome after major pediatric trauma. While we may infer that trauma systems and trauma centers that make special provisions for the needs of injured children are likely to achieve better outcomes than those that do not, we do not know who or what is specically responsible for this survival advantage. Although studies to date have lacked the statistical power to address these questions, the development and maintenance of a national trauma registry for children that is representative of the pediatric population as a whole will promote and permit the performance of such studies, and will allow further renement of existing systems of pediatric trauma care to better suit the needs of the United States injured children. The specic question of whether pediatric trauma patients can be optimally treated by adult trauma surgeons has been investigated by a number of authors. Knudson et al. and Fortune et al. in 1992, Rhodes et al. in 1993, Bensard et al. in 1994, and DAmelio et al. in 1995, in comparing, respectively, 353, 303, 1, 115,

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410, and 427 pediatric patients with the Multiple Trauma Outcome Study database regarding their demographics, mechanism of injury, Revised Trauma Score, surgical procedures, intensive care, Injury Severity Score (ISS), and outcome, found that their overall fatality rates, respectively, of 6%, 8.9% (mean ISS 15.6), 2.5% (mean ISS 11.1), 2%, and 4.2% (mean ISS 11.5) compared favorably with national standardswhile Partrick et al. in 2000 and Sherman et al. in 2001 found similar results with respect not only to mortality outcomes, but also to the management and outcomes of injuries to two specic body regions, the head and abdomen (4854). Taken together, these studies appear to demonstrate unequivocally that adult trauma surgeons can provide appropriate care for pediatric trauma patients. However, what is not mentioned in any of these reports is that all institutions involved in these studies had the benet of comprehensive pediatric inpatient facilities, including pediatric emergency care, pediatric intensive care, pediatric acute care, and perhaps most important, yet most frequently overlooked, pediatric nursing careindirectly supporting the notion that what is most critical in pediatric trauma care is proper emphasis on the special needs of pediatric patients throughout all phases of care, and validating the observation that when such provision is made, pediatric trauma patients can be expected to have optimal outcomes. In conclusion, the implications of these research ndings are clear. Trauma systems must assure that the special needs of pediatric patients are met throughout the entire continuum of trauma carefrom prevention, through access, ambulance care, emergency care, operative and intensive care, acute care, recovery, and rehabilitation. To ensure that these goals are met at the system level, regional trauma advisory committees should invite representatives from the pediatric trauma care community to participate in all their activities on a permanent basis, while to ensure they are met at the hospital level, all trauma center medical directors should assume personal responsibility to invite the participation of pediatric-capable trauma professionals to the care of the pediatric trauma patient. To this end, reliance on the latest editions of the American College of Surgeons Consultation for Trauma Systems and Resources for Optimal Care of the Injured Patient will ensure that the needs of injured children are met in the system and the hospital alike, the principles of which are described below with respect to the care of the pediatric trauma patient (17,55).

ELEMENTS OF CONTEMPORARY PEDIATRIC TRAUMA SYSTEM DESIGN Pediatric Trauma System The pediatric trauma system is part of the fully inclusive regional trauma system, each component of which is pediatric capable. The regional trauma center and, ideally, the regional pediatric trauma center are at the hub of the system. Area trauma centers may be needed in localities distant from the regional trauma center and must be capable of surgical management of pediatric trauma. All other hospitals in the region should participate as they are able but must at least be capable of initial resuscitation, stabilization, and transfer of pediatric trauma patients. Finally, there must be a regional trauma advisory committee that includes pediatric representation with the authority to develop and implement guidelines for triage of pediatric trauma patients within the system. The regional trauma system should also collaborate with the public health system in injury prevention and with local public health, public safety, and emergency management agencies in disaster planning.

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Pediatric Trauma Center The pediatric trauma center should be located in a trauma hospital with comprehensive pediatric services, such as a full-service general, university, or childrens hospital. This hospital must demonstrate an institutional commitment to pediatric trauma care, as evidenced by the provision of appropriate staff, equipment, and resources necessary to care for the most seriously injured pediatric trauma patients. Pediatric medical and surgical subspecialty services and units must be present and should include pediatric trauma surgery, pediatric emergency medicine, pediatric critical care, pediatric neurosurgery, pediatric orthopedics, and pediatric anesthesiology. Pediatric nursing and allied health professionals must also be present, and advanced life support training in trauma and pediatrics must be current for all staff who care for pediatric trauma patients. Finally, there must be an organized pediatric trauma service within the regional pediatric trauma center with separate medical leadership, nursing coordination, social services, and performance improvement. Regional pediatric trauma centers must also support education and research in pediatric trauma and provide leadership in pediatric trauma system coordination, including pediatric disaster management. EVIDENCE IN SUPPORT OF SPECIALIZED PRE-HOSPITAL CARE FOR PEDIATRIC TRAUMA Resuscitation There is scant literature on pre-hospital pediatric trauma resuscitation. Those studies that exist focus chiey on airway management, volume resuscitation, and cervical spine stabilization, and, collectively, suggest that less is more, that a scoop and run philosophy remains preferable to a stay and play approach for pediatric trauma patients, as is also true for adult trauma patientsespecially since pediatric resuscitation skills are infrequently used in pediatric trauma patients (56,57). Specically, it appears that none of the endotracheal intubation or medical antishock trousers or intravenous uid methods improves the survival of pediatric trauma patients, and that even under circumstances where volume resuscitation is utilized, the small volumes infused would be unlikely to have signicant physiologic benet. Furthermore, it appears that while cervical spine stabilization is critical for seriously head- and brain-injured patients, current methods are neither risk-free nor optimally designed to achieve proper neutral positioning in the majority of pediatric trauma patients. The effect of out-of-hospital pediatric endotracheal intubation on survival and neurological outcome was studied by Gausche et al. in 2000 (58). They conducted a prospective randomized trial of pre-hospital airway management (endotracheal intubation in 51% vs. bag and mask in 49%) in 830 consecutive pediatric patients less than 13 years of age. Mortality rates were similar between the two groups (26% vs. 31%, respectively), as was good neurological outcome (20% vs. 23%, respectively), including multiply injured and head-injured patients. However, while procedural complications were identical between the two groups (51% vs. 53%, respectively), scene times were longer for patients who were ventilated via tube rather than bag and mask (11 minutes vs. 9 minutes). In view of the relatively small numbers of head-injured patients in the above studythe very patients who might be expected to benet most from denitive airway controlpre-hospital endotracheal intubation for severe head injury in children was reviewed by Cooper et al. in 2001 (59). They performed a retrospective analysis

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of all 578 severe [Abbreviated Injury Scale (AIS) score  4] head injury patients reported to the National Pediatric Trauma Registry during its last ve years of operation who required pre-hospital airway management (endotracheal intubation in 83% vs. bag and mask in 17%). Once again, mortality rates were identical between the two groups (48% vs. 48%, respectively), intubated patients being older, more often transported by helicopter, and more often resuscitated with uid. As before, procedure or equipment failure or complications were identical between the two groupsas were functional outcomesbut injury complications occurred less often in intubated patients than in masked patients (58% vs. 71%, respectively), for reasons that could not be readily explained. The efcacy of medical antishock trouser (MAST) use in injured children who present in hypotensive shock was examined by the same group in 1992 (60). They reviewed the experience of the National Pediatric Trauma Registry over a four year period in 179 hypotensive (systolic blood pressure 80 mmHg) children (age 5 years), of whom 48 (27%) were treated with MAST. The MAST patients were somewhat older (12.6 years vs. 10.3 years) and more severely injured [Pediatric Trauma Score (PTS) 1.9 vs. 3.8, ISS 35.3 vs. 25.8] but were otherwise similar to controls. However, survival was dramatically lower in patients treated with MAST (25% vs. 48%), except among those with severe injuries (PTS  4, ISS  20) or who were severely hypotensive (systolic blood pressure 50 mmHg), who were neither helped nor hurt by their use, but whose injuries were of such great severity that survival was uncommon. The efcacy of pre-hospital volume resuscitation in injured children who present in hypotensive shock was also examined by this group in 1993 (61). They reviewed the experience of the National Pediatric Trauma Registry over a ve year period in 1727 hypotensive children (systolic blood pressure 80 mmHg < 5 years of age, systolic blood pressure 90 mmHg 5 years of age), of whom 386 (22%) were treated with intravenous uid in the eld. The uid patients were signicantly older (8.9 years vs. 3.7 years) and more severely injured (PTS 4.1 vs. 7.3, ISS 25.5 vs. 10.0), more severely head injured [Glasgow Coma Scale (GCS) 8 vs. 10], more hypotensive (systolic blood pressure 62 vs. 79), and more often victims of motor vehicle crashes and gunshot wounds but less often victims of falls. Once again, survival was signicantly lower in patients treated with uid (52% vs. 89%), a nding that was independent of age, injury severity, and systolic blood pressure, except among patients with severe injuries (ISS  20) or profound hypotension (systolic blood pressure 50 mmHg), most of whom died. The efcacy of intraosseous uid infusion either in the eld or in the emergency department in injured children who present in hypotensive shock was also examined by the group in 1993 (62). They reviewed the experience of the National Pediatric Trauma Registry over a ve year period in 405 hypotensive (systolic blood pressure 80 mmHg) children (age < 5 years), of whom 33 (8%) were treated with intraosseous uid. The intraosseous patients were far more severely injured (PTS 0.1 vs. 5.6, ISS 33.0 vs. 15.5), far more severely head injured (GCS 4 vs. 11), far more hypotensive (systolic blood pressure 29.0 vs. 67.0), but were similar in age and sex. As expected, survival was dramatically lower in patients treated with uid versus unmatched controls (12% vs. 80%), but was also signicantly lower in patients treated with uid versus controls matched by severity of injury (PTS 10% vs. 38%, ISS 7% vs. 29%) and degree of hypotension (systolic blood pressure <50 mmHg 0% vs. 18%, systolic blood pressure 50 mmHg 33% vs. 87%). The effectiveness of pre-hospital uid therapy in pediatric trauma patients was also reviewed by Teach et al. in 1995 (63). They reviewed the ambulance trip and

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emergency department records of 50 pediatric patients less than 18 years of age (average age 9.6 years) who received intravenous uid in the pre-hospital setting. They found that the combined total pre-hospital time (scene time plus transport time) did not differ whether the intravenous catheter was placed at the scene or in the ambulance (25.6 minutes vs. 25.5 minutes, respectively), while the average prehospital infusion volume was only 4.4 mL/kg (range 017 mL/kg), or less than 25% of the dose prescribed in regional advanced life support protocols. They also determined that of the 50 patients reviewed, the intervention was possibly benecial in two, possibly detrimental and one, and inconsequential in the remainder. Emergency transport and positioning of young children who have an injury of the cervical spine was investigated by Herzenberg et al. in 1989 (66). They found that in ten children less than seven years old, an unstable injury of the cervical spine had anterior angulation or translation, or both, on initial lateral radiographs that were made with the child supine on a standard backboard. Supine and lateral radiographs of 72 children who did not have a fracture also demonstrated more relative cervical kyphosis in younger children when they were in the supine position. They concluded that to prevent undesirable cervical exion in young children during emergency transport and radiography, a standard backboard should be modied to provide safer alignment of the cervical spine, either through use of a recess for the occiput or of a double mattress pad to raise the head. The respiratory effects of spinal immobilization in children were studied by Schafermeyer et al. in 1991 (67). They performed a prospective study of the restrictive effects of two spinal immobilization strapping techniques on the respiratory capacity of 51 normal, healthy children (age 615 years) by measuring forced vital capacity in the standing, supine, and fully immobilized positions. They found a 20% (range 459%) reduction in forced vital capacity, regardless of strapping technique. They concluded that spinal immobilization signicantly reduced respiratory capacity in children. Neutral cervical spine positioning was further researched by Nypaver et al. in 1994 (68). They measured the height of back elevation required to place the cervical spine in a neutral position in a convenience sample of children less than eight years old. They found that all children required elevation of the back for correct neutral position (mean height 25.5 mm, range 541 mm). They further concluded that children less than four years old required more elevation than older children (27 mm vs. 22 mm). Achieving neutral position with pediatric cervical spine immobilization was also examined by Curran et al. in 1995 (69). They conducted a prospective evaluation of current spine immobilization devices in achieving radiographic neutral positioning of the cervical spine in 118 pediatric trauma patients by obtaining lateral cervical spine radiographs while these patients remained fully immobilized. They found that 60% of patients had excessive kyphosis or lordosis, 50% were in excessive exion, and that no single device or technique (collar, backboard, towels and collar, and backboard and blocks were most frequently used) appeared to provide superior protection from angulation. Unfortunately, no single method or combination of methods consistently achieved a neutral position. The question of whether pre-hospital cervical spine immobilization can be safely avoided in pediatric patients with minor injuries has not been answered. Attempts were made by Jaffe et al. and Rachesky et al. in 1987 to develop clinical prediction rules that would reliably determine which of these patients had sufciently low risk of cervical spine injury to justify omission of cervical spine stabilization in the pre-hospital setting, but neither was sufciently accurate (68,69). However, the

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National Emergency X-Radiography Utilization Study (NEXUS) criteria for clinical prediction of cervical spine injury established by Hoffman et al. in 2000 were applied to pediatric trauma patients by Viccellio et al. in 2001 and appeared to perform well, with 100% sensitivity and negative predictive value (95% condence intervals of 87.8100% and 99.4100.0%, respectively) (70,71). However, the authors urged caution in applying the results due to the small size of the studylikely a wise recommendation in view of the known risks of spinal cord injury without radiographic abnormality (SCIWORA) and atlantoaxial instability, especially in patients with Downs syndrome (72,73). Triage Pediatric pre-hospital trauma triage criteria are based upon the American College of Surgeons Field Trauma Triage Decision Scheme, which includes anatomic, physiologic, mechanistic, and comorbid criteria, including age less than ve. The Pediatric Trauma Score was also developed as a eld triage tool and correlates closely with the Injury Severity Score as a predictor of mortality (74). However, the Revised Trauma Score performs nearly as well as the Pediatric Trauma Scoredespite the fact that it is based upon adult vital signspresumably because abnormalities in respiratory rate and Glasgow Coma Scale Score tend to correlate in seriously injured pediatric patients, most of whom have serious traumatic brain injury, thereby giving double weight to those components of the score most likely to be abnormal following head injury (75). Yet, both scores require calculation in the busy pre-hospital setting, calling for simpler tools requiring no added calculations that would minimize both undesirable over-triage and unacceptable under-triage. To assess patterns of pediatric trauma triage and patient transfer to regional pediatric trauma centers and proximate adult trauma centers based upon use of the anatomic, physiologic, and mechanistic criteria delineated in the American College of Surgeons Field Triage Decision Scheme, a review of 1307 pediatric trauma cases was conducted by Jubelirer et al. in 1990 (78). The study was performed in eight level-II trauma centers surrounding a major metropolitan statistical area that contained two regional pediatric trauma centers. They found that while 43 patients were transferred to the regional pediatric trauma centers based on local criteria, the remaining 1264 patients were treated in the level-II trauma centers, with outcomes that compared favorably to those in other published reports. They concluded that patients with moderate but not severe injuries (PTS > 8) could be successfully managed by level-II trauma centersalthough the observed mortality rate of 1.8% suggests that at least some patients who died, all of who clearly had serious injuries (PTS  8), might have fared better if pediatric trauma triage criteria had led them to a pediatric trauma center. The need for pediatric-specic triage criteria was reinforced following publication of the results of a statewide trauma triage study by Phillips et al. in 1996 (79). They performed a retrospective analysis of state trauma registry data and state hospital discharge data in a nine county region to determine if use of the state trauma triage scorecard based upon the American College of Surgeons Field Triage Decision Scheme resulted in appropriate categorization as major or minor trauma, according to standardized protocols developed by an expert medical panel. They found that of the 1505 pediatric cases available for analysis, which accounted for 9.2% of the total study population, 6.0% of all hospitalized cases, and 6.8% of all trauma deaths, there was a 15.2% over-triage rate and a 33.3% under-triage rate, well above the 5% target

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rates for acceptable over-triage and under-triage. They concluded that new pediatric triage instruments were needed to avoid unacceptable under-triage. To this end, a better alternative for predicting inpatient mortality for pediatric trauma patients with blunt injuries was reported by Hannan et al. in 2000 (78). They performed a retrospective review of 2923 seriously injured (ISS  8) pediatric patients (age  12 years) reported to a single states trauma registry over a two year period. They tested all variables from the Pediatric Trauma Score and the Revised Trauma Score, as well as the individual components of the GCS score, the AVPU Score, ISS, ICISS, and age specic systolic blood pressure, nding that the only signicant independent predictors of mortality were ICISS, a Best Motor Response of one from the Glasgow Coma Scale Score, and the Unresponsive category from the AVPU Scorethe latter two being readily available to pre-hospital personnel. Moreover, the sensitivity and specicity of both measures exceeded 90%. Pre-hospital triage in the injured pediatric patient was also studied by Engum et al. in 2000 (81). They performed a prospective analysis of 1295 pediatric trauma patients versus 1326 adult trauma patients who died in the emergency department, underwent operation, or were admitted to the intensive care unit, as indicators of the need for specialized trauma care. They found that the most accurate criteria for prediction of major injury were systolic blood pressure 90 mmHg, burn 15% of total body surface area, Glasgow Coma Scale Score 12, respiratory rate 29 breaths per minute, and paralysis, while less accurate criteria for major injury were fall >20 feet, penetrating trauma, vehicle ejection, paramedic judgment, vehicle rollover, and need for vehicle extrication. Using these criteria, they found an over-triage rate of 71% but an under-triage rate of 0%, with the Revised Trauma Score and Pediatric Trauma Score missing 30% and 45% of major trauma patients, respectively. The specic question of whether specialized tools for pediatric trauma team activation and for pediatric helicopter triage could improve pediatric trauma staff utilization and pediatric trauma survival rates, without excessive over-triage rates, has also been investigated. Sola et al. in 1994, in a study of 952 children treated at a regional pediatric trauma center over a one-year period, found that pediatric trauma triage criteria had a sensitivity of 86% in predicting which trauma patients would require either an operation or pediatric intensive care, while maintaining a specicity of 98% (82). Moront et al. in 1996, in a study of 3861 injured children treated at a regional pediatric trauma center over a four-year period, found that helicopter transport was associated with better survival rates than ground transport, and that pediatric helicopter triage criteria based on Glasgow Coma Scale Score and heart rate improved helicopter resource utilization without compromising care, although substantial over-triage rates were observed (83). However, Kotch and Burgess in 2002, in a study of 969 patients transported to a regional trauma center by helicopter over a ve-year period, of whom 143 patients were children, found no differences in triage scores, injury severities, or survival probabilities in children versus adults, although pediatric lengths of stay were slightly shorter (84).

ELEMENTS OF CONTEMPORARY PEDIATRIC PRE-HOSPITAL TRAUMA CARE Pediatric trauma resuscitation should begin as soon as possible after the injury occurs, ideally through pediatric-capable emergency medical dispatchers who provide pre-arrival instructions to lay rescuers at the scene. It continues upon the arrival

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of pre-hospital professionals, including rst responders, emergency medical technicians, and paramedics. Pre-hospital treatment protocols utilized by these emergency medical personnel should be conservative yet permissive, emphasizing basic life support modalities such as supplemental oxygen and assisted ventilation via bag and mask, only providing advanced life support interventions such as endotracheal intubation and volume resuscitation when appropriate (83). The emphasis in pediatric pre-hospital trauma care is on aggressive support of vital functions during what has been called the platinum half hour of early pediatric trauma care (J. A. Haller, personal communication, December 1, 2003). Pediatric trauma protocols utilized by emergency medical personnel begin with an analysis of scene safetyincluding a survey for hazardous materialsand, if the scene is safe, continue with formation of a general impression of the urgency of the patients condition, utilizing the Pediatric Assessment Triangle to obtain a rapid evaluation of the patients appearance, work of breathing, and circulation to skin. Pre-hospital trauma professionals next proceed to the primary survey, or initial assessment, of the airway, breathing, circulation, and disabilities, with an emphasis on detection and management of neuroventilatory rather than hemodynamic abnormalities, the former being some ve times more common in pediatric trauma patients than the latter. The secondary survey, or focused history and detailed physical examination, is performed nextbut is omitted entirely, or performed en route, if the patient is less than fully stable. Because of the need for specialized pediatric trauma care, injured children should be transported to the nearest pediatric-capable trauma center, keeping the child warm. Pre-hospital professionals are our pre-hospital pediatric trauma surgeons and must be fully trained in all aspects of pre-hospital pediatric trauma resuscitation if they are to be effective in this role. First responders currently receive 40 to 50 hours of training in oxygen administration, use of airway adjuncts, assisted ventilation via bag and mask, bleeding control, splinting, and immobilization, only six of which hours are in pediatric care (84). Emergency medical technicians currently receive 110 to 120 hours of training, including all of the above plus additional training in lifts, carries, and ambulance transport, only 10 of which hours are in pediatric care (85). Paramedics currently receive 1000 to 1200 hours of training, including all of the above plus additional training in endotracheal intubation, needle cricothyroidotomy, needle decompression of probable tension pneumothorax, and intravenous and intraosseous access for volume resuscitation, only 20 of which hours are in pediatrics (86). Pre-hospital professionals are taught utilizing National Standard Curricula developed for each level of practice, which in the future will be periodically revised on a ve- to seven-years cycle, based upon National EMS Education Standards, consistent with the EMS Education Agenda for the Future (87). An andragogical versus a pedagogical approach is taken to teaching, based upon modern principles of adult education, and the need to know versus what might be nice to know. The curricula are, for the most part, assessment-based rather than diagnosisbased, and thereby focus on presenting problems rather than underlying illnesses and injuries. Pediatric educational modules follow upon adult educational modules, to allow the limited pediatric curricular hours to be used most efciently, and should be regularly and generously supplemented by up-to-date continuing trauma education programs such as the Pre-hospital Trauma Life Support (PHTLS) course of the National Association of Emergency Medical Technicians and the American College of Surgeons, as well as up-to-date continuing pediatric education programs

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such as the Pediatric Emergencies for Pre-hospital Professionals (PEPP) course of the American Academy of Pediatrics, and the Pediatric Pre-hospital Care (PPC) course of the National Association of Emergency Medical Technicians (8890). Pediatric equipment is mandatory for the successful resuscitation of critically injured children in the pre-hospital setting. Minimum standards for pediatric equipment in ambulances at both the basic life support and advanced life support levels have been published by the National EMS for Children Resource Alliance Committee on Ambulance Equipment and Supplies, which were recently updated, and are summarized in Table 5 (13). Although medications required by children differ little from those needed by adults, drug dosages, for the most part, are determined on the basis of size. The use of color-coded tapes that key drug doses and equipment selection to body length has proved effective in the eld and is now standard equipment in most agencies (91). Pediatric interfacility transport is a key component of pediatric trauma care, and many pediatric comprehensive care centers have established specialized teams for interfacility transport of critically ill and injured patients for this purpose. However, pediatric interfacility transport is not risk-free, as adverse events such as plugged endotracheal tubes and loss of vascular access occur at nearly twice the rate during interfacility transport as in the pediatric intensive care unit, and 10 times

Table 5 Minimum Standards for Pediatric Equipment in Ambulances Minimum standards for pediatric equipment in Basic Life Support ambulances Pediatric stethoscope, infant/child attachments Pediatric blood pressure cuffs, infant/child sizes Disposable humidier(s) Pediatric simple/non-rebreathing oxygen masks, all sizes Pediatric face masks, all sizes Pediatric bag-valve devices, infant/child sizes Pediatric airway adjuncts, all sizes Pediatric suction catheters, all sizes Pediatric Yankauer device Pediatric extrication collars, all sizes Pediatric extrication equipment (including infant car seat) Pediatric limb splints, all sizes Minimum standards for pediatric equipment in Advanced Life Support ambulances All of the above, plus . . . Pediatric endotracheal tubes, all sizes Pediatric stylets, all sizes Pediatric laryngoscope blades, all sizes Pediatric Magill (Rovenstein) forceps Pediatric intravenous catheters, all sizes Pediatric intraosseous needles, all sizes Pediatric nasograstric tubes, all sizes Pediatric electriocardiogram electrodes Pediatric debrillator paddles, infant/child sizes Pediatric dosage-packed medications/uids Pediatric dosage/volume wall chart Mini-drip intravenous infusion sets

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more frequently with non-specialized teams than with specialized teams (92,93). At a minimum, transport providers must be capable of critical pediatric assessment and monitoring, and must be highly skilled in the techniques of pediatric endotracheal intubation and vascular access, as well as uid and drug administration in critically ill and injured children (94,95). Whenever possible, interfacility transport of such patients should be conducted by specialized pediatric transport teams staffed by physicians and nurses with special training in pediatric critical care treatment and transport (96,97). Pediatric ambulance patient transport involves both a different purpose and a different environment than pediatric automobile passenger transport. The ambulance patient compartment is open and large, contains numerous heavy pieces of equipment, and carries restrained patients and passengers and unrestrained providers in a wide variety of places and positions. However, in contrast to automobile passenger safety, formal standards are not yet developed regarding ambulance occupant protection. This unfortunate situation persists despite the documented lethal hazards of ambulance crashes, which are 10 times more common per passenger mile than automobile crashes (98). Pediatric ambulance patient transport, though inherently unsafe, can be made less hazardous through the use of safe driving practices and effective restraint of patients, passengers, providers, and equipment. Unfortunately, many commercially available restraint devices are ineffective but are not known to be so because they have been subjected only to static testing at the laboratory bench rather than dynamic testing in a moving ambulance (99). Fortunately, recent evidence suggests that safe restraint of a child occupant can be achieved through the use of a child safety seat when secured to the ambulance stretcher using two standard ambulance gurney belts (100). Yet, the most important step in ensuring safe transport of ill or injured pediatric patients is to ensure that all personnel, most especially ambulance drivers, regularly follow the Dos and Donts recently issued by the NHTSA and the EMS for Children Program, as shown in Table 6 (101).

Table 6 The Dos and Donts of Transporting Children in an Ambulance Dos Do drive cautiously at safe speeds observing trafc laws Do tightly secure all monitoring devices and other equipment Do ensure available restraint systems are used by EMTs and other occupants, including the patient Do transport children who are not patients, properly restrained, in an alternate passenger vehicle, whenever possible Do encourage utilization of the DOT NHTSA emergency vehicle operator course (EVOC), national standard curriculum Donts Do not drive at unsafe high speeds with rapid acceleration, decelerations, and turns Do not leave monitoring devices and other equipment unsecured in moving EMS vehicles Do not allow parents, caregivers, EMTs or other passengers to be unrestrained during transport Do not have the child/infant held in the parents, caregivers, or EMTs arms or lap during transport Do not allow emergency vehicles to be operated by persons who have not completed the DOT EVOC or equivalent

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SUMMARY Organizing the community for pediatric trauma requires not only specialized knowledge of the evaluation and management of childhood injury, including pediatric injury prevention and EMS for children, but also unwavering commitment to ensure that the specialized needs of injured children are met at every level of system organization. Mature understanding of the trauma system as a public good, and practiced application of the interpersonal and organizational skills necessary to lead and manage complex undertakings, are also mandatory for the trauma professional who seeks to inuence the provision of care in a given region. While the principles of pediatric trauma and EMS system design may be simple, they are not always easy to implement without a clear understanding that pediatric trauma care is a truly collaborative venture that requires the coordination of numerous professionals and services from many different disciplines and agencies, all of which have a stake in the care of the injured child. Yet, the benet to the community that chooses to organize itself for pediatric trauma care is self-evident, evenperhaps especiallyto those with whom the system itself may not interact or interface on a regular basis. For example, civic and business leaders have a major stake in the development and support of the community pediatric trauma system. Childhood injuries cost time and money, not only from the involved families, but from their employers and their insurance companies as well. There is ample ground to make common cause with such community partners, for whom the well-being of children is clearly no less important than to public health and trauma care professionals. Indeed, it is the one health care benet on which all agreethe need for systems and services that keep children healthy. REFERENCES
1. Haller JA, Shorter N, Miller D, et al. Organization and function of a regional pediatric trauma center: does a system of management improve outcome? J Trauma 1983; 23:691696. 2. Foltin GL, Cooper A. Medical operations: pediatric. In: Kuehl AE, ed. Pre-hospital Systems and Medical Oversight, 3rd ed. Dubuque: Kendall/Hunt Publishing Company, 2002:539555. 3. Harris BH, Barlow BA, Ballantine TV, et al. American Pediatric Surgical Association: principles of pediatric trauma care. J Pediatr Surg 1992; 27:423426. 4. Cooper A, Barlow B. The surgeon and EMSC. Pediatrics 1995; 96:184188. 5. Boyd DR. The history of emergency medical services (EMS) systems in the United States of America. In: Boyd DR, Edlich RF, Micik S, eds. Systems Approach to Emergency Medical Care. Norwalk: Appleton and Company, 1983:182. 6. Tsai A, Kallsen G. Epidemiology of pediatric pre-hospital care. Ann Emerg Med 1987; 16:284292. 7. Cooper A, Barlow B, Davidson L, et al. Epidemiology of pediatric trauma: importance of population-based statistics. J Pediatr Surg 1992; 27:149154. 8. Ludwig S, Fleisher G, Henretig F, et al. Pediatric training in emergency medicine residency programs. Ann Emerg Med 1982; 11:170173. 9. Seidel JS, Hornbein M, Yoshiyama K, et al. Emergency medical services and the pediatric patient: are the needs being met? Pediatrics 1984; 73:769772. 10. Seidel JS. Emergency medical services and the pediatric patient: are the needs being met? II. Training and equipping emergency medical services providers for pediatric emergencies. Pediatrics 1986; 78:808812.

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11. Committee on Pediatric Emergency Medical Services, Institute of Medicine, National Academy of Sciences. In: Durch JS, Lohr KN, eds. Emergency Medical Services for Children. Washington: National Academy Press, 1993. 12. Emergency Medical Services for Children National Resource Center. Emergency Medical Service for Children Five-Year Plan. Washington: Emergency Medical Services for Children National Resource Center, 1998. 13. Committee on Ambulance Equipment and Supplies, National Emergency Medical Services for Children Resource Alliance. Guidelines for pediatric equipment and supplies for basic life support and advanced life support ambulances. Ann Emerg Med 1996; 28:699701. 14. Mulligan-Smith D, OConnor RE, Markenson D. EMSC Partnership for Children: National Association of EMS Physicians Model Pediatric Protocols. Prehosp Emerg Care 2000; 4:111130. 15. Committee on Emergency Department Equipment and Supplies, National Emergency Medical Service for Children Resource Alliance. Guidelines for pediatric equipment and supplies for emergency departments. Ann Emerg Med 1998; 31:5457. 16. Committee on Pediatric Emergency Medicine, American Academy of Pediatrics and Pediatric Committee, American College of Emergency Physicians. Care of children in the emergency department: guidelines for preparedness. Pediatrics 2001; 107:777781. 17. Anonymous. Pediatric trauma. In: Committee on Trauma, American College of Surgeons: Resources for Optimal Care of the Injured Patient: 1999. Chicago: American College of Surgeons, 1999. 18. Anonymous. Pediatric trauma. In: Committee on Trauma, American College of Surgeons: Advanced Trauma Life Support Student Manual 1997 Edition. Chicago: American College of Surgeons, 1997:289312. 19. Anonymous. Trauma resuscitation and spinal immobilization. In: Hazinski MF, Zaritsky AL, Nadkarni VM, et al., eds. Providers Manual of Pediatric Advanced Life Support. Dallas: American Heart Association, 2002:253286. 20. Tepas JJ, Fallat ME, Moriarty TM. Trauma. In: Gausche-Hill M, Fuchs S, Yamamoto L, eds. Advanced Pediatric Life Support: The Pediatric Emergency Medicine Resource, 4th ed. Sudbury: Jones and Bartlett Publishers, 2003:268323. 21. Seidel JS. EMS-C in urban and rural areas: the California experience. In: Haller JA, ed. Emergency Medical Services for Children: Report of the Ninety-Seventh Ross Conference on Pediatric Research. Columbus: Ross Laboratories, 1989:2230. 22. New York City 911 Receiving Hospital Advisory Committee. New York City 911 Receiving Hospital Emergency Department Standards, 5th ed (revised). New York: New York City Emergency Medical Service, 1989. 23. National Center for Health Statistics, 2000. 24. Rice DP, MacKenzie EJ, et al. Cost of Injury in the United States: A Report to Congress. Atlanta: Centers for Disease Control, 1989:59. 25. Committee on Trauma and Committee on Shock, Division of Medical Sciences, National Research Council, National Academy of Sciences. Accidental Death and Disability: The Neglected Disease of Modern Society. Washington: National Academy of Sciences, 1966. 26. National Highway Trafc Safety Administration. Trauma System Agenda for the Future. Washington: National Highway Trafc Safety Administration, 2002. 27. Cooper G, Dawson D, Kaufmann C, et al. Trauma Systems Planning and Evaluation: A Model Approach to a Major Public Health Problem. Rockville: Health Resources and Services Administration, 2004. 28. Public Health Functions Steering Committee, United States Public Health Service. Public Health in America. Rockville: United States Public Health Service, 1994. 29. Committee for the Study of the Future of Public Health, Institute of Medicine, National Academy of Sciences. The Future of Public Health. Washington: National Academy Press, 1988.

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30a. Committee on Assuring the Health of the Public in the 21st Century, Institute of Medicine, National Academy of Sciences. The Future of the Publics Health in the 21st Century. Washington: National Academy Press, 1988. 30b. [Link]. 31. Davidson LL, Durkin MS, Kuhn L, et al. The impact of the safe kids/health neighborhoods injury prevention program in Harlem 1988 to 1991. Am J Public Health 1994; 84:580596, 1992. 32. Laraque D, Barlow B, Davidson L, et al. Central Harlem playground injury project: a model for change. Am J Public Health 1994; 84:16911692. 33. Laraque D, Barlow B, Durkin M, et al. Injury prevention in an urban setting: challenges and successes. Bull NY Acad Med 1995; 72:1630. 34. Durkin M, Kuhn L, Davidson L, et al. Epidemiology and prevention of severe assault and gun injuries to children in an urban community. J Trauma 1996; 41: 667673. 35. Durkin M, Olsen S, Barlow B, et al. The epidemiology of urban pediatric neurological trauma: evaluation of, and implications for, injury prevention programs. Neurosurgery 1998; 42:300310. 36. Durkin M, Laraque D, Lubman I, et al. Epidemiology and prevention of trafc injuries to urban children and adolescents. Pediatrics 1999; 103:e74. 37. Pollack MM, Alexander SR, Clarke N, et al. Improved outcomes from tertiary center pediatric intensive care: a statewide comparison of tertiary and nontertiary care facilities. Crit Care Med 1991; 19:150159. 38. Nakayama DK, Copes WS, Sacco WJ. Differences in pediatric trauma care among pediatric and nonpediatric centers. J Pediatr Surg 1992; 27:427431. 39. Hall JR, Reyes HM, Meller JL, et al. Traumatic death in urban children, revisited. Am J Dis Child 1993; 147: 102107. 40. Cooper A, Barlow B, DiScala C, et al. Efcacy of pediatric trauma care: results of a population-based study. J Pediatr Surg 1993; 28:299305. 41. Hall JR, Reyes HM, Meller JT, et al. Outcome for blunt trauma is best at a pediatric trauma center. J Pediatr Surg 1996; 31:7277. 42. Hulka F, Mullins RJ, Mann NC, et al. Inuence of a statewide trauma system on pediatric hospitalization and outcome. J Trauma 1997; 42:514519. 43. Hulka F. Pediatric trauma systems: critical distinctions. J Trauma 1999; 47:S85S87. 44. Potoka DA, Schall LC, Gardner MJ, et al. Impact of pediatric trauma centers on mortality in a statewide system. J Trauma 2000; 49:237245. 45. Potoka DA, Schall LC, Ford HR. Improved functional outcome for severely injured children treated at pediatric trauma centers. J Trauma 2001; 51:824834. 46. Osler TM, Vane DW, Tepas JJ, et al. Do pediatric trauma centers have better survival rates than adult trauma centers? An examination of the National Pediatric Trauma Registry. J Trauma 2001; 50:96101. 47. Farrell LS, Hannan EL, Cooper A. Severity of injury and mortality associated with pediatric blunt injuries: hospitals with pediatric intensive care units vs. other hospitals. Pediatr Crit Care Med. In press. 48. Knudson MM, Shagoury C, Lewis FR. Can adult trauma surgeons care for injured children? J Trauma 1992; 32:729739. 49. Fortune JM, Sanchez J, Graca L, et al. A pediatric trauma center without a pediatric surgeon: a four-year outcome analysis. J Trauma 1992; 33:130139. 50. Rhodes M, Smith S, Boorse D. Pediatric trauma patients in an adult trauma center. J Trauma 1993; 35:384393. 51. Bensard DD, McIntyre RC, Moore EE, et al. A critical analysis of acutely injured children managed in an adult level I trauma center. J Pediatr Surg 1994; 29:1118. 52. DAmelio LF, Hammond JS, Thomasseau J, et al. Adult trauma surgeons with pediatric commitment: a logical solution to the pediatric trauma manpower problem. Am Surg 1995; 61:968974.

