Emergency Medical Services: Clinical Practice and Systems Oversight [3rd Edition] 9781119756255, 1119756251, 9781119756248, 1119756243

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Emergency Medical Services Clinical Practice and Systems Oversight

Emergency Medical Services Clinical Practice and Systems Oversight Volume 1: Clinical Aspects of EMS

Third edition

Editor‐in‐Chief David C. Cone, MD Professor of Emergency Medicine Yale University School of Medicine New Haven, Connecticut

Editors Jane H. Brice, MD, MPH Professor of Emergency Medicine University of North Carolina at Chapel Hill Chapel Hill, North Carolina

Theodore R. Delbridge, MD, MPH Executive Director Maryland Institute for Emergency Medical Services Systems Baltimore, Maryland

J. Brent Myers, MD, MPH Chief Medical Officer ESO Associate Medical Director Wake County EMS Raleigh, North Carolina

This edition first published 2021 © 2021 John Wiley & Sons, Inc. A co‐publication between John Wiley & Sons, Inc and National Association of EMS Physicians® Edition History NAEMSP®, published by John Wiley and Sons, Ltd. by (2e, 2015); Previously published by Kendall Hunt Professional, 2009. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, except as permitted by law. Advice on how to obtain permission to reuse material from this title is available at http://www.wiley.com/go/permissions. The right of David C. Cone, Jane H. Brice, Theodore R. Delbridge, and J. Brent Myers to be identified as the authors of the editorial material in this work has been asserted in accordance with law. Registered Office(s) John Wiley & Sons, Inc., 111 River Street, Hoboken, NJ 07030, USA John Wiley & Sons Ltd, The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, UK Editorial Office 9600 Garsington Road, Oxford, OX4 2DQ, UK For details of our global editorial offices, customer services, and more information about Wiley products visit us at www.wiley.com. Wiley also publishes its books in a variety of electronic formats and by print‐on‐demand. Some content that appears in standard print versions of this book may not be available in other formats. Limit of Liability/Disclaimer of Warranty The contents of this work are intended to further general scientific research, understanding, and discussion only and are not intended and should not be relied upon as recommending or promoting scientific method, diagnosis, or treatment by physicians for any particular patient. In view of ongoing research, equipment modifications, changes in governmental regulations, and the constant flow of information relating to the use of medicines, equipment, and devices, the reader is urged to review and evaluate the information provided in the package insert or instructions for each medicine, equipment, or device for, among other things, any changes in the instructions or indication of usage and for added warnings and precautions. While the publisher and authors have used their best efforts in preparing this work, they make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifically disclaim all warranties, including without limitation any implied warranties of merchantability or fitness for a particular purpose. No warranty may be created or extended by sales representatives, written sales materials or promotional statements for this work. The fact that an organization, website, or product is referred to in this work as a citation and/or potential source of further information does not mean that the publisher and authors endorse the information or services the organization, website, or product may provide or recommendations it may make. This work is sold with the understanding that the publisher is not engaged in rendering professional services. The advice and strategies contained herein may not be suitable for your situation. You should consult with a specialist where appropriate. Further, readers should be aware that websites listed in this work may have changed or disappeared between when this work was written and when it is read. Neither the publisher nor authors shall be liable for any loss of profit or any other commercial damages, including but not limited to special, incidental, consequential, or other damages. Library of Congress Cataloging‐in‐Publication Data Names: Cone, David C., editor. | Brice, Jane H., editor. | Delbridge, Theodore R., editor. | Myers, J. Brent, editor. Title: Emergency medical services : clinical practice and systems oversight / edited by editor-in-chief, David C. Cone, editors, Jane H. Brice, Theodore R. Delbridge, J. Brent Myers. Other titles: Emergency medical services (Cone) Description: Third edition. | Hoboken, NJ : Wiley-Blackwell, 2021. | Includes bibliographical references and index. | Contents: v. 1. Clinical Aspects of EMS – v. 2. Medical Oversight of EMS. Identifiers: LCCN 2020054682 (print) | LCCN 2020054683 (ebook) | ISBN 9781119756248 (paperback) | ISBN 9781119756255 (adobe pdf) | ISBN 9781119756262 (epub) Subjects: MESH: Emergency Medical Services | Emergency Medicine Classification: LCC RA645.5 (print) | LCC RA645.5 (ebook) | NLM WX 215 | DDC 362.18–dc23 LC record available at https://lccn.loc.gov/2020054682 LC ebook record available at https://lccn.loc.gov/2020054683 Cover Design: Wiley Cover Image: © National Association of EMS Physicians Set in 9.5/12pt Minion pro by Straive, Pondicherry, India

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Contents

Contributors, viii Foreword, xiv Preface, xv About the Companion Site, xvi

12 Cardiac arrest systems of care, 120

Bryan McNally, Paul M. Middleton, Marcus E.H. Ong, and Gayathri Devi Nadarajan

13 Cardiac arrest: clinical management, 134

Jon C. Rittenberger and Vincent N. Mosesso, Jr.

Section IV: Medical Problems Volume 1: Clinical Aspects of EMS 1 History of emergency medical services, 1

Jon R. Krohmer

Section I: Airway 2 EMS airway management: system considerations, 21

Francis X. Guyette and Henry E. Wang

3 Airway procedures, 30

Jestin N. Carlson and Henry E. Wang

4 Airway management: special situations, 42

Brendan Anzalone and Henry E. Wang

Section II: Breathing 5 Respiratory distress, 51

Matthew R. Neth and Mohamud R. Daya

6 Oxygenation and ventilation, 61

Vincent N. Mosesso, Jr and Angus M. Jameson

Section III: Circulation 7 Hypotension and Shock, 71

Francis X. Guyette, Raymond L. Fowler, and Ronald N. Roth

8 Vascular access, 83

Bryan B. Kitch and Eric H. Beck

9 Chest pain and acute coronary syndromes, 90

Joseph P. Ornato, Michael R. Sayre, and James I. Syrett

14 The challenge of the undifferentiated patient, 147

Andrew Travers

15 Altered mental status, 152

Mariecely Luciano‐Feijoó and Jefferson G. Williams

16 Syncope, 158

David J. Schoenwetter

17 Seizures, 163

J. Stephen Huff

18 Stroke, 171

Timothy P. Chizmar and Janelle M. Martin

19 Abdominal pain, 181

Jeffrey D. Ferguson and Michael Ferras

20 Diabetic emergencies, 188

Mariecely Luciano‐Feijoó, José G. Cabañas, and Jane H. Brice

21 Allergic reactions, 194

Debra G. Perina and Briana N. Tully

22 Renal failure and dialysis, 199

Jocelyn M. De Guzman and Bryan B. Kitch

23 Infectious and communicable diseases, 208

Russell D. MacDonald

24 Choking, 222

Gregory H. Gilbert

25 Submersion injuries and drowning, 228

Robert Lowe

Section V: Trauma Problems

10 Cardiac dysrhythmias, 100

26 Trauma systems of care, 235

11 Cardiac procedures and managing technology, 108

27 Blunt trauma considerations, 240

Christian C. Knutsen and Donald M. Yealy Joanna L. Adams and David P. Thomson

James E. Winslow

Sabina A. Braithwaite and Noah Bernhardson v

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Contents

28 Motor vehicle crashes, 248

47 Treatment and evaluation of specific toxins, 383

29 Penetrating trauma, 254

Section VIII: Environmental Problems

Stewart C. Wang, Kristen Cunningham, Sven Holcombe, and Robert Kaufman Michelle Welsford and Clare Wallner

30 Traumatic Brain Injury, 264

Anjni Joiner

31 Electrical injuries, 271

Jeffrey Lubin

32 Blast injury, 278

Andre Pennardt and Emerson Franke

33 Thermal and chemical burns, 285

Richard B. Schwartz, Richard Cartie, Peter V. Bui, and Bradley Michael Golden

Michael C. Beuhler

48 Cold exposure illness and injury, 393

Jonnathan Busko

49 Heat‐related illness, 403

Gerald (Wook) Beltran

50 High‐altitude illnesses, 410

Hawnwan Philip Moy and Richard T. Benson II

51 Effects of flight, 416

David P. Thomson and Joanna L. Adams

52 Diving injury, 421

Katherine Couturier and Irfan Husain

34 Crush injury, 294

Roberto C. Portela and Nathan Roney

35 Hemorrhage control, 299

Jeremiah Escajeda

36 Orthopedic injuries, 307

Mary P. Mercer

37 Ocular trauma, 316

Eric Hawkins and Joseph Blackwell

38 Bites, stings, and envenomations, 321

Adam Frisch, Andrew King, and Stephanie O. Frisch

39 Field trauma triage, 327

Matthew Cobb and Aaron Dix

40 Trauma‐stabilizing procedures, 335

Benjamin A. Smith

Section VI: Obstetrics and Gynecology Problems 41 Physiology of pregnancy, 345

Rickquel Tripp

42 Emergencies of pregnancy, 350

Aiman Saleh and Joseph Grover

43 Normal childbirth, 357

Stephanie A. Crapo and David A. Kranc

44 Childbirth emergencies, 361

Angus M. Jameson and Micha Campbell

45 Perimortem cesarean section, 365

Christian Martin‐Gill

Section VII: Toxicological Problems 46 Principles of toxicology, 373

Christine M. Murphy

Section IX: Special Populations 53 The special needs of children, 433

Susan Fuchs

54 Pediatric medical priorities, 439

Toni Gross and J. Joelle Donofrio‐Odmann

55 Pediatric trauma priorities, 450

Jennifer N. Fishe

56 Technology‐dependent children, 454

Sylvia Owusu‐Ansah

57 Approach to the geriatric patient, 460

Michael Mancera, Michael Lohmeier, and Manish N. Shah

Section X: Special Considerations 58 Behavioral health emergencies, 469

Jay H. Reich and Anthony T. Ng

59 Bariatric patient challenges, 480

Jeremy T. Cushman

60 Intimate partner violence, 485

Elizabeth A. Donnelly, Dana S. Levin, and Betty Jo Barrett

61 Sexual assault, 493

Diane L. Miller and Karen D. Serrano

62 Child maltreatment, 498

Deborah Flowers and Molly Berkoff

63 Human Trafficking, 502

Ronna G. Miller, Asha K. Tharayil, Brian L. Miller, and Brandon B. Morshedi

Contents

64 Ethical challenges, 519

68 Point‐of‐care testing in EMS, 559

65 Death, dying, and end of life issues, 525

69 Ultrasound applications in the prehospital setting, 566

Dave W. Lu and James G. Adams Jennifer Cook, Aaron Case, Shannon Appy, Joshua Lupton, and Terri A. Schmidt

66 Family and bystanders, 541

Lynne Dees

67 Analgesia, 553

Richard A. Kamin and Mark X. Cicero

Alix J.E. Carter

Danielle Levine and Rachel Liu

Appendix, 574 Glossary, 579 Index, 591

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Contributors

James G. Adams, MD

Professor of Emergency Medicine Northwestern University Feinberg School of Medicine Chicago, Illinois

Joanna L. Adams, MS, MD

Clinical Assistant Professor of Emergency Medicine East Carolina University Brody School of Medicine Associate Medical Director Vidant EastCare Greenville, North Carolina

Brendan Anzalone, DO

Assistant Professor of Emergency Medicine University of Alabama at Birmingham Birmingham, Alabama

Shannon Appy, MD, MPH

Assistant Professor of Hospice and Palliative Medicine Oregon Health & Science University Portland, Oregon

Betty Jo Barrett, PhD, MSSW Associate Professor Women’s and Gender Studies University of Windsor Windsor, Ontario, Canada

Eric H. Beck, DO, MPH, Paramedic

Michael C. Beuhler, MD

Professor of Emergency Medicine Atrium Health Carolinas Medical Center Medical Director North Carolina Poison Control Charlotte, North Carolina

Joseph Blackwell, MD

Department of Emergency Medicine Carolinas Medical Center Charlotte, North Carolina

Sabina A. Braithwaite, MD, MPH, Paramedic Associate Professor of Emergency Medicine Washington University in St. Louis Medical Director AirEvac Lifeteam Missouri/Arkansas St. Louis, Missouri

Jane H. Brice, MD, MPH

Professor of Emergency Medicine University of North Carolina at Chapel Hill Chapel Hill, North Caroline

Peter V. Bui, MD

Instructor of Emergency Medicine Medical College of Georgia at Augusta University Augusta, Georgia

Department of Emergency Medicine Case Western Reserve University, School of Medicine Cleveland Medical Center, University Hospitals Health System Cleveland, Ohio

Jonnathan Busko, MD, MPH

Gerald (Wook) Beltran, DO, MPH

José G. Cabañas, MD, MPH

Associate Professor of Emergency Medicine University of Massachusetts Medical School ‐ Baystate Springfield, Massachusetts

Richard T. Benson II, MD Director and Medical Director Vance County EMS Henderson, North Carolina

Molly Berkoff, MD, MPH

Professor of Pediatrics University of North Carolina at Chapel Hill Chapel Hill, North Carolina

Noah Bernhardson, MD, Paramedic EMS Fellow Washington University in St. Louis Assistant Medical Director Mehlville (MO) Fire Protection District St. Louis, Missouri

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Emergency Department Medical Director St. Joseph Healthcare Bangor, Maine

Adjunct Associate Professor of Emergency Medicine University of North Carolina at Chapel Hill Director and Medical Director Wake County EMS System Raleigh, North Carolina

Micha Campbell, MD, MPH Clinical Instructor of Emergency Medicine University of Pittsburgh Assistant Director of EMS St. Clair Memorial Hospital Pittsburgh, Pennsylvania

Jestin N. Carlson, MD

National Director of Clinical Education U.S. Acute Care Solutions Department of Emergency Medicine Saint Vincent Hospital Erie, Pennsylvania

Contributors

Alix J.E. Carter, MD, MPH

Associate Professor of Emergency Medicine Dalhousie University Medical Director of Research EHS Nova Scotia Halifax, Nova Scotia Canada

Richard Cartie, MD

Director Pediatric Critical Care Services Joseph M. Still Burn Center Burn and Reconstructive Surgery Centers of America Augusta, Georgia

Aaron Case, MD

Emergency Medicine Providence Milwaukie Hospital Milwaukie, Oregon

Timothy P. Chizmar, MD

Maryland State EMS Medical Director Maryland Institute for Emergency Medical Services Systems Baltimore, Maryland

Mark X. Cicero, MD

Associate Professor of Pediatrics and Emergency Medicine Yale University School of Medicine New Haven, Connecticut

Matthew Cobb, MD

Mohamud R. Daya, MD, MS Professor of Emergency Medicine Oregon Health & Science University EMS Medical Director Tualatin Valley Fire & Rescue Portland, Oregon

Jocelyn M. De Guzman, MD

Clinical Assistant Professor of Emergency Medicine University of Tennessee College of Medicine Chattanooga Chattanooga, Tennessee

Lynne Dees, PhD, Paramedic Center for Prehospital Care David Geffen School of Medicine University of California at Los Angeles Los Angeles, California

Aaron Dix, Paramedic, MBA Prisma Health Emergency Medical Services Prisma Health Greenville, South Carolina

Elizabeth A. Donnelly, PhD, MPH, LICSW, EMT Associate Professor School of Social Work University of Windsor Windsor, Ontario, Canada

J. Joelle Donofrio‐Odmann, DO

Department of Emergency Medicine Prisma Health University Medical Group Prisma Health Greenville, South Carolina

Associate Clinical Professor of Pediatrics and Emergency Medicine University of California, San Diego Deputy Chief Medical Officer City of San Diego and San Diego Fire Department San Diego, California

Jennifer Cook

Jeremiah Escajeda, MD

Research Associate Oregon Health & Science University Portland, Oregon

Katherine Couturier, MD, MPH Instructor of Emergency Medicine Yale University School of Medicine New Haven, Connecticut

Stephanie A. Crapo, MD Department of Emergency Medicine Ridgecrest Regional Hospital Medical Director Liberty Ambulance Service Ridgecrest, California

Kristen Cunningham, MPA

MetroHealth Department of Emergency Medicine Cleveland, Ohio

Jeffrey D. Ferguson, MD

Associate Professor of Emergency Medicine Virginia Commonwealth University Medical Director Henrico County Division of Fire Richmond, Virginia

Michael Ferras, MD

Clinical Instructor of Emergency Medicine Virginia Commonwealth University Richmond, Virginia

Jennifer N. Fishe, MD

Program Director International Center for Automotive Medicine University of Michigan Ann Arbor, Michigan

Assistant Professor of Emergency Medicine University of Florida College of Medicine Associate Medical Director for Pediatrics Nassau County Fire Rescue Department Jacksonville, Florida

Jeremy T. Cushman, MD, MS, Paramedic

Deborah Flowers, MSN

Associate Professor of Emergency Medicine University of Rochester Medical Director Monroe County and City of Rochester Rochester, New York

Medical Services Coordinator Child Advocacy Centers of North Carolina Graham, North Carolina

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x

Contributors

Raymond L. Fowler, MD

J. Stephen Huff, MD

Emerson Franke, MD

Irfan Husain, MD, MPH

Adam Frisch, MD, MS

Angus M. Jameson, MD, MPH

Professor of Emergency Medicine University of Texas Southwestern Dallas, Texas

EMS Fellow Aventura Hospital Aventura, Florida

Assistant Professor of Emergency Medicine University of Pittsburgh Pittsburgh, Pennsylvania

Stephanie O. Frisch, PhD

Assistant Professor of Biomedical Informatics University of Pittsburgh Pittsburgh, Pennsylvania

Susan Fuchs, MD

Professor of Pediatrics (Emergency Medicine) Northwestern University Feinberg School of Medicine Chicago, Illinois

Gregory H. Gilbert, MD Medical Director San Mateo County EMS Redwood City, CA

Bradley Michael Golden, DO, AEMT Assistant Professor of Emergency Medicine Medical College of Georgia at Augusta University Augusta, Georgia

Toni Gross, MD, MPH

Clinical Associate Professor of Pediatrics Louisiana State University Health Sciences Center, New Orleans New Orleans, Louisiana

Joseph Grover, MD

Assistant Professor of Emergency Medicine University of North Carolina Medical Director Orange County EMS Chapel Hill, North Carolina

Francis X. Guyette, MD, MPH Associate Professor of Emergency Medicine University of Pittsburgh School of Medicine Medical Director STAT MedEvac Pittsburgh, Pennsylvania

Eric Hawkins, MD, MPH

Assistant Professor of Emergency Medicine Carolinas Medical Center Charlotte, North Carolina

Sven Holcombe, PhD

Crash Safety Engineer International Center for Automotive Medicine University of Michigan Ann Arbor, Michigan

Professor of Emergency Medicine and Neurology University of Virginia Charlottesville, Virginia

Assistant Professor of Emergency Medicine Emory University School of Medicine Atlanta, Georgia

Affiliate Assistant Professor USF Health‐Morsani College of Medicine Medical Director Pinellas County EMS Largo, Florida

Anjni Joiner, DO, MPH Assistant Professor of Surgery Duke University School of Medicine Medical Director Durham County EMS Durham, North Carolina

Richard A. Kamin, MD

Associate Professor of Emergency Medicine University of Connecticut Health Center Farmington, Connecticut

Robert Kaufman

Senior Crash Investigator International Center for Automotive Medicine University of Michigan Ann Arbor, Michigan

Andrew King, MD

Assistant Professor of Emergency Medicine Wayne State University Detroit, Michigan

Bryan B. Kitch, MD

Assistant Professor of Emergency Medicine Brody School of Medicine East Carolina University Greenville, North Carolina

Christian C. Knutsen, MD, MPH Assistant Professor of Emergency Medicine SUNY Upstate Medical University Syracuse, New York

David A. Kranc, MD

EMS Fellow UNC Health Department of Emergency Medicine Assistant Medical Director Calhoun County (SC) EMS Chapel Hill, North Carolina

Jon R. Krohmer, MD

Director Office of EMS National Highway Traffic Safety Administration US Department of Transportation Washington, DC

Contributors

Dana S. Levin, PhD, LMSW

Janelle M. Martin, MD

Danielle Levine, MD, MEd

Christian Martin‐Gill, MD, MPH

Associate Professor School of Social Work University of Windsor Windsor, Ontario, Canada

Instructor of Emergency Medicine Yale University School of Medicine New Haven, Connecticut

Rachel Liu, MD

Associate Professor of Emergency Medicine Yale University School of Medicine New Haven, Connecticut

Michael Lohmeier, MD

Associate Professor of Emergency Medicine University of Wisconsin‐Madison Medical Director UW Health Emergency Education Center Madison, Wisconsin

Robert Lowe, MD

Clinical Professor of Emergency Medicine Ohio University Heritage College of Osteopathic Medicine Medical Director Columbus Division of Fire Columbus, Ohio

Dave W. Lu, MD, MS, MBE

Associate Professor of Emergency Medicine University of Washington School of Medicine Seattle, Washington

Jeffrey Lubin, MD, MPH

Professor of Emergency Medicine Penn State Milton S. Hershey Medical Center Hershey, Pennsylvania

Mariecely Luciano‐Feijoó, MD Assistant Professor of Emergency Medicine University of North Carolina at Chapel Hill Chapel Hill, North Carolina

Joshua Lupton, MD, MPH, MPhil Clinical Instructor and Research Fellow Oregon Health & Science University Portland, Oregon

Russell D. MacDonald, MD, MPH

Professor of Emergency Medicine University of Toronto Medical Director Toronto Paramedic Services and Toronto Central Ambulance Communication Centre Toronto, Ontario, Canada

Michael Mancera, MD

Assistant Professor of Emergency Medicine University of Wisconsin‐Madison Medical Director Fitchrona and Middleton EMS Madison, Wisconsin

Jurisdictional/Regional EMS Medical Director Maryland Institute for Emergency Medical Services Systems Western Maryland Washington County, Maryland

Associate Professor of Emergency Medicine University of Pittsburgh Associate Medical Director STAT MedEvac Pittsburgh, Pennsylvania

Bryan McNally, MD, MPH Professor of Emergency Medicine Emory University School of Medicine Rollins School of Public Health Atlanta, Georgia

Mary P. Mercer, MD, MPH

Associate Professor of Emergency Medicine University of California San Francisco San Francisco, California

Paul M. Middleton, MBBS, MD, MMed Associate Professor of Emergency Medicine University of Sydney Director South Western Emergency Research Institute Sydney, New South Wales Australia

Brian L. Miller, MD

Assistant Professor of Emergency Medicine UT Southwestern Medical Center Deputy Medical Director UT Southwestern/Parkland BioTel EMS System Dallas, Texas

Diane L. Miller, MD, MS

Assistant Professor of Emergency Medicine University of North Carolina Medical Director North Carolina State Highway Patrol Chapel Hill, North Carolina

Ronna G. Miller, MD

Associate Professor of Emergency Medicine UT Southwestern Medical Center Assistant Medical Director UT Southwestern/Parkland BioTel EMS System Dallas, Texas

Brandon B. Morshedi, MD, DPT Assistant Professor of Emergency Medicine UT Southwestern Medical Center Deputy Medical Director UT Southwestern/Parkland BioTel EMS System Dallas, Texas

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xii

Contributors

Vincent N. Mosesso, Jr, MD

Sylvia Owusu‐Ansah, MD, MPH

Hawnwan Philip Moy, MD

Joseph P. Ornato, MD

Professor of Emergency Medicine University of Pittsburgh School of Medicine Medical Director UPMC Prehospital Care Pittsburgh, Pennsylvania

Assistant Professor of Emergency Medicine Washington University in Saint Louis St. Louis, Missouri

Christine M. Murphy, MD

Associate Professor of Emergency Medicine Carolinas Medical Center Charlotte, North Carolina

Gayathri Devi Nadarajan, MBBS Clinical Assistant Professor Duke‐NUS Medical School Consultant in Emergency Medicine Singapore General Hospital Singapore

Matthew R. Neth, MD

Assistant Professor of Emergency Medicine Oregon Health & Science University Associate EMS Medical Director Tualatin Valley Fire & Rescue Portland, Oregon

Anthony T. Ng, MD

Assistant Professor of Psychiatry Uniformed Service University of the Health Sciences Bethesda, Maryland

Andre Pennardt, MD

Professor of Emergency Medicine Augusta University Aventura Hospital and Medical Center Aventura, Florida

Debra G. Perina, MD

Professor of Emergency Medicine University of Virginia School of Medicine Charlottesville, Virginia

Roberto C. Portela, MD

Clinical Assistant Professor of Emergency Medicine Brody School of Medicine East Carolina University Medical Director Pitt County EMS Greenville, North Carolina

Marcus E.H. Ong, MBBS, MPH

Professor of Health Services and Systems Research Duke‐NUS Medical School Senior Consultant in Emergency Medicine Singapore General Hospital Singapore

Assistant Professor of Pediatrics University of Pittsburgh School of Medicine EMS Medical Director UPMC Children’s Hospital of Pittsburgh Pittsburgh, Pennsylvania

Professor of Emergency Medicine Virginia Commonwealth University Operational Medical Director Richmond Ambulance Service Richmond, Virginia

Jon C. Rittenberger, MD, MS Professor of Emergency Medicine Geisinger Commonwealth School of Medicine Danville, Pennsylvania

Nathan Roney, MD, MS EMS Fellow Brody School of Medicine East Carolina University Greenville, North Carolina

Ronald N. Roth, MD

Professor of Emergency Medicine University of Pittsburgh Medical Director City of Pittsburgh Department of Public Safety Pittsburgh, Pennsylvania

Aiman Saleh, MD

EMS Fellow University of North Carolina Assistant Medical Director Orange County EMS Chapel Hill, North Carolina

Michael R. Sayre, MD Professor of Emergency Medicine University of Washington Medical Director Seattle Fire Department Seattle, Washington

Terri A. Schmidt, MD, MS

Professor Emeritus of Emergency Medicine Oregon Health & Science University Portland, Oregon

David J. Schoenwetter, DO Medical Director Geisinger Life Flight Geisinger Health Danville, Pennsylvania

Richard B. Schwartz, MD

Professor of Emergency Medicine Medical College of Georgia at Augusta University Augusta, Georgia

Contributors

Karen D. Serrano, MD

Briana N. Tully, DO

Manish N. Shah, MD, MPH

Clare Wallner, MD, MCR

Clinical Assistant Professor of Emergency Medicine University of North Carolina Chapel Hill, North Carolina

Professor of Emergency Medicine University of Wisconsin‐Madison Madison, Wisconsin

Benjamin A. Smith, MD

Clinical Assistant Professor of Emergency Medicine University of North Carolina at Chapel Hill School of Medicine Medical Director AirLife NC Chapel Hill, North Carolina

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Clinical Instructor of Emergency Medicine University of Virginia School of Medicine Charlottesville, Virginia

Assistant Professor of Emergency Medicine McMaster University Associate Medical Director HHS Centre for Paramedic Education & Research Hamilton, Ontario, Canada

Henry E. Wang, MD, MS Professor of Emergency Medicine Ohio State University Columbus, Ohio

Stewart C. Wang, MD, PhD James I. Syrett, MD, MBA Oswego Health Oswego, New York Director of Prehospital Care Wayne County, New York

Asha K. Tharayil, MD Assistant Professor of Pediatrics UT Southwestern Medical Center Dallas, Texas

David P. Thomson, MS, MD, MPA Clinical Professor of Emergency Medicine East Carolina University Brody School of Medicine Medical Director Vidant EastCare Greenville, North Carolina

Andrew Travers, MD, MSc Professor of Emergency Medicine Dalhousie University Provincial Medical Director Emergency Health Services Nova Scotia Halifax, Nova Scotia, Canada

Rickquel Tripp, MD, MPH EMS Medical Director University of Pittsburgh Medical Center Pittsburgh, Pennsylvania

Professor of Surgery Director International Center for Automotive Medicine University of Michigan Ann Arbor, Michigan

Michelle Welsford, MD

Professor of Emergency Medicine McMaster University EMS Physician HHS Centre for Paramedic Education & Research Hamilton, Ontario, Canada

Jefferson G. Williams, MD, MPH

Clinical Assistant Professor of Emergency Medicine University of North Carolina Deputy Medical Director Wake County Department of Emergency Medical Services Raleigh, North Carolina

James E. Winslow, MD, MPH Associate Professor Wake Forest University Health Sciences Medical Director North Carolina Office of EMS Winston‐Salem, North Carolina

Donald M. Yealy, MD

Professor of Emergency Medicine, Medicine, and Clinical and Translational Sciences University of Pittsburgh School of Medicine Pittsburgh, Pennsylvania

Foreword

Emergency Medical Services: Clinical Practice and Systems Oversight is firmly established as the standard reference text for the medical subspecialty of EMS. Within the following pages is the distillation of the clinical practice of EMS medicine. This text provides the updated (2019) core content of the specialty for the next generation of EMS leaders, and provides an ongoing reference for the practicing clinician. NAEMSP extends its heartfelt thanks and gratitude to the editors, David Cone, Jane Brice, Ted Delbridge, and Brent Myers, for their tireless work; and to the authors for their important contributions that have brought this important body of knowledge to a third edition. Though in gestation for over three decades, the actual specialty of EMS medicine is still in its infancy. The success and the relevance of EMS medicine will succeed or fail by our stewardship in the coming years. The validation of a specialty solely by virtue of the hard‐won achievement of recognition by the house of medicine will not, by itself, lead to a general acknowledgement among our colleagues, communities, and local, state, and national leadership that EMS physicians are truly the leaders of this important facet of the health care system and, as such, possibly not realize that EMS is even part of the health care system! The inflection point may be seen when more communities become invested in seeing the outcomes and quality metrics of their EMS systems, and begin to require that medical oversight is provided by an EMS physician, in the same way that they would seek out qualified physicians for other aspects

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of their health care systems. We will know we are on track as medical directors evolve into chief medical officers, and more commonly become direct‐reports to mayors as opposed to dotted lines to middle management, expected to be in the C‐ suite meetings on the same level as other chief executives. We have the responsibility to become more deeply invested in local, state, and national political advocacy to have a voice on issues that affect our practice, our personnel, and our communities. The natural evolution of our specialty that seems out of reach at this point can become a positive “disruptive” force for health care. Those of you who are reading this text are those who will be responsible for the advancement of our specialty. The latest edition of the text will be published during an era that has seen the rise of a global pandemic, a true 100‐year event, the full scope and effects as yet unknown at the time of this writing. It is likely that there will be sustained changes in EMS as a result of the lessons learned. This third edition should serve as a solid foundation for what EMS is, and the principles within will provide guidance for what it can become. Although the post‐pandemic landscape remains unrevealed, what is known and what will unequivocally not change is the ethos of dedication, service, valor, and heroism demonstrated by EMS during this crisis. Michael Levy, MD President 2021 & 2022 National Association of EMS Physicians®

Preface

Since the earliest version of this textbook in 1989, the ­subspecialty of EMS medicine has evolved dramatically. In addition to increasing sophistication and application of expertise, EMS has developed to encompass a unique body of knowledge. Recognizing these features and an ongoing need to nurture the professionalism of those physicians who are and might become committed to EMS, the American Board of Medical Specialties recognized EMS as a subspecialty in 2010. The American Board of Emergency Medicine administered the first certification examination in 2013, and at this writing there are 880 ABEM‐ certified EMS physicians, with substantially more emergency physicians certified in EMS than in any other emergency medicine sub‐specialty. The Accreditation Council for Graduate Medical Education has accredited 71 EMS fellowship programs as of this writing. This third edition of Emergency Medical Services: Clinical Practice and Systems Oversight builds on the foundations of its predecessors: EMS Medical Directors Handbook (1989), Prehospital Systems and Medical Oversight (1994, 2002), and the first two editions of this book (2009 and 2015). As with the 2015 edition, this text is intended to be the primary textbook for EMS fellowship programs, structured around the 2019 version of the core content of EMS medicine [1], which forms the basis for the ABEM certification examination. The Appendix maps the current EMS fellowship core content to specific chapters for easy reference. Noting that the ABEM certification exam is

written to help assure the qualifications of the minimally qualified EMS physician who has attained “proficiency in managing the breadth of clinical conditions and operational aspects encountered by EMS systems in non‐traditional healthcare settings [2]”, this text is written at the “essentials‐plus” level. The intent is to cover the essential material that the exam candidate needs to know, with additional detail in key areas. We thank the dozens of authors who have generously donated their time and effort to this new edition, and the hundreds of authors and editors of the past editions, upon whose efforts this latest edition are built. D Cone J Brice T Delbridge B Myers April 2021

References 1 Delbridge TR, Dyer S, Goodloe JM, et al. The 2019 core content of emergency medical services medicine. Prehosp Emerg Care. 2020; 24:32–45. 2 American Board of Emergency Medicine. Emergency medical services. Available at: https://www.abem.org/public/become‐certified/ subspecialties/emergency‐medical‐services. Accessed February 22, 2021.

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About the Companion Site

This series is accompanied by a companion website: https://naemsp.org/career-development/textbooks/textbook-support-3rd-edition/  The website includes: • Videos Note: The videos are clearly signposted throughout the book. Look out for

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 .

CHAPTER 1

History of emergency medical services Jon R. Krohmer

Before 1966: Historical Perspectives The true origins of the concept of prehospital emergency care may not be clear, but there is no doubt that this philosophy has existed for centuries. Early hunters and warriors provided care for the injured. Although the methods used to staunch bleeding, stabilize fractures, and provide nourishment were primitive, the need for treatment was undoubtedly recognized. The basic elements of prehistoric response to injury still guide contemporary emergency medical services (EMS) activities. Recognition of the need for action led to the development of medical and surgical emergency treatment techniques. These techniques in turn made way for systems of communication, treatment, and transport, all geared toward reducing morbidity and mortality. The Edwin Smith Papyrus, written in 1500  bc, vividly describes triage and treatment protocols [1]. Reference to emergency care is also found in the Babylonian Code of Hammurabi, where a detailed protocol for treatment of the injured is described [2]. In the Old Testament, Elisha breathed into the mouth of a dead child and brought the child back to life [3]. The Good Samaritan not only treated the injured traveler but also instructed others to do likewise [4]. Greeks and Romans had surgeons present during battle to treat the wounded. The most direct evidence of modern prehospital systems is found in the efforts of Jean Dominique Larrey, Napoleon’s chief military physician. Larrey developed a prehospital system in which the injured were treated on the battlefield before using horse‐drawn wagons to carry them away [5]. In 1797, Larrey built “ambulance volantes” of two or four wheels to rescue the wounded. He introduced a new concept in military surgery: early transport from the battlefield to aid stations and then to the frontline hospital. This method is comparable to the way that modern physicians modified the military use of helicopters in the Korean and Vietnam wars. Larrey also initiated detailed treatment protocols, such as the early amputation of shattered limbs to prevent gangrene.

The Civil War is the starting point for what we know as EMS systems in the United States [6]. Learning from the lessons of the Napoleonic and Crimean wars, military physicians led by Joseph Barnes and Jonathan Letterman established an extensive system of prehospital care. The Union army trained medical corpsmen to provide treatment in the field. A transportation system, which included railroads, was developed to bring the wounded to medical facilities. However, the wounded received suboptimal treatment in these facilities, stirring Clara Barton’s crusade for better care [7]. The medical experiences of the Civil War stimulated the beginning of civilian urban ambulance services. The first were established in cities such as Cincinnati, New York, London, and Paris. Edward Dalton, Sanitary Superintendent of the Board of Health in New York City, established a city ambulance program in 1869. Dalton, a former surgeon in the Union Army, spearheaded the development of urban civilian ambulances to permit greater speed, enhance comfort, and increase maneuverability on city streets [8]. His ambulances carried medical equipment such as splints, bandages, straitjackets, and a stomach pump, as well as a medicine chest of antidotes, anesthetics, brandy, and morphine. By the turn of the century, physician interns accompanied the ambulances. Care was rendered and often the patient was left at home. Ambulance drivers had virtually no medical training. Our knowledge of turn‐of‐the‐century urban ambulance service comes from the writings of Emily Barringer, the first woman ambulance surgeon in New York City [9]. Further development of urban ambulance services continued in the years before World War I. Electric, steam, and gasoline‐powered carriages were used as ambulances. Calls for service were generally processed and dispatched by individual hospitals, although improved telegraph and telephone systems with signal boxes throughout New York City were developed to connect the police department and the hospitals. In some cities, the first ambulances and hospitals, in fact, were developed as part of the police department [10].

Emergency Medical Services: Clinical Practice and Systems Oversight, Third Edition. Volume 1: Clinical Aspects of EMS. Edited by David C. Cone, Jane H. Brice, Theodore R. Delbridge, and J. Brent Myers. © 2021 NAEMSP. Published 2021 by John Wiley & Sons, Inc.

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During World War I, the introduction of the Thomas traction splint for the stabilization of patients with leg fractures led to a decrease in morbidity and mortality. Between the two World Wars, ambulances began to be dispatched by mobile radios. In the 1920s, in Roanoke, Virginia, the first volunteer rescue squad was started. In many areas, volunteer rescue or ambulance squads gradually developed and provided an alternative to the local police department, fire department, or undertaker. In areas where medical resources were available, those ambulances were staffed with physicians, often interns. After the entry of America into World War II, the military demand for physicians pulled the interns from American ambulances, never to return, resulting in poorly trained staff and non‐standardized prehospital care. Postwar ambulances were underequipped hearses and similar vehicles staffed by untrained personnel. Half of the ambulances were operated by mortuary attendants, most of whom had never taken even a first aid course [11]. Throughout the 1950s and 1960s, two geographic patterns of ambulance service evolved. In cities, hospital‐based ambulances gradually coalesced into more centrally coordinated citywide programs, usually administered and staffed by the municipal hospital or fire department. In rural areas, funeral home hearses were sporadically replaced by a variety of units operated by the local fire department or a newly formed rescue squad. Additionally, in both urban and rural areas, a few profit‐making providers delivered transport services and occasionally contracted with local government to provide emergency prehospital services and transport. Before 1966, very little legislation and regulation applicable to ambulance services existed, limiting consistency among services. Ambulance attendants had relatively little formal training, and physician involvement at all levels was minimal. A number of factors combined in the mid‐1960s to stimulate a revolution in prehospital care. Advances in medical treatments led to a perception that decreases in mortality and morbidity were possible. Closed‐chest cardiopulmonary resuscitation (CPR), reported as successful in 1960 by W.B. Kouwenhoven and Peter Safar, was eventually adopted as the medical standard for cardiac arrest in the prehospital and hospital settings [12, 13]. New evidence that CPR, pharmaceuticals, and defibrillation could save lives immediately created a demand for physician providers of those interventions in both the hospital and prehospital environments. Throughout the 1960s, fundamental understanding of the pathophysiology of potentially fatal dysrhythmias expanded significantly. The use of rescue breathing and defibrillation was refined by Peter Safar, Leonard Cobb, Herbert Loon, and Eugene Nagel [14]. Safar persuaded many others that defibrillation and resuscitation were viable areas of medical research and clinical intervention. In 1966, Pantridge and Geddes pioneered and documented the use of a mobile coronary care ambulance for prehospital resuscitation of patients in Belfast, Northern Ireland. Their treatment protocols, originally developed for the treatment of

myocardial infarction in intensive care units, were moved into the field [15]. Because the physician‐led medical team was often with the patient at the time of cardiac arrest, the resuscitation rate was a remarkable 20%. Their “flying squads” added a dimension of heroic excitement to the job of being an ambulance attendant, and their performance data helped convince American city health officials and physicians that a more medically sophisticated prehospital advanced life support (ALS) system was possible.

1966: Accidental Death and Disability: The Neglected Disease of Modern Society The modern era of prehospital care in the United States began in 1966. In that year, recognition of an urgent need for improved care, the crucial element necessary for development of prehospital systems nationwide, was heralded by a report from the National Academy of Sciences National Research Council (NAS‐NRC), a non‐profit organization chartered by Congress to provide scientific advice to the nation. Accidental Death and Disability: The Neglected Disease of Modern Society (commonly referred to as the “white paper”) documented the enormous failure of the U. S. health care system to provide even minimal care for the emergency patient in both the prehospital and hospital settings. The NAS‐NRC report identified key issues and problems facing the United States in providing emergency care (Box  1.1). Its summary report listed recommendations that would serve as a blueprint for EMS and emergency medicine development, including such things as first aid training for the lay public, state‐level regulation of ambulance services, emergency department improvements, development of trauma registries, single nationwide phone number access for emergencies, and disaster planning [16]. This document established a benchmark against which to measure subsequent progress and change in emergency care. The 1966 NAS‐NRC document described the care provided by both prehospital services and hospital emergency departments as being woefully inadequate. In the prehospital arena, treatment protocols, trained medical personnel, rapid transportation, and modern communications concepts such as two‐way radios and emergency call numbers, were all identified as necessities that were simply not available to civilians. Although there were more than 7,000 accredited hospitals in the country at the time, very few were prepared to meet the increased demand for volume and clinical care that developed between 1945 and 1965. From 1958 to 1970, the annual number of emergency department visits increased from 18  million to more than 49  million [16]. In addition, emergency departments were staffed by the least experienced personnel, who had little education in the treatment of multiple injuries or critical medical emergencies. Early efforts of the American College of Surgeons (ACS) and the American Academy of Orthopedic Surgeons (AAOS) to improve emergency care were largely unsuccessful because interest

History of emergency medical services

Box 1.1  Key findings of the 1966 NAS‐NRC report

Inadequacies of Prehospital Care in 1966 1  The general public is insensitive to the magnitude of the problem of accidental death and injury. 2  Millions lack instruction in basic first aid. 3   Few are adequately trained in the advanced techniques of cardiopulmonary resuscitation, childbirth, or other life‐saving measures, yet every ambulance and rescue squad attendant, policeman, firefighter, paramedical worker, and worker in high‐ risk industry should be trained. 4  Local political authorities have neglected their responsibility to provide optimum emergency medical services. 5  Research on trauma has not been supported or identified at the National Institutes of Health on a level consistent with its importance as the fourth leading cause of death and a primary cause of disability. 6   The potentials of the U.S. Public Health Service Program in accident prevention and emergency medical services have not been fully exploited.

and support from the medical community were essentially non‐existent [17–20]. The 1966 NAS‐NRC document was the first to recommend that emergency facilities be categorized. It also emphasized aggressive clinical management of trauma, suggesting that local trauma systems develop databases, and that studies be instituted to designate select injuries to be incorporated in the epidemiological reports of the U.S. Public Health Service. Changes were also recommended concerning legal problems, autopsies, and disaster response reviews. Trauma research was especially emphasized, with the ultimate goal of establishing a National Institute of Trauma [16]. Another problem identified in the report was the broad gap between existing knowledge and operational activity. This white paper contains very good conceptual discussions that remain relevant for EMS physicians today. In addition to the NAS‐NRC white paper, other reports raised many similar issues. The President’s Commission on Highway Safety had previously published a report entitled Health, Medical Care, and Transportation of Injured, which recommended a national program to reduce deaths and injuries caused by highway crashes. Its findings were complemented by and consistent with the NAS‐NRC report [21]. The recommendations in both documents were used when the Highway Safety Act of 1966 was drafted. This law established the cabinet‐level Department of Transportation (DOT) and gave it legislative and financial authority to improve EMS. Specific emphasis was placed on developing a highway safety program, including standards and activities for improving both ambulance service and attendant training, with particular focus on motor vehicle crashes [22]. This focus led to improvements in both transportation capabilities and clinical care. The Highway Safety Act of 1966 also authorized funds to develop EMS standards and implement programs that would improve ambulance services. Matching funds were provided

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7  Data are lacking on how to determine the number of individuals whose lives are lost through injuries compounded by misguided attempts at rescue and first aid, absence of physicians at the scene of the injury, unsuitable ambulances with inadequate equipment and untrained attendants, lack of traffic control, or the lack of voice communication facilities. 8  Helicopter ambulances have not been adapted to civilian peacetime needs. 9  Emergency departments of hospitals are overcrowded, some are archaic, and there are no systematic surveys on which to base requirements for space, equipment, or staffing for present, let alone future, needs. 10  Fundamental research on shock and trauma is inadequately supported; medical and health related organizations have failed to join forces to apply knowledge already available to advanced treatment of trauma, or educate the public and inform Congress. Source: Adapted from Accidental Death and Disability: The Neglected Disease of Modern Society. Washington, DC: National Academy of Sciences, 1966.

for EMS demonstration projects and studies. All states were required to have highway safety programs in accordance with the regulatory standards promulgated by DOT. The standard on EMS required each state to develop regional EMS systems that could handle prehospital emergency medical needs. Ambulances, equipment, personnel, and administration costs were funded by the highway safety program. Regional financing, as opposed to county or state funding, was a new concept that would be echoed in federal health legislation throughout the remainder of the decade [22]. With the Highway Safety Act as a catalyst, DOT established a division of emergency medical care and contributed more than $142 million to regional EMS systems between 1968 and 1979. A total of roughly $10 million was spent on research alone, including $4.9 million for EMS demonstration projects. A number of other federal EMS initiatives in the late 1960s and early 1970s poured additional funds into EMS. This included $16 million in funding from the Health Services and Mental Health Administration, which had been designated as the lead EMS agency of the Department of Health, Education, and Welfare (DHEW), to areas of Arkansas, California, Florida, Illinois, and Ohio, for the development of model regional EMS systems [23]. In 1969, the Airlie House Conference proposed a hospital categorization scheme [24]. The American Medical Association (AMA) Commission on EMS urged facility categorization and published its own scheme, which identified staffing, equipment, services, and personnel types [25]. This became known as “horizontal categorization.” Although it was supported by professional and hospital associations, many hospitals and physicians feared hospitals in lower categories would suffer a loss of prestige, patients, or reimbursement. The DHEW EMS program developed a categorization scheme based on hospital‐wide care of specific disease processes. Known as “vertical categorization,”

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this concept was ultimately embraced by many regional programs as a major theme in the development of EMS systems. By the late 1960s, drugs, defibrillation, and personnel were available to improve prehospital care. As early as 1967, the first physician‐responder mobile programs morphed into “paramedic” programs staffed with non‐ physicians using physician‐monitored telemetry capabilities as a modification of the physician‐staffed approach by Pantridge in Belfast. The “Heartmobile” program, begun in 1969 in Columbus, Ohio, was initially staffed with a physician and three EMTs. Within 2 years, 22 highly trained (2,000‐hour program) paramedics provided the field care; the physician role became supervisory. Similarly, in Seattle, physicians supervised highly trained paramedics providing care in the field, increasing the survival rate of 10‐30% for prehospital cardiac arrest patients whose presenting rhythm was ventricular fibrillation. The Seattle model was also one in which fire department first‐ responders played a crucial role in building what is now called a chain of survival. In Dade County, Florida, rapid response of mobile paramedic units was combined with hospital physician direction via radio and telemetry for the first time [26]. In Brighton, England, non‐physician personnel provided field care without direct medical oversight. Electrocardiographic data were recorded continuously to permit retrospective review by a physician [27]. National professional organizations such as the ACS, the AAOS, the American Heart Association (AHA), and the American Society of Anesthesiologists, in concert with other groups, provided extensive medical input into the early development of EMS. New organizations were also formed to focus on EMS, including the AMA’s Commission on EMS, the AHA’s Committee on Community Emergency Health Services, the American Trauma Society, the Emergency Nurses Association, the Society of Critical Care Medicine, the National Registry of Emergency Medical Technicians (NREMT), and the American College of Emergency Physicians (ACEP). In the years prior to 1973, such groups made significant but uncoordinated efforts toward the reorganization, restructure, improvement, expansion, and politicization of EMS [24, 25, 28, 29]. One of the most difficult issues with the development of paramedic programs was that most medical practice acts prevented these non‐physicians from performing procedures and skills that had historically been restricted to physicians (and in some cases nurses). Early in the development of the Los Angeles County program, the physician leadership realized that they had to seek legislative changes to allow paramedics to provide the clinical care desired. Following prolonged and contentious discussions, the Wedworth‐Townsend Act was signed by Governor Ronald Reagan in 1970, the first paramedic act in the nation. Additional states followed that example over the next decade. The first widely recognized national awareness of the concept of paramedics and organized emergency medical services came

to national attention in 1971 with the syndicated television show EMERGENCY. This show depicted the activities of Los Angeles County Fire Department (LACFD) paramedics Johnny Gage and Roy Desoto providing care in the field, supported by the hospital staff at Rampart General Hospital (modeled after the Los Angeles County General Hospital) in the characters of doctors Kelly Bracket, Joe Early, and Mike Morton, and nurse Dixie McCall. With technical advisors LACFD Captain Jim Page and Drs J. Michael Criley and Ronald Stewart, the show gave the citizens of the United States the concept of ALS care in the field and during transport to a specialty care hospital facility. Although presenting very positive impressions of EMS, it also led communities to the misconception that this level of care was uniformly available around the country, an expectation not yet achieved. Having said that, this show was instrumental in helping move understanding of EMS forward and served as a model for EMS systems development and a desire by many viewers to become emergency care clinicians. In 1972, the NAS‐NRC published Roles and Resources of Federal Agencies in Support of Comprehensive Emergency Medical Services, which asserted that the federal government had not kept pace with efforts by professional and lay health organizations to upgrade EMS [30]. The document endorsed a more vigorous federal government role in the provision and upgrading of EMS. It recommended that President Nixon acknowledge the magnitude of the accidental death and disability problem previously reported by proposing action by the legislative and executive branches to ensure optimum universal emergency care. It urged the integration of all federal resources for delivery of emergency services under the direction of a single division of DHEW, which would have primary responsibility for the entire emergency medical program. It also recommended that the focal point for local emergency medical care be at the state level, and that all federal efforts be coordinated through regional EMS programs [30]. 1973: The Emergency Medical Services Systems Act By 1973, several major lessons had emerged from the demonstration projects and the various studies undertaken during the preceding 7 years. Although federal activities had been limited to the 1968 DHEW regional demonstration projects mentioned earlier, significant progress had been made. The projects proved that a regional EMS system approach could work. However, because systems research was not a component of the DHEW program, the demonstration projects did not prove that a regional approach, or for that matter any particular approach, was more effective than another. Many national organizations supported further federal involvement, both in establishing EMS program goals and in providing direct financial support. After several attempts at passing federal EMS legislation, a modified EMS bill was passed with support from numerous public and professional groups. President Nixon vetoed this bill in August 1973, based on the

History of emergency medical services

conservative philosophy that EMS was a service that should be provided by local government, and the federal government should neither underwrite operations nor purchase equipment. Additional congressional hearings led to the reintroduction of a bill proposing an extensive federal EMS program, based on the rationale that individual communities would not be able to develop regional systems without federal encouragement, guidelines, and funding. Finally, in November 1973, the Emergency Medical Services Systems Act was passed and signed. It was added as Title XII to the Public Health Service Act, to address EMS systems, research grants, and contracts. It also added a new section to the existing Title VII concerning EMS training grants [31]. The law was reauthorized in 1976, 1978, and 1979, with a continuing goal to encourage development of comprehensive regional EMS systems throughout the country. The available grant funds were divided among the four major portions of the EMS Systems Act: Section  1202  – ­Feasibility studies and planning; Section 1203 – Initial operations; Section  1204  –  Expansion and improvement; and Section  1205  –  Research. Applicants were encouraged to build on existing health resources, facilities, and personnel. The EMS regions were ultimately expected to become financially self‐sufficient. Therefore, a phase‐out of all federal funding initially targeted for 1979 was extended to 1982. This EMS program was administered in DHEW through the Division of Emergency Medical Services, with David Boyd, the medical director of the Illinois demonstration project, named as director. The law and subsequent regulations emphasized a regional systems approach, a trauma orientation, and a requirement that each funded system address the 15 “essential components” (Box 1.2). Medical oversight was not one of the 15 components, although subsequent regulations encouraged and then required medical oversight.

Box 1.2  The Fifteen Essential EMS Components.

1  Manpower 2  Training 3  Communications 4  Transportation 5  Facilities 6  Critical care units 7  Public safety agencies 8  Consumer participation 9  Access to care 10  Patient transfer 11  Coordinated patient record‐keeping 12  Public information and education 13  Review and evaluation 14  Disaster plan 15  Mutual aid Source: Washington, DC: Department of Health, Education, and Welfare, Division of Emergency Medical Services, 1973.

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1973–1978: Rapid Growth of EMS Systems In 1974, the Robert Wood Johnson Foundation allocated $15 million for EMS‐related activities, the largest single contribution for the development of health systems ever made in the United States by a non‐profit foundation. Forty‐four areas of the country received grants of up to $400,000 to develop EMS systems [32]. This money was intended to encourage communities to build regional EMS systems, emphasizing the overall goal of improving access to general medical care, in addition to the original focus on trauma. The money was provided over a 2‐year period to establish new demonstration projects and develop regional emergency medical communications systems [33]. In early 1974, a newly reorganized DHEW Division of Emergency Medical Services began implementing the legislative mandate. Adopted from earlier experiences, the basic principles were that an effective and comprehensive system must have resources sufficient in quality and quantity to meet a wide variety of demands, with the recognition that the discrete geographic regions established must have sufficient populations and resources to enable them to become self‐sufficient eventually. Each state was also to designate a coordinating agency for statewide EMS efforts. Ultimately, 304 EMS regions were established nationwide. By 1979, 17 regions were fully functional and independent of federal money. However, of the 304 geographic areas, 22 had no activity and 96 were still in the planning phase [34]. In the regulations, David Boyd strictly interpreted the congressional legislative intent of the EMS Systems Act to mandate that all regions adopt all 15 essential components of the legislation. Regions were limited to five grants, and with each year of funding, progress toward more sophisticated operational levels was expected. By the end of the third year of funding, regions were expected to have basic life support (BLS) capabilities, which required no physician involvement. ALS capability, which was expected to perform traditional physician activities and have physician oversight, was expected at the end of the fifth year. The use of BLS and ALS terminology in the regulations spread widely. However, the original definitions that corresponded directly to the funded emergency medical technician‐ambulance (EMT‐A) and paramedic levels of training quickly became elusive as states created variations in the EMT‐A and paramedic levels. Nationally, the EMT‐A level required no medical involvement, but some states such as Kentucky did extend medical oversight to BLS because of insurance laws – laws making medical care and transportation across a county line virtually impossible without a physician’s approval over the radio. Developing the geographic regions required to secure federal funding through the EMS Systems Act usually necessitated new EMS legislation at the state level. The state laws that developed throughout the 1970s varied markedly regarding the issues of

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medical oversight, overall operational authority, and financing. In some states, physician involvement was required. In others, medical oversight was not even mentioned in law or regulation. Often, responsibility for coordinating activities was assigned to a regional EMS council of physicians, prehospital personnel, insurance companies, and consumers who often had specific interests to protect. The level of physician input was inconsistent across the nation. Personnel A lack of appropriately trained emergency personnel at every level of care had been identified in the NAS‐NRC document [16]. After 1973, extensive effort and money were directed at addressing this educational deficiency. Serendipitously, a large number of medical corpsmen, physicians, and nurses were returning from Vietnam; they understood that trained non‐ physicians could perform life‐saving tasks in the field. Many argued that rapid transport and early surgery could improve civilian trauma practice as it had done on the battlefield.

Physicians

In 1966 the NAS‐NRC document stated, regarding emergency care, “No longer can responsibility be assigned to the least experienced member of the medical staff, or solely to specialists, who, by the nature of their training and experience, cannot render adequate care without the support of other staff members” [16]. Thus the importance of physician leadership and training in EMS was identified early. During the 25 years following World War II, increasing demands for care were placed on hospital emergency departments. As a result, groups of physicians began focusing on exclusively practicing and improving emergency care. They identified the academic discipline and scientific rigor necessary to define a separate medical specialty: emergency medicine. In 1968, ACEP was founded by those physicians interested in the organization and delivery of emergency medical care. In 1970, the first emergency medicine residency was established at the University of Cincinnati, and the first academic department of emergency medicine in a medical school was formed at the University of Southern California. Soon the directors of medical school hospital emergency departments founded the University Association for Emergency Medicine. Between 1972 and 1980, more than 740 residents completed training at 51 emergency medicine residencies throughout the country [35–37]. The first major step toward designation as a medical specialty occurred in 1973 when the AMA authorized a provisional Section of Emergency Medicine. In 1974, a Committee on Board Establishment was appointed, and a liaison Residency Endorsement Committee was formed [37]. Further impetus toward expansion of residency training in emergency medicine occurred with the formation of the American Board of Emergency Medicine (ABEM) in 1976 [38]. Before that time there was some hesitancy to create additional residency programs that might not lead to board certification.

In September 1979, emergency medicine was formally recognized as a specialty by the AMA Committee on Medical Education and the American Board of Medical Specialties. One of the strongest arguments in favor of the new specialty was that emergency physicians had a unique role in the oversight of prehospital medicine. ABEM gave its first certifying examination in 1980, which incidentally did not examine on any areas of prehospital care. Although emergency medicine, emergency nursing, and prehospital care were all nourished by the funds distributed between 1973 and 1982, the first full‐time EMS medical director was not appointed until April 1981 in New York City. Previously, all had been part‐time, and many had been simply functionaries. Shortly thereafter, cities like Salt Lake City and Houston followed New York’s lead, and appointed full‐time EMS medical directors. Even then, EMS as a physician career choice was perceived by many as perhaps a risky career undertaking.

Prehospital Clinicians

The Highway Safety Act of 1966 funded EMT‐A training and curriculum development. By 1982, there were approximately 100,000 people trained at the EMT‐A level. They were trained to provide basic, non‐invasive emergency care at the scene and during transport, including such skills as CPR, control of bleeding, ventilation, oxygen administration, fracture management, extrication, obstetric delivery, and patient transport. The educational requirements, which began as a 70‐hour curriculum published by the AAOS in 1969, soon grew to 81 hours of lectures, skills training, and hospital observation; most of the increase in those hours were due to the addition of training in the use of pneumatic anti‐shock garments or military anti‐shock trousers. After working for 6 months, graduates were allowed to take a national certifying examination administered by the NREMT. Founded in 1970, the NREMT developed a standardized examination for EMT‐A personnel as one requirement for maintaining registration. Many states began to recognize NREMT registration for the purposes of state certification or licensure or reciprocity ­between states [29]. While the EMT‐A quickly became a nationally recognized standard, the development of national consensus at the paramedic level was slower, with marked differences in training from locality to locality. Paramedic practices became somewhat ­formalized with the adoption of a DOT emergency medical technician‐paramedic (EMT‐P) curriculum in the late 1970s. By 1982, EMT‐P training ranged from a few hundred to 2,000 hours of educational and clinical experience. Typical clinical skills included cardiac defibrillation, endotracheal intubation, venipuncture, and the administration of a variety of drugs. The use of these skills was based on interpretation of history, clinical signs, and cardiac rhythm strips. Telemetric and voice communications with physicians were usually required prior to initiating advanced level care. In the early days of paramedics, extensive “online” direct medical oversight was mandatory for all calls in most systems. With time, this requirement was

History of emergency medical services

modified by the introduction of protocols allowing for greater use of standing orders [39]. However, a great deal of variation in the use of direct medical oversight remained. As early as 1980, paramedics in decentralized systems, such as New York’s, used many clinical protocols, most of which had few indications for mandatory direct medical oversight. On the other hand, as late as 1992, many centralized systems, such as the Houston Fire Department, had only a few standing orders (mainly for cardiac arrest) that did not require contemporaneous discussion with a direct medical oversight physician. The concept of the EMT‐intermediate (EMT‐I) evolved as a clinician level positioned somewhere between EMT‐A and EMT‐P. Airway management, intravenous therapy, fluid replacement, rhythm recognition, and defibrillation were the most common “advanced” skills included in the EMT‐I curriculum, though significant variation existed from state to state. To meet perceived unique needs of care capabilities from state to state, states developed several levels of EMT‐I, often in a modular progression with formal bridge courses. By 1979, formally recognized prehospital personnel existed at dozens of levels, with highly variable requirements for medical oversight. Public Education CPR training gradually became more widely accepted, as evidenced by participation in training programs throughout the country. As early as 1977, a Gallup poll reported that 12 million Americans had taken CPR courses and another 80 million were familiar with the technique and wanted formal training [6]. The success of public training was documented by many studies [40, 41]. The issues of whom to train and how to improve skill retention continue to be explored, as evidenced by the AHA/ International Liaison Committee on Resuscitation (ILCOR)’s Guidelines 2020 document, which contains significant changes in how the techniques of CPR and emergency cardiac care are taught to laypersons [42]. CPR guidelines based on ILCOR and AHA guidelines continue to be updated. Communications Before 1973, there were few communication systems available for emergency medical care. Only 1 in 20 ambulances had voice communications with a hospital, a universal emergency telephone number was not yet operational nationally, and telephones were not available on highways and rural roads. Centralized dispatch was uncommon and there were problems in communications because of community resistance, cost, and insufficient and variable technology. With DOT funding, major steps were taken toward overcoming these communication problems. National conferences, seminars, and public awareness programs advocated diverse methodologies for EMS communication systems. A communications manual published in 1972 provided technical systems information [43]. Although the first 9‐1‐1 call was placed in 1968, it was not until 1973 that the 9‐1‐1 universal emergency number was advocated as a national standard by DOT and the White House Office of Telecommunications. The

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Federal Communications Commission established rules and regulations for EMS communication and dedicated a limited number of radio frequencies for emergency systems. In 1977, DHEW issued guidelines for a model EMS communications plan [44]. EMS medical directors gradually began to appreciate the importance of more structured call receiving, patient prioritizing, and vehicle dispatching. Physicians were forced to look seriously at EMS operational issues that had previously been seen as neither critical nor medical [45]. Formalized emergency medical dispatch program development began in the mid‐late 1970s. On the other hand, telemetry as it had been pioneered by Gene Nagel in Florida was generally seen to be impractical, expensive, and unnecessary, and essentially disappeared over time. Transportation Transportation of the critically ill or injured patient rapidly improved after 1973. Although national standards for ambulance equipment were developed in the early 1960s, a 1965 survey of 900 cities reported that fewer than 23% had ordinances regulating ambulance services. An even smaller percentage required an attendant other than the driver, and only 72 cities reported training at the level of an American Red Cross advanced first aid course, the nearest thing to a standard ambulance attendant course before the advent of EMT‐A in 1969 [46]. The hearses and station wagons used in the 1960s did not allow personnel room to provide CPR or other treatments to critically ill patients. The vehicles were designed to carry coffins and horizontal loads, not a medical team and a sick patient. In the 1960s, two reports focused national attention on the hazardous conditions of the nation’s ambulances [16, 47]. In addition to inadequate policies, staff training, and communications, ambulance design was faulty, and equipment absent or inadequate. Morticians ran 50% of the ambulance services because they owned the only vehicles capable of carrying patients horizontally. No U.S. vehicle manufacturer built a vehicle that could be termed an ambulance. As early as 1970, DOT and the ACS had developed ambulance design and equipment recommendations [48, 49]. In 1973, DHEW released the comprehensive guide, Medical Requirements for Ambulance Design and Equipment, and a year later the U.S. General Services Administration issued federal specifications KKK‐A 1822 for ambulances [50]. Although the KKK specifications were originally developed for government procurement contracts, local EMS agencies were often politically obligated to meet or exceed the specifications when ordering new ambulances. A 1978 study described the status of ambulance services within 151 of the regions. Only 65% of the 13,790 ambulances in those regions met the federal KKK standards. Eighty‐one regions used paramedics and 72 had some type of air ambulance capability. Response time was often longer than 10 minutes in urban areas and as much as 30 minutes in rural areas [51].

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Hospitals When awarding grants for EMS under the EMS Systems Act, DHEW required regions to develop standards and guidelines for categorization of emergency departments in the following eight critical clinical groups: trauma, burns, spinal cord injuries, poisoning, cardiac, high‐risk infants, alcohol and drug abuse, and behavioral emergencies. Regions were required to identify the most appropriate receiving hospitals for each of these clinical problems. In reality, only a small portion of emergency facilities was functionally categorized, and in many cases the system did not work as described on paper. Hospital administrators resisted losing control, physicians feared surrendering clinical judgment, and both feared losing patient revenues. Despite this resistance, DHEW used EMS hospital categorization to restructure acute patient distribution along the lines of clinical capability rather than market share.