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53. Partrick DA, Moore EE, Bensard DD, et al. Operative management of injured children at an adult level I trauma center. J Trauma 2000; 48:894901. 54. Sherman HF, Landry VL, Jones LM. Should level I trauma centers be rated NC-17? J Trauma 2001; 50:784791. 55. American College of Surgeons Committee on Trauma. Consultation for Trauma Systems. Chicago: American College of Surgeons, 1996. 56. Su E, Mann NC, McCall M, et al. Use of resuscitation skills by paramedics caring for critically injured children in Oregon. Prehosp Emerg Care 1997; 1:123127. 57. Paul TR, Marias M, Pons PT, et al. Adult versus pediatric prehospital trauma care: is there a difference? J Trauma 1999; 47:455459. 58. Gausche M, Lewis RJ, Stratton SJ, et al. Effect of out-of-hospital pediatric endotracheal intubation on survival and neurological outcome: a controlled clinical trial. JAMA 2000; 283:783790. 59. Cooper A, DiScala C, Foltin G, et al. Prehospital endotracheal intubation for severe head injury in children: a reappraisal. Sem Pediatr Surg 2001; 10:36. 60. Cooper A, Barlow B, DiScala C, et al. Efcacy of MAST use in children who present in hypotensive shock. J Trauma 1992; 33:151. 61. Cooper A, Barlow B, DiScala C, et al. Efcacy of pre-hospital volume resuscitation in children who present in hypotensive shock. J Trauma 1993; 35:160. 62. Cooper A, Barlow B, DiScala C, et al. Efcacy of intraosseous infusions in infants and young children who present in hypotensive shock following major trauma. Presented at the Annual Meeting of the Surgical Section of the American Academy of Pediatrics, Washington, DC, October 1993. 63. Teach SJ, Antosia RE, Lund DP, et al. Prehospital uid therapy in pediatric trauma patients. Pediatr Emerg Care 1995; 11:58. 64. Herzenberg JE, Hensinger RN, Dedrick DK, et al. Emergency transport and positioning of young children who have an injury of the cervical spine. J Bone Joint Surg 1989; 71-A:1522. 65. Schafermeyer RW, Ribbeck BM, Gaskins J, et al. Respiratory effects of spinal immobilization in children. Ann Emerg Med 1991; 20:10171019. 66. Nypaver M, Treolar D. Neutral spine positioning in children. Ann Emerg Med 1994; 23:208211. 67. Curran C, Dietrich AM, Bowman MJ, et al. Pediatric cervical-spine immobilization: achieving neutral position? J Trauma 1995; 39:729732. 68. Jaffe DM, Binns H, Radkowski MA, et al. Developing a clinical algorithm for early management of cervical spine injury in child trauma victims. Ann Emerg Med 1987; 16:270276. 69. Rachesky I, Boyce WT, Duncan B, et al. Clinical prediction of cervical spine injuries in children: radiographic abnormalities. AJDC 1987; 141:199201. 70. Hoffman JR, Mower WR, Wolfson AB, et al. Validity of a set of clinical criteria to rule out injury to the cervical spine in patients with blunt trauma. N Engl J Med 2000; 343:9499. 71. Viccellio P, Simon H, Pressman BD, et al. A prospective multicenter study of cervical spine injury in children. Pediatrics 2001; 108:e20. 72. Pang D, Pollack IF. Spinal cord injury without radiographic abnormality in children the SCIWORA syndrome. J Trauma 1989; 29:654664. 73. Frost M, Huffer WE, Sze CI, et al. Cervical spine abnormalities in Down syndrome. Clin Neuropath 1999; 18:250259. 74. Tepas JJ, Mollitt DL, Talbert JL, et al. The pediatric trauma score as a predictor of injury severity in the injured child. J Pediatr Surg 1987; 22:1418. 75. Kaufmann CR, Maier RM, Rivara FP, et al. Evaluation of the pediatric trauma score. JAMA 1990; 263:6972. 76. Jubelirer RA, Agarwal NN, Beyer FC, et al. Pediatric trauma triage: review of 1,307 cases. J Trauma 1990; 30:15441547.

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77. Phillips S, Rond PC, Kelly SM, et al. The need for pediatric-specic triage criteria: results from the Florida Trauma Triage Study. Pediatr Emerg Care 1996; 12: 394399. 78. Hannan E, Farrell L, Meaker P, et al. Predicting inpatient mortality for pediatric blunt trauma patients: a better alternative. J Pediatr Surg 2000; 35:155159. 79. Engum SA, Mitchell MK, Scherer LR, et al. Prehospital triage in the injured pediatric patient. J Pediatr Surg 2000; 35:8287. 80. Sola JE, Scherer LR, Haller JA, et al. Criteria for safe cost-effective trauma triage: prehospital evaluation and distribution of injured children. J Pediatr Surg 1994; 29: 738741. 81. Moront ML, Gotschall CS, Eichelberger MR. Helicopter transport of injured children: system effectiveness and triage criteria. J Pediatr Surg 1996; 31:11831188. 82. Kotch SJ, Burgess BE. Helicopter transport of pediatric versus adult trauma patients. Prehosp Emerg Care 2002; 6:306308. 83. Foltin G, Salomon M, Tunik M, et al. Developing pediatric pre-hospital advanced life support: the New York City experience. Pediatr Emerg Care 1990; 6:141144. 84. National Highway Trafc Safety Administration. National Standard Curriculum for First Responders. Washington: National Highway Trafc Safety Administration, 1995. 85. National Highway Trafc Safety Administration. National Standard Curriculum for Emergency Medical Technician-Basics. Washington: National Highway Trafc Safety Administration, 1994. 86. National Highway Trafc Safety Administration. National Standard Curriculum for Emergency Medical Technician-Paramedics. Washington: National Highway Trafc Safety Administration, 1998. 87. National Highway Trafc Safety Administration. EMS Education Agenda for the Future. Washington: National Highway Trafc Safety Administration, 2001. 88. Prehospital Trauma Life Support Committee, National Association of Emergency Medical Technicians, in cooperation with the Committee on Trauma, American College of Surgeons, McSwain NE, Frame S, Salomone JP, eds. PHTLS: Basic and Advanced Prehospital Trauma Life Support, 5th ed. St Louis: Mosby, 2003. 89. Dieckmann R, Brownstein D, Gausche M, eds. Pediatric Emergencies for Prehospital Professionals (PEPP) Student Manual. Elk Grove Village and Sudbury: American Academy of Pediatrics and Jones and Bartlett Publishers, 2000. 90. Markenson DS. Pediatric Prehospital Care. Upper Saddle River: Prentice Hall, 2002. 91. Luten RC, Seidel JS, Lubitz DS, et al. A rapid method for estimating resuscitation drug doses from length in the pediatric age group. Ann Emerg Med 1988; 17:576581. 92. Kanter RK, Boeing NM, Hannan WP, et al. Excess morbidity associated with interhospital transport. Pediatrics 1992; 90:893898. 93. Edge WE, Kanter RK, Weigle CGM, et al. Reduction of morbidity in interhospital transport by specialized pediatric staff. Crit Care Med 1994; 22:11861191. 94. Smith DF, Hackel A. Selection criteria for pediatric critical care transport teams. Crit Care Med 1983; 11:1012. 95. MacNab AJ. Optimal escort for interhospital transport of pediatric emergencies. J Trauma 1991; 31:205209. 96. American Academy of Pediatrics Committee on Hospital Care. Guidelines for air and ground transport of pediatric patients. Pediatrics 1996; 78:943950. 97. Day S, McCloskey K, Orr R, et al. Pediatric interhospital critical care transport: consensus of a national leadership conference. Pediatrics 1991; 88:696704. 98. Kahn CA, Pirrallo RG, Kuhn EM. Characteristics of fatal ambulance crashes in the United States: an 11-year retrospective. Pre-hosp Emerg Care 2001; 5:261269. 99. Levick NR, Winston F, Aitken S, et al. Application of a dynamic testing procedure for ambulance pediatric restraint systems. Soc Automotive Eng Australasia 1998; 58:4551.

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100. Levick NR, Li G, Yannaccone J. Biomechanics of the patient compartment of ambulance vehicles under crash conditions: testing countermeasures to mitigate injury. Soc Automotive Eng Australasia 2001; 2001:173. 101. National Highway Trafc Safety Administration/Emergency Medical Services for Children/Health Resources and Services Administration. Dos and Donts of Transporting Children in an Ambulance: Fact Sheet. Washington: National Highway Trafc Safety Administration/Emergency Medical Services for Children/Health Resources and Services Administration, 1999.

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Organizing the Hospital for Pediatric Trauma Care
Max L. Ramenofsky
Geisinger Medical Center, Danville, Pennsylvania, U.S.A.

HISTORY OF TRAUMA CENTERS The development of trauma centers in the United States has a varied background, which takes its origins from many of the wars this country has fought. Many aspects, which are now considered to be integral parts of any trauma center, originated on the battleeld. Aspects such as immediate availability of surgeons who can provide immediate surgical care to trauma victims, facilities capable of providing any indicated treatment (Mobile Army Surgical Hospital units), pre-hospital personnel to identify and stabilize the victim in the eld and transport the patient to an emergency room capable of providing the indicated therapy, transport systems such as ground ambulances and helicopters to transport the victims, just to mention a few. All of these components originated in the U.S. military. The civilian trauma system originated in the State of Illinois in 1967 with the inception of the rst adult trauma center at Cook County Hospital under the leadership of Drs. Robert Freeark and Robert Baker. Shortly after this, Dr. R. Adams Cowley initiated the Shock Trauma Unit (Maryland Institure for Emergency Medical Services System) at the University of Maryland in Baltimore. Following closely on the heels of the rst two adult trauma centers, the U.S. Congress passed a number of emergency medical services systems acts, which dened many aspects of the things needed by a trauma system in the prehospital arena. These included the makeup of ambulances (equipment), the necessity for communications systems, which would allow pre-hospital personnel to speak with either an individual distant from or in a trauma receiving facility, and the training necessary for personnel in an ambulance unit, i.e., emergency medical technicians (EMTs), paramedics, etc. It is an interesting sidelight to note that prior to the passage of the various emergency medical services systems acts, many ambulance drivers were, in fact, funeral home directors.

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PEDIATRIC TRAUMA CENTERS It is of interest to note that in 1962 the rst Pediatric Trauma Center was established by Dr. Peter Kottmeier at the Kings County Hospital, in Brooklyn, New York, ve years before the rst adult trauma center opened its doors. Trauma care was further advanced in the United States by the American College of Surgeons (ACS), which in the early 1920s started the Committee on Trauma (COT). The purpose of the COT was to improve the care of the trauma victim by education. In February of 1984, the COT developed the rst resources or standards manual, which dened the standards of care necessary to treat trauma patients (1). These standards were primarily focused on the hospital resources necessary for this task. Not including the 1984 pamphlet, there have been four editions of this manual, the most current being entitled, Resources for the Optimum Care of the Injured Patient (25). The next edition is tentatively scheduled for publication in 2005. The ACS COT established the Verication Subcommittee in February of 1987. This subcommittees purpose was to verify compliance by hospitals wishing to become ACS-veried trauma centers, with the standards of care promulgated by the resources manual. The rst document describing the resources necessary to treat the injured child was published in the Journal of Trauma in 1982 (6). The COT rst included an appendix on Pediatric Trauma Care in their original 1984 pamphlet, Appendix J (1). The rst pediatric chapter in the ACS resource manual appeared in the 1987 edition (3). The COT has dened what is meant by the term pediatric trauma center by dividing trauma centers into levels. The highest level is a Level-I Pediatric Trauma Center located in a childrens hospital. A similar designation and quality of care may be present in a Level-I Adult Trauma Center with pediatric expertise. Childrens hospitals can also apply to become a Level-II Pediatric Trauma Center. By ACS standards, all trauma centers, regardless of their designation level, must have the ability to stabilize and transfer injured children when received in their institution.

PREPLANNING Before the rst patient is seen and treated in any institution that desires to become a trauma center or have a trauma unit, there is a great deal of organization that must be accomplished. The decision to apply for such a designation is the rst priority. This decision is not one that can be made by a single individual or department. The decision is one that must be embraced by the entire institution for the simple reason that trauma, by its very nature, is extremely disruptive to any hospitals schedule. Trauma is a disease that can and does occur at any and all times. The orderly carrying out of a busy operating room schedule can be disrupted because of the necessity of bringing an injured patient to the operating room at any time. Other resources such as laboratory and radiology are similarly disrupted due to the need for immediate results from the laboratory as well as immediate access to a computerized tomography scanner, magnetic resonance imaging, and/or interventional radiological procedures. The requirement for a designated and immediately available trauma team is similarly disruptive. Thus, it should be apparent that the decision to seek designation as a trauma center is one that requires agreement of many, if not all, departments within a busy hospital. The hospitals administration must agree and support this decision.

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Commitment The single most important component for any institution seeking a trauma designation is commitment. Commitment to provide the personnel, equipment, space, and all other resources necessary for treatment of the injured patient, 24 hours a day, seven days a week. Facilities The injured patient generally enters an institution through its emergency department (ED). Often the ED is very busy and crowded. An injured patient should not be expected to wait until a room opens before being seen. Thus a trauma room or resuscitation bay must always be available. This is an expense for the institution, but assessment and resuscitation must be available without delay. The makeup of such a room should include appropriate IV uids, catheters, surgical instrument sets, warming equipment, including a method to rapidly warm the entire room, medications and enough space for an entire team of physicians, nurses, and technicians to have easy access to the patient. Often a hospital that constructs a new trauma room will include a ceiling-mounted X-ray unit in the room. If not, there must be sufcient space for a portable X-ray machine to be wheeled into the space. For any institution that treats injured children, the Broselow System is a reasonable method of organizing the trauma room. This system provides colorcoded equipment such as airways, laryngoscopes, endotracheal tubes, suction catheters, vascular access devices, nasogastric (NG) tubes, urinary catheters, and chest tubes. The color-coding is based on the childs weight. In addition, the Broselow tape is a clever method of rapidly determining the childs weight based on height and can be used in the trauma room for quick determination of weight, IV-uid bolus infusion amounts, and emergency medications. The Broselow tape can be mounted in a Lucite holder and kept permanently in the room. When so mounted it measures roughly ve feet in length and does not have a tendency to be lost. The facilities necessary for an institution to become a trauma center are not limited to the emergency room. The institution must have immediate availability to CT scanning, angiography, interventional radiology, operating rooms, intensive care units, and patient oors. Another requirement is the availability of rehabilitation medicine. Radiology In addition to routine radiographic procedures such as chest, abdominal, extremity, and spine X rays, the institution must provide immediate access to CT scanning for the injured child. The CT scan is the major diagnostic modality utilized in both children and adults, and must always be available to the trauma patient.

Operating Room An operating room must always be available for the trauma patient. In a busy hospital this is difcult because this requirement decreases by one the number of rooms available for routine elective surgery. In addition to having an OR immediately available, personnel, including nurses, technicians, and anesthesiologists, must be immediately available 24/7.

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Pediatric Intensive Care Intensive care must be available for the injured child, preferably in a pediatric intensive care unit (PICU) with appropriately trained and trauma credentialed nurses. Should a PICU not be present, an intensive care unit may meet this requirement with appropriately trained and credentialed pediatric nurses. The equipment necessary for PICU care is well documented in the ACS resources manual.

Patient Floors There must be beds available on a pediatric oor for patients being admitted to the hospital with injuries. Nursing care must be adequate in this area as well.

Personnel The hospital personnel required for an institution to become a pediatric trauma center includes various physician specialties, pediatric-trained nurses working in certain specialized areas of the hospital, laboratory technicians, radiological technicians, and social workers. This is not a comprehensive list but is the basic catalogue of players.

Physicians The group of physicians immediately responsible for the care of an injured child is made up of the surgical specialties. Pediatric general surgery includes within its training the care of the injured child. The pediatric surgical team must include a leader of that team whose responsibility it is to organize the team. In the ED, this trauma team is expected to meet the patient on arrival. Once the patient has been placed in the resuscitation room, the team begins its work. Hopefully, the ED has been notied by the pre-hospital personnel of the cause of the injury, e.g., motor vehicle crash, gunshot wound, stab wound, fall, and is prepared to start the resuscitation phase. Occurring simultaneously with the resuscitation phase is the diagnostic phase. However, the team should be trained to the important fact that the diagnosis is less important than saving the life of the injured child. Thus, the team should be aware that the lack of a diagnosis should never impede the application of an indicated treatment. For example, if the patient cannot maintain their airway, the airway should be secured before the diagnosis of the cause of the unstable airway is determined. To reverse the process, and rst determine the cause of the unstable airway before treating, may result in the death of the patient. The composition of the team, in addition to the leader, is generally two other surgeons, an anesthesiologist or emergency medicine physician, and at least two nurses, one of who acts as the scribe. Absolute responsibility for the patient rests with the team leader. The team leader will have assigned specic duties to other members of the team. For example, the leader may assign the physician at the head of the patient and either the anesthesiologist or emergency medicine physician to manage the airway. The surgeon on the patients right side may be assigned the responsibility of evaluating the neck, chest, right-sided extremities, and the patients back. The surgeon on the left side may be assigned the duties of evaluating the abdomen and perineum,

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left-sided extremities, and neurological status. Such a setup provides for rapid and accurate initial assessment of the injured patient. Other physicians will be part of the trauma team but not necessarily part of the physician group who initially responds upon the patients arrival. Clearly, Orthopedic Surgery and Neurosurgery must be included in this group. Also, Plastic Surgery, Ear Nose Throat, Urology, and Ophthalmology will be required in specic cases. These individuals must be available on short notice at the behest of the trauma team leader. Nonsurgical physicians are also included in the requirements. Pediatric emergency medicine and pediatric intensive care physicians are included in this group, as are radiologists. Others whose expertise may be required include gastroenterologists, cardiologists, neurologists, infectious disease specialists, and general pediatricians. Nurses The nurses in the resuscitation room have established duties. One will serve the function of the scribe and will record everything that occurs with the patient. The second nurse prepares the room before the patient arrives, and makes sure that appropriate uids, chest tubes and chest evacuation apparatus, IV uids, urinary catheters, suture material, surgical trays, etc., are available and in the room. It is also this nurses responsibility to make sure that the room temperature is adequate so that hypothermia does not supervene. Intensive care nurses with education, training and/or experience, and expertise in pediatrics are required in the PICU setting. Methods of training are discussed later in this chapter. Laboratory and Radiological Technicians These technicians are an integral part of the trauma team meeting the patient in the ED. Most trauma centers have a routine laboratory panel that is ordered on every patient. Technicians being present at the time the patient arrives shortens the length of time the team must wait for various laboratory results. As with laboratory studies, most injured patients require, at a minimum, a specic group of X rays, including lateral cervical spine, chest, and abdominal lms. The presence of the X-ray technician with the X-ray machine shortens waiting time. When more sophisticated studies are warranted, such as CT scans or angiography, the technicians are helpful in organizing them.

Social Work The stress on a family resulting from a serious injury or death of a child is signicant. The presence of social services in the ED, should either occur, is comforting for the family and can function as a bridge for information when the trauma surgeons are busy providing the necessary care.

EDUCATION Physician education in trauma care is quite obvious for surgeons. Nearly all surgical specialties have, as part of their educational curriculum, a section devoted to care of

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the injured. Clearly, pediatric surgical training has a trauma component as mandated by the Residency Review Committee for Surgery. Most other surgical specialties have a similar requirement. The ACS Advanced Trauma Life Support (ATLS) Course for Physicians is, in many states, a requirement to participate in the care of injured children or injured patients in general (7). This course is a scaffold by which an injured child, or any injured patient, can be thoroughly evaluated and life-threatening injuries identied and treated. This requirement for ATLS has never been mandated by the ACS but has been mandated by many government agencies responsible for the individual states emergency medical services (EMS) or trauma laws. Nurses caring for the trauma patient are often required to have experience and/or training in trauma nursing. There are a number of courses offered by various organizations for trauma nursing. Advanced Trauma Care Nursing (ATCN) is the course provided by the Society of Trauma Nurses, and Trauma Nurse Care Course (TNCC) is provided by the Emergency Nursing Association. As with physicians, nurses are required to have one of these courses in order to care for injured patients. EMTs and paramedics often provide pre-hospital trauma care. The Pre-hospital Trauma Life Support (PHTLS) course is a pre-hospital course provided by the National Association of EMTs. This particular course parallels the ATLS course and provides physicians and pre-hospital personnel a common language by which care of the trauma patient can be expedited. The trauma center must take on the responsibility of educating its own personnel, surrounding institutions personnel, the pre-hospital system, and the general populace. General education for the public can take the form of trauma or injury prevention lectures, posters, and public service announcements.

SEVERITY PREDICTORS AND THE TIERED RESPONSE An essential element in organizing the hospital is to plan for what will actually happen when a trauma patient arrives. How is the commitment of the hospital and its staff put into action? There are two key components to this. The rst is to dene the patient at risk and to determine what resources are required in individual cases. The second is to dene the relative roles and responsibilities of the members of the hospital staff in the care of trauma patients. For these purposes most trauma centers divide their patients into three main groups (Table 1):  Category 1Patients with isolated, single-system injuries caused by lowenergy mechanisms. This group is by far the largest. They have simple fractures, soft tissue injuries, etc. They usually arrive by private conveyance. Rarely, these patients have signicant occult injuries such as a splenic laceration or an epidural hematoma. The ED staff can assess them and seek consultation when appropriate. They do not require a trauma team response.  Category 2: MechanismPatients at increased risk for multisystem or lifethreatening injuries without signicant anatomic or physiologic derangement. This group is dened mainly by mechanism of injury such as a fall from a great height or involvement in a high-energy motor vehicle collision with ejection, serious injuries or death of another occupant, rollover, or

Organizing the Hospital for Pediatric Trauma Care Table 1 Criteria for Triaging Pediatric Trauma Patients Category 1 No signicant mechanism of injury GCS 15 Normal pulse, BP, and respiratory rate Hemodynamically stable patient with an isolated extremity injury Category 2: Mechanism Blunt trauma with abdominal pain Suspected chest or abdominal injury Falls >20 feet Motor vehicle accident with ejection Motor vehicle accident with death in same compartment Rollover Prolonged extrication Category 3: Physiologic derangement Altered mental statusGCS 13 Airway or breathing compromise Hypotension Trauma arrest/CPR

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Multiple injuries (3 systems)

Penetrating injury to head, neck, chest, or abdomen Paralysis post injuryspinal cord injury Major extremity amputation

signicant intrusion into the passenger compartment. These patients typically arrive by ambulance. Although most do not have life- or limbthreatening injuries, many do. These patients demand careful assessment by trained and experienced trauma staff.  Category 3: Physiologic derangementPatients with obvious anatomic or physiologic derangement such as an amputation; penetrating injury to the head, neck, or trunk; coma; or shock. These patients also typically arrive by ambulance. These patients demand immediate careful assessment by the most highly trained and experienced trauma staff. The exact details of the eld triage criteria should be worked out locally. Engum et al. have shown that a system of eld triage based on anatomic and physiologic variables plus mechanism of injury provides a sensitive and safe system of triage (8). In Engums study, standard scoring systems such as the Revised Trauma Score and the Pediatric Trauma Score had unacceptably low sensitivities, missing approximately one-third and one-half of major trauma cases, respectively. A system for activating the receiving hospital staff is also necessary. Trauma responses should be tailored to the expected needs of the individual patient and based on objective information, either from the eld or referring hospital, which places the patient into one of the three categories described above. The rst category of patients with low-energy, single-system injuries can be handled by the ED staff on duty with referral to appropriate surgical services as required. The second and third groups with high-risk mechanisms or overt evidence of life-threatening injury both require trauma team activation and full assessment according to protocol. A trained and experienced trauma surgeon should direct the team, but the team should include other physicians, nurses, a respiratory therapist, a radiology technologist, a laboratory technician, a pharmacist, a social worker, and a chaplain. The roles of each member of the team vary depending on local circumstances, but they must be clearly dened.

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Many hospitals have revised or modied their team response for the second category of patients that meet mechanism-only criteria to avoid inefcient use of staff time and resources, what might be called false alarms. Dowd et al. have shown that patients who meet mechanism-only criteria are less likely to require a resuscitative intervention than those who meet anatomic and physiologic criteria, and therefore do not require full trauma team activation (9). They concluded that use of anatomic and physiologic criteria only for the highest level of trauma team activation results in increased specicity without sacricing sensitivity.

EMERGENCY MEDICAL SERVICES No trauma center or institution can exist without emergency medical services (EMS). By and large EMS is responsible for all pre-hospital care, including transportation to the trauma center. Pre-hospital personnel generally work under the medical license of a physician who is charged with providing pre-hospital care guidelines. The physician is often online with the in-eld ambulance personnel, receiving data and providing instructions to the emergency medical technicians in the eld. Other systems work by off-line medical control where there are specic protocols developed beforehand. EMS will generally transport a patient to a specic hospital or, in the case of injured child, to a pediatric trauma center. There must be telephone or radio communication with the receiving institution so that the trauma team can meet the patient in the ED on arrival. There must also be a method for the ED to communicate with the trauma team to alert them as to the mechanism of injury and types of injuries suffered by the victim. This can be accomplished in a variety of ways. Walkie-talkies are used in some systems, as are beepers. Most commonly today, cellular telephone communication is the method of choice. The various communication devices are, of course, an expense for the hospital. For any trauma center to succeed in its mission of providing appropriate and rapid care to an injured patient, the institution must be on good terms with the EMS system. The trauma center must always be aware of the fact that pre-hospital personnel work in the most difcult and primitive emergency room of all, the eld. The institution must provide appropriate feedback to these pre-hospital personnel so that the education of these individuals is steadily increased. This is often accomplished by run reviews, case studies, and lectures on specic topics. When errors are identied, alternatives should be suggested to help the prehospital personnel improve their performance. One common error is spending too much time in the eld trying to stabilize a patient who would be better served by rapid and temporary stabilization and rapid transport to the trauma center. Ambulances carry a limited amount of supplies. The hospital should provide needed supplies to a pre-hospital unit when requested. All of these courtesies will be rewarded by loyalty to the trauma center.

SUMMARY The decision to become a trauma center is one that takes signicant commitment from the entire institution. Commitment is the single most important aspect in becoming a trauma center. The institution must determine the specic type of

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trauma center it wishes to become based on the standards that apply to that particular state or region. The ACS resources document is generally a good place to start to put together all of the in-hospital systems that need to be in place prior to a site survey to verify that the institution meets all of the applicable standards. In most states, there is an entity in either the board of health or re department that has responsibility for verication. There are necessary equipment, space, personnel, and educational requirements that the institution must meet in order to function as a trauma center. It is neither cheap nor easy for an institution to meet the requirements, but if the hospital has the commitment to become a trauma center, it can be accomplished.

REFERENCES
1. The American College of Surgeons, Committee on Trauma. Hospital and Pre-Hospital Resources for Optimum Care of the Injured Patient and Appendices AJ. 1984. 2. The American College of Surgeons, Committee on Trauma. Resources for the Optimum Care of the Injured Patient. 1997. 3. The American College of Surgeons, Committee on Trauma. Resources for the Optimum Care of the Injured Patient. 1987. 4. The American College of Surgeons, Committee on Trauma. Resources for the Optimum Care of the Injured Patient. 1990. 5. The American College of Surgeons, Committee on Trauma. Resources for the Optimum Care of the Injured Patient. 1993. 6. Ramenofsky ML. Standards of care for the critically injured pediatric patient. J Trauma 1982; 22(11):921923. 7. The American College of Surgeons, Committee on Trauma. Advanced Trauma Life Support for Physicians. 1997. 8. Engum SA, Mitchell MK, Scherer LR, Gomez G, Jacobson L, Slotkin K, Grosfeld JL. Prehospital triage in the injured pediatric patient. J Pediatr Surg 2000; 35(1):8287. 9. Dowd MD, McAneney C, Lacher M, Ruddy RM. Maximizing the sensitivity and specicity of pediatric trauma team activation criteria. Acad Emerg Med 2000; 7(10): 11191125.

PART II: GENERAL PRINCIPLES OF RESUSCITATION AND SUPPORTIVE CARE

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The ABCs of Pediatric Trauma
Robert W. Letton
Pediatric Trauma and Burns, Brenner Childrens Hospital, Wake Forest University School of Medicine, Winston-Salem, North Carolina, U.S.A.

INTRODUCTION Pediatric multiple trauma victims present a unique set of problems to the emergency physician, pediatrician, or surgeon. Children rarely sustain lethal injury; however, delayed recognition and inappropriate management of the common problems encountered in the pediatric trauma patient can lead to a poor outcome. The ultimate common pathway leading to death in the injured child is profound shock: the inadequate delivery of oxygen to the tissues. It is therefore the goal of the initial phase of resuscitation to rapidly evaluate and treat any immediate life-threatening injuries that compromise tissue oxygenation. This is known in Advanced Trauma Life Support (ATLS) courses as the primary survey or the ABCs of trauma: airway, breathing, and circulation (1). Appropriate management of the ABCs is necessary for optimal outcome in pediatric trauma, regardless of whether it is managed in an adult or pediatric trauma center (2). In fact, with a relatively limited number of pediatric trauma centers, most improvements in pediatric trauma care are likely to come from improvements at combined trauma centers (3). When performing the primary survey of an injured child, one must keep in mind that frequent reassessment is mandatory. Children have tremendous physiologic reserve and may rapidly decompensate when their threshold level is crossed. Only by frequent evaluation and assessment can the physician detect and treat the child appropriately prior to decompensation. Before a child leaves the trauma room for a diagnostic procedure, they must have their ABCs assessed and stabilized. The computed tomography (CT) scanner is no place to lose an airway or require chest tube placement. As the trauma workup proceeds into the secondary survey, any deterioration in an otherwise stable trauma patient, whether adult or child, should prompt a reassessment of the ABCs. Performance of the primary survey is divided into the three separate stages of airway, breathing, and circulation only for discussion. In practice, it is a dynamic process in which the clinician must be aware that all three aspects occur together in real time. The procient physician managing pediatric or adult trauma must be able to evaluate all three simultaneously, not in sequence, and recognize that problems with the airway inuence breathing and circulation, and vice versa. It is
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the goal of this chapter to provide a framework upon which to base the initial management of the Golden Hour in pediatric trauma. A MEDLINE search was performed with a restriction to articles dealing with children (ages 1 to 12) published since 1990. Using the Eastern Association for the Surgery of Trauma guidelines, no class-I articles could be found. Mostly class-III articles and a few class-II articles were used as a basis for this review. Recommendations are based on current ATLS guidelines, with an attempt to include current evidence-based data as they relate to the primary survey in children.

ANATOMIC AND PHYSIOLOGIC CONSIDERATIONS Children differ from adults in several specic areas relevant to trauma care. Infants and young children, in particular, have a relatively large body-surface-area-to-body-cellmass ratio and are thus prone to developing hypothermia. This is particularly true when exposed for resuscitation or operation or when given large volumes of intravenous uids or blood products. To prevent hypothermia, it is important to keep injured children covered as much as possible and to have available warm blankets, heat lamps, room temperature controls, and uid warmers in resuscitation areas and operating rooms (OR). The childs vital signs and circulating blood volume also vary with age. This obviously affects the recognition and treatment of physiologic derangement. Young children have relatively large heads and are more likely to suffer head injuries, especially with deceleration mechanisms such as falls and motor vehicle trauma. Their craniums are also thinner and their brains are less completely myelinated, both of which tend to increase the severity of injury. Infants with open cranial sutures, larger subarachnoid space and cisterns, and greater extracellular space in the brain may tolerate expanding intracranial hematomas and cerebral edema better. The glottis lies in a more superior and anterior position relative to the pharynx. This makes orotracheal intubation much easier than nasotracheal intubation, especially in an emergency. In children up to about eight years of age, the airway is narrowest at the level of the cricoid cartilage. This is why uncuffed endotracheal tubes are generally used. Because it is narrower foreign material, uid or blood more easily occludes the childs airway. The fact that the trachea is relatively short increases the risk of malposition of endotracheal tubes because they are either too high or too low in the trachea. Tube position must be checked carefully at the time of intubation and monitored regularly thereafter. In children, the thorax is much more compliant to external forces and the vital organs are closer to the surface, both of which tend to increase the risk of blunt injury to the tracheobronchial tree, the heart, and great vessels. The elasticity of pediatric arteries and the normal absence of atherosclerosis offset this risk. In children, the mediastinum is more mobile so that an increase in pressure from a pneumothorax or hemothorax on one side is more apt to compromise both lungs. In the abdomen, the liver, spleen, and kidneys are less well protected by the ribs in children because the ribs are more pliable and because these organs are less well covered by the ribs.

AIRWAY The main reason for ensuring a stable airway is to provide effective oxygenation and ventilation while protecting the cervical spine and avoiding increases in intracranial

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pressure. Airway control is intimately related to cervical spine protection, but the scope of this chapter will be limited to managing the airway only. Any child involved in a signicant trauma should be assumed to have a cervical spine injury until proven otherwise. Movement of the neck, as is commonly employed to provide an airway, can convert a bony or ligamentous injury into a permanent disability. C-spine protection should be initiated at the scene and maintained in the emergency department. Any child that arrives without neck stabilization should be held with in-line traction or have an appropriate sized rigid cervical collar applied while the airway is evaluated. Anatomy and Assessment Several anatomic features predispose the child to potential airway obstruction. The childs head is relatively large and causes exion of the neck in the supine position. The tongue is larger in proportion to the rest of the oral cavity and predisposes the child to more rapid upper airway obstruction with posterior displacement of the tongue. Even a minimal amount of pressure on the submental soft tissue during bag-valve-mask ventilation can displace the tongue posteriorly and occlude the airway. The larynx is higher in the neck (C3-4) compared with that of the adult (C4-5); this alters the preferred angle of insertion of the laryngoscope blade and makes the cords appear to be more anterior. Cocking the laryngoscope, as is commonly practiced in adult intubation, will only push the cords more anterior and make intubation difcult. The infant epiglottis is short and angled away from the long axis of the trachea, increasing the difculty of its control with the laryngoscope blade. Infant vocal cords are more cartilaginous and easily injured when passing the endotracheal tube. The narrowest portion of the airway in the child is the subglottis, not the glottis, as in the adult. A tube that readily passes the cords in an infant may be too tight in the subglottis. Uncuffed tubes are often used for this reason, and an acceptable air leak should be heard at a pressure that is neither too low to allow adequate tidal volumes nor too high. The airways are much smaller and the supporting cartilage is less well developed, making the trachea more susceptible to obstruction from mucus, blood, or edema. In addition, the pediatric trachea is much shorter than the adult trachea, and advancing the tube too far into the right main stem bronchus is common. It can be difcult to recognize early airway obstruction in the child. Certainly the infant who is screaming or crying loudly and the older child who can converse with you have airways that are not in immediate jeopardy. The child who arrives comatose (Glasgow Coma Score less than 8) or with obvious laryngeal trauma has an airway that is in immediate danger. Often the child is obtunded. If spontaneous breathing is absent, the airway should be opened with a jaw thrust maneuver taking care to protect the C-spine. A nger sweep to rule out a foreign body should be performed. If no breathing effort is seen after this maneuver, hand ventilation with a mask should be initiated and preparation made to intubate the child. During assisted mask ventilation, the operator must take care not to place undue pressure on the base of the tongue, as this will occlude the airway. It is the metastable pediatric trauma patient that can present difculties in determining whether an airway is adequate. The patient may appear only slightly agitated, with nasal aring, stridor, and air hunger. The child with an innocent-appearing face and neck burn may have signicant airway edema. When in doubt, the following maneuvers should be attempted to secure the airway.

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Managing the Airway Studies investigating eld intubation have demonstrated complication rates as high as 25% (4). Appropriate mask ventilation can provide adequate gas exchange until one skilled in the task can intubate the child (5). Newer airway techniques, including the laryngeal mask airway (LMA), have been shown to be an effective temporary airway in children until secure endotracheal intubation can be performed in the emergency department (6). The LMA is placed in the posterior pharynx and advanced until it seals over the vocal cords and larynx. Excessive extension of the neck must be avoided in any airway technique. Oral and nasal airways do not protect the airway. In fact, their insertion can induce emesis. Nasal airways are too small to be effective in the child. An oral or nasal airway is, at best, a temporary technique to improve bag ventilation in preparation for endotracheal intubation. Oral endotracheal intubation is the gold standard for airway control. It is critical to maintain neutral alignment of the cervical spine during all airway manipulation. Even though nasotracheal intubation in adults requires less spine manipulation, in children it is difcult and time-consuming, and therefore has little role in the acutely injured child. The size of the nares is often not large enough for an appropriate-sized tube. In addition, the path that the tube has to follow to the cords is at a very acute angle, requiring direct laryngoscopy and forceps to accomplish. Enlarged tonsils and adenoids can bleed if blindly injured with the endotracheal tube. Children less than six years of age should receive an appropriately sized uncuffed endotracheal tube to minimize trauma to the cords and subglottic edema. Formulas exist for calculating endotracheal tube size (Table 1), but a quick reference is the size of the middle phalanx of the fth digit. The Broselow tape, which bases drug doses and weight on the childs length, also estimates endotracheal tube size (7). Stylets are helpful for pediatric intubation to give the tube a gentle J curve. The tip of the stylet should never be extended beyond the end of the tube, and a thin coat of lubricating jelly can aid in removing the stylet without extubating the child. Endotracheal Intubation The process of intubating a child can be harrowing for those not accustomed to it. Current ATLS recommendations call for a rapid sequence induction of sedation
Table 1 Endotracheal Tube Size in Relation to Age Age Term infant 6 months 1 year 2 years 4 years 6 years 8 years 10 years 12 years 14 years Adult Internal diameter (mm) 3.0 3.5 4.0 4.5 5.0 5.5 6.0 6.5 7.0 7.5 8.0

Note: May estimate tube internal diameter with formula: ID (mm) Age/4 4.

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and paralysis, especially in those with closed head injury and possible elevated intracranial pressure (1). Attempts to intubate a partially responsive, coughing, combative child will cause further elevation of the intracranial pressure. The use of drugs in rapid sequence induction must induce unconsciousness and paralysis, as well as blunt the intracranial pressure response (8). Our current choice of drugs for rapid sequence induction is listed in Table 2. Care should be taken if the patient is in shock not to induce hypotension with too much sedative. Paralysis should not be induced in the spontaneously breathing patient until the physician is capable of visualizing the cords. Gentle mask ventilation with cricoid pressure should be attempted to preoxygenate the child. In-line cervical immobilization with the collar opened anteriorly should provide adequate exposure. Rapid sequence induction is initiated after proper equipment is obtained and the child has been pre-oxygenated. This should include a bag and mask connected to high ow oxygen, suction, a laryngoscope with functioning bulb, and an endotracheal tube with stylet of appropriate size as well as tubes that are a half size larger and smaller than the estimated correct size. A Miller (straight) blade is most often easiest to use and should be gently inserted into the oropharynx and the tongue elevated anteriorly to visualize the cords. Avoid the temptation to cock the laryngoscope, as this will further displace the cords anteriorly and increase the likelihood of breaking or loosening an incisor. The tube should only be inserted a few centimeters past the vocal cords. The trachea is short and intubation of the right main stem bronchus can easily occur. The tube should be placed no deeper than three times the endotracheal tube size, in centimeters, from the lips. The Broselow tape will also specify a depth of insertion (7). Endotracheal tube position should be conrmed with a disposable capnometer, as well as auscultation of both lung elds and listening over the epigastrium for esophageal intubation. Breath sounds transmit easily in young children and listening in both axillae will give the best point of auscultation to determine if the breath sounds are equal. Symmetry of chest wall excursion with ventilation should be noted; diminished sounds and movement of the left side should be treated by withdrawing the tube 0.51 cm. If diminished sounds persist, a left-sided pneumothorax should be considered. Since the trachea is so short, movement of 1 cm in either direction can often displace the tube into an inappropriate position. Vigilance in securing the tube and constant checking of its position is mandatory. Current ATLS recommendations call for obtaining a chest X ray, as well as lateral C-spine and pelvis lms, at the end of the primary survey to conrm tube position as well as rule out injury (1).

Table 2 Drugs and Doses Commonly Used for Rapid Sequence Induction Drug class Short-acting sedatives Drug name Etomidate Pentothal Versed Rocuronium Vecuronium Succinylcholine Atropine Dose (mg/kg) 0.20.4 24 0.010.02 0.60.9 0.10.2 12 0.010.02

Short-acting paralytics

Vagolytic (infants)

Note: Avoid propofol and ketamine in children with elevated intracranial pressure. Sedatives and barbiturates can aggravate hypotension.

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Special Airway Situations Any child with a severe burn to the face and neck should be assumed to have an airway at jeopardy. Heat injury to the upper airway results in edema of the pharynx, larynx, and tongue that can rapidly occlude the airway. As tissues become more distorted, intubation can become more difcult. Furthermore, children injured in a conned space can have a compromised airway, even without obvious face and neck burns. Inhaled toxic fumes and particles can irritate the airway and cause edema. Prophylactic intubation is appropriate whenever heat injury to the upper airway is suspected, or if transportation to another facility is expected. It is much easier to remove a tube that is not needed than to obtain an airway emergently in a swollen burn victim. In addition, carbon monoxide poisoning is difcult to detect, as the pulse oximeter will continue to read high saturation. Tracheal intubation insures efcient delivery of oxygen under these circumstances. In the child with severe face or neck trauma, alternative maneuvers to endotracheal intubation may be necessary to secure the airway. A child with severe facial trauma that is able to maintain an airway should have a quick primary survey and all immediate life-threatening injuries addressed. The child should then be transported to the operating room where a formal tracheostomy can be performed. If the patient is unable to maintain an airway, a needle cricothyrotomy is preferred to a surgical cricothyrotomy, especially if the child is less than 10 years of age. Insertion of a 14-gauge needle or angiocath requires less skill and can provide a temporary airway until the child can have a formal tracheostomy in the operating room. Needle cricothyrotomy provides good oxygenation, although normocarbia can be difcult to maintain and therefore it should be converted to a surgical airway as soon as possible. Other alternatives, including ber opticassisted intubation and retrograde intubation or tracheostomies, are institution- and operator-dependent. Laryngeal trauma is rare in children but may need to be addressed with penetrating trauma or clothesline injuries sustained on bicycles and ATVs. Endotracheal intubation can potentially worsen the injury by causing complete separation of the trachea from the larynx and total loss of the airway. Signs and symptoms of laryngeal fracture include stridor, subcutaneous emphysema of the neck, pneumothorax, and hoarseness. If the child is able to maintain an airway, oxygen should be provided until a surgical airway can be obtained in the OR. Cricotracheal separation is an airway emergency that often requires immediate tracheostomy in the emergency department.

BREATHING Once an airway is secure, attention must next be directed toward injuries that affect ventilation and oxygenation. Most of these injuries comprise the immediate lifethreatening injuries of the chest. Although these will be discussed in detail elsewhere in this textbook, they must be mentioned now, as an adequate primary survey cant be performed without including these injuries in the differential diagnosis. Ventilation and oxygenation must occur in an effective manner, and if they are not, correctable causes should immediately be sought. The intubated child with stable blood pressure and good saturation likely does not have an immediately life-threatening chest injury, but can still have a potentially life-threatening chest injury. The intubated child that decompensates after intubation most likely has a life-threatening

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chest injury and must be managed appropriately to preserve a good outcome. The major life-threatening thoracic injuries include tension pneumothorax, open pneumothorax, massive hemothorax, ail chest, and cardiac tamponade. Other potentially life-threatening injuries to consider are simple pneumothorax, hemothorax, pulmonary contusion, tracheobronchial tree injuries, cardiac contusion, traumatic aortic disruption, aerophagia, and traumatic diaphragmatic injury (Table 3). Assessment and Monitoring Assessing adequacy of ventilation and oxygenation in a busy trauma bay can be problematic. The childs breathing should be observed, looking for symmetry of excursion or ail chest segments (rare in children). Auscultation can be difcult in a noisy emergency department, but the best point of auscultation to check for equality of breath sounds is in the axilla. Pneumothorax will initially result in loss of expiratory breath sounds, followed by the loss of inspiratory breath sounds. To distinguish the loss of breath sounds associated with a hemothorax versus a pneumothorax, percussion can be attempted; however, dullness and resonance to percussion can be difcult to appreciate in a noisy emergency department. Fortunately, both are initially treated with placement of a chest tube and are easy to distinguish afterwards. If the child is stable, a chest X ray can be obtained prior to initiating therapy. A decompensating child with decreased breath sounds should not wait for an X ray prior to decompression of the hemo/pneumothorax. Any child that has been intubated will require mechanical ventilation. In infants less than one year of age, pressure regulated ventilation is our preferred mode of ventilation in order to minimize iatrogenic barotrauma. A peak pressure is chosen such that the resulting tidal volume is 710 cm3/kg, and a rate of 20 to 40 is chosen and adjusted based on the pCO2 on an arterial blood gas. If the child has a closed head injury, the pCO2 should be maintained at approximately 3035 mmHg, otherwise a pCO2 of 40 mmHg is acceptable. In children over one year of age, volume control ventilation is our preferred method of ventilation. However, pulmonary compliance should be monitored closely, and if it acutely changes secondary to uid resuscitation, pulmonary contusion, or other causes, pressure control ventilation must be considered to minimize barotrauma as much as possible. Initial settings in volume control are similar in that a tidal volume of 710 cm3/kg is desired, but the older the child, the lower the rate necessary to maintain adequate ventilation. Most emergency departments are equipped with pulse oximeters, and many have capnometers to monitor end tidal CO2. Arterial blood gases are useful but can be difcult to obtain. If perfusion is adequate, arterial oxygen saturation can
Table 3 Potential Life-Threatening Injuries Addressed in Primary Survey Immediate life-threatening injuries Airway obstruction Tension pneumothorax Open pneumothorax Massive hemothorax Cardiac tamponade Flail chest Potential life-threatening injuries Simple pneumothorax Hemothorax Pulmonary contusion Tracheobronchial injury Cardiac contusion Aortic disruption Diaphragmatic rupture

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be monitored with pulse oximeters. The pulse oximeter is also useful for assessing poor circulation in that if the extremities are cool and the pulse oximeters will not register, hypovolemic shock is undoubtedly present and must be addressed. If the child is intubated, an end tidal CO2 monitor can be placed on the endotracheal tube. The absolute value on end tidal CO2 should be correlated to the pCO2 on blood gas initially, and changes in end tidal CO2 then are monitored and useful in guiding changes in ventilation. Disposable capnometers are available to conrm position of the endotracheal tube. However, continuous monitoring can be performed, which is especially useful for monitoring ventilation in the child with a closed head injury until an arterial line can be obtained in the intensive care unit. Tension Pneumothorax Trauma to the rib cage may result in rib fracture and parenchymal injury. A small parenchymal injury with air leak as well as a major tracheobronchial tear may result in pneumothorax. The child with a pneumothorax may have an asymptomatic simple pneumothorax or have severe respiratory distress secondary to an open or tension pneumothorax. Physical ndings of pneumothorax include an absence of breath sounds on one side of the chest, hyperresonance to percussion, subcutaneous emphysema, and tracheal deviation away from the affected side. Physical ndings may be very subtle. A tension pneumothorax occurs with progressive entry of air that is unable to escape from the pleural space. This compresses the ipsilateral lung and results in a shift of the mediastinum to the contralateral side. Since the mediastinum is so compliant, it shifts earlier in the course, resulting in decreased venous return and more rapid cardiovascular collapse in the child. An open pneumothorax allows communication between the environment and pleural space. Equilibration of atmospheric and pleural pressure occurs with collapse of the lung and less shift of the mediastinum. Because of the loss of negative inspiratory pressure, respiratory distress can occur due to decreased ventilation on the ipsilateral side. Massive hemothorax occurs secondary to parenchymal injury with severe vascular injury, or secondary to intercostal bleeding from rib fractures. This condition is more common with penetrating chest trauma than blunt chest trauma. Treatment of a tension pneumothorax is accomplished by insertion of a chest tube. Temporary relief can often be obtained with needle decompression. Any child that has had needle decompression of the chest needs an appropriate-sized chest tube placed as soon as possible. Children are more susceptible to the associated mediastinal shift than adults. Therefore, any child with acute cardiovascular collapse, especially if it occurs shortly after the initiation of positive pressure ventilation, should have needle decompression or tube thoracostomy performed bilaterally if it is unclear which side is the symptomatic side. If acute cardiovascular collapse occurs, this decompression should be performed prior to obtaining a conrmatory chest radiograph. Needle decompression of the second intercostal space anteriorly may alleviate the condition long enough to allow for completion of the primary survey prior to placing a chest tube. However, if needle decompression fails to reverse the collapse, a chest tube should immediately be placed. Clinically, a hemothorax may be difcult to distinguish from a tension pneumothorax; however, treatment is the same for both conditions and an X ray is not necessary prior to treatment. Massive hemothorax will not usually respond to needle decompression unless there is an associated tension pneumothorax component. A three-sided occlusive dressing that allows air to

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exit the pleural space on expiration and prevents its return on inspiration can treat open pneumothorax. With massive open pneumothorax, intubation and positive pressure ventilation may be necessary to overcome the defect. Tube Thoracostomy Even in emergency situations, chest tube placement should be performed aseptically. The skin should be prepared with an antiseptic and sterile towels draped to expose the appropriate chest. The most important landmark is the nipple, which should be visible after draping. Usually the fth or sixth interspace is located at the level of the nipple, and a skin incision is made one or two ngerbreadths below the nipple in the anterior axillary line after anesthesizing with 1% lidocaine. A hemostat is then used to tunnel the chest tube for 12 cm in the subcutaneous space. The hemostat is then inserted on top of the rib and pushed rmly until the pleural space is entered. If tension is present, this maneuver alone will alleviate the tension and restore hemodynamic stability. An appropriate-size chest tube is then inserted into the pleural space (Table 4). Many pediatric chest tubes come with a sharp trochar, which should never be used to blindly place the chest tube. The trochar can be safely used as a stylet to help guide the tube into the previous dissected tunnel and entrance into the pleural space. It should always be pulled back 12 cm from the end of the chest tube, but can then help stiffen the tube for easier placement. The other method of inserting the tube would be to remove the trochar completely, grasp the tube in the end of a hemostat, and direct it through the tract and into the pleural space. The tube should be gently inserted until it is felt contacting the apex, then withdrawn 2 cm and secured with a suture. Fogging of the tube should be noted on insertion, and tidal movement of the water seal chamber should be noted with ventilation. A chest X ray is always obtained to check tube position. Other Chest Injuries One must keep in mind that pneumothorax may be associated with more severe injuries of the tracheobronchial tree. A large continuous air leak after chest tube placement or continued respiratory distress may signal a larger tracheobronchial injury. Bronchoscopy in the operating room should be performed soon after the primary survey to diagnose the injury in those who fail to resolve their air leak, or who remain difcult to ventilate and oxygenate. If the air leak is on the left side, passing the endotracheal tube into the right main stem may temporarily allow adequate ventilation and oxygenation until it can be addressed operatively. Tidal volumes must be decreased and rate increased to avoid a pneumothorax on the right side as well. Blood loss from a massive hemothorax should continuously be
Table 4 Chest Tube Size (French) Size of patient (kg) <3 38 815 1640 >40 Pneumothorax 810 1012 1216 1620 2024 Hemothorax 1012 1216 1620 2028 2836

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monitored to avoid hypotension and determine the need for thoracotomy. In general, loss of more than 207 mL/kg of blood from the chest with continued bleeding should be addressed surgically. Although a true ail chest is rare in children, the compliance of the chest wall frequently allows impact to cause an occult pulmonary contusion without obvious rib fracture. This underlying pulmonary contusion and/or injury to the lung parenchyma can result in respiratory distress. A large pulmonary contusion can result in hypoxia from severe ventilationperfusion mismatch. Management of severe pulmonary contusion should aim to maintain the child in a state of euvolemia (9). Attempts to avoid pulmonary edema by keeping the child hypovolemic are likely to result in hemodynamic instability and worsen the ventilationperfusion mismatch. If the child is able to maintain saturation with spontaneous ventilation and supplemental oxygen, the contusion is best treated with aggressive pain management, including epidural catheter or rib blocks to provide adequate pain control for aggressive chest physiotherapy. If paradoxical motion is severe and the child is hypercarbic or hypoxic, a contusion or ail segment is best managed with intubation and positive pressure ventilation. Aggressive pulmonary toilet while intubated, sufcient tidal volume to prevent atelectasis, and maintaining a normovolemic state are ideal management. Positive end expiratory pressure is benecial, and positive pressure ventilation is often needed for two to three days before the patients chest wall is stable enough to allow for spontaneous ventilation. Potential life-threatening injuries, which usually do not manifest symptoms early in evaluation, include traumatic aortic rupture and diaphragmatic rupture. The mobile mediastinum that makes the child more susceptible to tracheobronchial injuries makes them less likely than the adult to sustain a torn aorta (10). Although rare, an aortic injury should be suspected especially in chest trauma with a signicant deceleration mechanism. Signs suggesting a torn aorta include the chest X ray ndings of a widened mediastinum, apical cap, left hemothorax, deviated left main stem bronchus, deviated nasogastric (NG) tube, or rst and second rib fractures. In a severely injured patient with multiple potential sources of hypotension, the presence of a widened mediastinum should not interfere with completion of the primary survey. There is the temptation to rush into repair of the aorta, due to its devastating consequences should it rupture. However, the unstable pelvis, bleeding liver and spleen, or open femur fracture must be addressed prior to placing the patient in a thoracotomy position for repair of the torn aorta (11). Hypotension induced by a torn aorta is acute in onset, extremely short in duration, and the patient expires rapidly. Diaphragmatic rupture can result from a fall from excessive height or crush injury to the chest and abdomen. Loss of diaphragmatic function as well as herniation of abdominal contents into the thorax can result in respiratory distress. It can present subtly on chest X ray with loss of left diaphragm border, or obvious loops of bowel can be seen in the chest. Axial cuts on CT scan can miss a small defect as well. A plain lm with NG tube in stomach noted above the diaphragm and/or UGI with bowel in the chest is diagnostic. Initial treatment in the primary survey should be placement of an NG tube to decompress the abdominal contents in the chest. The diaphragmatic defect is most often repaired from an abdominal approach. A nonlife-threatening condition common in pediatric trauma victims that can cause signicant respiratory distress is massive aerophagia. Small children that present to the emergency department crying and screaming can swallow a signicant quantity of air and induce massive gastric distension. This aerophagia can result in

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increased girth, respiratory compromise, and emesis with potential for aspiration. This can be rapidly cured by early insertion of an NG tube. Cardiac Injury/ER Thoracotomy Blunt injury to the heart is rare in the child; however, it must be assumed with any penetrating trauma to the chest, especially if the wound is potentially transmediastinal. If a childs cardiopulmonary status acutely deteriorates, bilateral chest tubes should be placed for the likely tension pneumothorax; if these fail to alleviate the condition, a pericardiocentesis should be performed. A positive pericardiocentesis for blood is an indication for urgent thoracotomy or sternotomy to identify and repair a cardiac injury. Myocardial contusion is rare in children, but can occur in adolescent drivers who may sustain a signicant chest impact from the steering wheel. Rarely is contusion severe enough that acute decompensation occurs. Emergency room thoracotomy is a topic of debate in the literature and in many trauma centers. Even though children have much greater physiologic reserve than adults, loss of vital signs that do not return with adequate Cardio Pulmonary Resuscitation prior to arrival in the emergency department (ED) is almost universally fatal. This is especially true when the injury is secondary to blunt trauma and does not warrant an emergency room (ER) thoracotomy. Over the years, a number of institutions have reviewed their success rate with ER thoracotomy in blunt trauma, and few if any survivors have been noted (12,13). Even those children whose vital signs return with CPR prior to arrival in the ED have a 25% survival rate, at best, and two-thirds of those that did survive had a signicant impairment in one or more activities of daily living (14). In contrast, an ER thoracotomy can be life saving with penetrating chest trauma when vital signs are not lost until the child arrives in the ED.

CIRCULATION After a patent airway is established and adequate ventilation has been insured, the diagnosis and management of shock takes precedence. Evaluation of circulation is a process that must be performed simultaneously with the assessment of the airway and breathing. Successful treatment of shock requires rapid recognition that the child is in shock and simultaneous treatment maneuvers. Direct pressure may be required to control external bleeding, especially from scalp, neck, and groin wounds. Long bone and pelvic fractures should be stabilized with traction and splinting. Pediatric Physiology In general, the physiologic concepts of hemorrhagic shock apply to both children and adults. However, children are unique in several aspects of anatomy and physiology that make recognition of shock more difcult, but at the same time provide them tremendous reserve to survive many injuries that adults would be unable to. Most notably, the variability in size and weight that one encounters in dealing with pediatric trauma poses a problem in insuring that appropriate equipment and medications will be available for the resuscitation of the child. Normal circulating blood volume in a child is 7% to 8% of total body weight, 7080 mL/kg. Although in relative terms the circulating volume is 20% greater than in adults, what may appear to be a small amount of blood loss can be very signicant

54 Table 5 Normal Vital Signs by Age Heart rate Weight (kg) (beats/min) 36 12 16 35 160180 160 120 100 Pressurea (mmHg) 6080 80 90 100 Respirations (breaths/min) 60 40 30 20

Letton

Age 06 months Infant Preschool Adolescent

a

Urine output (mL/kg/hr) 2 1.5 1 0.5

Systolic blood pressure should be 80 2 age (yrs). Source: Taken from Advanced Trauma Life Support for Doctors Instructor Manual.

in a young child. A 200-mL estimated blood loss in a 10-kg child is equal to 25% of their blood volume. Children also have a higher body-surface-area-to-mass ratio. This leads to an increase in insensible water loss that makes them susceptible to hypovolemia and increased heat loss, which can lead to hypothermia. In extremely young children, hypothermia is a major problem associated with trauma resuscitation. Hypothermia aggravates pulmonary hypertension, hypoxia, and acidosis and results in a signicant increase in oxygen consumption. The extremely compliant mediastinum makes infants and children more susceptible to wide swings induced by tension pneumothorax or hemothorax. Shifting of the mediastinum not only decreases venous return and cardiac output, but can also interfere with ventilatory capacity of the contralateral lung. The clinician evaluating pediatric trauma must be familiar with the wide variability in normal vital signs based on age. A pulse rate and blood pressure that are acceptable in an infant may indicate signicant hypovolemia in an adolescent (Table 5). The goal of management is to recognize that shock exists before the vital signs change. The signs of late hypovolemic shock are easy to recognize, but the clinical presentation of early shock requires a high index of suspicion. The clinician must rely on subtle ndings during the physical examination as well as the vital signs (Table 6).

Table 6 Systemic Response to Blood Loss in Pediatric Trauma Patients System Cardiac CNS <25% blood loss Tachycardia Lethargic, irritable, and confused 2545% blood loss Weak, thready pulse and tachycardia Changing level of consciousness and dulled response to pain Cyanotic, decreased capillary rell, and cold extremities Decreased urine output >45% blood loss Hypotension, tachycardia to bradycardia Comatose

Skin

Cool and clammy

Pale and cold

Renal

No decrease in output and increased specic gravity

No urine output

Source: From Chapter 10: Pediatric Trauma in Advanced Trauma Life Support for Doctors, Instructor Course Manual, American College of Surgeons Committee on Trauma, 6th Edition, Chicago, IL, 1997.

The ABCs of Pediatric Trauma

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Assessment Shock is a state in which there is inadequate delivery of oxygen to meet the demands of the child. Absolute values of blood pressure have little to do with dening the shock state. A child with normal blood pressure can be in shock, just as a child with low blood pressure can be well perfused and not in shock. The earliest warning signs that a child is in shock include signs of decreased skin perfusion (capillary rell, temperature, and color), central nervous system perfusion (lethargy, inappropriate response to painful procedures, and lack of recognition of parents), pulses (tachycardia and presence or absence of pulses), and falling blood pressure. With a quick physical exam, the physician should be able to readily estimate the degree of shock and estimate blood loss (Table 6). After the airway and breathing are secured, most astute trauma physicians palpate the childs feet or hands. A child that has warm feet with bounding pedal pulses is not in acute shock. A child with cool feet, weak and thready pedal pulses, depressed capillary rell, and mottled cool extremities is already in signicant shock. The child with hypotension and a markedly depressed mental status is in late shock with blood loss up to 40% of blood volume. Waiting until hypotension is present to begin treating shock is too late. There are no laboratory tests or X rays that can rapidly estimate the degree of blood loss and shock. In acute hemorrhage, the hemoglobin level does not change immediately, only after compensatory uid shifts have occurred and resuscitation has begun. The best laboratory predictor of shock and volume loss is the arterial base decit. Adult trauma surgeons have identied base decit as a predictor of survival, and recently this test has been demonstrated to be predictive of morbidity and mortality in pediatric trauma victims (1517). As anaerobic metabolism is increased in response to inadequate tissue perfusion, lactic acid is produced. Most anxious children hyperventilate, which helps compensate for the developing metabolic acidosis. If shock persists, the metabolic acidosis worsens. Sodium bicarbonate can improve the laboratory values obtained, but until the cause of shock is addressed and resuscitation is initiated, the overall clinical picture will not improve. Sodium bicarbonate has not been shown to improve survival and may aggravate any existing respiratory acidosis with increased CO2 production (18,19).

Intravenous Access In order to resuscitate the child from shock, intravenous access is a must. In the very young, this can pose more of a problem than obtaining the airway. At the same time that access is being established, blood should be drawn for a standard trauma laboratory panel. A specimen for typed and crossed blood must be sent early in the resuscitation. Establishing two large-bore peripheral intravenous catheters is clearly the rst choice for resuscitation (1). A short catheter should be chosen to minimize resistance to ow. This can be a daunting task in a small, hypovolemic child. Preferably, lines should be placed above and below the diaphragm. The most desirable sites for peripheral IV access include percutaneous IVs in the antecubital fossa, distal saphenous vein, or other peripheral vein. The veins are usually more supercial than initially anticipated. Another tip is to rotate the needle and angiocath 180 so that the bevel hooks under the venotomy and insures that the angiocath will thread into the vein. The most common cause of failure is not getting a ash of blood in the angiocath, but successfully threading it into the vein.

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Most authors and texts recommend a distal saphenous vein cutdown in the event that peripheral lines cannot be obtained. In the child less than one year of age, performance of a cutdown quickly may be a difcult task to those unaccustomed to doing this. When attempting a cutdown, a transverse incision is made over the vessel with a scalpel just anterior to the medial malleolus. The remainder of the dissection should be done bluntly with a small hemostat. The vessel is isolated with a suture, and often an angiocath can be inserted under direct vision using the stylet without making a venotomy. If the angiocath can be placed through the skin just below the incision and then directed into the vessel, it can be maintained more easily. Other options include a percutaneously placed central venous catheter. In elective circumstances, the jugular or subclavian approach would be preferred. However, in the emergency department environment, and with the possibility of cervical spine trauma, the risk of pneumothorax or spine injury may be prohibitory. Temporary cannulation of the femoral vein with a large-bore IV catheter or venous introducer can provide access as quickly as a cutdown in many instances. These catheters should be removed as soon as possible as long-term use of femoral catheters may be associated with an increased risk of venous thrombosis (20). The line must be placed as aseptically as possible, and many trauma surgeons demand that all lines placed in the eld or emergency department be removed once they are stable in the hospital. The groin is sterilely prepped and draped and the femoral pulse is palpated. With a nger over the palpable arterial pulse, the femoral vein is aspirated with a needle and syringe just medial to the palpable pulse. A wire is threaded by the Seldinger technique, and the line placed over the wire. Long multiple lumen catheters should be avoided due to the resistance to ow. A single lumen six French catheter introducer, if available, or even a large-bore angiocath should be sufcient for large volume resuscitation. In children less than six years old, intraosseous infusion provides a rapid and safe route of success. Blood products, uids, and medications can be given through this type of catheter (21,22). Although not a good long-term route of IV access, it allows the initiation of uid resuscitation, and with improved circulatory status, a peripheral route of venous access may become feasible. Complications with intraosseous needles are rare if placed appropriately. A 16- or 18-gauge bone marrow aspiration needle is placed in the tibia, 23 cm below the tibial tuberosity, angled slightly away from the growth plate. If the tibia is fractured, it can be placed in the femur 3 cm above the femoral condyle. In all pediatric trauma victims, percutaneous peripheral intravenous access should be attempted rst. If this fails in a child less than one, if a pediatric surgeon or intensivist is not available, an intraosseous line should be obtained and the child transferred as soon as possible. In the child one to six years of age, a percutaneous femoral line and/or saphenous vein cutdown may be feasible prior to resorting to an intraosseous line. Most children over six years of age have veins of sufcient size for percutaneous peripheral placement. If in extremis and access is difcult, a femoral central line or saphenous vein cutdown would be the best choices for access.

Resuscitation Once shock has been identied and intravenous access has been obtained, resuscitation should be initiated. Many algorithms for resuscitation exist, and most are based on

The ABCs of Pediatric Trauma

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Figure 1 Resuscitation ow diagram for the pediatric trauma patient. Source: From Advanced Trauma Life Support for Doctors Instructor Manual. Source: From Chapter 10: Pediatric Trauma in Advanced Trauma Life Support for Doctors, Instructor Course Manual, American College of Surgeons Committee on Trauma, 6th Edition, Chicago, IL, 1997.

ATLS recommendations (Fig. 1). Any injured child that shows clinical signs of hypovolemic shock should have prompt surgical consultation. A 20-mL/kg bolus of lactated ringers or normal saline is given as soon as shock is suspected. Response to this bolus is monitored. It may be repeated once or twice if perfusion is not improved. If after a second bolus of crystalloid the child is still clinically in shock, a 10-cm3/kg bolus of crossmatched packed red blood cells (or type specic or O-negative cells) should be given. At this point in the resuscitation, if the child is not in an institution capable of handling a hemodynamically unstable child, preparation for transfer should be initiated. Furthermore, if the surgeon responsible for the childs care has not been notied yet, surgical consultation is needed immediately. Children with stable spleen and liver lacerations, as well as stable fractures, will usually stabilize after a 10-cm3/kg bolus of packed cells. Those that do not and continue to exhibit signs of hypovolemic shock are likely to need their primary survey completed in the operating room. The primary survey is not complete until the child is hemodynamically stable and does not have an ongoing uid requirement. Until that time, if an adequate airway and ventilation are conrmed, hypovolemic shock must be assumed and a source sought and treated.

CONCLUSION Initial management of the pediatric trauma victim is similar to that of the adult trauma victim. However, it requires sufcient knowledge of the physiologic and anatomic differences between children and adults. Successful management requires adequate assessment and control of the airway, breathing, and circulation. Evaluation of the ABCs is a dynamic process that requires simultaneous assessment and resuscitation, as well as persistent reassessment until the child is hemodynamically

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stable. Although class-I and -II data are rare in the current literature, guidelines such as those developed through the ATLS program can be used to successfully manage most pediatric trauma victims.

REFERENCES
1. American College of Surgeons. Advanced Trauma Life Support for Doctors. Chicago, 1997. 2. Bensard DD, McIntyre RCJ, Moore EE, Moore FA. A critical analysis of acutely injured children managed in an adult level I trauma center. J Pediatr Surg 1900; 29:1118. 3. Knudson MM, Shagoury C, Lewis FR. Can adult trauma surgeons care for injured children? J Trauma Inj Infect Crit Care 1900; 32:729737. 4. Nakayama DK, Gardner MJ, Rowe MI. Emergency endotracheal intubation in pediatric trauma. Ann Surg 1900; 211:218223. 5. Gausche M, Lewis RJ, Stratton SJ, Haynes BE, Gunter CS, Goodrich SM, Poore PD, McCollough MD, Henderson DP, Pratt FD, Seidel JS. Effect of out-of-hospital pediatric endotracheal intubation on survival and neurological outcome: a controlled clinical trial [see comments] [published erratum appears in JAMA 2000 Jun 28; 283(24):3204]. JAMA 2000; 283(6):783790. 6. Martin SE, Ochsner MG, Jarman RH, Agudelo WE, Davis FE. Use of the laryngeal mask airway in air transport when intubation fails. J Trauma Inj Infect Crit Care 1900; 47:352357. 7. Lubitz DS, Seidel JS, Chameides L, Luten RC, Zaritsky AL, Campbell FW. A rapid method for estimating weight and resuscitation drug dosages from length in the pediatric age group. Ann Emerg Med 1901; 17:576581. 8. Nakayama DK, Waggoner T, Venkataraman ST, Gardner M, Lynch JM, Orr RA. The use of drugs in emergency airway management in pediatric trauma. Ann Surg 1900; 216:205211. 9. Allen GS, Cox CSJ. Pulmonary contusion in children: diagnosis and management [review] [67 Refs]. South Med J 1901; 91:10991106. 10. Lowe LH, Bulas DI, Eichelberger MD, Martin GR. Traumatic aortic injuries in children: radiologic evaluation. AJR 1900; American:3942. 11. Fabian TC, Davis KA, Gavant ML, Croce MA, Melton SM, Patton JHJ, Haan CK, Weiman DS, Pate JW. Prospective study of blunt aortic injury: helical CT is diagnostic and antihypertensive therapy reduces rupture. Ann Surg 1901; 227:666676. 12. Beaver BL, Colombani PM, Buck JR, Dudgeon DL, Bohrer SL, Haller JAJ. Efcacy of emergency room thoracotomy in pediatric trauma. J Pediatr Surg 1900; 22:1923. 13. Hazinski MF, Chahine AA, Holcomb GW, Morris JAJ. Outcome of cardiovascular collapse in pediatric blunt trauma. Ann Emerg Med 1900; 23:12291235. 14. Li G, Tang N, DiScala C, Meisel Z, Levick N, Kelen GD. Cardiopulmonary resuscitation in pediatric trauma patients: survival and functional outcome. J Trauma Inj Infect Crit Care 1900; 47:17. 15. Siegel JH, Rivkind AI, Dalal S, Goodarzi S. Early physiologic predictors of injury severity and death in blunt multiple trauma. Arch Surg 1901; 125:498508. 16. Rutherford EJ, Morris JAJ, Reed GW, Hall KS. Base decit straties mortality and determines therapy. J Trauma Inj Infect Crit Care 1901; 33:417423. 17. Kincaid E, Chang M, Letton R, Chen J, Meredith JW. Admission base decit in pediatric trauma: a study using the National Trauma Data Bank. J Trauma Inj Infect Crit Care 2001; 51:332335. 18. Iberti TJ, Kelly KM, Gentili DR, Rosen M, Katz DP, Premus G, Benjamin E. Effects of sodium bicarbonate in canine hemorrhagic shock. Crit Care Med 1901; 16:779782.

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19. Ushay HM, Notterman DA. Pharmacology of pediatric resuscitation [review] [129 Refs]. Pediatr Clin North Am 1901; 44:207233. 20. Talbott GA, Winters WD, Bratton SL, ORourke PP. A prospective study of femoral catheter-related thrombosis in children. Arch Pediatr Adolesc Med 1901; 149:288291. 21. Fiser DH. Intraosseous infusion [review] [59 Refs]. N Engl J Med 1901; 322:15791581. 22. Guy J, Haley K, Zuspan SJ. Use of intraosseous infusion in the pediatric trauma patient. J Pediatr Surg 1900; 28:158161.

5
Clearance of the Cervical Spine in Children
Brian D. Kenney
Department of Surgery, The Ohio State University, Columbus, Ohio, U.S.A.