1978–1981: EMS at Midpassage By 1978, many of the original problems and questions concerning EMS had come into focus. Many of the deficiencies identified in the 1966 NAS‐NRC report had been addressed, and progress was being made in many areas. Economic resources and political support were being contributed by local and state governments, private foundations, non‐profit organizations, and professional groups. However, there was still tremendous geographic variability regarding access to and distribution of services and accessibility, quality, and quantity of EMS resources. Basic questions concerning the effectiveness of the various components, system designs, and relationships still existed, and future funding was uncertain. In 1978, the NAS‐NRC released Emergency Medical Services at Midpassage, which stated, “EMS in the United States in midpassage [is] urgently in need of midcourse corrections but uncertain as to the best direction and degree.” The report was sharply critical of how the EMS Systems Act had been implemented by DHEW and recommended “research and evaluation directed both to questions of immediate importance to EMS system development and to long‐range questions. Without adequate investment in both types of research, EMS in the United States will be in the same position of uncertainty a generation hence as it is today” [52]. The report documented coordination problems among various governmental agencies, focusing particular concern on the multiple standards promulgated as a condition of funding. Some of the standards were conflicting; often they had never been evaluated [52]. Between 1974 and 1981, there were various sources of federal and private funds, and each grant often came with a new set of requirements. DOT established standards for ambulance design, personnel training, and other transportation elements, and DHEW announced seven critical care areas as the basis

for a systems approach and 15 components as modular elements for EMS design. A variety of private organizations also produced standards. With regard to the technique of CPR, the American Red Cross and the AHA established slightly different standards, criteria, and training requirements. By 1978, some states still had not enacted EMS legislation, whereas others had legislated specifically what prehospital clinicians could do, potentially hampering the flexibility needed for successful local development. Lack of national conformity or agreement precluded the development of universally accepted national standards in most areas of EMS. On 26 October 1978, a memorandum of understanding was signed by DOT and DHEW describing each organization’s responsibilities relating to development of EMS systems. The agreement was an attempt to coordinate government activities and assign national level responsibility for EMS development and direction. DOT, in coordination with DHEW, was to “develop uniform standards and procedures for the transportation phases of emergency care and response.” DHEW was responsible, in coordination with DOT, for developing “medical standards and procedures for initial, supportive, and definitive care phases of EMS systems.” Research and technical assistance were to be performed cooperatively, and both agencies agreed to exchange information and “establish joint working arrangements from time to time” [53]. Because the roots, constituencies, and operating philosophies of DOT and DHEW were markedly different, the 1978 agreement quickly failed. Over the four subsequent years, the lack of coordination continued [54]. In 1980, the EMS directors from each state banded together to form the National Association of State EMS Directors (now NASEMSO). With membership from all 50 states and the territories, it attempted to take a leadership role with regard to national EMS policy, and to collaborate on the development of effective, integrated, community‐based, and consistent EMS systems. Its strategy was to “achieve our mission by the participation of all the states and territories, by being a strong national voice for EMS, an acknowledged key resource for EMS information and policy, and a leader in developing and disseminating evidence‐based decisions and policy” (https://nasemso. org/about/overview). Financing By 1978, termination of federal funding in most regions was imminent, and the potential effect on operations and future development began to raise concerns. The 1976 and 1979 amendments to the EMS Systems Act reflected concerns about future funding and had consequently demanded evidence of financial self‐sufficiency as one basis for further support. DOT estimates of non‐federal monies spent annually between 1968 and 1980 ranged up to $800 million. In 1979, DHEW officials estimated in testimony that 90% of regions with paramedic service had achieved financial self‐ sufficiency by 1978 [44]. However, the Comptroller General, in

History of emergency medical services

a 1976 report entitled Progress in Developing Emergency Medical Services Systems, cited considerable inconsistency in the degree and duration of support provided by community resources [55]. A few years later, in 1979, the Comptroller General testified on the financial status of the EMS regions after analyzing grant applications under the 1976 amendments. By the 1980s, the discrepancy between DHEW’s and the Comptroller General’s estimates of financial self‐sufficiency of EMS systems suggested serious unrecognized difficulties in the continued underwriting of EMS systems. The financial demands on an EMS system were considerable, related to four major elements: prehospital care, hospital care, communications, and management. The specific costs varied by community. The original 1966 NAS‐NRC report estimated that ambulance services accounted for about one‐fourth of total EMS system costs, with 75% of that amount for personnel. Communications costs varied from 7% of total cost when there was integration with existing public services, to 35% when completely new systems needed to be established. Although management costs were high during the development phases, they were originally expected to account for less than 2% of the total cost during the operational phase [52]. Health insurance reimbursement did not keep pace with EMS costs, which presented a real problem for EMS providers. Health care benefits were often limited to hospital care and had maximum fixed reimbursements. For example, 20% of Blue Cross patients were not covered for emergency transport, and, of those covered, one‐third were only covered after a motor vehicle crash. EMS reimbursement was focused on the transportation aspect of the service, a financial problem that has continued to plague EMS. By 1982, the NAS‐NRC wrote, “Availability of advanced emergency care throughout the nation is a worthy objective, but the cost of such services may prohibit communities from obtaining them” [52]. Research A total of $22 million was appropriated between 1974 and 1979 for EMS research. The National Center for Health Services Research, in coordination with DHEW, funded various clinical and systems research projects. During the 1979 legislative hearings, testimony from DHEW and the leadership of academic research centers stressed the need for continued EMS research. Annual reports from DHEW detailed the types of research under way, the questions being studied, and the scope of long‐term and short‐term research projects funded under Section  1205 of Title XII [51]. These projects included “methods to measure the performance of EMS personnel, evaluate the benefits and the costs of ALS systems, examine the impact of categorization efforts, determine the clinical significance of response time, and explore the consequences of alternative system configurations and procedures” [56]. Other projects focused on “developing systems of quality assurance, designing and testing clinical algorithms, and examining the relationships between emergency

9

departments and their parent hospitals (including rural‐urban differences)” [56]. In early 1979, the Center for the Study of Emergency Health Services at the University of Pennsylvania urged continued support of EMS research. It claimed, “Dollars spent in EMS research have great potential to help control rising health care costs, [and can] have a significant and visible effect in preventing death and enhancing the quality of patient life following emergency events” [57]. The center suggested research identifying EMS cost control potentials because the phasing out of federal funds, coupled with the effects of local tax revolts, would certainly reduce financing. As the 1980s progressed, the demand for more efficient, effective systems would become universal. Managers of EMS systems, just like their counterparts elsewhere, needed to know which components of the system were crucial and which could be deleted if funding was limited. The answers to those questions were anything but clear. 1981: The Omnibus Budget Reconciliation Act Late in the summer of 1981, President Reagan signed comprehensive cost containment legislation that converted 25 Department of Health and Human Services (DHHS) [formerly the DHEW] funding programs into seven consolidated block grant programs [58]. EMS was included in the Preventive Health Block Grant, along with seven other programs such as rodent control and water fluoridation. Individual states were then left to determine how much money from the block grants would be distributed locally. Although existing EMS programs were temporarily guaranteed minimal support, a state could later decide to withdraw all block grant money from one or more regional EMS programs. This concept, simply a fundamental premise of conservative federal government, evolved quite differently in each state. As with decisions regarding how to implement clinician levels and assure competence, the funding process was generally quite political, with little direct input from the public or the EMS or medical communities. The 1976 Forward Plan for the Health Services Administration made it clear that, by 1982, all federal EMS system financial support would end, and regional EMS programs would be the responsibility of the regional agencies. The federal role was to be “one of technical assistance and coordination” [59]. These changes significantly curtailed federal funding for EMS program development and evolution. 1982–1996: Changing Federal Roles The public health initiative for developing a national EMS system came to a gradual, quiet, and unceremonious demise after the 1981 legislative changes. In most regions, the remnants of the old DHEW program were left to die off slowly under the cloud of confusion occasioned by the Preventive Health Block Grants formula. In most (but not all) states, EMS regional programs were lost in the shuffle of competing health programs while the Reagan administration systematically eliminated federal support for all such programs. In fact, in most jurisdictions

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the regional EMS momentum present throughout the 1970s simply evaporated. Paradoxically, some individuals involved in EMS saw the end of DHEW era as an opportunity to develop and implement alternative approaches that would not previously have been permitted [60]. Organizations such as the NREMT, the National Association of EMTs (NAEMT), and NASEMSO stepped into the vacuum and endeavored to provide some degree of national infrastructure and EMS identity. At the state level, state EMS agencies managed to keep the momentum by sponsoring well‐attended statewide conferences. At the federal level, the DOT continued its support of EMS activities. In 1984, the Emergency Services Bureau of the National Highway Traffic Safety Administration (NHTSA) was instrumental in creating the American Society for Testing and Materials (ASTM) Committee on Emergency Medical Services (F‐30). Through the ASTM, NHTSA sought to legitimize the promulgation of standards in many areas of EMS. Through a complex consensus process, thousands of ASTM technical standards were arrived at in many different industries, including construction and building. Although these standards have no federal mandate, they were often enforced at the local level, for example, in building codes. Since a confusing but enthusiastic beginning in 1984, more than 30 EMS‐related standards have been developed, including those for the EMT‐A curriculum, rotor‐wing and fixed‐wing medical aircraft, and EMS system organization. This last document outlined the roles and responsibilities of state, regional, and local EMS agencies. The resultant standards, although mandated by no authority, were considered by several state legislatures when state EMS laws or guidelines, written to obtain federal funding in the mid‐1970s, required updating. Many of the ASTM F‐30 standards have been withdrawn in recent years. The F‐30 Committee prospered as long as physician involvement was evident and decisive, but it was clearly NHTSA’s decision what standard to expedite and when. The NREMT, NAEMT, and other interest groups joined the physicians, each to protect themselves. Although many physicians and physician groups eventually tired of the F‐30 exercise, NHTSA preserved some semblance of a central authority at the federal level. As early as 1983, NHTSA began assuming some roles previously associated with old DHEW programs. Many of the original evaluation staff were hired on a part‐time basis to promote use of EMS management information systems. In 1988, NHTSA attempted to organize the electronic exchange of information among surviving EMS clearing houses, but those efforts eventually failed after 3 years. Because NHTSA had no specific legislative mandate to assume many of the roles previously performed by DHEW, some states tried to assume those roles but were often unsuccessful. One area that received less attention at the federal level was trauma research and systems development. That would remain so until the passage of the Trauma Care Systems Planning and Development Act in 1990

(Public Law 101‐590). This program was funded for several years by DHHS but subsequently also lost funding. It would be incorrect to view the period since 1982‐1996 as simply stagnant. It might be better characterized as a time when varying forces confused attempts by the federal government and national organizations to define and standardize EMS. During this time, neither an operational consensus nor a discrete EMS development philosophy emerged. Across the country, local activists battled others in pursuit of diminishing funds. By 1992, patients had clearly emerged as customers, and, by the beginning of the Clinton administration, EMS was as conceptually unified, standardized, efficient, expensive, and confused as the rest of American health care. The Clinton health care plan of 1993 barely mentioned ambulance services, and it did not address EMS systems at all. Emergency Medical Services for Children Program The Emergency Medical Services for Children (EMSC) program was first authorized and funded by the U.S. Congress in 1984 as a demonstration program under Public Law 98‐555. The EMSC program is administered by the DHHS Health Resources and Services Administration’s Maternal and Child Health Bureau; many of the EMSC programs are jointly funded by the Health Resources and Services Administration (HRSA) and NHTSA. This program is a national initiative designed to reduce child and youth disability and death caused by severe illness or injury [61] and serves as an example of a successful collaboration between government and academic forces. In the late 1970s, the Hawaii Medical Association laid the groundwork for the EMSC program by urging members of the American Academy of Pediatrics to develop multifaceted EMS programs that would decrease morbidity and mortality in children. It worked with Senator Daniel Inouye (D‐HI) and his staff to write legislation for a pediatric EMS initiative. In 1983, a particular incident demonstrated the need for these services. One of Senator Inouye’s senior staff members had an infant daughter who became critically ill. Her case showed the serious shortcomings of an average emergency department when caring for a child in crisis. A year later, Senators Orrin Hatch (Republican‐UT) and Lowell Weicker (Republican‐CT), backed by staff members with disturbing experiences of their own, joined Senator Inouye in sponsoring the first EMSC ­legislation. Initial funding from the EMSC program supported four state demonstration projects. These state projects developed some of the first strategies for addressing important pediatric emergency care issues, such as disseminating educational programs for prehospital and hospital‐based clinicians, establishing data collection processes to identify significant pediatric issues in the EMS system, and developing tools for assessing critically ill and injured children. In later years, additional states were funded to develop other strategies and to implement programs developed by their predecessors. This work progressed through the 1990s when all 50 states and the territories received funding to

History of emergency medical services

improve EMSC and integrate it into their existing EMS systems. In response to the available money, in many areas, prehospital care of children became the focus of all EMS innovation. After several years, with projects developing many useful and innovative approaches to taking care of children in the prehospital setting, a mechanism was needed to make these ideas and products more easily accessible to interested states. In 1991, two national resource centers were funded to provide technical assistance to states and to manage the dissemination of information and EMSC products. In 1995, the EMSC National Resource Center in Washington, DC was designated the single such center for the nation. Additionally, with the recognition of the dire need for research and the lack of qualified individuals in each state to perform it, a new center was funded, the National EMSC Data Analysis Resource Center (NEDARC) located at the University of Utah School of Medicine. Created through a cooperative agreement with the Maternal and Child Health Bureau, the NEDARC was established to “help states accelerate adoption of common EMS data definitions, and to enhance data collection and analysis throughout the country” [62]. As the 1980s ended, members of Congress requested information that justified continued funding of the EMSC program. The Institute of Medicine (IOM) of the National Academy of Sciences was commissioned in 1991 to conduct a study of the status of pediatric emergency medicine in the nation. A panel of experts was convened to review existing data and model systems of care, and to make recommendations as appropriate. The findings from this national study revealed continuing deficiencies in pediatric emergency care for many areas of the country and listed 22 recommendations for the improvement of pediatric emergency care nationwide [63]. These recommendations fell into the following categories: education and training, equipment and supplies, categorization and regionalization of hospital resources, communication and 9‐1‐1 systems, data collection, research, federal and state agencies and advisory groups, and federal funding. These findings convinced Congress to raise funding for the EMSC program. In response to the IOM report, the EMSC program developed a strategic plan. With the assistance of multiple professionals, including physicians, nurses, and prehospital clinicians, major goals and objectives were identified. The EMSC 5‐year plan for 1995–2000 served as a guideline for further development of the program [64]. The plan had 13 goals and 48 objectives. Each objective had a specific plan that identified national needs, suggested activities and mechanisms to achieve the objective, and listed potential partners. In 1998, the plan was updated with baseline data, refined objectives, and progress in completing activities [65]. EMS Physicians 1982‐1996 Throughout the 1970s, emergency physicians and the fledgling ACEP supported regional EMS programs. By 1983, emergency physicians and the embryonic state chapters of ACEP were

11

primarily focused on developing their new specialty and care in emergency departments. During this period, medical directors for EMS systems around the country increasingly began to publish articles in scientific journals on prehospital research and on their experiences with prehospital care. Gradually, they began to meet and, in the process, found many areas of common interest. After a series of organizational meetings that began in Hilton Head, South Carolina, in 1984, the National Association of EMS Physicians (NAEMSP) was created in 1985, with Dr Ron Stewart as its first president. By the late 1980s, emergency physician specialty groups such as ACEP and the Society for Academic Emergency Medicine also placed more emphasis on EMS and began to encourage EMS‐related activities among their members. Training 1982‐1996 In the early 1980s, NHTSA developed an EMT‐I curriculum and by 1992 developed the EMT‐B curriculum (EMT‐basic, formerly the EMT‐A level), which was a success and adopted by most states. The EMT‐B curriculum included the use of automated external defibrillators as recommended by the AHA [42] and assisting patients with their medications. The National EMS Training Blueprint Project Task Force, sponsored by the NREMT, began a process in 1993 to define more clearly the scope of practice of EMS personnel [66]. Transportation 1982‐1996 Encouraging the use of voluntary ambulance standards was common from 1983 to 1990. By 1990, issues of ambulance operations, safety, and optimal mode of response were starting to be a risk‐management concern and more services began to use medical priority dispatch systems. The number and availability of medical helicopters increased, but with as many as 44 air ambulance crashes in one year, safety concerns began to increase as well.

1996‐2008: The Role of the Federal Government Matures, the United States Faces Terrorism, and EMS is at the Breaking Point EMS Agenda for the Future In 1996, NHTSA and HRSA published the EMS Agenda for the Future [67]. This document was the culmination of a year‐long process to develop a common vision for the future of EMS. The federally funded project was coordinated by NAEMSP and NASEMSO with involvement of hundreds of other organizations and EMS‐interested individuals who provided input to the spirit and content of the agenda. In addition to describing a vision for the future of EMS, the document discusses 14 attributes of the EMS system and outlines steps that will enable progress toward realizing that vision (Box 1.3). Shortly after its

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Chapter 1

Box 1.3  EMS Agenda for the Future attributes of the EMS system.

•  Integration of health services •  EMS research •  Legislation and regulation •  System finance •  Human resources •  Medical direction •  Education systems •  Public education •  Prevention •  Public access •  Communication systems •  Clinical care •  Information systems •  Evaluation Source: Modified from [67].

initial publication, thousands of copies of the EMS Agenda for the Future had been distributed to guide EMS system‐related planning, policy creation, and decision‐making. EMS Education for the Future: A Systems Approach In December 1996, NHTSA held a conference to address the EMS education recommendations of the EMS Agenda for the Future report published earlier in the year. Over the next two years, an EMS Education Task Force was established. The goals were expanded to include defining the essential elements of a national EMS education system, as well as the education organizational and disciplinary interrelationships necessary to achieve the recommendations in the Agenda. The outcome of the Task Force was the document entitled the EMS Education for the Future: A Systems Approach [68]. It called for development of five components of an overall EMS education system following the model of medical education: a national EMS core content, a national EMS scope of practice model, national EMS education standards, national EMS education program accreditation, and national EMS certification. General responsibility for each of the components was assigned to specific disciplines of the EMS community: EMS core content – physicians; scope of practice  –  state regulators; ­ education standards  – EMS educators; national program accreditation  – educational programs; and certification – assumed by NREMT. Subsequent projects and documents for each of these areas were developed to fill those needs: • EMS Core Content publication – 2005; updated 2012 and 2019 • EMS Scope of Practice publication – 2005; updated 2019 • EMS Education Standards publication – 2009; planned update 2021 National Ambulance Fee Schedule Complaints about Medicare reimbursement for ambulance services based primarily on transportation of the patient increasingly became an issue during the 1990s. Specifically, there were

concerns about the lack of uniformity in reimbursement from region to region. The Balanced Budget Act of 1997 required the Health Care Financing Administration (HCFA) to commence a negotiated rule‐making process with industry groups and develop a national fee schedule for ambulance services. That process began in 1999 when HCFA established a rules committee that included HCFA, the American Ambulance Association, the International Association of Fire Chiefs, the International Association of Firefighters, the National Volunteer Fire Council, the AHA, the National Association of Counties, NASEMSO, the Association of Air Medical Services, and a single physician representing both ACEP and NAEMSP. The regulations and national fee schedule that resulted from the negotiated rule‐making process became effective on April 1, 2002 [69]. The fee schedule established seven national categories of reimbursement for ground ambulances: BLS (emergency and non‐emergency), ALS (emergency and non‐emergency), a second level of ALS for complex cases, paramedic ALS intercept, and specialty care transport. In addition, there were two categories for air medical transport: fixed‐wing and rotor‐wing. The final rule also included adjustments for regional wage differences as well as for services provided in rural areas where the cost per transport is generally higher due to the lower overall numbers of transports. Reimbursement, however, was still generally based on the need for transportation of the patient. A medical committee was established during the negotiated rule‐making process to develop a coding system for ambulance billing that would better convey to HCFA the medical necessity for transport and the need for ALS. This document was not an official component of the rule‐making process. However, the coding system was eventually adopted in 2005 by the Centers for Medicare and Medicaid Services as an “educational tool.” It was never made a requirement for reimbursement as was originally proposed [70]. National EMS Information System The collection and use of EMS data had been an issue of discussion since the mid‐1980s. In 2001, NASEMSO, in conjunction with its federal partners at NHTSA and the Trauma/EMS Systems program at HRSA, began developing a national EMS database, which ultimately lead to the National EMS Information System (NEMSIS). By 2003, a detailed data dictionary was completed. Information about each of the data elements, the variables, the definitions associated with the data elements, and how to deploy the elements in a database were described [71]. With funding from NHTSA, EMSC, and Centers for Disease Control and Prevention (CDC), the NEMSIS Technical Assistance Center was established under contract with NHTSA at the University of Utah School of Medicine in 2005. The mission of the Technical Assistance Center was to collaborate with the University of North Carolina at Chapel Hill, where previous EMS data activities were occurring, to provide support to the NEMSIS project.

History of emergency medical services

NEMSIS, with continued support from NHTSA, has continued to promote and develop the growth of EMS data collection and use. The EMS data elements have evolved based on input from the EMS community and subsequent versions of the data set have been released. In addition to defining the data elements and data dictionary, the NEMSIS program is responsible for working closely with EMS patient care record vendors, and it tests vendor products for compliance with the data standard. NEMSIS is using national level EMS data to support multiple research initiatives and is working closely with the CDC, CMS, and other federal agencies on EMS data issues. Working with EMS stakeholders, state EMS offices and data managers and vendors, NEMSIS is providing valuable information at the local, state, and national levels to support clinical, administrative and research activities. September 11, 2001 The attacks on the World Trade Center and the Pentagon on September 11, 2001 (9/11) changed the way Americans think about the world and the way they live. Efforts to enhance the capability to prevent and respond to terrorist attacks have become routine. Shortly after 9/11, the Department of Homeland Security (DHS) was established, as part of the largest and most expensive reorganization of the federal government in history. Congress began funding preparedness efforts with billions of dollars going to federal agencies, state and local governments, and private entities such as hospitals. Despite the massive funding for public safety and medical preparedness, reports have indicated that only a small percentage (less than 4%) of this funding ended up supporting EMS needs. Advocacy efforts by multiple stakeholders to increase federal funding for EMS, for both day‐to‐day services and preparedness, were largely unsuccessful. Advocates for EMS Recognizing the need for greater national advocacy for EMS, NASEMSO and NAEMSP formed a non‐profit organization, Advocates for EMS (AEMS), on October 22, 2002, for promoting, educating, and increasing awareness among decision makers in Washington on issues affecting EMS. Although there had been previous efforts to establish national EMS advocacy coalitions, none was able to sustain efforts for more than a few years. With support from the major EMS stakeholder organizations, AEMS continued to promote a more unified national EMS agenda for the next decade. However, special interest needs of several organizations ultimately led to the demise of AEMS, with various groups focusing on their specific interests. Federal Interagency Committee on EMS The Federal Interagency Committee on EMS (FICEMS, https:// www.ems.gov/ficems.html) has coordinated efforts between federal agencies on related EMS issues for decades. Although this forum provided an opportunity for collaboration between federal agencies on EMS issues, FICEMS lacked statutory authority and its representatives were not senior officials, which

13

often led to policy and implementation challenges. In 2005, Congress formally legislated a new FICEMS with senior representatives from DOT, DHS, DHHS, the Department of Defense, the Federal Communications Commission, and a single state EMS director. The role of FICEMS is to identify state and local EMS needs, to recommend new or expanded programs for improving EMS at all levels, and to streamline the process through which federal agencies support EMS. FICEMS has established a number of working groups to identify and address EMS issues facing the EMS community at all levels, and continues to coordinate federal initiatives. National EMS Advisory Council In 2007, the National EMS Advisory Council (NEMSAC, https://www.ems.gov/nemsac.html) was established by statute to provide advice and consult with FICEMS and the Secretary of Transportation regarding EMS issues affecting DOT. The council is composed of 25 individuals representing the major EMS disciplines, chosen for their expertise in those disciplines. They do not represent specific EMS organizations or employers. Working within established committees, the council identifies, researches, and produces advisory documents on topical issues with recommendations to FICEMS and DOT. Trends in Air Medical Services Air medical services in the United States struggled financially for a number of decades; the industry as a whole experienced only modest growth until 2000. However, by 2005, an estimated 700 air ambulances were in operation, more than double the number from a decade before. Unfortunately, that same growth was associated with a more than 200% increase in helicopter crashes. From 2000 to 2005, 60 people died in 84 crashes, and an estimated 10% of air ambulances in the United States had experienced crashes [72]. At the same time, the number of flights paid for by Medicare was up 58% from 2001, and during the same period Medicare payments for air ambulance transports doubled to $103 million [73]. This has led to a belief that the improved reimbursement for air medical services that came with the implementation of the national fee schedule in 2002 was a factor that contributed to this increase in the use of helicopters. Efforts by states to regulate air ambulance services have been hampered by legal challenges from the industry related to the Airline Deregulation Act of 1978. The act preempts states from regulating Federal Aviation Authority (FAA)‐licensed air transport services in ways that affect their rates, routes, or services. Although the FAA recognizes the role of states in regulating the medical aspects of air ambulance services, questions frequently arise as to what is medical and what is related to rates, routes, or services [74]. Institute of Medicine Report on the Future of Emergency Care In the decade from 1993 to 2002, the number of emergency departments and hospital inpatient beds in the United States declined

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Chapter 1

at the same time the number of patients coming to emergency departments increased by 26%. The IOM began a study of hospital‐based emergency care in 2003 that rapidly expanded to address long‐standing and significant issues related to EMS and emergency care for children. EMS systems were viewed as increasingly overburdened and underfunded. The result was a three‐ volume IOM report titled The Future of Emergency Care, which was released in 2006 [75]. Key findings of the report included the following: many emergency departments and trauma centers are overcrowded; emergency care is highly fragmented; critical specialists are often unavailable to provide emergency and trauma care; and EMS and emergency departments are not well equipped to handle pediatric care. Key recommendations of the report were to create coordinated, regionalized, and accountable emergency care systems; create a lead (federal) agency for emergency care; end emergency department boarding and diversion; increase funding for emergency care; enhance emergency care research; promote EMS workforce standards; and enhance pediatric presence throughout emergency care. The IOM report was the first major report on emergency care since the 1966 NAS‐NRC report. One recommendation of particular relevance to EMS physicians was the recommendation to create a subspecialty of EMS. Other recommendations of specific interest to EMS included developing national standards for the categorization of emergency care facilities; developing evidence‐based national model EMS protocols; increasing funding for EMS preparedness; states requiring national accreditation of paramedic education programs and national certification for state licensure; and EMS agencies having pediatric coordinators to ensure appropriate equipment, training, and services for children.

2009–2020: A Period of Incremental Progress Subspecialty in EMS Medicine Following decades of efforts and bolstered by a recommendation in the 2006 IOM report The Future of Emergency Care, ABEM successfully petitioned and the American Board of Medical Specialties approved a physician subspecialty in EMS on September 23, 2010. The ABEM website has the following description of the subspecialty: EMS is a medical subspecialty that involves prehospital emergency patient care, including initial patient stabilization, treatment, and transport in specially equipped ambulances or helicopters to hospitals. The purpose of EMS subspecialty certification is to standardize physician training and qualifications for EMS practice, improve patient safety and enhance the quality of emergency medical care provided to patients in the prehospital environment, and facilitate further integration of prehospital patient treatment into the continuum of patient care [76]. A task force developed and published an article entitled “The core content of EMS medicine” on January 10, 2012. It has since been updated [77]. The first certification examination was administered in October 2013. As of the fall of 2020, 831 physicians have been certified in EMS by ABEM [78].

EMS Clinician Education In 2009, NHTSA published the National EMS Education Standards. These are consistent with the principles of the 1996 EMS Education Agenda for the Future: A Systems Approach and establish the entry‐level educational competencies for the levels of EMS clinicians outlined in the National EMS Scope of Practice Model [79]. The current model has four levels of clinicians: emergency medical responder, emergency medical technician, advanced emergency medical technician, and paramedic. The EMT‐I that was established in 1999 was eliminated. The National EMS Education Standards replaced the earlier National Standard Curricula, enabling more diverse implementation methods and updates that are more frequent. A revision of the educational standards is expected to be published in 2021. Community Paramedicine There has been growing interest in the United States in expanding the role of paramedics to include the management of non‐urgent and urgent low‐acuity illnesses, monitoring patients with chronic illnesses at home, and performing other functions that do not involve the traditional EMS role of treating and transporting patients to emergency departments. While scientific evidence of the safety and effectiveness of such expanded roles is limited, the success of programs in Canada, England, and Australia has drawn the attention of governments and others interested in innovative models of health care delivery and incorporating non‐physician personnel, who are sometimes viewed as underused, into these models [80]. Legislation passed in Minnesota in 2011 (2011 Minn. Laws, Chap. #12) defines community paramedics and establishes a process for educating and certifying them. In 2012, a law was passed to enable reimbursement for community paramedic services under the medical assistance program and to study the cost and quality of the program (2012 Minn. Laws, Chap. #169). Also in 2012, the Maine legislature passed a law to establish pilot community paramedic projects (Chapter 562, Sec. 1 §84). Community paramedic programs also function in many areas of the United States. The National Association of EMTs has established an EMS 3.0 initiative to further promote the potential capabilities of EMS clinicians in providing appropriate care to support the national health care needs [81]. In further recognition of the potential services that EMS systems can appropriately provide, the Centers for Medicare and Medicaid Innovation Center recently initiated an Emergency Triage, Treatment and Transport (ET3) pilot program. Using nearly 200 pilot sites, the program is designed to investigate, over a 5‐year study period, the appropriateness and financial considerations of several models: treat in place (without transport), treat and referral for follow‐up, and transport to alternative destinations (other than an emergency department) [82]. National EMS Culture of Safety Project EMS is known to be a high‐risk profession; EMS personnel are 2.5 times more likely than the average worker to be killed on the job [83], and their transportation‐related injury rate is five times higher than average [84]. Additionally, there are patient safety concerns as outlined in the 1999 IOM report To Err is Human,

History of emergency medical services

as well as concerns about risks to EMS personnel, patients, and the community from ambulance crashes. In 2009, the National EMS Advisory Council recommended that NHTSA create a strategy for building a culture of safety in EMS. With support from the EMSC program at HRSA, NHTSA contracted with ACEP to develop a National EMS Culture of Safety Strategy that was published in October 2013 [85]. This initiative resulted in the formation of the National EMS Safety Council composed of multiple EMS stakeholder organizations to continue to focus on safety considerations for EMS clinicians.

EMS Agenda 2050 Twenty years after the publication of the 1996 Agenda, FICEMS and NEMSAC recommended to NHTSA that it was time to

ADAPTABLE AND INNOVATIVE Technologies, system designs, educational programs and other aspects of EMS systems are continuously evaluated in order to meet the evolving needs of people and communities. Innovative individuals and organizations are encouraged to test ideas in a safe and systematic way and to implement effective new programs.

SUSTAINABLE AND EFFICIENT EMS systems across the country have the resources they require to provide care in a fiscally responsible, sustainable framework that appropriately compensates clinicians. Efficient EMS systems provide value to the community, minimize waste and operate with transparency and accountability.

SOCIALLY EQUITABLE Access to care, quality of care and outcomes are not determined by age, socioeconomic status, gender, ethnicity, geography or other social determinants. Caregivers feel confident and prepared when caring for children, people who speak different languages, persons with disabilities or other populations that they may not interact with frequently. Figure 1.1  The six guiding principles of EMS Agenda 2050. Source: [86].

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review the status of the recommendations of the 1996 document. Based on those suggestions, the EMS Agenda 2050 team was established. Following community input, regional meetings around the country and discussions, the EMS Agenda 2050 was released in 2019 [86]. This document, projecting the EMS world in 2050, changed the patient‐centered focus of the 1996 document to a people‐centered focus to include not only the patient, but the patient’s family, community, and the EMS clinicians. Acknowledging the difficulty in predicting the clinical and technological capabilities that would be available in 2050, the goals of EMS systems at that time will be based on six guiding principles: adaptable and innovative, inherently safe and effective, integrated and seamless, reliable and prepared, socially equitable, and sustainable and efficient (Figure 1.1). These guiding principles have also been adopted as the tenets of NEMSAC.

INHERENTLY SAFE AND EFFECTIVE The entire EMS system is designed to be inherently safe in order to minimize exposure of people to injury, infections, illness or stress. Decisions are made with the safety of patients, their families, clinicians and the public as a priority. Clinical care and operations are based on the best available evidence, allowing systems to deliver effective service that focuses on outcomes determined by the entire community, including the individuals receiving care.

INTEGRATED AND SEAMLESS Healthcare systems, including EMS, are fully integrated. Additionally, local EMS services collaborate frequently with community partners, including public safety agencies, public health, social services and public works. Communication and coordination across the care continuum are seamless, leaving people with a feeling that one system, comprising many integrated parts, is caring for them and their families.

RELIABLE AND PREPARED EMS care is consistent, compassionate and guided by evidence—no matter when or where it is needed or who is providing the care. EMS systems are prepared for anything by being scalable and able to respond to fluctuations in day-to-day demand, as well as major events, both planned and unplanned.

16

Chapter 1

Acknowledgment This chapter was adapted from, and contains much of the original content of, the History of EMS Chapter authored by Robert Bass, MD, in the second edition of this volume.

References 1 Breasted JH. Historical medicine. Bull Hist Med. 1923; 3:58–78. 2 Major RH. A History of Medicine, vol. 1. Springfield, IL: Charles C. Thomas, 1954. 3 1 Kings 17:17–24. 4 Luke 10:25–37. 5 Garrison FH. An Introduction to the History of Medicine, 4th ed. Philadelphia: W.B. Saunders, 1929. 6 The Gallup Poll, Field Newspaper Syndicate, June 30, 1977. 7 Post CJ. Red Crossader. EMS. 1997; 64. 8 Haller JS Jr. The beginnings of urban ambulance service in the United States and England. J Emerg Med. 1990; 8(6):743–55. 9 Barringer ED. Bowery to Bellevue. New York: W.W. Norton & Co., 1950. 10 Answering the call: California’s EMS legacy. Siren (A publication of the California Ambulance Association) 2020; Summer:3–4. 11 Barkley KT. The history of the ambulance. Proc Int Cong Hist Med. 1974; 23:456–66. 12 Kouwenhoven WB, Jude JR, Knickerbocker GB. Closed chest cardiac massage. JAMA. 1960; 173:1064–7. 13 Safar P, Brown TC, Holtey WJ, Wilder RJ. Ventilation and circulation with closed‐chest cardiac massage in man. JAMA. 1961; 176:574–6. 14 Eisenberg MS. Life in the Balance: Emergency Medicine and the Quest to Reverse Sudden Death. New York, NY: Oxford University Press, 1997. 15 Pantridge JF, Geddes JS. A mobile intensive care unit in the management of myocardial infarction. Lancet. 1967; 2(7510): 271–3. 16 Committee on Trauma and Committee on Shock. Accidental Death and Disability: The Neglected Disease of Modern Society. Washington, DC: National Academies Press, 1966. 17 Committee on Trauma. Minimal equipment for ambulances. Bull Am Coll Surgs. 1961; 46:136–7. 18 Committee on Trauma. Minimal equipment for ambulances. Bull Am Coll Surg. 1967; 52:92–6. 19 Hampton OP. The systematic approach to emergency medical services. Arch Environ Health. 1970; 21(2):214–17. 20 Hampton OP. Transportation of the injured: a report. Bull Am Coll Surg. 1960; 45:55–9. 21 President’s Commission on Highway Safety. Health, Medical Care, and Transportation of Injured. Washington, DC: US Government Printing Office, 1965. 22 National Highway Safety Act of 1966 (US), PL No. 89–564. 23 Jelenko C, Frey CF. Emergency Medical Services: An Over View. Bowie, MD: Brady Company, 1976. 24 Committee on Trauma. Recommendations for an Approach to an Urgent National Problem. Proceedings of the Airlie Conference on Emergency Medical Services. Chicago, IL: American College of Surgeons, American Academy of Orthopedic Surgeons, 1969.

25 Commission of Emergency Medical Services. Recommendations of the Conference on the Guidelines for the Categorization of Hospital Emergency Capabilities. Chicago, IL: American Medical Association, 1971. 26 Nagel EL, Hirschman JC, Nussenfeld SR, Rankin D, Lundblad E. Telemetry medical command in coronary and other mobile emergency care systems. JAMA. 1970; 214(2):332–8. 27 Lewis RP, Stang JM, Fulkerson PK, Sampson KL, Scoles A, Warren JV. Effectiveness of advanced paramedics in a mobile coronary care system. JAMA. 1979; 241:1902–4. 28 American Heart Association, National Academy of Sciences, National Research Council. Cardiopulmonary resuscitation. JAMA. 1966; 198(4):372–9. 29 Boyd DR, Edlich RF, Micik S. Systems Approach to Emergency Care. Norwalk, CT: Appleton‐Century‐Crofts, 1983. 30 Committee on Emergency Medical Services. Roles and Resources of Federal Agencies in Support of Comprehensive Emergency Medical Services. Washington, DC: National Research Council, 1972. 31 Emergency Medical Services Systems Act of 1973 (US), PL No. 93–154, Title XII of the Public Health Service Act. 32 Diehl D. The Emergency Medical Services Program. Robert Wood Johnson Foundation Special Report, Number 2, 1977. 33 Robert Wood Johnson Foundation. National Competitive Program Grants for Regional Emergency Medical Communications Systems Administered in Cooperation with National Academy of Sciences. Program guidelines, 1973. 34 Lythcott GI. Statement before the Subcommittee on Health and Scientific Research Committee on Labor and Human Resources. In: United States Senate Hearing Report 24, Feb 1979. 35 Anwar AH, Hogan MH. Residency‐trained physicians: where have all the flowers gone? JACEP. 1979; 8(2):84–7. 36 Emergency Medicine Residents Association. A survey by EMRA, May 1980. 37 Liaison Residency Endorsement Committee. American College of Emergency Physicians. Information supplied June 1980. 38 American Board of Emergency Medicine. Eligibility Requirements. East Lansing, MI: ABEM, 1976. 39 Joint Review Committee on Educational Programs for EMT‐­ Paramedics. Essentials and Guidelines of an Accredited Educational Program for the Emergency Medical Technician‐Paramedic. Essentials adopted 1978, guidelines approved 1979. 40 Eisenberg MS, Berger L, Hallstrom A. Epidemiology of cardiac arrest and resuscitation in a suburban community. JACEP. 1979; 8(1):2–5. 41 McElroy CR. Citizen CPR: the role of the layperson in prehospital care. Top Emerg Med. 1980; 1(4):37–46. 42 American Heart Association in collaboration with International Liaison Committee on Resuscitation. Executive Summary: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Circulation 2020; 142:S2–S27. 43 National Highway Traffic Safety Administration. Communication: Guidelines for Emergency Medical Services. Washington, DC: U.S. Department of Transportation, 1972. 44 Emergency Medical Services Division, U.S. Department of Health, Education, and Welfare. HSA 77–2036, March 1977. 45 Kuehl AE, Kerr JT, Thompson JM. Urban emergency medical system: a consensus. Am J Emerg Med. 1984; 2:559–63. 46 Hampton OP. Present status of ambulance services in the United States. Bull Am Coll Surg. 1965; 50:177–9.

History of emergency medical services

47 Division of Medical Sciences National Research Council. Summary Report of the Task Force on Ambulance Services. Washington, DC: National Academy of Sciences, National Research Council, 1967. 48 American College of Surgeons Committee on Trauma. Essential equipment for ambulances. Bull Am Coll Surg. 1970; 55(5):7–13. 49 National Highway Traffic Safety Administration. Ambulance Design Criteria. Washington, DC: U.S. Government Printing Office, 1971. 50 Roemer R, Kramer C, Frink JE. Planning Urban Health Services: Jungle to System. New York, NY: Springer, 1975. 51 Answers to questions submitted by members of Subcommittee on Health and Scientific Research of the Committee on Labor and Human Resources. In: United States Senate Hearing Report 98– 100, Feb 1979. 52 Committee on Emergency Medical Services. Emergency Medical Services at Midpassage. Washington, DC: National Research Council, 1978. 53 Memorandum of understanding between the U.S. Department of Transportation and the U.S. Department of Health, Education, and Welfare. Procedures Relating to Emergency Medical Services Systems. Washington, DC: U.S. Government Printing Office, 1978. 54 Post CJ. Omaha Orange: A Popular History of EMS in America. Boston, MA: Jones and Bartlett, 1992. 55 Comptroller General of the United States. Progress in Developing Emergency Medical Services Systems. Washington, DC: U.S. Government Accountability Office, 1976: HRD 76–150;13. 56 Boyd DR. Emergency medical services systems evaluation. Statement submitted to the Subcommittee on Health and Scientific Research, Committee on Labor and Human Resources. In: United States Senate Hearing Report 47–57, Feb 1979. 57 Cayten GC. Testimony to the Subcommittee on Health and Scientific Research of the Committee on Labor and Human Resources. In: United States Senate Hearing Report 156–166, Feb 1979. 58 Omnibus Budget Reconciliation Act of 1981 (US), PL No. 97–35. 59 U.S. Department of Health, Education and Welfare. The Forward Plan for the Health Services Administration. Washington, DC: US Government Printing Office, 1976. 60 Page J. History and Legislation Panel. Phoenix, AZ: EMS Medical Directors’ Course, 1993. 61 Ball J. Emergency medical services for children. In: Foltin G, Tunik M, Cooper A, Markenson D, Treiber M, Karpeles T (eds). Teaching Resource for Instructors in Prehospital Pediatrics. New York, NY: Center for Pediatric Emergency Medicine, 2000. 62 National EMSC Data Analysis Resource Center. Who is NEDARC? Accessed October 15, 2020. Available at: https://www.nedarc.org/ nedarcCanHelp/whoIsNEDARC.html. 63 Durch JS, Lohr KN (eds). Emergency Medical Services for Children. Washington, DC: National Academy Press, 1993. 64 U.S. Department of Health and Human Services, Health Resources and Services Administration, Maternal and Child Health Bureau. 5‐Year Plan: Emergency Medical Services for Children, 1995‐2000. Washington, DC: Emergency Medical Services for Children National Resource Center, 1995. 65 U.S. Department of Health and Human Services, Health Resources and Services Administration, Maternal and Child Health Bureau. 5‐Year Plan: Midcourse Review, Emergency Medical Services for Children, 1995‐2000. Washington, DC: Emergency Medical Services for Children National Resource Center, 1998.

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66 National EMS Training Blueprint. Columbus, OH: National Registry of EMTs, 1993. 67 Emergency Medical Services Agenda for the Future. Washington, DC: U.S. Department of Transportation, National Highway Traffic and Safety Administration, 1996. 68 Emergency Medical Services Education Agenda for the Future: A Systems Approach. Washington, DC: U.S. Department of Transportation, National Highway Traffic and Safety Administration, 2000. 69 Centers for Medicare and Medicaid Services. Medicare Program: Payment of Ambulance Services, Fee Schedule; and Revision to Physician Certification Requirements for Coverage of Nonemergency Ambulance Services. 42 CFR Parts 410 and 414. Final Rule, 2002. 70 Department of Health and Human Services, Centers for Medicare and Medicaid Services. CMS Manual System, Pub 100‐4 Medicare Claims. Transmittal 395, Dec 2004. 71 Dawson DE. National Emergency Medical Services Information System (NEMSIS). Prehosp Emerg Care. 2006; 10(3):314–16. 72 Levin A, Davis R. Surge in crashes scars air ambulance industry. USA Today, July 17, 2005. Available from: https://usatoday30.usatoday. com/news/nation/2005‐07‐17‐air‐ambulance‐crashes_x.htm. 73 Meier B. As medical airlifts proliferate, the public price tag is rising. New York Times, May 3, 2005. Available from: https://www. nytimes.com/2005/05/03/business/as‐medical‐airlifts‐proliferate‐ the‐public‐price‐tag‐is‐rising.html. 74 McGinnis KK, Judge T, Nemitz B, et  al. Air medical services: future development as an integrated component of the emergency medical services (EMS) system: a guidance document by the Air ­Medical Task Force of the National Association of State EMS Officials, National Association of EMS Physicians, Association of Air Medical Services. Prehosp Emerg Care. 2007; 11(4):353–68. 75 Committee on the Future of Emergency Care in the United States Health System. Future of Emergency Care series, including: Emergency Medical Services: At the Crossroads; Emergency Care for Children: Growing Pains; Hospital‐Based Emergency Care: At  the Breaking Point. Washington, DC: National Academies Press, 2006. 76 American Board of Emergency Medicine. Emergency Medical Services. Available at: https://www.abem.org/public/become‐ certified/subspecialties/emergency‐medical‐services. Accessed October 15, 2020. 77 Perina DG, Pons PT, Blackwell TH, et al. The core content of EMS medicine. Prehosp Emerg Care. 2012; 16(3):309–22. 78 American Board of Emergency Medicine. Exam and certification statistics. Available at: https://www.abem.org/public/resources/ exam‐certification‐statistics. Accessed October 11, 2020. 79 National Highway Traffic Safety Administration. National EMS Scope of Practice Model. Washington, DC: U.S. Department of Transportation, National Highway Traffic Safety Administration, DOT HS 810 657; February 2007. 80 Bigham BL, Kennedy SM, Drennan I, Morrison LJ. Expanding paramedic scope of practice in the community: a systematic review of the literature. Prehosp Emerg Care. 2013; 17(3):361–72. 81 National Association of EMTs. EMS 3.0. Available at: http://naemt. org/initiatives/ems‐transformation. Accessed October 20, 2020. 82 Centers for Medicare and Medicaid Services, U.S. Department of Transportation. Emergency Triage, Treat, and Transport (ET3) Model. Available at: https://innovation.cms.gov/innovation‐ models/et3. Access October 20, 2020.

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83 Maguire BJ, Hunting KL, Smith GS, Levick NR. Occupational fatalities in emergency medical services: a hidden crisis. Ann Emerg Med. 2002; 40(6):625–32. 84 BJ. Transportation‐related injuries and fatalities among emergency medical technicians and paramedics. Prehosp Disaster Med 2011; 26(5):346–52.

85 American College of Emergency Physicians. Strategy for a National EMS Culture of Safety. 2013. Available at: www.emscultureofsafety. org. Accessed October 11, 2020. 86 EMS Agenda 2050. A People-Centered Vision. Available at: https:// www.ems.gov/projects/ems‐agenda‐2050.html. Accessed October 20, 2020.

SECTION I

Airway

CHAPTER 2

EMS airway management: system considerations Francis X. Guyette and Henry E. Wang

The skills of airway management: an illustrative vingnette A 34-year-old, 6-ft, 100-kg, unhelmeted male operator of an ATV is thrown from the vehicle. An air medical crew arrives, completes their survey, places the patient on a cardiac monitor, establishes a 20G peripheral IV, and starts a normal saline infusion. The patient’s Glasgow Coma Scale score is 7, systolic blood pressure 104/50 mmHg, pulse 128/min, respiratory rate 24/min, and oxygen saturation 94% on 15 liters per minute via non-rebreather mask. The crew assesses the patient’s airway using the LEMON method. They Look externally, noting a possible fractured jaw, and then Evaluate using the 3-3-2 rule, noting that they can place three fingers in the mouth, three fingers from the angle of the jaw to the mentum, and two fingers from the thyroid cartilage to the bottom of the jaw. The mandible is not receding. They assess Obstruction using a modified Mallampati, which provides a clear view of the posterior oropharynx and uvula when they suction blood from the mouth. Lastly, rather than assess neck Mobility, they remove the patient’s cervical collar and hold inline stabilization from below. They use an airway checklist to prepare for intubation. They check their bag-valve-mask, oxygen, and suction device. The IV is patent. The patient’s pulse oximetry, pulse rate, and blood pressure are normal. They deliver oxygen via nasal cannula at 15 liters per minute to provide apneic oxygenation. They prepare 8.0-mm and 7.5-mm endotracheal tubes. They inspect the 8.0-mm balloon and lubricate and insert a stylet. They turn on the video laryngoscope and begin recording. The crew connects a waveform capnograph and prepares a tube holder. They identify an appropriately sized

supraglottic airway and place it adjacent to the patient’s chest as a contingency. They administer rocuronium and ketamine and the patient is oxygenated with a BVM. Once the patient is no longer breathing, they place the video scope while suctioning, and pass the tube through the cords under visualization. They inflate the balloon and confirm placement by EtCO2 and five-point auscultation. They secure the tube with a tube holder, and reassess the patient to ensure stable vitals. The crew sedates the patient and places restraints to preclude self-extubation.

Introduction Airway management, including endotracheal intuabtion (ETI), is an essential intervention in prehospital care  [1, 2]. Airway management is a difficult process associated with potential adverse events. Numerous studies underscore the challenges in attaining and maintaining clinical proficiency. These observations underscore that airway management is not a discrete procedure but rather a comprehensive strategy of care that requires close, system‐level medical oversight. The most successful prehospital airway management programs incorporate multiple elements, including training, skills verification, equipment selection, decision support, continuing education, and total quaility management. The practicing EMS physician must be an expert in out‐of‐hospital airway management and must also be able to choose tools and skills necessary to best mitigate the specific risks within a given EMS system. The goal of this chapter is to describe the medical direction paradigms and considerations necessary for a high quality airway management program.

Emergency Medical Services: Clinical Practice and Systems Oversight, Third Edition. Volume 1: Clinical Aspects of EMS. Edited by David C. Cone, Jane H. Brice, Theodore R. Delbridge, and J. Brent Myers. © 2021 NAEMSP. Published 2021 by John Wiley & Sons, Inc.

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Chapter 2

Challenges of airway management in the field Airway management in the field comes with unique challenges that differ from those of the hospital setting. Prehospital airway management occurs in an uncontrolled environment where patients are severely ill and undifferentiated. The prior medical histories of EMS patients are frequently unknown. Prehospital patients may also be situated in awkward locations such as on the floor, on a bed, or in the wreckage of a car. Prehospital clinicians, including EMS physicians, have fewer monitoring and pharmacologic options than they do in the hospital. Certain options for in‐hospital airway management (e.g., calling for specialized equipment or seeking additional expertise) are not generally available in the field. These factors increase the complexity and difficulty of airway management and underscore the need for simple and efficient approaches. The EMS medical director must be aware of these distinctions and provide appropriate guidance. Which airway, when, and how? Successful prehospital airway management relies on the optimized combination of basic, advanced, and rescue airway interventions. EMS medical directors must choose strategies appropriate for the needs of their systems based on available personnel, resources, and environment. An exclusive focus on any one management technique will limit the clinicians’ abilities to adapt to difficult situations and failed procedures. Ideally, prehospital personnel should have a predefined algorithm to rapidly shift between management techniques to achieve successful airway management.

Considerations for basic airway interventions

Basic interventions provide the foundation of airway care for each patient and are the safety net when advanced airway interventions are unsuccessful. Basic airway management may be the preferred technique when the time and the risks associated with performing advanced airway maneuvers outweigh the benefits of a secure airway. For example, if caring for a severely injured patient, basic airway management may be preferable when the transport time to the hospital is short or when other interventions take priority (e.g., management of massive hemorrhage or tension pneumothorax). Another example is pediatric respiratory arrest, when most EMS clinicians are more comfortable and more facile with bag‐valve‐mask ventilation than with pediatric endotracheal intubation.

Considerations for endotracheal intubation

Despite its role in ALS and inclusion in paramedic‐level protocols for over 4 decades, the clinical benefit of ETI in the prehospital environment is unclear [3–6]. ETI is associated with several risks, including failed intubation, unrecognized esophageal intubation, hypoxia, hypotension, bradycardia, aspiration, and airway trauma. While the risks of ETI can be mitigated through

proper education and equipment, prehospital systems are often unable to make the substantial investments necessary to ensure a high degree of airway management safety. EMS medical directors must be prepared to properly educate and train their personnel in ETI, ensuring that they have the decision‐making and psychomotor skills necessary to perform the procedure. Many EMS medical directors believe that airway management training must include a minimum of didactic training on the indications, contraindications, and techniques for ETI, and simulated and live intubations in supervised environments. The EMS medical director must determine how to provide suitable training for and adequate current competency in ETI. Strategies may include defining a minimum number of yearly ETI experiences, focused training with simulation, and supervised experience in the operating room or emergency department. Dashboards summarizing training and clinical airway management experience can help to identify clinicians in need of additional training. In order to concentrate limited field experience opportunities, it may be appropriate to restrict the procedure to fewer people. When available, review of video laryngoscopy images may provide key learning opportunities [7]. ETI adjuncts such as the tracheal introducer (gum elastic bougie) and video laryngoscopy may improve intubation success but at the cost of added complexity. The latter point deserves emphasis. Each newly acquired airway device increases the burden of skill maintenance. If an adjunct is deployed, the EMS medical director should consider using the device on every intubation to facilitate integration and improve skill maintenance.

Is prehospital ETI associated with improved outcomes?

The association between prehospital ETI and patient outcome is unclear. Most studies entail observational analyses vulnerable to confounding by indication [8, 9]. However, select randomized clincial trials comparing ETI with other airway techniques provide important data and perspectives. Gausche et al. found no differences in survival or neurological outcome between children receiving ETI and those receiving bag‐valve‐mask ventilation (BVM)  [10]. Conducted in France and Belgium, the Cardiac Arrest Airway Management (CAAM) trial found no difference in survival between adult out‐of‐hospital cardiac arrests managed with ETI vs. BVM [11]. The AIRWAYS‐2 trial in the United Kingdom found no difference in survival or 30‐ day functional outcome between adult out‐of‐hospital cardiac arrest (OHCA) patients receiving ETI vs. i‐gel®  [12]. In the United States, the Pragmatic Airway Resuscitation Trial (PART) found improved 72‐hour survival among adult OHCA managed with the laryngeal tube vs. ETI [13].

Are adverse events common during prehospital ETI?

Several studies draw attention to previously unrecognized adverse events associated with prehospital ETI. Successful prehospital airway management strategies have placed strong emphasis on minimizing these and other adverse

EMS airway management: system considerations

events. Many of these adverse events have been detected only through enhanced monitoring technology and rigorous airway management review. Several studies describe complications of prehospital airway management including misplaced or dislodged endotracheal tubes  [14–17]. Using continuous EtCO2 has reduced the incidence of the unrecognized misplaced endotracheal tube. Prehospital ETI may distract from other important resuscitation tasks. For example, hyperventilation after successful ETI of cardiac arrest patients can compromise coronary perfusion during CPR chest compressions [18, 19]. Furthermore, conventional ETI efforts may increase CPR “hands‐off ” or no‐flow time (pauses in CPR to facilitate endotracheal intubation) compared with other airway devices  [20]. Models of high‐performance CPR now teach rescuers to defer airway management in favor of providing uninterupted compressions. Prehospital intubation has been associated with increased exposure to hypoxia, hypotension, and hypocapnia  [21, 22]. Iatrogenic oxygen desaturation or braydcardia is common during intubation attempts  [23]. Advanced age, preprocedural hypotension, and hypoxia are associated with peri‐intubation hypotension [24]. Hypoxia and bradycardia may be prevented by continuous monitoring of pulse oxymetry and provision of oxygen during apneia or supplemental ventilation  [25, 26]. Postprocedure hypocapnia may be mitigated by flow‐limiting bag ventilation, timing devices for respiration, or mechanical ventilation. EMS medical directors should anticipate these events and promulgate protocols that direct resuscitation prior to intubation and limit exposure to hypotension, hypoxia, and hypocarbia through continuous monitoring and appropriate intervention.

Should EMTs perform ETI?

The prior national EMT curriculum included ETI as an optional module [27]. However, the ability of EMTs to acquire and maintain clinical ETI skills remains unclear. Two independent studies of EMT ETI found suboptimal success rates (50  L/ min and a ventilatory rate of 20 breaths/min can deliver a tidal volume of 950  mL  [61, 62]. Aspiration is also a concern, but only limited data clinically quantify this problem  [63]. EMS

36

Chapter 3

Figure 3.10 Cricothyroidotomy.

personnel may also use a properly placed jet ventilation catheter to help convert to an open cricothyroidotomy.

Confirmation of airway placement After ETI, verification of endotracheal tube placement is essential  [64]. Tube placement verification is particularly important given the uncontrolled nature of the prehospital environment and the risks of unrecognized tube dislodgement or misplacement  [65–68]. Because of the amount of patient movement during prehospital care, EMS personnel must frequently, and preferably continuously, verify correct tube positioning. In addition to visualizing the endotracheal tube passing through the vocal cords into the trachea, endotracheal tube placement should be confirmed using multiple techniques. Auscultation is the most common method for verifying endotracheal tube placement. The rescuer auscultates both lung fields to verify the presence of breath sounds, and auscultates the epigastrium to verify the absence of gastric sounds. It is possible to be misled by transmitted sounds, however. Some low‐tech innovations have been helpful in the past. The esophageal intubation detector consists of a Toomey syringe with a special adaptor for the endotracheal tube. The esophageal detector device is a large, bulb‐type device (Figure 3.11). Both of these devices are based on the concept that the esophagus will collapse, producing resistance to a vacuum, while the trachea

Figure 3.11  Esophageal detector device.

will not collapse and will therefore not produce any resistance as the bulb or plunger produces suction. The most important technique for verifying endotracheal tube placement is detection of exhaled, or end‐tidal, carbon dioxide. There are currently three types of devices used for detecting end‐tidal carbon dioxide: 1) colorimetric end‐tidal carbon dioxide detector, 2) digital capnometer, and 3) waveform end‐tidal capnography.

Airway procedures

Figure 3.12  Colorimetric carbon dioxide detector.

The colorimetric end‐tidal carbon dioxide detector uses a chemically treated paper detector that changes color from purple to yellow when exposed to carbon dioxide (Figure 3.12). If the paper color remains purple, this suggests esophageal tube placement. Designed for single use, these devices can be used for only a limited duration (30 >40 Absent or biphasic wheezing

bpm, beats per minute; EtCO2, end‐tidal CO2 Source: Based on National Heart, Lung and Blood Institute, National Institutes of Health. Guidelines for the diagnosis and management of asthma (EPR‐3). 2007. National Heart, Lung, and Blood Institute; National Institutes of Health; US Department of Health and Human Services.

EtCO2 = 40

Figure 5.2  A capnogram depicting bronchospasm with a characteristic “shark fin” appearance. Source: Based on Egleston CV, Ben Aslam H, Lambert MA.

Capnography for monitoring non‐intubated spontaneously breathing patients in an emergency room setting. J Accid Emerg Med. 1997; 14:222–4.

Respiratory distress

If rapid sequence intubation is necessary for an asthma patient, the preferred induction agent is ketamine due to its inherent bronchodilator properties. Once intubated, ventilation should be provided at reduced volumes and rates to prevent air trapping and secondary barotrauma. The inspiratory‐to‐expiratory ratios should be adjusted to provide a prolonged expiratory phase. Permissive hypercarbia is generally well‐tolerated in these individuals. All NIPPV and intubated asthma patients should be monitored closely for signs of secondary barotrauma, such as tension pneumothorax and pneumomediastinum. Chronic obstructive pulmonary disease COPD is characterized by persistent expiratory airflow limitation. The underlying pathophysiology involves a complex process of chronic inflammation, remodeling of the small airways with the destruction of alveoli, and an increase in extracellular matrix production. The disease is manifested through a response to noxious particles and gases, including cigarette smoke and environmental pollutants, though genetic factors may also play a role [20, 35, 36]. It has significant social and economic effects and is the fourth leading cause of death in the United States [37–39]. Acute exacerbations are often precipitated by bacterial or viral respiratory tract infections, exposure to pollutants or allergens, or medication noncompliance. The clinical presentation is similar to that of asthma (Box 5.2). Patients typically develop worsening shortness of breath, more frequent and severe cough, and possibly increased sputum production [40]. Clinical examination often reveals wheezing. Patients with COPD should receive titrated oxygen with a goal to maintain SpO2 between 88% and 92%, which is associated with reduced mortality [16]. Continuous capnography can aid in the detection of impending respiratory failure. Increasing EtCO2 levels indicate a deteriorating condition. As with asthma, capnographic waveforms may take the form of a shark fin appearance (Figure 5.2) and can assist with the prehospital diagnosis and assessment of response to treatment [12]. As with asthma, the primary treatments during acute exacerbations are directed toward reversing airway obstruction with SABAs and anticholinergic agents [41]. Corticosteroids are associated with decreased rates of treatment failure and relapse [42]. Antibiotics are also important adjuvant therapy for COPD exacerbations and are associated with a reduction in treatment failure and mortality in selected patients  [43]. NIPPV has become established as a lifesaving therapy in the treatment of COPD exacerbations [20, 21, 44]. If it is necessary to intubate a COPD patient, appropriate settings for mechanical ventilation include decreased respiratory rates, lower tidal volumes, and an increased expiratory phase. As with asthma, these patients must be monitored closely for evidence of secondary barotrauma [21, 45]. Acute decompensated heart failure and SCAPE Heart failure results from a structural or functional cardiac abnormality that leads to impaired ventricular filling or cardiac output. Chronic heart failure is typically caused by myocardial ischemia, cardiomyopathy, longstanding uncontrolled hypertension, or

55

underlying valvular heart disease. A common way to classify heart failure is based on systolic function. Patients with impaired cardiac filling are classified as having heart failure with preserved ejection fraction, whereas those with poor cardiac output are classified as having heart failure with reduced ejection fraction [46]. It is estimated that more than 6.5 million adults are living with heart failure in the United States, although the number may be higher [47, 48]. The disease has major social and economic effects [49]. During an ADHF exacerbation, a stressor (e.g., acute MI, dysrhythmia, infection, dietary changes, or medication noncompliance) leads to an acute myocardial functional decline that overwhelms the body’s compensatory mechanisms. Symptoms of an acute exacerbation include increased shortness of breath, orthopnea, generalized weakness, and chest discomfort. Patients who are volume overloaded will often report increased bilateral lower extremity edema and weight gain. In some cases, patients will be hypotensive due to profoundly low cardiac output leading to cardiogenic shock. Clinical assessment classically reveals rales on auscultation of the lungs, which can help differentiate ADHF from a COPD exacerbation. The examination may also show jugular venous distension and edema (sacral, abdominal, lower extremity). SCAPE occurs when a heart failure patient rapidly develops a sympathetic overdrive and acute pulmonary edema. Contrary to ADHF, which develops over days to weeks, symptoms of SCAPE develop rapidly, typically over minutes to hours. Patients suffering from SCAPE may not be volume overloaded. Consequently, clinical examination may not show the classic signs of heart failure, such as pedal edema and jugular venous distension. Additional examination clues that can aid in a patient’s volume status assessment are listed in Box 5.2. Ultrasound may aid in the prehospital diagnosis of both ADHF exacerbation and SCAPE. B‐lines, vertical lines extending from the pleural line to the bottom of the ultrasound image, are indicative of interstitial fluid that can be seen with both ADHF and SCAPE (Figure 5.3) [9]. The presence of a pleural effusion on a prehospital chest ultrasound may be a novel prehospital marker for ADHF [50].

Figure 5.3  Ultrasound image depicting B‐lines, which may be seen in

ADHF and SCAPE.

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Prehospital management consists of positioning the patient in an upright posture, particularly if there is a concern for volume overload. This allows pleural effusions and edema to localize at the lung bases and venous blood to pool in the lower extremities, thereby reducing cardiac preload. Patients presenting with hypotension should prompt EMS clinicians to consider causes such as acute MI, in addition to other causes of shock (e.g., hypovolemic, distributive, or obstructive). If the cause of shock is due to low cardiac output, specific prehospital treatment might include inotropic and vasopressor medications such as epinephrine and norepinephrine. Patients may receive additional hemodynamic support from dobutamine and milrinone in the hospital. NIPPV should be used in patients in severe respiratory distress, assuming no contraindications exist (e.g., no spontaneous respirations, vomiting). Studies have demonstrated improvement of oxygenation and hemodynamics, decreased intubation rates, and decreased mortality  [51–53]. Continuous pressure at a level of 5‐10  cmH2O improves oxygenation by recruiting atelectatic and fluid‐filled alveoli and decreasing the work of breathing. The increase in intrathoracic pressure also alters hemodynamics by decreasing the transmural wall tension of the heart [54]. Nitrates are the mainstay pharmacologic treatment for patients who present with acute respiratory distress and pulmonary edema and who have adequate or elevated blood pressure. Nitroglycerin acts rapidly to dilate veins, allowing blood to distribute to the periphery, thereby decreasing cardiac preload. At higher doses, typically above 150‐250 μg/min, nitroglycerin also acts as an arterial vasodilator, decreasing cardiac afterload [55]. Studies of nitroglycerin use have shown relatively low rates of serious adverse effects ranging from 0.3% to 3.6% [56]. EMS clinicians must be cognizant of the potential interaction with all antierectile dysfunction phosphodiesterase‐inhibiting drugs (e.g., sildenafil), which are contraindications to the use of nitroglycerin. Caution is also advised if there is concern for an underlying right ventricular MI. This may be suspected if there is ST‐elevation in the inferior limb leads (II, III, aVF), especially when the elevation in lead III is greater than in lead II. A dose of 400 μg administered sublingually, given every 5  minutes, with frequent reassessment to ensure the maintenance of a systolic blood pressure of at least 100  mmHg, is often effective. Sublingual nitroglycerin also has the advantage of a rapid time to peak effect of 5 to 15 minutes and duration of action of less than 1 hour and can be used concurrently with NIPPV. Transdermal nitroglycerin paste is not recommended since its effectiveness is limited by slow absorption, which is further worsened by the presence of decreased skin perfusion during ADHF. Intravenous access should ideally be obtained before administering SL nitroglycerin, as it has the rare potential to produce hypotension and bradycardia [56]. However, the inability to obtain IV access should not preclude or delay its use. Intravenous bolus of high‐dose nitroglycerin is gaining traction as a treatment option in the emergency department and

prehospital settings and may be of particular benefit in patients with SCAPE  [57–59]. Intravenous administration facilitates a more rapid decline in afterload as compared to SL formulations. A case series demonstrated the feasibility and safety of IV bolus nitroglycerin when administered by paramedics and revealed improvements in systolic blood pressure and oxygen saturation upon emergency department arrival  [59]. One of the main indications for this therapy in this study was a systolic blood pressure >160  mmHg to avoid potential adverse events (e.g., hypotension). While studies have reported safety with bolus doses up to 2 mg for SCAPE, a reasonable starting dose is a 1 mg bolus with a repeat dose in 5 minutes if the blood pressure remains above 160 mmHg [57–60]. Loop diuretics (e.g., furosemide) are used primarily for patients with ADHF who are hypervolemic. Determining the appropriate patient to receive this treatment can be challenging prior to hospital arrival [6]. The time to peak drug response is about 30  minutes, with a prolonged duration of action. Diuretics also influence plasma electrolytes, which typically are not assessed in the field. Consequently, given the delayed onset of peak effect, protracted duration of action, and side effect profile, diuretics are rarely indicated in the prehospital setting [61]. The other treatment options (e.g., nitroglycerin and NIPPV) likely provide more benefit to the patient. Morphine, once a staple of therapy for ADHF and SCAPE, has also been largely supplanted by the other therapies. A review of the large ADHERE database found a significant association between receiving morphine and death, as well as several other adverse outcomes  [62]. One explanation may be that as morphine causes hypotension, it takes away the therapeutic room available for the use of other medications that could be used to reduce preload and afterload, such as nitroglycerin. In addition, as a respiratory depressant, morphine may decrease the respiratory drive of an already struggling patient and worsen hypoxemic respiratory failure [63]. Pneumonia and infectious respiratory disease In general, there are few specific field interventions for patients who are determined to have pulmonary infectious causes of their shortness of breath. Pneumonia treatment guidelines are universally focused on prompt diagnosis and early treatment with antibiotics. Pneumonia should be considered in patients with cough with or without fever. It is important to note that some of these diseases can be highly contagious, and it is recommended that personal respiratory protection (e.g., an N95  mask to protect against novel viruses as well as tuberculosis) is maintained when evaluating a respiratory distress patient who is suspected of having an infectious etiology. Treatment of these patients will typically consist of oxygen, NIPPV (if ventilation support is needed to improve oxygenation further), IV fluids (if hypotensive), and transport. Patients with known asthma or COPD who have reactive airways in response to infection may also benefit from bronchodilators. Many pneumonia patients may also

Respiratory distress

wheeze from underlying small airways infectious inflammatory processes and hence may respond to inhaled bronchodilators. Pulmonary embolus Pulmonary embolus is another clinical condition that can present to EMS clinicians with respiratory distress. Classic risk factors for venous thromboembolism (VTE) include the Virchow triad of venous stasis, trauma, and hypercoagulability. There are many risk factors for VTE, but the ones that have been clinically validated by Wells criteria and the PERC rule for risk stratification include recent surgery or immobilization of an extremity, malignancy, exogenous estrogen use, and prior DVT [64]. Other notable risk factors include genetic deficiency of anticlotting factors, pregnancy, obesity, and extended travel. Pulmonary embolus is a challenging clinical diagnosis because the manifestations can be subtle. The most common symptom is dyspnea, and the most common clinical signs are tachycardia and tachypnea. The pulmonary exam is usually unremarkable, although examination of the extremities, particularly the legs, may reveal swelling, erythema, and possibly pain in a limb with a DVT. With the increased use of peripherally inserted central venous catheters, pulmonary emboli are also reported more frequently because of upper extremity DVTs  [65]. Small emboli often present with respiratory distress. Larger emboli that cause lung infarction can present with findings such as pleuritic chest pain and hemoptysis, and those with massive saddle embolism cause findings suggestive of obstructive shock (Box 5.2). The latter can be detected by findings such as right axis deviation, right ventricle strain, and right bundle branch block on a 12‐lead ECG. Additional useful ECG features for pulmonary embolus include the presence of T‐wave inversions in both V1 and lead III, an S wave in lead I, and a Q wave and inverted T wave in lead III (S1Q3T3) [66]. Acute right ventricular dysfunction can also be visualized using portable ultrasonography. EMS treatment priorities include high‐flow oxygen, vascular access, and cardiac monitoring. A fluid bolus is reasonable in the patient who presents with a suspected massive pulmonary embolus and perfusion failure. In some patients, the presentation can take the form of a witnessed nontraumatic cardiac arrest with narrow complex pulseless electrical activity as the initial rhythm. The presence of respiratory distress, altered mental status, and a shock index (heart rate/systolic blood pressure) >0.8 have also been shown to be predictive of cardiac arrest in suspected pulmonary embolus patients [67]. A rapidly declining EtCO2 can also be a harbinger of impending arrest. Although the use of prehospital thrombolysis in these instances has been reported to be effective in selected cases, a randomized controlled clinical trial failed to show improved outcomes during cardiac arrest when t‐PA was administered compared to placebo for patients with refractory pulseless electrical activity [68, 69]. Pneumothorax Spontaneous pneumothorax is an uncommon condition that can present with acute respiratory distress. Risk factors for the

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development of a spontaneous pneumothorax include smoking history, underlying lung disease (e.g., COPD, tumor, infection, or a connective tissue disorder), positive‐pressure ventilation, and being male, with a tall, slender build [70]. A spontaneous pneumothorax is typically caused by rupture of the alveolar air sacs (i.e., subpleural bleb), leading to air accumulation between the parietal and visceral pleura, followed by variable collapse of the lung. Tension pneumothorax is a life‐threatening condition that occurs when the intrathoracic pressure increases due to air trapping from a valve‐like defect in the visceral pleura. This results in hemodynamic compromise from impaired venous return and decreased cardiac output. Symptoms of spontaneous pneumothorax include dyspnea and pleuritic chest pain. The examination may reveal tachycardia, unilateral decreased breath sounds on the affected side, asymmetrical chest rise, and chest wall crepitus. Patients with a suspected simple pneumothorax should be monitored closely for evidence of tension physiology such as worsening respiratory distress, hypoxia, and hypotension. Jugular venous distension and tracheal deviation are late findings of tension pneumothorax and should not be relied on to confirm this diagnosis. If available, ultrasound can be a valuable tool to assess for a potential pneumothorax, with both high sensitivity and specificity [10, 11]. Imaging will reveal an absence of lung sliding on the affected side. Intubated patients receiving positive‐pressure ventilation are at greater risk for developing a tension pneumothorax and should be monitored closely. Patients should be treated with supportive care, including oxygen, as indicated. If tension pneumothorax is suspected, immediate chest wall decompression is indicated. This can be achieved through needle or finger thoracostomy, depending on clinician scope of practice and training [71, 72]. (See Chapter 40.) Tracheotomy The patient with a tracheotomy presents a special circumstance when experiencing respiratory distress. An initial consideration is whether the distress is directly related to the tracheotomy itself. If not, then assessment and treatment should proceed as it would otherwise, with the added benefit of an effectively secured airway already in place. Respiratory distress related to tracheotomies generally relates to complications that manifest as airway obstructions. Commonly, secretions are the culprit, causing mucus plugging or drying inside the cannula and resulting in various degrees of obstruction. Initially, EMS clinicians should attempt to suction the airway through the inner cannula of the tracheotomy tube. Except in children, whose tracheotomy tubes have no inner cannula, the clinician can remove it if suctioning is inadequate. If there is no relief, the clinician should suction through the tracheotomy tube. Small aliquots of saline instilled into the tube may help loosen secretions to improve suctioning results. In the event that an appropriately sized suction catheter cannot be passed into a tracheotomy tube, it may also be removed with important considerations.