Immobilization of the cervical spine at the scene of the injury is an important part of the early care of pediatric trauma patients. Exclusion of injury and discontinuation of immobilization (cervical spine clearance), while relatively routine in the awake, asymptomatic patient, can be very challenging in small children or in patients with a decreased level of consciousness. Expeditious clearance of the cervical spine is important to avoid the possible complications of spinal immobilization, including decubiti and aspiration. While a pediatric neurosurgeon or orthopedist is involved early for a patient with closed head injury or obvious neurological decit, a pediatric surgeon, general trauma surgeon, or emergency room physician performs the majority of cervical spine assessments on trauma patients. Clinical assessment is the most important aspect of cervical spine evaluation, but a variety of imaging modalities, including plain radiography, computed tomography (CT), and magnetic resonance imaging (MRI) can assist the clinician with decisions about discontinuation of immobilization. The judicious use of these modalities attempts to discover all injuries while avoiding the overuse of radiologic procedures and prolonged immobilization. Spinal cord injury should be considered in any victim of major blunt trauma, especially with a history of head and neck trauma or signicant exion or extension injury of the neck. The incidence of cervical spine injuries among trauma victims is relatively low (1.62.2%) with a mean age around 10 years. Motor vehicle crashes are the leading cause of cervical spinal injury (52%) followed by sports (27%) and falls (15%) (1). Nearly 70% of pediatric injuries involve the upper cervical spine (C1C4); approximately one-half are fractures and one-quarter are dislocations (2). Compared to adults, pediatric trauma victims have fewer cervical spine fractures but a higher proportion of spinal cord injury without radiographic abnormality (SCIWORA). The greater elasticity and ligamentous laxity of the pediatric cervical spine provide some protection against bony injury, but may increase the risk of SCIWORA. The incidence of SCIWORA in children ranges from 19% to 38% with the highest incidence in younger children (1,2). Protection of the cervical spine should be part of the initial evaluation of patients with signicant trauma. Early cervical spine immobilization allows for attention to resuscitation (airway, breathing, and circulation). Soft collars do not provide immobilization and should not be used after acute injuries. A variety of hard
61

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Kenney

collars are in use, but those most commonly used are the Philadelphia collar and the Miami Junior. No direct comparative study of the differences between hard collar manufacturers is available. A detailed physical examination is conducted during the secondary survey to look for supercial injury over the spine, hematoma, malalignment, tenderness, and sensory or motor decit (3). Most alert children with spinal cord injury complain of neck pain or have tenderness along the bony cervical spine, while numbness, paresthesias, or evidence of a peripheral neurological decit are rare (4). Neurologic decits can manifest as paraplegia (lower extremity paralysis) or quadriplegia (paralysis of all four extremities) along with corresponding sensory decit. Rarely, patients may present with central cord syndrome in which upper extremity symptoms are evident with normal neurologic function of lower extremities. High spinal cord injury may lead to diaphragmatic paralysis, shock, or cardiopulmonary arrest (5). After stabilization and clinical evaluation, the physician must decide if radiological studies are needed. Several professional groups, including the Eastern Association for the Surgery of Trauma (EAST) and the American College of Radiology, have promulgated guidelines for the evaluation of the cervical spine in trauma patients (6,7). The guidelines are perhaps best documented by EAST, which performed a computerized search of the National Library of Medicines Medline database, looking at 20 years of citations with cervical spine in the title and subject words radiography, cervical vertebra, and/or trauma. The articles were classied according to study design. No randomized controlled trials (class I) and few prospective, nonrandomized (class II) studies were found. Recommendations were mainly based on retrospective studies (class III) that can be weakened by bias in patient selection, symptom detection, choice of diagnostic studies, or options for treatment. In addition, retrospective studies may be hampered by lack of complete patient follow-up. The published guidelines do not specically discuss pediatric trauma patients. Therefore, for this review, the Medline search was repeated using the same parameters with restriction to children (aged 118 years) and articles published since 1990. Recommendations concerning the evaluation of the cervical spine in children are based on the EAST guidelines as well as the more recent references with ndings related to children. The published guidelines are consistent with respect to patients who are completely asymptomatic with no physical ndings, normal mentation, and no distracting injuries, proposing that these patients do not require radiological evaluation. Recent studies support the conclusion that asymptomatic patients do not need screening radiography (810), but include few pediatric patients. One study of pediatric patients supported the view that fractures will usually manifest symptoms but the study included only eight injured patients and was restricted to falls of less than ve feet (11). All of these studies were retrospective, making comparison of clinical and radiologic ndings subject to signicant bias. For a valid comparison of clinical and radiologic evaluation, clinical ndings must be recorded prospectively, prior to radiographs. One such study was recently done primarily in adult patients (aged 1493 years) (12). Consecutive blunt trauma patients who were alert on admission (GCS 14 or 15) were evaluated for cervical spine injury. Symptoms and physical ndings were documented on study forms that were then placed in sealed envelopes prior to radiographic studies. Of the 2176 patients, 33 (1.6%) were found to have cervical spine injuries. Three missed injuries were seen in 1768 asymptomatic patients with normal clinical examination (sensitiv-

Clearance of the Cervical Spine in Children

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ity > 99%). In one of these, the fracture was also missed on screening lateral C-spine radiography, but was found with further radiography due to the onset of pain one day after admission. The sensitivity of radiography when blinded to clinical data was 61% as 13 of 33 injuries were missed. Radiography is clearly decient without clinical examination, but even when used together they are not perfect in immediately nding all injuries. A recent multicenter study prospectively tested cervical spine evaluation guidelines in a population of 34,069 adults and children who underwent radiography of the cervical spine after blunt trauma (13). The ve criteria in the decision rule that dened a low probability of injury (screening X rays unnecessary) were: no midline cervical tenderness, no focal neurological decits, normal alertness, no intoxication, and no painful distracting injuries. The study identied 12% of patients who could have avoided radiographic evaluation according to the decision rule. The screening tool was predictive in 810 of 818 patients who had radiographically documented cervical spine injury. Of the eight patients identied as low probability of injury who had a radiographically documented cervical injury, only two were felt to have a clinically signicant injury, according to predened criteria in the study. Unfortunately, the study did not extensively evaluate pediatric patients: only 2.5% of patients were eight years old or younger, and 1.3% of patients with cervical spine injuries were eight years old or younger. Patients who are asymptomatic with respect to the cervical spine (no cervical pain or tenderness; no neurologic decit), but have injuries that may distract their attention, should have cervical spine lms to screen for injury. One recent retrospective study questioned these recommendations, but the study population was small and did not include children (9). Most pediatric trauma patients do not meet all of the criteria for a low probability of injury and, therefore, should undergo screening radiological examination. Plain radiography may show bony deformity/fracture, malalignment (especially of the posterior aspect of vertebral bodies), asymmetry of distance between spinous processes, vertebral canal narrowing, or increased prevertebral soft tissue. A lateral C-spine radiograph is the minimal study for screening and must include the base of the occiput down to the upper portion of the rst thoracic vertebra (Fig. 1). The addition of odontoid and anterior/posterior views does increase sensitivity and specicity (14). Some have questioned the value of the anterior/posterior view when odontoid and lateral views are normal (15). Some authors would also include oblique views for screening. Many trauma patients (1015%) require more than the initial screening radiography to completely visualize the cervical spine (16,17). Supplemental swimmers views are sometimes required to visualize the lower cervical spine and its junction with thoracic vertebra. Axial CT scans with sagittal reconstruction can help to evaluate the extremes of the upper or lower cervical spine when they are difcult to see on plain lms or to elucidate abnormalities seen on plain radiography (Figs. 24). CT can also help with spurious abnormalities that are often seen in pediatric patients, including pseudosubluxation of C3 on C4 or skeletal growth centers (apical odontoid epiphyses and basilar odontoid synchondrosis) (18). Patients with symptoms of pain or tenderness whose initial screening radiographs are normal often undergo exion and extension lms in the erect position to evaluate for ligamentous injuries. EAST recommends these lms be obtained with the patient actively positioning the neck in extreme exion and extension (6). The value of these additional lms has been questioned in children (19). A careful

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Figure 1 Compression fracture, anterior, superior portion of C7 sustained by a 15-year-old who fell 8 feet from a swing.

retrospective comparison of static cervical lms followed by exion/extension lms concluded that the additional lms were not helpful when plain lms were normal (no acute abnormality and no loss of normal lordosis) (20). Other authors recommend MRI because of excellent detail of soft tissue injuries, including vessel injuries, ligament disruption, disc herniation, and spinal cord injury or hematoma (Fig. 5) (21,22). Fractures are not always seen on MRI, thus plain radiographs should precede MRI studies. No consensus exists for symptomatic patients in whom all studies are negative. Some authors recommend, in addition to neurosurgical consult, the use of a stiff collar for two weeks, followed by repeat clinical exam and plain radiography (16). Patients with neurological decits but no obvious abnormalities on plain X ray (SCIWORA) should undergo MRI of the cervical spine. In the evaluation of soft tissue or spinal cord injury, magnetic resonance is superior to plain radiography or CT scan (21,23). Early neurosurgical evaluation is needed for consideration of therapies that may improve outcome, such as systemic steroids or surgical decompression. Patients with closed head injury or obtundation are a special challenge for evaluation. Most of these patients undergo three-view screening X rays, but the

Clearance of the Cervical Spine in Children

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Figure 2 A 4-year-old who struck a table after jumping from a chair. The minimal anterior tilt of the odontoid process relative to the vertebral body of C2 was difcult to interpret because of the synchondrosis. The fracture was conrmed by the nding of abnormal irregular lucency along the base of the odontoid on a 3D reconstruction of thin-cut computed tomography.

adequacy and quality of these lms is frequently compromised by lack of cooperation. Blacksin and Lee suggest that inclusion of the upper cervical spine during cranial CT scan for the head injury (thin cut axial CT images through C1 and C2) can simplify this problem (24). Because not all patients had complete plain radiography, no direct comparison was made between the sensitivity of plain radiography versus CT. When C-spine abnormalities are seen on a limited upper cervical CT scan, the remainder of the C-spine must be evaluated to look for other injuries, either with plain C-spine lms or with CT scanning. Some have advocated routine complete cervical CT scanning in closed head injured or obtunded patients rather than or in addition to the lateral C-spine radiograph (25,26). In a prospective, blinded study of adult patients (17 years) who had both plain radiography and CT of the cervical spine, specicity was 100% for both studies, but sensitivity for CT was 90% versus only 60% for plain radiography (25). Of two injuries seen by plain radiography but not CT, both were considered stable. The fact that all of the injuries were seen by CT or plain radiography and that no patient suffered a delayed diagnosis suggests

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Figure 3 (A) Motor vehicle injury in a 17-year-old patient resulting in fractures through the posterior neural arch of C1 and pedicles of C2 with anterior displacement. (B) Further denition of fractures was aided by computed tomography.

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Figure 4 Cervical spine lm of a 10-year-old following a trampoline injury raised concern about possible subluxation of C2 relative to C3. Computed tomography showed no evidence of fracture or soft tissue swelling, which conrmed that the original ndings represented pseudosubluxation.

inadequate description of patient follow-up or retrospective inclusion of suspicious results as positive when later conrmed by other studies. Despite these limitations, CT is probably the most sensitive study for bony cervical injury in obtunded patients. Even after normal C-spine evaluation with plain radiographs or CT scan, physicians are reluctant to discontinue immobilization in patients who do not allow reliable clinical examination. Patients can be immobilized for 24 to 48 hours to allow time for improved wakefulness and repeat assessment. For patients who remain unreliable, one study suggests cervical exion and extension under uoroscopy with concomitant monitoring of somatosensory evoked potentials (SSEP): patients with normal studies were cleared; malalignment leads to a neurosurgical consultation; and abnormal SSEP leads to an MRI (27). Normal MRI allowed for clearance of the C-spine. The algorithm was complicated and included too few patients, but further studies are ongoing. The published guidelines promote thorough evaluations but also attempt to diminish the number of unnecessary radiographic examinations. Emergency centers vary greatly in the use of radiography to evaluate trauma patients. A recent survey showed a low of 15.6% of trauma patients evaluated with radiography at one center to a high of 91.5% (28). Differences in missed injuries were not observed but the study follow-up was poor. The validity of guidelines depends on the ability of clinicians to understand and properly apply criteria. In trying to implement clinical guidelines, the reliability of individual criteria was evaluated in a prospective study (29). Physicians showed substantial inter-rater reliability (high k scores) for evaluation of altered neurologic

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Figure 5 A 12-year-old with a trampoline injury and neck pain. (A) Computed tomography showed fracture of superior aspect of odontoid. (B) The 1-cm fragment was displaced anterior and inferior. (C) Magnetic resonance imaging revealed severe central canal stenosis at the cervical-medullary junction and edema within the cervical cord at the C2 and C3 levels. In addition, distension of the cerebrospinal uid spaces within the posterior fossa was evident, likely due to the degree of stenosis.

function (83.6%, Ks 0.58), intoxication (96.7%, Ks 0.86), posterior midline tenderness (89.3%, Ks 0.77), distracting injury (91.8%, Ks 0.77), and all criteria combined (87.7%, Ks 0.73). In another prospective study, emergency medical technicians (EMTs) were not able to reliably eliminate the possibility of spinal cord injury by use of a similar decision rule. Over half of patients who were cleared clinically by EMTs were immobilized by physicians and required radiography on arrival to the hospital. Low k scores between emergency physicians and EMTs were noted for several of the clinical criteria on which the decision rule was based, including: mechanism consistent with injury, reliable mental status, presence of distracting injury, neck pain or tenderness, neurologic decit, and neck pain with motion (30). The k scores were < 0.5 for all criteria except reliable mental status. Considered together these studies suggest that the implementation of guidelines for cervical spine evaluation requires clinical examination and sophisticated judgment by experienced physicians.

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Figure 6 Algorithm for clearance of the cervical spine in children.

Many different algorithms for clearance of the cervical spine have been published (16,27,30). The algorithms differ in a variety of ways: presenting symptoms, physical ndings, complexity of radiologic assessment, and nal disposition of patients. Considering the current interpretation of the published studies, an algorithm was developed that attempts to triage patients into separate categories to provide efcient care (Fig. 6). Expert interpretation is required at each decision point. The physician caring for trauma victims has many choices to aid in the evaluation of the cervical spine. Proper understanding of the epidemiology of the cervical spine injury, careful attention to the history of the traumatic incident, elucidation of current symptoms, a careful neurological examination, and judicious radiographic

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testing should allow appropriate care of these patients. The evaluation must be carried out in the context of a cervical spine that is immobilized to avoid the possibility of secondary injury.

REFERENCES
1. Brown RL, Brunn MA, Garcia VF. Cervical spine injuries in children: a review of 103 patients treated consecutively at a level-1 pediatric trauma center. J Pediatr Surg 2001; 36(8):11071114. 2. Kokoska ER, Keller MS, Rallo MC, Weber TR. Characteristics of pediatric cervical spine injuries. J Pediatr Surg 2001; 36(1):100105. 3. Subcommittee on Advanced Trauma Life Support of the American College of Surgeons. Spine and Spinal Cord Trauma. In: Advanced Trauma Life Support Manual. 6th ed. Chicago, 1997:263300. 4. Dietrich AM, Ginn-Pease ME, Bartkowski HM, King DR. Pediatric cervical spine fractures: predominantly subtle presentation. J Pediatr Surg 1991; 26:995999; discussion 9991000. 5. Bohn D, Armstrong D, Becker L, Humphreys R. Cervical spine injuries in children. J Trauma 1990; 30:463469. 6. Pasqual M. Practice management guidelines for trauma: EAST ad hoc committee on guideline development: identifying cervical spine instability after trauma. J Trauma 1998:945946. See also the practice management guidelines at [Link]. 7. American College of Radiology Appropriateness Criteria2 for cervical spine trauma at [Link]. 8. Velmahos GC, Theodorou D, Tatevossian R, Belzberg H, Cornwell EE 3rd, Berne TV, Asensio JA, Demetriades D. Radiographic cervical spine evaluation in the alert asymptomatic blunt trauma victim: much ado about nothing. J Trauma 1996; 40:768774. 9. Saddison D, Vanek VW, Racanelli JL. Clinical indications for cervical spine radiographs in alert trauma patients. Am Surg 1991; 57:366367. 10. Lindsey RW, Diliberti TC, Doherty BJ, Watson AB. Efcacy of radiographic evaluation of the cervical spine in emergency situations. South Med J 1993 Nov; 86(11):12531255. 11. Schwartz GR, Wright SW, Fein JA, Sugarman J, Pasternack J, Salhanick S. Pediatric cervical spine injury sustained in falls from low heights. Ann Emerg Med 1997; 30: 249252. Published erratum appears in Ann Emerg Med 1998 Jan; 31(1):141. 12. Gonzalez RP, Fried PO, Bukhalo M, Holevar MR, Falimirski ME. Role of clinical examination in screening for blunt cervical spine injury. J Am Coll Surg 1999; 189:152157. 13. Hoffman JR, Mower W, Wolfson AB, Todd KH, Zucker M. Validity of a set of clinical criteria to rule out injury to the cervical spine in patients with blunt trauma. NEJM 2000; 343(2):9499. 14. West OC, Anbari MM, Pilgram TK, Wilson AJ. Acute cervical spine trauma: diagnostic performance of single-view versus three-view radiographic screening. Radiology 1997; 204:819823. 15. Holliman CJ, Mayer JS, Cook RT Jr, Smith JS Jr. Is the anteroposterior cervical spine radiograph necessary in initial trauma screening? Am J Emerg Med 1991; 9:421425. 16. Banit DM, Grau G, Fisher JR. Evaluation of the acute cervical spine: a management algorithm. J Trauma 2000; 49:450456. 17. Moulton C, Grifths PD. The adequacy of cervical spine radiographs in the accident and emergency department. J R Soc Med 1993; 86:141143. 18. Subcommittee on Advanced Trauma Life Support of the American College of Surgeons. Pediatric Trauma. In: Advanced Trauma Life Support Manual. 6th ed. Chicago, 1997:353376.

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19. Dwek JR, Chung CB. Radiography of cervical spine injury in children: are exion-extension radiographs useful for acute trauma? AJR Am J Roentgenol 2000; 174:16171619. 20. Ralston ME, Chung K, Barnes P, Emans JB, Schutzman SA. Role of exion-extension radiographs in blunt pediatric cervical spine injury. Acad Emerg Med 2001; 8:237245. 21. Katzberg RW, Benedetti PF, Drake CM, Ivanovic M, Levine RA, Beatty CS, Nemzek WR, McFall RA, Ontell FK, Bishop DM, Poirier VC, Chong BW. Acute cervical spine injuries: prospective MR imaging assessment at a level-1 trauma center. Radiology 1999; 213:203212. 22. Benzel EC, Hart BL, Ball PA, Baldwin NG, Orrison WW, Espinosa MC. Magnetic resonance imaging for the evaluation of patients with occult cervical spine injury. J Neurosurg 1996; 85:824829. 23. Flanders AE, Schaefer DM, Doan HT, Mishkin MM, Gonzalez CF, Northrup BE. Acute cervical spine trauma: correlation of MR imaging ndings with degree of neurologic decit [see comments]. Radiology 1990; 177:2533. 24. Blacksin MF, Lee HJ. Frequency and signicance of fractures of the upper cervical spine detected by CT in patients with severe neck trauma. AJR Am J Roentgenol 1995; 165:12011204. 25. Berne JD, Velmahos GC, El-Tawil Q, Demetriades D, Asensio JA, Murray JA, Cornwell EE, Belzberg H, Berne TV. Value of complete cervical helical computed tomographic scanning in identifying cervical spine injury in the unevaluable blunt trauma patient with multiple injuries: a prospective study [see comments]. J Trauma 1999; 47:896902; discussion 902903. 26. Nunez DB Jr, Zuluaga A, Fuentes-Bernardo DA, Rivas LA, Becerra JL. Cervical spine trauma: how much more do we learn by routinely using helical CT? Radiographics 1996; 16:13071318; discussion 13181321. 27. Scarrow AM, Levy EI, Resnick DK, Adelson PD, Sclabassi RJ. Cervical spine evaluation in obtunded or comatose pediatric trauma patients: a pilot study. Pediatr Neurosurg 1999; 30:169175. 28. Stiell IG, Wells GA, Vandemheen K, Laupacis A, Brison R, Eisenhauer MA, Greenberg GH, MacPhail I, McKnight RD, Reardon M, Verbeek R, Worthington J, Lesiuk H. Variation in emergency department use of cervical spine radiography for alert, stable trauma patients. CMAJ 1997; 156:15371544. 29. Mahadevan S, Mower WR, Hoffman JR, Peeples N, Goldberg W, Sonner R. Interrater reliability of cervical spine injury criteria in patients with blunt trauma. Ann Emerg Med 1998; 31:197201. 30. Meldon SW, Brant TA, Cydulka RK, Collins TE, Shade BR. Out-of-hospital cervical spine clearance: agreement between emergency medical technicians and emergency physicians. J Trauma 1998; 45:10581061.

6
Trauma from Child Abuse
Charles S. Cox, Jr.
Department of Surgery, Division of Pediatric Surgery, University of Texas-Houston Medical School, Houston, Texas, U.S.A.

INTRODUCTION Caffey and Kempe rst focused the medical communitys attention on the problem of child abuse by identifying an association between long bone fractures and subdural hematomas in children. Further work led to Kempes symposium and article The Battered Child Syndrome (13). As awareness increased, it became clear that a constellation of injuries is associated with child abuse and that these injuries occur in patterns. Because the history is often unreliable or deliberately deceptive, the recognition of known patterns of injury and the judicious use of diagnostic imaging are important in the evaluation of these patients. Unfortunately, prospective, randomized, controlled trial data on child abuse are unavailable. Since the treatment of most of the injuries associated with child abuse is well described elsewhere in this and other texts, this chapter will not review the treatment of specic injuries. Instead, it will attempt to assist the practitioner in deciding whether identied injuries could be caused by the reported mechanism and in recognizing the unique associations that have been previously identied.

LITERATURE-BASED GUIDELINES The author examined the literature obtained from MEDLINE from 1990 to 2000 and classic articles from earlier time periods. There were no class-I papers. Thus, standards of care cannot be developed according to the denitions of evidence-based medicine. A few papers t into class II (prospectively collected data submitted to retrospective analysis). Most were class III. There is a vast amount of empirically derived information that is supported by class-III data.

EPIDEMIOLOGY Child abuse accounts for 3% to 4% of all traumatic injuries evaluated in pediatric trauma centers. However, abuse and assault result in the highest injury severity
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74 Table 1 Deaths Due to Child Abuse or Neglect Age <1 14 59 1014 Percent of all deaths 41% 49% 4% 2%

Cox

and mortality of all mechanisms of injury (National Pediatric Trauma Registry, 1998). Estimates of fatal child abuse and neglect have been tabulated using death certicate data and statistical modeling. Serious abuse occurs most often in children under ve years of age (Table 1) (4). The National Incidence Study of Child Abuse and Neglect studied the relative impact of demographic characteristics of the child, family structure, and economic variables on types of child abuse and neglect (5). Physically abused children were more likely to live in poverty with mothers who were unemployed. Race had little inuence on the likelihood of neglect or abuse.

INITIAL EVALUATION AND TREATMENT History The history of the presenting illness or injury is a critical component of the initial evaluation of inicted injury in children. The typical nding is a discrepant history that is modied over time as the caretaker adapts the history to developing medical information. Therefore, documentation of each interaction is important to catalog the evolution of the history during the hospitalization. Because the history is often unreliable, most injuries are discovered by physical exam and imaging studies. Clinical Presentation Unexplained Loss of Consciousness or Shock Seriously abused children are often evaluated for an unexplained loss of consciousness or shock. As with any life-threatening injury or clinical situation with hemodynamic instability, standard resuscitative interventions are employed. When the history is not consistent with the clinical scenario, or there are external signs of abuse, the evaluation should focus on imaging studies to dene the injury. Typically, computed tomography (CT) scanning of the head and of the abdomen and pelvis during the same radiographic session are useful for demonstrating intra- and extra-cranial pathology as well as visceral injury. The imaging studies help classify the mechanism and timing of injury. The evaluation of these children also includes retinal examination using indirect ophthalmoscopy by an ophthalmologist, soft tissue examination to evaluate for patterned bruising or burns, as well as careful palpation for point tenderness suggesting acute fractures. Children less than ve years old should also undergo a skeletal survey to evaluate for occult bony injuries. External and Soft Tissue Trauma Injuries to the skin and soft tissue include burns (contact and immersion), bruises, and patterned marks and scars. Patterns and locations of burns and bruises are often

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self-explanatory, e.g., clothing iron imprint directly on the back or thigh, or handshaped bruise on the cheek. All of these physical ndings can be correlated with the history. Pathologic bruising can be a source of confusion. This can usually be eliminated by routine coagulation studies. Bruises of the buttocks, perineum, or abdomen, or multiple bruises of varying ages, are suspicious for inicted injury. Inicted burns are usually either immersion or pattern-type injuries due to a hot object. Immersion burns often occur in a stocking/glove distribution or on the buttocks and posterior surfaces of the thighs, legs, and feet. Pattern burns such as those caused by an iron are rarely unintentional. Fractures Fractures are brought to the attention of the physician in three ways: (1) acute evaluation for fracture-related signs and symptoms, (2) incidental discovery of old fractures on another radiographic study, and (3) by skeletal survey. The most critical step in determining the etiology of the fracture is the correlation of the injury with the age and development of the child. Fracture patterns and their associations with intentional injury are discussed below. Imaging Studies Skeletal Survey All infants and children under ve years of age with suspected abuse should undergo a skeletal survey. Postmortem skeletal surveys should be performed on all children who die when abuse is suspected. High-detail systems with specic images should be performed, avoiding the baby-gram technique. Repeat imaging in one to two weeks may show injuries not readily apparent on the initial survey due to the development of fracture calluses. Nuclear Medicine Bone scintigraphy has been suggested as an alternative or complementary imaging method to plain radiographs for occult fractures associated with child abuse (68). There have been no denitive studies demonstrating the superiority of one over the other. The major value of radionuclide scintigraphy is its increased sensitivity for periosteal trauma of the extremities and trauma of complex anatomic structures such as the spine, ribs, and scapula. Thus, scintigraphy can further characterize or rule out multiple injuries in the child with a suspected mechanism of abuse. Neuroradiology CT of the brain is critical in the management of traumatic brain injury (TBI). Magnetic resonance (MR) imaging is less readily available in the acute setting. Thus CT is the primary imaging modality for central nervous system (CNS) trauma in most institutions. MR imaging can be useful in the less acute setting to more precisely dene chronic abnormalities. A class-II study compared two groups of patients with similar Glasgow Coma Scores and perinatal histories, categorizing the TBI as either accidental or inicted (9). Patients with inicted TBI had higher rates of subdural, interhemispheric, and convexity hemorrhages and signs of pre-existing abnormalities such as cerebral atrophy, subdural hygroma, and ex vacuo ventriculomegaly. Subdural hygroma occurred exclusively in patients with inicted TBI with atrophy, suggesting

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a previously undetected TBI. Intraparenchymal hemorrhage, shear injury, and skull fractures were more frequent after accidental TBI.

CNS INJURY Shaken-Infant Syndrome Caffey rst postulated a link between shaking infants and intracranial and intraocular hemorrhage without evidence of external trauma (1,2). This has become known as the shaken-infant syndrome or shaken-baby syndrome. Many infants with this syndrome also show signs of impact injury to the head, ranging from skull fractures to soft tissue injury. Thus, it is often referred to as the shaken-impact syndrome (10). Often these infants present with sudden death (SIDS), seizures, coma, or apnea. The risk of any child suffering non-accidental head injury by this mechanism in their rst year has been estimated to be one in 4000 (11). Intracranial hemorrhage and retinal hemorrhage are key elements of this syndrome. Associated ndings may include long bone fractures or rib fractures. In shaken-infant syndrome, the subdural hematoma is usually not associated with signs of external trauma. The cause of the subdural hematoma is avulsion of the venous bridges between the brain and dura due to the rapid acceleration and deceleration that occurs with violent shaking (2). External head trauma technically changes the classication of the injury to shaken-impact syndrome. There may also be associated skull fractures. Accidental subdural hematoma is rare in infants, and is not typically related to low-level (<4 feet) falls. In the absence of a highenergy mechanism of injury, such as a motor vehicle crash or fall from a signicant height, child abuse must be considered in every case of subdural hematoma in children. In the clinical scenario of reported minimal trauma in infants, the presence of a skull fracture without intracranial injury suggests accidental trauma, whereas skull fractures and intracranial bleeding or intracranial bleeding alone are highly suggestive of child abuse (12). A critical, although not mandatory, component of the diagnosis of shakeninfant syndrome is the presence of retinal hemorrhage. This nding must be evaluated and rigorously documented by an ophthalmologist. The validity of clinical information and diagnostic studies in shaken-infant cases is dependent on the completeness of the retinal examination. A full assessment includes indirect ophthalmoscopy to examine the peripheral retina. One study demonstrated that 29% of patients with retinal hemorrhages were not detected by non-ophthalmologists (13). Complete postmortem ocular evaluation (including the optic nerve) is the gold standard for the diagnosis of retinal hemorrhage (14). The mechanism that produces retinal hemorrhage is the subject of debate in the literature. One theory postulates that an abrupt increase in intracranial pressure results in venous obstruction and retinal hemorrhage. This may be augmented by abrupt increases in intrathoracic pressure due to thoracic compression. A second theory holds that acceleration/deceleration forces result in traction of the vitreous on the retina with hemorrhagic retinoschisis cavities. Numerous class-II and -III studies show that retinal hemorrhages occur only rarely (<5%) with severe head trauma and not at all with moderate or mild head trauma (15,16). Other causes of retinal hemorrhage in infants include birth trauma, cardiopulmonary resuscitation (CPR), hematological diseases, and ruptured vascular malformations. With rare exceptions, CPR does not cause retinal hemorrhage (14,1719). Bacon et al. and Kirschner and Stein each reported a case of retinal hemorrhage in an

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infant after vigorous resuscitation (20,21). Purtscher retinopathy, a lesion of diverse pathophysiolgic origin, is a rare cause of retinal hemorrhage. However, this is rarely the cause of retinal hemorrhage and should be interpreted in the context of the clinical presentation.

ABDOMINAL INJURY Although the true incidence of abdominal trauma as a result of child abuse is unknown, it is less common than burns, head injuries, and musculoskeletal injuries (22). The most common mechanism is a direct blow to the mid-epigastrum. This compresses the abdominal viscera against the thoracolumbar spine, which can in turn produce a burst injury to the intestine, pancreatic contusion or transection, duodenal hematoma or perforation, or mesenteric laceration (Figs. 1 and 2) (23,24). As with any blunt abdominal trauma, bleeding from a solid organ injury can also occur. Children with abdominal injuries tend to be older than those with shaken-infant/ shaken-impact syndrome. The mean age of children with severe intra-abdominal injuries is two years old. The mortality rate is 45% (23). Patients with abdominal injuries secondary to abuse often present in shock late after their injuries. The cornerstones of the diagnosis of these injuries are the physical exam and CT scan of the abdomen and pelvis. Ultrasound is less helpful. The focused abdominal sonography for trauma

Figure 1 Flat abdominal radiograph demonstrating massive free intraperitoneal air. This was due to a jejunal perforation from a direct blow to the mid-abdomen.

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Figure 2 Intra-operative photograph of the child whose radiographs are depicted in Figures 1 and 3. Note the avulsed proximal jejunum with perforation. The forceps are within the lumen of the avulsed segment, demonstrating the perforation. The child was struck in the midabdomen approximately 12 to 18 hours prior to presentation in hemorrhagic shock.

Figure 3 Skeletal survey demonstrating rib fractures with fracture calluses noted. These ndings were detected on the skeletal survey of the child whose injuries are shown in Figures 1 and 2. These old fractures and new injuries are pathognomonic of abuse.

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(FAST) exam may play a role in the prioritization of injury management in the multisystem injured child, but CT scanning provides more complete, organ specic information. Patients with other injuries from non-accidental mechanisms should undergo CT scanning of the abdomen and pelvis to evaluate for occult intra-abdominal injuries. While minor solid organ injuries in hemodynamically stable patients may be managed nonoperatively, patients with hemoperitoneum often present late after their injuries and in hypovolemic shock. The principles of management of abdominal injury due to blunt abdominal trauma have been applied successfully to these injuries.

FRACTURES AND FRACTURE PATTERNS Caffey recognized the pattern of fractures and head injury that are indicative of nonaccidental injury (1). Eighty percent of non-accidental fractures occur in children less than 18 months of age (25). In evaluating a child with one or more fractures, a careful history and physical exam, with particular focus on age and developmental milestones, are important. A critical comparison of the history with the physical ndings helps to determine the likelihood of fractures being intentionally inicted. The discovery of multiple fractures in different stages of healing or fractures inconsistent with the developmental age of the child or the reported mechanism should raise suspicion of non-accidental trauma. The presence of a non-accidental fracture places the child at high risk for subsequent injuries and child protective services (CPS) notications (26). Long Bone Fractures Femur Long bone fractures, without consideration of mechanism, age of the patient, or associated injuries, have a low specicity for child abuse (27). Spiral fractures have been classically viewed as pathognomonic of abuse in non-walking children. In a class-III study, Scherl et al. noted that the majority of fractures in children were transverse, and that this was also the most common pattern in cases of conrmed abuse. Because transverse fractures are often not felt to be caused by abuse, they are less frequently the subject of investigation (28). Perhaps the most important factor in assessing the probability of abuse with femur fractures is age. In children less than 12 months old, 60% to 80% of femoral fractures are related to abuse. In contrast, femoral fractures are almost never related to abuse in children older than two years of age (29,30). Humerus The location of the humeral fracture is the most important distinguishing feature to delineate between accidental and non-accidental fractures. In infants and toddlers, mid-shaft and metaphyseal fractures are more likely to be related to abuse, whereas supracondylar fractures are usually due to accidental falls (25,29). Rib Fractures Rib fractures are uncommon in childhood, mainly because it requires a high-energy impact to break a childs rib. Rib fractures are believed to result from anterior posterior thoracic compression during violent shaking (Fig. 3). It has been estimated that 85% to 100% of rib fractures in infants are due to abuse (29,31). Most reports

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state that fractures due to abuse occur in the posterior part of the rib near the costovertebral junction where the rib articulates with the transverse process (32). However, some studies claim that fractures caused by abuse can also occur in the anterior and lateral aspects of the rib (6). A postmortem radiologichistopathologic study using high resolution radiographic techniques demonstrated that the majority of rib fractures are not detected by routine skeletal surveys (33). CPR is often implicated as a cause of rib fractures in children. This arose from reports of rib fractures in adults after CPR (34). However, as is true for retinal hemorrhages from CPR, this association is either nonexistent or extremely rare in children. Class-II and -III data report that 0% to 3% of pediatric rib fractures result from CPR (6,7). Regardless of location, rib fractures are a marker for severe thoracic injury. If rib fractures are not explainable by a high-energy impact motor vehicle crash or autopedestrian injury) or intrinsic bone disease, then child abuse should be considered as a possible cause. STAIRWAY INJURIES AND LOW-LEVEL FALLS Stairway falls are common during childhood. As opposed to falls from a height, stairway falls are discretely quantiable without the confounding variable of hitting another object. Falls down stairways are often implicated as the mechanism of injury by caregivers after non-accidental trauma. Knowledge of the expected injury patterns and injury severity may provide a more objective basis for the diagnosis of nonaccidental trauma. Two class-II studies have specically addressed the issue of injury pattern after stairway-related injury (35,36). Both studies concluded that truncal injuries were rare (23%) and that head, neck, and distal extremity injuries were common (7090%). Importantly, multiple injuries involving more than one body region were rare. While extremity injuries are common, one class-III study of 363 children found no instances of femur fractures from a stairway or low-level fall (35). Indeed, intestinal perforation as a result of stairway falls has never been reported. A 29-year review of all English language publications demonstrated no intestinal perforations due to an unobstructed stairway fall (37). Therefore, intestinal perforation after a reported stairway fall should be viewed as highly suspicious.

PHYSICIAN RESPONSIBILITIES It is the duty of the examining physician to report all suspected cases of child abuse to CPS. It is not the duty of the physician to be absolutely certain that suspicious injuries or circumstances are related to abuse. Most large childrens facilities have child protection teams that consist of social workers, nurses, and physicians with expertise in this area. Following CPS notication, a written physicians statement is required to document the basis for the reasonable suspicion, the probable mechanism of injury, its severity, and the actual and anticipated medical consequences. The physician who prepares this statement must be prepared to testify about their ndings in court. Many physicians and CPS teams nd that medical photographs of the described injuries assist in communicating and memorializing the physical ndings in their report. Diseases such as osteogenesis imperfecta, Menkes syndrome (sex-linked recessive copper deciency), temporary brittle bone disease, and congenital syphilis can cause bony abnormalities that mimic the effects of child abuse (38,39). Hemophilia, purpura fulminans, or other disorders of coagulation may present with bruising and

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frank bleeding, suggesting trauma. The history may appear inconsistent with the physical exam if the examiner is unfamiliar with these diseases. HermanskyPudlak syndrome (functional platelet disorder) has presented with both subdural hematoma and retinal hemorrhage in an infant (40). Mongolian spots may be mistaken for contusions. Physicians accustomed to evaluating children for suspected abuse learn to recognize most of these diagnoses. In fatal cases, autopsy results can clarify the diagnosis. In nonfatal cases a pediatric specialist trained in the evaluation of child abuse should assess all children with suspected abuse to minimize the possibility of a mistaken diagnosis.

REFERENCES
1. Caffey J. Multiple fractures in the long bones of infants suffering from chronic subdural hematoma. Am J Res 1946; 56:163168. 2. Caffey J. On the theory and practice of shaking infants: its potential residual effects of permanent brain damage and mental retardation. Am J Dis Child 1972; 124:161169. 3. Kempe CH, Silverman FN, Steele BF, Droegemueller W, Silver HK. The battered-child syndrome. JAMA 1962; 181:1724. 4. McClain PW, Sacks JJ, Froehlke RG, Ewigman BG. Estimates of fatal child abuse and neglect, United States, 1979 through 1988. Pediatrics 1993; 91:338343. 5. Jones ED, McCurdy K. The links between types of maltreatment and demographic characteristics of children. Child Abuse Negl 1992; 16:201215. 6. Feldman KW, Brewer DK. Child abuse, cardiopulmonary resuscitation, and rib fractures. Pediatrics 1984; 73:339342. 7. Bush CM, Jones JS, Cohle SD, Johnson H. Pediatric injuries from cardiopulmonary resuscitation. Ann Emerg Med 1996; 28:4044. 8. Conway JJ, Collins M, Tanz RR, Radkowski MA, Anandappa E, Hernandez R, Freeman EL. The role of bone scintigraphy in detecting child abuse. Semin Nucl Med 1993; 23:321333. 9. Ewing-Cobbs L, Prasad M, Kramer L, Louis PT, Baumgartner J, Fletcher JM, Alpert BA. Acute neuroradiologic ndings in young children with inicted or noninicted traumatic brain injury. Childs Nerv Syst 2000; 16:2534. 10. Duhaime AC, Christian CW, Rorke LB, Zimmerman RA. Nonaccidental head injury in infantsthe shaken-baby syndrome. NEJM 1998; 338:18221829. 11. Barlow KM, Minns RA. Annual incidence of shaken impact syndrome in young children. Lancet 2000; 356:15711572. 12. Billmire ME, Myers PA. Serious head injury in infants: accident or abuse? Pediatrics 1985; 75:340342. 13. Kivlin JD, Simons KB, Laxoritz S, Ruttum MS. Shaken baby syndrome. Ophthalmology 2000; 107:12461254. 14. Gilliland MGF, Luckenbach MW. Are retinal hemorrhages found after resuscitation attempts? Am J Forensic Med Pathol 1993; 14:187192. 15. Duhaime AC, Alario AJ, Lewander WJ, Schut L, Sutton LN, Seidl TS, Nudelman S, Budenz D, Hertle R, Tsiaras W, Loporatio S. Head injury in very young children: mechanisms, injury types, and ophthalmologic ndings in 100 hospitalized patients younger than 2 years of age. Pediatrics 1992; 90:179185. 16. Buys Y, Levin AV, Enzenauer RW, Elder JE, Letourneau MA, Humphreys RP, Mian M, Morin JD. Retinal ndings after head trauma in infants and young children. Ophthalmology 1992; 99:17181723.

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17. Kanter RK. Retinal hemorrhage after cardiopulmonary resuscitation or child abuse. J Pediatr 1986; 108:430432. 18. Budenz DL, Farber MG, Mirchandani HG, Park H, Rorke LB. Ocular and optic nerve hemorrhages in abused infants with intracranial injuries. Ophthalmology 1994; 101:559565. 19. Goetting MG, Sowa B. Retinal hemorrhage after cardiopulmonary resuscitation in children: an etiologic reevaluation. Pediatrics 1990; 85:585588. 20. Bacon DJ, Sayer GC, Howe JW. Extensive retinal hemorrhages in infancy. An innocent cause. Br Med J 1978; 281:1. 21. Kirschner RH, Stein RJ. The mistaken diagnosis of child abuse. Am J Dis Child 1985; 139:873875. 22. Caniano DA, Beaver BL, Boles ET. Child abuse: an update on surgical management in 256 cases. Ann Surg 1986; 203:219224. 23. Cooper A, Floyd T, Barlow B. Major blunt abdominal trauma due to child abuse. J Trauma 1988; 28:14831485. 24. Tracy T, OConnor JP, Weber TR. Battered children with duodenal avulsion and transection. Am Surg 1993; 59:342345. 25. Worlock P, Stower M, Barbor P. Patterns of fractures in accidental and non-accidental injury in children: a comparative study. Br Med J 1986; 293:100103. 26. Skellern C, Wood D, Murphy JA, Crawford M. Non-accidental fractures in infants: risk of further abuse. J Paediatr Child Health 2000; 36:590592. 27. Cramer KE. Orthopaedic aspects of child abuse. Pediatr Clin North Am 1996; 43: 10351051. 28. Scherl SA, Miller L, Lively N, Russinoff S, Sullivan CM, Tornetta P. Accidental and nonaccidental femur fractures in children. Clin Orthop Res 2000; 376:96105. 29. Leventhal JM, Thomas SA, Roseneld NS, Markowitz RI. Fractures in young children. Distinguishing child abuse from unintentional injuries. AJDC 1993; 147:8792. 30. Thomas SA, Roseneld NS, Leventhal JM, Markowitz RI. Long bone fractures in young children: distinguishing accidental injuries from child abuse. Pediatrics 1991; 88: 471476. 31. Cadzow SP, Armstrong KL. Rib fractures in infants: Red Alert! The clinical features, investigations and child protection outcomes. Paediatr Child Health 2000; 36:322326. 32. Kleinmann PK. Diagnostic imaging in infant abuse. AJR 1990; 155:703712. 33. Kleinman PK, Marks SC, Nimkin K, Rayder SM, Kessler SC. Rib fractures in 31 abused infants: postmortem radiologic-histopathologic study. Radiology 1996; 200:807810. 34. Patterson RH, Burns WA, Janotta FS. Complications of external cardiac resuscitation: a retrospective review and survey of the literature. Med Ann Dist Columbia 1974; 43: 389394. 35. Joffe M, Ludwig S. Stairway injuries in children. Pediatrics 1988; 82:457461. 36. Chiaviello CT, Christoph RA, Bond GR. Stairway-related injuries in children. Pediatrics 1994; 94:679681. 37. Huntimer CM, Muret-Wagstaff S, Leland NL. Can falls on stairs result in small intestine perforations? Pediatrics 2000; 106:301305. 38. Miller ME, Hangartner TN. Temporary brittle bone disease: association with decreased fetal movement and osteopenia. Calcif Tissue Int 1999; 64:137143. 39. Paterson CR, Burns J, McAllion SJ. Osteogenesis imperfecta: the distinction from child abuse and the recognition of the variant form. Am J Med Genet 1993; 45:187192. 40. Russell-Eggitt IM, Thompson DA, Khair K, Liesner R, Hann IM. HermanskyPudlak syndrome presenting with subdural haematoma and retinal hemorrhages in infancy. J R Soc Med 2000; 93:591592.

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Fetal Trauma
Amir Kaviani, Dario Fauza, Moritz Ziegler, and Russell Jennings
Department of Surgery, The Childrens Hospital and Harvard Medical School, Boston, Massachusetts, U.S.A.

INTRODUCTION AND BACKGROUND Trauma is the leading non-obstetric cause of death in the pregnant patient (1). Approximately 7% of all pregnancies are complicated by trauma, and four of every 1000 pregnancies require hospital admission because of a traumatic injury (2). With an increasing number of women working outside the home during pregnancy, there has been a proportional increase in the number of pregnant patients treated for injuries resulting from motor vehicle crashes (3). The risk of injury from a violent crime during pregnancy also parallels that of the general population. In a large multicenter review, penetrating trauma was responsible for 20% of admissions of pregnant women to a trauma center (4). Blunt and penetrating trauma are associated with increased pregnancy complications, and higher severity of injury correlates with markedly higher fetal loss (5). Since the fetus and mother are intimately linked, as the fetus is dependent on the mother, maternal trauma may have a profound effect on fetal outcome. In the clinical setting, the gravid patient provokes a great deal of anxiety in caregivers for two main reasons. First, most trauma surgeons with experience caring for patients with life-threatening injuries have little experience in obstetrics; conversely most obstetrical specialists have little experience in dealing with trauma. Second, each decision made by the caregivers impacts at least two patients, and the potential mortality is 200% or greater. It is important to recognize that the fetus is completely dependent on the mother for survival and that the physiology of pregnancy is such that perfusion to the uterus may be severely compromised with little obvious change in maternal physiologic parameters. Advances in the eld of fetal therapy and intervention over the past two decades have led to increasing recognition of the fetus as a patient. This chapter will address some unique considerations associated with trauma during pregnancy in order to assist the surgeon, when called upon, in delivering optimal care to both mother and fetus.

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ANATOMIC AND PHYSIOLOGIC CHANGES ASSOCIATED WITH PREGNANCY General Considerations Treatment priorities for the pregnant trauma victim remain the same as in her nonpregnant counterpart, although stabilization and resuscitation must be modied to account for the anatomical and physiological changes associated with pregnancy. The rst step in resuscitation of the fetus is restoring the hemodynamics of the mother. With obvious signs of maternal hemodynamic instability, the chances of saving the fetus are less than 20% (6). The uterine vascular bed is without signicant autoregulatory control, and oxygen delivery across the placenta to the fetus is directly dependent on uterine perfusion pressure (7). Maternal hemorrhage and shock result in decreased uterine and placental perfusion, which ultimately leads to fetal hypoxia, bradycardia, and death (7). Cardiovascular and Hematopoietic Systems During pregnancy, maternal blood volume increases by 50% (8). Plasma volume increases by 30% to 45%. However, erythropoiesis does not keep pace with the changes in plasma volume, and red cell mass expands by only 10% to 15%, creating a physiologic anemia (8). Due to the increase in blood volume, hemodynamic instability may not become clinically apparent until blood loss approaches 2000 3000 mL, or 30% to 40% of circulating blood volume (9). Initially, the increase in blood volume protects the fetus. However, once hemodynamic instability becomes clinically apparent it implies a signicantly greater loss of blood and may require a much larger resuscitation volume than is otherwise suspected (8). Cardiac output begins to increase in the rst trimester, peaks at a level 50% greater than normal during mid-trimester, and is sustained at this level until delivery (8). An increase in the stroke volume and basal heart rate by 1015 beats/min contribute equally to the increase in cardiac output. Maternal systolic and diastolic blood pressures decrease steadily throughout pregnancy, reaching a nadir at 28 weeks gestation (10). Progesterone-induced vasodilation is one mechanism thought to be responsible for this effect (7). This combination of a physiologic decrease in blood pressure and increase in heart rate can confound efforts to assess the patients hemodynamic stability during the initial assessment. Further complicating the hemodynamic prole is the patients position at time of evaluation. When the patient is in the supine position, the inferior vena cava is partially compressed by the gravid uterus. This translates to a decrease in venous return, resulting in the supine hypotensive syndrome (11). This syndrome is marked by dizziness, pallor, tachycardia, sweating, and hypotension. In the supine position, partial aortic compression by the enlarged uterus also reduces uterine perfusion, further compromising blood ow to the fetus (12). Turning the mother onto the left lateral decubitus position and exion of the right hip partially restore the circulation and increase the cardiac output by 30% (12). A summary of the hemodynamic changes during pregnancy is provided in Table 1. Respiratory System Maternal oxygen consumption is increased by as much as 20% during pregnancy due to the metabolic demands of the growing breasts, uterus, placenta, and fetus.

Fetal Trauma Table 1 Hemodynamic Changes in the Third Trimester of Pregnancy Parameter Mean arterial pressure (mmHg) Pulmonary capillary wedge pressure (mmHg) Central venous pressure (mmHg) Heart rate (beats/min) Cardiac output (L/min) Systemic vascular resistance (dyne/sec/cm5) Pulmonary vascular resistance (dyne/sec/cm5) Serum colloid osmotic pressure (mmHg) Non-gravid 86 8 62 43 71 10 4.3 0.9 1530 520 119 47 20.8 1.0 Gravid 90 6 82 43 83 10 6.2 1.0 1210 266 78 22 18.0 1.5

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Change (%) NS NS NS 17% 43% 21% 34% 14%

Through an increase in tidal volume mediated partially by increased progesterone levels, minute ventilation increases by as much as 50% (7). This increase in tidal volume is offset partially by a decrease in residual volume and expiratory reserve volume owing to the upward displacement of the diaphragm (8). These two effects combine to decrease the functional residual capacity by about 18%, which renders the pregnant woman particularly intolerant to hypoventilation and apnea (8). The net result of these respiratory dynamics is an unchanged arterial partial pressure of oxygen (PaO2), a decreased partial pressure of carbon dioxide (PaCO2), and a compensatory decrease in plasma bicarbonate levels compared to the non-gravid state (13). Gastrointestinal System Increased circulating levels of estrogen and progesterone inhibit gastrointestinal motility and nutrient absorption throughout pregnancy (14). Gastrin production is also increased during pregnancy, mainly as a result of its production by the placenta (9). This leads to elevation of maternal gastric acid and enzyme production. In the second and third trimesters, increased progesterone levels inhibit cholecystokininmediated smooth muscle contraction in the gallbladder (14). This leads to impaired gallbladder emptying and, along with the increased concentration of cholesterol in bile during pregnancy, contributes to a higher incidence of gallstones (9). As the gravid uterus enlarges throughout pregnancy, it displaces other intraabdominal organs and increases intra-abdominal pressure. As expected, the signs and symptoms of injury to abdominal viscera during pregnancy will vary signicantly compared to the non-gravid state due to the shift in their position within the abdominal cavity. In addition, with progression of the pregnancy, stretching and diastasis of the rectus abdominus muscles may lead to loss of the usual guarding and muscular rigidity associated with intra-abdominal organ injury (6). These factors may contribute to physical exam ndings inconsistent with the degree of maternal injury and must be taken into account when examining the pregnant trauma victim. Endocrine System Throughout pregnancy, the placenta is a constant source of hormone production and is responsible for many of the associated hormonal changes. Progesterone, estrogen, and thyroid-stimulating hormone (TSH), adrenocorticotropic hormone

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(ACTH), human chorionic gonadotropic hormone (hCG), and human placental lactogen (hPL) are all produced by the placenta throughout pregnancy (15). The hPL enhances maternal lipolysis and inhibits maternal utilization of glucose, thereby making nutrients available to the fetus. In the maternal bloodstream, hPL functions as a physiologic antagonist of insulin and contributes to increased peripheral resistance to insulin (16). This results in increased maternal protein catabolism and ensures a constant supply of amino acids to the growing fetus (17). Renal System Maternal renal perfusion increases by up to 50% throughout pregnancy as maternal and fetal metabolic requirements increase signicantly (16). Maternal glomerular ltration rate is increased by up to 100% as a result of the increase in blood volume and cardiac output in pregnancy (18). This contributes to a steady decline in maternal blood urea nitrogen and creatinine, and hyperemia and enlargement of both kidneys, an effect mediated in part by progesterone-associated smooth muscle relaxation (18). In the third trimester, the increase in size of the uterus may contribute to compression of the ureters, resulting in hydroureters and hydronephrosis (18). Thus an intravenous pyelogram demonstrating a dilated renal collecting system may not be due to other abnormalities (6). As pregnancy progresses, the mothers bladder is gradually elevated out of the pelvis, and is therefore more susceptible to direct injury.

INITIAL EVALUATION AND MANAGEMENT Armed with a basic understanding of maternal and fetal anatomy and physiology, a physician faced with a pregnant trauma victim can modify the resuscitation and subsequent management to optimize outcome for both the mother and the fetus. Regardless of the estimated gestational age of the fetus, the physicians rst priority during the initial evaluation remains resuscitation and stabilization of the mother. Primary Survey The primary survey of the injured pregnant patient begins with assessment of the airway, breathing, and circulation. After establishing a patent airway, generous use of supplemental oxygen is advocated in order to prevent maternal and fetal hypoxia (19). Due to the differences between adult and fetal oxyhemoglobin dissociation curves, small decreases in maternal oxygen content are associated with signicant fetal hypoxia (20). If maternal circulatory compromise is suspected due to the mechanism of injury, the patient must be placed in the left lateral decubitus position with exion of the right hip to minimize mechanical aortocaval compression by the uterus. The mother with a suspected spinal injury can be secured on the backboard prior to initiating these positional maneuvers. Manual displacement of the uterus toward the left upper quadrant may be appropriate in cases where emergency room interventions such as intubation and placement of central venous lines are not easily accomplished in the lateral decubitus position. Once on the backboard, the board may be tipped 45 to the left in order to decompress the inferior vena cava and restore central venous pressure.

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Early in pregnancy, the diameter of the mothers chest increases by approximately 2 cm, primarily under the control of hormonal effects (9). As the uterus enlarges, upward displacement of the diaphragm may exceed 6 cm (9). These changes obscure the anatomy of the thoracic cavity, and care should be taken while attempting invasive procedures such as tube thoracostomy or thoracentesis, as standard placement in the fth and sixth intercostal spaces has been associated with both visceral organ and uterine perforation (21). As a rule, such tubes should be placed in the second or third intercostal spaces to avoid risk of injury to intra-abdominal organs. The physiologic hypervolemia of pregnancy may mask early signs of shock. Therefore, generous resuscitation with crystalloid is advocated in patients who appear normotensive on initial presentation (22). Even minor maternal trauma may be associated with increased circulating maternal catecholamines, resulting in uteroplacental vasoconstriction (7). Treatment of maternal hypotension with vasopressors should be avoided and used only as a last resort, understanding the implications for blood ow to the uterus and placenta and the potential for fetal compromise (11). Secondary Survey The secondary survey begins with a thorough history of the mother, including the obstetrical history, and is followed by a thorough physical examination. As part of this survey, fetal evaluation and monitoring are initiated and continued while management decisions are being made. A history of preterm labor, placenta previa, or placental abruption puts the pregnant patient at increased risk for recurrence of these conditions and must be elicited during the secondary survey (11). The obstetric history must include the starting date of the last menstrual period, date of the rst perception of fetal movement, expected date of delivery, and any complications associated with the current and previous pregnancies. An estimation of the gestational age and fetal maturity can be obtained by determination of uterine size by palpating the most superior aspect of the uterine fundus and comparing its location with known anatomical landmarks. This is especially useful when the history is not readily available due to maternal incapacitation or lack of adequate prenatal care. For example, a uterine fundus palpated midway between the umbilicus and the xyphoid process is consistent with an estimated fetal age of 24 to 26 weeks (23). This information may play a critical role in the decision making regarding early delivery. A gynecologic exam must be performed to indicate the status of the pregnancy. Vaginal bleeding, a bulging perineum, ruptured membranes, presence of contractions, and abnormalities of fetal heart rate and rhythm are all associated with increased risk to the pregnancy (23). Vaginal bleeding is abnormal prior to the onset of labor and may be associated with uterine injury, placental abruption, premature cervical dilation, or placenta previa (23). Bulging fetal membranes are caused by pressure from a presenting part of the fetus and are associated with spontaneous abortion early in pregnancy (11). The presence of cloudy green uid around the cervical os or perineum indicates rupture of the amniotic sac and may be associated with compression of the umbilical cord vessels (23). The presence of amniotic uid may be conrmed by the change in color of nitrazine paper from bluegreen to deep blue, and may be signicant in predicting potential for infection. However, differentiation of amniotic uid from urine may be difcult, and insertion of a Foley catheter is recommended if rupture of membranes is suspected to support the diagnosis. Uterine contractions are assessed by palpation of the abdominal wall overlying

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the uterine fundus and determination of the frequency, intensity, and duration of the contraction pattern. Beta agonists such as mitodrine may be used to control uterine contractions and progressing pregnancy without decreasing uterine perfusion. Strong contractions may be associated with true labor, and their presence indicates the need to prepare for delivery and resuscitation of the newborn (11).

Evaluation and Monitoring of the Fetus Fetal assessment begins with auscultation for fetal heart tones. The baseline fetal heart rate is dened as the rate in beats per minute around which the fetal heart rate oscillates for 10 or more minutes. The normal range is 120160 beats/min. Tachycardia is dened as a heart rate greater than 160 beats/min and is the initial fetal response to stress, hypoxia, and hypotension (24). Once fetal heart tones are detected by auscultation, continuous electronic fetal heart rate monitoring (EFM) is initiated for constant assessment of fetal well-being. Both internal and external techniques may be used to monitor the fetal heart (25). The internal approach is reserved for the near term fetus, and involves detection of the fetal QRS pulse by placement of an electrode directly on the presenting part of the fetus. This technique may be utilized in cases where the amniotic membranes are ruptured and provides more accurate information about variations in fetal cardiac activity (10). It is also associated with a higher incidence of infection and direct fetal injury (26). External monitoring involves Doppler ultrasonography to detect fetal heart wall motion. Its advantages include noninvasiveness and wide clinical applicability. However, motion artifacts associated with the fetal tracing may impair the reliability of this technique (26). Sudden fetal bradycardia is most commonly associated with acute fetal hypoxia and in the traumatized obstetric patient is often due to complete or partial placental abruption. Acute fetal bradycardia has also been associated with amniotic uid embolus syndrome, acute maternal respiratory insufciency, or eclamptic seizure (10). Late onset fetal tachycardia is commonly a result of overwhelming maternal infection and is often associated with maternal pyrexia and chorioamnionitis (7). Isolated fetal hemorrhage is not usually associated with a tachycardic response in the fetus, and persistent fetal tachycardia is not always a sign of uncontrolled bleeding from direct injury to the fetus (7). A normal fetal heart rate has a 95% correlation with adequate fetal perfusion and is the single best predictor of fetal survival after traumatic injury to the mother (27). The ideal duration of fetal monitoring after trauma has been a subject of debate by experts in the eld. Numerous studies have attempted to determine risk factors that affect pregnancy outcome and establish guidelines for fetal monitoring. Pearlman et al. in a prospective randomized trial of 85 injured pregnant patients found four hours of cardiotocographic monitoring to be a sensitive but not specic indicator of fetal survival (28). A recent study by Curet et al. identied risk factors for premature contractions, preterm labor, and fetal loss after traumatic injury during pregnancy (29). In this series, risk factors associated with fetal death included major mechanisms such as ejections, and collisions involving motorcycles or pedestrians. Maternal death, maternal tachycardia, abnormal fetal heart rate, lack of restraints, and maternal Injury Severity Score >9 were also associated with increased fetal mortality. Risk factors associated with premature contractions or labor in this study included gestational age >35 weeks, assaults, and pedestrian collisions. These

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authors concluded that patients with any of these risk factors should be monitored for at least 24 hours, and that stable patients without any risk factors or other reasons for further observation and monitoring could be safely discharged after six hours of fetal monitoring. Current guidelines of the American College of Surgeons Committee on Trauma recommend 24 hours of fetal monitoring for patients with frequent uterine activity (>6 contractions/hr), abdominal tenderness, vaginal bleeding, or hypotension (23). In patients with these ndings, obstetrical consultation should be obtained after the initial evaluation and resuscitation is complete.

Fetal Viability The presence of a viable fetus is a central point in the subsequent management of the injured pregnant patient. A fetus is considered viable when it has achieved 24 weeks of a 40-week gestation, as fetal lungs mature and become capable of gas exchange (29). With aggressive neonatal resuscitation and vigilant intensive care monitoring, approximately 50% of these fetuses survive, although morbidity remains high and is often attributed to intracranial hemorrhage, necrotizing enterocolitis, and respiratory distress syndrome (30). Real-time ultrasonography is the optimal method for measurement of parameters such as head size (circumference and biparietal diameter), abdominal circumference, and femur length (31). Palpation of the uterine fundus halfway between the umbilicus and the xyphoid process is also consistent with fetal viability (31).

DIAGNOSTIC STUDIES Keeping in mind the basic rule that preservation of fetal life is largely dependent on maternal stabilization, radiographic studies should not be foregone simply because of potential exposure of the fetus to ionizing radiation. In addition, adequate assessment of maternal injuries through imaging studies is usually possible without signicant teratogenic risk to the fetus. This risk is greatest during the process of organogenesis, which takes place between weeks 3 and 16 of gestation (3). The risk declines signicantly after this point, and radiation-induced injuries after the 20th week of gestation are rare. As a general rule, a direct-beam radiograph (i.e., abdomen, pelvis, and lumbar spine), delivers a dose of 0.05 Gray units (GY) (Table 2). An indirect lm (skull, chest, and extremities) is associated with a 0.001 GY dose of radiation. The radiation energy absorbed during a CT scan of the abdomen ranges from 0.02 to 0.026 GY. Magnetic resonance imaging does not involve ionizing radiation, and does not entail risk at any gestational age. Other variables that affect fetal exposure include shielding, exposure time, tube to lm distance, and unnecessary repetition of a study due to inadequate planning by the caregiver. Necessary radiographic examinations should be obtained according to the following guidelines: 1. Careful planning to obtain the minimum number of radiographs to obtain the maximum information. 2. Shielding the patients abdomen during the study with a lead apron. 3. Use of a dosimeter badge to keep track of total radiation exposure in a critically ill patient in whom a protracted intensive care unit stay is anticipated.

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MANAGEMENT STRATEGIES Blunt Trauma Automobile accidents account for the majority of cases of blunt trauma during pregnancy (23). Three-point restraints are effective in reducing severe maternal injuries, and are associated with increased fetal survival when compared to two-point restraints (32,33). Other causes of blunt trauma during pregnancy include falls and aggravated assaults. Due to the anatomic and physiologic changes that occur during pregnancy, different patterns of injury are observed in a pregnant patient with blunt thoracoabdominal injuries compared to her nonpregnant counterpart. The incidence of splenic injury and retroperitoneal hematoma is greater due to the increased intra-abdominal venous congestion associated with pregnancy (6). Conversely, the incidence of bowel injury in the mother is decreased, presumably as a result of the anatomic displacement of the intestines away from the lap belt distribution by the enlarged uterus (33). Severe lower abdominal trauma during pregnancy is often associated with direct injury to the fetus. This mechanism is usually associated with fetal skull fracture and resultant intracerebral hemorrhage (10). Pelvic fracture in the pregnant patient is associated with a high maternal and very high fetal mortality rate (34). An intact uterineplacental interface is essential for oxygen and nutrient delivery to the fetus. Even in the absence of direct fetal injury, severe fetal injury may result from abruptio placentae (27). Placental abruption refers to the abnormal separation of the placenta from the uterus, and in blunt trauma occurs as a result of the sudden increase in intrauterine pressure that results from sudden deceleration in a restrained patient (33). In addition, the uterus is thought to elongate on a vertical axis during deceleration, and deformation of the relatively elastic uterine musculature in relation to the more rigid placental tissue creates a shearing effect thought to contribute to placental separation. Abrubtio placentae complicates 1% to 5% of minor injuries, and 20% to 66% of major blunt traumatic injury (35). Clinical ndings associated with placental abruption include: vaginal bleeding, abdominal pain, tenderness, and uterine contractions. The reduced area of the uterineplacental interface for fetalmaternal gas exchange and nutrient delivery in these instances is thought to be responsible for resultant fetal hypoxia, prematurity, and death. One of the most serious complications associated with placental abruption is disseminated intravascular coagulation (DIC), which is thought to result from entry of thromboplastins from the injured placental tissue into the maternal circulation. The DIC in the injured pregnant patient is associated with a three- to ve-fold increase in fetal and maternal mortality (27). Thus, early diagnosis of placental abruption is necessary to avoid this serious complication. Although most patients suffering myometrial contusions will exhibit mild to moderate uterine contractions in the ensuing recovery period, uterine activity of greater than eight contractions per hour in the rst four hours after blunt trauma is associated with a 25% risk of placental abruption (36). The vast majority of trauma-related placental separations occur within the rst four hours after injury. However, delayed separations after 24 to 48 hours have been reported (35). Ultrasound can detect placental abruption with high sensitivity and specicity in the trauma setting (31). Computed tomography (CT), which may be used for maternal evaluation, can conrm the ultrasound ndings. In a study aimed at delineating factors affecting fetal outcome after blunt maternal trauma, Scorpio et al. reported that admission Injury Severity Scores (ISS) and bicarbonate levels were the best predictors of pregnancy outcome (37).

Fetal Trauma Table 2 Estimated Total Body Exposure to Radiation from Typical Imaging Modalities Procedure Chest X ray Skull X ray Cervical spine X ray (2 views) Intravenous pyelogram (IVP) Lumbar spine X ray (2 views) Thoracic spine X ray (2 views) Kidney/ureter/bladder (KUB) X ray Mammogram CT scan (head) CT scan (thorax) CT scan (abdomen/pelvis)

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Estimated dose (mSv) 0.08 0.40 0.50 1.20 2.00 3.00 4.50 4.50 1.002.00 11.0015.00 15.0025.00

The average ISS on admission for mothers who experienced fetal demise after blunt trauma was 31 and average bicarbonate level was 16.8, compared to 11 and 20.3, respectively, in cases where the fetus survived. After maternal resuscitation has been initiated and secondary survey begun, the management of the pregnant blunt trauma victim should proceed with three key considerations in mind: 1. The determination of gestational age in a stable patient is the key factor in determining the subsequent management of the mother and fetus. 2. The physiologic hypervolemia associated with pregnancy may mask ongoing intra-abdominal hemorrhage and hypotension. 3. The physical exam is unreliable due to the displacement of intra-abdominal organs by the enlarging uterus and related changes in peritoneal response to irritation from stretching of the abdominal wall. Penetrating Trauma Penetrating trauma during pregnancy is neither rare nor insignicant, accounting for up to 36% of maternal deaths (38). A review of several large series demonstrated that gunshot wounds suffered during pregnancy are associated with a maternal mortality rate of 4%, while fetal mortality in the same cases ranged between 40% and 70% (39). Undoubtedly, a portion of this mortality is due to prematurity from early delivery; however, delay in diagnosis of a potentially correctable lesion in a viable fetus contributes. Unlike blunt traumatic injury, where the cause of fetal demise is most often due to placental abruption, fetal death from penetrating injuries is most commonly associated with ongoing bleeding, hepatic injuries, and disruption of the central nervous system. A well-informed, multidisciplinary approach with participation of a fetal surgeon in the decision-making process may improve fetal survival and outcome in cases where fetal viability is threatened. Patterns of Injury Most cases of penetrating trauma during pregnancy result from violence against the mother (40). Other causes include attempted suicide and attempted abortion. The altered anatomy of intra-abdominal organs has important implications. Near term

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a penetrating injury inferior to the xyphoid process is associated with a high likelihood of uterine perforation, while injury to the thoracoabdominal areas bilaterally is associated with a high incidence of gastrointestinal organ injury due to crowding of the organs in this portion of the abdomen. Most cases of intentional gunshot wounds to the uterus are not associated with extrauterine organ injury. However, the chance of fetal injury is 60% to 90% (40).

Management of Penetrating Injuries The decision to operate in cases of penetrating trauma follows similar algorithms in pregnant and nonpregnant individuals: abdominal gunshot wounds require celiotomy, and stab wounds warrant exploratory laparotomy based on the assessment of the likelihood of entrance through the parietal peritoneum into the abdominal cavity (Fig. 1). A recent controversial report advocates conservative management of gunshot wounds to the lower abdomen in the gravid patient who is stable, provided certain conditions are met (40). These conditions are: 1. 2. 3. 4. 5. 6. The entrance wound is below the fundus. The bullet can be demonstrated to be within the uterus. The mother is stable. The abdominal examination is benign. There is no demonstrable blood in the gastrointestinal tract or urine. There is no indication for uterine evacuation.

These author recommendations are supported by the fact that only 19% of women who sustain gunshot wounds to the pregnant uterus will have associated intra-abdominal injuries with surgical signicance. Although these studies deserve consideration, the current prevailing opinion is that the gravid patient with an intra-abdominal gunshot wound must undergo

Figure 1 Algorithm for management of penetrating trauma in pregnancy.

Fetal Trauma Table 3 Indications for Emergency Caesarean Section Uncontrollable uterine hemorrhage Irreparable uterine injury Access to maternal injuries is obscured by uterus Maternal instability with a potentially viable fetus Systemic complications of pregnancy (eclampsia, DIC) Maternal death

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exploratory celiotomy. This view is supported for several reasons. The abdominal exam may be unreliable in pregnancy, and peritoneal signs resulting from hollow viscus injury may be masked. In addition, the risks associated with missing an intraabdominal injury usually outweigh those associated with anesthesia and celiotomy. In a stable woman with a previable fetus, abdominal exploration followed by hysterotomy by a fetal surgeon may reveal a fetal lesion, which can be repaired in utero, delaying delivery until fetal viability is achieved. Indications for fetal surgery are limited to ongoing hemorrhage in the fetus. Since the fetal abdominal cavity is sterile, a suspected hollow viscus injury in the fetus does not warrant exploration. However, uncontrollable fetal hemorrhage may result in fetal demise and may be amenable to correction in utero. Stab wounds to the abdomen during pregnancy are managed similarly in pregnant and nonpregnant patients: exploration is mandatory for patients who demonstrate obvious signs of intra-abdominal injury, including shock, peritonitis, and evisceration. In cases where indications for exploration are not clear, adjunctive diagnostic studies such as CT scanning and diagnostic peritoneal lavage aid in supporting the decision to operate. Once the decision to operate is made, a midline celiotomy is undertaken and usually provides adequate exposure. Careful retraction of the uterus may be necessary to improve exposure and must be performed with care to avoid aortocaval compression. Celiotomy alone does not warrant caesarean section since it prolongs the operation and increases blood loss by at least 1000 mL (41). Specic indications for emergency caesarean section are listed in Table 3. The risk of inducing labor by manipulation of the gravid uterus is very low (41). In cases where uterine injury is severe and hemorrhage uncontrollable, a caesarean section may be indicated to evacuate the uterus prior to hysterectomy or uterine repair.

Table 4 Postmortem Caesarean Section: Predictors of Successful Outcome Time between maternal death and delivery <5 min 510 min 1015 min 1520 min 2025 min Inuence on survival Excellent Good Fair Poor Unlikely

Duration of gestation: Fetal viability is dened as 24 weeks of gestation. This corresponds to a fundal height of approximately 2426 cm above the pubis or a uterus palpable midway between the umbilicus and costal margin. Under optimal conditions, the fetus has a 5060% estimated chance of survival without a major handicap; therefore, caesarean section is indicated shortly after maternal death.

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A postmortem caesarean section is indicated in cases where a dead or moribund woman is carrying a potentially viable fetus. A review of 120 successful postmortem caesarean sections found that 70% of surviving infants were delivered within ve minutes of maternal death. The same ndings have been conrmed by others and are listed in Table 4.

REFERENCES
1. Civil I, Schwaab C. Abdominal trauma. J Trauma 1988; 28:708710. 2. Perlow JH, Wigton T, Hart J, Strassner HT, Nageotte MP, Wolk BM. Birth trauma: a ve-year review of incidence and associated perinatal factors. J Reprod Med 1996; 41(10):754760. 3. Pearlman MD. Motor vechile crashes, pregnancy loss and preterm labor. Int J Gynaecol Obstet 1997; 57(2):127132. 4. Kissinger D, Rozycki G, Morris Jr. J, et al. Trauma in pregnancy: prediciting pregnancy outcome. Arch Surg 1991; 126(11):10791088. 5. Schiff MA, Holt VL. The injury severity score in pregnant trauma patients: predicting placental abruption and fetal death. J Trauma 2002; 53(5):946949. 6. Moise KL Jr, Belfort MA. Damage control for the obstetric patient. Surg Clin North Am 1997; 77(4):835852. 7. Harvey M. Physiologic changes of pregnancy. In: Harvey C, ed. Crit Care Obstetrical Nursing. Aspen: Gaithersburg, MD, 1991:123. 8. Lee W, Cotton D. Cardiorespiratory changes during pregnancy. In: Clark S, ed. Crit Care Obstetrics. Boston: Blackwell, 1991: 2. 9. Cunningham F, MacDonald P, Leveno K. Maternal Adaptations to pregnancy. In: Williams Obstetrics, ed. Appleton & Lange: Norwalk, CT, 1993 209216. 10. Colburn V. Trauma in pregnancy. J Perinat Neonatal Nurs 1999; 13(3):2132. 11. Connolly AM, Katz VL, McMahon MJ, et al. Trauma and pregnancy. Am J Perinatol 1997; 14(6):331336. 12. Bieniarz J, Branda L, Maqueda E. Aortocaval compression by the uterus in late pregnancy. Am J Obstet Gynecol 1968; 102:11061113. 13. Lavery JP, Staten-McCormick M. Management of moderate to severe trauma in pregnancy. Obstet Gynecol Clin North Am 1995; 22(1):6990. 14. Bynum T. Hepatic and Gastrointestinal disorders in pregnancy. Med Clin North Am 1977; 61:129134. 15. Gonzalez J, Elizondo G, Saldivar D. Pituitary gland growth during normal pregnancy: an in vivo study using management resonance imaging. Am J Med 1988; 85:217. 16. Lopez Bernal A, Watson SP, Phaneuf S, et al. Biochemistry and physiology of preterm labour and delivery. Baullieres Clin Obstet Gynaecol 1993; 7(3):523552. 17. Perelman RH. The infant of the diabetic mother. Pathphysiol manag Prim Care 1983; 10(4):751760. 18. Huddleston JF. Intrapartum fetal assessment. A review. Clin Perninatol 1999; 26(3): 549568. 19. Bobby PD, Santos AC. Effect of prolonged asphyxia on skin blood ow in fetal lambs. Obstet Gynecol 2000; 95(4):607611. 20. Parer JT, Livingston EG. What is fetal distress? Am J Obstet Gynecol 1990; 162(6): 14211425; discussion 14251427. 21. Gardeil F, Daly S, Turner MJ. Uterine rupture in pregnancy reviewed. Eur J Obstet Gynecol Reprod Biol 1994; 56(2):107110. 22. Hill DA, Lense JJ. Abdominal trauma in the pregnant patient. Am Fam Physician 1996; 53(4):12691274.