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The longer the tracheotomy has been in place, the more mature and stable the tract is. While the inner cannula can be safely removed, the tracheotomy tube should generally not be removed if the surgery to place it was recent, especially within 7 days. Risks include airway collapse and the potential to create a false passage during attempts to reintubate the stoma. In any case, the EMS clinician must be prepared for a difficult airway situation (see Chapter 3). Unless the tracheotomy was concomitant with laryngectomy, the patient may be intubated orally. He or she can also be reintubated through the existing stoma, using an appropriately sized endotracheal tube. A gum elastic bougie can be used to facilitate such a tube change. Bleeding from a tracheotomy can occur early or later after its placement. Bleeding at the site, until definitive hemostasis can be accomplished, may be controlled with application of hemostatic dressings. Bleeding within the airway, causing respiratory distress, may be cleared with suctioning through the tracheotomy inner cannula or tube. In critical circumstances, the tracheotomy tube may be removed so that the stoma can be reintubated with an endotracheal tube that is advanced distal to the site of bleeding to secure the airway. In some cases, the endotracheal tube cuff may also tamponade the bleeding source, and overinflation of the tracheotomy cuff or the endotracheal tube cuff may be considered. While tracheotomies provide a potential source of respiratory distress, it is important that their presence does not result in overlooking other causes, as discussed. If supplemental oxygen is necessary, humidification is appropriate to prevent drying of secretions.

Summary Respiratory distress is a very common complaint in the prehospital setting. The initial evaluation should be focused on identifying immediate threats to life and determining needs for immediate intervention, such as NIPPV, bag‐valve‐mask ventilation, or advanced airway management (supraglottic airway or endotracheal intubation). Once this evaluation is completed, efforts should be focused on attempting to determine the underlying cause of the problem. Respiratory distress may be caused by a primary pulmonary, cardiovascular, or infectious problem issue, or as part of the compensation for another nonpulmonary problem. In general, treatment should include titrated oxygen with cardiac rhythm, pulse oximetry, and waveform capnography monitoring while ensuring timely transport. In stable situations, the emphasis should focus on avoiding overtreatment and resisting the urge to give multiple medications in an undirected fashion. However, short‐acting inhaled bronchodilators should be initiated if there is a concern for bronchospasm, and nitrates should be considered as first‐line therapy in the patient with findings consistent with ADHF or SCAPE.

References 1 Baeder L. V2 911 Call Complaint vs EMS Provider Findings. National EMS Information System. Available at: https://wiki. utahdcc.org/confluence/x/nYAsAQ. Accessed August 10, 2020. 2 Prekker ME, Feemster LC, Hough CL, et al. The epidemiology and outcome of prehospital respiratory distress. Acad Emerg Med. 2014; 21:543–50. 3 Stiell IG, Spaite DW, Field B, et al. Advanced life support for out‐of‐ hospital respiratory distress. N Engl J Med. 2007; 356:2156–64. 4 Williams TA, Finn J, Fatovich D, Perkins GD, Summers Q, Jacobs I. Paramedic differentiation of asthma and COPD in the prehospital setting is difficult. Prehosp Emerg Care. 2015; 19:535–43. 5 Ackerman R, Waldron RL. Difficulty breathing: agreement of paramedic and emergency physician diagnoses. Prehosp Emerg Care. 2006; 10:77–80. 6 Jaronik J, Mikkelson P, Fales W, Overton DT. Evaluation of prehospital use of furosemide in patients with respiratory distress. Prehosp Emerg Care. 2006; 10:194–7. 7 DeVon HA, Penckofer S, Larimer K. The association of diabetes and older age with the absence of chest pain during acute coronary syndromes. West J Nurs Res. 2008; 30:130–44. 8 McSweeney JC, Cody M, O’Sullivan P, Elberson K, Moser DK, Garvin BJ. Women’s early warning symptoms of acute myocardial infarction. Circulation. 2003; 108:2619–23. 9 Laursen CB, Hanselmann A, Posth S, Mikkelsen S, Videbaek L, Berg H. Prehospital lung ultrasound for the diagnosis of cardiogenic pulmonary oedema: a pilot study. Scand J Trauma Resusc Emerg Med. 2016; 24:96. 10 Lichtenstein DA, Menu Y. A bedside ultrasound sign ruling out pneumothorax in the critically ill. Lung sliding. Chest. 1995; 108:1345–8. 11 Dulchavsky SA, Schwarz KL, Kirkpatrick AW, et  al. Prospective evaluation of thoracic ultrasound in the detection of pneumothorax. J Trauma. 2001; 50:201–5. 12 Egleston CV, Ben Aslam H, Lambert MA. Capnography for monitoring non‐intubated spontaneously breathing patients in an emergency room setting. J Accid Emerg Med. 1997; 14:222–4. 13 Manifold CA, Davids N, Villers LC, Wampler DA. Capnography for the nonintubated patient in the emergency setting. J Emerg Med. 2013; 45:626–32. 14 Hunter CL, Silvestri S, Ralls G, Papa L. Prehospital end‐tidal carbon dioxide differentiates between cardiac and obstructive causes of dyspnoea. Emerg Med J. 2015; 32:453–6. 15 Hunter C, Putman M, Foster J, et  al. Utilizing end‐tidal carbon dioxide to diagnose diabetic ketoacidosis in prehospital patients with hyperglycemia. Prehosp Disaster Med. 2020; 35:281–4. 16 Austin MA, Wills KE, Blizzard L, Walters EH, Wood‐Baker R. Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: randomised controlled trial. BMJ. 2010; 341:c5462. 17 Singer AJ, Emerman C, Char DM, et  al. Bronchodilator therapy in acute decompensated heart failure patients without a history of chronic obstructive pulmonary disease. Ann Emerg Med. 2008; 51:25–34. 18 Fisher AA, Davis MW, McGill DA. Acute myocardial infarction associated with albuterol. Ann Pharmacother. 2004; 38:2045–9. 19 Hodroge SS, Glenn M, Breyre A, et  al. Adult patients with respiratory distress: current evidence‐based recommendations for prehospital care. West J Emerg Med. 2020; 21:849–57.

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20 Williams TA, Finn J, Perkins GD, Jacobs IG. Prehospital continuous positive airway pressure for acute respiratory failure: a systematic review and meta‐analysis. Prehosp Emerg Care. 2013; 17:261–73. 21 Aguilar SA, Lee J, Dunford JV, et  al. Assessment of the addition of prehospital continuous positive airway pressure (CPAP) to an urban emergency medical services (EMS) system in persons with severe respiratory distress. J Emerg Med. 2013; 45:210–9. 22 Mal S, McLeod S, Iansavichene A, Dukelow A, Lewell M. Effect of out‐of‐hospital noninvasive positive‐pressure support ventilation in adult patients with severe respiratory distress: a systematic review and meta‐analysis. Ann Emerg Med. 2014;63(5):600–607. 23 Bledsoe BE, Anderson E, Hodnick R, Johnson L, Johnson S, Dievendorf E. Low‐fractional oxygen concentration continuous positive airway pressure is effective in the prehospital setting. Prehosp Emerg Care. 2012; 16:217–21. 24 US Centers for Disease Control and Prevention. Most recent national asthma data. Available at: https://www.cdc.gov/asthma/ most_recent_national_asthma_data.htm. 2020. Accessed August 10, 2020. 25 National Heart, Lung and Blood Institute, National Institutes of Health. Guidelines for the diagnosis and management of asthma (EPR‐3). Available at: www.nhlbi.nih.gov/guidelines/asthma/ index.htm. 2007. Accessed August 21, 2020. 26 Nagurka R, Bechmann S, Gluckman W, Scott SR, Compton S, Lamba S. Utility of initial prehospital end‐tidal carbon dioxide measurements to predict poor outcomes in adult asthmatic patients. Prehosp Emerg Care. 2014; 18:180–4. 27 Knapp B, Wood C. The prehospital administration of intravenous methylprednisolone lowers hospital admission rates for moderate to severe asthma. Prehosp Emerg Care. 2003; 7:423–6. 28 Gibbs MA, Camargo CA Jr., Rowe BH, Silverman RA. State of the art: therapeutic controversies in severe acute asthma. Acad Emerg Med. 2000; 7:800–15. 29 Nassif A, Ostermayer DG, Hoang KB, Claiborne MK, Camp EA, Shah MI. Implementation of a prehospital protocol change for asthmatic children. Prehosp Emerg Care. 2018; 22:457–65. 30 Conway J, Friedman B. Intravenous magnesium sulfate for acute asthma exacerbation in adults. Acad Emerg Med. Published online ahead of print June 23, 2020. doi: 10.1111/acem.14066. 31 Kew KM, Kirtchuk L, Michell CI. Intravenous magnesium sulfate for treating adults with acute asthma in the emergency department. Cochrane Database Syst Rev. 2014:CD010909. 32 Williams AM, Abramo TJ, Shah MV, et al. Safety and clinical findings of BiPAP utilization in children 20 kg or less for asthma exacerbations. Intensive Care Med. 2011;3 7:1338–43. 33 Beers SL, Abramo TJ, Bracken A, Wiebe RA. Bilevel positive airway pressure in the treatment of status asthmaticus in pediatrics. Am J Emerg Med. 2007; 25:6–9. 34 Thapamagar SB, Doshi V, Shenoy S, Ganesh A, Lankala S. Outcomes of noninvasive ventilation in obese patients with acute asthma exacerbations. Am J Ther. 2018; 25:e635–41. 35 Chung KF, Adcock IM. Multifaceted mechanisms in COPD: inflammation, immunity, and tissue repair and destruction. Eur Respir J. 2008; 31:1334–56. 36 Stoller JK, Aboussouan LS. Alpha1‐antitrypsin deficiency. Lancet 2005; 365:2225–36. 37 Heron M. Deaths: leading causes for 2017. Natl Vital Stat Rep. 2019; 68:1–77.

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38 Ford ES, Murphy LB, Khavjou O, Giles WH, Holt JB, Croft JB. Total and state‐specific medical and absenteeism costs of COPD among adults aged ≥18 years in the United States for 2010 and projections through 2020. Chest. 2015; 147:31–45. 39 Murray CJ, Atkinson C, Bhalla K, et  al. The state of US health, 1990‐2010: burden of diseases, injuries, and risk factors. JAMA. 2013; 310:591–608. 40 Global Initiative for Chronic Obstructive Pulmonary Disease. Global strategy for the diagnosis, management and prevention of chronic obstructive pulmonary disease: 2020 report. Available at: http://www.goldcopd.org. 2020. Accessed July 31, 2020. 41 Campbell IA, Colman SB, Mao JH, Prescott RJ, Weston CF. An open, prospective comparison of beta 2 agonists given via nebuliser, Nebuhaler, or pressurised inhaler by ambulance crew as emergency treatment. Thorax. 1995; 50:79–80. 42 Walters JA, Tan DJ, White CJ, Gibson PG, Wood‐Baker R, Walters EH. Systemic corticosteroids for acute exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev.. 2014:CD001288. 43 Ram FS, Rodriguez‐Roisin R, Granados‐Navarrete A, Garcia‐ Aymerich J, Barnes NC. Antibiotics for exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2006:CD004403. 44 Osadnik CR, Tee VS, Carson‐Chahhoud KV, Picot J, Wedzicha JA, Smith BJ. Non‐invasive ventilation for the management of acute hypercapnic respiratory failure due to exacerbation of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2017; 7:CD004104. 45 Celli BR. Update on the management of COPD. Chest. 2008; 133:1451–62. 46 Borlaug BA. Defining HFpEF: where do we draw the line? Eur Heart J 2016; 37:463–5. 47 Benjamin EJ, Blaha MJ, Chiuve SE, et  al. Heart disease and stroke statistics‐2017 update: a report from the American Heart Association. Circulation. 2017; 135:e146–e603. 48 McDonagh TA, Morrison CE, Lawrence A, et al. Symptomatic and asymptomatic left‐ventricular systolic dysfunction in an urban population. Lancet. 1997; 350:829–33. 49 Echouffo‐Tcheugui JB, Bishu KG, Fonarow GC, Egede LE. Trends in health care expenditure among US adults with heart failure: The Medical Expenditure Panel Survey 2002‐2011. Am Heart J. 2017; 186:63–72. 50 Neesse A, Jerrentrup A, Hoffmann S, et  al. Prehospital chest emergency sonography trial in Germany: a prospective study. Eur J Emerg Med. 2012; 19:161–6. 51 Kallio T, Kuisma M, Alaspaa A, Rosenberg PH. The use of prehospital continuous positive airway pressure treatment in presumed acute severe pulmonary edema. Prehosp Emerg Care. 2003; 7:209–13. 52 Thompson J, Petrie DA, Ackroyd‐Stolarz S, Bardua DJ. Out‐of‐ hospital continuous positive airway pressure ventilation versus usual care in acute respiratory failure: a randomized controlled trial. Ann Emerg Med. 2008; 52:232–41, e241. 53 Masip J, Roque M, Sanchez B, Fernandez R, Subirana M, Exposito JA. Noninvasive ventilation in acute cardiogenic pulmonary edema: systematic review and meta‐analysis. JAMA. 2005; 294:3124–30. 54 Naughton MT, Rahman MA, Hara K, Floras JS, Bradley TD. Effect of continuous positive airway pressure on intrathoracic and left ventricular transmural pressures in patients with congestive heart failure. Circulation. 1995; 91:1725–31.

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55 Levy PD, Bellou A. Acute heart failure treatment. Curr Emerg Hosp Med Rep. 2013; 1112–21. 56 Engelberg S, Singer AJ, Moldashel J, Sciammarella J, Thode HC, Henry M. Effects of prehospital nitroglycerin on hemodynamics and chest pain intensity. Prehosp Emerg Care. 2000; 4:290–3. 57 Levy P, Compton S, Welch R, et al. Treatment of severe decompensated heart failure with high‐dose intravenous nitroglycerin: a feasibility and outcome analysis. Ann Emerg Med. 2007; 50:144–52. 58 Wilson SS, Kwiatkowski GM, Millis SR, Purakal JD, Mahajan AP, Levy PD. Use of nitroglycerin by bolus prevents intensive care unit admission in patients with acute hypertensive heart failure. Am J Emerg Med. 2017; 35:126–31. 59 Patrick C, Ward B, Anderson J, et  al. Feasibility, effectiveness and safety of prehospital intravenous bolus dose nitroglycerin in patients with acute pulmonary edema. Prehosp Emerg Care. 2020:1–7. 60 Wang K, Samai K. Role of high‐dose intravenous nitrates in hypertensive acute heart failure. Am J Emerg Med 2020; 38:132–7. 61 Hoffman JR, Reynolds S. Comparison of nitroglycerin, morphine and furosemide in treatment of presumed pre‐hospital pulmonary edema. Chest. 1987; 92:586–93. 62 Peacock WF, Hollander JE, Diercks DB, Lopatin M, Fonarow G, Emerman CL. Morphine and outcomes in acute decompensated heart failure: an ADHERE analysis. Emerg Med. 2008; 25:205–9. 63 Gray A, Goodacre S, Seah M, Tilley S. Diuretic, opiate and nitrate use in severe acidotic acute cardiogenic pulmonary oedema: analysis from the 3CPO trial. QJM. 2010; 103:573–81.

64 Kline JA, Courtney DM, Kabrhel C, et al. Prospective multicenter evaluation of the pulmonary embolism rule‐out criteria. J Thromb Haemos. 2008; 6:772–80. 65 Lee JA, Zierler BK, Zierler RE. The risk factors and clinical outcomes of upper extremity deep vein thrombosis. Vasc Endovascular Surg. 2012; 46:139–44. 66 Kosuge M, Kimura K, Ishikawa T, et  al. Electrocardiographic differentiation between acute pulmonary embolism and acute coronary syndromes on the basis of negative T waves. Am J Cardio. 2007; 99:817–21. 67 Courtney DM, Kline JA. Prospective use of a clinical decision rule to identify pulmonary embolism as likely cause of outpatient cardiac arrest. Resuscitation. 2005; 65:57–64. 68 Perrott J, Henneberry RJ, Zed PJ. Thrombolytics for cardiac arrest: case report and systematic review of controlled trials. Ann Pharmacother. 2010; 44:2007–13. 69 Abu‐Laban RB, Christenson JM, Innes GD, et  al. Tissue plasminogen activator in cardiac arrest with pulseless electrical activity. N Engl J Med. 2002; 346:1522–8. 70 Bintcliffe O, Maskell N. Spontaneous pneumothorax. BMJ. 2014; 348:g2928. 71 Dickson RL, Gleisberg G, Aiken M, et  al. Emergency medical services simple thoracostomy for traumatic cardiac arrest: postimplementation experience in a ground‐based suburban/rural emergency medical services agency. J Emerg Med. 2018; 55:366–71. 72 Hannon L, St Clair T, Smith K, et  al. Finger thoracostomy in patients with chest trauma performed by paramedics on a helicopter emergency medical service. Emerg Med Australa. 2020; 32:650–6.

CHAPTER 6

Oxygenation and ventilation Vincent N. Mosesso, Jr and Angus M. Jameson

Introduction Oxygenation and ventilation are critical life‐sustaining functions, and their evaluation and management are primary components of emergency medical services (EMS) care. While these two parameters are related, they are distinct physiological functions that require independent assessment. The focus of this chapter is on diagnostic aids and management, and EMS physicians and other clinicians must develop and maintain expert physical examination skills for the proper assessment of these important processes. The astute EMS clinician will observe demeanor, mentation, ability to speak, ease and volume of air exchange, work of breathing, upper or lower airway obstruction, pulmonary congestion, and central and peripheral cyanosis. These findings should be considered together with diagnostic test results to determine the status of oxygenation and ventilation in an individual patient, whether intervention is needed, and, if so, which treatment modalities are indicated.

Assessment of Oxygenation Adequate oxygen delivery to body tissues is a necessity for life and is dependent on both the transfer of oxygen from the alveolar airspace to the blood and sufficient tissue perfusion with oxygenated blood. Oxygenation of the blood is dependent on a number of distinct factors, each of which can be impaired by various pathological processes (Table  6.1). Normal hemoglobin oxygen saturation in peripheral arterial blood is 96–99%. It is important to understand the relationship between oxygen saturation and the partial pressure of oxygen. This is depicted by the oxyhemoglobin dissociation curve (Figure 6.1). This curve demonstrates that above 90% the saturation percentage is very insensitive to changes in partial pressure of oxygen (PaO2) between 150  mmHg and 760 mmHg. This means that, especially in patients receiving supplemental oxygen, severe impairment of oxygen transfer

into the blood can occur without major changes in the saturation level and EMS clinicians can miss the physiological deterioration. Considered another way, if the partial pressure of oxygen in blood is at least 60 mmHg, hemoglobin is able to transport oxygen efficiently to the periphery. Several tools have been developed that can reliably measure oxygenation of blood in the prehospital environment. Portable devices are available that can measure oxygen content in arterial and venous blood samples (i.e., PaO2). However, because of cost and the need to perform vascular puncture, these devices are typically only used at selected special event venues and by critical care teams. Most commonly, oxygen levels in the field are determined by pulse oximetry (i.e., oxygen saturation, SpO2). This simple, noninvasive method reports the percentage of hemoglobin in arteriolar blood that is in a saturated state. It is important for prehospital clinicians to understand that standard pulse oximetry does not discriminate between hemoglobin saturated with oxygen and hemoglobin saturated with carbon monoxide (i.e., oxyhemoglobin versus carboxyhemoglobin). In cases of carbon monoxide exposure, pulse oximetry will be misleading to the unsuspecting clinician [1]. Newer‐generation devices are available that can measure carboxyhemoglobin levels distinct from oxyhemoglobin [2]. Pulse oximetry may be unreliable in states of low tissue perfusion, such as with shock or local vasoconstriction due to cold temperature. Additionally, as this technology relies on transmission and absorption of light waves, barriers such as fingernail polish or skin disease can interfere with accuracy. Measurement of tissue oxygenation saturation (StO2) uses near‐infrared light resorption to measure oxygen saturation of blood in the skin and underlying soft tissue. This enables assessment of oxygen delivery and consumption in local tissue rather than simply the amount of oxygen circulating in the arterial system, which is measured by pulse oximetry. While there are increasing reports of the utility of this technology, it is not yet in widespread clinical use due to cost, technical limitations, and lack of large clinical studies [3].

Emergency Medical Services: Clinical Practice and Systems Oversight, Third Edition. Volume 1: Clinical Aspects of EMS. Edited by David C. Cone, Jane H. Brice, Theodore R. Delbridge, and J. Brent Myers. © 2021 NAEMSP. Published 2021 by John Wiley & Sons, Inc.

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Table 6.1  Conditions that impair oxygen transfer in the lungs Box 6.1  Conditions that impair ventilation Physiological process

Pathological conditions

Partial pressure of oxygen in inhaled air Minute ventilation (volume of air inhaled per minute)

Displacement by other gases

Diffusion of oxygen across the alveolar membrane Perfusion of the alveoli

External compression of chest Muscle weakness (chest wall and/or diaphragm) Central nervous system control malfunction Decreased lung compliance Pneumothorax Hemothorax and pleural effusion Pneumonitis Alveolar and/or interstitial edema Decreased cardiac output Hypotension Shunting

100 90 80 70 SaO2

60 50 40 30 20 10 0

0

50

100 PaO2

150

200

Figure 6.1  Oxygen‐hemoglobin dissociation curve

Assessment of Ventilation Ventilation refers to the movement of air into and out of the lungs. It is measured as minute ventilation (volume of air exchanged per minute), which can be calculated by the equation, minute ventilation = tidal volume × respiratory rate. Normal ventilation ranges from 6 L/minute to 7 L/minute. Although hypoventilation can lead to decreased oxygenation and hemoglobin oxygen saturation, ventilatory effectiveness is better evaluated by how well carbon dioxide (CO2) is being eliminated. Ventilation can be compromised by a number of conditions (Box 6.1), and its assessment is of equal importance to that of oxygenation. Ventilatory function can be determined directly by measuring the volume of air inhaled or exhaled per minute, or indirectly by measuring the CO2 level in blood or exhaled air. The partial pressure of carbon dioxide (PaCO2, may be measured in either arterial or venous blood samples using portable devices, as both provide similar results). However, just as oxygen content in the blood is usually assessed by noninvasive modalities in out‐ of‐hospital settings, so too is CO2. Three types of devices are

•  Airway obstruction: ◆◆ Upper ◆◆ Lower (asthma, chronic obstructive pulmonary disease) •  Muscle weakness (may be neurological) •  Pleural effusion (large) •  Pneumothorax •  Sucking chest wound •  Diaphragmatic malfunction (e.g., rupture, paralysis) •  Pleuritic pain •  Medications and recreational substances: ◆◆ Opioids ◆◆ Sedatives ◆◆ Oxygen (in patients with hypoxic drive)

currently in use to detect and measure the presence and level of CO2 in exhaled air, which serves as a surrogate for the level of CO2 in blood. The simplest, but least useful, are semiquantitative colorimetric devices that use litmus paper to detect the acid generated by absorption of CO2 from exhaled air. These devices are compromised by prolonged exposure to air and by contamination from acidic gastric secretions. They may not be able to detect the extremely low levels of CO2 generated by patients in cardiac arrest. For these reasons, and due to the increasing availability of devices that can measure and continuously monitor exhaled CO2, colorimetric devices are being used less often than quantitative devices. Capnometry uses light absorption to measure the level of CO2 in exhaled air. Clinically, the level at the end of exhalation is the most useful value and is referred to as end‐tidal CO2 (EtCO2). This measurement reflects the CO2 content in alveolar gas and, therefore, in the pulmonary venous blood returning to the left heart. The EtCO2 level is typically 32–42 mmHg. It is 3–5 mmHg lower than the PaCO2 level in arterial blood, due to physiological alveolar dead space. Various clinical conditions such as poor pulmonary perfusion, greater than normal dead space (i.e., shunting and V/Q mismatch), and cuff or sampling device leak can widen this gap to 10–20 mmHg [4]. EtCO2 cannot be higher than the PaCO2, but may be significantly lower, and this should be considered when modifying manual or mechanical ventilation. Whenever possible, in critical care transport scenarios, for example, baseline PaCO2 may be obtained and compared to the EtCO2 level at the time of blood sampling. Venous PaCO2 is ­typically about 4 mmHg higher than arterial PaCO2 (range +10 to –2) [5]. Continuous waveform capnography provides additional information on the frequency of respirations and the flow rate of inhalation and exhalation by displaying a graphic depiction of measured expired CO2 over time. Flow rate is affected by airway mechanics, including obstruction and bronchospasm, and is reflected in changes in the shape of the involved phase of ventilation. EMS clinicians should have a good understanding of the interpretation of EtCO2 values as well as waveform morphology, as they both are altered by a variety of clinical conditions and may provide diagnostic information (Box 6.2) [6].

Oxygenation and ventilation

As a monitor of respiratory function, capnography is superior to pulse oximetry because it changes nearly immediately with changes in ventilation. On the other hand, hypoxia may be delayed by the body’s reserve and the physiology of hemoglobin oxygen dissociation, as discussed above. When capnography waveform analysis is included, a near real‐time assessment is possible and EMS clinicians may identify inadequacy of ventilation or the presence of various respiratory disease states, and they may glean information about circulatory and metabolic function as well. Impairment of ventilation is associated with rising EtCO2 values. When combined with waveform analysis, respiratory effort

Box 6.2  Factors that affect EtCO2

True decrease in blood PaCO2: •  Hyperventilation (primary or secondary) •  Shock/cardiac arrest (with constant ventilation) •  Hypothermia /decreased metabolism True increase in blood PaCO2: •  Hypoventilation •  Return of circulation after cardiac arrest •  Improved perfusion after severe shock •  Tourniquet release •  Administration of sodium bicarbonate •  Fever/increased metabolism •  Thyroid storm Increased gap between blood PaCO2 and EtCO2: •  Severe hypoventilation •  Increased alveolar dead space •  Decreased perfusion •  Disconnected or clogged tubing

(c)

30 20 10 0 –10

60 50 40 30 20 10 0

A

A

may also be monitored as to rate and depth of breathing. When respiratory rate or respiratory depth has become inadequate and EtCO2 values rise, clinicians can initiate or augment respiratory support prior to the development of hypoxia. In the prehospital environment, this application of waveform capnography is especially useful in monitoring respiratory status following the administration of opioid analgesics, benzodiazepines, and other medications capable of producing respiratory depression (Figure 6.2). Obstructive respiratory physiology is the most often described diagnosis made upon EtCO2 waveform analysis. Both chronic obstructive pulmonary disease (COPD) and asthma fall into this category, and the waveform produced will be similar. The classic description of this waveform is the “shark fin” morphology, consisting of a shallower upward sloping of the initial rise of the EtCO2 wave (Figure  6.2b). This represents a slower rate of exhalation. It may be considered analogous to the forced expiratory volume in one second measurement of the pulmonary function test. This slower exhalation is precipitated by collapse or partial occlusion of bronchioles in emphysema and chronic bronchitis and spasm in acute asthma attacks. As the condition improves following bronchodilation, the initial upward segment will become more vertical. However, in more severe cases, the numeric value or amount of EtCO2 will also rise, heralding respiratory insufficiency, and should lead the ­clinician to consider ventilatory support measures. Although less commonly employed, EtCO2 and waveform analysis may also be useful in assessment of metabolic derangements such as diabetic ketoacidosis and aspirin overdose. These conditions cause respiratory compensation of metabolic acidosis and will present with hyperventilation, typically with a decreasing level of EtCO2.

60 50 40 30 20 10 0 Time

(b)

B

Time

EtCO2 (mmHg)

EtCO2 (mmHg)

(a)

D

C

EtCO2 (mmHg)

EtCO2 (mmHg)

50 40

63

Time

(d)

60 50 40 30 20 10 0 Time

Figure 6.2  Capnography waveforms. (a) Normal waveform. Point A is beginning of expiration. A‐B is expiration of dead space air. B‐C shows rapid rise in level of CO2 as air from lungs is exhaled. C‐D is the plateau phase representing primarily alveolar air. D represents the value used for determination of EtCO2. D‐A represents inspiration. (b) Effect of bronchospasm. Note the slower rise in the CO2 level leading to the so‐called shark fin waveform. (c) Hypoventilation. (d) Hyperventilation

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Assisting Oxygenation and Ventilation While oxygenation and ventilation are distinct parameters, their assessment and management are often interdependent. Thus, we discuss them together. The initial and most basic treatment for inadequate oxygenation is the administration of supplemental oxygen to increase the relative amount, or fraction, of oxygen in inspired gases (i.e., FiO2). Oxygen should be provided to all patients with respiratory distress, with any clinical markers of respiratory compromise (e.g., altered mental status), or with measured inadequate oxygenation or ventilation. There is an increasing trend toward more selective application of oxygen with the growing recognition of oxygen toxicity. Most current guidelines and protocols endorse administering supplemental oxygen only if the oxygen saturation is less than 94%. Unnecessarily elevating the SpO2 above normal levels may in fact be harmful to patients experiencing neurological or cardiac insults associated with ischemic damage [7]. Patients with underlying pulmonary disease, such as COPD and interstitial fibrosis, may have oxygen saturations below 94% on a chronic basis. A subset of these patients will also have chronically high PaCO2 levels (hypercapnia), which lead to dependence on a hypoxic drive for ventilatory control and stimulation. Providing supplemental oxygen, especially at high flow rates, may contribute to respiratory depression and potentially produce apnea [8]. EMS clinicians must carefully assess and monitor these patients, administer oxygen if needed, and be prepared to assist ventilation. Oxygen should not be withheld from a hypoxic patient because of concern for their dependency on a hypoxic drive for breathing. Supplemental oxygen can be administered through various devices that deliver different ranges of oxygen concentration (Table  6.2). Most EMS systems carry nasal cannulas and non‐ rebreather facemasks, allowing clinicians to choose either a lower or a higher FiO2. When supplemental oxygen itself does not lead to adequate oxygenation of blood, noninvasive positive‐pressure ventilation (NIPPV) can be beneficial to supplement ventilatory function in addition to providing increased FiO2. This modality is most effective in patients with pulmonary edema, who have poor oxygen diffusion between alveolar air and the pulmonary capillary blood. Further, it is useful for patients with other conditions, including asthma, COPD, and pulmonary hypertension. NIPPV is described in more detail below.

Table 6.2  Devices for delivery of supplemental oxygen Device name

O2 flow rate (L/min)

FiO2 (approximate %)

Nasal cannula Simple face mask Partial rebreather mask Non‐rebreather mask Venturi mask Tracheostomy mask

1–6 5–12 8–15 8–15 4–15 10–15

24–44 35–55 35–60 60–95 24–50 35–60

While hypoxemia in the setting of adequate ventilation can be treated with supplemental oxygen and augmentation of ventilatory function, inadequate ventilation requires immediate intervention. The EMS clinician should rapidly determine the likely cause (Box  6.1) of the patient’s ventilatory insufficiency and determine if it can be quickly corrected. Examples of this are removal of upper airway obstruction, administration of bronchodilators for bronchospasm, sealing of sucking chest wounds, administration of naloxone for opioid overdose, and needle decompression of tension pneumothorax. Some conditions cannot be immediately alleviated, particularly in the prehospital setting, such as muscle weakness from Guillain‐Barré syndrome or severe physical fatigue, vital capacity reduction from a large pleural effusion, and non‐reversible drug toxicity. In other cases, medical interventions may not be sufficiently effective immediately, such as for acute pulmonary edema or severe asthma. Whenever ventilation is compromised and cannot be immediately alleviated, mechanical ventilatory support must be provided.

Noninvasive Positive‐Pressure Support Patients who are awake, protecting their airways, have respiratory drive, and can cooperate may be given ventilatory support with noninvasive modalities that provide positive airway pressure. These include continuous positive airway pressure (CPAP), which delivers constant pressure above that of the atmosphere throughout the ventilation cycle, and bi‐level positive airway pressure (BiPAP), which delivers different pressures during the inspiratory and expiratory phases. Portable devices for the delivery of CPAP in the prehospital setting are generally of three types. Two of these require a high‐pressure (50  psi) oxygen source. One continuously delivers oxygen under pressure to a mask with a pop‐off valve that opens when the desired pressure is reached. The other uses a controller that essentially acts as a demand valve, adjusting flow to maintain the desired pressure. The third type of device uses oxygen flow from a standard regulator and a Venturi valve to create a virtual valve resulting in elevated pressure. Usually, treatment is started at 5–10 cm H2O and increased as needed to a maximum of 20 cm H2O. Prehospital devices generally deliver near 100% FiO2, while more advanced devices allow the FiO2 to be titrated. Until recently, BiPAP has been only available to EMS personnel who carry full‐function mechanical ventilators, but newer devices can now provide this modality for the field. NIPPV has been shown to improve oxygen delivery. This is thought to be the result of the hydrostatic pressure effects of increasing the gas diffusion gradient, promoting displacement of fluid in the alveoli back into the capillary bed, and stenting open small bronchioles (which do not have cartilaginous walls), thereby increasing both the volume of air exchanged and the number of alveoli ventilated. NIPPV also decreases the work of breathing. The ultimate clinical effects are that patients

Oxygenation and ventilation

will often have improved oxygenation, improved ventilation, marked improvement in respiratory distress, and significantly lower likelihood of needing intubation and mechanical ventilation [9].

Expiratory PEEP value valve

Self-inflating bag

65

Air-inlet one-way valve & O2 reservoir socket Air-inlet & pressure release valves

Bag‐Valve‐Mask Ventilation Patients with marked respiratory failure may need more intensive ventilatory support than NIPPV. This is true for patients with inadequate ventilatory effort and those with depressed mental status who cannot protect their airways. Immediate assistance should be provided for these patients using a bag‐valve‐mask device to either assist spontaneous ventilations or provide full mechanical ventilation. Proper positioning (head and neck tilt, sniffing position), mechanical airway opening (jaw thrust or modified jaw thrust), and placement of a nasal or oral airway can markedly improve airflow. High‐flow oxygen should fill the bag device, preferably with a reservoir bag. Using this device can be difficult for a single clinician, using one hand to seal the mask and the other to squeeze the bag. Whenever possible, a two‐ person technique should be used, with one person using both hands and a jaw thrust maneuver to make a firm seal around the mask and open the airway, while the other person squeezes the bag. EMS clinicians must be cognizant of volume and rate when assisting ventilation. Patients who are severely hypoxic or hypercarbic may initially require hyperventilation, as do those with severe metabolic acidosis, such as from diabetic ketoacidosis or sepsis. However, absent such conditions, unnecessary hyperventilation will have detrimental effects, including decreased cerebral perfusion, venous return, and cardiac output, and metabolic impairment from respiratory alkalosis. Standard adult bags are typically 1,500–1,600 ml, so a full squeeze will provide excessive tidal volume and likely high peak airway pressure, and facilitate inadvertent hyperventilation. One study found that most adults could be ventilated with a pediatric bag, but a small adult size with 1,000 ml is available [10]. Some devices can be equipped with high inspiratory pressure pop‐off valves and positive end‐expiratory pressure (PEEP) valves (Figure  6.3). These adjuncts improve proper ventilation and oxygenation.

Mechanical Ventilation While bag‐valve‐mask ventilation can be an effective and life‐ saving initial measure, it is difficult to maintain effectiveness in the longer term, especially in a moving vehicle. Additionally, it provides no protection from aspiration of stomach contents, blood, or other secretions. When adequately trained personnel are available, a more definitive airway should be sought in patients who have marked depression of consciousness, inability to protect their airway, or who require full mechanical ventilatory support to maintain oxygenation and ventilation. Usually,

Face mask

Pop off valve

Oxygen inlet & tubing

Reservoir bag

Figure 6.3  Bag‐valve mask device

this entails placement of an endotracheal tube or a supraglottic advanced airway device (see Chapters 2 and 3). Patients can then be ventilated either manually (i.e., with a bag device) or with a portable mechanical ventilator. Management of mechanical ventilators is a complex topic and a comprehensive tutorial is beyond the scope of this chapter. However, a basic understanding of the modes, settings, and troubleshooting of mechanical ventilators is important. Mechanical ventilators are typically used in the prehospital setting by air medical services and by ground critical care teams during interfacility transports. Greater portability is facilitating their deployment within EMS systems for use during longer transports. EMS clinicians may also encounter patients who are chronically on ventilators in residential or long‐term care ­settings. Modes of Ventilation There are two basic modes of mechanical ventilation, volume control and pressure control, with multiple variations and combinations of these. Common modalities include assist control (AC), synchronized intermittent mandatory ventilation (SIMV), adaptive support ventilation (ASV), and pressure support (PS). The key to understanding these modes is recognizing that the time of the respiratory cycle (i.e., respiratory rate), tidal volume, flow rate, and pressure developed in the airways are all interdependent and affected by the individual patient’s airway physiology. In each of these modes, different combinations of these variables are controlled by the machine, and the patient’s respiratory function determines the uncontrolled variables. In AC mode, the ventilator delivers a set tidal volume with each breath. A default respiratory rate is set, but the patient may trigger breaths above that default rate. In AC mode, the machine will deliver the full set tidal volume on either a patient‐ or machine‐triggered breath. SIMV is very similar to AC, and, in fact, in patients without spontaneous respiratory effort the two are effectively identical. The major difference is that in SIMV the machine does not deliver the full set tidal volume in response to a patient‐triggered breath, but rather allows the patient’s effort to determine the volume of the breath. In SIMV

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mode, the ventilator will synchronize ventilator‐triggered breaths with patient‐triggered breaths, assuring that the set rate is met or exceeded. In both AC and SIMV modes, care must be taken to monitor the airway pressures developed during the respiratory cycle. In contrast, PS mode delivers a set inspiratory pressure above a baseline PEEP with each patient‐triggered breath. The patient’s respiratory drive determines the rate and the patient’s lung compliance and airway resistance determine the tidal volume developed. ASV combines several modes of ventilation in an adaptive manner dynamically to adjust levels and modes of support to the patient’s requirements. Ventilator Settings and Troubleshooting Once the mode of ventilation is selected, EMS clinicians will need to set several variables. In AC and SIMV modes, tidal volume, respiratory rate, and PEEP are all determined by the clinician. Tidal volumes are normally chosen to be 6–10  mL/ kg of ideal body weight based on patient height. Tidal volumes of 6–8 mL/kg are preferred for patients with acute respiratory distress syndrome, whereas 8–10 ml/kg may be better for other conditions such as trauma and COPD [11]. Respiratory rate should be adjusted based upon the patient’s clinical situation, with low tidal volume strategies usually associated with higher rates. Higher than standard minute ventilation should be assured in patients who are dependent upon respiratory compensation of a metabolic acidosis. PEEP may also be applied to improve oxygenation via mechanisms similar to NIPPV, discussed above, and is often initially set at 5–10  cm H2O. For patients with obstructive physiology (e.g., asthma and COPD), care should be taken to maximize expiratory time to avoid incomplete expiration and breath stacking, which can lead to increased airway pressures. If air trapping is suspected, excess pressure can be alleviated by disconnecting the endotracheal tube from the ventilator for a few seconds and compressing the patient’s chest. Peak inspiratory pressure (PIP) represents the maximum pressure developed during the inspiratory phase. Changes in PIP are a common source of ventilator alarms. Low PIP usually indicates a leak in the ventilator circuit. High PIP may represent either an increase in airway resistance (e.g., blocked tube, bronchospasm, secretions) or a decrease in lung compliance (e.g., pulmonary edema, atelectasis, pneumothorax, pleural effusion, hyperinflation). These two states can be distinguished by performing an inspiratory hold test to measure a plateau pressure. This test is performed by pressing the hold button on the ventilator for approximately 5  seconds during inspiration without allowing the patient to exhale. This effectively eliminates the airway resistance from the measured pressure and allows independent assessment of pressure being developed in the lungs with a given tidal volume. This is equivalent to a measurement of lung compliance. If the plateau pressure rises along with PEEP, clinicians should look for correctable causes of decreased lung compliance.

Pneumothorax Pneumothorax is air in the otherwise “virtual space” between the parietal and visceral pleurae. The volume and pressure of the air in this space determine the clinical effect, which can range from asymptomatic to life‐threatening. Early signs and symptoms may be subtle and the condition is often not expected. It is therefore important for EMS clinicians to maintain a high index of suspicion for pneumothorax in a variety of presenting complaints and to be aware of potential predisposing or associated conditions (Box 6.3). Patients may present with pleuritic pain, sudden onset of a sharp pain, minimal to severe shortness of breath, and hypoxemia. Physical exam findings that should prompt consideration of pneumothorax include decreased or absent unilateral breath sounds, subcutaneous emphysema, or evidence of thoracic trauma. Pulse oximetry may or may not decrease depending on the size of the pneumothorax and the underlying pulmonary function and comorbidities of the individual patient. Similarly, EtCO2 may or may not appreciably change and its interpretation may be further complicated by compensatory hyperventilation or other comorbid conditions. A potentially more sensitive indicator in patients already receiving mechanical ventilation may be decreases in tidal volumes and increases in peak ­pressures. Ultrasound, if available, can also be used to identify pneumothorax. The one case that must be recognized clinically is a tension pneumothorax. This occurs when the intrathoracic pressure is so great that ventilation and venous return to the heart are obstructed, leading to respiratory compromise and shock. Besides unilateral decreased or absent breath sounds and subcutaneous emphysema, tracheal deviation and jugular venous distension may be present, but these should not be relied upon. Tension physiology must be recognized and treated immediately. Tension pneumothorax must be treated immediately with needle thoracostomy (needle decompression). Following skin cleansing, a large‐bore intravenous catheter (14 gauge or larger) should be inserted through the chest wall. When the needle enters the pleural space, a rush of air is often heard. The needle is then removed, leaving the catheter in place. Patients may require decompression with several needle thoracostomies in

Box 6.3  Conditions associated with pneumothorax

Trauma: •  Blunt •  Penetrating Medical: •  Acute asthma, especially if cardiac arrest •  Chronic obstructive pulmonary disease or other underlying lung disease •  Decompression‐associated barotrauma •  Marfan syndrome (or marfanoid habitus) •  Thoracic endometriosis (catamenial)

Oxygenation and ventilation

the prehospital environment as air reaccumulates in the pleural space. Needle decompression traditionally was performed in the second intercostal space at the mid‐clavicular line. Increasing evidence has shown that use of this site is prone to great vessel injury and failure to reach the pleural space [12–14]. Therefore, the Committee on Trauma of the American College of Surgeons now recommends using the fourth or fifth intercostal space between the anterior and mid‐axillary lines [15]. The chest wall should never be penetrated inferior to the nipple line due to risk of splenic or hepatic puncture. Treatment failure is typically due to using too short a needle or the catheter becoming occluded, which requires placement of additional needle(s). The hub of the catheter should either be left open or attached to a Heimlich (one‐way) valve. Finger thoracostomy is an additional technique for emergent chest decompression [16, 17]. Some EMS physicians consider this more reliable than needle decompression and less likely to cause lung injury. This technique should be performed only by experienced EMS clinicians with specific training and credentialing. The procedure includes antisepsis of skin, identification of mid‐axillary line just above the nipple line, making a 3–4 cm skin incision with a scalpel, spreading subcutaneous and intercostal tissue with hemostats, and puncture of parietal pleura with finger. The site should then be covered as for a sucking chest wound. Vigilance for reaccumulation of the pneumothorax is essential just as after needle decompression. Subsequently, the patient should receive a formal thoracostomy tube placed on suction with water seal. This is typically deferred until arrival in the emergency department but may be considered in the prehospital setting under special circumstances (e.g., protracted transport interval) and if appropriately credentialed clinicians and resources are available. A patient with a penetrating wound to the chest should have an occlusive dressing applied with watchful monitoring for the development of tension physiology. If tension develops, the dressing should be immediately vented. Some types of occlusive dressings provide one‐way air flow (pleural space to environment) to prevent the accumulation of gas in the pleural space that leads to a tension pneumothorax. Alternatively, an occlusive dressing may be left unsealed on one side or corner, which allows it to act like a one‐way flap valve. A frequent concern with the management of patients with pneumothorax is air transport. Boyle’s law (P1 × V1 = P2 × V2) describes that the air in the pleural space will expand with decreasing atmospheric pressure associated with increasing altitude. The EMS clinician should be aware that helicopter transport is not typically associated with sufficient altitude to have a significant clinical effect. For example, most medical helicopters fly at 1,000–3,000  feet above the ground. But at 6,000  feet, an altitude sometimes associated with instrument flight conditions (e.g., inclement weather), the increase in size would be about 25% (e.g., V2 = P1 × V1/P2 = 760 mmHg × 100  cc/609 mmHg = 125 cc). The clinical effects of such an increase in pneumothorax size are very much patient specific, depending

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on such things as initial volume, lung compliance, and comorbid conditions. Patients generally should not be flown in fixed‐ wing aircraft (especially without cabin pressurization) without tube thoracostomy decompression.

Summary Oxygenation and ventilation are distinctly different but interrelated physiological processes. In general, adequate oxygenation requires sufficient ventilation to deliver gas to alveolar spaces, where oxygen can then enter pulmonary capillaries for transport to peripheral tissues. Pulse oximetry is a useful tool, except in cases of carbon monoxide poisoning, to help determine the extent of tissue oxygenation. Patients with respiratory distress or SpO2 less than 94% should receive supplemental oxygen. However, use of oxygen should not be indiscriminate. Ventilation is about gas moving in and out of the lungs. Clearly, it can occur without oxygen, and, in that sense, is a distinct process. The adequacy of ventilation is generally assessed in terms of minute ventilation. Waveform capnography is a useful tool to both monitor ventilation and evaluate its effectiveness. NIPPV may provide needed support to an awake patient with inadequate ventilation but intact respiratory drive. Mechanical ventilation is the maximum ventilatory support tool. Especially in a dynamic prehospital environment, vigilant monitoring is imperative to promptly identify and address deficiencies in ventilation and oxygenation and complications arising from their treatment.

References 1 Chan ED, Chan MM, Chan MM. Pulse oximetry: understanding its basic principles facilitates appreciation of its limitations. Respir Med. 2013; 107:789–99. 2 Barker SJ, Curry J, Redford D, Morgan S. Measurement of carboxyhemoglobin and methemoglobin by pulse oximetry. Anesthesiology. 2006; 105:892–7. 3 Samraj RS, Nicolas L. Near infrared spectroscopy (NIRS) derived tissue oxygenation in critical illness. Clin Invest Med. 2015;38(5): E285–95. 4 McSwain SD, Hamel DS, Smith PD, et  al. End‐tidal and arterial carbon dioxide measurements correlate across all levels of physiologic dead space. Respir Care. 2010; 55:288–93. 5 Byrne AL, Bennett M, Chatterji R, et  al. Peripheral venous and arterial blood gas analysis in adults: are they comparable? A systematic review and meta‐analysis. Respirology. 2014; 19:168–75. 6 Kodali BS. Capnography outside the operating rooms. Anesthesiology. 2013; 118:192–201. 7 Berg RA, Hemphill R, Abella BS. Part 5: Adult Basic Life Support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010; 122:S685–705. 8 Austin MA, Wills KE, Blizzard L, et al. Effect of high flow oxygen on mortality in chronic obstructive disease patients in the prehospital setting: randomized controlled trial. BMJ. 2013; 341:c5462.

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9 Williams B, Boyle M, Robertson N, Giddings C. When pressure is positive: a literature review of the prehospital use of ­continuous  positive airway pressure. Prehosp Disaster Med. 2013; 28:52–60. 10 Siegler J, Kroll M, Wojcik S, Moy HP. Can EMS providers provide appropriate tidal volumes in a simulated adult‐sized patient with a pediatric‐sized bag‐valve‐mask? Prehosp Emerg Care. 2017; 21:74–8. 11 Acute Respiratory Distress Syndrome Network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000; 342:1301–8. 12 Inaba K, Ives C, McClure K, et  al. Radiologic evaluation of alternative sites for needle decompression of tension pneumothorax. Arch Surg. 2012; 147:813–18.

13 Sanchez LD, Straszewski S, Saghir A, et al. Anterior versus lateral needle decompression of tension pneumothorax: comparison by computed tomography chest wall measurement. Acad Emerg Med. 2011; 18:1022–6. 14 Inaba K, Karamanos E, Skiada D, et al. Cadaveric comparison of the optimal site for needle decompression of tension pneumothorax by prehospital care providers. J Trauma. 2015; 79:1044–8. 15 American College of Surgeons, Committee on Trauma. Advanced Trauma Life Support: Student Course Manual. Chicago, IL: American College of Surgeons, 2018. 16 Jodie P, Hogg K. BET 2: Pre‐hospital finger thoracostomy in patients with chest trauma. Emerg Med J. 2017; 34:419. 17 Jodie P, Kerstin H. BET 1: Pre‐hospital finger thoracostomy in patients with traumatic cardiac arrest. Emerg Med J. 2017; 34:417–18.

SECTION III

Circulation

CHAPTER 7

Hypotension and Shock Francis X. Guyette, Raymond L. Fowler, and Ronald N. Roth

Introduction Shock is a life‐threatening physiological state characterized by decreased tissue perfusion and end‐organ tissue dysfunction, and is a significant predictor for complications including death  [1]. The presence of shock must be recognized and therapeutic interventions must be started early to prevent progression. Unfortunately, identification and treatment of shock in the out‐of‐hospital setting are fraught with many difficulties and potential pitfalls. Patient assessment is often limited by the challenging environment. The tools available for the diagnosis and treatment of shock in the field are limited. Even when shock is properly identified, the most appropriate management is often unknown or the subject of debate. In the field, identification of shock relies primarily on recognition of signs and symptoms, including tachycardia, poor skin perfusion, and altered mental status. Note that hypotension, arbitrarily defined at a systolic blood pressure (sBP) of less than 90 mmHg, is not an adequate definition of shock and may not adequately reflect the onset of tissue hypoperfusion [2]. Unfortunately, the early stages of compensated shock, with only subtle alterations in physical findings, are easily overlooked or misinterpreted by clinicians. Physiological changes associated with age, pregnancy, or treatment for medical conditions such as beta‐blockers for hypertension, may also mask or alter the body’s compensatory responses. As a result, the patient with severe shock may present with near‐normal vital signs.

Pathophysiology Shock is a complex physiological process defined as the widespread reduction in tissue perfusion leading to cellular and organ dysfunction and death. In the early stages of shock, a series of complex compensatory mechanisms act to preserve

critical organ perfusion [3]. In general, the following relationships drive this process:

Blood pressure Cardiac output

cardiac output peripheral vascular resistaance heart rate stroke volume

Any condition that lowers cardiac output or peripheral vascular resistance may decrease blood pressure. Alterations of heart rate (very low or very high) can lower cardiac output, and hence can reduce blood pressure secondary to decreased cardiac filling. Decreasing stroke volume may lower cardiac output with a possible reduction in perfusion as well. Cardiac output may be reduced by lower circulating blood volume (e.g., hemorrhage or dehydration), by damage to the heart (e.g., myocardial infarction or myocarditis), or by conditions obstructing blood flow through the thorax (e.g., tension pneumothorax, cardiac tamponade, or extensive pulmonary embolism). To aid in the evaluation and treatment of shock, it is often useful for the physician and emergency medical services (EMS) personnel to categorize the etiology of the shock condition [4]. Most EMS clinicians are familiar with the “pump‐pipes‐fluid” model of the cardiovascular system, with the pump representing the heart, pipes representing the vascular system, and fluid representing the blood [5]. Categorizing shock into four categories may help to organize assessments and management approaches. Accurate physical assessment is vital for the EMS clinician to determine the categories of the shock state (Table 7.1).

Evaluation The diagnosis of shock depends on a combination of key historical features and physical findings in the proper clinical setting. For example, tachycardia and hypotension in an elderly patient

Emergency Medical Services: Clinical Practice and Systems Oversight, Third Edition. Volume 1: Clinical Aspects of EMS. Edited by David C. Cone, Jane H. Brice, Theodore R. Delbridge, and J. Brent Myers. © 2021 NAEMSP. Published 2021 by John Wiley & Sons, Inc.

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Table 7.1  Categories of shock Type of shock

Disorder

Examples

Comments

Hypovolemic

Decreased intravascular fluid volume

A. External fluid loss Hemorrhage Gastrointestinal losses Renal losses Cutaneous loss B. Internal fluid loss Fractures Intestinal obstruction Hemothorax Hemoperitoneum Third spacing

Hypovolemic shock states, especially hemorrhagic shock, produce flat neck veins, tachycardia, and pallor

Distributive

Increased “pipe” size: peripheral vasodilation

A. Drug or toxin induced B.  Spinal cord injury C. Sepsis D.  Anaphylaxis E.  Hypoxia/anoxia

Distributive shock states usually show flat neck veins, tachycardia, and pallor. Neurogenic shock due to a cervical spinal cord injury tends to show flat neck veins, normal or low pulse rate, and pink skin

Obstruction

Pipe obstruction

A. Pulmonary embolism B.  Tension pneumothorax C. Cardiac tamponade D. Severe aortic stenosis E.   Venocaval obstruction

Obstructive shock states tend to produce jugular venous distension, tachycardia, and cyanosis

Cardiogenic

“Pump” problems

A. Myocardial infarction B.  Arrhythmias C. Cardiomyopathy D.  Acute valvular incompetence E.  Myocardial contusion F.  Myocardial infarction G. Cardiotoxic drugs/poisons

Cardiogenic shock states tend to produce jugular venous distension, tachycardia, and cyanosis

with fever, cough, and dyspnea may represent pneumonia with septic shock. Hemorrhagic shock should be suspected in a ­middle‐aged man with epigastric pain, hematemesis, melena, and hypotension. Hypotension, tachycardia, and an urticarial rash in a victim of a recent bee sting strongly suggest distributive shock secondary to anaphylaxis. Obstructive shock precipitated by a tension pneumothorax should be suspected in a patient with hypotensive trauma who has unilateral decreased breath sounds and tracheal deviation to the opposite side. An important problem in the prehospital diagnosis of shock is the frequent inaccuracy of field assessment. For example, in one analysis, emergency medical technicians (EMTs) made vital sign errors more than 20% of the time [6]. Subsequently, when critical medical decisions are based on the data gathered in the field, multiple assessments should be performed. EMS clinicians should look for the signs and symptoms of system‐wide reduction in tissue perfusion, such as tachycardia, tachypnea, mental status changes, and cool, clammy skin (Box 7.1). When available, adjunctive technologies can provide improved recognition and assessment of shock by revealing reductions in expired CO2, hypovolemia, obstruction or poor cardiac contractility, and elevated serum lactate levels. Vital signs that fall outside of expected ranges must be correlated with the overall clinical presentation. Vital signs have a broad range of normal values. They must be interpreted in the

Box 7.1  Signs and symptoms of shock

Cardiovascular •  Tachycardia, arrhythmias, hypotension •  Jugular venous distension in obstructive and cardiogenic shock states •  Tracheal deviation away from the affected side in tension ­pneumothorax Central nervous system •  Agitation, confusion •  Alterations in level of consciousness •  Coma Respiratory •  Tachypnea, dyspnea Skin •  Pallor, diaphoresis •  Cyanosis (in obstructive and cardiogenic shock cases), mottling

context of the individual patient. A petite 45‐kg, 16‐year‐old girl with lower abdominal pain with a reported blood pressure of 88 mmHg systolic by palpation may have a ruptured ectopic pregnancy, or may just be at her baseline blood pressure. An elderly patient with significant epistaxis may be hypertensive due to catecholamine release and vasoconstriction despite being relatively volume depleted. Consideration should be given to

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patient age, comorbid conditions, and medications that may affect the interpretation of vital signs. In the noisy field environment, EMS clinicians often measure blood pressure by palpation rather than auscultation. Blood pressure by palpation provides only an estimate of sBP  [7]. Without an auscultated diastolic pressure, the pulse pressure (the difference between systolic and diastolic pressure) cannot be calculated. A pulse pressure less than 30 mmHg or 25% of the sBP may provide an early clue to the presence of hypovolemic or obstructive shock [3]. Conversely, a wide pulse pressure may be indicative of distributive shock. Dividing the pulse rate by the sBP typically produces a ratio of approximately 0.5 to 0.8, which is called the “shock index.” When that ratio exceeds 0.9, then a shock state may be present [8]. Previously healthy patients with acute hypovolemic shock may maintain relatively normal vital signs with up to 25% blood volume loss [3]. Sympathetic nervous system stimulation with vasoconstriction and increased cardiac contractility may result in normal blood pressure in the face of decreasing intravascular volume, especially in the pediatric population. In some patients with intra‐abdominal bleeding (e.g., ruptured abdominal aneurysm, ectopic pregnancy), the pulse may be relatively bradycardic despite significant blood loss [9]. EMS personnel may equate “normal” vital signs with normal cardiovascular status  [5]. The field team may be lulled into a false sense of security initially if the early signs of shock are overlooked, and then they are caught off guard when the patient’s condition dramatically worsens during transport. Following trends in the vital signs may also help identify shock before patients reach abnormal vital sign triggers. Early recognition and aggressive treatment of shock may prevent progression to the later stages of shock that can result in the death of potentially salvageable patients [10]. Prehospital hypotension may predict in‐hospital morbidity and mortality in both trauma and medical patients  [11–13]. Medical patients may have a 30% higher mortality if there has been prehospital hypotension  [11]. Trauma patients with prehospital hypotension have similar outcomes, even with subsequent normotension in the emergency department. This emphasizes the importance and value of accurate in‐field assessments, so that the next echelon of patient care can be informed and aware of the potential for critical illness or injury. Despite their questionable value, orthostatic vital signs are often evaluated in the emergency department, and occasionally in the field. A positive orthostatic vital sign test for pulse rate would result in a pulse increase of 30 beats/min after 1 minute of standing [14]. Symptoms of lightheadedness or dizziness are considered a positive test. Occasionally, orthostatic vital signs are performed serendipitously by the patient who refuses treatment while lying down, then stands up to leave the scene, and suffers a syncopal or near‐syncopal episode. This demonstration of orthostatic hypotension is often helpful in convincing the patient to consent to treatment and transport. However, EMS clinicians should not routinely obtain orthostatic vital signs,

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and they should not equate absence of orthostatic response with euvolemia. Capillary refill, an easy test to perform in the field setting, is not a useful test for mild‐to‐moderate hypovolemia [15]. Moreover, environmental considerations, such as cold temperatures and adverse lighting conditions, also affect the accuracy of this technique for shock assessment. On‐scene estimates of blood loss by EMS clinicians may influence therapeutic interventions, including fluid administration. However, studies suggest that field clinicians are not accurate at estimating spilled blood volumes [16]. Hypoxia is a common manifestation of shock states. Patients in various stages of exsanguination may not have sufficient blood volume to perfuse adequately the body with oxygen. Unfortunately, pulse oximetry alone cannot detect the adequacy of oxygen delivery. Pulse oximetry may fail to detect a pulse (and give inaccurate oxygen saturation readings) when blood flow is reduced [15, 17]. Like pulse oximetry, capnography may also serve as an important tool in the evaluation and treatment of shock in the prehospital setting [18–21]. Exhaled end‐tidal carbon dioxide (EtCO2) levels vary inversely with minute ventilation, providing feedback regarding the effect of changes in ventilatory parameters  [22, 23]. Additionally, changes in EtCO2 are virtually immediate when the airway is obstructed or the endotracheal tube becomes dislodged  [24]. EtCO2 concentration may be influenced by factors other than ventilation. For example, levels are reduced when pulmonary perfusion decreases in shock, cardiac arrest, and pulmonary embolism [25–27]. EtCO2 is most useful as an indicator of perfusion when minute ventilation is held constant (e.g., when mechanical ventilation is applied)  [19, 25]. Under these conditions, changes in EtCO2 levels reliably indicate changes in pulmonary perfusion. In any patient suffering from a potential shock state, diminished EtCO2 should be a warning of the critical nature of the patient’s problem.

Additional Modalities to Assess Shock Use of portable ultrasound in the field can facilitate the recognition of immediately life‐threatening causes of shock including intra‐abdominal bleeding and cardiac tamponade. Many EMS agencies, primarily air medical services, have deployed point‐ of‐care ultrasound for field evaluations, including the focused assessment by sonography in trauma (FAST) examination, the EFAST incorporating a lung assessment for pneumothorax, and various shock protocols to assess volume status, a limited cardiac exam, or reversible causes of shock  [28]. Ultimately, the EMS medical director must determine if the cost and effort required to acquire the equipment, training, and performance of these skills translates into improved patient outcomes. The use of field ultrasound has the potential to worsen patient outcome if the procedure delays the time to definitive care, does not influence patient destination or care, or interferes with

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maintenance of critical parameters such as airway, ventilation, and hemorrhage control. There is growing interest in the use of biomarkers that can be employed to identify, monitor, and predict the outcome in shock [29]. Point‐of‐care testing devices make measurement of biomarkers in the field an attractive option. Elevation of serum lactate may reflect anaerobic tissue metabolism in acute sepsis and shock  [29, 30]. In the setting of infection, elevated lactic acid may indicate septic shock and the need for early goal‐ directed therapy. Elevated venous lactate is associated with increased mortality risk and the need for resuscitative care in trauma patients. Prehospital trauma research indicates that an elevated lactate level in the setting of trauma predicts the need for aggressive resuscitation  [31]. Serial lactate measurements may indicate the effectiveness of ongoing resuscitation [32]. Prehospital telemedicine holds the promise of providing access to the highest levels of care to patients and field clinicians by using EMS as a “telemedicine facilitator” (see Chapter 73). In the event that the patient is in profound shock or extremis, EMS clinicians can engage a wide range of expertise to help manage the patient [33]. Artificial intelligence technology (“assisted intelligence”) is also uniquely suited to prehospital medicine. Diagnostic algorithms can interpret trends in data and identify patients who are in compensated shock prior to clinical deterioration  [34]. Further recognition of those patterns may lead to individualized care in the form of direct decision support informing EMS clinicians in how to best care for their patients.

Treatment All treatment approaches to shock must include the following basic principles: 1.  Perform the initial assessment. 2.  Deal with issues identified during the initial assessment such as airway, breathing, and circulation issues, including active external bleeding. 3.  Determine the need for early definitive care: –– hemorrhage control and volume resuscitation –– needle thoracostomy –– electrical therapy for dysrhythmia –– invasive airway management. 4.  Maintain adequate oxygen saturation (SaO2 greater than 94%). 5.  Ensure adequate ventilation without hyperventilating. 6.  Monitor vital signs, ECG, oxygen saturation, capnography, and lactate (if available). 7.  Prevent additional injury or exacerbation of existing medical conditions. 8.  Protect the patient from the environment. 9.  Determine the etiology of the shock state and treat accordingly. 10.  Notify and transport to an appropriate facility.

Often the etiology of the patient’s shock state and the initial management options are clear from the history. For example, the out‐of‐hospital treatment of a young, previously healthy college student with hypotension secondary to severe vomiting and diarrhea includes intravenous (IV) fluids. The treatment of cardiogenic shock in an unresponsive elderly patient with ventricular tachycardia requires prompt cardioversion. Occasionally, the primary problem may be strongly suspected but not readily diagnosable or treatable in the field (e.g., pulmonary embolism). Less frequent, but most difficult to manage, is the patient in shock without an obvious cause. With the understanding of the limited treatment options in the prehospital setting (primarily fluids, inotropic agents, and vasopressors), field treatment may be individualized for the four categories of shock: hypovolemic, distributive, obstructive, and cardiogenic. Hypovolemic Shock Hypovolemic shock is the result of significant loss of intravascular volume resulting in hypotension. The many etiologies of hypovolemic shock include external fluid loss and shifting of fluids from the vascular system to a nonvascular body compartment. The treatment of hypotension and shock caused by hypovolemia is relatively straightforward. External bleeding should be controlled. Fluid replacement via vascular access is the mainstay of treatment. Unfortunately, the ideal fluid for the resuscitation of hypovolemic shock and the amount of fluids that should be provided remain controversial [35–37]. Distributive Shock Distributive shock, characterized by a decrease in systemic vascular resistance, is associated with abnormal distribution of microvascular blood flow [38]. Causes of distributive shock include sepsis, anaphylaxis, medication overdose, and acute neurological injury. The treatment of distributive shock involves the combination of vasoactive medications, which constrict the dilated vasculature, and fluids, which fill the expanded vascular tree. Commonly used vasoactive medications for distributive shock in the field include epinephrine, norepinephrine, and dopamine. Although epinephrine is easily administered via several routes (e.g., intramuscular, intravenous bolus, or infusion), the drug has significant adverse effects. Norepinephrine infusions are associated with a lower incidence of cardiac dysrhythmias than either dopamine or epinephrine  [39]. In addition, studies of cardiogenic shock suggest increased mortality associated with dopamine [40]. However, continuous infusions may be difficult to maintain without special infusion pumps. Anaphylaxis is a serious, generalized allergic or hypersensitivity reaction that can be of rapid onset (minutes to hours) and is potentially fatal. Mediators that have been implicated in the pathophysiology of anaphylaxis target the skin, digestive, respiratory, and cardiovascular systems (see Chapter  21)  [41]. With respect to the cardiovascular system, these mediators can precipitate hypotension, tachycardia, vasodilatation, and increased vascular permeability. These effects result in a decrease

Hypotension and Shock

in peripheral vascular resistance and an expanded vascular tree, precipitating distributive shock. In reality, mediators also contribute to decreased cardiac inotropic and chronotropic effects and fluid loss via edema, contributing to components of cardiogenic and hypovolemic shock, respectively [41]. The classic presentation of anaphylaxis – urticaria, shortness of breath, and hypotension precipitated by a bee sting, medication injection, or ingestion of a previously known allergen (e.g., peanut ingestion) – is rarely missed in the field. However, anaphylaxis presenting with hypotension but without a rash or an identifiable precipitant would be difficult to identify. Epinephrine is a nonselective agonist of all adrenergic receptors. These receptors are present within organ systems affected by anaphylaxis [42, 43]. By increasing peripheral resistance via α‐1 receptors and increasing cardiac output via β‐1 receptors, epinephrine helps to reverse the distributive shock state. The treatment of anaphylaxis is the administration of epinephrine as soon as the condition is recognized. The initial dose is typically injected intramuscularly in the lateral thigh as additional monitoring and intravenous access are obtained. The administration of antihistamines and steroids should never delay the administration of epinephrine. Prompt prehospital epinephrine injection is associated with a lower risk of hospitalization and fatality [41, 44]. Obstructive Shock Blood pressure is dependent on the maintenance of cardiac output. Any condition that inhibits venous return can be anticipated to decrease cardiac output and induce shock. A number of clinical conditions exist in which venous return to the thorax and heart are reduced. These conditions include tension ­pneumothorax, cardiac tamponade, and massive pulmonary embolism. Obstructive causes of shock are often difficult to diagnose and treat. Clinical signs of decreased venous return include neck vein distension and cyanosis, often in the setting of shock. Identifying these signs requires the clinician to complete an efficient, organized assessment. Shock in the setting of neck vein distention and cyanosis should lead the EMS clinician to suspect an obstructive condition as the cause. If possible, the obstruction should be resolved, such as by decompression of a tension pneumothorax. However, when the primary problem cannot be treated successfully in the field (e.g., massive pulmonary embolus or cardiac tamponade), intravenous fluids may be helpful in increasing preload and temporizing the condition. Cardiogenic Shock Causes of cardiogenic shock include arrhythmias, valvular heart disease, infection, cardiotoxic agents, and most commonly myocardial infarction. As a result, cardiogenic shock requires individualized treatment. Early revascularization among patients with myocardial infarction improves long‐term survival  [45]. Cardiogenic shock from severe dysrhythmias should be treated with appropriate electrical or pharmacological therapy. “Pump

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failure” is often difficult to diagnose and to treat without invasive monitoring. Adult patients without obvious pulmonary edema may benefit from fluid challenges of approximately 200‐300 mL of crystalloid. An improvement in the patient’s condition suggests that enhancing preload would be beneficial. A worsening of the patient’s condition with a modest fluid challenge, or the presence of obvious pulmonary edema on initial evaluation, suggests that fluid therapy would not be helpful. In such settings, treatment with inotropic agents or vasopressors, such as dobutamine or norepinephrine, would be more appropriate. Intravenous infusions are often difficult to manage in the field without an infusion pump and must be monitored closely. Less common causes of cardiogenic shock include beta‐ blocker and calcium channel blocker toxicity. Such agents block sympathomimetic receptors, impairing the body’s normal compensatory responses. These patients present with profound bradycardia and shock, often refractory to sympathomimetic treatment and fluid challenges due to the receptor blockade. Additional therapies may include IV glucagon or calcium, which facilitate heart rate stimulation and vasoconstriction through alternative cellular receptors. EMS agencies carry them for the treatment of hypoglycemia and hyperkalemia, respectively. Shock of Unclear Etiology In some clinical scenarios, the primary etiology for the patient’s shock state may be difficult to determine despite careful history taking and physical examination. Focused ultrasound may be helpful identifying hypovolemia (inferior vena cava), hemorrhage (FAST, aortic exam), obstructive shock (pneumothorax, cardiac tamponade, right heart strain consistent with pulmonary embolus), or cardiogenic shock (hypokinetic wall, valvular dysfunction), providing additional information for consideration of the cause of the condition. The primary treatment decision is whether to give fluids. In hypovolemic, distributive, and obstructive shock, fluids are an appropriate initial treatment for hypotension or other signs of shock. The caveat is that indiscriminate administration of large volumes of IV fluids may not improve patient outcomes. Some cases of cardiogenic shock may respond to fluids. However, fluids should not be given to patients in cardiogenic shock with pulmonary edema. When fluids are contraindicated, or they fail to improve the patient’s response, vasopressors or ionotropic agents may be indicated. The EMS clinician should exercise caution with respect to worsening cardiogenic shock when using vasopressors that increase afterload. Ionotropic agents (i.e., dobutamine) may also precipitate hypotension through afterload reduction. Fluids are also not appropriate when cardiogenic shock has been precipitated by a treatable arrhythmia. Response to fluid challenges (where appropriate) should dictate whether additional fluid challenges should be given or whether a trial of a sympathomimetic agent should be used. Some patients with shock may remain refractory to initial attempts at resuscitation. This response may reflect the need for definitive care in the hospital (e.g., thoracotomy, laparotomy). If, after vigorous field treatment, the patient remains hypotensive,

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it is prudent to consider other etiologies for the hypotension, including adrenal suppression, hypothyroidism, or various toxic agents. In some cases, patients with profound acidosis will not respond to vasopressors or inotropic agents, as their receptors are pH dependent. Administration of sodium bicarbonate, 1 mEq/kg IV, may improve perfusion by buffering acidosis and improving sensitivity to vasopressor activity. Use of vasopressin to supplement other vasopressors may also improve perfusion as it increases systemic vascular resistance even during acidosis. In cases of refractory shock or adrenal suppression, administration of steroids may also be of benefit. Hydrocortisone is ideal for this purpose, as patients may benefit from both mineralocorticoid and glucocorticoid properties. Methylprednisolone is far more widely available in the prehospital environment and may have some limited utility in refractory shock. Patients exposed to potent cellular toxins such as cyanide or hydrogen sulfide may present with refractory shock, requiring therapy with agent‐specific antidotes. Consider transport to a facility capable of mechanical support for patients with refractory shock. Pediatric Shock Recognition and management of shock in the pediatric population follow the same general principles as in adults, with a few notable exceptions [46]. Children in shock more commonly present with a low cardiac output and a relatively high systemic vascular resistance (SVR). This has been described as “cold shock,” as opposed to the low‐SVR state or “warm shock” frequently seen in adults. Children presenting in distributive shock usually require more aggressive fluid resuscitation with volumes of 60 cc/kg or more [47]. If children fail to respond to the initial fluid resuscitation, epinephrine is preferred as the first‐line vasopressor to counter the relatively low cardiac output seen in pediatric shock. Additional support for patients with low SVR and wide pulse pressure may be provided with norepinephrine or vasopressin. Dobutamine may provide inotropic and chronotropic support in patients with very low cardiac output and improve delivery of oxygen to tissues. Following initial treatment with fluids and vasoactive agents, pediatric patients may also benefit from adjunctive therapies for shock [46]. Early airway management should be considered, as children may use up to 40% of their cardiac output to support the work of breathing. Ketamine is the preferred induction agent, as it preserves cardiac output and will not result in the hypotension or adrenal suppression potentially seen with other induction agents. Hydrocortisone should be administered to children with adrenal insufficiency. Transport to an appropriate facility with pediatric critical care should be an important consideration.

Shock Interventions Fluids The treatment of shock must be customized to the individual EMS agency and geographic location. In the urban setting with

short transport times, the victim of a penetrating cardiac wound would probably benefit most from airway maintenance and rapid transport to the hospital. IV or intraosseous (IO) access could be attempted en route, if it will not delay delivery to definitive care [48]. On the other hand, with longer transport times in the rural setting, a similar patient might benefit from a carefully titrated crystalloid volume infusion during transport. Fluid delivery could be initiated while the patient is en route to the hospital, thereby prolonging neither scene time nor time until definitive care  [49]. In the patient who presents a difficult IV access problem, IO infusions may be attempted. Placing the IO needle in the humeral head may result in faster infusion rates than the proximal tibia. The ideal fluid for use in the field would be small in volume, portable, non‐allergenic, inexpensive, and would not interfere with clotting factors [35]. Unfortunately, this ideal fluid has yet to be discovered. Isotonic crystalloids are currently the fluid of choice for out‐of‐hospital resuscitation in the United States [1, 36, 49, 50]. Among critically ill patients requiring large volume resuscitation, there is a benefit of balanced crystalloid solutions over normal saline but there is insufficient evidence to recommend them for initial resuscitation. Moreover, as they are relatively hypotonic, they may be detrimental in traumatic brain injury [51]. Crystalloid fluids are inexpensive and widely available but may contribute to dilutional coagulopathy, hyperchloremic acidosis, and hypothermia when given in large volumes. Whole blood would arguably provide the greatest benefit as a resuscitative fluid in the setting of hemorrhagic shock but lacks availability due to issues of cost, storage, and limited supply. Use of blood products in the prehospital environment is generally limited to a few air medical services and EMS systems that carry blood for administration to victims of hemorrhagic shock. Prehospital administration of plasma reduces mortality in trauma victims but suffers the same limitations as blood administration [52]. Freeze‐ dried plasma that has a long shelf life and can be made readily available is being used outside the United States. It may become important in prehospital resuscitation [53–55]. The optimal volume of fluids to administer in the field is not known, especially in the trauma victim with uncontrolled hemorrhage  [36, 48, 49, 56–61]. Current trauma algorithms call for the administration of IV fluid for all major trauma victims. Insufficient fluid volume may allow exposure to increasing “doses” of hypotension, leading to worsening mortality from hypoperfusion [62]. Evidence suggests, however, that attempts at normalization of blood pressure with a large volume of fluids in a patient with uncontrolled hemorrhagic shock may be deleterious to patient outcome. Complications may include acidosis, dislodgement of blood clots, and dilution of clotting factors  [56]. In such a patient, it appears that the best course is to give sufficient crystalloid to maintain perfusion (such as a peripheral pulse and mentation) pending the delivery of the patient to the appropriate facility [57–59]. Extremity veins are the typical sites for venous access. External jugular veins are also useful in many patients. Few

Hypotension and Shock

EMS systems use central venous access. IO access has become so important as a method of vascular access that it is supported by a position statement from the National Association of EMS Physicians [63]. In patients in extremis or cases in which peripheral access is not immediately available, IO access may be preferred. Ventilation The patient in shock may require assisted ventilation. Venous return requires a relative negative pressure in the right atrium to ensure return of blood to the heart. Assisted ventilation using any of the typical techniques, such as bag‐valve‐mask ventilation, endotracheal intubation, or supraglottic devices, results in an increase in airway pressure, raising intrathoracic pressure. Patients in shock from any cause are extremely sensitive to increases in intrathoracic pressure. Studies in a swine hemorrhagic shock model showed that even modest increases in the rate of positive‐ pressure ventilation significantly reduce brain blood flow and oxygenation [64]. EMS personnel must carefully control the rate of assisted positive‐pressure ventilation in the shock patient, as overventilation is common. Generally, a one‐handed squeeze on the ventilation bag at a rate of approximately once every 8 seconds is reasonable for an adult, producing a minute ventilation of about 5 L/min. Minute ventilation should be adjusted to ensure an EtCO2 between 35 cmH2O and 45 cmH2O. Vasopressors Administration of vasoactive medications in combination with volume resuscitation may be required to reverse systemic hypoperfusion from shock. These agents increase vasoconstriction and may support inotropy and chronotropy  [65]. Although a wide variety of vasoactive agents are available in the hospital, the drugs carried by prehospital services are limited by local, regional, or statewide protocols or regulations. Historically, most services carried epinephrine and dopamine. Norepinephrine is increasingly used in place of dopamine, following randomized controlled trials demonstrating improved survival with norepinephrine over dopamine in cardiogenic and distributive shock  [40, 66]. Vasopressin, a potent vasoconstrictor that is effective at low pH, is available in some systems. It may be beneficial in patients with shock refractory to norepinephrine [67]. Among patients with hemorrhagic shock, vasopressin decreases blood product requirements, but additional studies are necessary to demonstrate improved patient‐centered outcomes [68]. The choice of vasopressor depends on the suspected underlying pathological process and the patient’s response to therapy. Unfortunately, in the field, the etiology of the shock state is often unclear, and close monitoring of vital signs is difficult. The administration of vasoactive agents in the field has multiple challenges including the need to calculate weight‐based dosages, mix and dilute drugs, and administer precise volumes. EMS clinicians should use calculators or templates or seek direct medical oversight. When available, portable IV infusion pumps should be used to ensure accurate and precise medication administration.

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An alternative to vasopressor infusions are boluses of vasopressors used to temporize patients in profound shock or peri‐arrest until the patient can be stabilized with volume or vasopressor infusions. Extrapolated from anesthesia practices to the emergency department, hypotension may be treated with boluses of phenylephrine or epinephrine [69]. Prehospital “push dose” vasopressors increase blood pressure but may increase mortality [70, 71]. Further research is necessary to identify the appropriate patient population, agent, and dose for prehospital push dose vasopressors. Other Medications Other agents used for shock resuscitation include corticosteroids, antibiotics, and inotropic agents  [72–74]. The role of these agents in out‐of‐hospital shock management remains unclear. It would be reasonable to administer steroids to shock victims with known adrenal insufficiency or chronic steroid use and refractory hypotension.

Controversies Shock Science The lack of definitive studies on the treatment of shock by EMS clinicians leaves the medical director without clear guidelines for treating these patients. As a result, considerable controversy exists with respect to many areas of the treatment of shock (especially traumatic shock) in the prehospital setting. The benefit of an EMS procedure must be weighed against potential risks. A major pitfall associated with shock treatment is that resuscitative interventions may delay definitive care. Pantridge and Geddes demonstrated that some aspects of definitive care, such as defibrillation and arrhythmia management, should be delivered in the field [75]. However, for trauma victims with uncontrolled internal hemorrhage, definitive care can only be provided in the hospital. Any field procedure that significantly delays delivery of definitive care must have proven value. For example, pneumatic anti‐shock garments were implemented in clinical EMS practice without supporting evidence, and then a formal assessment revealed that they actually worsened patient outcome in certain circumstances, particularly thoracic injury [76]. Sepsis Septic shock, an example of distributive shock, is characterized by life‐threatening organ dysfunction caused by a dysregulated host response to infection [77]. As one of the leading causes of death in the United States, EMS clinicians encounter patients with severe sepsis at a crude rate of 3.3 per 100 EMS patients, higher than that of acute myocardial infarction (2.3 per 100) or stroke (2.2 per 100) [78]. An estimated 30‐40% of all severe sepsis hospitalizations arrive at the emergency department via EMS [78–80]. EMS systems play an important role in the care of patients with cardiovascular disease, trauma, and stroke.

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However, a similar role with respect to the care of patients with sepsis has yet to be achieved. Like stroke and acute myocardial infarction, sepsis is a time‐sensitive illness with demonstrated improved survival with early treatment [78, 81, 82]. There are multiple challenges associated with identifying sepsis in the prehospital setting. EMS clinician knowledge and understanding of the condition is the first barrier  [83]. EMS protocols may include the presence of hypotension, respiratory distress, and altered mental status as criteria for invoking sepsis protocols. However, these findings may be missing in the prehospital patient with sepsis  [79, 84, 85]. While hypotension and fever are typical findings in septic patients, their presence is often missed in the prehospital setting [79, 86]. In addition, patients with alterations in physiological variables identified in the emergency department may have had normal vital signs in the field [79]. The lack of diagnostic tools in the field (e.g., point‐of‐care lactate, white blood cell count, urinalysis, chest x‐ray) makes the diagnosis of sepsis and determining a potential source of infection more challenging in the field. Of note, ETCO2 has been proposed as a surrogate for serum lactate levels. Inversely correlating with serum lactate, lower ETCO2 levels have been identified in patients with serious penetrating trauma and sepsis [32, 87–89]. Finally, attempts at developing prehospital scores or tools to identify patients with sepsis have had mixed results [82, 90–92]. In general, there is considerable variation in the sensitivity for EMS identification of sepsis, and EMS clinician impression alone is poor in the identification of these patients [93]. The emergency department care of the septic patient includes the early initiation of goal‐directed volume resuscitation and early antibiotics  [30, 81]. Vasopressors are initiated for fluid refractory hypotension or in patients with fluid overload, to maintain a mean arterial pressure of 65‐70  mmHg.  The role of empiric antibiotics in the field for presumed sepsis has yet to be defined and antibiotic administration is not in the scope of practice for many EMS clinicians. Fluids, vasopressors, and hemodynamic monitoring (vital signs) are generally achievable in the prehospital setting. A prehospital protocol for the treatment of patients with suspected sepsis not in congestive heart failure may include repeat fluid boluses of 500  mL, with reassessment between each bolus for blood pressure responsiveness and signs of respiratory distress secondary to fluid overload  [85, 87]. While crystalloids are the fluid of choice for the initial resuscitation of the septic patient, balanced salt solutions (e.g., lactated Ringer’s) may be preferred over normal saline [94]. The solution used for resuscitation will often be directed by what is carried on the ambulance. Prehospital fluid administration of any volume and even IV placement alone have been associated with decreased odds of in‐hospital mortality  [95]. In patients with hypotension secondary to sepsis, prehospital administration of fluids resulted in a lower in‐hospital mortality as compared to those without hypotension, but longer scene times resulted [93].

Vasopressors are an important part of the treatment of sepsis. Norepinephrine, epinephrine, and vasopressin can be used as single agents or in combination [96]. However, the use of dopamine is associated with increased mortality in septic shock [96]. Unfortunately, the administration of these vasoactive agents is best done via medication pumps. These pumps are expensive, require additional training for EMS clinicians, and are not in the scope of practice for some. Despite the many challenges, patients identified with sepsis in the prehospital setting have a decreased mortality compared with patients diagnosed later in the hospital [78, 82, 97]. There are three key steps for EMS to improve sepsis‐related outcomes: 1) Maintain high suspicion and recognize the potential for sepsis; 2) Initiate resuscitation with IV fluids; and 3) Provide a prehospital sepsis alert to the receiving hospital well before arrival. Improving identification of patients with serious infections may include a combination of EMS clinician impression along with physiological factors. Simply identifying potential patients with sepsis and alerting and transporting to the most appropriate facility – analogous to the care of myocardial infarction, trauma, and stroke – can improve survival. Hemorrhagic Shock Hemorrhage is a common cause of shock among trauma victims. Field clinical trials have suggested that volume resuscitation before controlling hemorrhage may be detrimental [36, 49, 56–58, 60]. Possible mechanisms for worse outcomes include dislodgement of clot, dilution of clotting factors, decreased oxygen‐carrying capacity of blood, hyperchloremic metabolic acidosis, and exacerbation of bleeding from injured vessels in the thorax or abdomen. Controlling external hemorrhage is essential for maintaining vascular volume. Direct pressure is usually sufficient to control external bleeding. Military and civilian experience suggests that tourniquets should be used early and ­liberally [98]. An assortment of topical hemostatic materials to be placed directly on the bleeding wound also exists [98–101] (see Chapter 35). Studies in Houston and San Diego suggest that mortality following traumatic hemorrhage is not influenced by prehospital administration of fluid [57, 59]. Survival to hospital discharge rates were not significantly different for patients receiving fluids versus patients not receiving fluids in the field. Both studies were performed in systems with relatively short scene and transport times. As discussed above, currently EMS clinicians are taught to administer only enough IV or IO fluids to restore a peripheral pulse or to reach a systolic blood pressure of 80–90  mmHg. However, the optimum target blood pressure for these patients remains undefined. Trauma victims with isolated head injuries who receive excessive fluids may develop worsened cerebral swelling. In addition, excess fluids may precipitate congestive heart failure in susceptible individuals or lead to impaired immune response following severe injury.

Hypotension and Shock

Conversely, the benefit of limited volume resuscitation has been derived from military and urban data with a predominance of penetrating injuries and young, healthy patients. This population may be more tolerant of hypovolemic resuscitation and benefit from relative hypotension while reducing the risk of clot dislodgement. Tranexamic acid (TXA) is a lysine derivative that blocks fibrinolysis. It has long been used to control hemorrhage during surgery [2]. In a randomized controlled study, TXA reduced mortality from traumatic hemorrhage if administered within 3 hours of the time of injury. Some EMS systems are beginning to use TXA to treat hemorrhagic shock. Evidence for its benefit is found in its early administration and in patients with severe shock or concomitant traumatic brain injury  [102]. Late administration of TXA has been associated with worse outcomes [103]. Attempts at establishing intravascular access in critically injured trauma victims may delay time to definitive care, especially in the urban setting [56, 104–107]. The majority of IV fluid studies have taken place in urban settings primarily with penetrating trauma victims and rapid transport times. The effectiveness of IV fluids for similar patients in the rural and wilderness settings remains undefined. The subject remains controversial, with several studies providing mixed messages [45, 56, 98–100, 105–108].

Protocol A treatment protocol for treating shock in the field should address the following factors: 1.  Performing the initial assessment. 2.  The definitive or life‐saving interventions appropriate for these patients. 3.  Access to definitive care without unnecessary prehospital delay. 4.  Resources to be used in the field. 5.  Skills of the various levels of EMS clinicians in the field. Protocols developed for the out‐of‐hospital treatment of shock must consider the heterogeneity of the disease state, the limited assessment and treatment options, and the environment in which the protocols will be applied. Protocols for the inner city may not be appropriate for the rural setting. The level of training and clinical experience of the EMS personnel must also be considered. Ideally, the EMS medical director should use evidence‐based medical decision making, drawing from best practices when developing treatment protocols.

Conclusion Shock must be correlated with the patient’s clinical condition, age, size, and present and past medical history. EMS clinicians must identify signs of decreased tissue perfusion when assessing for the

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presence of shock. Treatment modalities for shock are limited in the field, but include bleeding control, fluid administration, inotropic agents, and careful control of assisted ventilation. Although the mainstay of shock treatment is IV fluids, approaches should be individualized for different clinical scenarios. The potential benefits of shock care interventions must be weighed against the potential risks of delaying ­definitive care.

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36 Stern SA, Dronen SC, Birrer P, Wang X. Effect of blood pressure on hemorrhage volume and survival in a near‐fatal hemorrhage model incorporating a vascular injury. Ann Emerg Med 1993; 22:155–63. 37 Alderson P, Bunn F, Lefebvre C, et  al. Human albumin solution for resuscitation and volume expansion in critically ill patients. Cochrane Database Syst Rev. 2002; (1):CD001208. 38 Elbers PW, Ince C. Mechanisms of critical illness: classifying microcirculatory flow abnormalities in distributive shock. Crit Care. 2006; 10:221. 39 Patel GP, Grahe JS, Sperry M, et al. Efficacy and safety of dopamine versus norepinephrine in the management of septic shock. Shock. 2010; 33:375–80. 40 De Backer D, Biston P, Devriendt J, et al. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med. 2010; 362:779–89. 41 Reber LL, Hernandez JD, Galli SJ. The pathophysiology of anaphylaxis. J Allergy Clin Immunol. 2017; 140:335–48. 42 Shaker M, Kanaoka T, Feenan L, Greenhawt M. An economic evaluation of immediate vs non‐immediate activation of emergency medical services after epinephrine use for peanut‐induced anaphylaxis. Ann Allergy Asthma Immuno. 2019; 122:79–85. 43 Simons KJ, Simons FE. Epinephrine and its use in anaphylaxis: current issues. Curr Opin Allergy Clin Immunol. 2010; 10:354–61. 44 Simons FER, Simons KJ. Epinephrine (adrenaline) in anaphylaxis. Chem Immunol Allergy. 2010; 95:211–22. 45 Hochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. N Engl J Med. 1999; 341:625–34. 46 Aneja RK, Carcillo JA. Differences between adult and pediatric septic shock. Minerva Anestesiol. 2011; 77:986–92. 47 Kissoon N, Orr RA, Carcillo JA. Updated American College of Critical Care Medicine––pediatric advanced life support guidelines for management of pediatric and neonatal septic shock: r­ elevance to the emergency care clinician. Pediatr Emerg Care 2010; 26:867–9. 48 O’Connor RE, Domeier RM. An evaluation of the pneumatic anti– shock garment (PASG) in various clinical settings. Prehosp Emerg Care. 1997; 1:36–44. 49 Pepe PE, Eckstein M. Reappraising the prehospital care of the patient with major trauma. Emerg Med Clin North Am. 1998; 16:1–15. 50 Finfer S, Norton R, Bellomo R, Boyce N, French J, Myburgh J. The SAFE study: saline vs. albumin for fluid resuscitation in the critically ill. Vox Sang. 2004; 87(Suppl 2):123–31. 51 Semler MW, Self WH, Rice TW. Balanced crystalloids versus saline in critically ill adults. N Engl J Med. 2018; 378:1951. 52 Sperry JL, Guyette FX, Brown JB, et al. Prehospital plasma during air medical transport in trauma patients at risk for hemorrhagic shock. N Engl J Med. 2018; 379:315–26. 53 Pusateri AE, Butler FK, Shackelford SA, et al. The need for dried plasma – a national issue. Transfusion 2019; 59(Suppl 2):1587–92. 54 Shlaifer A, Siman‐Tov M, Radomislensky I, et  al. Prehospital administration of freeze‐dried plasma, is it the solution for trauma casualties? J Trauma Acute Care Surg. 2017; 83:675–82. 55 Sunde GA, Vikenes B, Strandenes G, et al. Freeze dried plasma and fresh red blood cells for civilian prehospital hemorrhagic shock resuscitation. J Trauma Acute Care. Surg. 2015; 78(6 Suppl 1):S26–30. 56 Bickell WH, Wall MJ, Jr., Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med. 1994; 331:1105–9.

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57 Kaweski SM, Sise MJ, Virgilio RW. The effect of prehospital fluids on survival in trauma patients. J Trauma. 1990; 30:1215–19. 58 Kowalenko T, Stern S, Dronen S, Wang X. Improved outcome with hypotensive resuscitation of uncontrolled hemorrhagic shock in a swine model. J Trauma. 1992; 33:349–362. 59 Martin RR, Bickell WH, Pepe PE, Burch JM, Mattox KL. Prospective evaluation of preoperative fluid resuscitation in hypotensive patients with penetrating truncal injury: a preliminary report. J Trauma. 1992; 33:354–61. 60 Silbergleit R, Satz W, McNamara RM, Lee DC, Schoffstall JM. Effect of permissive hypotension in continuous uncontrolled intra‐ abdominal hemorrhage. Acad Emerg Med. 1996; 3:922–6. 61 Smith JP, Bodai BI, Hill AS, Frey CF. Prehospital stabilization of  critically injured patients: a failed concept. J Trauma. 1985; 25:65–70. 62 Spaite DW, Hu C, Bobrow BJ, et al. Association of out‐of‐hospital hypotension depth and duration with traumatic brain injury mortality. Ann Emerg Med. 2017; 70:522–530.e21. 63 Fowler R, Gallagher JV, Isaacs SM, Ossman E, Pepe P, Wayne M. The role of intraosseous vascular access in the out‐of‐hospital environment (resource document to NAEMSP position statement). Prehosp Emerg Care. 2007; 11:63–6. 64 Yannopoulos D, Tang W, Roussos C, Aufderheide TP, Idris AH, Lurie KG. Reducing ventilation frequency during cardiopulmonary resuscitation in a porcine model of cardiac arrest. Respir Care. 2005; 50:628–35. 65 Neumar RW, Otto CW, Link MS, et  al. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010; 122(18 Suppl 3):S729–767. 66 Sakr Y, Reinhart K, Vincent JL, et al. Does dopamine administration in shock influence outcome? Results of the Sepsis Occurrence in Acutely ill Patients (SOAP) Study. Crit Care Med. 2006; 34:589–97. 67 Hajjar LA, Vincent JL, Barbosa Gomes, et  al. Vasopressin versus norepinephrine in patients with vasoplegic shock after cardiac surgery: the VANCS randomized controlled trial. Anesthesiology. 2017; 126:85–93. 68 Sims CA, Holena D, Kim P, et al. Effect of low‐dose supplementation of arginine vasopressin on need for blood product transfusions in patients with trauma and hemorrhagic shock: a randomized clinical trial. JAMA Surg. 2019; 154:994–1003. 69 Schwartz MB, Ferreira JA, Aaronson PM. The impact of push–dose phenylephrine use on subsequent preload expansion in the ED setting. Am J Emerg Med. 2016; 34:2419–22. 70 Nawrocki PS, Poremba M, Lawner BJ. Push dose epinephrine use in the management of hypotension during critical care transport. Prehosp Emerg Care. 2020; 24:188–95. 71 Guyette FX, Martin‐Gill C, Galli G, McQuaid N, Elmer J. Bolus dose epinephrine improves blood pressure but is associated with increased mortality in critical care transport. Prehosp Emerg Care. 2019; 23:764–71. 72 Sprung CL, Annane D, Keh D, et  al. Hydrocortisone therapy for patients with septic shock. N Engl J Med. 2008; 358:111–24. 73 Dellinger RP, Levy MM, Carlet JM, et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock: 2008. Intensive Care Med. 2008; 34:17–60. 74 Liu VX, Fielding‐SinghV, Greene JD, et al. The time of early antibiotics and hospital mortality in sepsis. Am J Respir Crit Care Med. 2017; 196:856–63.

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75 Pantridge JF, Geddes JS. A mobile intensive‐care unit in the management of myocardial infarction. Lancet. 1967; 2(7510):271–3. 76 Mattox KL, Bickell W, Pepe PE, Burch J, Feliciano D. Prospective MAST study in 911 patients. J Trauma. 1989; 29:1104–11. 77 Singer M, Deutschman CS, Seymour CW, et al. The third international consensus definitions for sepsis and septic shock (Sepsis‐3). JAMA. 2016; 315:801–10. 78 Seymour CW, Rea TD, Kahn JM, Walkey AJ, Yealy DM, Angus DC. Severe sepsis in pre‐hospital emergency care: analysis of incidence, care, and outcome. Am J Respir Crit Care Med. 2012; 186:1264–71. 79 Suffoletto B, Frisch A, Prabhu A, Kristan J, Guyette FX, Callaway CW. Prediction of serious infection during prehospital emergency care. Prehosp Emerg Care. 2011; 15:325–30. 80 Wang HE, Weaver MD, Shapiro NI, Yealy DM. Opportunities for emergency medical services care of sepsis. Resuscitation. 2010; 81:193–7. 81 Rivers E, Nguyen B, Havstad S, et al. Early goal‐directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001; 345:1368–77. 82 Robson W, Nutbeam T, Daniels R. Sepsis: a need for prehospital intervention? Emerg Med J. 2009; 26:535–8. 83 Seymour CW, Carlbom D, Engelberg RA, et al. Understanding of sepsis among emergency medical services: a survey study. J Emerg Med. 2012; 42:666–77. 84 Seymour CW, Band RA, Cooke CR, et al. Out‐of‐hospital characteristics and care of patients with severe sepsis: a cohort study. J Crit Care. 2010; 25:553–62. 85 Pennsylvania Department of Health, Bureau of Emergency Medical Services. Pennsylvania Statewide Advanced Life Support Protocols. Harrisburg, PA: Department of Health, 2019. 86 Olander A, Andersson H, Sundler AJ, Bremer A, Ljungstrom L, Andersson Hagiwara M. Prehospital characteristics among patients with sepsis: a comparison between patients with or without adverse outcome. BMC Emerg Med. 2019; 19:43. 87 Grover J, Vacarelli M, Williams J, Cabanas JG. Greater emphasis: Wake County, NC, strives for prehospital recognition and treatment of sepsis. JEMS. 2016; 41:50–3. 88 McGillicuddy DC, Tang A, Cataldo L, Gusev J, Shapiro NI. Evaluation of end‐tidal carbon dioxide role in predicting elevated SOFA scores and lactic acidosis. Intern Emerg Med. 2009; 4:41–4. 89 Hunter CL, Silvestri S, Dean M, Falk JL, Papa L. End‐tidal carbon dioxide is associated with mortality and lactate in patients with suspected sepsis. Am J Emerg Med. 2013; 31:64–71. 90 Green RS, Travers AH, Cain E, et  al. Paramedic recognition of sepsis in the prehospital setting: a prospective observational study. Emerg Med Int. 2016; 2016:6717261. 91 Baez AA, Cochon L. Acute Care Diagnostics Collaboration: assessment of a Bayesian clinical decision model integrating the Prehospital Sepsis Score and point‐of‐care lactate. Am J Emerg Med. 2016; 34:193–6. 92 Shu E, Ives Tallman C, Frye W, et al. Pre‐hospital qSOFA as a predictor of sepsis and mortality. Am J Emerg Med. 2019; 37:1273–8. 93 Lane D, Ichelson RI, Drennan IR, Scales DC. Prehospital management and identification of sepsis by emergency medical services: a systematic review. Emerg Med J. 2016; 33:408–13. 94 Sethi M, Owyang CG, Meyers C, Parekh R, Shah KH, Manini AF. Choice of resuscitative fluids and mortality in emergency department patients with sepsis. Am J Emerg Med. 2018; 36:625–9.

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102 CRASH‐2 Collaborators. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH‐2): a randomised, placebo‐controlled trial. Lancet. 2010; 376(9734):23–32. 103 CRASH‐2 Collaborators. The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH‐2 randomised controlled trial. Lancet. 2011; 377(9771):1096–101. 104 Bickell WH. Are victims of injury sometimes victimized by attempts at fluid resuscitation? Ann Emerg Med. 1993; 22:225–6. 105 Henderson RA, Thomson DP, Bahrs BA, Norman MP. Unnecessary intravenous access in the emergency setting. Prehosp Emerg Care. 1998; 2:312–16. 106 Sampalis JS, Tamim H, Denis R, et  al. Ineffectiveness of on‐site intravenous lines: is prehospital time the culprit? J Trauma. 1997; 43:608–15. 107 Seamon MJ, Fisher CA, Gaughan J, et al. Prehospital procedures before emergency department thoracotomy: “scoop and run” saves lives. J Trauma. 2007; 63:113–20. 108 Jacobs LM, Sinclair A, Beiser A, D’Agostino RB. Prehospital advanced life support: benefits in trauma. J Trauma. 1984; 24:8–13.

CHAPTER 8

Vascular access Bryan B. Kitch and Eric H. Beck

Introduction While discussions continue concerning the utility of obtaining prehospital vascular access, the skill remains a standard taught to EMS clinicians and is a mainstay of contemporary emergency care. Methods of access include peripheral and central intravenous (IV) catheterization and intraosseous (IO) needle, depending on the local scope of practice and the qualifications of EMS personnel. The fluids and medications administered through these various routes depend on the clinical situation and local EMS convention. Those specifics are discussed throughout the clinical chapters of this text.

Benefits Similar to its benefit in the emergency department (ED) or any other acute care setting, vascular access provides an avenue for medical intervention by the EMS clinician. Early prehospital initi­ ation of treatment for cardiac arrest, cardiac arrhythmia, and sepsis has been shown to be beneficial for patients [1–3]. For the more stable, yet ill or distressed patient, the initiation of an IV for symp­ tomatic treatment of nausea, pain, or dehydration can help initiate the continuum of care that will likely progress in the ED. Treatment of potentially reversible conditions like hypoglycemia and opiod overdose in the prehospital setting can prevent deterioration of the patient’s condition and potentially negate the need for trans­ port. Vascular access also facilitates advanced care, such as rapid sequence intubation and the administration of vasopressors and thrombolytics. The collection of blood samples for point of care or laboratory diagnostics is an additional, albeit secondary, benefit.

Risks Obtaining vascular access involves inherent risks to the cli­ nician, including blood exposure and needlestick injury. Whether it is attempted on‐scene or in transit, the prehospital

environment is often characterized by poor lighting, limited space, and movement in the rear of an ambulance. This offers less than ideal conditions in which to handle lancets, IV and IO needles, and other sharp supplies. A combative and/or confused patient can add to the difficulty. Transmission of HIV, hepatitis B, and hepatitis C remains a constant threat to EMS personnel, with the risks of infection following needlestick injury estimated at 0.3%, 6%–30%, and 1.8%, respectively [4]. Consistent use of universal precautions is imperative to reduce the likelihood of occupational exposures. Potential risks to the patient include bleeding, damage to adjacent structures, infection, and throm­ bosis, and these risks will be discussed later. Establishing an IV is often part of EMS protocols. In many cases protocols allow for EMS clinician assessment and judg­ ment regarding whether or not an IV is necessary. One study revealed that while over 50% of the patients who arrived at an ED via EMS had IVs in place, almost 80% of those IVs were not used in the prehospital setting. The tendency to err on the side of caution to avoid scrutiny for perceived undertreatment seemed to contribute to the discrepancy [5]. Another study sim­ ilarly found that protocols seemed to drive the decision to start an IV, as opposed to an actual need for administration of medi­ cines or fluids [6]. Medical oversight is indicated to continually evaluate the appropriateness of “precautionary” IVs in the con­ texts of potential risks and costs to the system and to patients. Several studies in trauma situations have revealed a lack of significant benefit regarding prehospital vascular access. The classic EMS mantra of “two large bore IVs” for trauma patients has been muted by concern for increased on‐scene times and delayed transport to definitive medical care. Two studies have demonstrated high success rates when IVs were attempted in transit without delaying transport [7, 8]. However, guidelines provided by the Eastern Association for the Surgery of Trauma regarding prehospital IV placement or IV fluid administration for either penetrating or blunt injury patients are based on find­ ings that no benefit is provided [9]. Multiple research studies

Emergency Medical Services: Clinical Practice and Systems Oversight, Third Edition. Volume 1: Clinical Aspects of EMS. Edited by David C. Cone, Jane H. Brice, Theodore R. Delbridge, and J. Brent Myers. © 2021 NAEMSP. Published 2021 by John Wiley & Sons, Inc.

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have suggested that routine administration of IV fluids may not be helpful and, in fact, can be harmful in the prehospital setting [10, 11]. Another study endorsed “scoop and run” transport for EMS, as it found that each prehospital procedure before ED tho­ racotomy compounded a reduction in the odds of survival [12].

PERIPHERAL IV ACCESS History In 1656, Sir Christopher Wren injected opium into the veins of dogs using a quill and bladder, making him the founder of modern IV therapy. Until the 1950s, reusable steel needles were used, but the introduction of over‐the‐needle plastic IV catheters replaced indwelling metal needles, improving operator safety and allowing more patient comfort, rapid flow, and reduced infiltration [13, 14]. Flow through the catheter is based on Poiseuille’s law, dealing with pressure and resistance. The pertinent determinants of the equation include the radius of the catheter and the cath­ eter length. Flow is directly proportional to the radius to the fourth power (r4) and inversely proportional to catheter length. As such, a large gauge, short IV catheter can profoundly improve the potential flow rate over a smaller gauge, longer catheter. Typical locations for peripheral IV access include the ante­ cubital fossa, veins in the forearm and dorsum of the hand and foot, external jugular vein, and scalp veins.

Figure 8.1  IV starting equipment.

Technique (See Video Clip 8.1)

1. Preparation When the decision to pursue vascular access is made, the prepara­ tion for the procedure is just as important as the skill itself. Striv­ ing for speed in the prehospital setting, assumptions regarding the patient’s health, or other neglectful behavior deviating from the practice of universal precautions can result in occupational exposure. When possible, wash hands prior to putting on gloves. Prepare the equipment (Figure 8.1). An IV start kit is optimal (tourniquet, alcohol wipe or other cleaner, tape or a commer­ cially available adhesive device). Select an IV needle with a catheter (Figure 8.2), saline lock, saline flush, and/or IV fluids. Check the IV catheter for integrity. Prepare the patient for the procedure. When appropriate, dis­ cuss with the patient the reason for the procedure along with risks and benefits. Unless a true emergency exists or the patient is not able to make his or her own decisions, verbal consent should be obtained. 2. Site selection Position the patient’s extremity to help straighten the desired vein. Apply the tourniquet proximal to the targeted area (Figure 8.3). When possible, look distally first to allow additional, more proximal attempts on the same extremity, if necessary. Once the tourniquet is applied, have the patient pump his or her fist open and closed several times to help the vasculature become engorged. Feel for a soft, spongy, nonpulsatile vessel.

Figure 8.2  18‐ and 20‐gauge IV catheters with needles.

3. Clean the site Use an alcohol pad, betadine, chlorhexidine, or a similar anti­ septic product to clean the proposed IV site. Allow the area to dry. 4. Insertion of the IV Hold the skin taut with one hand while inserting the needle with the dominant hand. Approach the vessel as shallow as possible (less than 30 degrees angle to the skin) with the bevel of the needle facing up or away from the patient. Once a “pop” is felt and/or a flash of blood is seen in the reservoir of the IV needle, advance the needle slightly further, and slowly slide the catheter over the needle, cannulating the vessel with the plastic catheter while not moving the needle itself (Figure 8.4). 5. Removing the needle Hold firm pressure over the tip of the cannulated plastic cath­ eter while the needle is withdrawn from the hub of the catheter. If applicable, push the button to retract the needle to its safe position and set it away. The needle needs to be disposed of in a sharps container as soon as the IV is secured.

Vascular access

Figure 8.3  Position of tourniquet proximal to target vein.

Figure 8.4  “Flash” of blood indicating that needle is within the vein’s lumen and catheter should be advanced over the needle.

6. Securing the IV Attach the saline lock and flush the lock with saline, or attach IV fluid tubing directly to the hub of the catheter. Secure the cath­ eter hub with tape or a commercially available securing device. Check for signs of infiltration (i.e., localized swelling, inability to flush the catheter, pain). The technique for cannulating the external jugular vein is similar. The needle is inserted in a caudad direction, but no tourniquet is used. Instead, the index finger of the nondomi­ nant hand can be used to apply gentle pressure to the external jugular vein just above the clavicle to facilitate venous engorge­ ment. Care should be taken to avoid placing a needle puncture too low in the neck (i.e., at or immediately above the clavicle) to avoid lung injury. Blind attempts when the external jugular vein is not readily apparent are not advised due to potential for serious injury to surrounding structures (Figure 8.5). Contraindications to intravenous access relate mainly to site selection. Sites with burns, cellulitis, trauma, and other condi­ tions that compromise the integrity of the overlying skin should

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Figure 8.5  External jugular vein.

be avoided. Extremities on the side of a recent mastectomy or lymphatic chain removal, those that contain known throm­ boses, and those that contain permanent modifications for dialysis access should be used only when all other options have been exhausted. Special consideration must be given to patients with known bleeding disorders and those who are taking med­ ications that may alter coagulation. In such cases, the ability to compress the vein used for an IV attempt is important to limit excessive bleeding. Maintenance of vascular access in the prehospital setting may often prove difficult as perspiration, dirt, and water reduce the effectiveness of tape and adhesive dressings used to secure ­the catheter. Combative or confused patients can also intentionally or unintentionally dislodge their IV access during transport, and may require additional verbal instruction and reminders along with extra padding and support to maintain the line. Gauze wraps, elastic bandages, and arm boards are just a few examples of adjuncts used to protect and optimally posi­ tion venous access.

Intraosseous Access IO devices function to access the intramedullary vessels found in the marrow of spongy bone that lead to the central circulation of the body. The IO needle, embedded in the bony structure, is protected by the noncollapsible periosteum, solving any prob­ lems with patency that may be encountered with IVs during vasoconstriction and low‐flow states found in, for example, sepsis and cardiac arrest. IO access is currently attainable with manual, impact‐driven, and powered drill methods. The gauge and length of some of the commercially available products vary for adult and pediatric patients. The commonly available EZ‐IOTM uses a 15‐mm‐long needle for children under 39 kg, while 25‐mm and 45‐mm lengths are available for patients 40 kg or greater. All are 15 gauge. The sites of insertion vary by manufacturer recom­ mendations, but locations may include the proximal tibia, distal

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tibia, proximal humerus, and sternum. Contraindications to IO access are generally site specific and include infection of the overlying skin, fracture at or above the IO site, vascular compro­ mise, and previous surgery or significant deformity of the bone. Previous sternotomy, suspected sternal fracture, and CPR with chest compressions preclude sternal IO access. Potential com­ plications include osteomyelitis, fat emboli, fracture, growth plate injury, compartment syndrome, infection, and extravasa­ tion resulting in local tissue injury and swelling [15–17]. Drinker and Lund in the 1920s were the first to use IO vascular access in the sternum of animal models, demonstrating that the fluid given did indeed reach intravascular circulation. Josefson followed in 1934, reporting the first IO use in humans. Soon after, in the 1940s, the first use of the IO was documented in the pediatric population. While its use among military personnel during WWII was advocated when IV access was delayed or difficult, the development of the over‐the‐needle PVC IV cath­ eter by Massa in the 1950s temporarily curtailed use of the IO. The reemergence of the IO in the 1980s in the Pediatric Advance Life Support and Advanced Pediatric Life Support courses sup­ ported its use after failed IV attempts. More recent guidelines from the American Heart Association advocate for the use of IOs as first‐line access in pediatric emergencies and as the first alternative in adult cardiac arrest, including in out‐of‐hospital settings [13, 15, 16, 18]. Several studies have demonstrated the success of obtaining vascular access through IOs after failed or difficult attempts at IV access. IO vascular access has demonstrated high first‐ attempt success rates and overall success rates of 90% and greater in adults and children [17]. The advantages of the com­ mercially available battery‐powered driver used in the study included its short learning curve, ability to easily penetrate thick cortical bone given its power source, and rapid drug delivery into the systemic circulation [19]. IO access has been proven to be as quick and effective as IV access [20]. In patients with inac­ cessible peripheral veins, IO access is faster and more successful than central IV lines [21]. Most medications given through the peripheral IV can be given through an IO, with bioequivalence proven between the two routes [22]. IO has been shown to have clinically comparable time to peak drug concentration as compared to central IV access [18]. Wilderness, tactical, disaster, and other specialty EMS groups may encounter situations requiring early consideration of the use of the IO for vascular access. Austere conditions, limited access to an entrapped patient, or cumbersome gear and clothing of both patient and clinician can inhibit efforts to ini­ tiate peripheral IV access. One study demonstrated significantly shorter times to IO access compared to IV access when EMS cli­ nicians donned chemical, biological, radiological, and nuclear protective equipment [23]. IO access is recommended during any resuscitation when IV access is not attainable [15]. Pediatric IO placement mirrors the adult procedure with minimal additional considerations. As IV access in a critically

ill child can be difficult and anxiety provoking for the EMS cli­ nician, many pediatric emergency practitioners elect to use IO after fewer failed attempts than would be tolerated in an adult. Additionally, IO placement in a moving child requires less fine motor dexterity than IV catheter placement and may be suc­ cessful when traditional calming and redirection techniques are unsuccessful. The pediatric patient also offers several addi­ tional sites for placement, such as the distal femur and the iliac crest. However, as these sites are not commonly used in adults, training and protocols may be more effective using similar ana­ tomical landmarks across all patients.

Technique (See Video Clip 8.2)

1. Preparation Wash hands, don the appropriate personal protective equip­ ment (PPE), and prepare the equipment (Figure 8.6) 2. Identify the landmarks and site • Humeral head – Keep the arm adducted with the palm pro­ nated. Palpate the proximal humerus and locate the greater tuberosity, which will be the site of insertion. • Proximal Tibia  –  Identify the tibial tuberosity. The site of insertion should be two finger breadths below and just medial to this landmark. • Distal tibia – Abduct and externally rotate the hip. Palpate the flat portion of bone just proximal to the medial malleolus. 3. Clean the site Cleanse the targeted area with alcohol prep, betadine, chlorhex­ idine, or other antiseptic. Allow the site to dry. 4. Insert the IO Insert the IO needle into the skin overlying the desired location until bone is reached. Insert the needle through the cortex into the marrow either manually or per device‐specific instructions. The needle should be relatively stable and freestanding in the bone if inserted appropriately.

Figure 8.6  Intraosseous equipment.

Vascular access

5. Assess IO patency Remove the trocar and dispose of it in a sharps container. Attach a syringe or IO‐specific tubing and assess for patency of the IO. Monitor the extremity for extravasation. Attach IV fluids if indi­ cated; use a pressure bag or manually push fluids via syringe to achieve desired infusion rates. 6. Secure the IO needle Stabilize the IO needle in place with gauze and tape or a com­ mercially available device. In a non‐urgent setting, lidocaine or other anesthetic drugs may be injected into the area of the proposed IO insertion.

Central intravenous access Prehospital central venous access is a procedure sometimes per­ formed by advanced‐level paramedics, nurses, and EMS phy­ sicians. Usually in the form of a large 8.5 French single lumen catheter, the route provides rapid access to the central venous circulation for fluid resuscitation, blood product administration, and medications. Central venous access may be the preferable option when attempts at peripheral and IO lines have failed or are contraindicated, but its prehospital use is sparsely reported (Figure  8.7). Central venous line placement by air medical transport teams has been reported [22]. Similarly, one report documented the performance of 115 prehospital central lines placed by field‐response EMS physicians over a 3‐year period [23]. Another describes central venous catheters being placed in the prehospital setting quickly and safely by EMS physicians in systems that employ this model, such as those in Europe [24]. Critical care teams are often responsible for maintenance of these lines during interfacility transport, so familiarity with this form of vascular access is important. The internal jugular, subclavian, and femoral veins are options for central venous access. Traumatic injuries above the diaphragm often dictate a femoral location. Attempts for access in the internal jugular and subclavian veins have a risk of pneumothorax, which

Figure 8.7  Central venous catheter kit.

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should be considered if the patient acutely decompensates during the procedure. Placement of a central line, especially in the upper body, often causes an interruption of CPR efforts [21]. Risks of bleeding from venous or inadvertent arterial puncture, infection, thrombosis, and nerve damage also exist [19]. The prehospital environment makes it nearly impossible to preserve sterile tech­ nique. Given that these lines are performed as “code” lines under emergency, semisterile (similar to a peripheral IV line) condi­ tions, it should be expected that the line would be removed and another one placed if the patient survives to the ED.

Special considerations Accessing dialysis catheters and indwelling catheters In the prehospital setting, dialysis catheters, infusion ports, and other long‐term artificial structures should not be considered as first‐line options for gaining vascular access unless carefully con­ sidered by the medical director and other relevant consultants. The health of these difficult access patients often depends on fre­ quent IV access and medication administration. Improper use of these routes may result in serious consequences. Alternative forms of vascular access or medication routes should be consid­ ered. In the case that the EMS clinician must access these types of catheters, special attention must be paid to the specific technique for accessing each device found in the community, as subtle but important differences exist across a range of device types and manufacturers. The most important tenets of accessing an exist­ ing device revolve around maintaining a sterile procedure, as line infection often leads to substantial morbidity. Additionally, many indwelling catheters are filled with a fluid such as saline or heparin when not in use. Care must be taken to properly remove and discard this solution to avoid contamination of blood sam­ ples or systemic administration of an active medication. Other Alternative Vascular Access Points Saphenous vein cutdown is a last‐resort access method. In a direct comparison with cadaveric models, paramedic students performed IO access more rapidly, successfully, and with less complications than venous cutdown [25]. Hypodermocyclis is the interstitial or subcutaneous administra­ tion of fluids into the body. This method is much slower than an intravenous infusion, but it is safe and effective as an alternative method of hydration in the geriatric population [26]. Hyal­ uronidase‐facilitated subcutaneous infusion can also be used in a mass casualty incident or disaster response scenario where there may be a limited number of practitioners treating a large number of patients [27]. Pediatric considerations The pain and anxiety in the pediatric patient associated with vascular access is often a difficult matter to address in the pre­ hospital setting. The need for rapid vascular access in a critically

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ill child along varying transport times does not typically allow for some of the pharmacological options for relieving the pain of IV insertion that are available in the ED and hospital setting. Various commercially available creams, gels, and patches often require several minutes up to an hour of application time to be effective. Local infiltration of lidocaine with either a small‐ gauge needle or needle‐free system such as the J‐Tip has quicker anesthetic delivery but requires a second, often psychologically traumatizing, needle puncture or startling noise caused by pres­ surized CO2. If the child is stable enough to consider the use of these pain‐reducing interventions, vascular access may poten­ tially be deferred to arrival to the hospital. Medical oversight and training for pediatric patient care should focus on helping the EMS clinician distinguish the stable patient from the criti­ cally ill one who would benefit from early vascular access [28]. Additionally, for many EMS clinicians IV attempts for young children are infrequent and often difficult. Training may be needed to improve technical skills and confidence to increase success [29].

Ultrasound‐guided IV access In ED care, ultrasound technology has become a useful tool to improve IV access success. Previously, patients who were unable to be cannulated by more traditional methods were often subject to more invasive procedures such as cutdowns or central lines, posing an increased level of risk. The growing widespread avail­ ability of ultrasound technology has found a role to augment the ability of clinicians to obtain IV access in a less‐­invasive fashion. While a detailed instruction is beyond the scope of this text, ultrasound techniques can be used in a static fashion to identify the location of a suitable vein when one cannot be seen or palpated. The vein is then accessed by the usual techniques. Alternatively, a dynamic approach is often used, wherein the clinician uses ultrasound to visualize the needle tip and subse­ quently the catheter entering the vein, ­confirming placement. The materials and methods are largely similar to standard peripheral access techniques, with the exception of the need for an ultrasound machine, gel, and longer length catheters for accessing deeper veins. Multiple studies have been performed analyzing the efficacy, speed, patency, and complications of ultrasound‐guided IV access. Across several inpatient and ED environments, ultra­ sound‐guided peripheral access shows trends toward being a comparable or preferable modality with regard to risk of failure, number of attempts, and procedure time [30]. There is clear demonstration of reduction of central line use when ultra­ sound is available to facilitate peripheral IV placement [31]. Success of ultrasound peripheral IV attempts was noninferior to the external jugular approach in those who failed traditional attempts [32]. With regard to prehospital use of this technology, barriers to implementation remain but are much less prominent than in

previous years. Ultrasound machines remain expensive, and when accounting for rugged storage solutions, most devices require a nontrivial amount of physical space. Handheld ultrasound devices have been produced in recent years and may allow for fea­ sibility studies of EMS‐initiated ultrasound‐facilitated IV access. As other applications for ultrasound are studied and implemented for prehospital use, the ability to gain vascular access may be an added benefit of the technology, even if not purchased for that primary purpose. As several other modalities are equivalent to if not faster than ultrasound‐guided peripheral IV placement, this technology may find a greater stronghold in alternative practice environments or in systems permissive of longer on‐scene times or for long‐distance or critical care transport (see Chapter 69).

Conclusion Vascular access is a common procedure for EMS clinicians. In some cases it is to facilitate administration of needed medica­ tions or resuscitative fluids. In other cases, IVs are placed as a precautionary lifeline in case such measures are eventually needed. Many IVs are not used prior to arrival at an ED. It is important for EMS clinicians to possess the necessary skills and equipment to initiate vascular access under a myriad of condi­ tions. Furthermore, this is an area that is appropriate for moni­ toring and evaluating from a quality improvement perspective, including both decision making and technical skill domains.

References 1 Seymour CW, Cooke CR, Hebert PL, Rea TD. Intravenous access during out‐of‐hospital emergency care of noninjured patients: a population‐based outcome study. Ann Emerg Med. 2012; 59:296–303. 2 Band RA, Gaieski DF, Hylton JH, Shofer FS, Goyal M, Meisel ZF. Arriving by emergency medical services improves time to treatment endpoints for patients with severe sepsis or septic shock. Acad Emerg Med. 2011; 18:934–40. 3 Rittenberger JC, Bost JE, Menegazzi JJ. Time to give the first medi­ cation during resuscitation in out‐of‐hospital cardiac arrest. Resuscitation. 2006; 70:201–6. 4 Harris SA, Nicolai LA. Occupational exposures in emergency medical service providers and knowledge of and compliance with universal precautions. Am J Infect Control. 2010; 38:86–94. 5 Kuzma K, Sporer KA, Michael GE, Youngblood GM. When are prehospital intravenous catheters used for treatment? J Emerg Med. 2009; 36:357–62. 6 Stratton SJ. Rethinking out‐of‐hospital intravenous access. Ann Emerg Med. 2012; 59:304–6. 7 Jones SE, Nesper TP, Alcouloumre E. Prehospital intravenous line placement: a prospective study. Ann Emerg Med. 1989; 18:244–6. 8 Slovis CM, Herr EW, Londorf D, Little TD, Alexander BR, Guth­ mann RJ. Success rates for initiation of intravenous therapy en route by prehospital care providers. Am J Emerg Med. 1990; 8:305–7. 9 Cotton BA, Jerome R, Collier BR, et al. Guidelines for prehospital fluid resuscitation in the injured patient. J Trauma. 2009; 67:389–402.

Vascular access

10 Bickell WH, Wall Jr MJ, Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med. 1994; 331:1105–9. 11 Haut ER, Kalish BT, Cotton BA, et  al. Prehospital intravenous fluid administration is associated with higher mortality in trauma patients: A national trauma data bank analysis. Ann Surg 2011; 253:371–7. 12 Seamon MJ, Fisher CA, Gaughan J, et  al. Prehospital procedures before emergency department thoracotomy: “scoop and run” saves lives. J Trauma. 2007; 63:113–20. 13 Millam D. The history of intravenous therapy. J Intraven Nurs. 1996; 19:5–14. 14 Rivera A, Strauss K, Van Zundert A, Mortier E. The history of peripheral intravenous catheters: How little plastic tubes revolu­ tionized medicine. Acta Anaesthesiol Belg. 2005; 56:271. 15 Fowler R, Gallagher JV, Isaacs SM, Ossman E, Pepe P, Wayne M. The role of intraosseous vascular access in the out‐of‐hospital envi­ ronment (resource document to NAEMSP position statement). Prehosp Emerg Care. 2007; 11:63–6. 16 Weiser G, Hoffmann Y, Galbraith R, Shavit I. Current advances in intraosseous infusion–a systematic review. Resuscitation. 2012; 83:20–6. 17 Santos D, Carron PN, Yersin B, Pasquier M. EZ‐IO(R) intraosse­ ous device implementation in a pre‐hospital emergency service: A prospective study and review of the literature. Resuscitation. 2013; 84:440–5. 18 Hoskins SL. Pharmacokinetics of intraosseous and central venous drug delivery during cardiopulmonary resuscitation. Resuscitation. 2012; 83:107–12. 19 Gazin N, Auger H, Jabre P, et  al. Efficacy and safety of the EZ‐ IO™ intraosseous device: out‐of‐hospital implementation of a management algorithm for difficult vascular access. Resuscitation. 2011; 82:126–9. 20 Reades R, Studnek JR, Garrett JS, Vandeventer S, Blackwell T. Comparison of first‐attempt success between tibial and humeral intraosseous insertions during out‐of‐hospital cardiac arrest. Prehosp Emerg Care. 2011; 15:278–81. 21 Leidel BA, Kirchhoff C, Bogner V, Braunstein V, Biberthaler P, Kanz K. Comparison of intraosseous versus central venous vascular

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access in adults under resuscitation in the emergency department with inaccessible peripheral veins. Resuscitation. 2012; 83:40–5. 22 Von Hoff DD, Kuhn JG, Burris III HA, Miller LJ. Does intraosse­ ous equal intravenous? A pharmacokinetic study. Am J Emerg Med. 2008; 26:31–8. 23 Lamhaut L, Dagron C, Apriotesei R, et al. Comparison of intrave­ nous and intraosseous access by pre‐hospital medical emergency personnel with and without CBRN protective equipment. Resuscitation. 2010; 81:65–8. 24 Fyntanidou B, Fortounis K, Amaniti K, et  al. The use of central venous catheters during emergency prehospital care: a 2‐year expe­ rience. Eur J Emerg Med. 2009; 16:194–8. 25 Hubble MW, Trigg DC. Training prehospital personnel in saphe­ nous vein cutdown and intraosseous access techniques. Prehosp Emerg Care. 2001; 5:181–9. 26 Molloy DM, Cunje A. Hypodermoclysis in the care of older adults. Can Fam Physician. 1992; 38:2038–2043. 27 Arthur AO, Goodloe JM, Thomas SH. Subcutaneous fluid administration: a potentially useful tool in prehospital care. Emerg Med Int. 2012:904521. doi: 10.1155/2012/904521. Epub 2012 May 9. 28 Zempsky WT. Pharmacologic approaches for reducing venous access pain in children. Pediatrics. 2008; 122(Suppl 3):S140–53. 29 Myers LA, Arteaga GM, Kolb LJ, Lohse CM, Russi CS. Prehospital peripheral intravenous vascular access success rates in children. Prehosp Emerg Care. 2013; 17:425–8. 30 Heinrichs J, Fritze Z, Vandermeer B, Klassen T, Curtis S. Ultrasono­ graphically guided peripheral intravenous cannulation of children and adults: a systematic review and meta‐analysis. Ann Emerg Med. 2013; 61:444–454. e1. 31 Shokoohi H, Boniface K, McCarthy M, et al. Ultrasound‐guided peripheral intravenous access program is associated with a marked reduction in central venous catheter use in non‐criti­ cally ill emergency department patients. Ann Emerg Med. 2013; 61:198–203. 32 Costantino TG, Kirtz JF, Satz WA. Ultrasound‐guided peripheral venous access vs. the external jugular vein as the initial approach to the patient with difficult vascular access. J Emerg Med. 2010; 39:462–7.

CHAPTER 9

Chest pain and acute coronary syndromes Joseph P. Ornato, Michael R. Sayre, and James I. Syrett

Introduction In the United States, someone experiences a myocardial infarction every 26 seconds, and alarmingly, the disease claims one life each minute [1]. Heart disease accounts for twice as many deaths in the United States as are attributed to unintentional injuries, which has major implications for EMS systems [2]. About half of individuals who suffer acute myocardial infarctions (AMI) are transported to the hospital by EMS, and many more patients call EMS for help because they are experiencing chest pain [3]. The prehospital management of chest pain has improved with better clinical examination, earlier administration of effective medications, and the broad use of 12‐lead ECGs to detect acute coronary syndromes (ACS) and myocardial infarction more accurately before arrival in the emergency department (ED) [4]. Because more rapid reperfusion during acute myocardial infarction improves heart function and patient survival, EMS and health care systems have focused on developing strategies to identify chest pain patients with myocardial infarction quickly and to provide effective treatment while transporting them directly to definitive care [5–7]. The goals of management for patients with chest pain include rapid identification of the patient with ACS, relief of symptoms, and transport to an appropriate hospital. This chapter will cover the assessment and treatment of patients with the chief complaint of chest pain and will focus on the scientific basis for prehospital medical care of those patients. It will also review common conditions that can cause chest pain.

General approach When evaluating a patient with a complaint of chest pain, EMS professionals should begin by assessing the patient’s stability and then obtain a basic clinical history and examination. Early in the assessment, an EMS clinician should apply a cardiac monitor to rapidly identify dysrhythmias, perform a diagnostic 12‐lead ECG,

and administer specific treatment depending on the results of the initial evaluation. Because only a small minority of the patients with chest pain actually have ACS, maintaining vigilance in this assessment and diagnostic routine can be difficult [8]. Complete accuracy in the diagnosis of chest pain is not always possible in any setting, not even in the hospital [9]. The prehospital clinician should not expect to diagnose a patient with a complaint of chest pain definitively. A careful history can lead the clinician to a correct “category” of diagnosis much of the time. As a general approach, the patient should be treated as if he or she has the most likely serious illness consistent with the signs and symptoms. Discomfort due to cardiac ischemia is usually, but not always, substernal and may radiate to the shoulder, either arm, both arms, upper abdomen, back, or jaw [9, 10]. Other symptoms such as nausea and diaphoresis are commonly present but do not accurately predict the presence or absence of ACS. Cardiac disease is most often seen beginning in middle‐aged men and older women. However, even younger adults under the age of 40 with chest pain but no cardiac risk factors and a normal ECG have a 1%–2% risk of ACS [11]. Taking a focused history using the “PQRST method” can be helpful (Box 9.1).

Box 9.1  Historical aspects of chest discomfort: the PQRST method

P:  What provoked the pain or what was the patient doing when the pain started? Q: What is the quality of the pain; burning, aching, squeezing, or stabbing? R:  Is there any radiation of the pain; does it go to the neck, jaw, arm, or back? S:  How severe is the pain? On a scale of 1 to 10, with 10 being the worst pain in one’s life, what is the pain now, and how has it changed? T:  What are the temporal aspects of the pain? How long has it been present? Has it occurred before? When?

Emergency Medical Services: Clinical Practice and Systems Oversight, Third Edition. Volume 1: Clinical Aspects of EMS. Edited by David C. Cone, Jane H. Brice, Theodore R. Delbridge, and J. Brent Myers. © 2021 NAEMSP. Published 2021 by John Wiley & Sons, Inc.

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There are many causes of chest pain, and their incidence changes depending on the characteristics of the population being studied. Patients calling on EMS are more likely to have acute myocardial infarction or other serious causes of chest pain than are patients in the general ED population [3]. Although the majority of this chapter focuses on the management of an ACS, other causes of chest pain are present more commonly.

Role of emergency medical dispatch Prehospital care of the patient with a complaint of chest pain begins at emergency medical dispatch. Identification of patients suspected to have ACS allows an EMS system to send advanced level clinicians to the patient. Many EMS systems with both basic and advanced level ambulances use a trained emergency medical call taker who asks the caller a series of questions to determine the nature of the emergency and the likelihood that advanced level care will be needed (see Chapter 88). A retrospective cohort study from England took a rigorous approach to determining the accuracy of one set of dispatcher questions in identifying patients with ACS [12]. Approximately 8% of calls at the “9‐9‐9” center were classified as “chest pain.” Subsequent chart review at the hospital identified all patients with the ultimate diagnosis of ACS and found that this represented only 0.6% of all 9‐9‐9 patients. Approximately 80% of the ACS patients were classified correctly as chest pain at the dispatch level. Another 7% were classified in a variety of other categories that still received a paramedic level response (e.g., severe respiratory distress). Sensitivity of the dispatch system for detecting ACS was 71% and specificity was 93%. However, a great deal of over‐triage occurred, and the positive predictive value of the dispatch system for detecting ACS was only 6%. Additional refinement of the dispatch question sequence to reduce over‐triage seems possible. The emergency dispatch question sequence for stroke performs much better, with a positive predictive value of 42% and a similar sensitivity to ACS at 83% [13]. Although an ACS patient can present with a variety of clinical symptoms, a study in Utah revealed that more than half of patients proven to have AMI complained of chest pain or a breathing complaint at the point of dispatch [14]. The percentage of AMIs significantly increased for patients aged 35 years and older and varied significantly by sex, dispatch level, and chief complaint. The American Heart Association (AHA) and American College of Cardiology (ACC) recommend that emergency medical dispatchers prompt patients with nontraumatic chest pain to take aspirin if they have no contraindications while awaiting EMS arrival [15, 16]. This recommendation is based on extrapolation from data showing that patients who take aspirin before hospital arrival are less likely to die, and it is likely quite safe [17].

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The 12‐lead electrocardiogram The 12‐lead ECG remains the quickest method of detecting myocardial ischemia or infarction. Although ECGs have been used to diagnose ACS since 1932, the technology has now advanced to the point that a prehospital ECG can be done quickly and accurately and can be sent wirelessly to the receiving hospital at a relatively low cost. Additional benefit can be gained by having the prehospital ECG become the first of a series of ECGs, increasing the sensitivity of diagnosis of coronary syndromes [18]. Performing a prehospital ECG on a patient exhibiting signs and symptoms of ACS is a Class I AHA/ACC recommendation [15, 16]. This recommendation is based on evidence demonstrating that, despite minimal increased time spent on scene for patients receiving ECGs, the time to definitive treatment for ST‐ elevation myocardial infarction (STEMI) with fibrinolysis or percutaneous coronary intervention (PCI) is shortened overall, with a significant reduction in mortality [19]. Prehospital electrocardiogram interpretation With the ease of obtaining a prehospital 12‐lead ECG comes the need for its accurate interpretation. Precise interpretations can influence decisions to transport patients to more appropriate but more distant facilities, as well as immediate management strategies on hospital arrival. A 12‐lead ECG is required to diagnose STEMI and can often provide evidence that ACS is present (see Figure 9.1). Currently, three methods of out‐of‐hospital ECG interpretation exist: computer algorithms integrated into the ECG machine, direct interpretation by paramedics, or wireless transmission of the ECG to a physician for interpretation. One, two, or all three can be used in a given EMS system. All prehospital 12‐lead ECG machines contain computer programs that will interpret the ECG, and the machines can be configured to print the interpretation on the ECG. If this technology is sufficiently sensitive and specific for STEMI, the EMS clinicians would theoretically not require education in interpretation, which would allow EMS systems to use advanced and basic‐level personnel to acquire 12‐lead ECGs. Additional benefits of using the computer’s interpretation include avoidance of the technical issues and cost of establishing base stations dedicated to receiving incoming ECGs, as well as the provision of consistent interpretation that does not depend on the variable skills and experience of EMS clinicians. Many prehospital 12‐ lead ECG systems use computerized interpretation systems that have high specificity, but the computer interpretation alone can miss up to 20% of true STEMI events [20]. Despite the high specificity, many emergency physicians and cardiologists do not place enough trust in the computer interpretation alone to routinely activate the cardiac catheterization PCI team that can provide rapid reperfusion treatment for a STEMI patient [21]. EMS clinician interpretation is another option. Additional extensive education is required, and interpretation accuracy can be affected by both experience and interest in the subject

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Figure 9.1  A prehospital 12‐lead ECG showing atrial fibrillation with a rapid ventricular rate and widespread ST‐segment elevation diagnostic for acute myocardial infarction. The ability of EMS clinicians to activate the hospital cardiac catheterization laboratory directly from the scene upon making such a diagnosis, and transport such a patient directly to the laboratory, has been demonstrated to decrease time to definitive care by PCI. Source: Courtesy of Dare County [North Carolina] Emergency Medical Services.

matter [22]. Although several studies have shown that trained paramedics can accurately interpret the presence of STEMI, experience also plays an important role [23–25]. When a paramedic identifies and reports “tombstones” on the 12‐lead ECG, experienced physicians are powerfully motivated to take action. The third method of interpretation is by transmission of the acquired ECG to a base station for interpretation by a physician. This method has generally been used as the criterion standard when comparing other methods of interpretation, and its accuracy has been shown to be slightly better than other methods. It relies both on the availability of the interpreting physician and on an infrastructure that facilitates reliable ECG transmission. In one observational cohort study, positive predictive value of prehospital 12‐lead ECGs was improved by transmitting them to emergency physicians compared with interpretation solely by paramedics [25]. In some cases, systems have been developed that enable simultaneous transmission of the 12‐lead ECG to the receiving ED and to an interventional cardiologist on call [26]. These systems have the potential to decrease treatment times further because both the ED staff and the PCI team are activated early. The AHA Guidelines state that the ECG may be transmitted for remote interpretation by a physician or screened for STEMI by properly trained paramedics, with or without the assistance of computer interpretation [15]. Advance notification should be provided to the receiving hospital for patients identified as having STEMI. Implementation of 12‐lead ECG diagnostic programs with concurrent medically directed quality management is recommended. No diagnostic test is perfect, and the 12‐lead ECG is no exception. A number of conditions other than acute myocardial infarction can cause ST‐segment elevation, such as left bundle branch block and hyperkalemia (Box 9.2) [27]. Some of the differences between STEMI and the mimics of acute ST‐segment elevation are subtle and easily missed.