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23. Stone IK. Trauma in the obstetric patient. Obstet Gynecol Clin North Am 1999; 26(3):459467. 24. Keunen H, Hassart TH. Fetal arterial pressure and heart rate changes in surviving and non-surviving immature fetal sheep following brief-repeated total umbilical cord occlusions. Eur J Obstet Gynecol Reprod Biol 1999; 87(2):151157. 25. Kaiser G. Do electronic fetal heart rate monitors improve delivery outcomes? J Florida Med Assoc 1991; 78:303. 26. Goeschen K. Fetal monitoring be combined CTG and FBA. J Perinat Med 1996; 24(1):3741. 27. George ER, Vanderkwaakm T, Scholten DJ. Factors inuencing pregnancy after trauma. AM Surg 1992; 58(9):594598; discussion 598. 28. Pearlman MD. A prospective controlled study of outcome after trauma during pregnancy. Am J Obstet Gynecol 1990; 162(6):15021510. 29. Curet M. Predictors of outcome in trauma during pregnancy: identication of patients who can be monitored for less than 6 hours. J Trauma 2000; 49:1825. 30. Solum T. Management of the extreme premature delivery. J Perinat Med 1991; 19(Suppl 1):317320. 31. Ma OJ, Mateer JR, DeBehnke DJ. Use of ultrasonography for the evalutation of pregnant trauma patients. J Trauma 1996; 40(4):665668. 32. Wolf M. A restrospective cohort study of seatbeat use pregnancy outcome after a motor vehicle crash. J Trauma 1993; 34:116121. 33. Towery R. Evaluation of pregnant women after blunt injury. J Trauma 1993; 35:731735. 34. Leggon RE, Wood GC, Indeck MC. Pelvic fractures in pregnancy: factors inuencing maternal and fetal outcomes. J Trauma 2002; 53(4):796804. 35. Rogers FB, Rozycki GS, Osler TM, et al. A multi-institutional study of factors associated with fetal death in injured pregnant patients. Arch Surg 1999; 134(11):12741277. 36. Green J. Placenta previa and abruption placentae. In: Creasy R, Resnik R, eds. Maternalfetal Medicine. WB Saunders: Philadelphia, 1994:602624. 37. Scorpio R, Esposito TJ. Blunt trauma during pregnancy: factors affecting fetal outcome. J Trauma 1992; 32:213217. 38. Fildes J, Reed L, Jones N, Martin M. Trauma: the leading cause of maternal death. J Trauma 1992; 32(5):643645. 39. Pierson R, Mihalovitz H, Thomas L, Beatty R. Penetrating abdominal wounds in pregnancy. Ann Emerg Med 1986; 15(10):12321234. 40. Franger AL, Buchsbaum HJ, Peaceman AM. Abdominal gunshot wounds in pregnancy. AM J Obstet Gynecol 1989; 160:11241128. 41. Ritter J. Postmortem caesarean section. IAMA 1961; 175:715.

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Imaging the Injured Child
David Tuggle
The Section of Pediatric Surgery, Department of Surgery, University of Oklahoma College of Medicine, Oklahoma City, Oklahoma, U.S.A.

Michele A. Markley
Chris Everts Childrens Hospital, Fort Lauderdale, Florida, U.S.A.

INTRODUCTION For many reasons, ranging from normal childhood activity to motor vehicle crashes and child abuse, fractures and soft tissue injuries are common in children almost to the point that they are part of growing up in our modern world. Radiological assessment has played an ever-increasing role in the management of these injuries since the early days of X-ray use. In our efforts to bring children back to their normal state of health, diagnostic images now play an essential part in accurately diagnosing injuries and monitoring how they respond to treatment. As technology has evolved, pediatric trauma care has led the eld in some areas and lagged behind in others. Because of the differences between adults and children in anatomy, physiology, and tissue and wound healing, and in the spectrum of injuries that they suffer, the exact role of imaging studies will also differ.

LITERATURE-BASED GUIDELINES A National Library of Medicine search of over 1000 articles revealed very few randomized prospective trials that specically address the use of imaging modalities in pediatric trauma (15). The vast majority of published articles concerning imaging of the injured child are nonrandomized and uncontrolled, i.e., type-II studies. There are considerably more studies overall concerning imaging in trauma in the adult population as compared to children. These are cited where applicable. Most clinicians caring for injured children would likely agree that computed tomography (CT) is the standard for imaging pediatric trauma patients with suspected or known intracranial injuries and/or abdominal solid organ injuries (levelII recommendation) (6,7). Similarly, clinicians agree that a chest radiograph should be the most common rst imaging study of the chest (level-II recommendation) (Table 1), and plain radiographs of an injured extremity are the standard of initial
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Tuggle and Markley Table 1 Pathology Potentially Noted on Chest X Ray Bony thorax for fracture Ribs Clavicles Vertebrae Scapulae Sternum Soft tissues Emphysema Opacication Foreign object Lung elds Pneumothorax Hemothorax Consolidation Lung contusion Foreign bodies Mediastinum Pneumomediastinum-airway rupture Widening of the mediastinum-aortic rupture Shift of the mediastinum-tension pneumo/hemothorax Foreign body Cardiac silhouette Cardiac tamponade

investigation for suspected fractures (level-II recommendation) (1). Arteriography is most often considered the gold standard for diagnosing arterial injuries (level-II recommendation). Aside from these generally accepted standards, other imaging modalities are typically left to the discretion of the treating surgeon. TYPES OF STUDIES Initial Radiographs in the Emergency Department Plain X rays are the initial radiologic diagnostic tests in use in emergency departments today. The initial physical examination of the child determines which studies should be performed and when. While the patient is undergoing resuscitation in the emergency department, the diagnosis of injuries is begun with standard radiographs, usually performed with a portable X-ray machine or one dedicated to the trauma room, thus avoiding movement of the patient. The most frequently ordered initial imaging studies in the emergency department include plain radiographs of the chest, abdomen, pelvis, cervical spine, and extremities (Fig. 1). Thoracic and lumbar spinal X rays are commonly ordered when neurologic injuries are suspected, or when the physical examination reveals point tenderness over the spine. Detecting a pneumothorax, pneumoperitoneum, pelvic fracture, or long bone fracture is an important component of the initial care of a traumatized child. As experience and technology have expanded, some previously common studies have been shown to be of limited use. Plain X rays of the skull may document fractures, but they have little value in directing management of the head injured child, with the excepted situations of penetrating injury and suspected child abuse (8,9). Wang and colleagues have documented the poor predictive power of plain skull

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Figure 1 Gunshot wound to the chest in a 13-year-old male. Note the pulmonary contusion and foreign object.

radiographs in determining intracranial bleeding in children with mild head injury (Glasgow Coma Scale of 1314) (10). Intravenous pyelography has been used to document injuries of the urinary system, but its usefulness is also limited. It does not allow for grading of renal, ureteral, or bladder injuries, or for determining the presence of other intra-abdominal injuries. Similarly, nuclear isotope scanning has little utility in the initial workup of the severely injured child. The grading of injuries is also uncertain and not all organs are evaluated. Skull lms, intravenous pyelography, and radionuclide studies have now been supplanted by CT scanning in most cases.

Ultrasound Ultrasound has been used extensively since it became widely available. In the United States, radiologists traditionally perform sonographic imaging, while in Europe and Asia surgeons commonly perform it. In the past decade, surgeon-directed ultrasonography has been popularized in the United States. Several recent studies by adult and pediatric trauma surgeons have attempted to determine the role of Focused Acute Sonography for Trauma, also called Focused Abdominal Sonography for Trauma (FAST) in the evaluation of the injured child. The most common FAST evaluation examines the heart, right and left upper quadrants, and the pelvis for uid. Some surgeons include an evaluation of the thorax for uid in the pleural space and for pneumothorax. Review of the National Library of Medicine revealed three prospective trials of the use of FAST in children (35), as well as other studies providing

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Figure 2 Positive right upper quadrant ultrasound for trauma in a 4-year-old child. White arrow denotes uid (dark area) between the liver and kidney.

useful data (6,1113). In some studies, a radiologist performed the FAST, while other publications have evaluated surgeon-directed ultrasonography. The technique of B-mode ultrasound in the hands of an experienced ultrasonographer should be as accurate in detecting blood in the abdomen as CT scanning or diagnostic peritoneal lavage (DPL) (Fig. 2) (1416). In a collected series of over 4900 patients, surgeons who performed ultrasound to detect hemoperitoneum and visceral injury demonstrated a sensitivity of 93.4%, a specicity of 98.7%, and an accuracy of 97.5% (1417). This can be compared to a group of 1043 patients in whom the ultrasonographic study was performed by radiologists. This collected series showed a sensitivity of 90.8%, a specicity of 99.2%, and an accuracy of 97.8% (11,1821). Both of these series include adults and children. Garcia et al. (5) have suggested that sonography for the sole purpose of establishing the presence of free intracavitary uid in the child is of questionable usefulness as it does not necessarily identify the specic organ injured nor the grade of the injury. They suggest that some solid organ injuries will be missed if free uid alone is the indication for abdominal CT scan. Currently, nonradiologist-directed ultrasound is considered an extension of the physical examination and not a conclusive diagnostic study. Although its sensitivity, specicity, and accuracy are high, it is used mostly as a screening tool to determine the need for more in-depth imaging studies or invasive evaluation. The typical FAST examination takes three to ve minutes when performed by a physician experienced in its use. A 3.5 MHz probe is used for children over 10 kg, while either a 3.5 or a 5 MHz probe can be used for children under 10 kg. The relative lack of subcutaneous tissue in most children makes this an easy study to perform on children compared to adolescents and adults. Obvious benets of the FAST evaluation include its portability, eliminating the need to transport the child to the radiology suite, and the fact that it limits the childs radiation exposure.

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The American College of Surgeons in conjunction with emergency medicine groups is in the process of establishing training guidelines and teaching programs for FAST evaluation. The American College of Surgeons has developed a program that provides basic education in ultrasound physics and technique, as well as some advanced courses in FAST evaluation of the abdomen and other regions of the body. In the near future, it is foreseeable that surgical training programs, in which the trainee is responsible for the care of the injured child, will likely include emergency ultrasound as part of their curriculum. However, due to the current lack of availability of FAST training and uncertainty of the usefulness of the technique at present, ultrasound evaluation of the injured child is of secondary importance in the initial workup of the pediatric trauma patient at this time. Vascular ultrasound studies, with color Doppler, are useful in detecting vascular injuries in children. These studies use 7 MHz (or higher) transducers with color capability. The use of color Doppler ultrasound may help to avoid the complications associated with arteriography in children with tiny blood vessels. As the quality of these devices has improved, the need for arteriography and the risk of vascular injury are increasingly avoided. Computed Tomography The CT scan is the accepted diagnostic imaging study of choice in the vast majority of stable injured children suspected of having a potentially life-threatening injury. The newer CT scanners have a gantry, which encircles the patient and rotates continuously in the same direction. During scanning, data acquisition is combined with continuous movement of the patient through the gantry. The path of the radiation is described as a spiral or helix, giving rise to the name spiral or helical CT. These scanners acquire data very quickly, allowing them to scan a fairly large volume or length in a short period of time. The rapidity of the scanner is advantageous for a number of reasons: 1. Motion artifact is reduced as the patient can often hold his breath for the entire study. 2. Optimal use of intravenous contrast enhancement is allowed. 3. The test is quicker than conventional CT scanning, resulting in higher resolution in the same study time. 4. The data obtained from spiral CT are best for 3D imaging because of the lack of motion artifacts. The CT scans of the head, abdomen, and chest are considered the standard of care for the evaluation of an internal injury in a stable, traumatized child. The majority of children with suspected intra-abdominal injuries should have a CT scan performed prior to instituting operative or nonoperative treatment unless an absolute indication for surgery is present (Fig. 3). A lap belt injury, a bicycle handlebar injury, or child abuse are the mechanisms most often associated with blunt intestinal injury. Unstable children in the emergency department are either taken directly to the operating room or evaluated by other modalities such as DPL or ultrasound. It is generally observed that a high percentage of CT scans on injured children will reveal no injuries. Ruess et al. evaluated the CT scans of 1500 consecutive children evaluated for blunt abdominal trauma (22). Abnormal CT scans were seen in only 26% of patients. A normal study was found to strongly predict a lack of deterioration in that only one delayed laparotomy was required in the 1112 children with a normal CT. In addition, a CT scan affected the decision to operate on children with a solid viscus injury in a very small subset of patients (5 of 1500 CT scans).

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Figure 3 The CT scan of a patient with spleen injury and blood in the abdomen, noted by arrow.

Despite the liberal use of head CT scans, it is possible for the child with a severe neurological injury to have a normal initial scan, or for a child to develop late manifestation of a neurologic injury or cerebral edema despite an initial normal study (23). The optimal technique of performing an emergency CT scan on an injured child and the use of contrast material remain unclear. Most institutions perform an initial head CT scan without intravenous contrast. The use of intravenous contrast during a CT scan for intrathoracic or intra-abdominal trauma improves its diagnostic accuracy, but is not required and can be omitted during the initial scan, depending upon the experience and protocols of the particular trauma center. The benet of using oral contrast for an abdominal CT scan in injured children is also a matter of debate. In a randomized, prospective adult clinical trial, the addition of oral contrast to an acute abdominal CT scan for trauma was found to be unnecessary and to cause delay in the time to CT scanning (24). In a review of 2162 patients with blunt trauma and an abdominal CT scan, Tsang et al. found that all seven patients with an intestinal perforation had studies that showed neither extraluminal air nor extraluminal oral contrast (25). In some centers, due to the length of time needed to ll the bowel with contrast and the resultant full stomach, which is thought to promote vomiting with aspiration, gastrointestinal (GI) contrast is avoided in the initial CT scan of the abdomen in the injured child. However, others suggest that it improves the accuracy of abdominal CT scans when intestinal or retroperitoneal injury is suspected, and that oral contrast administration is safe with minimal risk of aspiration (26,27). In summary, the use of GI contrast in emergency CT scans of the abdomen for trauma is a matter of institutional preference at the present time. Evidence, on CT scan, of intra-abdominal injuries requiring operative correction may be subtle (Fig. 4). While the ndings of free intraperitoneal or retroperitoneal air, extraluminal GI contrast medium, a bowel wall defect and active hemorrhage are often obvious and have a high correlation with intestinal injury requiring operative intervention, potentially life-threatening intestinal injuries may be manifest only by

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Figure 4 Blunt abdominal trauma in an 8-year-old male. The arrow indicates a complete transection of the tail of the pancreas, 12 hours after injury.

focal bowel wall thickening or peritoneal uid accumulation without solid organ injury (28,29). Other less specic ndings associated with intestinal injuries include mesenteric stranding, uid at the mesenteric root, focal hematomas, mesenteric pseudoaneurysm, and the hypoperfusion complex (Table 2). Magnetic Resonance Magnetic resonance imaging (MRI) is most often utilized for the patient with a suspected or conrmed neurologic injury. It is also useful in the evaluation of complex
Table 2 The CT Findings That Correlate with the Need for Surgery High correlation Free intraperitoneal or retroperitoneal air Extraluminal GI contrast medium Bowel wall defect Active hemorrhage Potential correlation Focal bowel wall thickening Peritoneal uid accumulation without solid organ injury Nonspecic ndings Mesenteric stranding Fluid at the mesenteric root Focal hematomas Mesenteric pseudoaneurysm Hypoperfusion complex

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orthopedic injuries, especially of the spine, pelvis, and joints. The MRI is rarely indicated as a primary study in the acute setting. It is especially helpful in patients with neurologic abnormalities whose X rays and CT scans are normal and to conrm clinically suspected fractures in children with no abnormality on standard radiographs (30,31). Some investigators advocate MRI to evaluate patients with traumatic aortic rupture, suggesting that in patients who would otherwise be managed with observation and delayed surgical intervention, it is the ideal modality with which to follow the patient prior to repair (32). The use of magnetic resonance cholangiopancreatography (MRCP) has not been extensively investigated with respect to pediatric pancreatic injuries, but we have found it a valuable imaging technique. Angiography and Interventional Radiology Vascular imaging studies are useful when large vessel injuries, especially those of arteries, are suspected. While pediatric vascular injuries are rare, they are often subtle in presentation and can be difcult to repair. Blunt injury of the aorta is best evaluated with angiography. It is the standard to which other diagnostic tests are compared (7). Spiral or helical chest CT scans are useful screening or diagnostic studies, but if indeterminate, the surgeon should rely on arteriography for diagnosis. A wide assortment of vascular injuries may be managed by the interventional radiologists use of endovascular transcatheter therapies. The intentional occlusion of a vessel using particulate matter is the current FDA-approved radiologic treatment for some vascular injuries. Using catheters as small as 2F or 3F, tiny vessels can be permanently occluded with a variety of microcoils, beads, or Gelfoam Pharmacia and UpJohn Company, Michigan, U.S.A. Embolic therapy for vascular injuries in children should be considered when surgical control of the vessel or vessels would be difcult or impossible, and only expendable vessels would be permanently occluded. This technique should be considered damage control angiography (33). Vascular injuries of the head and neck, pelvis, liver, spleen, kidney, retroperitoneum, and extremities are all amenable to transvascular embolic management (3440). In addition, interventional radiologic management of pancreatic injuries, intrathoracic uid collections, and intra-abdominal infections is now widely accepted (4143). This image-based approach to managing complex complications of trauma should be included in the armamentarium of the physician treating the injured child. In summary, the radiologic study of the injured child is a vital component of the diagnostic evaluation that begins as the patient enters the trauma system. As imaging modalities improve with technical advancements, the ability to quickly diagnose injuries will likely keep pace. REFERENCES
1. Klassen TP, Ropp LJ, Sutcliffe T, Blouin R, Dulberg C, Raman S, Li MM. A randomized, controlled trial of radiograph ordering for extremity trauma in a pediatric emergency department. Ann Emerg Med 1993; 22(10):15241529. 2. Sharieff GQ, Kanegaye J, Wallace CD, McCaslin RI, Harley JR. Can portable bedside uoroscopy replace standard, post-reduction radiographs in the management of pediatric fractures? Pediatr Emerg Care 1999; 15(4):249251. 3. Thourani VH, Pettitt BJ, Schmidt JA, Cooper WA, Rozycki GS. Validation of surgeonperformed emergency abdominal ultrasonography in pediatric trauma patients. J Pediatr Surg 1998; 33(2):322328.

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4. Krupnick AS, Teitelbaum DH, Geiger JD, Strouse PJ, Cox CS, Blane C, Polley TZ. Use of abdominal ultrasonography to assess pediatric splenic trauma. Potential pitfalls in the diagnosis. Ann Surg 1997; 227(4):408414. 5. Emery KH, Mcaneney CM, Racadio JM, Johnson ND, Evora DK, Garcia VK. Absent peritoneal uid on screening trauma ultrasonography in children: a prospective comparison with computed tomography. J Pediatr Surg 2001; 36(4):565569. 6. Patel JC, Tepas JJ III. The efcacy of focused abdominal sonography for trauma (FAST): a screening tool in the assessment of injured children. J Pediatr Surg 1999; 34(1): 4447. 7. Nagy K, Fabian T, Rodman G, Fulda G, Rodriguez A, Mirvis S. Guidelines for the diagnosis and management of blunt aortic injury: an EAST Practice Management Guidelines Work Group Study. J Trauma 2000; 48(6):11281143. 8. Merten DF, Carpenter BLM. Radiologic imaging of inicted injury in the child abuse syndrome. Pediatr Clin North Am 1990; 37:815937. 9. Lloyd DA, Carty H, Patterson M, Butcher CK, Roe D. Predictive value of skull radiography for intracranial injury in children with blunt head injury. Lancet 1997; 349: 821824. 10. Wang MY, Grifth P, Sterling J, McComb JG, Levy ML. A prospective populationbased study of pediatric trauma patients with mild alterations in consciousness (GCS 1314). Neurosurgery 2000; 46(5):10931099. 11. Mutabagani KH, Coley BD, Zumberge N, McCarthy DW, Besner GE, Caniano DA, Cooney DR. Preliminary experience with focused abdominal sonography for trauma (FAST) in children: is it useful? J Pediatr Surg 1999; 34(1):4852. 12. Coley BD, Mutabagani KH, Martin LC, Zumberge N, Cooney DR, Caniano DA, Besner GE, Groner JI, Shiels WE II. Focused abdominal sonography for trauma (FAST) in children for blunt abdominal trauma. J Trauma 2000; 48(5):902906. 13. Suthers SE, Albrecht R, Foley D, Mantor PC, Pufnbarger NK, Jones SK, Tuggle DW. Surgeon-directed ultrasound for trauma is a predictor of intra-abdominal injury in children. Am Surg 2004; 70(2):164167. 14. Kimura A, Otsuka T. Emergency Center ultrasonography in the evaluation of hemoperitoneum: a prospective study. J Trauma 1991; 31:2023. 15. Tso P, Rodriguez A, Cooper C, Militello P, Mirvis S, Badellino MM, Boulanger BR, Foss FA Jr, Hinson DM, Mighty HE, et al. Sonography in blunt abdominal trauma: a preliminary progress report. J Trauma 1992; 33:3943. 16. Hoffman R, Nerlich M, Muggia-Sullam M, Pohlemann T, Wippermann B, Regel G, Tscherne H. Blunt abdominal trauma in cases of multiple trauma evaluated by ultrasonography: a prospective analysis of 291 patients. J Trauma 1992; 32:452458. 17. Rozycki GS, Ochsner MG, Jafn JH, Dinsmore BJ, Champion HR. Prospective evaluation of surgeons use of ultrasound in trauma patients. J Trauma 1993; 34:516526. 18. Luks FI, Lemire A, St. Vil D, Di Lorenzo M, Filiatruat D, Ouimet A. Blunt abdominal trauma in children: the practical value of ultrasonography. J Trauma 1993; 34:607610. 19. Sarkisian AE, Khondkarian A, Amirbekian NM, Bagdasarian NB, Khojayan RL, Oganesian YT. Sonographic screening of mass casualties for abdominal and renal injuries following the 1988 Armenian earthquake. J Trauma 1991; 31:247250. 20. Bode PJ, Niezen RA, Van Vugt AB, Schipper J. Abdominal ultrasound as a reliable indicator for conclusive laparotomy in blunt abdominal trauma. J Trauma 1993; 34:2731. 21. Shackford SR. Credentialing, Liability, and Turf Wars. American College of SurgeonsUltrasound Instructors Course, April 2001; 45. 22. Ruess L, Sivit CJ, Eichelberger MR, Gotschall CS, Taylor GA. Blunt Abdominal Trauma in Children: impact of CT on Operative and Nonoperative Management. AJR 1997; 169:10111014. 23. O Sullivan MG, Statham PF, Jones PA, Miller JD, Dearden NM, Piper IR, Anderson SI, Housley A, Andrews PJ, Midgley S. Role of intracranial pressure monitoring

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Tuggle and Markley in severely head injured patients without signs of intracranial hypertension on initial computerized tomography. J Neurosurg 1994; 80:4650. Stafford RE, McGonigal MD, Weigelt JA, Johnson TJ. Oral contrast solution and computed tomography for blunt abdominal trauma: a randomized study. Arch Surg 1999; 134(6):622626. Tsang BD, Panacek EA, Brant WE, Wisner DH. Effect of oral contrast administration for abdominal computed tomography in the evaluation of acute blunt trauma. Ann Emerg Med 1997; 30(1):713. Federle MP, Yagan N, Peitzman AB, Krugh J. Abdominal Trauma: use of oral contrast material for CT is safe. Radiology 1997; 205:9193. Lim-Dunham JE, Narra J, Benya EC, Donaldson JS. Aspiration after administration of oral contrast material in children undergoing abdominal CT for trauma. AJR 1997; 169:10151018. Strouse PJ, Close BJ, Marshall KW, Cywes R. CT of bowel and mesenteric trauma in children. Radiographics 1999; 19:12371250. Cox TD, Kuhn JP. CT scan of bowel trauma in the pediatric patient. Radiol Clin North Am 1996; 34(4):807818. Felsberg GJ, Tien RD, Osumi AK, Cardenas CA. Utility of MR imaging in pediatric spinal cord injury. Pediatr Radiol 1995; 25(2):131135. Naranja RJ Jr, Gregg JR, Dormans JP, Drummond DS, Davidson RS, Hahn M. Pediatric fracture without radiographic abnormality. Description and signicance. Clin Orthop 1997; 342:141146. Fattori R, Celletti F, Bertaccini P, Galli R, Pacini D, Pierangeli A, Gavelli G. Delayed surgery of traumatic aortic rupture. Role of magnetic resonance imaging. Circulation 1996; 94(11):28652870. Ben-Menachem Y. Exploratory and interventional angiography in severe trauma: present and future procedure of choice. Radiographics 1996; 16(4):963967. Sclafani AP, Sclafani SJ. Angiography and transcatheter arterial embolization of vascular injuries of the face and neck. Laryngoscope 1996; 106:168173. Agolini SF, Shah K, Jaffe J, Newcomb J, Rhodes M, Reed JF III. Arterial embolization is a rapid and effective technique for controlling pelvic fracture hemorrhage. J Trauma 1997; 43(3):395399. Schwartz RA, Teitelbaum GP, Katz MD, Pentecost MJ. Effectiveness of transcatheter embolization in the control of hepatic vascular injuries. J Vasc Interv Radiol 1993; 4(3):359365. Davis KA, Fabian TC, Croce MA, Gavant ML, Flick PA, Minard G, Kudsk KA, Pritchard FE. Improved success in nonoperative management of blunt splenic injuries: embolization of splenic artery pseudoaneurysms. J Trauma 1998; 44(6):10081013. Corr P, Hacking G. Embolization in traumatic intrarenal vascular injuries. Clin Radiol 1991; 43(4):262264. Velmahos GC, Chahwan S, Falabella A, Hanks SE, Demetriades D. Angiographic embolization for intraperitoneal and retroperitoneal injuries. World J Surg 2000; 24(5):539545. Schwartz MR, Weaver FA, Bauer M, Siegel A, Yellin AE. Rening the indications for arteriography in penetrating extremity trauma: a prospective analysis. J Vasc Surg 1993; 17(1):116122. Wales PW, Shuckett B, Kim PC. Long-term outcome after nonoperative management of complete traumatic pancreatic transection in children. J Pediatr Surg 2001; 36(5):823827. Moulton JS. Image-guided management of complicated pleural uid collections. Radiol Clin North Am 2000; 38(2):345374. van Sonnenberg E, Wittich GR, Goodacre BW, Casola G, DAgostino HB. Percutaneous abscess drainage: update. World J Surg 2001; 3(25):362369.

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Transfusion Therapy in Injured Children
Denis D. Bensard
The Childrens Hospital, The University of Colorado, Denver, Colorado, U.S.A.

INTRODUCTION Historical Perspective The beginnings of transfusion therapy may be traced to Harveys discovery of the systemic circulation in 1628. In 1667 Jean Baptiste Denis reported the transfusion of lambs blood to a 15-year-old boy. Lacking a full understanding of the implications of blood infusion, repeated deaths followed and transfusion was abandoned. The use of blood transfusion remained dormant for the next 150 years until James Blundell recognized that only human blood should be used for human transfusion. Yet, deaths continued to occur, most likely due to blood incompatibility and hemolytic transfusion reaction. In 1900, Karl Landsteiner determined the heterogeneity of blood and the importance of blood groups, a discovery for which he would later win the Nobel Prize. The integration of Landsteiners work in blood typing into effective therapy was limited by technical factors such as poor vascular access and frequent clotting of blood due to the lack of understanding of coagulation (1). In the decades that followed, techniques for reliable venous access were improved and sodium citrate was discovered as an effective anticoagulant, permitting storage of blood until transfused. World War II served as a catalyst for further developments, leading to the concept of blood banking and blood service organizations to procure blood. The Viet Nam War led to integration of transfusion therapy into the acute care of injured patients. Resuscitation times decreased and operative intervention occurred earlier, relative to previous conicts. Improvements in the treatment of wartime casualties were quickly incorporated into the management of civilian injuries. The rapid expansion of transfusion therapy abruptly ended when it became apparent that blood components could transmit potentially fatal viral pathogens. Viral transmission associated with blood exposure prompted efforts at more effective screening of blood and highlighted the importance of the judicious use of blood products. In the 1980s red blood cell and component transfusion began to stabilize, in contrast to the exponential increase observed in the preceding decades. Approximately 10 million

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red cell units were transfused in the United States in 1980, peaking at 12.2 million units in 1986, and subsequently declining to 11.4 million units in 1997 (2). LITERATURE-BASED GUIDELINES A computerized search of MEDLINE from 1990 to 2002 was performed and the following summarizes a review of the literature regarding the indications, results, and complications of transfusion therapy. Few randomized, controlled studies of transfusion practices have been conducted (class I) (37). The majority of studies represent class-II evidence (nonrandomized, controlled trials; controlled observational studies; or uncontrolled observational studies) and class-III evidence (expert opinion) developed in consensus conferences (813). Approximately 22 million blood component units are currently transfused annually in the United States, with the major portion administered to surgical patients. At an average cost $150 per unit transfused, transfusion therapy is expensive. In the United States, approximately $2 billion is spent annually for blood transfusion; the cost actually may be as high as $7 billion per year if indirect costs due to inefcient transfusion practices and complications are included (12,14). The risk of a transfusion-related complication ranges from 1:100 for a minor allergic reaction to 1:30,000 for hepatitis C infection to 1:250,000 for a fatal acute hemolytic reaction (2). The risks of transfusion therapy led to efforts to reduce and develop guidelines for its use. Like prior National Institute of Health (NIH) consensus conferences, the Blood Management Practice Guidelines Conference Group and the American Society of Anesthesiologists Task Force on Blood Component Therapy concluded that no single measure is capable of replacing clinical judgment regarding transfusion practices (812). With respect to red cell transfusion, there appears to be no single criterion for transfusion, such as a hemoglobin concentration of less than 10 mg/dL. Acknowledging that blood transfusion carries a documented risk for infection, adverse events, and potential immunologic effects, these groups recommend that blood transfusion should be kept to a minimum and that alternative blood substitutes be developed. EPIDEMIOLOGY An audit of blood component use in the United States showed that 11,107,000 red blood cell (RBC) units (42.8 units per 1000), 7,866,000 platelet units (16.5 units per 1000), and 2,621,000 fresh frozen plasma (FFP) units (10.1 units per 1000) were transfused in 1994 (15). The prevalence of transfusion therapy in injured children is less clear. In a review of children treated in the emergency department (ED) of a pediatric trauma center over a four-month period, 20 units of blood were transfused to 2 of 38 (5%) children suffering major trauma (14). Review of the National Pediatric Trauma Registry (NPTR, October 2000) demonstrates that, of the 39,681 children in the database, 3453 (0.9%) received blood component therapy. This low incidence of transfusion is likely due, in part, to the mild (ISS 19) to moderate (ISS 1019) injury severity, which comprises 90% of the children within the NPTR. Selected injured children with multiple injury or severe solid organ injury will require blood transfusion. In a population of severely injured children, ISS > 25, GCS < 7, immediate blood transfusion >20 mL/kg, and Pediatric Trauma Score < 4

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were all independent risk factors for death. The probability of death was 0.63 in those children with all threshold values (16). A review of 832 children with isolated splenic or liver injury treated in 32 pediatric surgical centers demonstrated that incidence of transfusion and laparotomy increased with the computed tomography (CT) grade of injury [transfused (%)/laparotomy(%)]: grade I 1.8/0; grade II 5.2/1; grade III 10.1/2.7; and grade IV 26.6/12.6 (17). Nonoperative management is now the accepted treatment of solid organ injury in the hemodynamically stable child (17,18). The fear of excessive transfusion has led some to question this form of management. Using decision analysis, Feliciano concluded that the nonoperative management of splenic injuries was associated with an increased mortality from transfusion-related deaths (19). These concerns seem unfounded in children, since a number of studies demonstrate that the operative management of splenic and liver injuries is associated with a greater transfusion requirement than nonoperative management (2022). Moreover, the tendency to transfuse children with solid organ injury appears to be declining (23). In a series of children treated over a six-year period with liver or splenic injury, Bond found that transfusion rates during the latter half of the study declined from 50% to 19% for hepatic injuries, despite increasing grade of injury, and 57% to 23% for splenic injuries with comparable injury grade (24). Similar trends have been observed in the management of injured adults (25). Although children with multiple injuries appear to have a higher transfusion requirement, we found that the frequency of transfusion declined from 67% to 35% during the last decade in children with multiple intra-abdominal injuries (21,23). Isolated orthopedic injuries rarely require transfusion in children unless other injuries are present or they involve major disruption of the pelvic ring (2628). In summary, while it appears that the need for transfusion in children is low, severely and multiply injured children are more likely to require blood component therapy.

PATHOPHYSIOLOGY Hypovolemic shock due to acute blood loss is the most common form of shock observed in injured children. By denition, shock represents a state of inadequate tissue perfusion to maintain normal cellular and organ function. The maintenance or restoration of normal oxygen delivery (DO2) to tissues, not an arbitrary hemoglobin value, should be the primary therapeutic goal of red blood cell transfusion. The DO2 is dened as the product of blood ow (cardiac output) and arterial oxygen content (CaO2). At or near the critical DO2 point, two parameters that reect tissue perfusion begin to change: (i) lactate level increases, and (ii) the oxygen extraction ratio (OER), dened as oxygen consumption/DO2, increases. Increases in the OER and lactate below the critical DO2 point represent a physiologic transfusion trigger (29). Interventions to improve DO2 are directed to maximize carbon monooxide (CO) and O2 carrying capacity. In the setting of traumatic shock, cardiac output is optimized rst by increasing preload with uid resuscitation. Reducing afterload or supplementing cardiac contractility may become necessary if uid resuscitation alone fails. If efforts to improve cardiac output are insufcient to improve DO2, then oxygen content may be targeted. Oxygen-carrying capacity depends on several variables [CaO2 1.36 hemoglobin saturation (%) 0.0034 PaO2], but hemoglobin concentration is the principal determinant. An acute decrease in hemoglobin produces

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Figure 1 Changes in oxygen delivery (DO2) with changes in hemoglobin (Hb) concentration and oxygen saturation (SaO2). Note the effect of decreased SaO2 on the need to increase cardiac output (CO) to maintain normal global DO2. Correction of SaO2 will measurably decrease CO. Source: From Ref. 29.

a drop in DO2 unless there is a compensatory increase in cardiac output (Fig. 1). A healthy individual may tolerate up to a 40% decrease in blood volume by increasing heart rate, redistributing uid from the extravascular space to the intravascular space, reducing blood viscosity, and increasing oxygen extraction. Ensuring complete oxygen saturation with the augmentation of inspired oxygen is easily accomplished with the addition of supplemental oxygen. In general, the healthy patient can compensate as hemoglobin falls to 5 g/dL, but below this level compensatory responses begin to fail. They become inadequate at levels below 3.5 g/dL. The mortality rate exceeds 50% for hemoglobin concentration less than 3 g/dL (30). In the setting of refractory shock and maximized cardiac output, increasing the hemoglobin concentration with blood transfusion becomes necessary. The actual utilization of oxygen by tissues is oxygen consumption. When oxygen consumption exceeds oxygen availability, anaerobic metabolism begins and lactate production increases. In hemorrhagic shock, reduced O2-carrying capacity and blood volume contraction exist at the same time. Restoration of blood volume by crystalloid infusion can reestablish cardiac output. Current experience suggests that otherwise healthy patients with hemoglobin values of less than 10 g/dL rarely require transfusion. Studies in Jehovahs Witness patients who refuse blood transfusion demonstrate that extremely low hemoglobin levels can be tolerated (31). In surgical patients who refuse blood, Carson found that no deaths occurred among patients with hemoglobin levels >6 g/dL and blood loss less than 500 mL (32). The critical principle in the management of the trauma patient is the restoration of DO2 and correction or avoidance of tissue hypoxia. The decision to augment DO2 in the setting of hemorrhagic shock with the administration of blood depends upon the severity of preexisting blood loss, the degree of ongoing blood losses, and the individuals compensatory ability to maintain the balance of DO2 to consump-

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tion. The optimal transfusion trigger remains elusive, but healthy patients tolerate hemoglobin as low as 7 g/dL if adequately resuscitated and without ongoing blood loss. In a study of healthy volunteers, acute isovolemic reduction of hemoglobin to 5 g/dL results in increased heart rate, stroke volume, and cardiac index and a slight increase in oxygen consumption, but does not produce evidence of inadequate systemic DO2 or increased lactate production (33). The same is true of euvolemic patients undergoing elective surgical procedures (32). In an elderly population undergoing surgical repair of hip fracture, a hemoglobin concentration of >8 g/dL had no apparent effect upon 30- or 90-day mortality (34). Together these studies demonstrate that in diverse populations of patients, low hemoglobin is well tolerated, even in patients undergoing surgery, if intravascular volume is maintained and cardiac function is satisfactory. In the setting of trauma, the adequacy of resuscitation is guided by the restoration of normal vital signs and organ perfusion. The use of lactate measurements to detect inadequate tissue perfusion and, therefore, inadequate resuscitation is helpful in selected situations. Minimally invasive measures of tissue oxygenation, skeletal muscle oximetry, or gastric tonometry, as well as the more invasive techniques of central vascular monitoring, have been used in an attempt to identify the endpoints of resuscitation. Yet, no single parameter exists to dene the optimal transfusion trigger, and the decision to transfuse must be made on a case-by-case basis. COMPONENT THERAPY At the time of collection blood is typically fractionated into its constitutive components of red blood cells, platelets, plasma, cryoprecipitate, and concentrated clotting factors. Component therapy allows the more efcient use of donated blood and avoids the undesirable effects of whole blood due to antibodyantigen reactions to platelets and white blood cells. For these reasons, whole blood is rarely transfused. Packed Red Blood Cells (PRBCs) Red blood cells are obtained by removing the supernatant plasma from 450 mL of whole blood after centrifugation and anticoagulation. The average volume of 1 unit of PRBCs is approximately 250 mL with a hematocrit of 60%. Small amounts of clotting factors and platelets are present but nonfunctional. Red blood cell infusion is indicated to increase RBC mass and therefore oxygen transport. Blood volume varies with age, ranging from 90 to 100 mL/kg in the premature infant to 70 mL/kg in children over one year of age. Therefore, blood should be administered in boluses of 10 mL/kg in infants and small children. Consensus Guidelines for Transfusion of Red Blood Cells 1. The use of a single hemoglobin trigger for all patients and other approaches that fail to consider all-important physiologic and surgical factors affecting oxygenation are not recommended. 2. Transfusion is rarely indicated when hemoglobin is >10 g/dL but generally indicated when the hemoglobin is <6 g/dL when the anemia is acute. 3. The determination of whether intermediate hemoglobin concentrations (610 g/dL) justify or require RBC transfusion should be based on the patients risk for complications of inadequate oxygenation (9,12,13).