Box 9.2  Causes of ST‐segment elevation on 12‐lead electrocardiogram

•  Acute myocardial infarction •  Normal ST‐segment elevation and normal variants •  Left bundle branch block •  Acute pericarditis and myocarditis •  Hyperkalemia •  Brugada syndrome and arrhythmogenic right ventricular ­cardiomyopathy •  Pulmonary embolism •  Transthoracic cardioversion •  Prinzmetal angina Source: Based on ref. [27].

Medications Several medications are important for EMS management of the patient with chest pain. Providing the chest pain patient with medication for relief of pain whenever safe and feasible and regardless of the etiology of the pain is fundamental. Treatment of pain reduces anxiety in addition to relieving the patient’s discomfort. For ACS patients, treatment of pain can reduce catecholamine levels and thus improve the balance between oxygen demand and supply for ischemic cardiac muscle. Oxygen Despite its historical use, the evidence review leading up to the AHA Guidelines does not recommend the routine use of oxygen therapy in patients with uncomplicated AMI or ACS who have no signs of hypoxemia or heart failure [15]. Among patients with STEMI and without hypoxia, a randomized trial comparing supplemental oxygen versus no supplemental oxygen, initially in the EMS setting and continued into the hospital, showed no evidence of benefit and larger infarct size among those given

Chest pain and acute coronary syndromes

oxygen [28]. The guidelines do, however, recommend oxygen administration if the patient is dyspneic or has an arterial oxyhemoglobin saturation 220/minute) should be either cardioverted with 100 J or treated with adenosine plus prepared for cardioversion. If the rate rises greater than 250/minute, cardioversion is the best choice given the risk of deterioration. Irregular narrow‐ complex tachydysrhythmia greater than 220/minute deserves countershock promptly as previously noted (50‐100 J). Stable wide‐complex tachydysrhythmias Wide‐complex tachydysrhythmia can be due to VT or SVT with abnormal conduction. Until proven otherwise, assume any new wide‐complex tachydysrhythmia is due to VT. Hospital data suggest that about two thirds of patients with new wide‐complex tachydysrhythmias have VT. With a history of previous myocardial infarction, the frequency of VT increases to 90%. Although it is possible to assemble evidence to detect supraventricular rhythms from a detailed examination and 12‐lead ECG, these data are not easily obtained in the field. Thus, actions in managing wide‐complex tachydysrhythmia should either treat or cause no harm in VT. All unstable patients with wide‐complex tachydysrhythmia should be cardioverted with 100 J, with escalating energy doses if needed. When stable or borderline, a few simple measures can help stratify patients. Observing this group is always an option, intervening only if conditions worsen. If P waves precede each QRS complex during a stable wide‐complex tachydysrhythmia with a rate of 140/minute or less, a supraventricular source is likely, especially sinus or atrial tachycardia, although VT is a remote possibility. Treatment focuses on correcting any potential causes (e.g., pain, hypovolemia, or hypoxemia) and observation. Irregular QRS complexes suggest atrial fibrillation or multifocal atrial tachycardia. Neither requires field rhythm‐directed

therapy in stable patients, although other actions (e.g., oxygen, bronchodilators) may be needed. When no clear P‐QRS relationship exists, differentiating between SVT and VT is difficult during a wide‐complex tachydysrhythmia. These key features help decide a clinical course of action: • A patient with new‐onset wide‐complex tachydysrhythmia and a history of previous myocardial infarction or VT very likely will have VT. • VT will often not slow during vagal maneuvers. Therefore, slowing of a wide‐complex tachydysrhythmia during these efforts suggests SVT. However, the absence of change does not diagnose VT. • Most VT does not respond to adenosine, whereas SVT usually slows or terminates. Conversely, lidocaine has little effect on most SVT and terminates 75% to 85% of VT. • VT is usually regular and rarely seen at a rate of greater than 220/minute. Any chaotic wide‐complex tachydysrhythmia should be considered atrial fibrillation with abnormal conduction. When a chaotic wide‐complex tachydysrhythmia at a rate of greater than 220/minute occurs, atrial fibrillation from Wolff‐Parkinson‐White syndrome is present. This rhythm is prone to deterioration. From these clinical observations, the following scheme can be used in approaching a stable or borderline (one minor sign or symptom of instability alone) patient with a wide‐complex tachydysrhythmia: • All stable patients with regular wide‐complex tachydysrhythmia at a rate of 120 to 220/minute should attempt or receive vagal maneuvers. Those who slow but then elevate again should receive adenosine (6‐12  mg IV). If no slowing with vagal maneuvers occurs, one of three paths should be taken: • Young (age 120/minute). Magnesium sulfate, 2 g as a rapid IV bolus, is also suggested for those who fail countershock. In children, TdP is rare, inherited, and treated with slowing heart rate. A more practical problem is mistaking VT or VF for TdP. VT and VF often display some changes in QRS complex appearance. EMS clinicians may mistake these variations for the classic, but rare, QRS twisting. If recurrent polymorphic VT occurs in a patient with one or more of the aforementioned risks, treatment should be started. Otherwise, orders and protocols should focus on the treatment of common VT. Rhythm disturbances in renal failure patients This group is often affected by metabolic derangements that alter rhythms, in addition to having high rates of underlying heart disease. Hyperkalemia is a common complication of renal failure that can cause a bradycardia or a wide‐complex

Figure 10.1  The classic one‐lead ECG appearance (lead II here) of torsades de pointes. Note the shifting of the QRS complex axis and appearance.

All air ambulances will have at least three crewmembers (pilot and two medical attendants)

All air ambulances will have at least three crewmembers (pilot and two medical attendants)

Paratransit transportation means comparable transportation services required by the Americans with Disabilities Act A for people with disabilities who are unable to use fixed route transportation systems.

Evacuation of hospital patients may require care that exceeds most paramedic training

Notes

NOTE: Type refers to FEMA’s methods for the categorization and description of resources that are commonly exchanged in disasters via mutual aid, by capacity and/or capability. Source: Based on FEMA Resource Typing Library Tool v1.5.3. Available at: https://rtlt.preptoolkit.fema.gov/Public/Combined

Depends on the model of aircraft, but assume no more than two litters for planning purposes.

Rotor‐wing for medical facilities to medical facilities or from medical facility to airport of embarkation (APOE) Good for short and intermediate distances but for planning purposes no more than 150 miles. The goal is to be able to deliver the patients quickly and return to provide additional lifts as needed

Depends on the model of aircraft, but assume one litter for planning purposes.

Commercial air ambulances (fixed wing) Type 1 – Critical care and ALS, 2 or more litter patients Type 2 – Critical care and ALS, 1 litter patient Type 3 – Neonatal specific

Road conditions   IAW FEMA contract, the one‐way distance to transport paratransit passengers shall not exceed 250 miles

Good for short or intermediate distances for wheelchair patients

Determine the seat requirement. The contractor determines the number of vehicles required based on seat requirements.

Experience and qualification of medical crew.   Equipment onboard   Oxygen   Weather conditions   Crew rest: Usually 10 hours in a 24‐hour period. Good for intermediate Experience and and long distances, but for planning qualification of medical crew. purposes no more than 150 miles.   The goal is to be able and deliver the Equipment onboard patients   quickly and return to provide Oxygen additional lifts as   needed Weather conditions   Crew rest: Usually 10 hours in a 24‐ hour period.

Oxygen     Road conditions

One critical or two stable patients per Good for short or ambulance intermediate distances no more than 250 miles.

Limiting factor

Ambulances (ground) Type I – ALS non‐HAZMAT Type II – BLS non‐HAZMAT Type III – Bariatric ALS, non‐ HAZMAT Type IV – ALS/critical care transport, non‐ HAZMAT Paratransit vehicles Type I – Sedan/minivan (1‐7 seats) Type II – Minibus (8‐26 seats) Type III – transit bus (>26 seats) Type IV – Wheelchair van (1‐9 seats with wheelchair lift) Type V – ADA minibus (10‐26 seats with wheelchair lift) Type VI – ADA transit bus Commercial air ambulances (rotary) Type 1 – Critical care and ALS, 2 or more litter patients Type 2 – Critical care and ALS, 1 litter patient Type 3 – Neonatal specific

Distance

Planning factor

Mode

Cardiac dysrhythmias

rhythm, although the latter is usually not above a rate of 100 to 120/minute and often much slower. Treatment should include IV calcium, high‐dose nebulized albuterol, and insulin plus glucose. Albuterol rapidly (but temporarily) shifts potassium into the cells and should be part of protocols for any renal failure patient with new‐onset symptomatic bradycardia or a wide‐ complex rhythm. Insulin and glucose also work quickly, but insulin is rarely available in the field. If used, however, insulin and glucose infusions are best done with direct medical oversight supervision due to the risk of hypoglycemia. Lidocaine can cause asystole in the presence of hyperkalemia. The role of other agents, including amiodarone, is unknown in the rare event of hyperkalemia and new‐onset wide‐complex tachydysrhythmia [14]. If a rhythm‐specific intervention is needed in unstable patients with suspected hyperkalemia, electricity (pacing for slow, countershock for fast rates) is a safe choice.

Protocols When developing protocols, focus on the simple data and steps. For example, both the bradycardia and tachycardia protocols should start with a division between “stable/no symptoms” and “symptomatic and unstable or borderline.” Those in the “stable/no symptoms” category should be observed, expeditiously transported, and monitored, with precautionary IV insertion and, if needed, oxygen. As a corollary, unstable patients with bradycardia or tachycardia should receive prompt electrical therapy (pacing or countershock), airway support, monitoring, and IV insertion occurring either in tandem with or after electrical therapy. EMS clinicians should save rhythm strips and give sedation if possible, but not withhold lifesaving treatment trying to “get a good strip” or titrating sedation. Unless the signs of instability are subtle, medical oversight contact should follow the initial treatment of unstable patients.

Summary Evaluate prehospital dysrhythmias in patients in a way tailored to the time restraints, physical limitations, and outcome needs that are specific to the field setting. Decision trees should be simple and effective, focusing on treating patients and not rhythms per se. Protocols must identify and treat all unstable patients. Those without symptoms or with trivial symptoms do not require

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rhythm‐directed therapies. For symptomatic but stable patients, a few key steps should be taken to help manage each case.

References 1 Neumar RW, Shuster M, Callaway CW, et  al. Executive summary: 2015 American Heart Association guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2015; 132: S315–67. 2 Yealy DM, Kosowsky J. Dysrhythmias. In Walls R, Hockberger R, Gausche‐Hill M editors. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 9th ed. Philadelphia, PA: Elsevier/Saunders, 2018. 3 McCabe J, Menegazzi JJ, Adhar G, Paris PM. Intravenous adenosine in the prehospital treatment of supraventricular tachycardia. Ann Emerg Med. 1992; 21:358–61. 4 American Heart Association. Part 6: Electrical therapies: automated external defibrillators, defibrillation, cardioversion, and pacing. Circulation. 2010; 112:S706–19. 5 Scholten M, Szili‐Torok T, Klootwijk P, Jordaens L. Comparison of monophasic and biphasic shocks for transthoracic cardioversion of atrial fibrillation. Heart. 2003; 89:1032–4. 6 Tanabe S, Yasunaga H, Ogawa T, et  al. Comparison of outcomes after use of biphasic or monophasic defibrillators among out‐of‐ hospital cardiac arrest patients. Circ Cardiovasc Qual Outcomes. 2012; 5:689–96. 7 Hedges JR, Syverud SA, Dalsey WC, et  al. Prehospital trial of emergency transcutaneous pacing. Circulation. 1987; 76:1337–40. 8 Paris PM, Stewart RD, Kaplan RM, Whipkey R. Transcutaneous pacing for bradyasystolic cardiac arrest in prehospital care. Ann Emerg Med. 1985; 14:320–3. 9 Dorian P, Case D, Schwartz B, et al. Amiodarone as compared with lidocaine for shock‐resistant ventricular fibrillation. N Engl J Med. 2002; 346:884–90. 10 Wrenn K. Management strategies in wide QRS complex tachycardia. Am J Emerg Med. 1991; 9: 592–7. 11 Wilber DJ, Baerman J, Olshansky B, et al. Adenosine sensitive ventricular tachycardia: clinical characteristics and response to catheter ablation. Circulation. 1993; 87:126–34. 12 O’Toole KS, Heller MB, Menegazzi JJ, Paris PM. Intravenous verapamil in the treatment of paroxysmal supraventricular tachycardia. Ann Emerg Med. 1990; 19:279–85. 13 Wang HE, O’Connor RE, Megargel RE, et al. The use of diltiazem for treating rapid atrial fibrillation in the out‐of‐hospital setting. Ann Emerg Med. 2001; 37:38–45. 14 McLean SA, Paul ID, Spector PS. Lidocaine‐induced conduction disturbance in patients with systemic hyperkalemia. Ann Emerg Med. 2000; 36: 626–7.

CHAPTER 11

Cardiac procedures and managing technology Joanna L. Adams and David P. Thomson

Introduction Cardiovascular collapse can occur from either mechanical pump failure or electrical failure. As technology continues to produce devices and procedures to support these patients, the EMS clinician is likely to encounter patients reliant on this technology. Many of these patients are managed by critical care teams during interfacility transports. There are also many patients who are dependent on these cardiac devices living outside the hospital who are encountered by prehospital EMS practitioners. Familiarity with these devices and how to troubleshoot them is paramount to appropriate care of these technology‐dependent patients by the EMS system. There are also procedures that the EMS physician should be knowledgeable about that can be used to stabilize patients suffering from cardiovascular collapse in the prehospital setting.

Short‐term mechanical circulatory support devices Categories of short‐term mechanical circulatory support devices used to manage acute cardiogenic shock include intra‐aortic balloon pumps (IABPs), non‐IABP percutaneous mechanical circulatory support devices, extracorporeal membrane oxygenator (ECMO) pumps, and nonpercutaneous centrifugal pumps (cardiopulmonary bypass). Each improves end‐organ perfusion, reduces intracardiac filling pressures, reduces left ventricular volumes and myocardial oxygen consumption, and augments coronary perfusion. Each type of device results in specific complexities and challenges during interfacility transport. Often, the required expertise necessitates that an experienced team be involved. Teams may be composed of critical care paramedics, nurses, and physicians who are specially trained to address complications with these devices and able to support the patient in the event of device failure. For example, in the case of ECMO, it

is important that a perfusionist or other specialist is part of the team and dedicated to managing the pump [1]. Intra‐aortic balloon pump The IABP is used to help stabilize acutely ill cardiac patients. Its role is to provide support until short‐term recovery or definitive care. The IABP works by decreasing cardiac afterload, augmenting diastolic perfusion pressure, and increasing coronary artery perfusion [2]. The decrease in afterload reduces the workload on the heart, and the improved coronary artery circulation can increase oxygen supply to the myocardium. EMS clinicians will encounter IABP patients during interfacility transfers, often for more advanced cardiac care or surgery. The most common indications for an IABP are acute myocardial infarction, cardiogenic shock, ventricular aneurysm, left ventricular failure, valve or papillary muscle rupture, or a combination of these factors [3]. Absolute contraindications for an IABP include aortic dissection, abdominal aortic aneurysm, and aortic valve incompetence. Relative contraindications include bleeding disorders and atherosclerosis [2]. The IABP catheter is inserted via the femoral artery and then advanced into the thoracic aorta. The tip of the balloon should be positioned 1‐2 cm distal to the origin of the subclavian artery and must be above the branches of the renal arteries. If the balloon is not placed correctly, occlusion of coronary, subclavian, or renal arteries could occur [2]. On a chest x‐ray, the tip of the catheter should be visible between the second and third intercostal space. When inflated, the balloon should not completely occlude the aortic lumen, as this can damage the aortic wall, and blood components [2]. Most devices have different‐sized balloons to be used based on patient weight or height. It is important to ensure the appropriate balloon volume is being used. IABP function is dependent on precise timing. The balloon is cycled in conjunction with the cardiac cycle. It is important to remember the balloon is inflated during diastole, and deflated just prior to systole. While the balloon is inflated,

Emergency Medical Services: Clinical Practice and Systems Oversight, Third Edition. Volume 1: Clinical Aspects of EMS. Edited by David C. Cone, Jane H. Brice, Theodore R. Delbridge, and J. Brent Myers. © 2021 NAEMSP. Published 2021 by John Wiley & Sons, Inc.

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blood is pushed both back toward the heart, as well as distal in the aorta. The result is increased blood flow to coronary and carotid arteries and increased systemic perfusion. The balloon is deflated very rapidly, and this rapid loss of volume reduces the pressure in the aorta. The result is that the left ventricle does not contract as strenuously as it would otherwise. Cardiac workload and myocardial oxygen demands are subsequently reduced. If the timing is not correct, these advantages are lost, and the patient may be harmed [2]. An IABP can use different triggers to time inflation and deflation cycles. Most use the ECG or the arterial pressure waveform as a trigger. The IABP may also have an internal trigger in the event of cardiac arrest. To use the arterial pressure as a trigger the patient must have an arterial pressure catheter that is connected to the balloon pump. Some IABP devices have specialized fiber optic connectors to measure arterial pressures. The ECG can also be used as a trigger mode. Most devices have an “automatic” trigger mode, where the pump automatically switches between trigger modes if needed. An example would be a switch between ECG and arterial pressure modes if the ECG signal is lost. Most

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modern pumps can also compensate for arrhythmias such as atrial fibrillation and pacing modes [2]. With the trigger mode established, attention should focus on timing. Most patients are transported with a 1:1 frequency, where each cardiac cycle is assisted. In order to assess timing, it may be helpful to place the device in a 1:2 frequency (every other cardiac cycle is assisted) to get a better picture of the arterial pressure waveform landmarks. For transport, the operator should ensure that the balloon is set to inflate at the dicrotic notch and to deflate during the next isovolumetric contraction phase (Figure  11.1). The dicrotic notch phase on the arterial pressure waveform represents aortic valve closure and diastole. Once the timing is correct, the device can be placed back into a 1:1 frequency and put in the “automatic” mode if available [2]. Potential complications include limb ischemia, compartment syndrome, aortic dissection, bleeding, thrombocytopenia and red blood cell destruction, gas embolus, infection, and cardiac decompensation from improper timing. (Additional introduction to IABP can be found at https://www.youtube.com/ watch?v=NYeA‐3AAQB4&t=100s).

Figure 11.1  IABP arterial pressure tracings with 1:1 augmentation and 2:1 augmentation respectively. A. Diastolic augmentation with increased coronary

perfusion. B. Assisted aortic end‐diastolic pressure with decreased myocardial oxygen demand. C. Assisted systole. D. Unassisted aortic end‐diastolic pressure. E. Unassisted systole.

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The interfacility transport team should examine the patient with particular attention to the insertion site, as well as to the extremity distal to the site. The insertion site should be examined for bleeding or protruding balloon. The catheter tubing should be examined for any blood or blood flecks, and for kinking. The limb should be examined for signs of ischemia. Any problems must be corrected before transport. Fresh ECG leads should be applied to the patient. The referring hospital balloon pump should not be disconnected or shut off until the transport pump is connected and tested. The transport balloon pump should be plugged into an outlet during this time and not run on battery power. The pump should also be plugged into the aircraft or ambulance power inverter during transport. Pure battery operation should be used only to transport the patient from the vehicle to the in‐hospital destination. Special caution must be taken when transferring a patient from one model of IABP to another. There may be a difference in the balloon size, and an adapter may be needed to connect a “Brand A” catheter to a “Brand B” IABP. The balloon size should be noted and adjusted on the pump if necessary. In the event of cardiac arrest, the IABP will lose all trigger modes, give a “Trigger Arrest” alarm, and then stop counterpulsation. If not addressed, this could result in a thrombus formation. When CPR is initiated, the IABP should be switched to “Arterial Trigger.” Effective CPR should allow the IABP to function from the arterial pressures. In the event that arterial pressures are not sufficient, the IABP should be switched to an internal trigger. This last resort tactic provides asynchronous counterpulsation and helps prevent clot formation. “Internal Trigger” mode should be stopped if there is a return of circulation and the ECG or arterial pressure mode is restarted [3]. In the event of IABP failure during transport, a large Luer‐ lock syringe should be attached to the quick connector to aspirate the balloon for blood. If there is blood, then the balloon has lost integrity. Injection of anything into it will result in an aortic arterial injection. If no blood is found, use air to inflate the balloon to the volume capacity of the balloon. Then quickly aspirate the air and deflate the balloon. Repeat four to five times every 5 to 10 minutes to reduce the likelihood of thrombus formation until the pump can be repaired or replaced [2]. Non‐IABP percutaneous mechanical circulatory support devices In addition to IABPs, there are other devices that are inserted percutaneously for temporary support of patients in acute cardiogenic shock. Unlike the IABP that improves the conditions for left ventricular function, these percutaneously placed left ventricular assist devices (pLVAD) directly assist the left ventricle. Among the most common of these devices is a transaortic intraventricular pump (Impella®) and extracorporeal pumps, including a left atrium to aorta pump (TandemHeart®) and right atrium to aorta pump (ECMO) [4]. The transaortic intraventricular pump is an axial flow pump that is inserted into the femoral artery and advanced in

a retrograde fashion through the aortic valve and into the left ventricle. The device sits across the aortic valve and contains an inflow and outflow orifice. Between them is an impeller, a propeller that provides continuous blood flow from the left ventricle to the ascending aorta. Correct catheter positioning across the aortic valve is necessary for pump function. Blood is pumped from the left ventricle into the aortic root, unloading the left ventricle. This increases cardiac output and mean arterial pressure and decreases left ventricular end‐diastolic pressure, myocardial workload, and oxygen consumption [4]. The power connections for the pump motor and sensors are all contained within the catheter and connected to an external console that controls the pump and purge system. The controller console monitors both the catheter position and function of the impeller. It does not require pressure timing or electrocardiogram timing like the IABP, making it ideal for patients with arrhythmias. In addition to providing information on the location of the catheter and the flow rate of the impeller, the controller console also provides alarms related to suction events and purge pressure issues [4]. EMS clinicians are most likely to encounter these devices during interfacility transport of critical care patients. They are generally placed in patients with cardiogenic shock following acute myocardial infarction. Like the IABP, the positioning of the catheter is critical. The catheter location should be confirmed visually as sutured at a specific depth, in addition to reviewing the placement signal on the controller console. If repositioning of the catheter needs to be performed, the referring physician should do it prior to attempting transport. If the catheter becomes dislodged during transport, it should not be repositioned. Alternative support may be required. The pump also contains a purge system that prevents blood from entering the motor. It should be closely monitored during transport. Only transport teams knowledgeable about these devices should transport them without a specialist to manage the device. Knowledge about how to interpret the placement signal and how to troubleshoot the alarms by administering intravenous fluids, titrating vasopressors, or adjusting the flow of the impeller is important to a safe transport [5]. Patients with a transaortic intraventricular pump have been safely transferred between hospitals [1]. It seems likely that EMS clinicians providing critical care transport will encounter more patients with similar devices over time. There is some uncertainty about mortality outcome benefits compared to, for example, IABP therapy. However, technological advances continue, and some centers preferentially use transaortic microaxial‐flow LVADs with acceptable mortality and complication rates in place of more invasive devices [6, 7]. The left atrium to aorta extracorporeal centrifugal pump is placed percutaneously through the femoral vein. The cannula is passed via a transseptal puncture through the intra‐atrial septum from the right atrium to left atrium where oxygenated blood is aspirated. A second outflow cannula is placed that returns the blood to the femoral artery. Advantages compared to the IABP

Cardiac procedures and managing technology

and transaortic intraventricular pump are improved unloading of the left ventricle with improved cardiac output. This pump also bypasses the left ventricle and aortic valve and can therefore be useful for patients with left ventricular thrombus or aortic stenosis [8]. Like the transaortic intraventricular pump, this device results in improved hemodynamic profiles but with less certain short‐term mortality benefits. The disadvantage of this extracorporeal centrifugal pump is the transseptal puncture, requiring a surgeon or experienced interventional cardiologist for placement. This approach also increases complications associated with potential iatrogenic cardiac injury [8]. Similar to other devices, an understanding of how to troubleshoot this device and manage the complications is imperative for safe transport. Extracorporeal membrane oxygenation ECMO devices provide prolonged mechanical support by pumping blood and by exchanging oxygen and carbon dioxide in the blood prior to its return to the patient. Thus, ECMO may be helpful during both circulatory failure and pulmonary failure. There are two main types of ECMO support, venoarterial (VA) and venovenous (VV). VA ECMO drains venous blood via a venous cannula, oxygenates the blood in the ECMO circuit, and pumps the oxygenated blood into a large artery via an arterial cannula, bypassing both the heart and lungs. VA ECMO is used for both cardiac and pulmonary failure. VV ECMO oxygenates the blood and returns it to the body to be circulated by the heart, requiring adequate function of the both the right and left heart. VV ECMO is used during respiratory failure. Cannulation for VA and VV ECMO differs in both their locations of access and who generally performs the procedure. For VA ECMO the venous cannula can be inserted into the right atrium via the internal jugular vein, or less commonly, via a femoral vein to the inferior vena cava and then right atrium. Venous cannulation can be performed via open incision, but it can also be placed via Seldinger technique. The arterial cannulation for VA ECMO can be performed via the right carotid artery, the femoral artery, or via a transthoracic approach by directly cannulating the aorta. There are benefits and downsides to each location, for example leg ischemia in femoral cannulation or neurologic compromise in carotid cannulation. VV ECMO cannulation usually involves the right internal jugular vein or femoral veins and may involve anywhere from one to multiple sites of cannulation for venous drainage. There are cannulas that can be placed in the right internal jugular vein with multiple lumens that can drain deoxygenated blood and return oxygenated blood from a single cannulation point. Indications for ECMO include acute, reversible, severe respiratory or cardiac failure unresponsive to conventional management. A few examples for VV ECMO include neonates with respiratory failure following meconium aspiration, severe influenza‐associated acute respiratory distress syndrome, and near-drowning with inability to oxygenate the patient. Some examples for VA ECMO include drug overdoses,

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massive pulmonary embolism, and witnessed cardiac arrest with refractory ventricular arrhythmias. Absolute contraindications to ECMO include patients with advanced, untreatable, or irreversible disease like advanced malignancy, nonrecoverable cardiac disease (and not transplant candidates), or irreversible brain injury. Some relative contraindications may include elderly patients, multiorgan failure, and bleeding diathesis. EMS physicians may encounter ECMO devices in the setting of critical care transport. Some medical centers are able to cannulate patients but are unable to provide additional services they may require once on ECMO, necessitating transport. Other hospitals do not have ECMO cannulation capabilities, and surgeons or intensivists with training in ECMO cannulation are sometimes transported to the outlying hospital to cannulate the patient prior to transport. ECMO has been initiated in the prehospital setting as a treatment of refractory cardiac arrest, one of the most notable cases being at The Louvre in Paris [9]. Pilot projects are being conducted to determine the feasibility of implementing systematic initiation of ECMO in the field for cases of refractory cardiac arrest. Such efforts require substantial investments in developing the necessary multidisciplined team to conduct the resuscitation, cannulate the patient, and manage the technology. Transporting ECMO patients is a complex undertaking that requires planning [10]. Specialized equipment, as well as equipment mounts, may be required depending on the mode of travel [10]. The size and composition of the transport team should also be determined in advance. Some ECMO programs include a cannulation team that goes out ahead of the transport team. Transport teams may include a perfusionist to manage the ECMO device and a physician to provide direct medical oversight. Conversations between the transport team and the referring and receiving institutions should occur prior to patient contact to arrange for needed supplies and equipment in order to prevent delays. Without question, these are resource‐ intensive cases.

Long‐term mechanical circulatory support devices Ventricular assist devices Ventricular assist devices (VAD) commonly refer to surgically implanted pumps that are intended to assist one or both ventricles of the heart. They are most often placed in patients with severe congestive heart failure. Devices include left ventricular assist devices (LVADs), right ventricular assist devices (RVADs), and biventricular assist devices. The most common is the LVAD, with a cannula placed in the apex of the left ventricle, blood flow to the pump, and flow back through a cannula into the ascending aorta. Thus, the device assists the ventricle in moving blood through the circulatory system [3]. VADs were first developed in the 1960s. Technological advances made them more portable, but the patient was still

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confined to the hospital. In the 1990s, fully portable devices were developed that allowed VAD patients to be discharged from the hospital [11, 12]. VADs are most commonly used as a bridge to cardiac transplantation, but they also may be used as a bridge during a reversible cardiac condition or as a permanent destination therapy. There are two types of VAD patients. There are those with nonportable devices who require critical care transport with a perfusionist. Alternatively, those with portable VADs may be living at home where prehospital EMS clinicians may be called. Currently, there are four generations of VADs with features that vary (Box 11.1). First‐generation devices mimic the pumping action of the left ventricle via the use of diaphragms or pusher plates that cause blood to be sucked into the left ventricle and expelled into the aorta. This mechanism results in pulsatile blood flow. The patient will have a pulse and blood pressure that can be measured [12]. The pumps are powered by electricity and can be either electromechanical or pneumatic. Electromechanical pumps use an electromagnetic pusher plate to drive the blood, whereas pneumatic devices use air pressure to move the blood. Pneumatic devices may come with a hand pump to be used in the event of device or power failure [11]. Second‐generation LVADs have continuous‐flow rotary pumps. If the device only assists with the work of the left ventricle, the underlying heart function may result in a palpable pulse. If the LVAD is fully replacing the function of the ventricle, there may not be a palpable pulse. As with other technological advances, these devices offer advantages in size, ease of implantation, and durability. The number of moving parts has been reduced to one: the impeller. Second‐generation LVADs are subdivided into devices with axial pumps and those with radial (centrifugal) pumps [11] (Figure 11.2).

Axial pumps use a corkscrew and the Archimedes principle against gravity. The inflow and outflow pumps are in line with the impeller, resulting in a smaller size pump. In contrast, centrifugal pumps have the inflow and outflow cannulas at right angles to the flow. Right angles allow for less suction, which can decrease the risk of the ventricle collapsing around the inflow cannula or distortion of the interventricular septum. Both can result in right ventricular failure [11]. These continuous‐flow devices are found in 90% of patients with LVADs. Continuous‐flow devices have been shown to produce superior organ perfusion than first‐generation, pulsatile, devices [13]. Third‐generation LVADs represent a further technological step forward. They can use continuous flow, axial flow, or centrifugal pumps. The impeller is driven by electromagnets. This results in no contact between the impeller and the sides of the pump. Benefits include less trauma to blood components and less thrombus formation. The devices are also quieter and can last longer [11]. Fourth‐generation LVADs, currently in testing and trials, are exploring further advances in technology, including wireless monitoring and elimination of the driveline. This would remove the cabling from the pump, which must travel through the skin in order to connect to the power source. As driveline infections are a major source of LVAD complications, driveline removal could result in significantly less morbidity [11].

HeartMate battery worn externally in holster

HeartMate battery worn externally in holster Aorta Heart

Box 11.1  Examples of LVADs by generation

First generation (pulsatile blood flow) •  Berlin Heart ECXOR (Berlin Heart AG) •  HeartMate XVE (Abbott Laboratories) •  Thoratec PVAD (Abbott)

Second generation (continuous flow) •  HeartMate II (Abbott Laboratories) •  Jarvik 2000 (Jarvik Heart)

Power lead

Percutaneous lead exiting body

Power lead HeartMate II LVAS or “heart pump”

Third generation (centrifugal flow) •  Berlin Heart INCOR (Berlin Heart AG) •  CentriMag (Abbott Laboratories) •  HeartMate III (Abbott Laboratories) •  HeartWare HVAD Pump (Medtronic)

Fourth generation •  HeartAssist 5 (ReliantHeart Inc.)

HeartMate IILVAS system controller Figure 11.2  HeartMate II LVAD. LVAS, left ventricular assist system.

Source: Reproduced with permission of the Thoratec Corporation.

Cardiac procedures and managing technology

The results of these advancements in technology are devices that allow the patient to leave the hospital and function at home. Prior to discharge the patient and family are given extensive training on the operation and maintenance of the device and how to troubleshoot problems and alarms. The patient is followed by a hospital team and is given written instructions for EMS practitioners, which outline the device operation, emergency interventions, and hospital contact information [14]. LVAD complications can be divided into two categories: device problems and patient problems (Box 11.2). The most common problems consist of neurologic events, bleeding, and cardiac arrhythmias. Neurologic events include acute strokes and transient ischemic attacks. Thrombotic and hemorrhagic events can occur. The incidence of stroke in VAD patients has been reported ranging from 8% to 25%. The risk is increased for patients with stroke histories and those who have had device‐ related infections [11]. The most commonly experienced forms of bleeding include epistaxis, gastrointestinal bleeding, and hematoma formation. Bleeding can result from trauma to blood components, from acquired von Willebrand disease, or from iatrogenic anticoagulation [15]. Most patients are given anticoagulants or antiplatelet drugs to reduce the risk of thrombus formation [16]. LVAD patients are also at increased risk of arrhythmias. Patients may have atrial fibrillation, often as a result of underlying disease. The LVAD will provide left ventricle support, but the loss of atrial “kick” may affect right ventricular function. LVAD patients may also suffer from ventricular arrhythmias. These arrhythmias may result from underlying disease, from irritation of the myocardium by the device, or from ventricular collapse or septal deviation from excessive pump function. Some patients may require an implanted cardioverter defibrillator [11, 16]. Infection is the most common complication, with infection rates ranging from 18% to 59% among LVAD patients.

Box 11.2  Complications encountered in LVAD patients

LVAD‐specific complications •  Suction event •  Pump thrombosis •  Pump complications: failure, stoppage, driveline damage

LVAD‐associated complications •  Infection ○○ Device‐related (i.e., endocarditis) ○○ Device‐specific (i.e., driveline and VAD pump pocket infection) ○○ Non‐LVAD infection (i.e., urinary tract infection, pneumonia) •  Bleeding (i.e., gastrointestinal bleeding) •  Cerebrovascular pathology: ischemic or hemorrhagic stroke •  Hemolysis •  New right ventricular failure •  Dysrhythmia •  Aortic regurgitation

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Infection is second only to heart failure as a cause of mortality in these patients. Infections can present at the surgical site, the driveline, the pump pocket, or the pump itself in the form of endocarditis [17]. Device‐specific problems can manifest as device failure (fortunately rare) or from battery or cable connection issues. Suction events can occur when there is not enough volume in the left ventricle to support the speed of the pump. This causes the intake cannula to collapse and subsequent ventricular arrhythmias [11]. LVADs in place for a long time can become dislodged, resulting in incomplete left ventricle emptying, right ventricular failure, and arrhythmias. LVADs may also have thrombotic complications, causing problems ranging from dyspnea to cardiogenic shock [18, 19]. While EMS clinician interactions with LVAD patients may be infrequent, these patients are high acuity and tend to have high rates of hospital admission [20]. It is beneficial for EMS systems to be aware of LVAD patients in their service areas, and have device reference cards and VAD specialist contact information accessible [21]. Hospital policies may indicate that a VAD specialist be sent to the scene to evaluate the device in the event of a problem. This situation could then result in a delay in patient transport while the VAD specialist is en route. If the patient is having a time‐sensitive medical issue not related to the device, a medical oversight decision may need to be made regarding transport. For example, perhaps a portable LVAD patient is having an acute stroke or GI bleed and no LVAD issues, but the EMS crew is not familiar with the LVAD. The medical oversight physician will need to weigh the risks of delay of transport while waiting on the VAD specialist to arrive versus the risk of an LVAD complication during the EMS transport. The LVAD patient in distress might be having an issue with the device, an exacerbation of the underlying cardiac disease, or an unrelated medical event. The initial EMS assessment should be to determine if the issue is LVAD‐related or not (Figure 11.3). If the event does not seem to be LVAD‐related, then local protocols or medical oversight should be consulted for further guidance. The next step is to determine the type of LVAD involved. The patient and caregiver should have device information available. This information should include whether the patient can receive electrical therapy and whether or not CPR can be performed. Obviously, these questions need immediate answers [11, 21]. EMS personnel must determine if the device provides pulsatile flow or continuous flow. A patient with a pulsatile flow device should have a palpable pulse and blood pressure. P­ulsatile‐pump LVAD failure requires the use of a hand pump to produce blood flow. A patient with a continuous‐flow device will have no detectable pulse. A functioning pump should make a humming sound on auscultation [11]. In the event of device malfunction, the LVAD should generate a series of auditory and visual alarms. These alarms will be device‐ and manufacturer‐ specific. The patient, caregiver, and device literature should be used to determine alarm causes. Power alarms may be triggered by low voltage in the batteries, necessitating battery changes, or,

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Rapid Assessment of VAD Patient

(Check for signs of life. Do not expect or try to feel for a pulse)

Unresponsive & not breathing normally

Loud alarm from external controller?

Address respiratory issues per local protocols

No

Humming sound audible (placing stethoscope over heart)? No Yes

Responsive & breathing normally

Unresponsive & breathing normally

Loud alarm from external controller? Yes

Assume LVAD failure.

(start ventilation when possible) Try to restart device: 1. Expose controller, power source and driveline 2. Expose driveline attached to controller 3. Ensure batteries or other power source securely attached 4. Check battery charge and replace batteries with charged batteries or attach to main power if available.

No

Humming sound audible (placing stethoscope over heart)? Yes Patient now responsive?

(Do not expect to measure a BP or use pulse ox) No

If in VF or VT then defibrillate

5. Attach charged battery to spare controller and detach driveline from controller attached to patient and connect it to new controller 6. Consider cable fracture, gently manipulate driveline to restore connection ***if pulatile device, hand pump if BP and pulse absent***

LVAD Restarted? (Humming sound audible?)

No

If circulation still not adequate then consider CPR/ACLS

Yes

Assess for hypovolemia and consider IV fluids May elevate legs to increase LVAD blood flow Proceed with local protocols and transfer to VAD center if possible

Figure 11.3  Emergency assessment of a patient with an LVAD.

in the case of a pulsatile device power failure, hand pumping. Low‐flow pump alarms most likely result from hypovolemia, which indicate the need for IV fluids or blood products. Other alarms may indicate cable disconnections that require troubleshooting. Transport should not be delayed to perform these interventions [11].

Patients with continuous‐flow devices may not have reliable pulse oximetry readings due to low pulse pressures. As noted, a continuous‐flow device will not produce a palpable pulse or a measureable blood pressure. The EMS clinician will need to use other signs to assess perfusion, such as skin color, absence or presence of diaphoresis, and mental status changes. The patient

Cardiac procedures and managing technology

should be placed on a cardiac monitor, and a 12‐lead ECG should be performed if possible, though the LVAD will create electrical noise on the ECG tracing. LVAD patients should also be exposed to examine for cable disconnections. The driveline skin site should not be routinely examined unless absolutely necessary, due to risk of infection. Clothes should not be cut with shears as there is risk of cutting the cables with disastrous results. For the same reasons, the patient should be moved carefully to prevent dislodgment. Patients showing signs and symptoms of another illness, such as stroke, should be assessed in the usual fashion, regardless of the assist device. Patients with evidence of hemodynamic compromise or hypoperfusion should have large‐bore IV access, and be volume resuscitated. Vasopressors are not generally a good initial therapy, as many problems are volume‐related, and vasopressors will increase afterload, which can worsen pump flow [11]. Arrhythmias should only be treated if they are symptomatic. An LVAD patient with full left ventricle support may be able to tolerate ventricular tachycardia or fibrillation. If the arrhythmia requires treatment, the usual therapies can be used for rate control and rhythm conversion. The patient can also receive electrical therapy [11]. Defibrillator pads should not be placed over the device. Some devices may require that the system controller cables be disconnected prior to defibrillation to prevent damage to the electronics. The patient should also be examined for the presence of an implantable cardioverter defibrillator (ICD), which should provide the appropriate treatment in the event of ventricular arrhythmia [22]. The decision of when to perform CPR can be a major conundrum in treating these patients. Knowledge of the device type and function is crucial. Patients with first‐generation LVADs producing pulsatile flow should not receive chest compressions. Instead the hand pump should be used. Second‐generation and later continuous‐flow devices will not have a hand pump. Chest compressions carry the risk that they may dislodge the device, resulting in exsanguination and death. On the other hand, if the LVAD is not pumping, the underlying left ventricle will not have the ability to maintain perfusion of organ systems. Patient survival is not likely. Lack of compressions may also result in a thrombus formation in the pump, resulting in obstruction to pump flow, and potential downstream embolic events. Awareness by EMS clinicians of the patient’s advanced directives regarding resuscitation may be important, as these patients have chronic severe disease. Ideally, device information, patient wishes and treatment plans, and contact information should be prepared prior to initial discharge from the hospital. In the event of an EMS contact with a patient who is hypoperfused and has a nonfunctioning pump, an attempt may be made to contact the LVAD coordinator for further recommendations. If the coordinator cannot be reached, and the patient is to be resuscitated, compressions should be started and transport initiated per local protocols [11].

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The LVAD patient should be transported to the hospital that placed the device if possible. These hospitals are usually tertiary care centers and should be capable of managing not only LVAD complications but also other issues, such as stroke or GI bleeding. If there are distance issues, air medical transport should be considered. This can shorten transit time and also provide critical care services. Regardless of transport mode, the LVAD patient should be transported with all device equipment, batteries, controllers, documentation, and caregivers (if possible).

Electrical cardiac support devices EMS personnel may also encounter patients in the field with short‐term electrical support devices, such as wearable cardioverter defibrillators (WCDs), or long‐term, implanted cardiac devices, such as implantable cardioverter defibrillators (ICDs) and pacemakers. The approach to a patient with an electrical cardiac support device who is suffering from a medical condition is to determine if the problem results from the device or the underlying medical condition. While these devices are generally safe and effective, thousands of patients have been affected by pacemaker and ICD malfunctions [23]. Pacemakers Cardiac pacemakers are implanted in patients who suffer from bradycardic dysrhythmias. If the patient’s intrinsic rhythm falls below a set target, the pacemaker will provide an electrical stimulus to the myocardium. Pacemakers are designated with a five‐letter code; the first three letters are referred to most often. The first letter indicates the chamber paced, the second letter indicates the chamber sensed, and the third letter the response after sensing (Box 11.3) [24, 25]. Pacemakers can be single chamber or dual chamber.

Box 11.3  Pacemaker codes

•  AOO •  AAI •  VOO •  VVI •  DOO •  DDI •  DDD

Atrial pace; no sense, no inhibitions Atrial pace; atrial sense, inhibited by atrial beat Ventricular pace; no sense, no inhibitions Ventricular pace; ventricular sense, inhibited by ventricular beat Dual chamber pace; no sense, no inhibitions Dual chamber pace; ventricular sense, inhibited by ventricular beat Dual chamber pace; dual chamber sense, inhibited by either chamber

Sources: Mulpuru SK, Madhavan M, McLeod CJ, Cha YM, Friedman PA. Cardiac pacemakers: function, troubleshooting, and management: part 1 of a 2‐part series. J Am Coll Cardiol. 2017; 69:189–210; Kenny T. The Nuts and Bolts of Implantable Device Therapy Pacemakers. Hoboken, NJ: Wiley & Sons, Ltd. 2015. Chapter 13, Pacemaker modes and codes; pp 140–52.

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The more common single‐chamber pacemaker is VVI, which paces the ventricle, senses the ventricle, and inhibits the output pulse if intrinsic ventricular activity is detected. The more common dual‐chamber pacemaker is DDD, which paces and senses in both the atrium and ventricle and has dual response to sensed intrinsic activity [25]. The EMS physician who responds to a pacemaker patient with a clinical issue should determine if the device is the problem.

Vital signs and cardiac monitoring are the best tools. The first determinant is the heart rate. If the patient is markedly bradycardic, the pacemaker is presumed to have failed (Figure 11.4). The patient will require hemodynamic support, which may include external cardiac pacing. If external pacing is indicated, care should be taken to not cover the implanted device with the external pads. If the patient is tachycardic, the physician will need to determine if the pacemaker is firing inappropriately or

Figure 11.4  The first ECG depicts failure of electrical capture with pacer spikes not associated with QRS complexes and a ventricular escape rhythm,

while the second ECG shows the same patient with electrical capture with a QRS complex with every pacer spike.

Cardiac procedures and managing technology

if there is another medical cause. The presence of pacer spikes prior to every tachycardic beat is the best indicator of a pacemaker issue. The next step is to determine what therapy is needed. Optimally, the patient can be transported to a facility where the implanted device can be interrogated by an electrophysiologist, preferably at the hospital where the device was implanted. If the patient’s clinical condition requires more emergent intervention, a special magnet can be held over the pacemaker to suspend inappropriate pacing. The magnet will not turn the pacemaker off, but it will trigger the device to pace at an asynchronous (fixed) rate depending on the device and manufacturer [26]. A DDD pacemaker will pace at DOO, a VVI device will pace at VOO, and an AII device will pace as AOO [26]. Magnet therapy is only effective when the magnet is on the skin over the pacemaker. In the event that magnet therapy is ineffective, it is theoretically possible to cut the pacemaker wires. However, this would be difficult in the field, may permanently damage the device, and should not be performed unless as a last resort. Temporary transvenous pacemakers may also be encountered by the EMS physician during interfacility transports. Transvenous pacemakers are placed in the hospital setting in patients with unstable bradycardic dysrhythmias unresponsive to medical therapy or transcutaneous pacing. The pacer wires are generally placed via the right internal jugular vein or the left subclavian vein and are attached to a pacing generator that generally allows for adjustment of the pacing rate, sensitivity, and energy output. Members of the transport team should be familiar with the specific pacing generator technology and how to troubleshoot it with regard to adjusting those settings. If the sensitivity is too low, the pacer may detect vibrations of transport, interpret them as R waves, and thus will not appropriately pace the patient. Consequently, if the sensitivity is set too high, it may not detect the underlying rhythm and will pace in an asynchronous mode. Implantable cardioverter defibrillators ICDs are a first‐line therapy for many patients at risk for sudden cardiac death (SCD). They are usually implanted in the left infraclavicular region and are typically palpable. All patients with these devices get identification cards that note the manufacturer and device model. ICDs have four main functions: 1) sensing atrial and ventricular signals, 2) classification of those signals into programmable heart rate zones, 3) administration of electrical therapy to terminate ventricular tachycardia or ventricular fibrillation, and 4) pacing for bradycardia or cardiac resynchronization therapy (equivalent to a standard pacemaker) [27]. If ventricular fibrillation or ventricular tachycardia is detected, shocks of 1 to 40 joules can be delivered [27]. Although this is less energy than external defibrillation or ­cardioversion, the shock can still be painful to the patient. The EMS physician will most likely encounter one of three possible scenarios with a patient who is suffering from an

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ICD‐related cardiac event. The first is device failure in the event of a ventricular arrhythmia. The second is an appropriately functioning device in the setting of a ventricular arrhythmia. The third possibility is the ICD delivering shocks inappropriately in the absence of a ventricular arrhythmia. The first steps in all cases are assessment of mental status, vital signs, and cardiac monitoring. If the patient has an unstable ventricular arrhythmia, and the ICD does not fire, it should be assumed the device is nonfunctional and resuscitation protocols should be followed. If external defibrillation is needed, the defibrillator pads should not be placed over the implanted device. If the patient has a ventricular rhythm and the ICD is giving appropriate shocks, care should be focused on additional treatment of the arrhythmia, as well as rapid transport to the hospital. The patient may benefit from analgesia and possibly sedation in the event of multiple shocks. External electrical therapy should not be needed. In the third scenario, the ICD is giving inappropriate shocks in the absence of a ventricular arrhythmia. Some ICDs are programmed to simply detect an elevated rate and not specifically detect ventricular arrhythmias. Inappropriate shocks are most often induced by T‐wave oversensing in which the high amplitude T‐wave is interpreted as another QRS complex leading to double counting. This can also occur during CPR when compressions can trigger an inappropriate shock [28]. As with pacemaker malfunctions, ideally the device can be interrogated by an electrophysiologist at the receiving hospital. In the event the patient’s condition requires emergent intervention to stop inappropriate shocks, a special magnet can be placed over the device. The magnet will suspend detection of ventricular fibrillation and ventricular tachycardia and should stop the shocks. The magnet will not stop the pacemaker function of the ICD or place the pacemaker in asynchronous (fixed) mode [27]. In the event a magnet is used, cardiac monitoring is required because the ICD will no longer be able to sense nor shock arrhythmias. Magnet therapy is only effective while the magnet is secured to the skin over the device. It may also be prudent to apply external defibrillator pads during transport. As with a pacemaker, cutting the lead wires of an ICD will most likely permanently damage the device, is difficult to perform in the field, and is not recommended short of a dire last resort. Wearable cardioverter defibrillator While ICDs have been shown to improve survival from SCD, placement is not always feasible. Ventricular fibrillation and ventricular tachycardia are the most common arrhythmias associated with SCD. The WCD can be used as a bridge to ICD placement or a bridge for short‐term protection against SCD when cardiac recovery is expected [29]. The WCD is a vest‐type garment with an inner layer containing sensing and energy delivering electrodes in direct contact with the patient’s skin. The holster of the vest contains the monitor, battery packs, and other device contents not in contact with the patient’s skin. The convex, resin‐insulated electrodes sense

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the patient’s electrical activity and the processor is programmed to detect shockable ventricular arrhythmias and initiate defibrillation if appropriate. The vest alerts the patient to the activation of the shock delivery algorithm via audible alarms and through vibration signals. This gives the patient the opportunity to deactivate the process by pressing two buttons simultaneously if they are alert. If not deactivated, gel is ejected between the electrodes and patient’s skin and a shock between 75 and 150 joules is delivered. The vest contains a lithium‐ion battery pack that provides continuous power for 24 hours [29]. Some of the issues related to the success rate of WCDs in preventing SCD is patient compliance. The device should be worn at all times. It should only be removed when bathing and then only if someone is present to initiate lifesaving measures as appropriate. The device has been redesigned to make it more comfortable and lightweight. The sense of security that the WCD provides also contributes to patient compliance [29]. The trials to date have reported a 75% success rate of WCDs providing appropriate shock therapy. Like ICDs, however, the WCDs also produce inappropriate shocks when ventricular arrhythmia is not present. Although WCDs have built‐in patient response buttons to prevent inappropriate shocks, shocks are still delivered because patients forget how to deactivate the device. Patients also do not receive appropriate shocks due to incorrect positioning of the device or its electrodes [29]. When an EMS clinician encounters a WCD patient, a standard evaluation should be conducted. CPR can be performed with the device in place. However, if it is broadcasting an imminent shock, stop CPR. The device should be allowed to complete the defibrillation of the unconscious patient prior to proceeding. If external defibrillation is available, external pads can be placed after disconnecting the monitor from the electrode belt, or the vest can be removed altogether. Prior to removing the vest, the battery should be removed to prevent an inadvertent shock.

Pericardiocentesis Pericardiocentesis may be indicated during resuscitation for pulseless electrical activity (PEA). If the PEA is the result of cardiac tamponade, pericardiocentesis may reverse that condition. Cardiac tamponade may be difficult to diagnose in the out‐of‐hospital setting. Tamponade may be suspected based on the patient’s clinical presentation. Prior to cardiac arrest, the patient may develop Beck’s triad of jugular venous distension, hypotension, and muffled heart sounds. If available, portable ultrasound can be used to detect tamponade. Successful pericardiocentesis has been performed in the out‐of‐hospital setting by both EMS physicians and critical care transport teams [30, 31]. It should be used as a final resort when all other therapies have failed [32]. For procedure details, see Chapter 40. Aspiration of blood that does not clot suggests removal from the pericardial space, as opposed to intraventricular blood. Successful pericardiocentesis and the correction

of the tamponade physiology should lead to restoration of spontaneous circulation.

Conclusion Technological advances in both electrical and mechanical cardiac support devices mean that more people are living with them, including people in their homes. Thus, familiarity by EMS clinicians is important to effect optional care and safe transport. Critical patients who are being supported by IABPs, ECMO, or nonportable VADs require special attention by expert teams when they must be transferred from one facility to another. Among the team members must be a specialist in managing the support device. Planning is key to moving patients safely and effectively. EMS clinicians are likely to encounter patients with portable VADs, even if infrequently. Ideally, they would know of such patients in their communities before they are summoned for an emergency condition. In any case, they should be able to rapidly identify the presence of a VAD and the need for determination of whether or not pulsatile flow is expected. Patients with VAD‐related problems often require fluid resuscitation, unless the issue is a rare pump failure or power failure. In those cases, the dedicated hand pump should be used to restore blood flow or CPR initiated if the VAD has no hand pump. For problems not immediately indicating a VAD malfunction, such as stroke or GI bleeding, the patient should be treated as he or she would be in the absence of the VAD. It is prudent to attempt to get the patient to the hospital where the VAD was placed if feasible and appropriate. EMS clinicians should be aware when their patient has a pacemaker or ICD. If the patient’s problem relates to a cardiac dysrhythmia, it is important to assess the ICD or pacemaker function. With a magnet, function can be suspended if it is emitting inappropriate, excessive electrical impulses or shocks. EMS physicians should be capable of performing pericardiocentesis. Although ultrasound may be a helpful adjunct, the procedure can done using anatomical landmarks.

Acknowledgment We acknowledge T.J. Doyle, MD, MPH, author of this chapter in the prior edition.

References 1 Blumen IJ. Principles and Direction of Air Medical Transport Advancing Air and Ground Critical Care Transport Medicine. Salt Lake City, UT: Air Medical Physician Association, 2015. 2 Arrow International. An Introduction to Intra‐Aortic Balloon Pumping. Reading, PA: Arrow International, 2005.

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3 Air and Surface Transport Nurses Association. Mechanically assisted cardiovascular transport. Flight and Ground Transport Nursing Core Curriculum. Air and Surface Transport Nurses Association, Denver, CO, 2006. pp. 205–10. 4 Burzotta A, Carlo T, Doshi SN, et al. Impella ventricular support in clinical practice: Collaborative viewpoint from a European expert user group. Int J Cardiol. 2015; 201:684–91. 5 ABIOMED, Inc. Impella Program Protocols & Tools. Danvers, MA: ABIOMED, Inc., 2019. 6 Ouweneel DM, Eriksen E, Sjauw KD, et  al. Percutaneous mechanical circulatory support versus intra‐aortic balloon pump in cardiogenic shock after acute myocardial infarction. J Am Coll Cardiol. 2017; 69:278–87. 7 Lemaire A, Anderson MB, Lee LY, et  al. The Impella device for acute mechanical circulatory support in patients in cardiogenic shock. Ann Thorac Surg. 2014; 97:133–8. 8 Ergle K, Parto P, Krim SR. Percutaneous ventricular assist devices: a novel approach in the management of patients with acute cardiogenic shock. Ochsner J. 2016; 16:243–9. 9 Lamhaut L, Hutin A, Deutsch J, et  al. Extracorporeal cardio­ pulmonary resuscitation (ECPR) in the prehospital setting: an illustrative case of ECPR performed in the Louvre Museum. Prehosp Emerg Care. 2017; 21:386–9. 10 Burns BJ, Habig K, Reid C, et al. Logistics and safety of extracorporeal membrane oxygenation in medical retrieval. Prehosp Emerg Care. 2011; 15:246–53. 11 Mecham CC. Prehospital assessment and management of patients with ventricular assist devices. Prehosp Emerg Care. 2013; 17:223–9. 12 Meyers TJ, Dasse KA, Macris MP, Poirer VL, Cloy MJ, Frazier OH. Use of a left ventricular assist device in an outpatient setting. ASAIO J 2001; 47:590–5. 13 Long B, Robertson J, Koyfman A, Brady W. Left ventricular assist devices and their complications: a review for emergency clinicians. Am J Emerg Med. 2019; 37:1562–70. 14 Hoshi H, Shinshi T, Takatani S. Third‐generation blood pumps with mechanical non‐contact magnetic bearings. Artif Organ. 2006; 30:324–28. 15 Geisen U, Heilmann C, Beyersdorf F, et al. Non‐surgical bleeding in patients with ventricular assist devices could be explained by acquired Von Willebrand disease. Eur J Cardiothorac Surg. 2008; 33:679–84. 16 Kato TS, Schulze PC, Yang J, et al. Pre‐operative and post‐operative risk factors associated with neurologic complications in patients with advanced heart failure supported by a left ventricular assist device. J Heart Lung Transplant. 2012; 31:1–8. 17 Califano S, Pagani FD, Malani PN. Left ventricular assist device associated infections. Infect Dis Clin North Am. 2012; 26:77–87. 18 Kiernan MS, Pham DC, DeNofrio D, Kapur NK. Management of HeartWare left ventricular assist device thrombosis using

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intracavitary thrombolytics. J Thorac Cardiovasc Surg. 2011; 142:712–4. 19 Felix SE, Martina JR, Kirkels JH, et al. Continuous flow left ventricular assist device support in patients with advanced heart failure: Points of interest for daily management. Eur J Heart Fail. 2012; 14: 351–6. 20 Goebel M, Tainter C, Kahn C, et al. An urban 9‐1‐1 system’s experience with left ventricular assist device patients. Prehosp Emerg Care. 2018; 23:560–5. 21 Schweiger M, Vierecke J, Stiegler P, Prenner G, Tscheliessnigg KH, Wasler A. Prehospital care of left ventricular assist device patients by emergency medical services. Prehosp Emerg Care. 2012; 16:560– 3. 22 Boyle A. Arrhythmias in patients with ventricular assist devices. Curr Opin Cardiol. 2012; 27:13–18. 23 Maisel WH, Moynahan M, Zuckerman BD, et  al. Pacemaker and ICD generator malfunctions analysis of Food and Drug Administration Annual Reports. JAMA. 2006; 295:1901–6. 24 Mulpuru SK, Madhavan M, McLeod CJ, Cha YM, Friedman PA. Cardiac pacemakers: function, troubleshooting, and management: part 1 of a 2‐part series. J Am Coll Cardiol. 2017; 69:189–210. 25 Kenny T. The Nuts and Bolts of Implantable Device Therapy Pacemakers. Hoboken, NJ: Wiley & Sons, Ltd, 2015. Chapter 13, Pacemaker modes and codes; p. 140–52. 26 Jacob S, Panaich SS, Maheshwari R, Haddad JW, Padanilam BZ, John SK. Clinical applications of magnets on cardiac rhythm management devices. Europace.2011; 13(9):1222‐1230. 27 Stevenson, WG, Chaitman BR, Ellenbogen KA, et  al. Clinical assessment and management of patients with implanted cardioverter‐defibrillators presenting to non‐electrophysiologists. Circulation 2004; 110:3866–69. 28 Cmorej P, Smrzova E, Peran D, Bulikova T. CPR Induced inappropriate shocks from a subcutaneous implantable cardioverter defibrillator during out‐of‐hospital cardiac arrest. Prehosp Emerg Care. 2020; 24:85–89. 29 Agarwal J, Narcisse D, Khouzam N, Khouzam RN. Wearable cardioverter defibrillator “The Lifevest”: device design, limitations, and areas of improvement. J Am Coll Cardiol 2018; 42:45–55. 30 Byhahn C, Bingold TM, Zwissler B, Maier M, Walcher F. Prehospital ultrasound detects pericardial tamponade in a pregnant victim of stabbing assault. Resuscitation. 2008; 76:146–8. 31 Kaniecki DM. Pericardiocentesis in an ambulance: a case report and lessons learned. Air Med J. 2019; 38:382–5. 32 Thomson D, Cooney D. Procedures. In: Emergency Medical Services: Clinical Practice and Systems Oversight. Cone DC, O’Connor RE, Fowler RL, editors. Volume 1, Clinical Aspects of Prehospital Medicine, Krohmer JR, Sahni R, Schwartz B, Wang HE, editors. Overland Park, KS: National Association of EMS Physicians, 2009.

CHAPTER 12

Cardiac arrest systems of care Bryan McNally, Paul M. Middleton, Marcus E.H. Ong, and Gayathri Devi Nadarajan

Introduction The original motivations to develop emergency medical services (EMS) systems were to improve the care of patients suffering from major trauma and out‐of‐hospital cardiac arrest (OHCA). Physicians and resuscitation researchers often focus on patient‐level perspectives of cardiac arrest care (e.g., specific drugs or treatment algorithms). However, the most important factors determining OHCA survival involve the systems of community care. Recognition that OHCA survival depended on the time intervals from collapse to initiation of CPR and to defibrillation spurred extensive EMS and public safety efforts to achieve faster response and earlier defibrillation. These efforts included the use of firefighters and police officers as first‐responders, training emergency medical technicians (EMTs) to perform defibrillation, and strategic deployment of advanced life support units (systems status management). However, there were, and remain, inherent logistical limits to first‐responder speed. Development of the automated external defibrillator (AED) led to the concept of public‐access defibrillation (PAD) [1]. The AED emphasized the potential of immediate bystander action in the management of cardiac arrest. Every EMS medical director, manager, and clinician must recognize the importance of this principle. EMS personnel and hospital staff have less influence on OHCA survival than do bystander CPR and AED use (Figure 12.1) [2]. OHCA survival when there is bystander CPR and an AED is used may be as high as 33‐50% [3–5]. State‐ level data from the Cardiac Arrest Registry to Enhance Survival (CARES) program (https://mycares.net), including OHCA incidence and survival rates, demonstrate the effect of bystander interventions early in the “chain of survival” (Table 12.1) [6]. Optimal OHCA survival depends on a comprehensive community‐based approach that includes collecting essential OHCA outcome data as part of a continuous quality improvement program to improve care. Programs like CARES and the Pan Asian Resuscitation Outcomes Study (http://www.scri.edu. sg/index.php/networks‐paros) provide communities with the

necessary tools to collect OHCA data in an ongoing efficient manner, enabling benchmarking and gauging effectiveness in a real‐world environment [4,7–8]. In King County, Washington, the Resuscitation Academy (http://www.resuscitationacademy. com) was created to help communities develop local quality assurance programs through a 3‐day fellowship program designed specifically for EMS clinicians, administrators, and medical directors. Implementation of a community systems‐based approach is as important a role for EMS agencies as the direct patient care they deliver. This chapter provides an overview of the system‐ level considerations in cardiac arrest resuscitation and care.

Epidemiology of Cardiac Arrest The annual incidence of OHCA in the United States is estimated between 166,000 and 450,000 cases [5, 9–10]. The reported incidence varies with the source of the data and definitions used. Precise epidemiological information is limited because the Centers for Disease Control and Prevention does not consider OHCA a reportable disease [11]. The rate of OHCA disability adjusted life years is 1347 per 100,000 population, which ranks third in the United States behind ischemic heart disease and low back and neck pain [12]. Many cardiac arrests are due to ventricular fibrillation (VF) or ventricular tachycardia (VT), but the proportion remaining in shockable rhythms on EMS arrival varies with the time from collapse to initial assessment. Studies based on patients who are hospitalized report shockable rhythms in about 75% of cases, whereas EMS studies report figures ranging from 24% to 60% [4, 13–18]. EMS data suggest that the rate of out‐of‐hospital VF/ VT may be decreasing, but the overall incidence of OHCA is not [19–22]. However, studies with rhythms recorded by on‐site defibrillators continue to identify VF/VT as the most common initial rhythm. VF/VT was the presenting rhythm in 61% of arrests in the casino trial and 59% of the patients in the PAD trial [23, 24].

Emergency Medical Services: Clinical Practice and Systems Oversight, Third Edition. Volume 1: Clinical Aspects of EMS. Edited by David C. Cone, Jane H. Brice, Theodore R. Delbridge, and J. Brent Myers. © 2021 NAEMSP. Published 2021 by John Wiley & Sons, Inc.

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Variable

121

Adjusted Odds Ratio (95% CI)

Age 15 s Platelet count 22 CT shows evidence of large MCA territory infarction (sulcal effacement or blurring of gray‐white junction in greater than one third of MCA territory)

Relative contraindications for the 3‐ to 4.5‐h treat­ ment window History of prior stroke and diabetes mellitus NIH Stroke Scale >25 Oral anticoagulant use regardless of INR Age >80 years INR, international normalized ratio; MCA, middle cerebral artery; NIH, National Institutes of Health; aPTT, activated partial thromboplastin time. Source: Miller J, Hartwell C, Lewandowski C. 2012, Stroke treatment using intravenous and intra‐arterial tissue plasminogen activator. Curr Treat Options Cardiovasc Med. 2012; 14:273–83. © 2012, Springer Nature.

after a stroke, and studies have indicated that hypertension usually resolves spontaneously within a few hours. Yet, systolic blood pressure greater than 185 mmHg has been associated with increased risk of ICH among patients who subsequently receive fibrinolytic therapy. Blood pressure control is also postulated to be helpful in reducing hematoma expansion among ICH patients. In general, blood pressure management is best deferred until the patient is in a more controlled environment, such as an ED, where invasive monitoring is possible. If there are compelling reasons to lower a patient’s blood pressure in the field, such as coexisting pulmonary edema, for example, great care must be taken not to over‐correct. A suitable initial

target is a 10% reduction of systolic blood pressure, but not lower than 150 mmHg. Some literature suggests that placing the patient supine may increase cerebral perfusion, but it also increases intracranial pressure, and this remains an area of uncertainty and investigation. Obviously, supine positioning is not advised in a patient who has clinical evidence of elevated intracranial pressure. As always, the risk of aspiration must be considered as well [13]. Ultimately, the goals for prehospital care of the stroke patients include rapid evaluation, stabilization, neurologic examination, and expedited transport to an appropriate destination hospital [15]. Early communication to the destination hospital is important. Studies have shown that such notification gives time for the stroke team to arrive in the ED and decreases the time from ED arrival to computed tomography (CT) imaging and increased rates of IV tissue plasminogen activator (tPA) administration [16, 17].