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Washed Red Blood Cells After the red blood cells have been separated they are washed with isotonic saline solution. This process removes nearly all white cells, platelets, plasma proteins, and debris. The resultant product signicantly decreases antigenicity and nonhemolytic febrile reactions caused by recipient antibodies to leukocyte antigens. Washed red blood cells are reserved for patients suffering complications of previous transfusion because of the increased processing time and cost. There appears to be a dose-dependent relationship between early blood transfusion and the later development of multiple organ failure (MOF) (35). Sauaia found that transfusion of greater than six units of PRBC within the rst 12 hours postinjury is an independent risk factor for the development of MOF (36). The lipid fraction in the stored blood, which increases with storage time, has been implicated as a mechanism for this phenomenon (37). Zalen demonstrated that trauma patients were more likely to develop MOF if transfused blood is >14 or >21 days old (38). Platelets A unit of platelet concentrate is extracted from the platelet rich plasma of one unit of whole blood to yield 5 1010 platelets in 60 mL of plasma. Platelets may be stored up to ve days. The product will retain 70% of platelet viability and 80% of the original clotting factor activity. Platelet transfusion is indicated to correct clinically signicant thrombocytopenia. Platelet concentrates contain white cells and may cause febrile reactions due to white cell antigens. However, since platelets are stored near room temperature, the risk of bacterial infection due to contamination should be considered. In children, transfusion of one unit of platelets per m2 increases the platelet count 20,000, with an average platelet survival of six to seven days. The usual dosage is: less than 5 years 13 units; 510 years 45 units; and greater than 10 years 6 units. Consensus Guidelines for the Transfusion of Platelets 1. Surgical patients with microvascular bleeding usually require platelet transfusion if the platelet count is less than 50,000/mL and rarely require therapy if it is greater than 100,000/mL; with intermediate platelet counts the determination should be based on the patients risk for more signicant bleeding. 2. Platelet transfusion may be indicated despite an apparently adequate platelet count if there is known platelet dysfunction and microvascular bleeding (10,12,13). Fresh Frozen Plasma When a unit of whole blood is fractionated the plasma components are frozen. Coagulation factors are present in the levels obtained from fresh whole blood. Storage at 18 C preserves clotting factor activity. The time to prepare and thaw FFP for transfusion is 30 to 45 minutes. Unfortunately, FFP is often overused for ongoing bleeding when more specic or more effective therapy is available. The NIH Consensus Conference concluded that 90% of FFP is given for inappropriate indications (8). Microvascular bleeding in the trauma patient typically results from massive transfusion, thrombocytopenia, and/or consumption of brinogen, none

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of which is readily corrected with FFP. The FFP transfusion should be reserved for the bleeding patient with a coagulation defect caused by liver disease, coumadin, or congenital factor deciency. The FFP should never be used for volume expansion. The FFP carries the same risk of transfusion-transmitted disease as blood. In infants and small children FFP is administered in 10 mL/kg boluses. Consensus Guidelines for the Transfusion of Fresh Frozen Plasma 1. The urgent reversal of coumadin therapy 2. Correction of known coagulation factor deciencies for which specic concentrates are unavailable 3. Correction of microvascular bleeding in the presence of elevated (>1.5 times normal) prothrombin time (PT) or partial thromboblastin time (PTT) 4. Correction of microvascular bleeding secondary to coagulation factor deciency in patients transfused with more than one blood volume and when PT/PTT measurements cannot be obtained in a timely fashion 5. FFP is contraindicated for augmentation of plasma volume or albumin concentration (8,12,13). Cryoprecipitate Cryoprecipitate is prepared from individual donors and contains concentrated factor VIII, von Willebrand Factor (vWF), and brinogen. Freezing of plasma to 80 C and then rewarming to 4 C allows separation of the precipitate, which contains 200 mg of brinogen, 150 units of factor VIII/vWF and 100 units of factor VIII. Since it is usually administered as a pooled product obtained from individual donors, cryoprecipitate carries the greatest risk of transfusion-transmitted disease. A typical adult dose (10 units) represents 10 donor exposures. Cryoprecipitate is the only concentrated form of brinogen and is therefore indicated for patients with dysbrinogenemia, hypobrinogenemia, or consumptive coagulopathy. In the past cryoprecipitate was used for patients with hemophilia A and von Willebrand disease but today specic factor replacement is available for these patients. Cryoprecipitate may also be used for brin glue, but commerciall brin glue preparations are now available, which substantially reduce the risk of transfusion-transmitted disease. Consensus Guidelines for the Transfusion of Cryoprecipitate 1. Correction of microvascular bleeding in massively transfused patients with brinogen concentrations less than 80100 mg/dL or when brinogen concentrations cannot be measured in a timely fashion (12,13) EMERGENCY MANAGEMENT Acute Resuscitation Hemorrhagic shock is the most common form of shock observed in injured children. Rapid identication and treatment of hemorrhagic shock is one of the core principles in the ABCs of trauma resuscitation. In a study of all trauma deaths occurring in the city and county of Denver, exsanguination was the second leading cause of acute (<48 hours) deaths (39). In the acute phase of resuscitation, the recognition of acute blood loss and shock is dependent upon an accurate assessment of clinical indices of organ function and perfusion. The American College of Surgeons Committee on

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Table 1 Classication of Hemorrhagic Shock in the Injured Child and the Probability of Blood Transfusion Based on Clinical Assessment Class I 1530% >100 Normal Mild Combative Cool 510 0.51 mL/kg >120 Hypotension Moderate Confused Mottled 1015 <0.5 mL/kg None Remain abnormal 3040% Class II Class III Class IV >40% >140 Severe hypotension Severe Lethargic Pallor >20 Negligible

<15%

Blood loss [blood volume (%)] Clinical ndings Heart rate Blood pressure Respirations (tachypnea) Mentation Skin Capillary rell (sec) Urine output Resuscitation Response to initial uids Vital signs

<100 Normal No Anxious Warm <5 13 mL/kg

Rapid Return to normal

Blood preparation Blood transfusion risk

Type and crossmatch Low

Transient Improvement, then recurrent tachycardia, hypotension Type-specic Moderatehigh

O-negative Immediate

Source: Modied from Ref. 40.

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Trauma has developed a useful classication of hemorrhagic shock based on systemic signs (Table 1) (40). Estimates of blood loss are based on parameters of cardiovascular, respiratory, central nervous system, and renal function. Furthermore, the response to initial uid resuscitation suggests the degree of blood loss, the rate of ongoing bleeding, and the likelihood of the need for blood transfusion. A rapid response to uid administration suggests minimal blood loss (class I) and a low probability of blood transfusion. A transient response suggests moderate and ongoing blood loss (classes II and III) and a moderate to high need for blood. If no response to initial uid resuscitation is observed then severe blood loss (class IV) is likely and immediate transfusion is indicated. If signs and symptoms of shock are present, a bolus of 20 mL/kg of crystalloid solution is rapidly administered and assessment repeated. If signs of shock continue another crystalloid bolus is given. External hemorrhage should be controlled with pressure and fractures splinted to reduce ongoing blood loss. Minimal or no response to crystalloid administration and the absence of obvious bleeding suggests internal hemorrhage. In this setting acute blood transfusion is indicated. O-negative or noncrossmatched-type PRBCs are administered in 1020 mL/kg boluses and preparation is made for prompt operative intervention to control further blood loss. The use of O-negative or noncrossmatched-type specic blood is equally safe for emergency volume resuscitation but should be reserved only for these situations. Fully crossmatched blood is associated with the lowest risk of unexpected hemolytic reactions, but generally requires 30 to 45 minutes to prepare. In lifethreatening situations blood resuscitation should not be delayed while awaiting crossmatch. It must be kept in mind that the use of greater than one-half blood volume of O-negative blood complicates later crossmatching. If the patient is subsequently given type-specic blood there is a signicant risk of hemolytic transfusion reaction. For this reason, the use of O-negative blood should be limited to less than 25% of the estimated blood volume. In situations when this is not possible, O-negative blood should be continued until the patient is stable. Massive Transfusion Selected patients will suffer near exsanguination and require massive transfusion until hemorrhage is controlled. The mortality in patients requiring massive transfusion following blunt trauma exceeds 50%. Half of these succumb within the rst 24 hours (41). Long-term outcome in survivors appears excellent (42). Transfusion of greater than one blood volume within a 24-hour period is dened as massive transfusion and associated with a number of hematologic complications. The primary complication following transfusion to this degree is coagulopathy. As blood loss approaches 1.5 blood volumes, platelets and clotting factors become diluted. Platelet count decreases to approximately 40% from baseline with replacement of one blood volume, 60% with two blood volumes, and 70% with three blood volumes. Microvascular bleeding generally occurs at a platelet count <50,000/mL. Clinically important dilution of clotting factors also occurs after replacement of 1.5 blood volumes. A PT or PTT value >1.8 times control is 96% specic for microvascular bleeding. Conversely, a PT < 1.3 times control has a 94% predictive value for the absence of microvascular bleeding. The most sensitive predictors of microvascular bleeding are platelet count less than 50,000/mL and a brinogen less than 0.5 g/L (43). Microvascular bleeding in the setting of massive transfusion is most likely due to signicant thrombocytopenia, clotting

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factor dilution, and hypobrinogenemia and is therefore an indication for platelet, factor, and brinogen replacement.

DEFINITIVE MANAGEMENT Operative Intervention Perhaps the most effective measure to limit blood transfusion therapy is the elimination of further bleeding by surgical intervention. Any child with suspected thoracic, abdominal, or vascular injury who is refractory to resuscitation should be taken promptly to the operating room. Given the success of nonoperative management of solid organ injury in children, one must be vigilant in recognizing the child who is continuing to bleed and requires operative therapy. In general, any child with a known solid organ injury in the abdomen who remains hemodynamically unstable despite adequate uid resuscitation, or requires >1/2 blood volume replacement within the rst 24 hours, has continuing bleeding and requires a laparotomy. Clinical variables in patients with splenic injury suggesting the need for surgical intervention include hypotension in the eld or ED, tachycardia in the ED, initial hematocrit less than 30, multiple injuries, or the need for blood transfusion in the ED (44). Once operative control is achieved, additional measures can be employed to reduce the need for blood transfusion. The use of uid warmers, heated ventilatory circuits, and active warming devices reduce the risk of hypothermia and the coagulopathy associated with decreased body temperature. Further surgical measures and techniques like argon beam coagulation, collagen hemostatic agents, brin sealant, abdominal packing, vascular isolation, or arteriography with embolization have all been effectively employed in the management of surgical bleeding. The basis for deciding to transfuse the patient intraoperatively is less clear. Remember, elective surgical procedures have been safely performed in adults with severe anemia (hemoglobin <7 g/dL) who refuse blood on religious grounds, provided normovolemia is maintained (34). The decision to transfuse should be based on an assessment of the patients condition, estimate of blood loss prior to surgical control, and ongoing blood loss. Endpoints of Resuscitation The conventional endpoints of resuscitationreturn of normal heart rate, blood pressure, and urine outputmay be all that are necessary in the previously healthy injured child with normal cardiopulmonary function. Base decit (BD) and lactate appear to accurately reect the hemodynamic and tissue perfusion changes associated with hemorrhagic shock. Increases in BD parallel oxygen transport parameters such as a-v O2 difference, DO2, and oxygen consumption. Similarly, lactate levels and BD can be used to guide resuscitation (45,46). Injury survivors with moderate to severe BD improve their BD within four hours and normalize their BD by 16 hours. Nonsurvivors fail to improve their BD to 6 or better, despite ongoing resuscitation (46). Moreover, transfusion requirements appear increased with more severe BD. In severely injured patients, transfusions were required within 24 hours of admission in 72% of patients with a BD  6 versus 18% of patients with a BD  6 (45). Endpoints of resuscitation should not rely solely on BD or lactate level. Mikulascheck demonstrated that if treatment decisions were guided by BD or anion gap, incorrect treatment would occur in up to one-half of patients (47).

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Persistent lactic acidosis suggests occult hypoperfusion. In a prospective study of trauma patients with two consecutive lactic acid levels >2.5 mmol/L who underwent invasive monitoring and resuscitation, Blow found a correlation between lactic acidosis and poor cardiac performance. Patients with persistent hypoperfusion despite resuscitative efforts demonstrated 43% mortality (48). The normalization of end organ and tissue perfusion as measured by serum lactate is perhaps the most reliable perfusion marker available (49). Recovery The recovery phase of injury until the time of discharge is the period when the greatest reduction in transfusion can be accomplished without compromising the patient. In the absence of ongoing blood loss, equilibration of the uid compartments rarely produces signicant changes in the hematocrit. Critically ill patients with hemoglobin concentrations less than 9 g/dL, randomized to a restrictive strategy in which transfusion was administered only for hemoglobin less than 7 g/dL or to a liberal transfusion strategy in which hemoglobin concentrations were maintained greater than 10 g/dL, demonstrated that a restrictive strategy of red cell transfusion results in a lower 30-day mortality in patients who are <55 years of age, less acutely ill, and without signicant cardiac disease (7). During the recovery period the decision to transfuse should be made only on the basis of symptoms or signs of ischemia. In general, children are not at risk for myocardial ischemia and rarely manifest signs of anemia (dyspnea, fatigue, and tachycardia). Blood draws should be minimized or eliminated, particularly if the patient is afebrile, asymptomatic, and tolerating a diet. In children with isolated splenic injury, Sha found that after an initial drop in hematocrit within the rst 24 hours post-injury, the hematocrit remained stable and returned to baseline by day six (23).

COMPLICATIONS OF TRANSFUSION Transfusion Reaction Transfusion reactions may be broadly classied into nonhemolytic and hemolytic reactions. Nonhemolytic reactions are common (1:100) and occur as the result of an allergic reaction to white blood cells or plasma proteins. In general, nonhemolytic reactions are mild, causing only fever, urticaria, and skin rash. In rare instances, life-threatening severe bronchospasm and anaphylaxis can occur. If a nonhemolytic transfusion reaction is suspected, the transfusion should be discontinued and the symptoms managed with antihistamines, epinephrine, and steroids, as indicated. Hemolytic transfusion reactions may be acute or delayed. Hemolysis occurs when recipient antibodies react with donor red blood cell antigens. Delayed reactions (1:1000) result from antibodies to the transfused blood that arose from prior transfusion or isoimmunization from pregnancy and were not detected by routine antibody assay. Fatal acute hemolytic reactions (1:250,0001:1,000,000) are caused by ABO incompatibility and most often result from either clerical or administration errors. Delayed hemolytic transfusion reactions (1:260,000) should also be considered serious and potentially life threatening. They accounted for 10% of all transfusion deaths between 1976 and 1985 (2). A hemolytic transfusion reaction is characterized

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by the rapid onset of fever, chills, rigors, chest or abdominal pain progressing to respiratory distress, and circulatory shock. Hemoglobin is present in the plasma and urine. Renal failure may ensue. Once recognized, the transfusion should immediately be discontinued. Aggressive resuscitation should be instituted to support the circulation and achieve a urine output of >60 mL/hr.

Transfusion-Transmitted Disease Viral infection, the most feared complication, is the most common cause of late death from transfusion (Table 2). The rst descriptions of transfusion-associated HIV infection occurred in late 1982. Improved screening and detection has reduced the current frequency of HIV infection to approximately to 1/250,000 1/2,000,000 units. The most common serious viral infection is hepatitis C (HCV), estimated to occur in 1/30,0001/150,000 units. Eighty-ve percent of posttransfusion HCV infections become chronic, 20% of infected patients develop cirrhosis, and 1% progress to hepatocellular carcinoma. Hepatitis B (HBV) infection is estimated to occur in 1/30,0001/250,000 units. In 1975 new screening tests were implemented, reducing transfusion-transmitted HBV infection. The HBV now accounts for only 10% of all cases of posttransfusion hepatitis. Acute disease develops in 35% of persons infected with HBV. Up to 10% will develop chronic infection. Bacterial infection due to contamination most often occurs following platelet transfusion (1/12,000 units), but can also occur following RBC transfusion (1/500,00 units). The difference in frequency is attributed to storage of platelets at 2024 C, which facilitate bacterial growth, while red blood cells are generally stored at much lower temperatures. The most common organism associated with RBC contamination is Yersinia enterocolitica, while Staphylococcus aureus, Klebsiella pneumoniae, Serratia marcescens, and S. epidermidis infections are most frequently observed in platelet-associated infection (2).

Metabolic Complications Children may be more susceptible than adults to metabolic complications with rapid transfusion because of the higher ratio of transfused blood-to-blood volume.

Table 2 Estimated Risks of Transfusion per Unit in the United States (1999) Febrile reaction Bacterial contamination Platelets Red blood cells Viral infection Hepatitis A Hepatitis B Hepatitis C HIV Delayed hemolytic transfusion reaction Fatal hemolytic transfusion reaction
Source: Adapted from Ref. 2.

1:100 1:12,000 1:500,000 1:1,000,000 1:30,0001:250,000 1:30,0001:150,000 1:200,0001:2,000,000 1:1000 1:250,0001:1,000,000

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Children are prone to hypothermia and may become profoundly hypothermic with the infusion of cold uids and blood products. Hypothermia not only increases metabolic demand but also worsens coagulopathy. Infants and small children should be maintained in a warm environment and given warmed uids and blood products. Rapid infusion can also produce severe electrolyte disturbances. Hypocalcemia or hyperkalemia may arise after large- or rapid-volume infusion and, therefore, serum electrolytes should be periodically evaluated.

RED BLOOD CELL SUBSTITUTES Due to the risks and costs of blood transfusion, efforts have been directed toward the development of hemoglobin-based red cell substitutes. Red cell substitutes do not transmit viral pathogens and have lower viscosities than blood while maintaining the same-oxygen carrying capacity of allogenic blood. Free hemoglobin has an extremely high oxygen afnity that renders it ineffective for tissue oxygenation. Furthermore, once outside the protective red cell membrane the hemoglobin tetramer disassociates into its component a and b dimers, which are potentially nephrotoxic. Polymerization of bovine, human, and recombinant hemoglobin results in synthetic hemoglobin with a P50 of natural hemoglobin, a plasma half-life up to 30 hours, and normal oncotic pressure (50). The absence of a red cell membrane eliminates the need for blood typing and crossmatching, as well as the immunologic effects attributed to surface antigens or white blood cells, platelets, and debris present in red blood cell units. One unit (500 mL) of synthetic, polymerized, stroma-free hemoglobin (Poly SFH-P) is characterized by hemoglobin concentration of 10 g/dL, P50 of 2830 torr and t1/2 of one day. A phase-II trial of Poly SFH-P demonstrated its safe use in acute trauma (51). A prospective, randomized trial of Poly SFHP in trauma patients demonstrated that the use of a red blood cell substitute for the treatment of acute blood loss reduced the need for red blood cell transfusion, while maintaining parameters of oxygen transport (4). The most recent trial of Poly SFH-P conrms the ability of red blood cell substitutes to maintain oxygencarrying capacity in the setting of acute hemorrhagic shock, even with transfusion requirements up to 20 units (52). Mortality (25%) was substantially lowered at critical hemoglobin levels 3 g/dL relative to historic controls (64.5%) who refused red blood cells on religious grounds. Remarkably 9/12 patients who sustained lethal blood loss (RBC Hb  1 g/dL) survived with the administration of Poly SFH-P and resultant total hemoglobin concentration (RBC Hb Poly SFH-P) 710 g/dL. Although these results are encouraging, the abrupt end of the diaspirin crosslinked hemoglobin (DCLHb) trial suggests that the various red blood substitutes under development are not homogenous. Unlike the Poly SFH-P trials, a phase-II trial of DCLHb administration was associated with a 72% increase in morbidity (Multiple Organ Dysfunction Score) and a threefold fold increase in mortality in the treatment group (46%) relative to the control group (17%) (53). It is speculated that selected red blood substitutes (e.g., DCLHb) bind nitric oxide, which causes the undesirable side effects of vasoconstriction and pulmonary hypertension. Nevertheless, efforts to develop a safe and effective red cell substitute continue given the advantages of a readily available, oxygen-carrying, resuscitative uid that eliminates the delay and risks of allogenic blood.

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42. Wudel JH, Morris JA Jr, Yates K, Wilson A, Bass SM. Massive transfusion: outcome in blunt trauma patients. J Trauma 1991; 31(1):17. 43. Ciavarella D, Reed F, Counts R. Clotting factor levels and the risk of diffuse microvascular bleeding in the massively transfused patient. Br J Haematol 1987; 67:365368. 44. Cathey KL, Brady WJ Jr, Butler K, Blow O, Cephas GA, Young JS. Blunt splenic trauma: characteristics of patients requiring urgent laparotomy. Am Surg 1998; 64(5):450454. 45. Davis JW, Parks SN, Kaups KL, Gladen HE, ODonnell-Nicol S. Admission base decit predicts transfusion requirements and risk of complications. J Trauma 1996; 41(5):769 774. 46. Davis JW, Kaups KL, Parks SN. Base decit is superior to pH in evaluating clearance of acidosis after traumatic shock. J Trauma 1998; 44(1):114118. 47. Mikulaschek A, Henry SM, Donovan R, Scalea TM. Serum lactate is not predicted by anion gap or base excess after trauma resuscitation. J Trauma 1996; 40(2):218222. 48. Blow O, Magliore L, Claridge JA, Butler K, Young JS. The golden hour and the silver day: detection and correction of occult hypoperfusion within 24 hours improves outcome from major trauma. J Trauma 1999; 47(5):964969. 49. Dabrowski G, Steinberg S, Ferrara J, Flint L. A critical assessment of endpoints of shock resuscitation. Surg Clinics N Amer 2000; 80:825844. 50. Creteur J, Sibbald W, Vincent J. Hemoglobin solutions-not just red blood cell substitutes. Crit Care Med 2000; 28:30253034. 51. Gould SA, Moore EE, Moore FA, Haenel JB, Burch JM, Sehgal H, Sehgal L, DeWoskin R, Moss GS. Clinical utility of human polymerized hemoglobin as a blood substitute after acute trauma and urgent surgery. J Trauma 1997; 43(2):325331. 52. Gould SA, Moore EE, Hoyt DB, Ness PM, Norris EJ, Carson JL, Hides GA, Freeman I, DeWoskin R, Moss GS. The life-sustaining capacity of human polymerized hemoglobin when red cells might be unavailable. J Am Coll Surg 2002; 195:445455. 53. Sloan EP, Koenigsberg M, Gens D, Cipolle M, Runge J, Mallory MN, Rodman GJ. Disaspirin cross-linked hemoglobin (DCHLb) in the treatment of severe traumatic hemorrhagic shock: a randomized controlled efcacy trial. JAMA 1999; 282:18571864.

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Pediatric ICU Management
Cameron Mantor, Nikola Pufnbarger, and David Tuggle
The Section of Pediatric Surgery, Department of Surgery, University of Oklahoma College of Medicine, Oklahoma City, Oklahoma, U.S.A.

ICU CARE Trauma continues to be the leading cause of death in the rst several decades of life. Those surviving an accident but suffering from signicant trauma will frequently need intensive care. The criteria for intensive care unit (ICU) admission will vary from institution to institution, but some commonality can be suggested. Those with multi-system trauma or hemodynamic instability will benet from intensive care. Others with a Pediatric Trauma Score of seven or less; isolated but signicant head trauma and an altered mental status; liver, or splenic lacerations of grade III or greater; signicant pancreatic injuries, multiple orthopedic injuries; and injuries, that may not be readily cared for on the ward because of local institutional factors may best be cared for initially in the ICU. MONITORING Basic monitoring is required for all pediatric trauma patients in the ICU. This includes measurement of vital signs: determination of heart rate and respiratory rate, continuous electrocardiography, noninvasive blood pressure determination, and temperature measurement. According to recent pediatric literature, pulse oximetry should be considered a fth vital sign, and capnography should also be included for intubated patients (1). Cardiovascular Monitoring Usually, noninvasive blood pressure monitoring is utilized in the pediatric population. Noninvasive monitoring in the child may be quite accurate if the proper cuff size is utilized. The American Heart Association has set guidelines for proper cuff t. They recommend a cuff whose width is 40% of the circumference at the midpoint of the limb or 20% greater than the diameter of the extremity (2). The attending trauma team must also be aware of the age-related norms for blood pressures (Table 1).

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BP <60 <75 <85 <90

In most modern pediatric intensive care units (PICU), automated arterial blood pressure devices are utilized. These units measure heart rate and systolic, diastolic, and mean arterial blood pressure. Pitfalls of noninvasive monitoring include: 1. Diastolic pressures tend to be slightly higher with the noninvasive devices. 2. Dysrhythmias and wide variations in blood pressure over a short time frame may be missed. Access for invasive blood pressure monitoring may be accomplished in all children. This is performed either through percutaneous arterial cannulation or by arterial cutdown. The usual site in children is the radial artery. However, in an emergent situation in a crowded trauma bay, the ICU, or operating room the quickest access may be percutaneous cannulation of the femoral artery (3). After stabilization in the PICU the arterial site may be changed to the radial artery. Pitfalls of invasive monitoring include limb ischemia (femoral artery), cannula compression, and kinking or clot formation. It is therefore wise to correlate invasive with noninvasive monitoring in the critically ill trauma patient. Benets of invasive monitoring include continuous direct waveform display of the arterial blood pressure and access for arterial blood sampling for blood gases. Electrocardiography (ECG) monitors the heart rate and rhythm of cardiac conduction. Rhythm disturbances associated with trauma may include atrial tachycardia, ventricular tachycardia (subarachnoid hemorrhage), persistent sinus bradycardia (cerebral hypoxia/arrest at the scene/airway obstruction/tracheal disruption/increased intracranial pressure secondary to head trauma/hypothermia due to cold exposure), and sinus tachycardia (hypovolemic shock). Also, many teenage trauma patients have taken drugs that alter the ECG: tricyclic antidepressants, cocaine, opiates, and amphetamines. Oxygen Saturation Pulse oximetry is currently being advocated as an accurate, simple, and noninvasive method of measuring the oxygen saturation of arterial blood. It is based on the spectrophotometry of oxygenated hemoglobin, which absorbs infrared light at the 940 nm wavelength and transmits red light at the 660 nm wavelength. The pulse oximetry probe has two light-emitting diodes that pass light at these wavelengths through the perfused tissue to a photodetector on the other side. The photodiode then compares the amount of infrared, red, and ambient light that reaches it and calculates the oxygen saturation (SaO2) (2). A small sensor (probe) is placed on the nger, toe, earlobe, forehead, or any convenient place. Most devices demonstrate the SaO2 as well as pulse rate continuously. The pulse oximeter has been demonstrated to reect moderate hypoxia (SaO2 < 89%) before an increase in ventilatory drive is demonstrated (1). This, as well as its noninvasive, continuous monitoring of the SaO2, has made it a critical

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component of PICU monitoring in the pediatric trauma patient. It provides a continuous reection of hemoglobin saturation and provides the trauma surgeon with knowledge that sufcient oxygen is being delivered to the injured tissues. A disadvantage of pulse oximetry has been decreased accuracy at low saturations (dened as SaO2 < 7075%). New generations of pulse oximeters perform better without deterioration of performance at saturations <75%. However, it is still recommended that frequent measurements of PaO2 should be done at lower saturations (4). If the oxygen saturation is below 70% on multiple pulse oximeter determinations then the arterial blood should be sampled because the true oxygen saturation is usually underestimated by most oximeters. Other disadvantages of some pulse oximeter models include motion artifact, placement of sensor below blood pressure cuff, and poor tissue perfusion of a distal extremity (3,5). When elevations of carboxyhemoglobin (COHb) are seen in the setting of carbon monooxide (CO) poisoning, the pulse oximetry reading remains in the normal range, despite markedly reduced actual oxygenated hemoglobin (O2Hb). This is because COHb does not absorb light at the infrared wavelength (940 nm), while it does transmit red light (wavelength 640 nm). As a result, the pulse oximeter cannot differentiate between the COHb and O2Hb at the red wavelength, and the combined value is applied to the calculation of the oxygen saturation. As a result, the pulse oximeter overestimates the actual oxyhemoglobin saturation (SaO2) so that it is unreliable in patients with CO poisoning (6). Ventilation End tidal carbon dioxide (EtCO2) monitoring, known as capnometry, is a noninvasive method for measuring the PaCO2 in expired gas. Similar to pulse oximetry-measuring devices, the exhaled gas passing through a sampling chamber, which has an infrared light source on one side and a photodetector on the other, measures the carbon dioxide (CO2). CO2 absorbs light at the infrared wavelength (940 nm). The CO2 present in the expired gas may be calculated from the amount of infrared light that reaches the photodetector . EtCO2 is a reection of alveolar ventilation, metabolic rate, and the pulmonary circulation. It also may be helpful in transport of the injured patient to and from the PICU for early detection of endotracheal tube dislodgment (7). It is currently recommended by several sources, including the American Academy of Pediatrics, that all children who are intubated and being transported have an EtCO2 (8).

MANAGEMENT OF PICU TRANSFUSIONS In the unstable trauma patient, hemoglobin and hematocrit should be measured every four hours and one hour after every transfusion until vital signs stabilize and urine output is adequate. To restore blood volume and O2-carrying capacity to a pediatric trauma patient that has lost a large volume of blood, it is essential to transfuse one unit quickly in larger children (>25 kg) or 1015 mL/kg of blood in smaller children. Packed red blood cells are the product of choice for patients with moderate acute blood loss. For severe hemorrhage, plasma substitutes are required when packed red blood cells are transfused to compensate for dilution of coagulation proteins. Massive transfusions that involve replacing an amount of blood equal to the patients blood volume in 24 hours involve several risks. These include citrate toxicity, electrolyte imbalance, and decreased release of oxygen to the tissues resulting

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from decreased 2,3 disphosglycerate content, pulmonary microembolism, decreased core temperature, and thrombocytopenia/disseminated intravascular coagulation (DIC). The total blood volume in a child is approximately 75 mL/kg. If this amount of blood has been given to a child in a 24-hour period or less then early treatment of the side effects of massive transfusion should be initiated. For every blood volume lost, it is often necessary to administer fresh frozen plasma (20 mL/kg), sodium bicarbonate (13 meq/kg if pH <7.3), calcium chloride 10% (1020 mg/kg if ionized calcium <2), and platelets (platelet count <50,000/uL). In children, 0.1 unit of platelet concentrate/kg usually increases the platlets an increment of 40,000/uL (3,9). Transfusion pumps equipped with warming units should be used when large amounts of blood and crystalloid are transfused to decrease the incidence of hypothermia. In addition, most PICU beds have thermal blankets and external warming sources to minimize heat loss.

NUTRITION Although gastric and colonic motility may be impaired for several days after trauma or stress, small intestinal motility and absorptive function remain intact. A prospective, randomized study by Moore and Jones demonstrated that enterally fed patients had fewer complications after major abdominal trauma than patients receiving total parenteral nutrition (10). A recent study by Jackson, et al. demonstrated that early enteral feeding in PICU patients was feasible, well tolerated, and cost-effective without the risk of aspiration or abdominal distension. Bedside nasal jejunal tubes were passed and caloric requirements were met within 48 hours in most patients (11,12). Placement of the tubes may be checked by portable kidney, ureter, and bladder (KUB) lms and, if passage is difcult, may be performed under uoroscopic guidance with minimal sedation in the uoroscopy suite. In conclusion, elemental feedings should be initiated early in the pediatric trauma patient and are preferred over parenteral nutrition. If full enteral feeds are not tolerated then parenteral nutrition should be instituted to meet the caloric needs of the patient, and a small amount of jejunal feeds can be continued to maintain gut integrity. COMMONLY USED MEDICATIONS Table 2 shows the commonly used medications.

ACUTE RESPIRATORY FAILURE Acute lung injury leading to respiratory insufciency is a frequent complication found in the trauma patient. Its etiology is varied and includes atelectasis, aspiration, infection, the acute respiratory distress syndrome (ARDS) as well as others. Of these ARDS has the most potential for signicant morbidity and mortality. Therapy may be as simple as supplying oxygen and pulmonary physiotherapy or as complicated as providing extracorporeal life support (ECLS). The pulmonary injury preceding ARDS may be direct (pulmonary contusion and smoke inhalation) or indirect (shock and sepsis). It is important to understand the differences in both their effects as well as how each can be best treated.

Pediatric ICU Management Table 2 Commonly Used Medications Pressors Dopamine

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Low dose Intermediate High

Dobutamine Epinephrine Analgesics Fentanyl Morphine Sedation Ativan Ketamine Versed Paralysis Cisatracurium Vecuronium Bronchodilators Albuterol Racemic epinephrine

25 mcg/kg/min 515 mcg/kg/min 20 mcg/kg/min 215 mcg/kg/min 0.11.0 mcg/kg/min 15 mcg/kg/hr 0.050.2 mg/kg/hr 0.050.2 mg/kg/hr 0.52 mg/kg 0.050.2 mg/kg/hr 12 mcg/kg/min 0.050.1 mg/kg/hr 0.0515 mg/kg nebulized q 4 hr 0.05 cc/kg/dose dilated to 3 cc NS nebulized q 4 hr

Pathophysiology In an early description Asbaugh et al. termed the clinical picture of progressive hypoxemia, tachypnea, and generalized patchy pulmonary inltrates, in the absence of cardiac failure ARDS (13). These signs and symptoms are usually presented within one to four days of the original inciting event. This clinical entity describes a nal common pathway with denable lung pathology from a wide spectrum of signicant injuries. Early beliefs were that ARDS results in a disseminated and homogeneous pulmonary process, as suggested by conventional chest X rays (CXR) (Fig. 1). It has since been shown with computed tomography (CT) that this is not so (Fig. 2) (14,15). CT scans in patients with ARDS reveal the presence of atelectasis and edema in the more dependent portions of the lungs. This is felt to be due to compression of lung tissue. Nondependent portions of the lungs have an increase in edema but are well aerated and thus receive an inordinate amount of the minute ventilation. This is because gases all ow via the path of least resistance. As the syndrome progresses, so does the opacication on CXR. Gattionni et al. showed that as little as one third of the lung is actually ventilated and called this condition baby lung (16). Mechanical ventilation in this clinical setting leads to regional over-distension of nondependent lung, reduces capillary perfusion, increases pulmonary dead space, and exacerbates the already present ventilation perfusion mismatch. It has also been shown that mechanical ventilation itself can lead to lung injury (17,18). Initially termed barotrauma, this injury may more appropriately be due to volutrauma. Webb and Tierny have also shown that regional over-distension of alveoli with mechanical ventilation leads to injury (19). This is most closely associated with high peak inspiratory pressures, greater than 40 cm H2O, and repeated opening and closing of collapsed alveoli. This alveolar over-distension leads to stress failure of alveolar capillary membranes, which leads to increased microvascular permeability and edema. Although the evidence is circumstantial, it is felt that this volutrauma

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Figure 1 Chest X ray CXR showing diffuse bilateral pulmonary inltrates.

on top of the existing ARDS signicantly complicates the syndrome. A recent multicenter study showed a signicant difference in mortality and ventilator days when lung protective strategies (tidal volume <6 cc/kg and plateau pressures <30 cm H2O) were used (20). Etiology Two groups of patients with ARDS are differentiated by the etiology of their pulmonary disease. A primary lung insult such as pneumonia may lead to a reduction in lung but not chest wall compliance. Here, consolidation is the main pathology. These patients are less responsive to lung recruitment measures such as positive end expiratory pressure (PEEP) and prone positioning. These patients are more susceptible to regional

Figure 2 CT scan showing the inhomogeneity of ARDS.

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hyperination so that peak pressures must be watched very closely. Indirect causes of ARDS, such as trauma and sepsis, lead to secondary lung injury. These patients have a reduction in both their lung and chest wall compliance. The major pathologic ndings are interstitial edema and alveolar collapse. These patients are usually more responsive to PEEP and prone positioning. If not careful, however, these measures may put them at risk for hemodynamic instability. Diagnosis Making the diagnosis of ARDS is not usually difcult if one considers it in those patients who have suffered signicant trauma or develop sepsis or pneumonia following trauma. Physicians do not universally agree on all of the necessary ndings but there are some commonalities. The American European Consensus Conference attempted to simplify this and includes: 1. 2. 3. 4. an acute onset, a PaO2/ fraction of expired oxygen (FiO2) <300, bilateral pulmonary inltrates on CXR, pulmonary capillary wedge pressure (PCWP) <18 mmHg or no clinical evidence of left atrial hypertension (21).