Definitive treatment options Sussman and Fitch reported the first use of IV thrombolytics to treat acute ischemic stroke in the late 1950s [18]. However, early studies using either streptokinase or urokinase resulted in high incidences of ICH. Therefore, these therapeutic agents were abandoned for the treatment of stroke until the 1970s, when advanced imaging technology could rule out the possibility of ICH prior to thrombolytic administration and allow for a more definitive diagnosis of ischemic stroke. Unfortunately, high rates of ICH secondary to streptokinase treatment persisted in later trials, and ultimately led to the early termination of the Multicenter Acute Stroke Trial‐Italy (MAST‐I) and Multicenter Acute Stroke Trial‐Europe (MAST‐E) in the mid‐1990s, as well as the abandonment of streptokinase as a viable ischemic stroke treatment option [19]. Around the same time as the MAST‐E trial, several trials of tPA, which was thought to have a better risk–benefit profile compared to other thrombolytics, were conducted and failed to demonstrate favorable outcomes. However, it was felt that the use of tPA held promise if a correct dose and the right population of patients were selected [19]. In 1995, the NINDS trial demonstrated improved functional outcomes at 3 months as measured by the National Institutes of Health Stroke Scale score, the modified Rankin score (mRS), and other neurologic assessment tools in highly selected ischemic stroke patients treated within 3 hours of symptom onset [20]. Patients treated with tPA were 30% more likely to have minimal to no disability at 3 months compared with patients treated with placebo (absolute benefit of 12%; number needed to treat [NNT] = 8), which was found to persist at 12 months [20, 21]. Based upon these findings, in 1996, the U.S. Food and Drug Administration approved the use of intravenous tPA for the treatment of acute ischemic stroke within 3 hours of the onset of symptoms [19]. One criticism of the NINDS trial was that patients treated with tPA had less severe stroke scores than the placebo group, which altered the measured outcome. However,

Stroke

after further analysis, it was determined that the difference in the stroke severity did not account for the differences [22]. Additionally, evidence has emerged supporting the extension of the 3‐hour treatment window to 4.5 hours [23]. The European Cooperative Acute Stroke Study (ECASS III) randomized patients to tPA or placebo within 4.5 hours of symptom onset and found that patients receiving tPA were significantly more likely to have favorable outcomes (52.4% vs. 45.2%; NNT = 14) [23]. Equally as important, among patients who present within the treatment time windows for tPA, those treated sooner have much better odds of having good outcomes. Specifically, patients treated up to 90 minutes from symptom onset have an odds ratio (OR) of having improved functional outcomes of 2.6 (NNT = 4.5), compared to an OR of 1.6 (NNT = 9) for those treated between 91 and 180 minutes, and an OR of 1.3 (NNT = 14.1) for those treated between 181 and 270 minutes [23]. It is the general consensus and the recommendation of the AHA/ ASA that tPA be given in the setting of acute ischemic stroke when it can be performed by personnel trained in the care of acute stroke and without protocol violations [9]. Intra‐arterial tPA and endovascular thrombectomy are two other options for stroke patients who fall outside of the 4.5 hour window or who have not substantially improved after IV tPA therapy [23]. The decision to use intra‐arterial tPA is made after angiographic imaging and requires an interventional neuroradiologist with specific expertise. The PROACT II (Prolyse in Acute Cerebral Thromboembolism) study evaluated the safety and efficacy of this procedure using prourokinase injected into middle cerebral artery occlusions. The study results indicated that there was a significant improvement in outcome (measured as independent function at 90 days) in 40% of patients in the treated group, compared with 25% of patients in the placebo group [24]. For patients with ischemic stroke due to large vessel occlusion (LVO), endovascular thrombectomy has emerged as a promising therapeutic intervention. In the Endovascular Therapy Following Imaging Evaluation for Ischemic Stroke (DEFUSE‐3) trial, investigators assessed functional outcomes for patients treated for a proximal middle cerebral artery or internal carotid artery occlusion with endovascular therapy plus standard medical therapy (endovascular‐therapy group) versus standard medical therapy alone (medical‐therapy group). Patients were treated within 6 to 16 hours since they were last known well. The trial was stopped early for efficacy after 182 patients were randomized. In the endovascular‐therapy group, there was a significantly higher proportion of patients (45% vs. 17% in the medical‐therapy group, p < 0.001) who were functionally independent at 90 days, defined as a mRS score of 0 to 2. Furthermore, the 90‐day mortality rate was lower at 14% in the endovascular‐therapy group versus 26% in the medical‐therapy group (p = 0.05). Notably, there was no significant difference between groups in the frequency of symptomatic intracranial hemorrhage (7% vs. 4%, p = 0.75) or serious adverse events (43% vs. 53%, p = 0.18) [25]. A second group of investigators (DAWN Trial Investigators) evaluated the efficacy of thrombectomy from 6 to 24 hours since

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the patient was last known well. Of the 206 patients enrolled, 107 were assigned to the thrombectomy group and 99 to the standard care group. The rate of functional independence (mRS 0 to 2) at 90 days was 49% in the thrombectomy group and 13% in the standard care group (adjusted difference 33 percentage points; 95% credible interval, 24 to 44; posterior probability of superiority > 0.99). The rate of intracranial hemorrhage did not significantly differ between the two groups (6% in thrombectomy group and 3% in standard care group, p = 0.50) [26]. As endovascular treatments provide greater clinical benefit for LVO strokes, it will become more important for EMS clinicians to be able to risk stratify and transport these patients to larger centers. Among prehospital stroke scores, none are perfect in predicting LVO strokes. In a study of 138 patients, a CPSS (Table  18.1) equal to 3 reliably predicted an LVO (OR 5.7, 95% CI 2.3‐14.1). Among patients with a CPSS = 3, 72.7% had an LVO, compared with 34.3% of patients with CPSS ≤2 (p < 0.0001) [27]. In another study of 440 patients, the Rapid Arterial oCclusion Evaluation (RACE) scale was found to have acceptable discrimination with a RACE score ≥5 having a sensitivity of 66% and specificity of 72% (positive predictive value [PPV] 47%, negative predictive value 86%) (Table 18.3). However, sensitivity and PPV were lower than Table 18.3  Rapid Arterial Occlusion Evaluation (RACE) Scale Item

Facial palsy Absent Mild Moderate to severe Arm motor function Normal to mild Moderate Severe Leg motor function Normal to mild Moderate Severe Head and gaze deviation Absent Present Aphasia* (if right hemiparesis) Performs both tasks correctly Performs 1 task correctly Performs neither tasks Agnosia† (if left hemiparesis) Patient recognizes his/her arm and the impairment Does not recognized his/her arm or the impairment Does not recognize his/her arm nor the impairment Score total

RACE score

NIHSS score equivalence

0 1 2

0 1 2–3

0 1 2

0–1 2 3–4

0 1 2

0–1 2 3–4

0 1

0 1–2

0 1 2

0 1 2

0

0

1

1

2

2

0–9

Source: Perez de la Ossa N, Carrera D, Gorchs M, et al. Design and validation of a prehospital stroke scale to predict large arterial occlusion. Stroke. 2014; 45:87–91. Used with Permission of Wolters Kluwer.

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Box 18.3  Time interval goals for fibrinolytic therapy

Arrival via EMS at the closest ED capable of delivering fibrinolytic as soon as safely possible EMS should provide notification while en route to receiving hospital for suspected stroke patients Rapid assessment by stroke team or emergency physician Completion of computed tomography (CT) scan within 20 minutes Administration of fibrinolytic (tPA) within 60 minutes of arrival to ED and within 4.5 hours of symptom onset for eligible patients Source: Modified from Powers WJ, Rabinstein AA, Ackerson T, et al. 2018 Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2018; 49:e46–e99.

in the original validation study, and further work is needed to determine the optimal prehospital screening tool for identification of LVO [28]. All of these treatments for stroke have potentially devastating complications, the most noteworthy being intracranial bleeding. In addition, these interventions have several exclusion criteria that must be considered when selecting patients, but are beyond the scope of this chapter. Nonetheless, it is important that EMS clinicians have at least a general understanding of available stroke treatments, as well as the rationale for accurate and rapid identification of the stroke victim. Box 18.3 describes the current AHA/ASA time‐to‐ treatment goals related to IV tPA. Ideally, the time window from ED arrival to drug administration should not exceed 60 minutes [9].

EMS transport Given the narrow time windows of opportunity associated with the various interventional stroke therapies and the clearly demonstrated benefit of earlier treatment, EMS is a critical link to ensuring that patients arrive at facilities capable of treating strokes in an expedited manner. Numerous studies have shown that stroke patients accessing the EMS system have a significantly greater chance of timely arrival at an emergency department, which in turn, can promote higher thrombolytic treatment rates [29–32]. More specifically, the California Acute Stroke Prototype Registry (CASPR) collected data from several California hospitals to identify factors that resulted in delayed presentation for treatment. This study indicated that if patients experiencing stroke symptoms (that did not occur overnight) had called EMS immediately, the percentage eligible for tPA would have increased from 4.3% to 28.6% [33]. Furthermore, one randomized trial examining the effect of an

intervention comprised of a prehospital stroke assessment tool, an ambulance protocol for hospital bypass for potential thrombolysis‐eligible patients, and prehospital notification of the acute stroke team demonstrated a significant increase in thrombolytic administration. In this study, the time from symptom onset to ED arrival decreased from 150 minutes to 90 minutes, and the proportion of patients receiving tPA increased from 4.7% to 21.4% after the intervention, with 43% of patients having minimal to no disability at 3 months [34]. Knowledge of the stroke treatment capabilities among area hospitals is quite important. Health care facilities that are not stroke centers may be able to administer tPA, but often lack the capability to perform more invasive procedures such as intra‐ arterial tPA administration or endovascular thrombectomy [24, 35]. These procedures require an interventional neuroradiologist. In addition, dedicated personnel must be available quickly and trained in the evaluation of stroke. The staffing of EDs throughout the country still varies widely, as does the relative stroke experience of practitioners. Designation by The Joint Commission indicates that a hospital has been evaluated and found to be compliant with specific national guidelines [36, 37]. Currently, The Joint Commission certifies hospitals at the following levels: Acute Stroke Ready Hospital, Primary Stroke Center, Thrombectomy‐Capable Stroke Center, and Comprehensive Stroke Center [38, 39]. The process of certifying hospitals as stroke centers depends on whether they meet specific criteria defined by The Joint Commission, which include availability of a stroke team, neurology consultation, and diagnostic and therapeutic capabilities (Table  18.4) [38]. Acute Stroke Ready Hospitals are able to deliver thrombolytics and promptly transfer patients to a higher‐level center. Primary Stroke Centers have committed to the rapid assessment and treatment with IV thrombolytics as well as an ability to admit acute stroke patients. A designation of Thrombectomy‐Capable or Comprehensive Stroke Center indicates those hospitals are uniquely equipped and staffed to treat the more complex stroke cases. Each EMS agency must evaluate the community it serves, including its available resources, and then work to develop appropriate patient care guidelines for the evaluation and treatment of stroke patients. This should be done in conjunction with the local and regional health care facilities. It should be determined whether the local community hospital is capable of managing acute stroke victims. Hospital transport destinations should be predetermined based on time and distance variables. In addition, air medical transport may be considered, including direct air medical evacuation of stroke patients from the scene. Air medical transport may be an appropriate option if the ground EMS transport time is expected to exceed 1 hour, and the air medical crew could arrive at a stroke center in time to facilitate appropriate evaluation and treatment within the therapeutic window. In making such a decision, it is important to consider all the elements of air medical response that consume time, including lift time, flight time, time for patient evaluation, and time to load and unload. Guidelines that include air

Table 18.4  Joint Commission stroke center comparison ASRH

PSC

TSC

CSC

Eligibility

Stroke protocols based on evidence‐based standards

Stroke protocols based on evidence‐ based standards

•• Stroke protocols based on evidence‐based standards •• Performed at least 15 mechanical thrombectomy procedures over past 12 months (or over 30 in past 24 months)

•• Stroke protocols based on evidence‐based standards •• Performed at least 15 mechanical thrombectomy procedures over past 12 months (or over 30 in past 24 months)

Program Medical Director

Possesses sufficient knowledge of cerebrovascular disease

Possesses sufficient knowledge of cerebrovascular disease

Possesses background in neurology

Possesses extensive expertise 24/7

Acute Stroke Team

Available 24/7, at bedside within 15 min

Available 24/7, at bedside within 15 min

Available 24/7, at bedside within 15 min

Available 24/7, at bedside within 15 min

EMS Collaboration

Access to EMS protocols

Access to EMS protocols

Access to EMS protocols, routing plans, records from transfer

Access to EMS protocols, routing plans, records from transfer

Stroke Unit

No designated beds for stroke patients

Has designated beds for acute stroke patients

Has Neuro ICU and on‐site critical care 24/7

Has Neuro ICU and on‐site neurointensivist 24/7

Diagnostic Capabilities

CT, labs 24/7 (MRI 24/7 if used)

CT, MRI (if used), labs 24/7; CTA and MRA; at least one cardiac imaging modality

CT, MRI, labs, CTA, MRA, catheter angiography 24/7; cranial and duplex ultrasound; TEE

CT, MRI, labs, CTA, MRA, catheter angiography 24/7; cranial and duplex ultrasound; TEE

Neurologist Accessibility

24/7 in person or via telemed

24/7 in person or via telemed

24/7 in person or via telemed; call schedule

Meets needs of multiple complex stroke patients; 24/7 call schedule

Neurosurgical Services

Within 3 hours via transfer

Within 2 hours; OR available 24/7 that provides neurosurgery

Within 2 hours; OR available 24/7 that provides neurosurgery

24/7 availability; neurointerventionist; neuroradiologist; neurologist; neurosurgeon

Treatment Capabilities

IV thrombolytics and transfer

IV thrombolytics and medical management

IV and IA thrombolytics; mechanical thrombectomy

IV thrombolytics; endovascular therapy; microsurgical clipping of aneurysms, stenting, and carotid surgery

Research

N/A

N/A

N/A

Participates in IRB‐approved stroke research

ACRS, Acute Stroke Ready; PSC, Primary Stroke Center; TSC, Thrombectomy‐Capable Stroke Center; CSC, Comprehensive Stroke Center. Source: Adapted from The Joint Commission ‐ The Stroke Certification Programs – Program Concept 2019. https://www.jointcommission.org/‐/media/tjc/documents/accred‐and‐cert/certification/certification‐by‐setting/stroke/dsc‐stroke‐grid‐comparison‐chart. pdf. Accessed 8/7/2020.

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medical dispatch based on telecommunicator information may be considered, specifically for rural areas without local health facilities capable of stroke interventions. Air medical transport of stroke patients in rural areas may facilitate access to thrombolytic treatment or thrombectomy for LVO strokes. Many hospitals and their EDs, especially smaller rural facilities, still lack resources and refined processes for rapidly evaluating possible stroke patients and administering tPA. In some cases, using air medical services markedly increases the proportion of patients treated with thrombolytics [40]. It seems clear that the role of medical helicopter transport as part of regional systems of care is expanding [41].

Innovations in prehospital stroke management Some regions are trialing the concept of mobile stroke units in an effort to improve the time to tPA or other intervention. A mobile stroke unit ambulance allows for the early administration of tPA in a prehospital setting through the ability to perform the neurologic evaluation and obtain CT imaging in a mobile unit. Most exist in urban areas, though the need for timely stroke evaluation and intervention points to significant potential in rural settings as well. Rural areas may use a rendezvous approach, in which EMS clinicians from a rural site bring the patient toward a stroke center, but meet and transfer care of the patient to the mobile stroke unit along the way. The mobile stroke unit crew often has telemedicine capabilities, linking EMS clinicians to additional resources within the affiliated stroke center [42]. One of the earliest such programs on the east coast of the United States was established by New York Presbyterian Hospital in 2016. This particular mobile stroke unit crew consisted of two paramedics, one radiology technologist, and one vascular neurologist. During the 7‐month pilot, 49 patients were transported, with diagnoses of acute ischemic stroke among 49% of those patients; tPA was administered to 32.6% of the patients transported. This program focused on the complete integration of the affiliated stroke centers’ information systems into a mobile unit, the first of its kind known to do so [43]. In February of 2017, the Edmonton Stroke Program in Canada implemented a rural mobile stroke unit, affiliated with the University of Alberta Hospital in Edmonton. The crew consisted of a stroke fellow, a radiology technologist, a registered nurse, a primary care paramedic, and an advance care paramedic. The unit was dispatched to rendezvous with EMS crews arriving from rural scene calls or rural EDs. The patient was then transferred into the mobile stroke unit for neurologic evaluation and CT imaging; the unit had the ability to administer tPA if appropriate. At last published report, 68 patients had been evaluated and 17 (25%) received tPA. An additional 28 patients were transferred to the stroke center for further evaluation [42]. Initial experiences indicate that mobile stroke units, in the settings in which they have been deployed, result in earlier

administration of tPA. No increased additional risk of complicating ICH has been noted. It remains difficult to determine the long‐term clinical outcome benefit, primarily due to the small patient numbers in most studies. Interest in broadening the use of mobile stroke units continues, including the introduction of CT angiography and perfusion, as well as the treatment of other neurological emergencies. Additionally, with advancements in telemedicine technologies, the ability to transition mobile stroke unit staffing to paramedics may also exist [42]. Emphasis is growing on endovascular thrombectomy for patients with LVO strokes. Current evaluations are focusing on the direct transport of select patients to thrombectomy‐capable and comprehensive stroke centers. However, although bypassing a closer primary stroke center reduces the time to potential thrombectomy, it may also delay the administration of IV thrombolytics. If there is a paucity of stroke centers capable of performing thrombectomy in a given geographical area, EMS transport times may be prolonged when using a bypass strategy. In addition, the optimal stroke scale for EMS identification of LVO stroke patients who may benefit from direct transport to a thrombectomy‐capable center needs additional research. Recent investigation suggests that patients with suspected LVO stroke may benefit from being redirected to a comprehensive stroke center if additional transport time is 72 hours, and burns > 72 hours old are at increased risk of severe hyperkalemia with the use of depolarizing NMBAs due to an upregulation of acetylcholine receptors. Fatal arrhythmias can develop within minutes and the EMS clinician must recognize and appropriately initiate treatment as discussed above. It is recommended that nondepolarizing NMBAs such as rocuronium be used instead for this patient population should RSI be required [39].

Signs of peritonitis for the prehospital clinician include a change in the fluid coming from the catheter during a fluid exchange or purulent drainage from the catheter insertion site [31]. The fluid used for dialysis in peritoneal dialysis often contains high amounts of glucose, drawing water out of the body. In rare cases, patients can absorb the glucose and present with a hyperglycemic, hyperosmolar state and resulting critical illness from the same [32].

Special considerations

Renal failure and dialysis

Use of dialysis access for resuscitation The use of an ESRD patient’s dialysis access in the prehospital setting should be reserved for the critical, rapidly decompensating patient when intravenous and intraosseous access cannot be obtained during resuscitation efforts. While the risks of complications (e.g., thrombosis, infection) may ultimately result in the loss of the patient’s graft, fistula, or catheter, these issues can be dealt with later, pending the patient’s survival. Both AV fistulas and AV grafts can be accessed in a fashion similar to starting a peripheral intravenous line. Gloves, eye protection, and a mask should be used along with aseptic technique to the extent possible. A tourniquet should be loosely applied to the axilla proximal to the access site, tight enough to cause the vessel to engorge, and be removed immediately after cannulation of the fistula or graft. A large‐bore needle (14, 16, or 18 gauge) with or without an angiocatheter should be inserted into the fistula at 20‐35 degrees (45 degrees for graft access) until a flash of blood is seen. The needle should be advanced 3‐4 mm before flattening the angle of insertion flat against the skin and threading the needle alone or with a catheter until the hub rests against the insertion site. The line needs to be secured in place. Due to the high‐velocity blood flow in the graft and fistula, saline lock tubing and a pressure bag for fluids will be needed, especially for access using an angiocatheter. When appropriate, the EMS clinician should assess for a thrill at the access site and relay this information to the receiving facility [40]. Dialysis catheters, whether tunneled or nontunneled, essentially function as central lines. The dialysis catheter usually has two lumens attached to two ports, red and blue. The red port is considered arterial and the blue port venous, tasked with bringing filtered blood from the dialysis machine back to the heart. A third port, white in color, may be present specifically for blood draws and medication administration. In the absence of the white port, the blue “venous” port should be used for emergency administration of drugs and fluids. Personal protective equipment should be donned to keep the procedure as sterile as possible. The port cap should be cleaned with chlorhexidine or alcohol, and the lumen should be clamped while the cap is removed. After cleaning the catheter hub, a syringe should be attached, and the lumen unclamped. As information regarding the locking fluid present in the catheter will likely not be immediately available to the EMS clinician, fluid and blood should be withdrawn with a 10 cc syringe and wasted before administration of medications. This is to prevent inadvertent systemic administration of the locking solution. The lumen should be flushed and clamped after drug administration. Replacement of locking fluid and caps can occur in the hospital setting. During emergency transport from a dialysis center, the staff at the facility may leave the ESRD patient’s vascular device accessed. EMS personnel should be aware of this as a potential site for emergency drug administration and should protect the access point from trauma.

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EMS pearls Focused history When the EMS clinician encounters a dialysis patient, a set of focused questions to the patient and any family/dialysis clinic staff present can be quite helpful to subsequent treatment teams. • Dialysis schedule – Knowing what days of the week the patient has dialysis, as well as the day of the most recent session is useful. • Length of sessions – Attempt to determine how many hours each dialysis session is, as well as if the patient is completing the full length each time, with attention to the last session. If transporting from the dialysis center, it is important to determine whether the session was completed, partial, or not even started. • Volume status  –  Each patients should have a known “dry weight,” which is the ideal euvolemic weight. Additionally, knowing the patient’s current weight can greatly help with fluid status assessment. The patient or dialysis center staff may also be able to state how much weight/fluid is removed with each dialysis and/or the current net fluid volume. • Vital signs – Dialysis patients may have “abnormal” vital signs at baseline. If so, careful documentation of the patient’s baseline heart rate and blood pressure is important. Refrain from using the limb on the same side of hemodialysis access to prevent complications like thrombosis. • Urine output status – Whether or not an ESRD patient is still able to make urine for diuresis is often helpful in treatment decisions of the fluid overloaded patient. Destination selection Should a patient with ESRD require transport, it may be necessary to choose a destination hospital that can care for his or her needs. Even if the patient is not presenting to EMS for a dialysis‐related complaint, should he or she require admission, renal replacement therapy will be required, eventually. The greater risk of coronary artery disease and stroke may necessitate specialty care more often than in the otherwise healthy nondialysis patient. Local protocols may be developed to address this specific patient population and its particular needs. Resource planning The individual in the community who is dialysis dependent requires unique resources for his or her survival. While under normal conditions the patient likely has established mechanisms for obtaining transportation and treatment, this system can be disrupted in the case of a disaster or disruptive weather event. The local emergency management agency should work alongside EMS medical directors and the dialysis providers to develop contingency plans appropriate for the local environment. Large dialysis center networks may operate a central command/tracking system that can be a resource for planning and disaster management. Other government and local agencies will need to contribute to this planning process, as operation of a hemodialysis machine requires infrastructure that is easily

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disrupted. Identification and registry of the patients who will require emergent dialysis services in times of need can allow for continued access to life‐sustaining care. Convalescent Transportation Hemodialysis patients have a frequent need for transportation to a medical facility for regular treatment sessions. Patients may require assistance in this regard, relying on nonemergency transportation services. There exists a wide variety in the training level of personnel handling this form of transportation. People in this field may become well acquainted with their “regular” dialysis patients and be able to recognize subtle changes in their condition, which may require diversion to a higher level of care. Protocols should be established to assist in the recognition of emergencies in this high‐risk population. If the particular transport unit does not possess the capabilities to care for emergency medical conditions, personnel should know the best method of accessing the resources required to do so.

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13 Montague BT, Ouellette JR, Buller GK. Retrospective review of the frequency of ECG changes in hyperkalemia. Clin J Am Soc Nephrol. 2008; 3:324–30. 14 Dépret F, Peacock WF, Liu KD, et al. Management of hyperkalemia in the acutely ill patient. Ann Intensive Care. 2019; 9:1–16. 15 Einhorn LM, Zhan M, Hsu VD, et al. The frequency of hyperkalemia and its significance in chronic kidney disease. Arch Intern Med. 2009; 169:1156–62. 16 Yu AS, Gupta A. Hypermagnesemia: causes, symptoms, and treatment. In: Goldfarb DS, editor. UpToDate [Internet]. Waltham, MA: UpToDate; 2020. Accessed August 20, 2020. 17 Dad T, Sarnak MJ. Pericarditis and pericardial effusions in end‐ stage renal disease. Semin Dial. 2016; 29:366–73. 18 Ahmadmehrabi S, Wilson Tang WH. Hemodialysis‐induced cardiovascular disease. Semin Dial. 2018; 31:258–67. 19 National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases. United States Renal Data System. 2018 USRDS Annual Data Report: Epidemiology of Kidney Disease in the United States. Bethesda, MD: NIH, 2018. 20 Murray AM, Seliger S, Lakshminarayan K, et  al. Incidence of stroke before and after dialysis initiation in older patients. J Am Soc Nephrol. 2013; 24:1166–73. 21 Galbusera M, Remuzzi G, Boccardo P. Treatment of bleeding in dialysis patients. Semin Dial. 2009; 22:279–86. 22 Kato S, Chmielewski M, Honda H, et  al. Aspects of immune dysfunction in end‐stage renal disease. Clin J Am Soc Nephrol. 2008; 3:152633. 23 Rajdev K, Leifer L, Sandhu G, et al. Fluid resuscitation in patients with end‐stage renal disease on hemodialysis presenting with severe sepsis or septic shock: a case control study. J Crit Care. 2020; 55:157–62. 24 Khan RA, Khan NA, Bauer SR, et al. Association between volume of fluid resuscitation and intubation in high‐risk patients with sepsis, heart failure, end‐stage renal disease, and cirrhosis. Chest. 2020; 157:286–92. 25 McMullen JT, Gadboid JA. Patient trapped kneeling for 18 hours has more than leg ischemia. JEMS [Internet]. 2016 [cited Aug 24, 2020]; 41. Available from: https://www.jems.com/journal/. 26 Whiffin ANH, Spangler JD, Dhir K, et  al. Bathroom entrapment leading to cardiac arrest from crush syndrome. Prehosp Emerg Care. 2019; 23:90–93. 27 Mirski MA, Lele AV, Fitzsimmons L, Toung TJ. Diagnosis and  treatment of vascular air embolism. Anesthesiology. 2007; 106:164–77. 28 Wolfson AB, Singer I. Hemodialysis‐related emergencies–part 1. J Emerg Med. 1987; 5:533–43. 29 Wangsgard C, Cabrera D. 2015. How to stop a post‐dialysis site bleeding. [Blog] Available at: https://emblog.mayo.edu/2015/04/27/ how‐to‐stop‐a‐post‐dialysis‐site‐bleeding. Accessed July 23, 2020. 30 Tuchman S, Khademian P, Mistry K. Dialysis disequilibrium syndrome occurring during continuous renal replacement therapy. Clin Kidney. J 2013; 6:526–29. 31 Szeto C, Li, P. Peritoneal Dialysis‐Associated Peritonitis. Clin J Am Soc Nephrol. 2019; 14:1100–1105. 32 Boyer J, Gill GN, Epstein FH. Hyperglycemia and hyperosmolality complicating peritoneal dialysis. Ann Intern Med. 1967; 67:568–72. 33 Menez S, Jaar BG. Missed hemodialysis treatments: a modifiable but unequal burden in the world. Am J Kidney Dis. 2018; 72:P625–27.

Renal failure and dialysis

34 Kutner NG, Zhang R, McClellan WM, et al. Psychosocial predictors of non‐compliance in haemodialysis and peritoneal dialysis patients. Nephrol Dial Transplant. 2002; 17:93–9. 35 Leggat JE, Orzol SM, Hulbert‐Shearon TE, et  al. Noncompliance in hemodialysis: predictors and survival analysis. Am J Kidney Dis. 1998; 32:139–45. 36 Gehm L, Propp DA. Pulmonary edema in the renal failure patient. Am J Emerg Med. 1989; 7:336–9. 37 Wilcox CS. New insights into diuretic use in patients with chronic renal disease. J Am Soc Nephrol. 2002; 13:798–805.

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38 Rafique Z, Chouihed T, Mebazaa, et  al. Current treatment and unmet needs of hyperkalemia in the emergency department. Eur Heart J Suppl. 2019; 21(Suppl A):A12–A19. 39 Martyn JA, Richtsfeld M. Succinylcholine‐induced hyperkalemia in acquired pathologic states: etiologic factors and molecular mechanisms. Anesthesiology. 2006; 104:158–69. 40 Manning, M. Use of dialysis access in emergent situations. J Emerg Nurs. 2008; 34:37–40.

CHAPTER 23

Infectious and communicable diseases Russell D. MacDonald

Introduction Emergency medical services (EMS) clinicians are typically the first health care workers to encounter sudden illnesses and other health emergencies in the community, placing them at risk of communicable and infectious diseases. The U.S. Occupational Safety and Health Administration identifies more than 1.2 million community‐based first‐response personnel, including law enforcement, fire, and EMS clinicians, who are at risk for infectious exposure [1]. While infectious and communicable disease preparedness may not have previously been a priority in some EMS agencies, the 2003 severe acute respiratory syndrome (SARS) outbreaks made it one. During the SARS outbreaks in Toronto and Taipei, EMS personnel were exposed to and contracted SARS in significant numbers, resulting in one paramedic fatality. The loss of paramedics available for work due to exposure, quarantine, and illness affected the ability to maintain staffing during the outbreak and highlighted the need for EMS systems to adequately prepare and protect the workforce from potential exposures [2–4]. The 2020 global pandemic due to the novel coronavirus 2019 (SARS‐CoV2 or 2019‐nCoV) highlighted the need for robust EMS infection prevention and control practices to protect personnel and maintain system integrity. Efforts must be multifaceted to account for potential exposures in the workplace from patients, co‐workers, and the public. Additionally, contingency planning must account for the possibility of temporary losses of significant portions of the workforce at times when demands on the EMS system are increased.

EMS Clinician and Patient An infectious disease results from the invasion of a host by disease producing organisms, such as bacteria, viruses, fungi, or parasites. A communicable (or contagious) disease is one that

can be transmitted from one source (i.e., person or animal) to another, by contact with the infected individual or bodily fluids, contact with contaminated surfaces or objects, or ingestion of contaminated food or water, or by contact with disease vectors such as mosquitos, fleas, or mice. Not all infectious diseases are communicable. For example, malaria and schistosomiasis are spread by contact with disease vectors. These are not typically considered to be communicable or contagious diseases because they cannot be spread by direct contact with an infected person. On the other hand, chickenpox is an infectious disease that is also highly communicable, because it can be easily transmitted from one person to another. The mode of transmission is the mechanism by which an agent is transferred to the host. Modes of transmission include contact transmission (direct, indirect, droplet), airborne, vector‐borne, or common vehicle (food, equipment). Contact transmission is the most common mode of transmission in the EMS setting and can be effectively prevented using routine practices. Direct contact transmission occurs when there is direct contact between an infected or colonized individual and a susceptible host. Transmission may occur, for example, by biting, kissing, or sexual contact. Indirect contact occurs when there is passive transfer of an infectious agent to a susceptible host through a contaminated intermediate object. This can occur if contaminated hands, equipment, or surfaces are not appropriately washed and decontaminated after patient contacts. Examples of diseases transmitted by direct or indirect contact include human immunodeficiency virus (HIV), hepatitis, and methicillin‐resistant Staphylococcus aureus (MRSA). Droplet transmission is a form of contact transmission requiring special attention. It refers to large droplets generated from the respiratory tract of a patient when coughing or sneezing, or during invasive airway procedures such as intubation and suctioning. These droplets are propelled and may be deposited on the mucous membranes of the susceptible host. The droplets may also settle in the immediate environment, and the infectious agents may remain viable for prolonged periods,

Emergency Medical Services: Clinical Practice and Systems Oversight, Third Edition. Volume 1: Clinical Aspects of EMS. Edited by David C. Cone, Jane H. Brice, Theodore R. Delbridge, and J. Brent Myers. © 2021 NAEMSP. Published 2021 by John Wiley & Sons, Inc.

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to be later transmitted by indirect contact. Examples of diseases transmitted by droplet transmission include meningitis, influenza, rhinovirus, respiratory syncytial virus, and coronavirus diseases. Airborne transmission refers to the spread of infectious agents to susceptible hosts through the air. In this case, infectious agents are contained in very small droplets that can remain suspended in the air for prolonged periods. These agents are dispersed widely by air currents and can be inhaled by a susceptible host located at some distance from the source. Examples of airborne transmission diseases include measles (rubeola), varicella (chicken pox), and tuberculosis. Vector‐borne transmission refers to the spread of infectious agents by means of an insect or animal (the “vector”). Examples of vector‐borne illnesses include rabies, where the infected animal is the vector, and West Nile virus or malaria, where infected mosquitos are the vectors. Transmission of vector‐ borne illness does not occur between patients and EMS personnel. Common vehicle transmission refers to the spread of infectious agents by a single contaminated source to multiple hosts. This can result in large outbreaks of disease. Examples of this type of transmission include contaminated water sources (Escherichia coli); contaminated food (Salmonella); or contaminated medication, medical equipment, or intravenous solutions.

identify patients with symptoms of fever, chills, cough, shortness of breath, or diarrhea. The call‐taker can also determine if the patient location, such as nursing home, group home, or other institutional setting, poses a potential risk to the responding personnel. This information appropriately conveyed to EMS clinicians helps them prepare and determine what precautions are necessary before they make patient contact. When patient contact is made, personnel should continue to determine if the patient has a potential risk for a communicable disease. A brief history and physical examination can help raise suspicion. The following screening questions may help identify a patient with a communicable disease: • Do you have a new or worsening cough or shortness of breath? • Do you have a fever, shakes, or chills? • Do you have a sore throat, runny nose, or nasal congestion? • Do you have nausea, vomiting, or diarrhea? • Do you have a headache or muscle pains? • Have you had an abnormal temperature (above 38 degrees C)? • Have you been in close contact with anyone who is ill or known to have a communicable disease? • Have you been in contact with anyone who has traveled to an area affected by a communicable disease outbreak? A screening physical examination will also identify obvious signs of a communicable disease. This may include a rash, skin lesions, or draining wounds.

General Approach and Patient Assessment

Specific Illnesses

The risk of communicable disease is not as apparent as other physical risks, such as road traffic, power lines, firearms, or chemical agents. EMS personnel must use the same heightened level of suspicion and precaution whenever approaching a patient. All personnel must take appropriate precautions when a patient presents with any signs or symptoms potentially due to an infectious or communicable disease. All EMS and first responder agencies must provide appropriate training that prepares personnel to identify at‐risk patients and to use personal protective equipment (PPE). Table 23.1 outlines suggested PPE based on procedure or intervention. Table  23.2 provides suggested precautions based on the suspected infection. Appropriate use of PPE is tantamount to implementation of isolation as it might be described in a hospital setting. One important principal difference is that the patient’s location is far less static. Thus, it is important that personnel, EMS and hospital alike, soon to come in proximity to the patient, have enough forewarning to enable them similarly to prepare with appropriate PPE. Further, in the case of a receiving hospital, advance notice may facilitate preparation of an optimal isolated receiving area for an infectious patient. The risk assessment begins with information from the public safety answering point, prior to making patient contact. Call‐ taking procedures should include basic screening to identify potential communicable disease threats. The screening can

Influenza Influenza classically presents with the abrupt onset of fever, usually 38‐40 degrees C, sore throat, nonproductive cough, myalgias, headache, and chills. Influenza is caused by a virus with three subtypes in humans: A, B, and C. Influenza A causes more severe disease and is mainly responsible for pandemics. It has different subtypes determined by surface antigens H (hemagglutinin) and N (neuraminidase). Influenza B causes more mild disease and mainly affects children. Influenza C rarely causes human illness and is not associated with epidemics [3]. Influenza transmission occurs primarily through droplets when a person coughs or sneezes but may also occur indirectly by contact with surfaces contaminated by respiratory secretions. Handwashing and shielding coughs and sneezes help to prevent spread. Influenza is transmissible from 1  day before symptom onset to approximately 5 days after symptoms begin and may last up to 10 days in children. Time from infection to development of symptoms is 1‐4 days [4]. Influenza has been responsible for at least 31 pandemics in history. The most lethal “Spanish flu” pandemic of 1918‐1919 is estimated to have caused 50  million deaths globally with 700,000 of those deaths occurring in the United States in a single year. In this pandemic, deaths occurred mainly in healthy 20‐ 40‐year‐olds, which differs from the usual pattern of mortality

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Table 23.1  Suggested Personal Protective Equipment Based on Procedure or Intervention Intervention

Gloves

Facial and Eye Protectiona

Gowns

Drawing blood or starting an IV/IO line Controlling minor bleeding with pressure or dressing minor skin wound Contact with patient with cough or vomiting Needle thoracostomy Tracheal intubation Oral or nasal suctioning

Yes Yes

No No

No No

Yes Yes Yes Yes

Yes Yes Yes Yes

Controlling arterial or heavy venous hemorrhage Emergency childbirth Known infection or colonization with antibiotic‐resistant organism (VRE, MRSA, etc.) Disinfecting or cleaning contaminated equipment or transport vehicle

Yes Yes Yes

Yes Yes No (unless cough present) Yes

Yes (if febrile respiratory illness or vomiting) Yes (if febrile respiratory illness present) Yes (if febrile respiratory illness present) Yes (if febrile respiratory illness or vomiting present) Yes Yes Yes

Yes

Yes

When in doubt: always use the maximum, not the minimum, PPE  If an aerosol‐generating medical procedure is anticipated or the patient is known to have a communicable disease that is known to be spread by the airborne route, an N95 respirator is the preferred mask to be worn by personnel treating or in close proximity to the patient.

a

Table 23.2  Suggested Precautions Based on Suspected Infection Level 1a

Level 2b

Level 3c

Abscesses Diarrhea Hepatitis A Hepatitis E Cytomegalovirus Herpes simplex

Chicken pox Common cold Croup Diphtheria Epiglotitis German measles (rubella)

Herpes zoster Lice Viral meningitis Scabies Syphilis

Red measles Herpes zoster Infectious mononucleosis Meningitis, meningococcal Meningitis, Haemophilus influenza Mumps Pharyngitis Pneumonia Streptococcus Tuberculosis Whooping cough

AIDSd Clostridium difficilee Hepatitis Bd Hepatitis Cd Hepatitis Dd Coronavirusesf during known outbreaks or when virus known to be producing rapid person‐to‐person spread Influenza (if contact with respiratory secretions is likely) Viral hemorrhagic feversg (Ebola, Marburg, Crimean‐Congo, Lassa)

 Gloves and handwashing.  Level 1 plus mask (N95 if airborne or high‐risk pathogen) and full face shield. c  Level 2 plus disposable impermeable gown. d  Level 3 if exposure to blood or body fluid is anticipated; otherwise, Level 1 precautions are appropriate. e  Level 2 is adequate is there is no risk of soiling clothes or uniform. However, if the patient has any risk of soiling, Level 3 precautions are necessary. f  Although transmission of coronaviruses (SARS, MERS, COVID‐19) may be considered to be similar to other highly contagious viral agents listed requiring Level 2 precautions, these viruses require Level 3 precautions, particularly in outbreak situations. In addition, special precautions may be required when transporting patients with coronaviruses. g  Special precautions are required when transporting patients who are symptomatic with known of suspected viral hemorrhagic fevers. a

b

and morbidity in young children and the elderly during seasonal outbreaks of influenza. Annual vaccination is the best way to prevent influenza, because vaccination can be given well before influenza virus exposures occur and can provide safe and effective immunity throughout the influenza season. Influenza vaccine is the

principal means of preventing morbidity and mortality. The vaccine changes yearly based on the antigenic and genetic composition of circulating strains of influenza A and B found in January to March, when influenza reaches its peak activity. When the vaccine strain is similar to the circulating strain, influenza vaccine is effective in preventing illness among 70‐90% of those

Infectious and communicable diseases

younger than 65 years who are vaccinated. Among those aged 65 years and older, the vaccine is 30‐40% effective in preventing illness, 50‐60% effective in preventing hospitalization, and up to 80% effective in preventing death. EMS personnel should be immunized annually, ideally as soon as the vaccine is ­available locally. Six licensed prescription influenza antiviral drugs are approved by the U.S. Food and Drug Administration (FDA), four of which (oseltamivir, zanamivir, peramivir, and baloxavir marboxil) were recommended for the 2019‐2020 influenza season. When used for prevention of influenza, they can be 70‐90% effective. However, antiviral agents should be used as an adjunct to vaccination, and not replace it. The Centers for Disease Control and Prevention (CDC) does not recommend widespread, routine, or pre‐exposure use of antiviral medications for chemoprophylaxis except under specific circumstances [3]. These include short‐term pre‐exposure chemoprophylaxis for unvaccinated health care personnel who are in close contact with persons at high risk of developing influenza complications during periods of influenza activity, when influenza vaccination is contraindicated or unavailable and these high‐risk persons are unable to take antiviral chemoprophylaxis. In addition, there is some weak evidence to suggest that antiviral post‐exposure chemoprophylaxis for unvaccinated EMS personnel can be used during periods of influenza activity when influenza vaccination is contraindicated or unavailable [5, 6]. If post‐exposure chemoprophylaxis is given, it should be administered as soon as possible after exposure, ideally no later than 48 hours. In the setting of an influenza outbreak, EMS systems may opt to restrict duties for EMS clinicians who are not immunized or who have not yet received prophylactic antiviral therapy, in attempts to prevent spread of influenza. Avian Influenza Wild birds carry a type of influenza A virus, called avian influenza virus, in their intestines, and usually do not get ill from it. However, avian influenza virus can make domesticated birds, including chickens, turkeys, and ducks, quite ill and can lead to death. Although avian influenza virus is chiefly found in birds, infection in humans from contact with infected poultry has been reported since 1996. A particular subtype of avian influenza A virus, H5N1, is highly contagious and deadly among birds. In 1997 in Hong Kong, an outbreak of avian influenza H5N1 occurred not only in poultry, but also in 18 humans, six of whom died. In subsequent infections of avian influenza H5N1 in humans, more than half of those infected with the virus have died. In contrast to seasonal influenza, most cases of avian influenza H5N1 have occurred in young adults and healthy children who have been exposed to infected poultry, or surfaces contaminated with H5N1 virus. Although transmission of avian influenza H5N1 from human to human is rare, inefficient, and not sustained, there is concern that the H5N1 virus could adapt and acquire the ability for

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sustained transmission in the human population. If the H5N1 virus could gain the ability to transmit easily from person to person, a global influenza pandemic could occur. As of June 2020, there were a cumulative 861 cases of human cases of H5N1 reported to the World Health Organization, resulting in 455 deaths. A number of vaccines are currently available for H5N1, the first approved in 2007 and the latest in 2020. Given that the H5N1 virus continually mutates, the best protection for new strains of H5N1 will depend on a vaccine specifically produced for any future virus strain. The H5N1 virus is resistant to the adamantanes, but sensitive to the neuraminidase inhibitors (e.g., oseltamivir, zanamivir) [5]. In April 2009, a novel influenza A (H1N1) virus caused respiratory illness across North America and many areas of the world. The 2009 influenza A (H1N1), while similar to other H1N1 viruses, was genetically and antigenically distinct. Influenza morbidity caused by the 2009 pandemic influenza A (H1N1) remained above seasonal baselines throughout spring and summer and was the first pandemic since 1968. Data from epidemiologic studies conducted during the 2009 influenza A (H1N1) pandemic indicate that the risk for influenza complications among adults aged 19‐64  years who had 2009 pandemic influenza A (H1N1) was greater than typically occurs for seasonal influenza [6]. Avian influenza A (H7N9) virus is a subtype of influenza viruses not previously seen in either animals or people until it was found in China in February 2013. Since its discovery, infections in both humans and birds have been identified. While it has not been reported in birds outside China, its low pathogenicity in birds makes it difficult to identify international spread. Most of the cases of human H7N9 virus infections have reported recent exposure to live poultry or potentially contaminated environments, especially markets where live birds have been sold. Since its discovery, there have been 1,568 confirmed cases and 616 deaths due to H7N9 [7]. The disease is of concern because most people who become infected have become severely ill. This virus does not appear to transmit easily from person to person, and sustained human‐to‐human transmission has not been reported. Asymptomatic and mild infections have been detected, but the underlying rate of such infections is not well understood [8]. There is no current vaccine for H7N9. As with H5N1, neuraminidase inhibitors are effective against H7N9, but adamantanes are not [9]. Tuberculosis Tuberculosis (TB) is caused by the Mycobacterium tuberculosis complex. The majority of active TB is pulmonary (70%), while the remainder is extra‐pulmonary (30%). Patients with active pulmonary TB will typically present with cough, scant amounts of non‐purulent sputum, and possibly hemoptysis. Systemic signs such as weight loss, loss of appetite, chills, night sweats, fever, and fatigue may also be present. EMS clinicians are unlikely to distinguish pulmonary TB from other respiratory illnesses. However, certain risk factors may alert them to the possibility

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of tuberculosis. These are immigration from a high‐prevalence country, homelessness, exposure to active pulmonary TB, silicosis, HIV infection, chronic renal failure, cancer, transplant recipient, or any other immunosuppressed state [10, 11]. About half of the world’s TB cases, and two‐thirds of all new cases, come from eight countries: Bangladesh, China, India, Indonesia, Nigeria, Pakistan, Philippines, and South Africa [12, 13]. Active pulmonary TB is transmitted via droplet nuclei from people with pulmonary tuberculosis during coughing, sneezing, speaking, or singing. Procedures such as intubation or bronchoscopies are high risk for the transmission of TB. Respiratory secretions on a surface rapidly lose the potential for infection. The probability of infection is related to duration of exposure, distance from the infected person, concentration if bacilli in droplets, ventilation in the room, and the susceptibility of the exposed person. Effective medical therapy eliminates communicability within 2‐4 weeks of starting treatment [14]. If transporting a patient who is known or suspected to have TB, respiratory precautions should be followed by EMS clinicians, including use of N95 respirators, as these types are necessary for infections that are spread via the airborne route. Patients should cover their mouths when coughing or sneezing or wear a surgical mask. In the event of suspected exposure to a patient with active pulmonary tuberculosis, report the case and the exposure to the EMS system or public health authority. Close contacts should be monitored for the development of active TB symptoms. Two tuberculin skin tests should be performed, based on public health recommendations, on those closely exposed to patients with active TB [15]. Because the incubation period after contact ranges from 2 to 10 weeks, the first test is typically done as soon as possible after exposure, and the second test is typically done eight to 12 weeks after the exposure. If the EMS clinician or contact develops either active TB with symptoms or latent asymptomatic TB, as diagnosed with a new positive TB skin test, treatment should be offered. There are several treatment regimens for latent TB infection [13]. The CDC and the National Tuberculosis Controllers Association recommend either 3  months of once‐weekly isoniazid plus rifapentine, 4  months of daily rifampin alone, or 3  months of daily isoniazid plus rifampin. Short‐course regimens are effective, safe, and have higher completion rates than traditional 6‐ to 9‐month courses of isoniazid monotherapy. They also have lower risk of hepatotoxicity. For active TB, a four‐ drug regimen typically includes isoniazid, rifampin, pyrazinamide, and ethambutol, with an intensive phase of all four drugs daily for 8  weeks, followed by a continuation phase including isoniazid and rifampin daily for an additional 18  weeks [16]. Several forms of multi‐drug‐resistant TB and extensively drug‐ resistant TB have been identified [17]. Multi‐drug‐resistant TB is treatable and curable by using second‐line drugs. However, second‐line treatment options are limited and require extensive chemotherapy (up to 2 years of treatment) with medicines that are expensive and toxic. These forms require aggressive, multi‐ drug regimens for prolonged periods, and are dependent on

the organism’s patterns of drug sensitivity and resistance. In all cases, a physician skilled in management of TB must initiate and monitor treatment and provide suitable follow‐up. Tuberculosis is a reportable disease, and public health officials must be notified to ensure appropriate follow‐up and contact tracing. Coronaviruses Coronaviruses are a large family of RNA viruses that may cause illness in animals or humans. Seven known coronaviruses cause human infections. Three are highly pathogenic. These include SARS, Middle East respiratory syndrome (MERS), and the recently discovered coronavirus, SARS‐CoV2 (2019‐nCoV), which causes the disease COVID‐19. Each has generated a large‐scale public health response. In humans, these coronaviruses typically manifest as respiratory infections ranging from mild symptoms to more severe presentations leading to pneumonia, acute respiratory distress syndrome, respiratory failure, and death. Zoonotic transmission to humans likely occurs from civet cats (SARS), dromedary camels (MERS), and bats (SARS‐ CoV2). It is difficult to distinguish coronavirus infections from other respiratory infections because patients present with symptoms similar to those of other febrile respiratory illnesses [18, 19]. Fever is the most common and earliest symptom of coronavirus infection, often accompanied by headache, malaise, or myalgia. Among patients with coronavirus infection, high fever, diarrhea, and vomiting are more common when compared with patients with other respiratory illnesses [20]. Cough occurs later in the course of disease and patients are less likely to have rhinorrhea or sore throat as compared to other lower respiratory tract illnesses [21]. The virus is typically found in respiratory secretions but can also be isolated in other body fluids such as urine and fecal matter. Transmission is typically via droplet spread from respiratory secretions. Thus, intubation and procedures that aerosolize respiratory secretions pose high risk. Since clinical features alone cannot reliably distinguish coronavirus infections from other respiratory illnesses, knowledge of contacts is essential [22]. Potential contact with patients known to have coronavirus infection, contact within coronavirus‐affected areas, or linkage to a cluster of pneumonia cases should be obtained in the history [23]. Development of effective drug therapies and vaccines specifically for coronavirus infections is the subject of a global effort in light of the SARS-CoV2 pandemic. The first coronavirus infection was recognized as a global threat in mid‐March 2003 due to outbreaks in Toronto Canada, Singapore, Vietnam, Taiwan, and China [24]. The first of these known cases of SARS occurred in Guangdong province, China, in November 2002 [25, 26]. The World Health Organization reported the last human chain of transmission of SARS to be broken in July 2003. The case‐fatality rate for SARS is approximately 8%, usually due to respiratory failure. The case‐fatality rate is less than 1% for SARS patients younger than 24 years and up to 50% for those 65  years and older or those with comorbid illness [27]. There are no confirmed cases of transmission

Infectious and communicable diseases

from asymptomatic cases. There have not been any cases of SARS infections anywhere in the world since a 2004 outbreak in China, where two researchers contracted SARS while working in a virology institute where experiments using live and inactivated SARS coronavirus were carried out [28]. A second novel coronavirus related to SARS, MERS‐CoV, emerged in 2012. The origins of the virus are not fully understood, but according to the analysis of different virus genomes it is believed to have originated in bats and later transmitted to camels at some point. MERS‐CoV is transferred to humans from infected dromedary camels through direct or indirect contact. Human‐to‐human transmission is possible, but only a few such transmissions have been found among family members living in the same household. In health care settings, human‐to‐human transmission appears to be more frequent. However, the virus has not been shown to spread in a sustained way. MERS‐CoV has been identified in several countries in the Middle East, Africa, South Asia, and the United States. In total, 27 countries have reported 2562 cases since the virus’s initial discovery in 2012, including the latest outbreak in Saudi Arabia in 2020. There have been 881 known deaths due to the infection and related complications. On December 31, 2019, the Medical Administration of Wuhan Municipal Health Committee in Hubei Province, China issued an urgent notice regarding patients requiring hospitalization due to pneumonia of unknown cause. Of the 27 cases, seven were critically ill. Health officials determined that one or more patients had been in a local seafood market prior to becoming ill. Chinese officials notified the World Health Organization of this cluster on January 3, 2020, and 6  days later reported the outbreak was due to a newly identified coronavirus. The viral genetic sequence was published two days later, and the first reported case of this novel coronavirus outside China was identified on January 13, 2020. Within less than 2 weeks, the virus was identified in patients in several countries in Asia, Western Europe, and the United States. By January 30, the World Health Organization declared the novel coronavirus, SARS‐CoV2, a public health emergency of international concern. The disease resulting from SARS‐CoV2 infection was termed coronavirus infectious disease 2019 (COVID‐19). The average incubation period ranges from 2 to 12 days, with a median of 5‐6 days. The most common symptoms of COVID‐19 are fever, dry cough, and tiredness. Other symptoms that are less common and may affect some patients include aches and pains, nasal

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congestion, headache, conjunctivitis, sore throat, diarrhea, loss of taste or smell, a rash on the skin, and discoloration of fingers or toes. These symptoms are usually mild and begin gradually. Some people who become infected may have very mild or no symptoms. The diagnosis can be suspected on clinical grounds and confirmed by viral testing that detects viral RNA. The virus is spread primarily from person to person through small droplets from the nose or mouth, when a person with COVID‐19 coughs, sneezes, or speaks. The droplets can also land on objects and surfaces, be picked up by contact with these objects or surfaces, and become infective when one’s eyes, nose, or mouth are touched. Asymptomatic spread of the virus from person to person may also occur. The majority of people with COVID‐19 experience mild to moderate respiratory illness and recover without requiring special treatment. Older people, and those with underlying medical problems like cardiovascular disease, diabetes, chronic respiratory disease, and cancer are more likely to develop serious illness. Overall mortality for COVID‐19 infection is approximately 2.2%. Table 23.3 compares the burden of disease related to coronavirus infections with influenza outbreaks. Several therapeutic agents have been evaluated for the treatment of COVID‐19. Remdesivir, an inhibitor of the viral RNA‐dependent RNA polymerase known to be effective against SARS and MERS, may also be effective in treatment of COVID‐19 [29–31]. Given the global nature of this pandemic, major efforts at developing vaccines have resulted in a number of vaccines now being available [32]. If coronavirus infection is suspected, EMS clinicians must follow all routine practices and some additional precautions [33]. This includes an initial assessment for any signs or symptoms of a respiratory infection or potential coronavirus risk factors. The initial assessment should be done from distance of at least 2  meters (6  feet) from the patient, if possible. Patient contact should be minimized, to the extent possible, until PPE is in place and a facemask is on the patient. EMS systems may also elect to limit or avoid any procedures that may increase risk to EMS personnel. These include tracheal intubation, deep suctioning, use of non‐invasive ventilatory support (continuous or bi‐level positive airway pressure), administration of nebulized medication, and any other procedure that may aerosolize respiratory secretions. During the SARS outbreaks, paramedics did not perform aerosol‐generating medical procedures in the

Table 23.3  Comparison of coronavirus infections, seasonal influenza, and 1918 pandemic influenza

R0b Total cases Deaths Case fatality rate (%)

SARS

MERS

COVID‐19a

Seasonal influenza (annual)

1918 pandemic influenza

3 8906 744 8.4

1.9‐3.9 2562 881 34.4

1.95‐3.28 131,909,792 2,854,276 2.2

0.9‐2.1 1 billion 389,000 0.04

1.4‐2.8 500 million 50 million 10

 As of April 5, 2021 [63].  Basic reproduction number: number of new cases that can develop from one confirmed case. Sources: From [62–67].

a

b

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prehospital setting to limit possible disease transmission [34]. If an aerosol‐generating medical procedure is anticipated, personnel should use N95 respirators as part of their PPE. Oxygen masks, bag‐valve‐mask ventilators, and other respiratory or ventilatory equipment should be equipped to filter expired air. Finally, EMS personnel and systems should notify the receiving facility of a patient suspected of coronavirus, permitting hospital staff to have appropriate PPE in place and a suitable isolation room prepared for the patient [35, 36].

Biological Weapons The CDC categorizes bioterrorism agents as shown in Box 23.1 [37]. Some of the listed agents, such as botulinum toxin and ricin, are not infectious diseases, but rather biological toxins. Anthrax The symptoms of anthrax are determined by the route of transmission of the bacterium, Bacillus anthracis, which causes the infection. There are three forms of anthrax: cutaneous, gastrointestinal, and inhalational [38, 39]. Cutaneous anthrax presents as a small, painless, pruritic papule, which progresses to a vesicle that ruptures and erodes, leaving a necrotic ulcer that later gets covered with a black, painless eschar. Pathognomonic features of anthrax include the presence of an eschar, lack of pain, and edema out of proportion

Box 23.1  Centers for Disease Control and Prevention categorization of bioterrorism agents

Category A High‐priority agents include organisms that pose a risk to national security because they: •  can be easily disseminated or transmitted from person to person •  result in high mortality rates and have the potential for major public health impact •  might cause public panic and social disruption; and •  require special action for public health preparedness. Anthrax (Bacillus anthracis) Botulism (Clostridium botulinum toxin) Plague (Yersinia pestis) Smallpox (variola major) Tularemia (Francisella tularensis) Viral hemorrhagic fevers (filoviruses, e.g., Ebola, Marburg, and arenaviruses, e.g., Lassa, Machupo)

Category B Second highest priority agents include those that: •  are moderately easy to disseminate •  result in moderate morbidity rates and low mortality rates; and •  require specific enhancements of CDC’s diagnostic capacity and enhanced disease surveillance. Brucellosis (Brucella species)

to the size of the lesion. Associated symptoms include swelling of adjacent lymph nodes, fever, malaise, and headache. Cutaneous anthrax is caused by B. anthracis entering a cut or abrasion in exposed areas of the body such as the face, neck, arms, and hands. The case‐fatality rate can be as high as 20% without antibiotic therapy, but 1% with therapy. Gastrointestinal anthrax presents with symptoms that are more non‐specific. There are two forms: oropharyngeal and intestinal. Oropharyngeal anthrax starts with edematous lesions at the base of the tongue or tonsils that progress to necrotic ulcers with a pseudomembrane. Sore throat, fever, cervical adenopathy, and profound oropharyngeal edema are associated symptoms. The intestinal form of anthrax initially presents with fever, nausea, vomiting, and abdominal pain and tenderness that may progress to hematemesis, bloody diarrhea, and abdominal swelling from hemorrhagic ascites. Gastrointestinal anthrax is caused by consumption of meat contaminated with anthrax. The case‐fatality rate of gastrointestinal anthrax is estimated to be 25‐60%. Inhalational anthrax initially causes non‐specific symptoms that mimic influenza. These early symptoms are low‐grade fever, non‐productive cough, malaise, and myalgias. Two to three days later, the patient rapidly progresses to severe dyspnea, profuse sweating, high fever, cyanosis, and shock. As many as half of patients develop hemorrhagic meningitis. It is critical that EMS personnel attempt to distinguish any influenza‐like illness from anthrax, because of the narrow window

Epsilon toxin of Clostridium perfringens Food safety threats (e.g. Salmonella species, Escherichia coli  O157:H7, Shigella) Glanders (Burkholderia mallei) Melioidosis (Burkholderia pseudomallei) Psittacosis (Chlamydia psittaci) Q fever (Coxiella burnetii) Ricin toxin from Ricinus communis (castor beans) Staphylococcal enterotoxin B Typhus fever (Rickettsia prowazekii) Viral encephalitis (alphaviruses, e.g., Venezuelan equine encephalitis, eastern equine encephalitis, western equine encephalitis) Water safety threats (e.g., Vibrio cholerae, Cryptosporidium  ­parvum)

Category C Third highest priority agents include emerging pathogens that could be engineered for mass dissemination in the future because of: •  availability •  ease of production and dissemination •  potential for high morbidity and mortality rates and major health impact •  emerging infectious diseases such as Nipah virus and hantavirus. Source: Based on Centers for Disease Control and Prevention. Bioterrorism Agents/Diseases [37].

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of opportunity for successful treatment. Nasal congestion and rhinorrhea are not common with inhalational anthrax, but more common with influenza‐like illness. Further, shortness of breath is more common in inhalational anthrax and less common with influenza‐like illness. Chest x‐ray demonstrates mediastinal widening or pleural effusion. These findings are the most accurate predictors of inhalational anthrax. Inhalational anthrax can be caused by inhalation of spores, commonly seen following intentional release of aerosolized anthrax, or from the processing of materials from infected animals, such as goat hair. The case‐fatality rate of inhalational anthrax can be as high as 97% without antibiotics and remain as high as 75% despite antibiotic treatment. Human‐to‐human transmission of any form of anthrax is rare. A vaccine for anthrax is licensed in the United States and is administered in a five‐dose schedule with annual boosters thereafter [40]. A second vaccine is currently in clinical trials. Vaccination is not currently recommended for emergency first responders or medical personnel. However, it may be indicated for certain military personnel, laboratory workers who work with high concentrations of B. anthracis, and people such as farmers, veterinarians, and livestock handlers who might handle infected animals or contaminated animal products. In cases of deliberate use of anthrax as a biological weapon, first responders should wear full‐face respirators with high efficiency particulate air filters or self‐contained breathing apparatus, gloves, and splash protection. If clothing is contaminated, it should be removed and placed in plastic bags. Soap and copious amounts of water should be used to decontaminate skin, and bleach should be applied for 10‐15  minutes in a ­one‐to‐ten dilution if there is gross contamination. If exposure to aerosolized anthrax occurs, post‐exposure prophylaxis (PEP) with ciprofloxacin or doxycycline should begin and continue for 60 days. Patients suspected of being infected with anthrax and requiring hospitalization should be immediately started on IV antibiotics [41–43]. Vaccination for PEP should be administered because of the persistence of anthrax spores in the lungs. Three licensed anthrax antitoxins are available from the U.S. Strategic National Stockpile. All work by binding to protective antigen, which blocks movement of toxins into cells and therefore the effects of toxins within the cells. Antitoxin use is indicated in all adults and children for the treatment of inhalation anthrax due to B. anthracis, in combination with other appropriate post‐exposure treatments. Quarantine is not indicated for individuals exposed to anthrax as they are not contagious. A clinical framework and medical countermeasure is available that outlines an approach to an anthrax mass casualty incident [44]. Botulism Botulism is caused by a neurotoxin produced by Clostridium botulinum, which ultimately leads to a flaccid paralysis. There are four forms of botulism based on site of toxin production: food‐borne, wound, intestinal, and inhalational [45].

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In food‐borne botulism, early symptoms are non‐specific and gastrointestinal, including nausea, vomiting, and diarrhea. This may progress to blurred vision, double vision, dry mouth, and difficulty in swallowing, breathing, and speaking. Descending muscle paralysis occurs, starting with shoulders, and progressing to upper arms, lower arms, thighs, and then calves. Respiratory muscle paralysis ultimately leads to death. Food‐ borne botulism is caused by the ingestion of C. botulinum toxin present in contaminated food, or by deliberate contamination as a biologic weapon. The case‐fatality rate in the US is 5‐10%. Intestinal botulism is rare and occurs mainly in infants. It causes a striking loss of head control, diminished suckling and crying ability, constipation, and respiratory failure. Intestinal botulism occurs with ingestion of botulism spores, rather than ingestion of toxin. Spores, which may come from honey, food, and dust, germinate in the colon [45]. The case‐fatality rate of hospitalized cases is less than 1%. Wound botulism causes the same symptoms as food‐borne botulism. This is rare and is caused by spores entering an open wound from soil or gravel. Inhalational botulism is the most common form in the case of use of botulinum toxin as a biologic weapon. Symptoms are the same as food‐borne botulism, but the incubation period may be longer. Botulism is not transmitted person to person. Therefore, EMS personnel should use standard precautions when caring for patients with suspected or known botulism. No special equipment is required. In the case of suspected aerosol exposure to the toxin, clothing should be removed and placed in plastic bags, and the exposed person should shower thoroughly. Treatment in the prehospital setting consists of supportive care and transport to the hospital. Botulinum antitoxin administered as soon as possible will arrest progression of symptoms but will not reverse paralysis. Recovery follows the regeneration of new neuromuscular connections. Treatment for wound botulism may also include antibiotic therapy and wound debridement to remove the source of toxin‑producing bacteria. Plague Plague is caused by the bacterium Yersinia pestis. The incubation period is typically 1‐6 days, with non‐specific initial signs and symptoms, including fever, chills, sore throat, malaise, and headache. Tender, swollen, warm, and suppurative lymph nodes, mainly in the inguinal area, often follow. Patients infected with the plague may progress to septicemia, meningitis, pneumonia, or shock. Untreated plague has a case‐fatality rate of 50‐90%; if treated, mortality is 15%. Plague is transmitted to humans by bites, scratches, respiratory droplets, or by direct skin contact. Bites from infected rat fleas are the most frequent source of transmission, but bites or scratches from cats may also transmit plague. Direct contact with tissue or body fluids of a plague‐infected sick or dead animal can lead to transmission to humans through a break in the skin [46].

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For patients with pneumonic plague, strict isolation is indicated with precautions against airborne spread until 48  hours after the start of antibiotic therapy. Close contacts of patients infected with pneumonic plague should receive chemoprophylaxis and be placed under surveillance for 7 days. Articles soiled with sputum or purulent discharges should be disinfected. Yersinia pestis could be used as a potential biological weapon leading to pneumonic plague [47]. In case of deliberate use as a biological weapon, plague bacilli would be transmitted via aerosolized airborne droplets. Many patients presenting with fever and cough, particularly hemoptysis in a fulminant course with high case fatality, should raise suspicions for a biological weapon [48–50]. Smallpox Smallpox is a disease caused by the variola virus. The last naturally occurring cases of smallpox were identified in 1977, and in 1980 the World Health Organization declared smallpox officially eradicated from the planet. However, there remain two sources of smallpox virus in storage and for research purposes, one in the United States and one in Russia. Any new cases of smallpox will be a medical and public health emergency. Strict respiratory and contact isolation of confirmed or suspected smallpox cases are essential to prevent spread of this virus. There are four main clinical forms of smallpox: ordinary smallpox (variola major), modified‐type smallpox, malignant smallpox, and hemorrhagic smallpox [51, 52]. All forms of smallpox infection begin with an incubation period usually lasting between 10 and 14 days. During this time, the infected person does not have symptoms, is not contagious, and may feel fine. Symptoms begin with a prodrome that typically lasts 2‐4  days, starting abruptly with fever, headache, abdominal pain, nausea, vomiting, muscle pain, headache, and malaise. In patients with pale‐skins, an erythematous or petechial rash may be visible. Ordinary smallpox is the most common and severe form of disease, accounting for over 85% of cases during the smallpox era. After the prodrome, mucous membrane lesions called enanthem begin in the mouth. This consists of red spots on the tongue and mucosa that enlarge and ulcerate quickly, followed by a rash on the face. The rash then progresses from the proximal extremities to the distal extremities and trunk within 24 hours. The macules progress to papules, vesicles, pustules, and crusts. Crusts later separate leaving depigmented skin and pitted scars. The case‐fatality rate for ordinary smallpox is about 30%. Transmission of smallpox is via virus inhalation from airborne droplets or fine particle aerosols from the oral, pharyngeal, or nasal mucosa of an infected person, physical contact with an infected person, or with contaminated articles through skin inoculation. Medical personnel in contact with suspected or confirmed smallpox cases should be wearing N95 respirators and should take other standard precautions. All bedding and clothing should be autoclaved or laundered in hot water with bleach.

Treatment of smallpox patients generally involves supportive care. Smallpox vaccines can prevent or lessen the severity of disease if given within 2‐3 days of the initial exposure. They may decrease symptoms if given within the first week of exposure. There are antiviral therapies shown to be effective against poxviruses, including variola. However, no treatment has been tested and proven effective for people who are sick from smallpox. Given that smallpox no longer exists as a naturally occurring disease, even a single suspected or known case should be considered an outbreak and public health authorities must be alerted immediately. Tularemia Tularemia, caused by the bacterium Francisella tularensis, has various clinical manifestations related to the route of introduction. People can become infected in several ways, including tick and deer fly bites, skin contact with infected animals and their carcasses, eating insufficiently cooked contaminated meat, drinking contaminated water, inhaling contaminated aerosols or agricultural and landscaping dust, and bioterrorism. The incubation period is usually 3‐5 days, but can range from 1 to 14 days. All forms of tularemia result in a sudden onset of non‐ specific influenza‐like symptoms, including high fever, cough, sore throat, chills, headache, and generalized body aches. Sometimes, nausea, vomiting, and diarrhea may also occur. All forms may lead to sepsis, pneumonia, and meningitis. The clinical forms include ulceroglandular, glandular, oculoglandular septic, oropharyngeal, and pneumonic [53]. Ulceroglandular tularemia is the most common form. It begins at the skin site of the bite of a tick or fly. A papule appears that becomes pustular, later ulcerates, and finally develops into an eschar. Regional lymph nodes become swollen, painful, and tender and rarely suppurate and discharge purulent material. Glandular tularemia has no skin involvement, only regional lymphadenopathy similar to ulceroglandular disease. Oculoglandular tularemia is caused by the bacillus entering the eye.  Conjunctival ulceration occurs followed by regional lymphadenopathy of the cervical and pre‐auricular nodes. Septic tularemia begins with non‐specific symptoms of fever, nausea, vomiting, and abdominal pain, eventually leading to confusion, coma, multisystem organ failure, and septic shock. Oropharyngeal tularemia is caused by consumption of contaminated water or food, leading to exudative pharyngitis, which may be accompanied by oral ulceration. Abdominal pain, diarrhea, and vomiting may accompany this type. Regional lymphadenopathy occurs, affecting the cervical and retropharyngeal nodes. Pneumonic tularemia may be caused by lung exposure to an infective aerosol from soil, grain, or hay. An infective aerosol can also result from a bioterrorist attack. The clinical presentation may be cough, pleuritic pain, and rarely dyspnea. Despite the lungs being the primary route of entry, it is not uncommon for tularemic pneumonia to present as non‐specific systemic signs without respiratory symptoms, and often a normal chest x‐ray.

Infectious and communicable diseases

There is no documented person‐person transmission of tularemia. Routine precautions are adequate when transporting and caring for patients. The vehicle and equipment, however, must be thoroughly cleaned and decontaminated after patient transport. Antibiotics such as streptomycin or gentamycin are effective, and antibiotics for treating patients infected with tularemia in a bioterrorist event are included in the national pharmaceutical stockpile maintained by the CDC.

Viral Hemorrhagic Fevers Viral hemorrhagic fevers are caused by different families of viruses and lead to similar clinical syndromes. In the case of bioterrorist attack, it is essential that first‐responders are able to recognize the illness associated with the intentional release of the biological agent. In hemorrhagic fever, the initial signs and symptoms are nonspecific and include high fever, headache, muscle aches, and severe fatigue. There may be associated gastrointestinal symptoms of nausea, vomiting, diarrhea, and abdominal pain. Respiratory symptoms of cough and sore throat may also occur. Approximately 5 days after the onset of illness, a truncal maculopapular rash develops in most patients. As the disease progresses, bleeding occurs from internal organs, the mouth, eyes, ears, and from under the skin, as evidenced by petechiae and ecchymosis. Shock, coma, seizures and kidney failure may ensue in severe cases. Viral hemorrhagic fevers are caused by viruses in four families: arenaviruses, bunyaviruses, flaviviruses, and filoviruses, causing diseases such as Ebola hemorrhagic fever, hantavirus pulmonary syndrome, Lassa fever, Marburg hemorrhagic fever, hemorrhagic fever with renal syndrome, and Crimean‐ Congo hemorrhagic fever [54]. Transmission occurs when humans have direct contact with infected animals, mainly rodents, or are bitten by a mosquito or tick vector. Once a person has become infected, some viruses can be transmitted from person to person, mainly by close contact with infected people, but also indirectly by objects contaminated with infected body fluids. Transmission of viral hemorrhagic fever mainly occurs in the latter stage of illness when the patient suffers vomiting, diarrhea, shock, and hemorrhage. In the case of Ebola virus, there are reports of transmission within a few days of the onset of fever. The incubation period ranges from 2 days to 3 weeks, and no transmission has been documented during the incubation period. To prevent infection, contact with rodents, and bites from ticks and mosquitos, should be prevented. Person‐to‐person transmission can be prevented by strict adherence to routine precautions. If clinicians are exposed to viral hemorrhagic fever, they should be placed under surveillance for fever. In addition, patients with known or suspected viral hemorrhagic fever must be isolated. While this is not possible in the EMS setting, the

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transporting vehicle can serve to isolate the patient from the scene and while in transit. During the 2018 outbreak of Ebola in the Democratic Republic of the Congo, four investigational treatments were initially available to treat confirmed patients. Of these, patients receiving one of two investigational antiviral drugs had higher overall survival. While these two drugs are not currently licensed by the U.S. FDA, they are currently in use in other countries for patients with Ebola. In December 2019, Ebola Zaire vaccine, live (Ervebo®, Merck Sharp & Dohme Corp.) became the first FDA‐approved vaccine for the prevention of Ebola. Another investigational vaccine was introduced under a research protocol in 2019 to combat an Ebola outbreak in the Democratic Republic of the Congo. This vaccine requires two doses, with an initial dose followed by a booster 56 days later. The CDC has prepared a number of documents specific to viral hemorrhagic fever, with detailed and comprehensive strategies to prevent spread and protect health care workers and provide guidance to EMS agencies and personnel [55, 56]. In collaboration with the CDC, the National Ebola Training and Education Center offers training, resources, readiness assessments, and expertise to help prepare for pandemics and other emerging threats related to infectious disease outbreaks [57] (Figure 23.1). Finally, to strengthen the United States’ infectious disease response capability, ten special regional treatment centers were established in 2015 to treat patients with Ebola or other severe, highly infectious diseases. These facilities have enhanced capabilities to receive special pathogen patients, and have the capacity for at least ten patients with high‐risk infectious diseases (Figure 23.2).

Figure 23.1  Health care workers exiting a containerized biocontainment

system. Source: Photo courtesy of U.S. Department of Health and Human Services Office of the Assistant Secretary for Preparedness and Response.

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avoid patient contact from 10  days after the exposure (the incubation period) until day 21 [58]. An exposure is defined as a breach of contact precautions (such as localized direct contact with uncovered lesions) and/or breach of airborne precautions (chickenpox or disseminated zoster). If an unprotected exposure occurs to a nonimmune health care professional, unless that person is pregnant or immunocompromised, the vaccine should be given within 3‐5 days. For people exposed to VZV who are nonimmune or cannot receive the varicella vaccine, varicella zoster immune globulin can prevent varicella from developing or lessen the severity of the disease. It should be given as soon as possible after exposure. Oral acyclovir or valacyclovir treatment should be considered in certain groups at increased risk for moderate to severe illness. These high‐risk groups include healthy people older than 12  years, people with chronic cutaneous or pulmonary disorders, people receiving long‐term salicylate therapy, and people receiving short, intermittent, or aerosolized courses of corticosteroids. Some physicians may elect to use oral acyclovir or valacyclovir for secondary cases within a household. Oral therapy should be given within the first 24 hours after the varicella rash starts, but is not recommended for use in otherwise healthy children experiencing typical varicella without complications. Figure 23.2  Transport team arrives with a patient at the dedicated entrance

of a Regional Ebola and Other Special Pathogen Treatment Center. Source: Photo courtesy of U.S. Department of Health and Human Services, Office of the Assistant Secretary for Preparedness and Response. public domain photos from the U.S. federal government.

Varicella Zoster Virus Varicella zoster virus (VZV) causes two distinct diseases: chickenpox and “shingles” (herpes zoster). Acute chickenpox is highly contagious and usually runs its course in about a week or two, producing immunity, but VZV is not eliminated from the body. The virus becomes dormant in the sensory ganglia and may reactivate decades later to produce zoster [58]. To decrease the incidence of chickenpox in adults who were never exposed to VZV as a child, routine childhood vaccination began in 1995. The full vaccine regimen (two doses) is 90‐100% protective against chickenpox, and virtually 100% effective against severe disease [58]. Serologic screening for VZV immunoglobulin G is indicated for adult health care workers who do not have a documented history of chickenpox. VZV is common, so ensuring EMS clinicians are immune prior to patient care is important and cost effective. Only immune health care personnel should care for patients with chickenpox or shingles. If a pregnant EMS clinician has a documented history of chickenpox or has positive titers, she is considered to be immune and can care for patients. Both she and the fetus are protected. Nonimmune adults exposed to either chickenpox or zoster can develop acute chickenpox, including potential complications of pneumonia, encephalitis, and death. Nonimmune personnel exposed to chicken pox or disseminated zoster must

Meningococcal Meningitis Neisseria meningitidis, or meningococcus, can be acquired from an infected patient if a mask is not worn [59–61]. All health care workers should understand that preventing transmission of meningococcus requires adherence to droplet precautions and that it is not an airborne‐transmitted disease. The illness has a high case‐fatality rate (10%) [61]. Patients are considered infectious for one week before the onset of symptoms and for 24 hours after effective treatment begins. PEP should be administered when close, unprotected (no mask) contact occurs, such as while performing unprotected mouth‐to‐mouth resuscitation on an infected patient, or if splash/splatter of secretions into mucous membranes occurs, as with suctioning, intubation, vomiting, coughing, or endotracheal tube management. Simple proximity to the patient does not qualify as close contact, unless the EMS clinician was less than 3  feet from the patient for more than 8  hours [61]. Because many patients having symptoms consistent with N. meningitidis infection are actually infected with other viruses or organisms, PEP should be given only after substantial exposure (as defined above) to a patient with culture‐ or Gram stain‐proven meningococcus. There is time to determine if N. meningitidis is present before empirically administering prophylaxis to many EMS personnel unnecessarily. PEP for meningococcus should start within 24  hours but may begin up to 10  days after exposure. PEP options include ceftriaxone, ciprofloxacin, or rifampin. Exposed workers may return to duty 24 hours after PEP begins. The EMS medical director plays an important role in ensuring that prehospital personnel are treated quickly and appropriately

Infectious and communicable diseases

when a true exposure to N. meningitidis has occurred. Often, one of the following situations occurs: 1.  A crew transports a patient suspected of having meningitis to an emergency department and calls the infection control officer with concerns about exposure. 2.  Hospital infection control personnel attempt to contact exposed prehospital personnel involved with treatment/transport of an inpatient now diagnosed with meningococcus. Usually, the infection control officer is directly involved, but the medical director can assist hospital infection control, occupational health service, and emergency department personnel by including prehospital clinicians in the pool of exposed workers. The designated infection control officer should gather specific information, confirming which (if any) prehospital personnel were close enough to the patient to warrant having them report for evaluation and possible PEP administration. Routine vaccination is not recommended for any specific health care worker group, including fire and EMS personnel. However, certain groups of people, who may also be EMS clinicians, are appropriate to consider for vaccination if they have not already received it. They include 19‐ to 55‐year‐olds living in college dormitories or other congregate settings, military recruits, microbiologists routinely exposed to isolates of N. meningitides, travelers to or residents of countries in which N. meningitidis meningitis is hyperendemic or epidemic, individuals with terminal complement‐component deficiencies, and individuals with anatomic or functional asplenia.

Conclusion EMS clinicians, by the nature of their work on the front lines of the health care system, have unique opportunities to encounter undifferentiated patients with infectious and communicable diseases. Vigilance in recognizing symptoms and signs of these illnesses is an important aspect of their work. First and foremost, EMS clinicians must be aware of the potential risks posed by communicable diseases and ensure they are consistent in using appropriate tools, in the form of PPE, to attenuate those risks.

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23 Booth CM, Matukas LM, Tomlinson GA, et  al. Clinical features and short‐term outcomes of 144 patients with SARS in the greater Toronto area. JAMA. 2003; 289:2801–9. 24 Dwosh H, Hong H, Austgarden D, et al. Identification and containment of an outbreak of SARS in a community hospital. Can Med Assoc J. 2003; 168:1415–20. 25 He J‐F, Peng G‐W, Zheng H‐Z, et  al. [An epidemiological study on the index cases of severe acute respiratory syndrome which occurred in different cities in Guangdong province]. Zhonghua Liu Xing Bing Xue Za Zhi. 2003; 347–9. 26 Guan Y, Zheng BJ, He YQ, et al. Isolation and characterization of viruses related to the SARS coronavirus from animals in southern China. Science. 2003; 302:276–8. 27 Poutanen SM, Low DE, Henry B, et  al. Identification of SARS in Canada. N Engl J Med. 2003; 348:1995–2005. 28 World Health Organization. China’s latest SARS outbreak has been contained, but biosafety concerns remain. Update 7, 18 May 2004. Available at http://www.who.int/csr/don/2004_05_18a/en. Accessed February 14, 2021. 29 Sheahan TP, Sims AC, Leist SR, et al. Comparative therapeutic efficacy of remdesivir and combination lopinavir, ritonavir, and interferon beta against MERS‐CoV. Nat Commun. 2020; 11:222. 30 Brown AJ, Won JJ, Graham RL, et al. Broad spectrum antiviral remdesivir inhibits human endemic and zoonotic deltacoronaviruses with a highly divergent RNA dependent RNA polymerase. Antiviral Res. 2019; 169:104541. 31 Beigel JH, Romashek KM, Dodd LE, et al. Remdesivir for the treatment of Covid‐19 – final report. N Engl J Med. 2020; 383: 1813–26. 32 World Health Organization. COVID-19 vaccines. Available at https://www.who.int/emergencies/diseases/novel-coronavirus2019/covid-19-vaccines. Accessed April 5, 2021.. 33 Centers for Disease Control and Prevention. Interim guidance for emergency medical services (EMS) systems and 911 public safety answering points (PSAPs) for COVID‐19 in the United States. Available at: https://www.cdc.gov/coronavirus/2019‐ncov/hcp/ guidance‐for‐ems.html. Accessed February 14, 2021. 34 Verbeek PR, Schwartz B, Burgess RJ. Should paramedics intubate patients with SARS‐like symptoms? Can Med Assoc J. 2003; 169:199–200. 35 Interdisciplinary Respiratory Protection Study Group. Protecting health care workers from SARS and other respiratory pathogens: A review of the infection control literature. AJIC. 2005; 33:114–21. 36 Chen MI, Chow AL, Earnest A, et al. Clinical and epidemiological predictors of transmission in Severe Acute Respiratory Syndrome (SARS). BMC Infect Dis. 2006; 6:151. 37 Centers for Disease Control and Prevention. Bioterrorism agents/ diseases. Last reviewed: April 4, 2018. Available at: https:// emergency.cdc.gov/agent/agentlist‐category.asp. Accessed February 14, 2021. 38 Inglesby TV, O’Toole T, Henderson DA, et al. Anthrax as a biological weapon, 2002. Update recommendations for management. JAMA. 2002; 287:2236–52. 39 Bell DM, Kozarsky PE, Stephens DS. Clinical issues in the prophylaxis, diagnosis, and treatment of anthrax. Emerg Infect Dis. 2002; 8:222–5.

40 Bower WA, Schiffer J, Atmar RL, et  al. Use of anthrax vaccine in the United States: recommendations of the Advisory Committee on Immunization Practices, 2019. MMWR Recomm Rep 2019; 68:1–14. 41 Anthrax. In: Heyman DL, ed. Control of Communicable Diseases Manual. 20th ed. Washington, DC: APHA Press, 2015. 42 Shadomy SV, Rosenstein NE. Anthrax. In: Wallace RB, ed. Maxcy‐ Rosenau‐Last Public Health and Preventive Medicine. 15th ed. USA: McGraw‐Hill Medical, 2007. pp. 427–31. 43 Anthrax. In: Atkinson W, Hamborsky J, McIntyre L, Wolfe S, eds. Epidemiology and Prevention of Vaccine‐Preventable Diseases, 13th ed. Washington, DC: Public Health Foundation, 2015. 44 Bower WA, Hendricks K, Pillai S, Guarnizo J, Meaney‐Delman D. Clinical framework and medical countermeasure use during an anthrax mass‐casualty incident. CDC Recommendations . MMWR Recomm Rep. 2015; 64(RR‐4):1–22. 45 American Academy of Pediatrics. Botulism and infant botulism (Clostridium botulinum). In: Pickering LK, Baker CJ, Kimberlin DW, Long SS, eds. Red Book: 2009 Report of the Committee on Infectious Diseases. 28th ed. Elk Grove Village, IL: American Academy of Pediatrics; 2009, pp. 259–61. 46 Gage KL, Beard CB. Plague. In: Cohen J, Powderly W, Opal S, eds. Infectious Diseases. 4th ed. Mosby, Ltd., London, 2017. pp. 1078–84. 47 Inglesby TV, Dennis DT, Henderson DA, Bartlett JG, Ascher MS, Eitzen E. Plague as a biological weapon: Medical and public health management. JAMA. 2000; 283:2281–90. 48 Plague. In: Heyman DL, ed. Control of Communicable Diseases Manual. 20th ed. Washington, American Public Health Association, 2015. 49 Staples JE. Plague. In: Wallace RB. Maxcy‐Rosenau‐Last Public Health and Preventive Medicine. 15th ed. USA: McGraw‐Hill Medical, 2007, pp. 370–3. 50 Centers for Disease Control and Prevention. Plague. Resources for clinicians. Available at: https://www.cdc.gov/plague/healthcare/ clinicians.html. Last reviewed February 10, 2020. Accessed February 14, 2021. 51 Centers for Disease Control and Prevention. Smallpox. For clinicians. Available at: https://www.cdc.gov/smallpox/clinicians/index. html. Last reviewed October 8, 2019. Accessed February 14, 2021. 52 World Health Organization. Smallpox. Clinical diagnosis. Available at: https://www.who.int/csr/disease/smallpox/clinical‐diagnosis/en. Accessed February 14, 2021. 53 Dennis DT, Ingelsby TV, Henderson DA, et  al. Tularemia as a biological weapon. Medical and public health management. JAMA. 2001; 285:2763–73. 54 Centers for Disease Control and Prevention. Viral hemorrhagic fevers. Available at: https://www.cdc.gov/vhf. Last reviewed January 29, 2014. Accessed February 14, 2021. 55 Centers for Disease Control and Prevention. Ebola (Ebola virus disease). For clinicians. Last reviewed: August 30, 2018. Available at: https://www.cdc.gov/vhf/ebola/clinicians/index.html. Accessed February 14, 2021. 56 Centers for Disease Control and Prevention. Ebola (Ebola virus disease). Emergency services. Last reviewed: January 28, 2016. Available at: https://www.cdc.gov/vhf/ebola/clinicians/emergency‐ services/index.html. Accessed February 14, 2021. 57 Kratochvil CJ, Evans L, Ribner BS, et al. The National Ebola Training and Education Center: preparing the United States for Ebola and other special pathogens. Health Secur. 2017; 15(3):253–60.

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58 Kuhar DT, Carrico R, Cox K. Infection Control in Healthcare Personnel: Infrastructure and Routine Practices for Occupational Infection Prevention and Control Services. Washington, DC: Centers for Disease Control and Prevention, 2019. 59 Centers for Disease Control and Prevention. Immunization of health‐care personnel: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. 2011; 60(RR‐7):1–45. 60 Gardner P. Clinical practice: prevention of meningococcal disease. N Engl J Med. 2006;355:1466–73. 61 Centers for Disease Control and Prevention. Prevention and control of meningococcal disease: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. 2005; 54(RR‐07):1–21. 62 Liu Y, Gayle AA, Wilder‐Smith A, Rocklöv J. The reproductive number of COVID‐19 is higher compared to SARS coronavirus. J Travel Med. 2020; 27(2):taaa021.

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63 World Health Organization. WHO Coronavirus Disease (COVID‐19) Dashboard. Available at: https://covid19.who.int. Accessed April 5, 2021. 64 Centers for Disease Control and Prevention. 1918 pandemic (H1N1 virus). Available at: https://www.cdc.gov/flu/pandemic‐ resources/1918‐pandemic‐h1n1.html. Last reviewed March 20, 2019. Accessed February 15, 2021. 65 World Health Organization. Influenza (seasonal). Available at: https://www.who.int/news‐room/fact‐sheets/detail/influenza‐ (seasonal). November 6, 2018. Accessed February 15, 2021. 66 Paget J, Spreeuwenberg P, Charu V, et  al. Global mortality associated with seasonal influenza epidemics: new burden estimates and predictors from the GLaMOR project. J Glob Health. 2019; 9:020421. 67 Centers for Disease Control and Prevention. Disease burden of influenza. Available at: https://www.cdc.gov/flu/about/burden/index.html. Last reviewed October 5, 2020. Accessed February 15, 2021.

CHAPTER 24

Choking Gregory H. Gilbert

Introduction Choking emergencies are important in EMS because of their time‐sensitive nature. Victims of choking can rapidly progress from airway obstruction to loss of consciousness and cardiac arrest. Bystanders must act quickly to resolve true choking episodes. EMS personnel will likely arrive on scene several minutes after the onset of choking. Therefore, they must be prepared to manage a patient in advanced stages of crisis. Choking is an emergency that must be solved on scene; there is limited value in bringing an unresolved choking victim to the emergency department for definitive treatment [1].

Pathophysiology and epidemiology Choking results from obstruction of the trachea by a foreign object. It is the nature of the so‐called “café coronary” that occurs during or shortly after a meal [2]. Although most choking episodes are associated with food, nonedible objects may also cause airway occlusion, particularly in children who may inadvertently aspirate coins, toys, or other objects. Choking can occur with liquids as well as solid substances [3]. Although most obstructions occur in the hypopharynx, a small foreign body may lodge in either bronchus, causing selective obstruction of a lung or lung segment. Because the right bronchus travels more directly off the trachea, most selective obstructions involve the right lung. These tend to be nonfatal and are much more common in the pediatric population (Table 24.1) [4]. Choking may be classified as partial or complete. A complete obstruction impairs the ability to breathe, to talk, and to cough and is an immediate life threat. A partial obstruction results in incomplete occlusion of the airway. In these instances, the individual may still be able to breathe,

talk, or cough. A complete occlusion generally mandates immediate intervention such as the Heimlich maneuver, or direct laryngoscopy if ALS personnel are present. Other less invasive maneuvers may be appropriate in individuals with partial obstruction. However, in instances of partial obstruction with compromised air exchange, cyanosis, or loss of consciousness, the rescuer must approach the case as though it involves a complete airway obstruction [5]. The incidence of choking varies with age. For pediatrics, the majority are witnessed by the caregiver. While most of the 12,435 annual ED visits for pediatric choking episodes are nonfatal, there are approximately 175 deaths annually in the United States (Figure  24.1). Children younger than 1 year of age are most likely to choke, with food and liquids causing most of these episodes. While food remains the most common and dangerous, toddlers ages 1 to 4 years have the highest incidence of choking on nonfood items such as coins, latex balloons, or toys. The U.S. Consumer Product Safety Commission has instituted monitoring systems, legislation, and regulations to protect children from nonfood items, but no similar interventions exist for preventing food‐related choking in children or adults. Hard candy, gum, nuts. and hot dogs are just some of the high‐risk foods [3–6]. Choking incidence rises again at age 60 years from concurrent conditions impairing chewing and coordinated swallowing (e.g., Alzheimer dementia, stroke, drinking alcohol, poor dentition, seizure, or Parkinson disease). A prior choking episode significantly increases the chances of future choking [2, 4, 7]. Reviewing the epidemiology of choking victims in these at‐ risk groups provides valuable information. Japan found that 10% of fatal choking incidents came from mochi rice and 25% of those deaths occurred in a 3‐day window around the New Year [8]. Community education regarding this danger, coupled with first aid and CPR training for the community and caregivers, led to fewer choking deaths in subsequent years [9].

Emergency Medical Services: Clinical Practice and Systems Oversight, Third Edition. Volume 1: Clinical Aspects of EMS. Edited by David C. Cone, Jane H. Brice, Theodore R. Delbridge, and J. Brent Myers. © 2021 NAEMSP. Published 2021 by John Wiley & Sons, Inc.

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Table 24.1  Ten leading causes of nonfatal injury emergency department visits 2001–2018 Age Groups Rank

1

1‐4

5‐9

10‐14

15‐24

25‐34

35‐44

45‐54

55‐64

65+

All Ages

1

Unintentional Fall 2,312,376

Unintentional Fall 15,301,388

Unintentional Fall 11,351,088

Unintentional Fall 10,580,755

Unintentional Fall 13,530,813

Unintentional Fall 13,552,907

Unintentional Fall 15,410,152

Unintentional Fall 14,444,824

Unintentional Fall 41,481,463

Unintentional Fall 153,068,392

2

Unintentional Struck by/Against 554,993 Unintentional Other Bite/Sting 221,793 Unintentional Foreign Body 176,287 Unintentional Fire/Burn 173,831

Unintentional Struck by/Against 6,295,205 Unintentional Other Bite/Sting 2,617,647 Unintentional Foreign Body 2,219,957 Unintentional Cut/Pierce 1,469,752 Unintentional Overexertion 1,368,694

Unintentional Struck by/Against 7,140,347 Unintentional Cut/Pierce 1,996,896 Unintentional Other Bite/Sting 1,771,965 Unintentional Pedal Cyclist 1,473,465 Unintentional Overexertion 1,408,912

Unintentional MV‐Occupant 13,417,475 Unintentional Overexertion 12,495,035 Unintentional Cut/Pierce 8,038,092 Unintentional Other Specified 4,325,205

Unintentional Overexertion 11,576,122 Unintentional Struck by/Against 11,385,533 Unintentional MV‐Occupant 10,287,114 Unintentional Cut/Pierce 7,510,102 Unintentional Other Specified 4,700,730

Unintentional Overexertion 10,229,414 Unintentional Struck by/Against 9,014,836 Unintentional MV‐Occupant 7,756,641 Unintentional Cut/Pierce 5,972,740 Unintentional Other Specified 4,487,109

Unintentional Overexertion 7,848,208 Unintentional Struck by/Against 7,165,831 Unintentional MV‐Occupant 6,304,279 Unintentional Cut/Pierce 4,929,580 Unintentional Other Specified 4,755,187

Unintentional Struck by/Against 4,311,610 Unintentional Overexertion 4,203,366 Unintentional MV‐Occupant 3,914,121 Unintentional Cut/Pierce 3,087,781 Unintentional Other Specified 2,662,423

Unintentional Struck by/Against 4,575,935 Unintentional Overexertion 3,566,705 Unintentional MV‐Occupant 3,486,633 Unintentional Cut/Pierce 2,481,957 Unintentional Other Bite/Sting 1,547,982

Unintentional Struck by/Against 77,580,582 Unintentional Overexertion 57,789,568 Unintentional MV‐Occupant 48,532,866 Unintentional Cut/Pierce 37,971,682 Unintentional Other Specified 24,073,540

Unintentional MV‐Occupant 1,137,559

Unintentional Struck by/Against 10,100,827 Unintentional Overexertion 4,994,013 Unintentional Cut/Pierce 2,372,524 Unintentional Pedal Cyclist 1,852,108 Unintentional Unknown/ Unspecified 1,683,118 Unintentional MV‐Occupant 1,489,226

Unintentional Struck by/Against 17,032,229 Unintentional Fall 15,093,453

Unintentional Other Bite/Sting 3,077,272

Unintentional Poisoning 3,111,629

Unintentional Poisoning 3,171,028

Unintentional Poisoning 3,505,168

Unintentional Poisoning 2,112,594

Unintentional Poisoning 1,541,853

Unintentional Other Bite/Sting 19,639,678

Unintentional Unknown/ Unspecified 2,803,012 Unintentional Poisoning 2,618,135

Unintentional Other Bite/Sting 2,955,740

Unintentional Other Bite/Sting 2,483,965

Unintentional Other Bite/Sting 2,304,759

Unintentional Other Bite/Sting 1,543,999

Unintentional Other Specified 1,253,339

Unintentional Poisoning 17,312,604

Unintentional Unknown/ Unspecified 1,965,206 Unintentional Other Transport 1,632,185

Unintentional Unknown/ Unspecified 1,614,575 Unintentional Other Transport 1,370,966

Unintentional Unknown/ Unspecified 1,379,338 Unintentional Other Transport 1,199,661

Unintentional Unknown/ Unspecified 870,767 Unintentional Other Transport 804,555

Unintentional Other Transport 1,184,565

Unintentional Unknown/ Unspecified 13,025,036 Unintentional Foreign Body 10,499,348

3

4

5

6

Unintentional Other Specified 143,148

7

Unintentional Inhalation/ Suffocation 123,256 Unintentional Cut/Pierce 110,208

Unintentional Other Specified 972,698

Unintentional Unintentional Fire/Burn 942,001 Foreign Body 1,033,269

Unintentional Other Bite/Sting 1,114,168

9

Unintentional Overexertion 97,398

Unintentional Poisoning 794,638

Unintentional Dog Bite 783,098

Unintentional Other Transport 938,352

10

Unintentional Unknown/ Unspecified 95,379

Unintentional Unknown/ Unspecified 785,575

Unintentional Other Transport 715,729

Unintentional Dog Bite 623,628

8

Unintentional Other Transport 2,079,784

Source: National Center for Injury Prevention and Control, Centers for Disease Control and Prevention.

Unintentional Unknown/ Unspecified 1,142,504

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Chapter 24

Unintentional MV Traffic Unintentional Poisoning Unintentional Fall Unintentional Suffocation Unintentional Unspecified Unintentional Drowning Unintentional Fire/burn Unintentional Natural/ Environment Unintentional Other Spec., classifiable Unintentional Other Land Transport All Others 0.0

5.0

10.0

15.0

20.0

25.0

30.0

35.0

Figure 24.1  Proportions of unintentional injury deaths in the United States 2001‐2018. Unintentional suffocation, including choking, is the fourth leading

cause of death from unintentional injury for all age groups. Source: National Center for Injury Prevention and Control, Centers for Disease Control and Prevention.

Patient assessment Because complete or partial airway obstruction may rapidly lead to cardiopulmonary arrest, expeditious recognition of choking is essential. Ideally, bystanders will recognize and immediately treat choking victims. Emergency medical dispatchers should assist 9‐1‐1 callers in providing effective interventions. Delay of recognition and treatment until EMS arrival will likely result in clinical deterioration. Patients suffering from complete airway obstruction usually present with classic signs, including aphonia, hands to the throat, and hyperemia of the face. Other more serious signs include altered mental status, cyanosis, and unconsciousness. Many conscious choking victims will exhibit the universal choking sign and will nod in affirmation to the question, “Are you choking?” [10]. Partial airway obstruction may be more difficult to assess, especially in pediatric patients. These individuals may still have partial speaking ability. In many cases, the victim may exhibit paroxysmal coughing, drooling, stridor, or poor feeding. Common conditions mimicking foreign body aspiration include pneumonia, asthma, croup, and reactive airway disease [11, 12]. An esophageal foreign body may also cause or mimic airway obstruction. Vital signs, pulse oximetry, and other diagnostic tools are not typically useful in establishing the severity of a choking episode. In one series, 10% of admitted adult choking patients had normal prehospital vital signs [13].

Management The clinical course and subsequent deterioration due to choking progress rapidly. In ideal circumstances, bystanders should resolve the airway obstruction, because even the promptest EMS agencies will not arrive in time to perform needed interventions.

Patients presenting with complete airway obstruction should receive abdominal thrusts or the Heimlich maneuver [11, 14, 15]. In the classic Heimlich procedure, the rescuer positions him or herself behind the sitting or standing patient, placing his or her arms around the chest at the level of the epigastrium. The rescuer places one fist against the epigastrium, using the other hand to apply quick upwards thrusts. The rescuer repeats the process until the obstruction clears [15]. Studies of a circumferential “horizontal” abdominal thrust with the same hand placement as the Heimlich, but with straight backward thrust, has shown similar airway pressures as for the Heimlich. Since this approach is below the ribcage, there is less likelihood to damage the internal organs or ribs [16]. For the unconscious patient, current Advanced Cardiac Life Support (ACLS) guidelines recommend performing standard CPR chest compressions [10]. The only caveat is that before giving breaths, rescuers should look inside the mouth to visualize and remove any foreign bodies. Abdominal compressions and blind finger sweeps are no longer recommended for unconscious persons [10, 11]. For infants less than 1 year of age, the rescuer typically positions the victim with the head downward, alternating back blows with chest compressions. Bulb suction, visualized finger sweeps, and back blows often work well without the need for chest compressions [10, 11, 17]. EMS personnel responding to a choking emergency must be prepared to manage the advanced stages of crisis and must act quickly on arriving at the scene. Bystanders may have failed to recognize that the patient is choking, leading emergency medical dispatchers to miscategorize the call as a condition other than choking (e.g., respiratory distress, chest pain, or unconscious person) due to inaccurate or incomplete information from the 9‐1‐1 caller. Bystanders may have already made unsuccessful attempts to clear the obstruction

Choking

with the Heimlich maneuver. The patient may be unconscious or in cardiac arrest. On confirming the presence of complete airway obstruction, rescuers should perform the Heimlich maneuver or chest compressions [10, 11, 18]. In cases of partial airway obstruction, rescuers should monitor for signs of cyanosis, inadequate breathing, or unconsciousness, signifying the need to immediately provide the Heimlich maneuver or chest compressions. If the Heimlich maneuver does not resolve the obstruction, ALS personnel may attempt to directly visualize the airway with a laryngoscope, making efforts to remove visualized foreign bodies using Magill forceps [19]. A table maneuver where the choking person is laid prone over a table, head and arms hanging over the side, and then receives sharp back blows from the rescuer between the scapula, has been successful in case studies [20]. Using a head down, inverted approach allows gravity to help expel the foreign body as seen in children, provided it can be done safely and without injuring the rescuer or victim [21]. Foreign bodies below the vocal cords may be more problematic. Anecdotal reports suggest using a rigid suction catheter in these situations. A cadaver study and case studies are promising for a portable, nonpowered, suction generating device called the LifeVac® that provides pressures far greater than any of the aforementioned techniques [22]. Although data in this area are lacking, intubation is risky in these cases and may further lodge the foreign body. As a last resort, rescuers may consider performing cricothyroidotomy or transtracheal jet ventilation. This approach will only work if the surgical airway is placed below the foreign body. There are anecdotal reports of using high‐pressure jet ventilation to eject entrapped foreign bodies. However, there are no organized reports of choking management using cricothyroidotomy or jet ventilation. For patients with partial airway obstructions, there are additional management options. The patient should be encouraged to cough and expel the object. High‐flow supplemental oxygen may be appropriate, although the sensation of the mask may make the patient feel uncomfortable, aggravating the situation. If the patient is able to adequately move air, it may be acceptable, and even preferable, to carefully transport the patient to the hospital for definitive care. In these cases, close monitoring of vital signs, oxygen saturation, respiratory effort, and level of consciousness are essential. Monitoring end‐tidal carbon dioxide may also help to reveal early clinical deterioration, though research data on this are lacking. EMS personnel should provide advanced notification to the receiving facility so that the emergency department can prepare its equipment and summon appropriate personnel. Because this is an airway emergency, it typically makes the most sense to go to the nearest hospital. At the receiving hospital, the patient may require urgent sedation, direct or video laryngoscopy, or surgical airway intervention

225

by an emergency physician, otolaryngologist, anesthesiologist, or surgeon. Many emergency departments have a ­“difficult airway” algorithm that involves summoning various specialists to provide assistance in these emergency airway situations. Many postchoking victims refuse EMS care and/or transport. In general, however, it is recommended that patients who have their choking resolved before EMS arrival, or by EMS clinicians, be transported to the hospital for further evaluation to ensure that no complications have occurred [10, 13, 15]. This recommendation is based primarily on case reports of laryngospasm, pulmonary edema, anoxic brain injury, and retained foreign body occurring after choking episodes. In addition, there are case reports of damaged internal organs following abdominal and chest thrusts [23]. A patient who persists in refusing transport should be made aware of these possible risks. As a final consideration, an anaphylactic reaction may masquerade as an upper airway obstruction, especially if the patient has recently eaten nuts [24]. If the history and presentation are suggestive of this situation, EMS clinicians should consider therapy with epinephrine and antihistamines.

Medical oversight considerations Deterioration after complete airway obstruction occurs so rapidly that direct medical oversight by phone or radio likely provides minimal value. In cases of partial obstruction, direct medical oversight may provide useful guidance regarding management and receiving hospital options. The most important consideration is to educate EMS personnel to recognize signs and symptoms of partial and complete obstruction. As bystander intervention is essential in treating choking, EMS community outreach and education efforts are equally important. Prevention through activity with regulating authorities can lead to altering or relabeling objects or foods known to be significant choking risks [5, 6, 8, 9]. EMS physician presence at the scene may potentially play a role in select complicated choking cases. Patients with partial airway obstructions may prove to be difficult to manage, requiring a fine balance between supportive care and skilled airway intervention. An on‐scene EMS physician may facilitate selection of optimal treatment strategies. In the event of complete airway obstruction unresolved by basic techniques, an on‐scene EMS physician may be best qualified to perform advanced airway interventions, such as direct or video laryngoscopy and foreign body removal, rapid sequence intubation, or cricothyroidotomy. In all cases, the EMS physician’s value will be greatest if he or she is present at the earliest stages of the event—before complete airway obstruction or anoxic injury.

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Controversies The most important controversies in choking management are the use of back blows and chest thrusts. The Heimlich Institute opposes both of these techniques. The American Heart Association (AHA) recommends these interventions if the Heimlich maneuver fails, and the American Red Cross (ARC) also advocates for both [10, 11, 25]. The AHA and the ARC recommend chest thrusts instead of the Heimlich maneuver for unconscious, pregnant, and obese patients and for children less than 1 year of age. Critics note that back blows can cause the object to lodge deeper and waste valuable time better spent performing the Heimlich maneuver. In a recent study, the Heimlich maneuver was 86.5% effective at removing an obstruction [13]. Back blows may prove effective in children less than 5 years of age [17]. Chest thrusts are associated with significantly higher morbidity and mortality than the Heimlich maneuver and should probably be reserved for the most serious choking victims [26]. Some of these controversies may be answered as the MOCHI study is getting underway in Japan and scheduled to conclude in 2023 [27].

Summary Medical directors can be most successful by being active and providing community education. ACLS‐ and Pediatric Advanced Life Support–trained public and EMS clinicians have improved choking survival rates beyond 95% [10, 11]. Expeditious recognition and treatment of choking are essential and should ideally be accomplished by bystanders. EMS personnel arriving on the scene should be prepared to manage a patient in extremis. Patients with partial airway obstructions may tolerate supportive care and rapid transport to the hospital. All choking victims should receive transport to the hospital for evaluation. An observational cohort trial underway in Japan, MOCHI, may provide answers to many of the controversies surrounding foreign body airway obstructions.

References 1 Igarashi Y, Yokobori S, Yoshino Y, Masuno T, Miyauchi M, Yokota H. Prehospital removal improves neurological outcomes in the elderly patient with foreign body airway obstruction. Am J Emerg Med. 2017; 35:1396–9. 2 Blaas V, Manhart J, Port A, Keil W, Buttner A. An autopsy approach to bolus deaths. J Forensic Leg Med. 2016; 42:82–87. 3 Brkic F, Umihanic S, Altumbabic H, et al. Death as a consequence of  foreign body aspiration in children. Review Med Arch. 2018; 72:220–3. 4 Centers for Disease Control and Prevention Web‐Based Injury Statistics Query and Reporting System (WISQARS)]. Available at: https://www.cdc.gov/injury/wisqars/. Accessed August 1, 2020.

5 Committee on Injury, Violence, and Poison Prevention, American Academy of Pediatrics. Policy statement– prevention of choking among children. Pediatrics. 2010; 125:601–7. 6 Chapin M, Rochette L, Annest J, Haileyesus T, Conner K, Smith G. Nonfatal choking on food among children 14 years or younger in the United States, 2001‐2009. Pediatrics. 2013; 123:275–81. 7 Hemsley B, Steel J, Sheppard J, Malandraki G, Bryant L, Balandin S. Dying for a meal: an integrative review of characteristics of choking incidents and recommendations to prevent fatal and nonfatal choking across populations. Am J Speech Lang Pathol. 2019; 28:1283–97. 8 Kiyohara K, Sakai T, Nishiyama C, et al. Epidemiology of out‐of‐ hospital cardiac arrest due to suffocation focusing on suffocation due to Japanese rice cake: a population‐based observational study from the Utstein Osaka Project. J Epidemiol. 2018; 28:67–74. 9 Taniguchi Y, Iwagami M, Sakata N, Watanabe T, Abe K, Tamiya N. Epidemiology of food choking deaths in Japan: time trends and regional variations. J Epidemiol. 2021. Published online ahead of print, June 13, 2020. doi: 10.2188/jea.JE20200057. 10 Olasveengen TM, Mancini ME, Perkins GD, et  al. Adult Basic Life Support: 2020 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Circulation. 2020; 116:S41–S91. 11 Topjian AA, Raymond TT, Atkins D, et al. Part 4: Pediatric Basic and Advanced Life Support: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Circulation. 2020; 116:S469–S523. 12 Karande S, Vaideeswar P, Muranjan M. Muddy clinical waters: a missed betel nut in the bronchus. BMJ Case Rep. 2015; 2015:bcr2015212919. 13 Soroudi A, Shipp HE, Stepanski BM, et  al. Adult foreign body airway obstruction in the prehospital setting. Prehosp Emerg Care. 2007; 11:25–29. 14 Pavitt M, Nevett, J, Swanton L, et al. London ambulance source data on choking incidence for the calendar year 2016: an observational study. BMJ Open Resp Res. 2017; 4:e000215. 15 Heimlich HJ. A life‐saving maneuver to prevent food‐choking. JAMA. 1975; 234:398–401. 16 Pavitt M, Swanton L, Hind M, et  al. Choking on a foreign body: a physiological study of the effectiveness of abdominal thrust manoeuvers to increase thoracic pressure. Thorax. 2017; 72:576–8. 17 Vilke GM, Smith AM, Ray LU, Steen PJ, Murrin PA, Chan TC. Airway obstruction in children aged less than 5 years: the prehospital experience. Prehosp Emerg Care. 2004; 8:196–99. 18 Kinoshita, K, Azuhata, T, Kawano, D, Kawahara, Y. Relationships between pre‐hospital characteristics and outcome in victims of foreign body airway obstruction during meals. Resuscitation. 2015; 88:63–67. 19 Sakai T, Kitamura T, Iwami T, et  al. Effectiveness of prehospital Magill forces use for out‐of‐hospital cardiac arrest due to foreign body airway obstruction in Osaka City. Scand J Trauma Resusc Emerg Med. 2014; 22:53. 20 Blain H, Bonnafous M, Grovalet N, Jonquet O, David M. The table maneuver: a procedure used with success in four cases of unconscious choking older subjects. Am J Med, 2010; 123:1150.e7–9. 21 Luczak A. Effect of body position on relief of foreign body from the airway. AIMS Public Health. 2019; 6:154–9.

Choking

22 Patel P, Shapiro N. Portable, non‐powered, suction‐generating device for management of life‐threatening aerodigestive tract foreign bodies: novel prototype and literature review. Int J Pediatr Otorhinolaryngol. 2019; 118:31–5. 23 Lee K, Wu Y, Ho S. Silent aortic dissection after the Heimlich maneuver: a case report. J Emerg Med. 2019; 56:210–12. 24 Nguyen AD, Gern JE. Food allergy masquerading as foreign body obstruction. Ann Allergy Asthma Immunol. 2003; 90:271–2. 25 Heimlich HJ, Patrick EA. The Heimlich maneuver: best technique for saving any choking victim’s life. Postgrad Med. 1990;87:38–48,53.

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26 Dupont V, Rougé‐Maillart C, Gaudin A, Jeanneteau A, Jousset N, Malbranque S. Left diaphragm laceration due to cardiopulmonary resuscitation. J Forensic Sci. 2016; 61:1135–38. 27 Norii T, Igarashi Y, Sung‐Ho K, et  al. Protocol for a nationwide prospective, observational cohort study of foreign body airway obstruction in Japan: the MOCHI registry. BMJ Open. 2020; 10:e039689.

CHAPTER 25

Submersion injuries and drowning Robert Lowe

Introduction Drowning is the process of experiencing respiratory i­mpairment from submersion/immersion in liquid  [1]. Drowning outcomes are referred to as one of three categories: death, morbidity, and no morbidity. Historically, various modifiers have been used both medically and in the lay press. The use of terms such as wet, dry, near, and secondary are not acceptable medical classifications, though their use in older literature may contribute to their continued application. In addition, the EMS medical director and EMS systems, and their efforts in public education, must be aware of lay terms being misappropriated. Terms such as dry drowning have been rampantly misapplied in social media. Lastly, submersion is defined as the passage of the airway beneath the surface of a liquid, while immersion is defined as liquid splashes about the face or airway [1, 2]. The definition excludes water rescue if there is no respiratory component.

Epidemiology Drowning remains a leading cause of unintentional death and unintentional injury [2]. The Centers for Disease Control and Prevention place the incidence of nonfatal drowning between 4,000 and 7,000 cases per year  [3–7]. Fatal drownings in the United States range from 3,200 and 6,000 cases per year [3, 6, 7]. The incidence of nonfatal drownings range from one to four times that of fatal drownings [5]. Greater than 50% of all drownings require hospitalization [3]. Drowning is a leading cause of unintentional injury for ages 1–4 and ages 15–19 years [4]. Among infants less than 1 year old, most drownings occur in the bathtub  [8]. For children less than 4 years old, most drownings occur in private pools. For ages greater than 15 years, the predominant drowning location includes natural water settings such as beaches and

lakes [9]. Fatalities are higher for victims less than 4 years old. C­ompared with females, males have twice the rate of nonfatal and five times the rate of fatal drownings [3]. More than half of adolescent and adult drownings involve alcohol or illicit substance use [9, 10]. Accomplished swimmers comprise approximately 35% of persons under the age of 20 years who suffer death by drowning  [11]. Preexisting medical conditions may play a role as well, as noted in children with seizures having a fourfold increase in drowning risk compared to the general population [5, 12]. Drowning accidents involving children commonly result from lapses in adult supervision. In the majority of child drownings, the child was under the care of one or both parents and was “out of sight” for less than 5 minutes [10]. While surveyed pool owners favor CPR requirements, fewer than half of these households actually have CPR‐qualified individuals. Of pool owners favoring isolation fencing around pools, only one third had their pool fenced. The risk of drowning or near‐drowning is three to four times higher in unfenced pools than fenced pools [7]. Epidemiologic and public health data highlight the role of education, planning, and other community level interventions in drowning prevention. Estimates of preventable drowning deaths are as high as 80% [5]. Many EMS systems participate in drowning prevention efforts, such as education and water safety programs, but to date little data are available regarding the effect of these efforts on the rates or outcomes of drowning.

Pathophysiology of drowning Classically, drowning begins as a period of panic and struggle, but in a minority of cases, such as those involving trauma or seizure, the initial phase may be different [10, 13]. Death from drowning ultimately results from respiratory compromise, hypoxia, and cardiac arrest. Successful resuscitation after a d­rowning‐induced cardiac arrest is rare.

Emergency Medical Services: Clinical Practice and Systems Oversight, Third Edition. Volume 1: Clinical Aspects of EMS. Edited by David C. Cone, Jane H. Brice, Theodore R. Delbridge, and J. Brent Myers. © 2021 NAEMSP. Published 2021 by John Wiley & Sons, Inc.

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Cerebral hypoxia plays a significant role in the functional recovery of the victim. Many drowning survivors suffer some permanent neurologic damage, with up to 10% suffering severe lasting effects  [15, 16]. The duration of hypoxia is correlated with submersion time and is an important determinant of recovery  [14, 15, 17]. Another important consideration is the neuroprotective effect of hypothermia. The medical literature and the lay press are replete with examples of survival after lengthy submersion in frigid or near‐freezing water. While cold water submersion does not guarantee survival, it may play a significant role in management decisions during and after the resuscitation [14, 18].

Clinical management Dispatch life support Public safety answering point telecommunicators should provide dispatch life support, including standard respiratory and cardiopulmonary arrest instructions. Minimizing delays in delivering instructions is essential. DeNicola found that 42% of children drowning in home swimming pools were rescued by bystanders but did not have CPR initiated until EMS personnel arrived [7]. The use of an AED is appropriate and should be included when such a device is available. A less‐clear area is whether telecommunicators should direct callers to rescue drowning victims. All water rescues involve risk and may potentially result in additional victims. Scene and crowd control The first step in successful drowning management is rapid extrication of the victim from the water. Scene safety is paramount, especially in natural water and moving water scenarios. Rescuers not specifically trained in water rescue should not attempt extrication or rescue in moving water. Crowd control and prevention of secondary victims are essential. Drownings are dramatic events. Depending on the setting (public pool, hotel pool, natural water setting), a large number of bystanders may be present. Bystanders acting as rescuers may inadvertently become secondary victims, especially in natural water settings or in large groups that include nonswimmers. Rescuers should liberally request and use crowd control resources. Management of the drowning victim in cardiac arrest The most dramatic clinical presentation of drowning is cardiopulmonary arrest. Rescuers should initiate standard cardiac arrest protocols for drowning victims. CPR should begin as soon as practical, with some advocating initiation of CPR while still in the water [11]. Airway management should begin immediately with bag‐valve‐mask ventilation [18]. Typically, extrication from the water should not be delayed for more definitive airway management. Once extricated from the water,

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additional airway procedures consistent with cardiac arrest protocols may be considered. Rescuers should anticipate vomiting, which may occur in up to 86% of drowning victims receiving rescue breathing and chest compressions [18, 19]. Maneuvers to clear water from the lungs, such as laying the patient prone and lifting the arms behind the back toward the head, are outdated, not indicated, and should not be performed [7, 9, 13, 18]. Cardiac arrest treatment algorithms do not require modification for drowning victims. While experts have historically emphasized minimizing movement in the severely hypothermic patient to avoid precipitating ventricular dysrhythmias, this recommendation seems to be based more on theory and conjecture than data. Advanced airway management is appropriate. Airway interventions while in the water are fraught with difficulty and risk of aspiration and delay of CPR initiation. While each scene may pose a unique risk‐benefit analysis around patient access and timely egress, typically anything more than basic maneuvers should be deferred to accomplish rapid extrication and initiation of full resuscitation efforts. In the severely hypothermic patient, advanced airway placement may allow for warmed, humidified ventilation. Vascular access and drug therapy should follow standard resuscitation protocols. Some have raised concern that medications may reach toxic levels in the circulation due to decreased metabolism in the severely hypothermic patient [20]. However, little scientific evidence distinguishes drug metabolism in hypothermic versus normothermic cardiac arrest patients. Despite this concern, most guidelines recommend minor alterations of cardiac arrest protocols for patients with hypothermia  [20]. Specifically, in moderate hypothermia (30°C‐34°C), rescuers may increase the time interval between doses of intravenous medications. Rescuers should also perform active external rewarming for moderate to severe hypothermia. For severe hypothermia (30°C  [21]. The determination of an accurate core temperature in the field setting is difficult, and rescuers should act based upon the best available clinical information. Management of non‐cardiac arrest drowning Airway management, hemodynamic stabilization, and transport are the mainstays of treatment. These individuals may be apneic, hypotensive, or hypothermic, and should receive appropriate resuscitative interventions. These victims have high potential for pulmonary injury and should receive emergency department evaluation even if relatively asymptomatic at the scene. Over half of initial nonfatal drowning victims ultimately require hospital admission. These patients should be transported and evaluated, as their conditions can deteriorate rapidly. Initial presentations can be misleading, and refusal of transport should be strongly discouraged [7, 11]. Field management should focus on evaluation and management of oxygenation. Monitoring of pulse oximetry,

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cardiac rhythms, vital signs, and overall neurologic status are warranted. Monitoring end‐tidal CO2 may also be helpful. Noninvasive positive‐pressure ventilation for the conscious breathing patient is being increasingly advocated [11, 22]. Rapid deterioration in ventilation, oxygenation, or ability to protect the airway may mandate additional airway interventions consistent with medical respiratory distress protocols. Secondary aspiration from vomiting is a risk in the deteriorating drowning victim. Intravenous access should be established in most drownings. Consideration should be given to potential concurrent trauma. Victims may have had concurrent medical conditions that triggered the event, such as hypoglycemia, seizures, and cardiac dysrhythmias. These should be addressed and treated appropriately. Management of concurrent trauma Many drownings occur concurrently with other major trauma. For example, an individual may sustain a cervical or spinal cord injury after diving into shallow water. Swimmers in lakes have sustained traumatic brain injuries or penetrating trauma after being struck by motor boats. An important consideration for drowning victims is the potential for cervical spine injury. Such injuries were identified among 11 of 143 pediatric drowning cases in a series from a pediatric trauma center, and 11 of 2,244 drowning victims in a separate series [8, 21]. All cervical spine injury patients had worrisome mechanisms of injury (e.g., diving, high‐impact, or assault). EMS rescuers should consider cervical spine injuries in diving, high‐impact (e.g., dive from a height), and whitewater submersion injuries. However, the rescuers must weigh the risks and benefits of cervical immobilization. For example, cervical immobilization may be dangerous and difficult in swiftwater rescues  [20]. American Heart Association guidelines support the position that routine stabilization of the cervical spine is not necessary unless the circumstances leading to the submersion episode indicate that trauma is likely. Drowning circumstances potentially linked to cervical injury include a history of diving, water slide use, concern for alcohol intoxication, or physical signs of injury  [18]. The decision to initiate spine immobilization while in the water is a risk‐benefit decision for the patient and rescue team. An absence of identified risk for cervical injury precludes the need for spine immobilization in or out of the water. Swimming pools in particular may be a more appropriate setting for floating back boards or baskets and application of cervical collars without undue risk to the patient or the rescue team. Swiftwater environments may require a more limited cervical spine control maneuver and rapid extrication to water’s edge prior to application of spinal motion restriction devices. In all events, if secondary concerns for cervical injury are discovered by examination or history, cervical spine protection measures should be instituted. Rewarming of drowning victims Rewarming is appropriate for severely hypothermic patients. Initial temperature management begins with removing the patient from the offending environment, the water. The

resuscitation effort should continue in a warmed environment. EMS clinicians should prewarm the ambulance if possible. To prevent further heat loss, the patient’s wet clothing should be removed. Additional rewarming techniques are commonly classified as active external rewarming and active internal rewarming. Active external rewarming includes the use of warm packs, warm water packs, forced air, thermal blankets, warmed oxygen, and warmed IV infusions. Care should be exercised to avoid secondary thermal injury from warm packs against the skin. There is concern for a paradoxical drop in the core temperature due to vasodilatation of the peripheral vasculature during rewarming. Vigilant hemodynamic monitoring is important  [12]. Active internal rewarming, including peritoneal lavage with warmed fluids, esophageal tubes for rewarming, chest lavage with warm fluids via chest tubes, and cardiac bypass or extracorporeal circulation, are generally beyond the scope of EMS. Historically, the advice was to rewarm by whatever means available, and to do so aggressively during the resuscitation. However, the old adage “A victim is not dead until warm and dead” may require reconsideration. Mounting evidence has shown that induced hypothermia after return of spontaneous circulation may impart some neurological benefit for ventricular fibrillation and possibly other causes of cardiac arrest (see Chapters  12 and  13). It would seem logical that a drowning victim may benefit from induced or continued hypothermia  [5, 11]. Additionally, guidelines now indicate a target core temperature of 32°C‐34°C after return of spontaneous circulation in cardiac arrest due to accidental hypothermia [20]. In the absence of specific drowning data, and the success of hypothermia in general cardiac arrest, the historic practice of aggressive rewarming is being questioned. There are calls to abandon the practice [23]. There is a paucity of published data or recommendations about resuscitation of drowning victims in hot water. Destination decisions Patients in cardiac arrest should be transported to the nearest emergency facility. Patients with perfusing rhythms may benefit from transport to a specialized facility (e.g., trauma or pediatric center), if feasible. While some victims have concurrent trauma, those without obvious injuries or significant mechanisms of injury do not require trauma center care [23].

Grief reactions Drownings are unexpected events, often in young and healthy people. Relatives and bystanders may express significant grief from these events. As noted previously, the greatest number of victims are young children. After the incident, attention should be paid to possible grief reactions among rescue personnel so that appropriate referral or interventions can be implemented.

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References 1 van Beeck EF, Branche CM, Szpilman D, et  al. A new definition of drowning; towards documentation and prevention of a global public health problem. Bull World Health Org. 2005; 83:853–6. 2 Schmidt AC, Sempsrott JR, Hawkins SC, et  al. Wilderness Medical Society clinical practice guidelines for the treatment and prevention of drowning: 2019 update. Wilderness Environ Med. 2019;30:S70–86. 3 Centers for Disease Control and Prevention. Drowning–United States, 2005–2009. MMWR. 2012;61:344–7. 4 Centers for Disease Control and Prevention. Unintentional Drowning: Get the Facts. https://www.cdc.gov/homeandrecreational safety/water‐safety/waterinjuries‐factsheet.html. Accessed October 2, 2020. 5 Meyer RJ, Theodorou AA, Berg RA. Childhood drowning. Ped Rev. 2006; 27:163–9. 6 Hwang V, Shofer FS, Durbin DR, Baren JM. Prevalence of traumatic injuries in drowning and near drowning in children and adolescents. Arch Pediatr Adolesc Med. 2003; 157:50. 7 DeNicola LK, Falk JL, Swanson ME, Gayle MO, Kissoon N. Submersion injuries in children and adults. Crit Care Clin. 1997; 13:477–502. 8 Brenner RA, Trumble AC, Smith GS, Kessler EP, Overpeck MD. Where children drown, United States 1995. Pediatrics. 2001; 108:85–89. 9 Olshaker JS. Submersion. Emerg Med Clin N Am. 2004; 22:357–67. 10 Moon RE, Long RJ. Drowning and near‐drowning. Emerg Med. 2002; 14: 377–86. 11 Layton AJ, Modell JH. Drowning; update 2009. Anesthesiology. 2009; 110:1390–1401.

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12 Orlowski JP, Rothner D, Leuders H. Submersion accidents in children with epilepsy. Am J Dis Child. 1982; 136:777–80. 13 Ibsen LM, Koch T. Submersion and asphyxial injury. Crit Care Med. 2002; 30:S402–8. 14 Gheen KM. Near drowning and cold water submersion. Semin Pedatr Surg. 2001; 10:26–7. 15 Burfor AE, Ryan LM, Stone BJ, Hirshon JM, Klein BL. Drowning and near‐drowning in children and adolescents: a succinct review for emergency physicians and nurses. Pediatr Emerg Care. 2005; 21:610–11. 16 Quan L. Near‐drowning. Pediatr Rev. 1999; 20:255–60. 17 Quan L, Bierens JJ, Lis R, et al. Predicating outcomes of drowning at the scene: a systemic review and meta‐analyses. Resuscitation. 2016; 104:63–75. 18 Vanden Hoek TL, Morrison LJ, Shuster M, et  al. Drowning. Part 12.11: Cardiac arrest in special situations: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010; 122:S829–61. 19 Manolios N, Mackie I. Drowning and near‐drowning on Australian beaches patrolled by life‐savers: a 10‐year study, 1973‐1983. Med J Aust. 1988; 148:165–71. 20 Vanden Hoek TL, Morrison LJ, Shuster M, et  al. Hypothermia. Part 12.9: Cardiac arrest in special situations: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010; 122:S829–61. 21 Watson RS, Cummings P, Quan L, Bratton S, Weiss NS. Cervical spine injuries among submersion victims. J Trauma. 2001; 51:658–62. 22 Tropjian AA, Berg RA, Joost JL, et  al. Brain resuscitation in the drowning victim, Neurocrit Care. 2012; 17:441–67. 23 Hunn ES, Helmer SD, Reyes J, et al. Patterns of injury in drowning patients–do these patients need a trauma team? Kas J Med. 2020; 13:165–78.

SECTION V

Trauma Problems

CHAPTER 26

Trauma systems of care James E. Winslow

In its broadest sense, a trauma system consists of an organized approach to managing patients who have suffered acute injury, across the continuum from initial medical care through rehabilitation, as well as injury prevention activities aimed at those at risk of suffering trauma. While the trauma system should be integrated with both public health and emergency management, there is significant overlap between trauma and EMS systems [1]. This chapter will focus primarily on the close interaction between these two systems.

Box 26.1    Criteria for statewide trauma systems

•  Legal authority for designation •  Formal process for designation •  Use of American College of Surgeon’s standards •  Use of nonbiased survey teams (from out‐of‐area) •  Number of trauma centers based upon population or volume •  Triage criteria that permit direct transport to a trauma center •  Monitoring of system performance •  Full geographic coverage Source: Based on ref. [3].

Trauma system organization The World Health Organization criteria to define a fully developed trauma system includes requirements for prehospital care, education and training, facility‐based trauma care, and quality assurance. Requirements for prehospital care include formal oversight of EMS by a lead agency, a universal access number, and legislative mechanisms to regulate EMS and provide universal EMS coverage. Education and training standards for EMS should be set. Licensing and renewal requirements for EMS clinicians must be in place. A mechanism for verification and accreditation of trauma centers through either governmental entity or professional organizations should exist, as well as a lead agency with a mandate to supervise all trauma care. Quality assurance is critical and should be established for both prehospital and facility‐based services [2]. In the United States, trauma systems are typically organized at the state level, although some larger counties may have sophisticated systems (e.g., San Diego County, CA). In 1988, West and colleagues described the ideal criteria for a statewide trauma care system (Box 26.1) [3]. State laws generally delegate authority for trauma centers designation to a state agency, such as a Department of Health, and describe the process by which hospitals may seek designation. Because of their close relationship, most state trauma offices are colocated with the state Office of EMS.

While most states use the standards promulgated by the American College of Surgeons Committee on Trauma (ACS‐ COT), some states opt to draft their own trauma center criteria. The term designation refers to authorization from a state agency for an institution to represent itself to the public as a trauma center, while verification refers to the inspection by a nonbiased team of experts (usually from outside the community) who have confirmed that all necessary services and processes are in place to meet the ACS‐COT (or equivalent) standards. In the ideal trauma system, the lead agency would have authority to designate trauma centers based upon need, rather than simply approving any facility that desires designation in a competitive, free‐market approach. Research by Ciesla demonstrates that the addition of trauma centers into a trauma system where there is no established need may increase costs without improving patient care [1]. Need for additional trauma centers should be based on the population of a geographic area, the volume of trauma patients encountered, or proximity to other designated centers. Trauma centers regularly caring for large numbers of patients maintain readiness, and patient management becomes routine, while those with insufficient practice, especially of the seriously injured, may struggle to maintain organizational processes and procedural skills.

Emergency Medical Services: Clinical Practice and Systems Oversight, Third Edition. Volume 1: Clinical Aspects of EMS. Edited by David C. Cone, Jane H. Brice, Theodore R. Delbridge, and J. Brent Myers. © 2021 NAEMSP. Published 2021 by John Wiley & Sons, Inc.

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Performance improvement is a key trauma system component. Trauma registry data are pooled on a system‐wide basis and analyzed. ACS‐COT has developed the Trauma Quality Improvement Project (TQIP), which conducts risk‐adjusted analysis of trauma center outcomes through voluntarily submitted data. By presenting its data as observed‐to‐expected ratios, TQIP allows centers to voluntarily benchmark themselves to other centers across the country. TQIP allows high‐performing trauma centers (low observed‐to‐expected ratios) to share best practices with lower‐performing facilities (high observed‐to‐expected ratios). Most states have trauma advisory committees comprised of individuals representing stakeholder sectors involved in trauma care. Providing oversight and advice to the state trauma office on matters related to trauma system improvements, advisory committees often draft or approve state trauma plans that serve as a strategic blueprint for enhancing the system over time. Often the state trauma advisory committee assists the state in determining how governmental funding will be distributed to trauma system stakeholders. Governmental funding offsets the expensive costs of maintaining trauma center readiness and data collection for trauma registries and aids with uncompensated care delivered by trauma centers. State funding may also provide education to individuals who care for trauma patients, or purchase needed equipment.

Trauma care facilities Trauma centers represent an essential component of trauma systems. A trauma center is an institution committed to the care of injured patients across the spectrum of initial resuscitation through rehabilitation, including operative management and critical care. A trauma center is a unique blend of personnel (surgeons and other physician specialists, nurses, and allied health care workers), equipment, and processes including robust ongoing performance improvement programs. The physicians, nurses, therapists, and technologists must work together as a cohesive team, under the direction of the trauma surgeon. The most widely accepted criteria for trauma center designation are those promulgated by the ACS‐COT [4]. These include the following: • Level III trauma center‐ A Level III trauma center is responsible for rapidly assessing trauma patients, initiating resuscitation, providing emergency operative care, and stabilizing the patient. A Level III trauma center must be well integrated into a larger regional trauma system with transfer agreements in place to facilitate the rapid transfer of trauma patients. In isolated areas without rapid access to a Level I or II trauma center, a Level III trauma center is expected to take a leadership role in local education and prevention. In a Level III center, general surgeons must be immediately available while orthopedic surgeons, radiologists, and anesthesia personnel must be on call [4].

• Level II trauma center‐ A Level II trauma center can manage more complex cases. Trauma surgeons must be available within 15 minutes of arrival for the most critically injured patients. In addition to the criteria from Level III centers, a Level II center must include on‐call physicians in the following specialties: neurosurgery, hand surgery, cardiac surgery, thoracic surgery, vascular surgery, microvascular surgery, plastic surgery, urology, obstetrics/gynecology, ophthalmology, oral/maxillofacial surgery, cardiology, gastroenterology, infectious disease, pulmonology, nephrology, and critical care medicine [4]. • Level I trauma center‐ A Level I trauma center is the highest‐level trauma center. To maintain the highest level of proficiency, the American College of Surgeons requires that a Level I trauma center admit at least 1,200 patients a year or have 240 admissions with an Injury Severity Score of greater than 15. A Level I trauma center has the same level of surgical specialists as a Level II center. Level I trauma centers are also expected to have an increased emphasis on injury prevention and are therefore required to employ a full‐time injury prevention coordinator. In addition to providing the most comprehensive trauma care, a Level I facility serves as a regional referral resource and a leader in the regional trauma system. As part of its teaching responsibilities, a Level I center must participate in training of surgical residents and conduct Advanced Trauma Life Support courses. Level I facilities must also have an ongoing research program related to injury [4]. When first conceived, trauma systems verification was limited to three levels and was seen as an exclusive system, allowing only hospitals with certain minimal capabilities to participate. In response, ACS‐COT added the Level IV trauma facility. The Level IV is a smaller hospital with limited capabilities that is viewed as a resuscitation point in a community lacking Level I–III trauma centers. Following initial stabilization at a Level IV center, the injured patient should be transferred to a higher level of care. Level IV centers round out an inclusive trauma system and the ability to provide full geographic coverage. The American College of Surgeons has recently advanced the idea of an inclusive trauma system and recognizes that all hospitals regardless of trauma center status care for injured patients. An inclusive trauma system includes all hospitals and assists with trauma education, providing feedback on care, developing standards of care, and transfer agreements [4].

Communications Functional communication systems (e.g., the 9‐1‐1 system), a key aspect of both EMS and trauma systems, enable trained telecommunicators to provide prearrival instructions for lay bystanders (e.g., direct pressure or tourniquet application for hemorrhage control) while EMS is responding. Telecommunicators also gather information from callers or first responders

Trauma systems of care

regarding specialized personnel or equipment needs, such as extrication or hazardous materials experts. For the most critically injured patients, rapid response and transport result in an expeditious patient arrival at the trauma center. Radio communications between the public safety answering point and the responding and transporting EMS units, as well as between the EMS units and the receiving facility, facilitate response, and transport. Prompt trauma center notification of the impending arrival of a seriously injured patient allows the facility to assemble its trauma team prior to patient arrival. Mass casualty events, such as the terrorist attacks of September 11, 2001, illustrated the vulnerabilities of public service communication when many agencies (e.g., law enforcement, fire, and EMS) were unable to communicate with each other. Emergency management organizations have focused significant resources on increasing interoperability, resulting in enhanced communication between first responders to improve mass casualty response. Many state trauma and EMS agencies host web‐based tools for receiving facility status (open versus on diversion, etc.). Some web‐based systems are robust enough to indicate the number of available beds, permitting a rapid assessment of surge capacity in a disaster.

Emergency response Trauma and EMS systems overlap to the greatest extent in emergency response, from EMS dispatch to patient arrival at the receiving facility. “Getting the right patient to the right place in the right amount of time” truly describes the challenge faced by EMS clinicians when caring for trauma patients. “Field triage” represents the decision making to select which injured patients (“the right patient”) require transport to a trauma center (“the right place”). In 2006 and again in 2011, the Centers for Disease Control and Prevention assembled national expert panels to review evidence and revise the field triage algorithm [5]. “The right amount of time” includes decisions regarding scene interventions and time, and determining the best mode of transport, namely ground EMS versus air medical services. While air medical transport can move an injured patient from a distant scene to a trauma center significantly faster than ground transport, ground transportation may be more expeditious when the patient is located closer to the trauma center (within ~10 miles), because of the time required to set up a landing zone and power up and power down helicopter engines. Trauma surgeons and EMS physicians should have input into regional protocols regarding transport modality of injured patients. EMS personnel may be called upon to transport patients from the initial receiving facility (perhaps a nontrauma center) to a trauma center. The care required en route (basic life support versus advanced life support versus specialty care), distance, and need for rapid transfer are the major determinants of whether ground or air transport is used. In some jurisdictions,

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the transferring facility may need to send a nurse to accompany the patient if care that exceeds the scope of practice of the EMS personnel is required. All ACS‐COT verified trauma centers must participate in public and professional education. Standardized trauma training courses for EMS personnel exist, including Prehospital Trauma Life Support and International Trauma Life Support. Many EMS systems require personnel to maintain current certification in one of these programs, which provides an opportunity for nurses and physicians from trauma centers to share their expertise in managing trauma patients. Some trauma centers provide case reviews for EMS personnel, offering follow‐up on diagnostic procedures and management after arrival at the facility, in combination with reinforcement of basic trauma care principles.