Clinical Course There is a series of phases in the course of ARDS. The initial phase is characterized by tachypnea and dyspnea with hypocarbia from hyperventilation. The partial pressure of oxygen (pO2) is usually normal. Microscopically there is neutrophil sequestration and platelet aggregation within the pulmonary vasculature. Within 12 to 24 hours progressive hypoxemia and worsening respiratory symptoms develop. A chest X ray will show bilateral inltrates. There is worsening endothelial injury and increased permeability with leaky capillaries. Neutrophils marginate to the interstitium, where there is already an abnormally high protein content. Damage to the alveolar epithelial integrity continues and uid oods the alveolar space. There is continued brin and platelet aggregation and worsening microvascular occlusion. At this point the clinical entity is still reversible if the initiating factors are discovered, treated, and eliminated. The next phase occurs if there are repeated or sustained insults. This takes place over the next several days. Respiratory failure continues with an increase in the ventilation perfusion mismatch and intrapulmonary shunting. Hypoxemia is now more severe and less responsive to increases in FiO2. This necessitates increased ventilation support in the face of worsening pulmonary compliance. Continued inltration with neutrophils and now mononuclear cells, lymphocytes, and broblasts worsen the interstitial milieu. Surfactant destruction occurs as well as further alveolar collapse. Macrophages release monokines, which activate other inammatory cells, thus worsening the entire picture. The nal phase is more chronic in nature. There is a worsening pulmonary brosis, and with recurrent pneumonias, lung compliance and gas exchange fail to improve. The usual endpoint is signicant morbidity if not mortality. Management There is no specic therapy for ARDS. Most measures are directed towards support of the patients respiratory status as well as the treatment of any underlying problems, such as pneumonia and sepsis. In the past most respiratory therapies were directed

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toward normalization of blood gases. Today, most critical care physicians attempt to achieve adequate gas exchange and prevent further lung injury, which may assist with lung healing. Mechanical ventilation is probably the most important supportive therapy in treating patients with ARDS. Criteria for its utilization include hypoxemia unresponsive to supplemental O2 and the need to recruit atelectatic alveoli. On occasion continuous positive airway pressure (CPAP) will be adequate; however, there are several limitations with this type of assistance. It requires a very tight-tting mask and a very cooperative patient. If the amount of pressure required exceeds 10 cm H2O, then the success rate is not high. Oxygenation Once a patient requires mechanical ventilation, manipulating the FiO2 and the positive end-expiratory pressure is used in an attempt to treat hypoxemia. Increasing the FiO2 does not always work. This is especially true when there is signicant shunting within the lungs. In this situation utilizing PEEP may be benecial. It may be used to recruit atelectatic alveoli, increase functional residual capacity, decrease the shunt fraction, increase the volume of ventilated parenchyma, redistribute alveolar edema, and decrease diffusion distances (22). The PEEP is only supportive, however, and is not therapeutic. Its prophylactic use probably does not change the course of ARDS. It does not decrease the amount of alveolar edema and at high levels >1012 cm H2O it may be detrimental. It increases mean airway pressure and intrathoracic pressure and decreases venous return, which may lead to a decrease in cardiac output. It may also impact intracranial pressure as well as hepatic and renal perfusion. These complications are rare if PEEP is kept below 10 cm H2O. If higher levels of PEEP are necessary then the use of a SwanGanz catheter or oximetric pulmonary artery catheter should be considered. The best level of PEEP can be calculated from static pressure volume curves (Fig. 3) (23). Looking at the lower and higher inection points facilitates setting both the best PEEP and peak inspiratory pressures. This limits overdistension on inspiration and alveolar collapse on expiration, which may prevent the alveolar stretch injury associated with repeated opening and closing of alveoli with ination and deation.

Figure 3 An ination pressure versus volume curve showing the upper (peak inspiratory pressure point) and lower (ideal PEEP) inection points.

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Ventilation In the past, average volumes of 1015 cc/kg were used in attempts to adequately ventilate patients. More recently evidence suggests that this is more than is really necessary (20). Six to ten cc/kg may be adequate. Much of the consolidated lung will not ventilate, so the portions of lung that can be ventilated are actually overstretched and damaged. We attempt to keep our peak inspiratory pressures <40. In some trauma patients (indirect lung injury) it is the chest wall that may be noncompliant. If this is the case then higher pressures may be better tolerated and necessary. The ability to maintain gas exchange is often difcult while staying within airway pressure and tidal volume guidelines. The question to ask is whether to change the guidelines or gas exchange expectations. Normocapnia may not be possible and it may be necessary to accept higher levels of partial pressure exected by CO2 in mmHg (pCO2). This idea of permissive hypercapnia is not new. Sudden elevations in pCO2, however, are also detrimental and result in cardiac depression, increases in intracranial pressure, and may worsen intracellular acidosis. An absolute endpoint is uncertain but a pH as low as 7.2 seems to be well tolerated. This often requires heavy sedation and even paralysis.

Ventilation Modes The two common modes of ventilation are based on airway pressure and tidal volume, respectively. Each has advantages and disadvantages. Pressure control allows for rapid variable ow and provides peak inspiratory pressure throughout the entirety of the inspiratory time. Volume control allows for a constant tidal volume and minute ventilation regardless of the changes in pulmonary compliance. There are some new modes that allow for a combination of both and also allow for changes breath to breath. Pressure-regulated volume control is one that sets a target tidal volume and inspiratory time and allows the ventilator to adjust the ow rate. Waveform and peak inspiratory pressure vary from breath to breath as pulmonary compliance, resistance, and patient cooperation change. This is our preferred method of ventilation in the more critical patients with ARDS. High-frequency ventilation allows for continual high airway pressures, very low tidal volumes, and very fast rates. Gas exchange occurs via Brownian motion. These modes are helpful as trials when other modes fail, as well as in cases of persistent pneumothoraces or chronic bronchopleural stulas. Their efcacy in the pediatric patient with ARDS has not been shown.

Prone Positioning Prone positioning was tried rst by Brian 25 years ago and seems to be quite popular in Europe (24). The idea is to reduce ventilation perfusion inequality by redistributing blood ow from unventilated areas of lung to those with a more normal ventilationperfusion ratio (V/Q) match. It may also recruit previously atelectatic lung areas. The patient is rotated from the supine to the prone position on a schedule whose time interval varies from institution to institution from every hour to once a day. Patient repositioning is labor-intensive and this effort must be monitored closely. Pressure points must be protected and the most common complication is dislodgement of lines and endotracheal tubes, which can be a serious problem if the patient has just been placed in the prone position.

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Nitric Oxide Nitric oxide (NO), initially named endothelium-derived relaxing factor, has been shown to dilate pulmonary arteries and has been used extensively in treating pulmonary hypertension. Its use in ARDS is based on two principles. First is the treatment of pulmonary hypertension, and the second is to direct blood ow towards ventilated alveoli, thus decreasing the ventilation perfusion mismatch. Initially, studies by Roissant et al. showed an improvement in oxygenation, reduced pulmonary artery pressure, and reduced shunt fraction (25). It appears though the ideal dose range is between 1 and 10 ppm (26). Its use is well tolerated and the adverse reactions are few and limited. Papazian demonstrated a benecial effect of inhaled NO when combined with prone positioning (27). Each modality increased the PaO2/FiO2, but the highest change was found when the two were combined. Partial Liquid Ventilation Peruorocarbons have been investigated for years due to their signicant afnity for oxygen. Recently, they have been used clinically in treating ARDS in both Phase 2 and 3 trials. Perubron is one such chemical that has low viscosity, low surface tension, high density, and a high oxygen solubility and CO2-carrying ability. Partial liquid ventilation is a technique where a volume of chemical equal to the functional residual capacity of a patient is used in combination with conventional ventilation. The peruorocarbons high density assists its ability to collect in the dependent portions of the lung, which are poorly ventilated. With this characteristic it has been shown to displace alveolar transudate within the dependent consolidated lung, thus recruiting alveoli. Exudate is then lavaged out of the lung, clearing cellular debris and mucous plugs. The most recent multicenter trial looking at its use in ARDS in adults has closed and the data are not yet available. Steroids Corticosteroids have been shown to modulate a number of mediators, which participate in the inammatory cascade that is a component of ARDS. Most agree that their use in the early phases of ARDS has no benet. We believe, however, that their efcacy in the later broproliferative phase of ARDS has still not been answered. Meduri et al. has shown positive effects of their use in those who have failed to respond to conventional ventilation after seven days (28). Extracorporeal Membrane Oxygenation (ECMO) When all of the above interventional modalities fail to show improvement in patients with ARDS, their survival has most likely been reduced to 20% to 30%. A trial of ECMO is warranted in this instance and some would argue that it should be considered sooner rather that later. The survival as reported by the Extracorporeal Life Support Organization is between 50% and 60% in, pediatric patients with respiratory failure (29). In short, ECMO supports the patients pulmonary function (venovenous) or pulmonary and cardiac function (venoarterial) in hopes that lung rest and healing can take place. It is not in the scope of this chapter to explain in detail the intricacies of ECMO, which can be found in one of the textbooks written on this subject (30).

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REFERENCES
1. Mower WR, Sachs C, Nicklin EL, Myers G, Kearin KT, Baraff LJ. Pulse oximetry as a fth pediatric vital sign. Pediatrics 1997; 99:681686. 2. Stafford MA. Cardiovascular physiology and care. In: ONeill JA, Rowe ML, Grosfeld EW, Fonkalsrud EW, Coran AG, eds. Pediatric Surgery. Vol. 1. St. Louis: Mosby-Year Book Inc., 1998. 3. American College of Surgeons, Advanced Trauma Life Support for Physicians, 6th ed. 1997. 4. Carter BC, Carlin JB, Tibballs J, Mead H, Hochmann M, Osborne A. Accuracy of two pulse oximeters at low arterial hemoglobin-oxygen saturation. Crit Care Med 1998; 26:11281133. 5. Tremper KK. Pulse Oximetrys nal frontier. Crit Care Med 2000; 28:16841685. 6. Bozeman WP, Myers RA, Barish RA. Conrmation of the pulse oximetry gap in carbon monoxide poisoning. Ann Emerg Med 1997; 30:608611. 7. Bhende MS, Karr VA, Wilsie DC, Orr RA. Evaluation of a portable infrared end-tidal carbon dioxide monitor during pediatric interhospital transport. Pediatrics 1995; 95:875878. 8. Task Force on Interhospital Transport, American Academy of Pediatrics. Guidelines for air and ground transportation of neonatal and pediatric patients. Elk Grove Village, IL: American Academy of Pediatrics, 1993. 9. Hutchinson RJ. Surgical implications of hematologic disease. In: ONeill JA, Rowe ML, Grosfeld EW, Fonkalsrud EW, Coran AG, eds. Pediatric Surgery. Vol. 1. St. Louis: Mosby-Year Book Inc., 1998. 10. Moore E, Jones T. Benets of immediate jejunostomy feeding after major abdominal trauma: A prospective, randomized study. J Trauma 1986; 26:874880. 11. Chellis MJ, Sanders SV, Webster H, Dean JM, Jackson D. Early enteral feeding in the pediatric intensive care unit. J Parenter Enteral Nutr 1996; 20:7173. 12. Panadero E, Lopez-Herce J, Caro L, Sanchez A, Cueto E, Bustinza A, Moral R, Carrillo A, Sancho L. Transpyloric enteral feeding in critically III children. J Pediatr Gastroenterol Nutr 1998; 26:4348. 13. Ashbaugh DG, Bigelow DB, Petty TL, Levine BE. Adult respiratory distress. Lancet 1967; 2:319323. 14. Pelosi P, Crotti S, Brazzi L. Computed tomography in adult respiratory distress syndrome: what it has taught us? Eur Respir J 1996; 9:10551062. 15. Gattinoni L, Pesenti A, Torresin A, Baglioni S, Rivolta M, Rossi F, Scarani F, Marcolin R, Cappelletti G. Adult respiratory distress syndrome proles by computed tomography. J Thorac Imag 1986; 1:2530. 16. Gattiononi L, Pesenti A, Bombino M, Baglioni S, Rivolta M, Rossi F, Rossi G, Fumangalli R, Marcolin R, Mascheroni D. Relationships between lung computed tomographic density, gas exchange and PEEP in acute respiratory failure. Anesthesiology 1988; 69:824832. 17. Dreyfuss D, Saumon G. Ventilator-induced lung injury-Lessons from experimental studies. Am J Respir Crit Care Med 1998; 157:294323. 18. Parker JC, Hernandez LA, Peevy KJ. Mechanisms of ventilator-induced lung injury. Crit Care Med 1993; 21:131143. 19. Webb HH, Tierney DF. Experimental pulmonary edema due to intermittent positive pressure ventilation with high ination pressures: Protection by positive end-expiratory pressures. Am Rev Respir Dis 1974; 110:556565. 20. The Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with conventional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000; 342(18):13011308. 21. Bernard GR, Artigas A, Bringham KL, Carlet J, Falke K, Hudson L, Lamy M, LeGall JR, Morris A, Spragg R. The American-European consensus conference on ARDS. Am J Respir Crit Care Med 1994; 149:818.

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22. Pepe PE, Hudson LD, Carrico CJ. Early application of positive end-expiratory pressure in patients at risk for adult respiratory distress syndrome. N Engl J Med 1984; 311:281. 23. Levy P, Similowski T, Corbeil C. A method for studying the static-pressure volume curves of the respiratory system during mechanical ventilation. J Crit Care 1989; 4:8389. 24. Hormann C, Benzer H, Baum M, Wicke K, Putensen C, Putz G, Hartlieb S. The Prone Position for ARDS. Anaesthesist 1994; 43(7):45462. 25. Rossaint R, Falke KJ, Lopez F, Slama K, Pison U, Zapol WM. Inhaled nitric oxide for the adult respiratory distress syndrome. N Engl J Med 1993; 328:399405. 26. BigatelIo LM, Hurdord WE, Kacmarek RM, Roberts JD, Zapol WM. Prolonged inhilation of low concentrations of nitric oxide in patients with severe adult respiratory distress syndrome: Effects on pulmonary hemodynamics and oxygenation. Anesthesiology 1994; 80:761770. 27. Papazian L, Bregeon F, Gaillat F, Thirion X, Gainnier M, Gregoire R, Saux P, Gouin F, Jammes Y, Auffray J. Respective and combined effects of prone position and inhaled nitric oxide in patients with acute respiratory distress syndrome. Am J Respir Crit Care Med 1998; 157:580585. 28. Meduri GU, Headley AS, Golden E, Carson SJ, Umberger RA, Kelso T, Tolley EA. Effect of prolonged methylprednisolone therapy in unresolving acute respiratory distress syndrome: A randomized controlled trial. JAMA 1998; 280:159165. 29. Extracorporeal Life Support Organization, International Summary, January 2002. 30. Zwischenberger J, Bartlett R. Extracorporeal Cardiopulmonary Support in Critical Care. Extracorporeal Life Support Organization, 1995.

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Nutritional Support for the Pediatric Trauma Patient
Tom Jaksic and Biren P. Modi
Department of Surgery, Childrens Hospital Boston, Boston, Massachusetts, U.S.A.

INTRODUCTION Trauma is accompanied by a set of metabolic aberrations that are profound but predictable. Over 65 years ago Sir David Cuthbertson described the fundamental aspects of this metabolic response to injury in adults (1). Although the metabolic sequelae of trauma in children qualitatively resemble those of adults, marked quantitative differences exist. An understanding of the metabolic events that accompany trauma is the rst step in nutritional support therapy. An individualized determination of nutrient requirements must be made and an appropriate route of delivery selected. Nutritional support of the injured child should be instituted promptly and be designed to limit the deleterious consequences of structural protein loss while facilitating wound healing and the immune response.

THE METABOLIC RESPONSE TO TRAUMA During the period immediately following severe injury, aggressive uid, electrolyte, and blood replacement is often required for survival. This period is termed the ebb phase of the metabolic response to trauma and is characterized by a decrease in cardiac output and a reduction in metabolic rate. Once the patient has been adequately resuscitated, the ow phase of injury is entered. The metabolic response during the ow phase is summarized in Figure 1 and consists of an increase in net muscle protein breakdown and the enhanced movement of amino acids through the circulation. This provides the amino acids needed for the rapid synthesis of proteins for the inammatory response and tissue repair. Those amino acids not used for protein synthesis are channeled through the liver to create glucose from their carbon skeletons by gluconeogenesis. Glucose requirements are effectively met by this mechanism. In a coupled hepatic process the amino portions of the amino acids are cleaved and detoxied by the urea cycle. There is a marked rise in the circulation of hepatically derived acute-phase proteins (i.e., C-reactive protein, brinogen,
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Figure 1 Substrate metabolism in patients following major trauma.

haptoglobin, alpha-1 antitrypsin, and alpha-1 acid glycoprotein) and a concomitant decrease in hepatically derived nutrient transport proteins such as albumin and retinolbinding protein. The metabolic response to major trauma is associated with a consistent hormonal and cytokine prole regardless of the specic pattern of injury. Traumatized patients demonstrate a very transient decrease in insulin concentrations followed by a persistent elevation. Despite higher insulin levels, which, in theory, should promote anabolism, accelerated net protein breakdown continues. This may be explained, in part, by the elevated concentrations of the catabolic hormones (glucagon, catecholamines, and cortisol) found during the period of acute injury. Increases in the cytokines interleukin-6 (IL-6) and tumor necrosis factor, both of which are released by activated macrophages, also occur. IL-6 levels are correlated with increased protein turnover, protein catabolism and the synthesis of acute phase proteins, and increased mortality

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(2,3). The release of IL-2, IL-8, gamma interferon, and many growth factors is also known to augment the immunologic and hormonal response to injury. The catabolism of skeletal muscle to generate the amino acids needed for wound healing and to produce glucose for energy production is an excellent shortterm adaptation in children. However, it cannot be sustained for long periods due to the lack of body protein stores. The progressive loss of skeletal muscle protein leads to respiratory compromise, cardiac dysfunction, increased susceptibility to infection and, ultimately, increased mortality (4). Hence minimizing the protein loss associated with trauma is of major clinical importance. METABOLIC RESERVES The most striking difference in body composition between the healthy adult and the healthy child is the quantity of protein available in times of injury. As a percentage of body weight the protein stores of adults are twice those of neonates (Table 1). Lipid stores are also decreased in children compared to adults, while carbohydrate reserves are constant across age groups. Not only do neonates and children have reduced stores, they have much higher baseline requirements. The resting energy expenditure for neonates is up to three times that for adults, and protein requirements may be 3.5 times the requirement for adults (8). Thus, critically ill children are more susceptible to the deleterious effects of protracted catabolic stress. The prompt institution of nutritional support, as soon as the patient has been adequately resuscitated, is prudent. In general, any child with signicant trauma who will not be eating adequately within three days should be considered for nutritional support. NUTRITIONAL NEEDS Once a decision has been made to commence nutritional support in the injured child an accurate individualized determination of nutrient requirements is needed. This assessment should include estimates of protein, total energy, carbohydrate, lipid, electrolyte, and micronutrient needs. Protein Requirements Amino acids are the key building blocks required for growth and tissue repair. The vast majority of amino acids reside in proteins, with the remainder being in the free amino acid pool. Proteins themselves are not static as they are continually degraded and synthesized in a process termed protein turnover. The reutilization of amino acids released from protein breakdown is extensive. Protein turnover contributes to
Table 1 The Body Composition of Neonates, Children, and Non-obese Adults as a Percent of Total Body Weight Age Neonates Children (age 10 years) Adults Protein (%) 11 15 18 Fat (%) 14 17 19 Carbohydrates (%) 0.4 0.4 0.4

Source: Based upon the data of Refs. 57.

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protein synthesis more than twice the amount of amino acids derived from protein intake. In traumatized children, such as those with severe burn injury, or in ill children with cardiorespiratory failure requiring extracorporeal membrane oxygenation (ECMO), protein turnover is twice that of normal children (9). Generally, in severe illness amino acids are redistributed away from skeletal muscle to injured tissues, cells involved in the inammatory response, and the liver. Acutely needed enzymes, serum proteins, and glucose (by way of gluconeogenesis) are thus synthesized. A salient advantage of high-protein turnover is that it allows for the immediate synthesis of proteins needed for the inammatory response and tissue repair. The process does require energy, hence either an increase in resting energy expenditure or a redistribution of energy normally used for growth is required. Although critically ill children demonstrate both an increase in whole-body protein degradation and wholebody synthesis, it is the former that predominates. Thus, these patients manifest net negative protein balance, which clinically may be noted by weight loss and skeletal muscle wasting. The catabolism of skeletal muscle to generate glucose is necessary as glucose is the preferred energy source for the brain, red blood cells, and renal medulla. Illness enhances gluconeogenesis in adults, children, and neonates. On a per kilogram body weight basis, gluconeogenesis seems to be particularly elevated in very small children (presumably because of their relatively large brain-to-body-weight ratio) (10). Interestingly, the provision of dietary glucose is relatively ineffective in quelling endogenous glucose production in the stressed state (11). Without elimination of the inciting stress for catabolism, the progressive loss of diaphragmatic and intercostal muscle as well as cardiac muscle may cause cardiopulmonary failure. Fortunately, amino acid supplementation does improve protein balance. The mechanism for this change in ill patients appears to be an increase in protein synthesis with little change in protein degradation (12). The amount of protein required to optimally enhance protein accretion is higher in unwell than in healthy children. Infants demonstrate 25% higher protein degradation after surgery, 100% increase in urinary nitrogen excretion with bacterial sepsis, and 100% increase in protein breakdown if they are ill enough to require ECMO (9). The provision of dietary protein sufcient to optimize protein synthesis, facilitate wound healing and the inammatory response, as well as to preserve skeletal muscle protein mass, is the single most important nutritional intervention in injured children. The quantity of protein (or amino acid solution) administered in critical illness should be 23 g/kg/day for infants up to the age of one year and 1.5 g/kg/day for older children. Certain severely stressed states (i.e., severe burn injury) may require additional protein supplementation (2.02.5 g/kg/day). Excessive protein administration should be avoided because toxicity, particularly in patients with marginal renal and hepatic function, is possible. Even relatively well neonates fed protein allotments of 6 g/kg/day have developed azotemia, pyrexia, a higher incidence of strabismus, and lower IQ (13,14). Two important issues regarding the protein metabolism of critically ill children remain to be elucidated. At present there is no specic recommendation possible regarding any special amino acid composition that may be of specic benet to severely injured children (15). The use of enteral glutamine supplementation (with and without other immune enhancing nutrients such as arginine, omega-3 fatty acids, and nucleotides) has been used in an effort to limit septic complications associated with trauma. However, this approach remains investigational and larger-scale studies are needed (16,17). Similarly, quelling the extreme protein catabolism found

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in children with major injuries utilizing hormonal modulation, particularly insulin administration, is also being actively investigated (18). Energy Requirements A careful appraisal of energy requirements in critically ill children is required as both too much and too little energy may have potentially deleterious consequences. Inadequate caloric intake will result in poor protein retention, especially if protein administration is marginal. In contradistinction, the provision of excess glucose calories in critically ill patients results in increased carbon dioxide (CO2) production rates (hence exacerbating ventilatory failure) and a possible paradoxical increase in net protein degradation (15,19). The severity and duration of the illness or injury governs the energy needs of critically ill patients. Recent data suggest that energy needs are far less than previously thought for most types of trauma. The resting energy expenditure in the ow phase of injury is increased by 50% in children with severe burns. However, it returns to normal during convalescence (20). If illness increases work of breathing, such as in neonates with bronchopulmonary dysplasia, a persistent elevation in energy expenditure up to 25% over expected values is evident (21). Newborns undergoing major operations have only a transient 20% increase in energy expenditure that returns to baseline levels within 12 hours and remains at baseline unless major complications develop (22,23). Adequate anesthetic and analgesic management also plays a signicant role in muting the stress response, as evidenced by neonates undergoing patent ductus arteriosus (PDA) ligation who do not manifest any discernable increase in resting energy expenditure postoperatively with fentanyl anesthesia and subsequent intravenous analgesia (24). Adult intensive care unit patients also do not have an elevation of resting energy expenditure over expected values (25). Head injury produces a variable elevation in resting energy expenditure, presumably due to a marked rise in circulating catecholamines. Again patients who are sedated, in phenobarbitol coma, or have been given neuromuscular relaxants manifest no such elevation in energy expenditure (26). Total energy requirements include resting energy expenditure, energy needed for physical activity, and diet-induced thermogenesis. Resting energy expenditure itself includes the caloric requirement for growth. Although critically ill children have increased protein turnover, their growth is often halted during extreme physiologic stress. Additionally, levels of physical activity are typically low following severe injury. The mean energy expenditures of critically ill neonates on ECMO were found to be nearly identical to age- and diet-matched, non-stressed controls (27). The critically ill cohort did, however, have a greater variability in energy expenditure (27). Further, a surfeit of calories in critically ill neonates does not necessarily result in improved protein accretion (15). Thus, for practical purposes the recommended dietary caloric intake for healthy children affords a reasonable starting point for critically injured patients (28). Table 2 outlines safe caloric provisions for injured children at various ages. Enterally fed traumatized children, as a rule, require a further 10% increment in calories due to obligate malabsorption. In any injured child with protracted illness the actual measurement of resting energy expenditure, by portable indirect calorimetry, is advised due to the high-interindividual variability in energy expenditure. Predictive equations used in conjunction with stress factors to account for degree of illness have been shown to be inaccurate in determining individual energy expenditures in intensive care unit patients and are not recommended (25).

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Jaksic and Modi Table 2 Estimated Energy Requirements for Neonates, Children, and Non-obese Adolescents Age (year) 04 46 68 810 1012 1218 Estimated energy requirement (kcal/kg/day) 100 90 80 70 60 50

Once protein needs have been met, both carbohydrate and lipid energy sources have similar benecial effects on net protein synthesis in ill patients (29). A rational partitioning of these energy-yielding substrates is predicated upon the knowledge of carbohydrate and lipid utilization in trauma. Carbohydrate Requirements Glucose production and availability is a priority in ill children. Injured and septic adults have a threefold increase in glucose turnover and oxidation and an elevation in gluconeogenesis (30,31). An important feature of the metabolic stress response is that the provision of dietary glucose does not halt gluconeogenesis; consequently, the catabolism of muscle proteins continues (11). It is clear, however, that a combination of glucose and amino acids effectively improves protein balance in illness primarily by augmenting protein synthesis (32). In early nutritional support regimens for surgical patients, glucose and amino acid formulations with minimal lipid (the minimum needed to obviate fatty acid deciency) were often utilized. Energy allotments well over normal dietary requirements were also often given. The excess glucose was converted to fat, resulting in a net generation of CO2. The synthesis of fat from glucose has a respiratory quotient (RQ), dened as the ratio of CO2 produced to O2 consumed, of about 8.7. In clinical situations, this high RQ is not attained, as glucose is never purely used for fatty acid synthesis. Nonetheless, the provision of excess glucose results in an elevated RQ increasing the ventilatory burden for the child. The mean RQ in postsurgical neonates fed a high glucose diet is approximately 1.0, while comparable neonates fed with less glucose, and lipids at 4.0 g/kg/day, have an RQ of 0.83 (29). In contrast to glucose metabolism, excess lipids are merely stored as triglycerides and do not result in an augmentation of CO2 production. Utilizing high glucose total parenteral nutrition, hypermetabolic adult patients fed excess caloric allotments have a 30% increase in O2 consumption, a 57% rise in CO2 production, and 71% elevation in minute ventilation (19). Thus, avoidance of overfeeding and the utilization of a mixed fuel system of nutrition employing both glucose and lipids to yield energy is theoretically and practically useful in stressed patients, many of who also have respiratory failure. Such an approach also often obviates problems with hyperglycemia in the relatively insulin-resistant ill child. Lipid Requirements Lipid metabolism, like protein and carbohydrate metabolism, is generally accelerated by illness and trauma (32). Initially, during the brief ebb phase following

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trauma or in early septic shock, lipid utilization is compromised and triglyceride levels rise as the metabolism of intravenously administered lipids falls. In the ow phase of the injury response, adult patients demonstrate lipid turnover rates that are two- to fourfold higher than comparable controls and proportionate to the degree of injury (33,34). The increased lipid turnover after injury involves the cycling of free fatty acids and glycerol into the synthesis and hydrolysis of triglycerides. Both metabolic processes result in a stream of substrates through the plasma pool that may be reected in a modest elevation in the resting metabolic rate. Approximately 30% to 40% of the released fatty acids are oxidized for energy, which results in RQ values post-injury in the vicinity of 0.8. This suggests that free fatty acids are, in fact, the prime source of energy in trauma patients. When subjected to uncomplicated abdominal surgery, infants and children have a reduction in RQ and a decline in plasma triglycerides, implying an increased oxidation of free fatty acids (35). The glycerol, released along with the free fatty acids from triglycerides, may be converted to pyruvate that is then, in turn, utilized as a glucose precursor. As with other catabolic processes in illness and trauma, the provision of dietary glucose does not decrease glycerol clearance nor diminish lipid recycling. Normal ketone body metabolism is markedly altered by severe injury. Acetyl coenzyme A (CoA) is the product of incomplete fatty acid and pyruvate oxidation, which through a condensation reaction within the hepatocyte forms the ketone bodies acetoacetate and B-hydroxybutyrate. In starved healthy subjects, a major adaptation to preserve skeletal muscle mass is the use of ketone bodies generated by the liver as an energy source for the brain (which cannot directly oxidize free fatty acids). However, in the three-day period following trauma there is a negligible elevation in serum ketone body levels when compared to healthy fasting subjects (36). This observation may be understood in light of serum insulin levels, as ketogenesis is inhibited by even low concentrations of the hormone, a phenomenon evident to physicians in the absence of ketotic problems in type II diabetes. Hence, the high insulin concentrations seen in severe injury ablate the ketotic adaptation to starvation. The energy needs of the injured patient are met largely by the mobilization and oxidation of free fatty acids. However, ill children have limited lipid stores. Thus, they may evolve biochemical essential fatty acid deciency within one week if administered a fat free diet (37,38). In infants, linoleic and linolenic acid are considered essential, with arachidonic acid and docosahexaenoic acid deemed as possibly, conditionally essential. When there is a lack of dietary linoleic acid, the formation of arachidonic acid (a tetraene) by desaturation and chain elongation cannot occur and the same pathway entrains available to oleic acid to form 5,8,11-eicosatrienoic acid (a triene). A triene-to-tetraene ratio of greater than 0.4 suggests essential fatty acid deciency. The clinical syndrome consists of dermatitis, alopecia, thrombocytopenia, susceptibility to bacterial infection, and failure to thrive (37,38). To obviate essential fatty acid deciency in injured children, a sufcient allotment of linoleic acid and linolenic acid is recommended. The parenteral provision of commercially available lipid solutions to traumatized children obviates the risk of essential fatty acid deciency and results in improved protein utilization without signicantly increasing carbon dioxide production or metabolic rate (39). These advantages are balanced by some potential risks of excess administration: hypertriglyceridemia, increased infections, and decreased alveolar oxygen diffusion capacity (4042). Although the evidence is far from conclusive, the possible adverse effects of lipid administration have resulted in most centers

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starting lipid supplementation in ill children at 0.5 gm/kg/day, and advancing over a period of days to 24 gm/kg/day, while closely monitoring triglyceride levels. Lipid administration is usually restricted to a maximum of 30% to 40% of total calories, although this practice has not been validated by clinical trials.

Electrolyte Requirements Electrolyte requirements (Na, K, Cl, HCO3, Ca2) must be evaluated frequently in the critically injured patient. Simultaneous serum and urine electrolyte determinations often yield information regarding the renal conservation of particular salts. In addition to routine electrolyte monitoring, careful attention to phosphate and magnesium levels is needed as hypophosphatemia may lead to thrombocytopenia and respiratory muscle dysfunction, while magnesium deciency can cause cardiac arrhythmias. Renal failure will result in the retention of phosphate, so nutritional allotments must be reduced accordingly. Frequently, head injured patients have an iatrogenically induced respiratory alkalosis. If a metabolic alkalosis is also present due to active diuresis or gastric suction, Cl administration should be used to correct the alkalosis. Alkalemia tends to inhibit respiratory effort, drive potassium into cells, and decrease ionized calcium by increasing the afnity of albumin for calcium. Metabolic acidosis is sometimes present in traumatized children with hypotension or ischemic injuries. The provision of acetate instead of Cl in the parenteral nutrition solution may combat this metabolic problem. The provision of excess acetate at 1 milliequivalent/kg over 24 hours is usually a safe adjunct to other measures to limit metabolic acidosis.

Vitamin and Trace Mineral Requirements Vitamin and trace mineral metabolism in injured pediatric patients has not been well studied. For the neonate and child, the fat-soluble vitamins A, D, E, and K, as well as the water-soluble vitamins ascorbic acid, thiamine, riboavin, pyridoxine, niacin, pantothenate, biotin, folate, and vitamin B12 are all required and are routinely administered. Since vitamins are not stoichiometrically consumed in biochemical reactions but rather act as catalysts, the administration of large supplements of vitamins in stressed states is not logical. The trace minerals that are required for normal development are zinc, iron, copper, selenium, manganese, iodide, molybdenum, and chromium. Trace minerals are usually used in the synthesis of the active sites of an ubiquitous and extraordinarily important class of enzymes called metalloenzymes. Like vitamins, metalloenzymes act as catalysts. Hence, unless there are excessive losses such as enhanced zinc loss with severe diarrhea, large nutritional requirements would not be anticipated in illness. The vitamin and trace mineral needs of healthy children and neonates are well dened in the literature (28). These levels have been used in traumatized patients, and little evidence exists that they are nutritionally inadequate. In children with severe hepatic failure, copper and manganese accumulation occurs; thus, parenteral trace mineral supplementation should be limited to once per week. The pharmacologic use of vitamins and trace minerals in pediatric illness is controversial. Reviews of both vitamin and trace mineral toxicity clearly demonstrate that excessive dosage is a health risk (43,44).

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ROUTES OF NUTRIENT PROVISION In the traumatized child the enteral route of nutrient provision is preferable to the parenteral route whenever the gastrointestinal tract is functional. Enteral nutrition is physiologic, safer, and cheaper (45). If there is a concern regarding aspiration, the use of post-pyloric feeding tubes placed at the bedside or by interventional radiology is a very useful adjunct to the nutritional management of the injured child. Continuous feedings using standard 1 kcal/mL formulas can adequately nourish the majority of patients. Carefully controlling the enteral infusion rate and avoiding bolus feeding until tolerance is established usually obviate diarrhea. If diarrhea persists stool cultures are sent for routine pathogens and Clostridium difcile toxin. At the time of extubation, feeds are held for a period of 6 to 12 hours. It is also our policy not to feed patients enterally who are hypotensive or have evidence of bowel obstruction in order to limit the risk of spontaneous small bowel necrosis associated with rapid enteral feeding (46). If the gastrointestinal tract is not functional and parenteral nutrition is necessary, central venous access is sought so that concentrated solutions that obviate uid overload can be safely administered. Percutaneously placed intravenous lines that are threaded centrally are the preferred means of administration. Central access may be placed at the bedside in most intensive care unit patients. Groin lines are not favored for nutritional therapy, because of their propensity for infection. Once gastrointestinal activity has been reestablished the patient can usually be converted to enteral nutrition within a two- to three-day time period.

SUMMARY Injured children are particularly susceptible to the loss of lean body mass and its attendant increased morbidity and mortality. Critical illness results in increased protein, carbohydrate, and lipid utilization and net negative protein balance. The judicious administration of carbohydrates, lipids, vitamins, trace minerals, and particularly protein, preferably through an enteral route, can optimize wound healing and reduce or even eliminate the consequences of this catabolic response.

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6. Foman SJ, Haschke F, Zeigler EE, Nelson SE. Body composition of reference children from birth to age 10 years. Am J Clin Nutr 1982; 35:11691175. 7. Munro HN. Nutrition and muscle protein metabolism. Fed Proc 1978; 37:22812282. 8. Kashyap S, Schulze KF, Forsyth M, Dell RB, Ramakrishnan R, Heird WC. Growth, nutrient retention, and metabolic response in low birth weight infants fed varying intakes of protein and energy. J Pediatr 1988; 113:713721. 9. Keshen TH, Miller RG, Jahoor F, Jaksic T. Stable isotopic quantitation of protein metabolism and energy expenditure in neonates on and post extra corporeal life support. J Pediatr Surg 1997; 32:958963. 10. Keshen T, Miller R, Jahoor R, Jaksic T, Reeds PJ. Glucose production and gluconeogenesis are negatively related to body weight in mechanically ventilated, very low birth weight neonates. Ped Res 1997; 41:132138. 11. Long CL, Kinney JM, Geiger JW. Non-supressibility of gluconeon