Medical oversight EMS medical oversight is divided into direct and indirect oversight. Direct oversight involves providing instructions to prehospital care clinicians via radio or telephone, or in person on‐scene. In the early days of advanced life support in the prehospital setting, direct medical oversight was heavily used with the thought that close communication between the receiving or base station physician and EMS clinicians was essential for quality care. Because of the time involved in contacting a physician, direct medical oversight may be associated with longer prehospital times. Focus has shifted toward indirect medical oversight, wherein EMS clinicians follow written protocols or treatment guidelines, each focused on a specific condition or chief complaint. As emergency departments are typically staffed by emergency physicians, direct oversight is almost always provided by emergency physicians rather than trauma surgeons. EMS physicians in many systems are physically present in the field, providing direct patient care, monitoring care, and providing orders for EMS personal. Most trauma surgeons have limited exposure to prehospital care, unless they worked as EMS clinicians in previous employment. As a result, trauma surgeons may have a limited understanding of prehospital care delivery and the unusual circumstances under which EMS clinicians must render care. For this reason, EMS physicians must be integral participants in the oversight of their respective trauma systems. Trauma surgeons should actively collaborate with EMS physicians in the development and review of EMS trauma protocols. As a part of a robust performance improvement program, each trauma system should review prehospital care provided to patients transported within the system. Feedback and focused education should be provided to the transporting EMS agencies. Similarly, trauma performance improvement committees should invite representatives from EMS services to participate in their meetings. Audit filter examples for prehospital trauma care evaluation are listed in Box 26.2 [6].

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Box 26.2    Audit filters for prehospital trauma care

•  Lack of adequate airway •  Misplaced endotracheal tube •  Hypoxia (SpO2 < 90%) upon patient arrival •  Inability to control external hemorrhage (e.g., no tourniquet applied to an extremity) •  Spinal immobilization performed for penetrating torso trauma •  Scene time >10 minutes for critical patient •  Appropriateness of needle decompression of pleural cavity •  Failure to transport a critically injured patient to the closest appropriate facility Source: From ref. [6].

Data collection Data collection is an essential component of the trauma system. All trauma centers are required to maintain trauma registries, containing key information regarding the trauma patients managed at their facilities. Data from these institutional trauma centers are pooled on a system level, either regionally or statewide. Many centers voluntarily submit data to the National Trauma Data Bank (NTDB). In some trauma systems, all hospitals, including nontrauma centers, are required to provide information about the injured patients for whom they care, as not all injured patients require management at trauma centers. Systems can evaluate under‐triage of trauma patients, which occurs when patients requiring trauma center capabilities are transported to hospitals that are not trauma centers. The ACS‐ COT believes a highly functioning trauma system has an under‐ triage rate of 5% or lower, and sets the acceptable over‐triage rate at between 25% and 35% [4]. A strong performance improvement effort requires a strong data collection system. Robust data collection allows a trauma center or system to identify opportunities for process change to result in improved care. In fact, progressive trauma systems have adopted a public health model of three core phases: assessment, policy development, and assurance. The assessment phase consists of data collection followed by data analysis. Once problems are identified, solutions are proposed and implemented in the policy development phase. In the assurance phase, additional data are collected to confirm that the implemented intervention is producing the desired effect (e.g., lowering complications). These three phases create a never‐ending loop of performance improvement wherein the trauma center or system continually strives to provide better and better care. Research is an important use of trauma registry data, providing a rich repository of data for retrospective studies comparing different management options and their respective outcomes. Linkages between EMS records and hospital or system trauma registries allow for analysis of the relationship between EMS and trauma system. Efforts to link the National

EMS Information System with the NTDB will permit robust analysis of prehospital intervention and system design effect on trauma outcomes.

Emergency management Emergency management focuses on the care of citizens affected by disaster. Modern emergency management systems use an all‐hazards approach rather than developing responses depending upon the disaster type. Because most disasters result in injury, close cooperation and interaction between emergency management and trauma programs is required. Internal trauma center strategies to open extra beds create disaster surge capacity. Planning is essential for successful disaster response. Along with emergency management colleagues, trauma program leaders should periodically test trauma center readiness by conducting disaster drills. Drills should ideally be held on different days and shifts to ensure all members are properly prepared. Similarly, trauma systems and corresponding emergency management agencies should evaluate system preparedness through drills that include numerous simulated patients, multiple EMS and first responder agencies, regional emergency management personnel, and multiple facilities. Drills can uncover potential system weaknesses while emphasizing the need for system coordination and communication.

Injury prevention Injury prevention represents an aspect of integration between the public health model and the trauma system. In this model, trauma is viewed as a disease, and efforts are focused on prevention. Trauma registry data, either from trauma centers or systems, illuminate common causes of injury (e.g., motor vehicle crashes or falls) and at‐risk groups (e.g., children or the elderly). Interventions to prevent or ameliorate injury are conceived and implemented. Further analysis monitors the effect of prevention strategies. In some EMS systems, EMS professionals routinely participate in injury prevention activities, such as distribution of car seats and educating parents on their use, or providing evaluations of homes of the elderly looking for conditions that may lead to falls, such as throw rugs or lack of antislips mat in bathtubs.

Summary Trauma is a leading cause of death for individuals aged 1 to 44 years. Significant overlap exists between trauma and EMS systems, community public health, and emergency management. Although each have different objectives, the synergy between systems of care leads to great strides toward achieving optimal care of injured patients on a regional basis.

Trauma systems of care

References 1 Ciesla DJ, Pracht EE, Leitz PT, Spain DA, Staudenmayer KL, Tepas JJ 3rd. The trauma ecosystem: the impact and economics of new trauma centers on a mature statewide trauma system. J Trauma Acute Care Surg. 2017; 82:1014–22. 2 Dijkink S, Nederpelt CJ, Krijnen P, Velmahos GC, Schipper IB. Trauma systems around the world: a systematic overview. J Trauma Acute Care Surg. 2017; 83:917–25. 3 West JG, Williams MJ, Trunkey DD, Wolferth CC. Trauma systems: current status–future challenges. JAMA. 1988; 259:3597‐–600.

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4 American College of Surgeons Committee on Trauma. Resources for Optimal Care of the Injured Patient 2014, 6th ed. Chicago: American College of Surgeons, 2014. 5 Sasser SM, Hunt RC, Faul M, et  al. Guidelines for field triage of injured patients: recommendations of the national expert panel on field triage, 2011. MMWR. 2012; 61:1–20. 6 Salomone JP, Salomone JA. Prehospital care. In: Mattox KL, Moore EE, Feliciano DV, editors. Trauma. 7th ed. New York: McGraw‐Hill, 2013.

CHAPTER 27

Blunt trauma considerations Sabina A. Braithwaite and Noah Bernhardson

Introduction Trauma is a disease whose severity is largely dictated by time and energy kinematics: time to definitive care, including operative intervention when required in a minority of cases, and energy mechanically transferred to the body to produce injury. Appropriate integration of out‐of‐hospital and in‐hospital management of trauma can significantly decrease overall morbidity and mortality. Studies continue to clarify which out‐ of‐hospital interventions truly benefit the patient and which interventions may worsen outcomes or delay more effective care options. Specifics on how mechanisms of injury, injury severity, available resources, clinician training level, method and timing of transport, and choice of specialty center destination affect management and outcome of trauma patients have become clearer in recent years. Controversy exists regarding how to best balance the need for expeditious patient transfer from the out‐ of‐hospital environment to in‐hospital definitive care with the patient’s need for critical or time‐sensitive interventions prior to hospital arrival. A growing body of evidence is further refining what interventions and parameters improve outcomes in specific subpopulations of trauma patients. In short, trauma is a multifaceted disease that requires application of new scientific knowledge to the individual patient’s care within a systems‐ thinking context to provide optimal patient management in the practice of EMS medicine.

Effect on EMS Proper assessment and management of blunt traumatic injuries are among the core skills for EMS physicians, paramedics, and EMTs. The physical demands and adverse environments encountered by EMS clinicians while managing the trauma patient can be considerable stressors. Even in these difficult circumstances, the ability to adapt the core trauma evaluation and management concepts to any patient situation is paramount.

EMS system structure elements, including public safety answering point (PSAP) capabilities with advanced automatic crash notification (AACN) integration, response unit tracking, automatic dispatching, ALS versus BLS, staffing level, air medical resources, and regional integration with hospitals all contribute to a system’s ability to improve outcomes for the trauma patient. Scientific comparison of different operational models is just beginning to demonstrate which may provide the greatest benefit to specific patient populations [1]. Long‐held beliefs in the importance of ALS interventions in the field (such as IV access for fluid resuscitation and endotracheal intubation) have been called into question  [2]. It may be that severely injured patients in areas with prompt access to designated trauma centers are best served by primary application of the basic skills of hemorrhage control, airway support, and rapid transport to the appropriate level trauma center.

Training for EMS clinicians The central concepts for EMS clinicians caring for trauma patients include: 1.  A foundation of thorough training on a consistent, organized patient assessment algorithm that can be applied to any trauma patient, regardless of injury severity. The algorithm should provide a hierarchical approach that focuses on identification and management of life threats, through properly sequenced evaluation and integrated management options for actual and potential injuries. Frequent reassessments and ability to integrate new information and recognize trends that require urgent intervention are essential. 2.  Efficient, appropriate use of local resources (e.g., air transport, hazardous materials, specialized rescue) and knowledge of hospital capabilities and destination policies (e.g., trauma center, pediatric trauma center, specialty burn care center). These can improve patient outcomes in patients with significant, time‐critical injuries. EMS systems should have

Emergency Medical Services: Clinical Practice and Systems Oversight, Third Edition. Volume 1: Clinical Aspects of EMS. Edited by David C. Cone, Jane H. Brice, Theodore R. Delbridge, and J. Brent Myers. © 2021 NAEMSP. Published 2021 by John Wiley & Sons, Inc.

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policies and procedures to identify such patients and promote primary transport to the most appropriate facility. The regionalization of care concept pioneered by trauma systems has shown that getting the right patient to the right place at the right time can improve outcomes  [3–5]. This model is now being imitated effectively in nontrauma disease processes and patient populations such as acute myocardial infarction and stroke (see Chapter 72, Emergency Care Regionalization) [6–8]. 3.  Correct application of spinal motion restriction, splinting, fluid resuscitation, and pain management to limit additional morbidity. 4.  Knowing how and when to properly use high‐risk low‐frequency invasive procedures such as cricothyrotomy or needle/ finger thoracostomy. This is essential for patient safety and care (Chapter 40, Trauma Stabilizing Procedures). 5.  Emphasis on universal precautions against blood and body fluid exposure and scene safety training with every patient interaction. The added potential hazards at traumatic injury scenes, such as traffic hazards, power lines, heavy machinery, and unsafe structures may pose a serious ongoing threat to rescuers. 6.  Limiting scene time to under 10  minutes for critical or unstable trauma patients and “rapid transport to the highest level of care.” This is encouraged in the National Model EMS Clinical Guidelines  [9]. Prolonged out‐of‐hospital time is associated with worse outcomes in critically ill patient populations [10, 11]. Monitoring and reinforcing proper application of these core concepts through performance measurement and improvement (Chapter 113, Defining and Measuring Quality), together with adequate practice on infrequently used psychomotor skills, are important parts of medical oversight and can affect patient morbidity and mortality. Realistic, relevant, integrated assessment and management scenario‐based training, potentially including high‐fidelity simulation, has been demonstrated to improve skill consistency and retention and may improve the ability of clinicians to translate didactics into clinical performance [12].

Resuscitation and initial assessment From 2015 to 2018, motor vehicle collisions were the fourth leading cause of unintentional nonfatal injury and the third leading cause of unintentional fatal injury in adults in the United States [13]. As a result, expertise in rapid and safe extrication of patients from motor vehicles of all types is critical. Even while still entrapped, it is essential that patient assessment and management be initiated for critical patients to ensure that life threats are addressed promptly and that adequate oxygenation, prevention of hypotension, and management of pain remain as focal points throughout their care. Extrication‐related issues that may affect management and timeliness of transport are addressed in Chapter 28, Motor Vehicle Crashes.

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The mechanism of injury, while not entirely predictive of actual injury sustained, can suggest potential for specific injuries that may be encountered during the assessment and management of the blunt trauma patient in the field. The importance of integration of local EMS and hospital resources, and tailoring guidelines to optimize patient care within these parameters, cannot be overemphasized. Blunt trauma management differs significantly from that for penetrating trauma, which is addressed in Chapter 29, Penetrating Trauma. Except for control of life‐threatening hemorrhage and support of airway and oxygenation/ventilation, all other interventions should take place en route to definitive care, and limiting scene time to 10  minutes or less should be the goal for critical or unstable patients. The primary survey The goal of the primary survey is to identify and address any immediate life threats while the critical patient is promptly packaged for transport to an appropriate trauma center. With increased availability of vehicle telemetry and traffic camera data in PSAPs, assessment and anticipation of needs based on patient mechanism of injury, potential notification of additional needed resources, and other local considerations can begin even before first responder arrival on the scene. AACN will increasingly integrate with EMS to provide objective prearrival information in motor vehicle collisions, potentially tailoring data‐driven resource allocation based on actual mechanism and patient information [14]. Vehicle telemetry can be used to predict injury severity based on multiple data points, including change in velocity, number of impacts, rollover, seatbelt usage, type of vehicle, and direction of force. With the advent of AACN, communication between the PSAP and the telemetric service provider center allows the PSAP to directly view current vehicle data and, in some cases, to directly view video from in‐vehicle or responder cameras [15]. Scene photography may also help convey aspects of mechanism of injury to the receiving physician as long as patient confidentiality is respected  [16]. Telemedicine applications are being further developed that allow concurrent assessment by EMS and receiving emergency physicians; these may facilitate triage and expedite care at the receiving facility for a number of time‐sensitive medical complaints, including trauma. Once patient contact is safely made, attention to discovering life threats through an organized approach is essential. Attention to arterial or exsanguinating hemorrhage control, establishing or maintaining airway patency, correcting oxygenation or ventilation failure, and avoiding or managing shock from blunt trauma are key aspects of the primary survey. In the severely injured patient with possible survival, the only survey to be done on‐scene is the primary survey. It has been shown that increased scene time and increased field procedures are associated with greater mortality in both penetrating and blunt trauma mechanisms. A recent study of blunt and penetrating trauma patients directly transported by ground

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to Level I or Level II trauma centers demonstrated that only 35.3% of patient encounters met the goal of 10 minutes or less, but did not provide specific subanalysis of critical or unstable patient groups [17]. The secondary survey The secondary survey, like the primary survey, is conducted using an organized, consistent approach. It differs substantially from the primary survey in its detail. The secondary survey is a methodical head‐to‐toe assessment exam designed to identify injuries that are not immediate life threats that may be obscured by visually distracting injury or primary survey life threat discovery. While important for all trauma patients, when emergent management priorities are identified in the primary survey and require frequent reassessment, the secondary survey may not be performed until after arrival at the destination trauma center for some critical patients. Omission of the secondary survey for this reason is not incorrect and may represent a conscious prioritization by an astute EMS clinician to focus on immediate life threats identified in the primary survey. The role of basic life support, advanced life support, and prehospital critical care assets Scientific debate continues over the value of out‐of‐hospital ALS in general, and for trauma care interventions including endotracheal intubation and crystalloid fluid resuscitation specifically  [18, 19]. Selection bias and significant variability in system elements and capabilities preclude a definite answer from existing literature at this time. Some evidence‐based EMS practice recommendations have been extrapolated from the in‐hospital literature, and their ability to translate into patient benefit in the out‐of‐hospital environment has yet to be demonstrated. Absent evidence to the contrary, EMS has applied what are thought to be time‐sensitive interventions that have demonstrated efficacy in the emergency department and other critical care environments. However, a large‐scale before‐and‐ after study of ALS has cast significant doubt on the use of ALS in trauma  [2]. An evaluation of the difference between ALS and BLS care on the outcomes of blunt trauma patients demonstrated that there is no evidence of mortality benefit with ALS versus BLS prehospital care [20]. While there are more recent papers on the effect of ALS in penetrating trauma, research in the setting of blunt trauma is sparse.

Constellations of blunt traumatic injury There are a number of recognized patterns of blunt trauma injury. For example, displaced sternal fractures are associated with a high risk of associated head, spinal, rib, and cardiac injury [21]. The likelihood of intra‐abdominal injury to motor vehicle occupants increases significantly at speeds greater than 12 mph and exceeds 5% at 20 mph. Extensive abdominal injury evaluation due to mechanism of injury alone appears

unwarranted in the absence of associated head, spine, chest, or leg injury [22]. Scapular fractures are commonly associated with rib and lower and upper extremity injury resulting from the high kinetic energy transfer, but not with blunt traumatic aortic injury  [23]. Facial fractures due to assault and motor vehicle crashes are associated with intracerebral and pulmonary injuries, with a high percentage of these patients requiring intubation during their inpatient courses  [24]. Obesity (body mass index > 30  kg/m2) is associated with a risk for longer hospital and intensive care length of stay and higher mortality in critical blunt trauma patients. Interestingly, head injuries are decreased in this population  [25]. Specific recommendations on management of traumatic brain injury and spine injuries are addressed in Chapters 30 and 36, respectively.

Issues in specific patient populations Blunt trauma in pregnancy Trauma is a leading cause for maternal mortality [26]. Pregnant trauma patients should be managed with the maxim “what’s best for mom is best for baby.” Supporting maternal oxygenation and perfusion is most likely to produce a positive outcome for both patients whenever possible. Blunt abdominal trauma is the leading form of injury in the pregnant patient. One retrospective study found that most pregnant blunt trauma patients were in the third trimester, with the majority due to motor vehicle collisions, followed by falls as the second most common etiology [27]. The majority of fetal deaths are due to motor vehicle collisions, with abruptio placentae and abdominal penetrating trauma as other common causes [28]. A study of hospitalized pregnant trauma patients, 80% of whom were involved in motor vehicle collisions, showed that predictors for fetal loss included higher injury severity score, maternal death, lower Glasgow Coma Scale score, abdominal abbreviated injury scale score greater than 3, vaginal bleeding, and shock with significant base excess. Morbidity, mortality, and hospital length of stay were not significantly different in pregnant versus nonpregnant matched case controls [29]. One small study showed the overall immediate complication rate to be low, most commonly preterm labor and placental abruption  [30]. However, an increase in long‐term complications was noted as well, with more severe trauma, multiple gestation, vaginal bleeding, and uterine contractions all being independent risk factors. Recent guidance from the obstetric literature emphasizes an algorithmic approach to these patients at all care levels, including the prehospital setting, in order to ensure optimal outcomes [27]. Destination choice may be affected by potential fetal viability and immediate need for neonatal specialty care. Estimating potential viability at greater than 24 to 26 weeks gestation by history or palpation of the uterine fundus above the umbilicus can facilitate this decision‐making process [29]. Patients at greater than 20 weeks estimated gestational age should be placed with

Blunt trauma considerations

the left side elevated 15 degrees, or up to 30 degrees of reverse Trendelenburg positioning, to relieve pressure on the great vessels, preventing supine hypotension and subsequent significant loss of preload and cardiac output [31]. Although normal pregnancy‐related changes in vital signs can imitate early shock, proactive oxygenation, fluid resuscitation, and monitoring are indicated to minimize risk of uterine hypoperfusion and fetal distress. Emergent Caesarian sections are extremely rare and should be reserved for salvageable infants in select situations, performed by adequate, trained staff including emergency physicians and obstetricians (Chapter 45, Peri‐Mortem Cesarean Section). Geriatric trauma CDC field triage criteria use age 55 as the break where patient management considerations change in recognition of the increased risk of death from trauma after that age (see Chapter 39 for additional information on field trauma triage). With an ever‐growing geriatric population, awareness of special considerations is important, particularly in trauma [32]. Geriatric patients are more likely to have intra‐abdominal injuries with concurrent head, leg, or chest injuries, regardless of motor vehicle collision speed. Falls, even from heights less than 3 feet, are a frequent cause of blunt trauma in the geriatric population [33]. Associated spinal injury risk is significant, complicated by the lack of sensitivity of physical exam criteria such as NEXUS in determining need for spinal motion restriction [34, 35]. In the geriatric population, mechanism of injury is often less severe, and geriatric blunt trauma has a higher incidence of occult injury. Furthermore, age‐related changes in geriatric physiology and medication use can further complicate patient assessment and lull clinicians into a false sense of security [36, 37]. Multiple measures of injury severity in elderly patients such as the Glasgow Coma Scale have been shown to be unreliable in predicting severe injury  [38]. Additional specific physiological changes and considerations for the geriatric patient are addressed in Chapter  57. Because of these considerations, under‐triage of geriatric trauma patients is significant, and more conservative triage algorithms  [39–41] have been advocated to limit morbidity and mortality in this population and assure prompt management at trauma centers rather than delayed secondary transfer  [42]. Geriatric trauma patients are not addressed as a unique population in the current National Model EMS Clinical Guidelines, but based on the current evidence, a more conservative approach to blunt trauma and potential spinal injury in this population is warranted. Pediatric trauma Blunt trauma in children has been noted to have some specific and unique injury patterns due to the anatomic differences in head circumference, airway size, cervical spine, etc. There are specific injury patterns unique to this age group that are well defined in the medical literature such as Waddell’s Triad,

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handlebar injury, and nonaccidental trauma  [43–45]. Specific recommendations on pediatric trauma and injury patterns are addressed in Chapter 55.

Medical oversight issues in trauma Among the most important aspects of medical oversight is teaching the ability to effect a prompt and smooth patient transition from scene to hospital. Guidelines for management should be evidence‐based whenever possible and should take into consideration neighboring regions, hospital practice, and other regional specialty resources. Physician participation in regional and state medical oversight committees helps add clinical practice consistency while taking into consideration specific agency and clinician capabilities, which may vary significantly within a locality. Monitoring of current literature and research allows the medical director to modify guidelines in keeping with national trends as tempered by local capabilities. Networking with specialty physicians helps assure that EMS is aligned with inpatient care, using complementary technology and practice that will facilitate and expedite optimal patient outcomes both in and out of hospital. Such networking will help limit “us‐versus‐them” attitudes toward EMS and reinforce that EMS is an equal and essential professional partner in the emergency health care team, dedicated to the same basic principles as the inpatient team. In the case of trauma care, having specific, agreed‐upon regional hospital triage criteria and guidelines on issues such as airway management, fluid resuscitation, medication management, spinal motion restriction, and trauma alert categories all facilitate uniformity of in‐hospital and out‐of‐hospital care. Ongoing monitoring of performance on established criteria, such as scene time in high‐priority trauma [46], and informed modification of practice, can positively affect patient outcomes [47].

Guidelines for out‐of‐hospital management Guidelines for management of the trauma patient should be focused on providing necessary interventions, together with rapid transport to the closest appropriate facility. Triage guidelines should also direct trauma patients requiring specific specialty care to regional facilities with special capabilities such as pediatric trauma, burn care, hyperbaric therapy, and extremity replantation. Protocols and guidelines should incorporate these considerations so patients are directed to the most appropriate facilities from the scene. Air medical transport Transport of trauma patients by helicopter has become increasingly common in the United States in recent years. Its positive effect on saving the lives of combat casualties is well documented, though its effect on outcomes in specific civilian patient

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populations is still being studied. Staffing models vary significantly between the U.S., European, and Australian systems. As a result, utilization rates, patient selection and injury severity, and effect on‐scene time and mortality are difficult to compare between these models [48]. There is significant concern that air medical transport may not uniformly provide added patient benefit for a number of reasons, including poor triage by field clinicians  [49]. Studies have demonstrated an up to 85% over‐triage rate with an early discharge rate of 35%  [50]. Systems should implement guidelines to appropriately integrate valuable air medical assets into their trauma systems, particularly given the cost and potential additional risks to both crew and patient  [51, 52]. A study of cost efficacy of helicopter EMS relative to ground EMS demonstrated that a minimum of a 15% relative risk reduction in mortality or disability is necessary for cost‐effectiveness. Statewide field triage criteria on helicopter EMS use which increase acuity of patients transported by helicopter have been demonstrated to reduce over‐triage and improve overall trauma patient outcomes while decreasing helicopter utilization. Additionally it has been shown that when an appropriate trauma center is within 15‐45  minutes, rapid ground EMS transport bypassing non‐trauma centers and going directly to the appropriate trauma center decreases mortality rate in hemodynamically unstable patients compared to those transported via helicopter [53–55]. Hospital destination Patient outcomes are significantly better at trauma centers than at non‐trauma centers. Both in‐hospital and 1‐year adjusted case fatality and relative death risk rates for moderately to severely injured patients reflect a 25% reduction in fatality risk  [56]. Studies support the importance of rapid transport to a regional trauma center where definitive care can be rendered [57]. With the exception of safety issues, inability to secure an unstable airway, and extrication issues, there is generally no indication for prolonging scene times, particularly in the severely traumatized patient. It is crucial that the out‐of‐hospital clinician rapidly and accurately identify the subset of trauma patients who may most benefit from trauma center management. The field triage decision scheme is fully described in Chapter  39. The most current version has shown efficacy, and de‐emphasizes trauma scoring, relying instead on progressive assessment of patient physiology, injury anatomy, mechanism, and special circumstances to provide trauma center destination guidance. Clinician judgment has been introduced as a factor in decision‐making for transport to regional trauma centers in the field triage decision scheme. Trauma scores and mechanism of injury should not override clinician judgment and divert a patient away from a trauma center [58]. Intriguing new research raises questions on structure of hospital trauma systems. Inclusive systems, in which each facility in a region or state participates to the extent of it capabilities, are compared with exclusive systems, in which a limited number of high‐level centers receive the majority of patients.

In one study, the odds of triage to a regional trauma center and inpatient mortality were similar in both groups; however, the most inclusive systems were associated with the lowest odds of death [59]. As trauma and specialty centers deal with more issues with overcrowding, transportation directly to an appropriate facility will become increasingly important. Use of central communications with real‐time hospital capacity data can significantly reduce mortality and costs to the health care system by reducing secondary transfer [60]. Trauma scoring Trauma scoring systems were first developed to attempt to quantify severity of injury and guide appropriate triage of patients to trauma centers. A variety of scoring systems exist, but their use is likely greater for research purposes than for patient care in the field [61]. Multiple different scoring systems and permutations have been developed and continue to evolve to assist in predicting injury, need for emergent surgery, and outcomes [62, 63]. The Revised Trauma Score (RTS) is one of the more common trauma scoring systems (Table 27.1). It combines the Glasgow Coma Scale score with respiratory rate and systolic blood pressure. Some systems, including the RTS and the Injury Severity Score, as well as derivations such as the survival risk ratio, have been used to predict patient outcome [64–67]. Prognostic studies have demonstrated that vital signs alone are poor predictors of trauma outcomes. Other indicators such as shock index (heart rate divided by systolic blood pressure), adjusted shock index (shock index times age), and pulse max index (heart rate divided by maximum heart rate) are better predictors of 48‐hour mortality  [68, 69]. Each trauma system must determine acceptable levels of over‐triage and under‐triage and how to best achieve these goals through ongoing quality improvement and surveillance.

Prevention and other public health issues Trauma is largely a preventable disease with a tremendous cost to society. Although it affects all age groups, it is particularly devastating to the young and remains the major killer of Table 27.1  Revised Trauma Score RR/min

SBP (mmHg)

GCS

RTS points

10–29 >29 6–9 1–5 0

>89 76–89 50–75 1–49 0

13–15 9–12 6–8 4–5 3

4 3 2 1 0

GCS = Glasgow Coma Scale; RR = respiratory rate; SBP = systolic blood pressure. Source: Adapted from Champion HR, Sacco WJ, Copes WS, Gann DS, Gennarelli TA, Flanagan ME. A revision of the Trauma Score. J Trauma. 1989; 29:623–9, with permission from Lippincott, Williams and Wilkins.

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North Americans under 40 years of age. As part of their role as advocates for their entire community’s health status, EMS physicians and systems must play an active role in injury prevention. Participation in community‐based programs to encourage safer behaviors and risk reduction can reduce the number of injured persons. Programs such as helmet use [70], cycle and pool safety, proper use of car seats, and use of seat belts have all helped to reduce the number and severity of injuries [71–73]. Programs targeting lay management of exsanguinating hemorrhage, active shooter drills, safe storage of firearms, reduction in drunk driving, and home safety assessments for elders can have positive effects on the community and may be led at the local, state, or national level. Local EMS systems or community partnerships may link to these resources without having to commit large amounts of financial or personnel support. This also represents an opportunity to put forward a proactive, positive “public face” for the EMS agency involved. The leadership for this effort must involve EMS physician medical oversight. The Centers for Disease Control’s Injury and Violence Prevention and Control page (www.cdc.gov/injury) is an excellent resource. See also Chapter 93, EMS–Public Health Interface Prevention, for additional information.

References 1 Iirola TT, Laaksonen MI, Vahlberg TJ, Palve HK. Effect of physician‐ staffed helicopter emergency medical service on blunt trauma patient survival and prehospital care. Eur J Emerg Med. 2006; 13:335–9. 2 Stiell IG, Nesbitt LP, Pickett W, et  al. The OPALS major trauma study: impact of advanced life‐support on survival and morbidity. CMAJ. 2008; 178:1141–52. 3 Middleton JM, Sharwood LN, Cameron P, et  al. Right care, right time, right place: improving outcomes for people with spinal cord injury through early access to intervention and improved access to specialised care: study protocol. BMC Health Serv Res. 2014; 14:600. 4 Boyd DR. A symposium on the Illinois trauma program: a systems approach to the care of the critically injured. J Trauma. 1973; 13:275–6. 5 Hick JL. Right care, right place, right time. Regional systems of care are the best way to ensure patients with emergent conditions have the best outcomes. Minnesota Med. 2015; 98:32–3. 6 Lorch SA, Millman AM, Zhang X, Even‐Shoshan O, Silber JH. Impact of admission‐day crowding on the length of stay of pediatric hospitalizations. Pediatrics. 2008; 121:e718–30. 7 Jollis JG, Al‐Khalidi HR, Roettig ML, et al. Impact of regionalization of ST‐segment‐elevation myocardial infarction care on treatment times and outcomes for emergency medical services‐transported patients presenting to hospitals with percutaneous coronary intervention: Mission: Lifeline Accelerator‐2. Circulation. 2018; 137:376–87. 8 Kahn JM, Branas CC, Schwab CW, Asch DA. Regionalization of medical critical care: what can we learn from the trauma experience? Crit Care Med. 2008; 36:3085–8. 9 National Association of State EMS Officials. National Model EMS Clinical Guidelines, version 2.2. 2019. Available at: https://nasemso. org/projects/model‐ems‐clinical‐guidelines/. Accessed September 23, 2020.

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10 Sampalis JS, Denis R, Lavoie A, et al. Trauma care regionalization: A process‐outcome evaluation. J Trauma. 1999; 46:565–81. 11 Brown JB, Rosengart MR, Forsythe RM, et al. Not all prehospital time is equal: Influence of scene time on mortality. J Trauma Acute Care Surg. 2016; 81:93–100. 12 Holcomb JB, Dumire RD, Crommett JW, et al. Evaluation of trauma team performance using an advanced human patient simulator for resuscitation training. J Trauma. 2002; 52:1078–86. 13 US Centers for Disease Control and Prevention. Web‐based Injury Statistics Query and Reporting System (WISQARS). Available at: https://www.cdc.gov/injury/wisqars/index.html. Accessed September 23, 2020. 14 Matsumoto H, Mashiko K, Hara Y, et  al. Dispatch of helicopter emergency medical services via advanced automatic collision notification. J Emerg Med. 2016; 50:437–43. 15 Transportation Safety Advancement Group. Advanced Collision Notification White Paper. 2019. Availble at: http://www.tsag‐its. org/wp‐content/uploads/2019/05/AACN‐Whitepaper‐Final.pdf. Accessed September 23, 2020. 16 Bennett TD, Kaufman R, Schiff M, Mock C, Quan L. Crash analysis of lower extremity injuries in children restrained in forward‐facing car seats during front and rear impacts. J Trauma. 2006; 61:592–7. 17 Ruelas OS, Tschautscher CF, Lohse CM, Sztajnkrycer MD. Analysis of prehospital scene times and interventions on mortality outcomes in a national cohort of penetrating and blunt trauma patients. Prehosp Emerg Care. 2018; 22:691–7. 18 Davis DP, Koprowicz KM, Newgard CD, et  al. The relationship between out‐of‐hospital airway management and outcome among trauma patients with Glasgow Coma Scale Scores of 8 or less. Prehosp Emerg Care. 2011; 15:184–92. 19 Kasotakis G, Sideris A, Yang Y, de Moya M, Alam H, King DR, et al. Aggressive early crystalloid resuscitation adversely affects outcomes in adult blunt trauma patients: an analysis of the Glue Grant database. J Trauma Acute Care Surg. 2013; 74:1215–21; discussion 1221–1222. 20 Jayaraman S, Sethi D, Wong R. Advanced training in trauma life support for ambulance crews. Cochrane Database Syst Rev. 2014; 2014:Cd003109. 21 von Garrel T, Ince A, Junge A, Schnabel M, Bahrs C. The sternal fracture: radiographic analysis of 200 fractures with special reference to concomitant injuries. J Trauma. 2004; 57:837–44. 22 Brasel KJ, Nirula R. What mechanism justifies abdominal evaluation in motor vehicle crashes? J Trauma. 2005; 59:1057–61. 23 Brown CV, Velmahos G, Wang D, Kennedy S, Demetriades D, Rhee P. Association of scapular fractures and blunt thoracic aortic injury: fact or fiction? American Surgeon. 2005; 71:54–57. 24 Alvi A, Doherty T, Lewen G. Facial fractures and concomitant injuries in trauma patients. Laryngoscope. 2003; 113:102–6. 25 Brown CVR, Neville AL, Rhee P, Salim A, Velmahos GC, Demetriades D. The impact of obesity on the outcomes of 1,153 critically injured blunt trauma patients. J Trauma. 2005; 59:1048–51. 26 Romero VC, Pearlman M. Maternal mortality due to trauma. Sem Perinatology. 2012; 36:60–67. 27 Greco PS, Day LJ, Pearlman MD. Guidance for evaluation and management of blunt abdominal trauma in pregnancy. Obstet Gynecol. 2019; 134:1343–57. 28 Mattox KL, Goetzl L. Trauma in pregnancy.[see comment]. Crit Care Med. 2005; 33:S385–9.

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29 Shah KH, Simons RK, Holbrook T, Fortlage D, Winchell RJ, Hoyt DB. Trauma in pregnancy: maternal and fetal outcomes. J Trauma. 1998; 45:83–86. 30 Melamed N, Aviram A, Silver M, et al. Pregnancy course and outcome following blunt trauma. J Maternal‐Fetal & Neonatal Med. 2012; 25:1612–7. 31 Cusick SS, Tibbles CD. Trauma in pregnancy. Emerg Med Clin NA. 2007; 25:861–72. 32 Mitra B, Cameron PA. Optimising management of the elderly trauma patient. Injury. 2012; 43:973–5. 33 Jawa RS, Singer AJ, Rutigliano DN, et al. Spinal fractures in older adult patients admitted after low‐level falls: 10‐year incidence and outcomes. J Am Geriatr Soc. 2017; 65:909–15. 34 Paykin G, O’Reilly G, Ackland HM, Mitra B. The NEXUS criteria are insufficient to exclude cervical spine fractures in older blunt trauma patients. Injury. 2017; 48:1020–4. 35 Tran J, Jeanmonod D, Agresti D, Hamden K, Jeanmonod RK. Prospective validation of modified NEXUS cervical spine injury criteria in low‐risk elderly fall patients. West J Emerg Med. 2016; 17:252–7. 36 Oyetunji TA, Chang DC, Crompton JG, et al. Redefining hypotension in the elderly: normotension is not reassuring. Arch Surg. 2011; 146:865–9. 37 Brown JB, Gestring ML, Forsythe RM, et al. Systolic blood pressure criteria in the National Trauma Triage Protocol for geriatric trauma: 110 is the new 90. J Trauma Acute Care Surg. 2015; 78:352–9. 38 Kehoe A, Rennie S, Smith JE. Glasgow Coma Scale is unreliable for the prediction of severe head injury in elderly trauma patients. Emerg Med J. 2015; 32:613–5. 39 Ichwan B, Darbha S, Shah MN, et al. Geriatric‐specific triage criteria are more sensitive than standard adult criteria in identifying need for trauma center care in injured older adults. Ann Emerg Med. 2015; 65:92–100.e3. 40 Nishijima DK, Gaona SD, Waechter T, et al. Out‐of‐hospital triage of older adults with head injury: a retrospective study of the effect of adding "anticoagulation or antiplatelet medication use" as a criterion. Ann Emerg Med. 2017; 70:127–38e6. 41 Wasserman EB, Shah MN, Jones CM, et al. Identification of a neurologic scale that optimizes EMS detection of older adult traumatic brain injury patients who require transport to a trauma center. Prehosp Emerg Care. 2015; 19:202–2. 42 Caterino JM, Brown NV, Hamilton MW, et al. Effect of geriatric‐specific trauma triage criteria on outcomes in injured older adults: a statewide retrospective cohort study. J Am Geriatr Soc. 2016; 64:1944–51. 43 Mikrogianakis A, Grant V. The kids are alright: pediatric trauma pearls. Emerg Med Clin North Am. 2018; 36:237–57. 44 Sarioglu FC, Sahin H, Pekcevik Y, Sarioglu O, Oztekin O. Pediatric head trauma: an extensive review on imaging requisites and unique imaging findings. Eur J Trauma Emerg Surg. 2018; 44:351–68. 45 Christian CW, American Academy of Pediatrics Committee on Child Abuse and Neglect. The evaluation of suspected child physical abuse. Pediatrics. 2015; 135:e1337–54. 46 Eckstein M, Alo K. The effect of a quality improvement program on paramedic on‐scene times for patients with penetrating trauma. Acad Emerg Med. 1999; 6:191–5. 47 Gage AM, Traven N, Rivara FP, Jurkovich GJ, Arbabi S. Compliance with Centers for Disease Control and Prevention field triage guidelines in an established trauma system. J Amer Coll Surg. 2012; 215:148–54; discussion 154–6.

48 Ringburg AN, Spanjersberg WR, Frankema SP, Steyerberg EW, Patka P, Schipper IB. Helicopter emergency medical services (HEMS): impact on on‐scene times. J Trauma. 2007; 63:258–62. 49 Bledsoe BE, Wesley AK, Eckstein M, Dunn TM, O’Keefe MF. Helicopter scene transport of trauma patients with nonlife‐threatening injuries: a meta‐analysis. J Trauma. 2006; 60:1257–66. 50 Miyagi H, Evans DC, Werman HA. Are there field triage criteria that can predict low‐yield air medical transports? Prehosp Disaster Med. 2019; 34:596–603. 51 Thomson DP, Thomas SH. Guidelines for air medical dispatch. Prehosp Emerg Care. 2003; 7:265. 52 Floccare DJ, Stuhlmiller DFE, Braithwaite SA, et  al. Appropriate and safe utilization of helicopter emergency medical services: a joint position statement with resource document. Prehosp Emerg Care. 2013; 17:521–5. 53 Delgado MK, Staudenmayer KL, Wang NE, et  al. Cost‐effectiveness of helicopter versus ground emergency medical services for trauma scene transport in the United States. Ann Emerg Med. 2013; 62:351–64. 54 Hirshon JM, Galvagno SM Jr., Comer A, et  al. Maryland’s helicopter emergency medical services experience from 2001 to 2011: system improvements and patients’ outcomes. Ann Emerg Med. 2016; 67:332–40. 55 Taylor BN, Rasnake N, McNutt K, McKnight CL, Daley BJ. Rapid ground transport of trauma patients: a  moderate distance from trauma center improves survival. J Surg Res. 2018; 232:318–24. 56 MacKenzie EJ, Rivara FP, Jurkovich GJ, et al. A national evaluation of the effect of trauma‐center care on mortality. New Eng J Med. 2006; 354:366–78. 57 Driscoll P, Kent A. The effect of scene time on survival. Trauma. 1999;1:23–30. 58 Newgard CD, Kampp M, Nelson M, et  al. Deciphering the use and predictive value of "emergency medical services provider judgment" in out‐of‐hospital trauma triage: a multisite, mixed methods assessment. J Trauma. 2012; 72:1239–48. 59 Utter GH, Maier RV, Rivara FP, Mock CN, Jurkovich GJ, Nathens AB. Inclusive trauma systems: do they improve triage or outcomes of the severely injured? J Trauma. 2006; 60:529–35. 60 Martinez B, Owings JT, Hector C, et  al. Association between compliance with triage directions from an organized state trauma system and trauma outcomes. J Am Coll Surg. 2017; 225:508–15. 61 Gabbe BJ, Cameron PA, Finch CF. Is the Revised Trauma Score still useful? ANZ J Surg. 2003; 73:944–8. 62 Moore L, Lavoie A, LeSage N, et  al. Statistical validation of the Revised Trauma Score. J Trauma. 2006; 60:305–11. 63 Moore L, Lavoie A, Abdous B, et  al. Unification of the Revised Trauma Score. J Trauma. 2006; 61:718–22. 64 Millham FH, LaMorte WW. Factors associated with mortality in trauma: re‐evaluation of the TRISS method using the National Trauma Data Bank. J Trauma. 2004; 56:1090–6. 65 Clarke JR, Ragone AV, Greenwald L. Comparisons of survival predictions using survival risk ratios based on International Classification of Diseases, Ninth Revision and Abbreviated Injury Scale trauma diagnosis codes. J Trauma. 2005; 59:563–7. 66 Hannan EL, Farrell LS. Predicting trauma inpatient mortality in an administrative database: an investigation of survival risk ratios using New York data. J Trauma. 2007; 62:964–8.

Blunt trauma considerations

67 Champion HR, Sacco WJ, Copes WS, Gann DS, Gennarelli TA, Flanagan ME. A revision of the Trauma Score. J Trauma. 1989; 29:623–9. 68 Bruijns SR, Guly HR, Bouamra O, Lecky F, Lee WA. The value of traditional vital signs, shock index, and age‐based markers in predicting trauma mortality. J Trauma Acute Care Surg. 2013; 74:1432–7. 69 Kim SY, Hong KJ, Shin SD, et  al. Validation of the Shock Index, Modified Shock Index, and Age Shock Index for predicting mortality of geriatric trauma patients in emergency departments. J Korean Med Sci. 2016; 31:2026–32. 70 Konkin DE, Garraway N, Hameed SM, et  al. Population‐based analysis of severe injuries from nonmotorized wheeled vehicles. Am J Surg. 2006; 191:615–8.

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71 Elkbuli A, Dowd B, Spano PJ 2nd, Hai S, Boneva D, McKenney M. The association between seatbelt use and trauma outcomes: Does body mass index matter? Am J Emerg Med. 2019; 37:1716–9. 72 Soori H, Nasermoadeli A, Ainy E, Hassani SA, Mehmandar MR. Association between mandatory seatbelt laws and road traffic injuries in Iran. Southeast Asian J Trop Med Public Health. 2011; 42:1540–5. 73 Di Saverio S, Gambale G, Coccolini F, et  al. Changes in the outcomes of severe trauma patients from 15‐year experience in a Western European trauma ICU of Emilia Romagna region (1996‐2010). Langenbecks Arch Surg. 2014; 399:109–26.

CHAPTER 28

Motor vehicle crashes Stewart C. Wang, Kristen Cunningham, Sven Holcombe, and Robert Kaufman

Introduction Death by motor vehicle crash (MVC) is currently the third leading cause of death for all Americans [1]. In the U.S. Department of Transportation’s National Highway Traffic Safety Administration’s revised 2014 report, the economic and societal annual costs associated with traffic crashes were $836 billion [2]. Over the past decade (2009‐2018), motor vehicle‐related death and injury rates have only slightly decreased. In 2009, the occupant fatality rate per 100 million vehicle miles of travel was 1.15; and in 2018 it was 1.13. The most significant change during this period is that the proportion of nonoccupant fatalities (pedestrian, pedalcyclists, motorcyclists) has increased from 14% to 20%. Overall, MVCs continually remain a burden to society with nearly 6.5 million crashes occurring in the United States during 2017 that resulted in about 2.7 million injuries and just over 34,000 deaths [3].

Effect on EMS In the United States, someone dies in an MVC every 16 minutes [3]. Moreover, fatal crashes are far outnumbered by crashes with nonfatal but serious injuries requiring urgent medical attention. Therefore, a significant percentage of EMS calls relate to MVCs. While many crashes involve only single vehicles, there may be multiple occupants in that vehicle. In a crash involving more than two vehicles, more EMS resources may be required. Likewise, if public transportation, such as trains or busses, are involved, the need for those resources is greatly expanded. The hazards present at the scene of the MVC are many and varied. Continued high‐speed traffic flow on freeways represents a significant threat to the safety of the rescue crews. Spilled fuel can result in a fire risk, and broken glass and sharp metal edges can also prove hazardous to the unprotected EMS responder. Grounded power lines and hazardous materials being transported on the roadway present additional risk.

EMS physicians and other clinicians may not have the personal protective gear to operate in such environments. Fire department response is often required to address situational hazards. Rural or smaller agencies may not have the heavy extrication equipment necessary to access trapped patients. Regardless of whether the EMS system is fire department–based, additional resources (e.g., rescue, law enforcement) are often needed at the scene of MVCs.

MVC injury biomechanics During a crash, different parts of an occupant’s body are subjected to sudden acceleration or deceleration. Injury results when tissues are disrupted by local concentrations of physical force generated by a crash event. Morbidity and mortality occur when vital organs absorb energy beyond their tolerance. The ability to tolerate physical forces varies considerably from individual to individual. Clinically, it is important to remember that those at either end of the age spectrum (children and the elderly) are particularly sensitive to serious injury due to the reduced ability of their tissues to absorb energy. Acceleration and deceleration are defined as changes in velocity over time, measured in g‐forces (the weight of objects in earth’s gravitational field). In healthy, nonelderly, adult individuals, the upper end of transient g‐force that can be tolerated is about 30g [4]. Both speed and stopping distance contribute to the overall g‐force experienced during an MVC. The force of gravity increases by the speed squared, while doubling the stopping distance cuts it by half. Automotive safety equipment such as seat belts, airbags, and vehicle deformation (crumple) zones effectively increase the stopping distance for the vehicle occupant during a crash. Four possible collisions occur during a MVC: 1.  The vehicle strikes another object and the crushing of the vehicle’s structure absorbs energy. Vehicles with a greater capacity to deform absorb more energy and effectively

Emergency Medical Services: Clinical Practice and Systems Oversight, Third Edition. Volume 1: Clinical Aspects of EMS. Edited by David C. Cone, Jane H. Brice, Theodore R. Delbridge, and J. Brent Myers. © 2021 NAEMSP. Published 2021 by John Wiley & Sons, Inc.

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increase the stopping distance. During this phase, the occupants continue in motion. 2.  A second collision occurs as a passenger strikes the vehicle’s interior or loads the restraint system such as seatbelt and airbags. 3.  Internal organs continue in motion until they forcefully interact with adjacent musculoskeletal structures. 4.  Loose objects and unrestrained occupants can strike the person, resulting in further injury [4]. Poor automotive design, absence of airbags, and lack of seat belt use decrease the stopping distance and thereby increase the g‐force experienced by a vehicle occupant.

Safety restraints Inertia causes occupants of a car to be moving the same speed as the car. In a crash, the car comes to an abrupt halt (in tenths of a second) and the occupants inside continue at the speed the car was traveling until their bodies are stopped by objects such as the windshield, instrument panel, or steering wheel, if they are not wearing seatbelts. Stopping an object’s momentum requires force acting over time. A seat belt, anchored to the vehicle, is designed to apply the stopping force to more durable parts of the body over a longer period, allowing the occupant to “ride down” the crash as the vehicle crumple zones crush and absorb the energy, and helps protect the body from serious injuries. In contrast, unrestrained occupants do not get the additional “ride down” time and, at higher speed, impact the vehicle interior with weaker parts of the body, for example, upper abdomen and chest to steering wheel. The use of three‐point seatbelts reduces the risk of fatal injury in passenger car occupants by 45% and the risk of moderate‐to‐ critical injury by 50%. The risks are reduced by 60% and 65%, respectively, for light truck occupants [5]. Airbags spread the force required to stop the occupants over a large part of their bodies, minimizing local concentrations of force that can disrupt tissues and cause injury. The airbag deploys into the space between the passenger and the frontal or side components of a vehicle and deploys in a fraction of a second. Even with the small amount of space and time, the system can activate to allow the passenger to distribute the force across the body rather than allowing an abrupt halt to the occupant’s motion against hard and irregular vehicle interior structures.

MVC types Even with the most advanced vehicle restraint systems, crash injuries still occur. Injuries are caused by physical forces, and the direction and magnitude of these forces are dependent on the configuration of the crash. Therefore, the type of crash (e.g., frontal, side, rollover) largely determines the injury patterns seen. Properly evaluating the crash scenario will help

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EMS physicians, and other clinicians predict the most likely injuries they will need to treat. Relaying accurate information about the crash event to the medical team will enable the proper assessment and care of the patient in the emergency department. Major crash types include planar crashes, rollovers, and a host of unusual crashes. Frontal crashes make up about 56% of all fatal crashes, and side impacts account for 23%. Rollovers tend to be the most highly injurious, comprising 30% of all the fatalities in single vehicle type crashes [6]. Each of these crash types involves its own injury patterns and concerns. Planar crashes These crashes are characterized by forces occurring in two dimensions, x and y (flat). They include frontal, side, and rear impacts. Additionally, any of these crashes can be further classified as a narrow impact crash. Typically, this means the vehicle strikes a narrow object, such as a tree or light pole, which then crushes into the vehicle further than would be the case if the vehicle struck a broad object. Frontal Automotive manufacturers have created “crush zones” to deal with this most common type of crash. The front of the vehicle is designed to absorb the energy from the crash and to minimize intrusion of vehicle structure into the occupant compartment. In assessing a crash, it is very important to differentiate between damage to the exterior of the vehicle and intrusion of vehicle structure into the passenger compartment of the vehicle. Significant intrusion of vehicle structure into the interior of the passenger compartment is much more predictive of serious occupant injury than external vehicle damage. Since the advent of frontal airbags, head and facial injuries have become much less common. While chest injuries such as rib fractures are still quite common, particularly in the elderly, incidences of aortic and heart injuries have substantially decreased. Currently, the most common serious injuries observed in frontal crashes affect these body regions in descending order of frequency: lower extremities, pelvis, thorax, head, and abdomen. Side Most side‐impact crashes involve two vehicles, a “bullet vehicle” that strikes the “struck vehicle” in the side. In assessing and describing side‐impact occupants, it is important to determine whether they were “near‐side” or “far‐side” occupants relative to the crash location. Near‐side occupants are at greater risk for severe injury. It is also important to remember that side‐impact crashes are generally far more dangerous than frontal crashes. Therefore, when arriving at the scene of a side impact crash, barring extenuating circumstances, medical priority should typically be given to the near‐side occupants of the struck vehicle, followed by the far‐side occupants, and then the front seat occupants of the bullet vehicle, and finally the rear seat occupants of the bullet vehicle.

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Side impacts, those that strike the right or left planes of the vehicle, can be further characterized as being L‐type (i.e., striking in front of or behind the passenger compartment) or T‐type (i.e., striking the passenger compartment). The T‐type side‐impact crashes are more dangerous for vehicle occupants than L‐type. Side impacts tend to be more severe as there is less space for “crush zones” and therefore very little way of absorbing energy. Narrow T‐type side‐impact cases are particularly dangerous for the occupants as there is far greater intrusion into the passenger compartment. There has been an increase in side protection in the form of curtain and seat‐mounted airbags; however, these safety features are far from common in the fleet. Currently, the most common serious injuries observed in side crashes affect these body regions in decreasing order of frequency: head, thorax, pelvis, and abdomen. Rear For vehicle occupants, this is generally the least dangerous of the planar impacts. The large crush zone in the back of many vehicles tends to absorb much of the energy of the incoming vehicle. In addition, the occupants are protected by broad surfaces of their seats. Rollover crashes Rollover crashes are characterized by forces occurring in three dimensions: x, y, and z. There is a specific type of rollover, called an arrested rollover, which indicates that the vehicle’s rolling motion was abruptly stopped by a fixed object such as a utility pole or tree. Arrested rolls are associated with greater intrusion of vehicle structure into the passenger compartment and a greater risk of injury to the occupants. Restraint use has a huge effect on injury risk and patterns in rollover crashes. Rollovers are problematic for the occupants as the rotation during the rollover event throws them upward and outward. As the roof strikes the ground, the occupants dive toward the roof. If the roll continues, occupants may slide out of their shoulder belts and continue to be thrown around the interior of the vehicle outward toward the side windows. As a result, ejection, or even partial ejection, of the occupant is much more likely in rollovers than other crash types. Complete or partial ejection of the occupants is associated with the most severe injuries and must be suspected in all rollovers due to the movement experienced by the occupants. Indeed, EMS findings of complete or partial ejection are a field triage criterion. Finding complex lacerations with road debris or “road rash” on any part of the body constitutes “partial ejection” and means that the occupant has come into contact with solid structures (e.g., ground, tree) outside the vehicle. Due to the likelihood of occupant ejection in rollover crashes, it is very important that EMS canvass a large area around the vehicle to detect ejected occupants. In addition, the vehicle damage makes this type of crash hard to assess, adding to the complexity of these cases. Roof intrusion is an important indicator of potential

injury in rollover crashes. A rule of thumb is that there is approximately 2 feet of distance between the bottom of the window/ top of door panel and the roof. If half of that distance is gone, there has been 12 inches of downward roof intrusion. The most common serious injuries observed in rollovers affect these body regions in descending order: thorax, abdomen, head, spine, and extremities. Unusual crashes Further complicating matters are other unusual types of crashes. These types include incompatibility between the vehicles involved in the crash (e.g., a large pickup truck striking a compact car), underride (e.g., a passenger vehicle rear‐ending a semitrailer and traveling under the restraining bar), and override (e.g., a semi crashing into a passenger vehicle and driving up and over the back of the passenger vehicle). Incompatibility between vehicles involved in a crash is based on three elements: mass, stiffness, and geometry. In the United States, the popularity of SUVs and trucks with their greater height, stiffness, and weight has increased the risk of injuries suffered by occupants of the vehicles they strike in a crash. These vehicles are designed to perform heavy‐duty functions and consequently they can be dangerous to the occupants of lighter vehicles. In addition, their stiffness makes them less able to protect their own occupants in severe crashes, as they are less able to absorb some of the crash energy. Incompatible side impacts are especially problematic as they compromise the ability of a struck vehicle’s safety systems to properly sense the crash and protect occupants, thus increasing the risk and severity of injuries. The occupants of the more vulnerable vehicle frequently sustain injuries higher in the body, such as the head and chest. These injuries can compromise the ABCs (airway, breathing, circulation) that are the medical priority during initial assessment. Rapid response and proper triage are therefore essential. Ejection can be a problem in these crashes as well. Partial ejection, where part of an occupant’s body strikes something outside the vehicle, such as an intruding hood of a striking vehicle, or even a tree branch, is associated with very high risk of serious injury and thus is a criterion for transport to the highest level of care available. Any crash may contain elements of several of these types, confounding EMS clinicians, physicians, and crash investigators.

Crashes involving vulnerable road users In addition to occupants of vehicles, there are other vulnerable (nonoccupant) populations sharing the roadways including pedestrians, pedalcyclists, and motorcyclists [6]. While overall injury and death have trended down over the past couple of decades for motor vehicle occupants, the opposite is true for vulnerable road users. Recently, these populations have experienced growing fatalities and injuries in the United States

Motor vehicle crashes

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Table 28.1  Morbidity and mortality for vulnerable road users

Pedestrians Fatalities Injuries Pedalcyclist Fatalities Injuries Motorcyclist Fatalities Injuries

2014

2015

2016

2017

2018

4,910 65,000   729 50,000   4,594 92,000

  5,494 70,000   829 45,000   5,029 89,000

  6,080 86,000   853 64,000   5,337 104,000

  6,075 71,000   806 50,000   5,229 89,000

  6,283 75,000   857 47,000   4,985 82,000

(Table  28.1) [7]. Additionally, these nonoccupants tend to be more seriously injured when involved in crashes than vehicle occupants as they do not have the protection offered by a motor vehicle.

EMS crash assessment priorities When approaching the scene of a crash, there are things to look for [8]: • Unrestrained occupant(s) • Possibly ejected occupants ○○ Complex open wounds ○○ Empty child safety seat ○○ Broken window or windshield ○○ Rollover • Intrusion into the occupant space The intrusion criterion for high‐risk auto crashes is 12 inches at the occupant seating location or 18 inches at any interior location within the vehicle. One key rule of thumb to remember is that a seat is approximately 24 by 24 inches. Therefore, if vehicle structure intrusion is such that only half the normal seat width remains, the occupant seated there is at high risk of serious injury (20% risk of ISS 15+). In addition, the foot well area is approximately 24 by 24 inches and the lower part of the dashboard is approximately 12 inches from the front edge of the seat. If a leg is entrapped between the dash and the front of the seat, there has been 12 inches of intrusion (Figures 28.1 and 28.2). The crash and vehicle information at the scene is essential to properly triaging the patient, and this information can predict the most likely injuries. Properly relaying this information to the medical team will enable the proper assessment and care of the patient. Extrication First responders understand that the quicker they remove occupants from a damaged vehicle and get them to treatment, the better their outcomes will be. It is imperative that clinical care begins at the scene and is a priority during the extrication process.

Figure 28.1  View from left side of driver’s toe pan intrusion. Source:

International Center for Automotive Medicine. Reproduced with permission of ICAM.

Integration of EMS into the incident command structure at an MVC can ensure that clinical care of the patient is not underemphasized during extrication. Whenever safely possible, it is desirable to have an EMS clinician (wearing appropriate personal protective equipment) inside the vehicle with the patient while extrication proceeds. Field Triage At the scene of any MVC or other event involving traumatic injury, EMS physicians and other clinicians must identify those patients who are at greatest risk for severe injury and then choose the most appropriate facility to which to transport them within the trauma system. This decision process is known as “field triage” and is based on an algorithm called a “decision scheme.” The first Field Triage Decision Scheme was published by the American College of Surgeons in 1986 [9], with subsequent updates in 1990, 1993, 1999, 2006, and 2012 [10]. See Chapter 39: Field Trauma Triage, for a detailed discussion of this topic. Guidelines for Field Triage of Injured Patients have also been published by the Centers for Disease Control and Prevention and is available on their website [11].

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There are clues that an airbag restraint system may be present. Sometimes there is a label on the visor, instrument panel, or window. A small, low glove box can indicate a large dash‐ mounted airbag. Tags or letters may be embossed on the areas containing an airbag restraint system, such as the seats, pillars, roof rails, or instrument panel. Some tags to be alert for include: SIR, ARS, SRS, Airbag, SIPS, HPS, ACRS, ITS, and KAS. Rescue workers should treat nondeployed airbag restraint systems as explosive devices: • Disconnect the battery • Disconnect any airbag restraint system connectors found • Do not place any objects against the module • Do not cut into the module • Do not strike a sensor, module, or diagnostic module Figure 28.2  View through sunroof of door panel intrusion into driver’s

seat. Source: International Center for Automotive Medicine. Reproduced with permission of ICAM.

Unique MVC problems There are many hazards involved in dealing with MVCs. In many cases, EMS physicians and other clinicians will be watching for traffic and avoiding the usual detritus that comes from a crash, such as broken glass, spilled fuel, and jagged metal pieces. They must also be ready to protect themselves from bodily fluids and blood‐borne pathogens. Batteries Many of the systems in today’s vehicle fleet contain electronic control units, which can include controls for airbags, door locks, electronic windows, seats, and telematics. Gasoline‐hybrid vehicles also have high‐voltage cables, which are identifiable by the use of orange insulation [12]. For this reason, an important initial step for EMS physicians and responders arriving on scene is to make sure the ignition is off, remove the key, and disconnect the battery. This shuts down the power source for all electronic control units and avoids any chance of injuries from the electrical components of the vehicle. Airbags EMS physicians and responders need to be especially careful about nondeployed airbags. There have been cases where EMS personnel have been injured when an airbag deployed as they were extricating the patient. There are several reasons an airbag restraint system may not have deployed during the crash. For instance, frontal airbags are designed to not deploy in rollover, rear, or side impacts. Side airbags are not designed to deploy in frontal or rear impacts. If the right front passenger seat is not occupied, the firing of those airbags may have been suppressed by design. In some cases, the collision may not have been severe enough to set the airbag off, or there could be a system malfunction that prevented the bags from deploying.

Emerging technology Advanced automatic crash notification Vehicles in the fleet have a large number of sensors. Some of them monitor the presence of an occupant. Others monitor for data suggesting a crash may be occurring. These data are constantly analyzed by the computer systems within the vehicle, and in the event of a crash, the computers will trigger the deployment of the safety systems in the optimal configuration for the type and severity of the crash being detected. In the case of many vehicles, some of these data will be sent via cellular networks to alert emergency responders and provide useful information that can improve postcrash care for the occupants. The ability to send this information is called Advanced Automatic Crash Notification (AACN) [13]. Currently, crashes calculated as severe enough to be associated with a 20% or greater risk of ISS 15 injury to the occupants are highlighted by telemetry providers who flag these potentially serious crashes to public safety answering points so that EMS can be better prepared prior to arrival on scene, as well as to prioritize responses between multiple incidents.

Available education The International Center for Automotive Medicine at the University of Michigan has created a website dedicated to training law enforcement, EMS, and medical personnel. This website is located at www.crashedu.org and contains various educational modules for first responders to obtain training. Continuing medical education credits are also available.

References 1 Kochanek K, Murphy S, Xu J, Arias E. Deaths: final data for 2017. Natl Vital Stat Reports. 2019; 68. https://www.cdc.gov/nchs/data/ nvsr/nvsr68/nvsr68_09‐508.pdf. 2 Blincoe L, Miller TR, Zaloshnja E, Lawrence BA. The Economic and Societal Impact of Motor Vehicle Crashes, 2010 (Revised). Report No.

Motor vehicle crashes

DOT HS 812 013. Washington, DC: National Highway Traffic Safety Administration, 2015. 3 National Highway Traffic Safety Administration. Traffic Safety Facts: 2017 and 2018 Data Overviews. Washington, DC: U.S. Department of Transportation, National Highway Traffic Safety Administration, 2019. 4 Peterson T, Tilman Jolly B, Runge J, Hunt R. Motor vehicle safety: current concepts and challenges for emergency physicians. Ann Emerg Med. 1999; 34:384–93. 5 National Highway Traffic Safety Administration. 2017 Data: Occupant Protection in Passenger Vehicles. Washington, DC: U.S. Department of Transportation, National Highway Traffic Safety Administration, 2019. 6 Insurance Institute for Highway Safety. Fatality Facts 2018: Passenger vehicle occupants. Washington, DC: Insurance Institute for Highway Safety, Highway Loss Data Institute, 2020. 7 National Highway Traffic Safety Administration. Pedestrians. Washington, DC: U.S. Department of Transportation, 2020. 8 International Center for Automotive Medicine. CrashEdu: Crash Response Training. Ann Arbor, Michigan: International Center

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for Automotive Medicine, 2013. Available at: http://crashedu. org/. 9 Mackersie R. History of trauma field triage development and the American College of Surgeons criteria. Prehosp Emerg Care. 2006; 10:287–94. 10 American College of Surgeons. Resources for optimal care of the injured patient: an update. Task Force of the Committee on Trauma, American College of Surgeons. Bull Am Coll Surg. 1990; 75:20–29. 11 Sasser SM, Hunt RC, Faul M, et  al. Guidelines for field triage of injured patients: recommendations of the national expert panel on field triage, 2011. MMWR Recomm Rep 2012; 61:1–20. 12 Morris B. Holmatro’s Vehicle Extrication Techniques. Glen Burnie, MD: Icone Graphic, 2006. 13 International Center for Automotive Medicine. AACN Telemetry: What It Is and How Do I Use It? Ann Arbor, Michigan: International Center for Automotive Medicine, 2013. Available at: http://crashedu.org/ems/mod15/. Accessed September 15, 2020.

CHAPTER 29

Penetrating trauma Michelle Welsford and Clare Wallner

Introduction Trauma (injury) is the leading cause of death for North Americans aged 1 to 34 years and is only surpassed by cancer and cardiovascular disease in older adults. Penetrating trauma has significant morbidity and mortality and is a common cause for activation of EMS. Injuries due to firearms are particularly lethal and require rapid assessment and decision making in the field to mitigate injury. In 2017, there were 276,689 deaths in Canada (7.5/1000 population) and 769 deaths associated with firearms (0.02/1000 population), 75% of which were intentional self‐harm, 23% homicides, and 2% unintentional [1]. In the United States in 2017 there were 2,813,503 deaths (8.6/1000 population) of which 38,882 were firearm‐related deaths (0.12/1000 population). Intentional self‐harm was 61%, homicides were 27%, and unintentional were 12% [2]. Other potential causes of penetrating trauma include knives, arrows, nails, glass, wood, and wire. Penetrating trauma can also occur with shrapnel from explosions as well as with foreign objects flying in motor vehicle collisions. The type of weapon or projectile, the way in which the object imparts its energy on the human body, and the location of impact dictate the type and severity of injury.

Physics and mechanics of penetrating trauma Two physical concepts explain injury associated with penetrating trauma. The energy associated with a moving object is defined by kinetic energy = ½ × mass × velocity2. Kinetic injury explains why a small and light projectile (e.g., a bullet) can result in devastating injury. Because the projectile energy is related to the velocity squared, doubling the velocity results in a fourfold increase in kinetic energy; if velocity increases by a factor of 4,

kinetic energy increases by a factor of 16. In penetrating trauma, the projectile imparts kinetic energy to the victim’s body, resulting in injury. The second concept is the law of conservation of energy: Energy cannot be created or destroyed but only transferred from one form to another. When a projectile enters the body and remains there, all the projectile’s kinetic energy has been transferred to the body. If a projectile travels through the body, the energy transferred to the body is equal to the kinetic energy of the object before entering minus its energy on leaving the body. Weapons can usually be classified based on the amount of energy carried by the projectile: • Low energy: knives, hand‐launched missiles. • Medium energy: handguns, smaller bullets, lower velocities (200–400 m/s). • High energy: military or hunting rifles, larger bullets, higher velocities (600–1000 m/s) [3]. Ballistics The study of the movement and behavior of projectiles is ballistics. Trajectory ballistics describes the projectile after launch, whereas terminal ballistics focuses on how the projectile acts when it hits its target, the latter being more clinically relevant. Several factors affect terminal ballistics, including missile size, velocity, missile shape, deformity, and stability. Size As a general rule, the larger the missile the more damage caused by direct contact between the missile and tissue. Larger missiles generally have a greater surface area and impart more energy faster. Bullet size is measured by the inside diameter of the gun barrel either in millimeters (e.g., 9 mm) or hundredths of an inch (e.g., 44 caliber). Magnum rounds refer to those with more gunpowder than a normal round, which increases the muzzle velocity and thus the bullet energy by 20% to 60% (Figure 29.1) [3, 4].

Emergency Medical Services: Clinical Practice and Systems Oversight, Third Edition. Volume 1: Clinical Aspects of EMS. Edited by David C. Cone, Jane H. Brice, Theodore R. Delbridge, and J. Brent Myers. © 2021 NAEMSP. Published 2021 by John Wiley & Sons, Inc.

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Velocity Missiles traveling through air encounter resistance or drag. Drag increases exponentially with velocity and is inversely proportional to mass. Clinically, this implies that the damage caused by a missile at short range will be greater than one fired at longer range and that heavier missiles are able to maintain their velocity better than light ones. For practical purposes, the impact velocity of bullets will be the same as the muzzle velocity at 45 meters for low‐energy firearms, such as handguns, and 90 meters for higher‐velocity weapons, such as rifles [4]. Shape and deformation The energy imparted by a missile is related to its shape. Missiles that are blunt (i.e., have a higher cross‐sectional area) experience more resistance and impart energy to tissues quickly, whereas sharper missiles cut through tissues more effectively and release

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energy over a longer period of time and distance. In addition, projectiles may deform on impact, increasing the bullet’s cross‐ sectional area (Figure  29.2). This mushrooming effect raises the resistance between the missile and tissues, thus increasing the energy transfer rate. Some missiles fragment on impact, increasing the rate of energy exchange, as the total surface area of the fragments is greater than that of the original missile. Stability Contrary to popular belief, bullets often do not travel in a direct line and may tumble or wobble (yaw) in their course, often decreasing the velocity and accuracy of the missile. If it tumbles or yaws after hitting tissue, the bullet’s surface area with respect to tissue is increased, thereby increasing the amount and rate of energy transfer [4], and thus the extent of injury (Figure 29.3).

y-axis

z-axis v Bullet axis

Yaw of repose

Figure 29.1  Bullets of various lengths and diameters, compared with an

AA battery. Source: Reproduced with permission of Robert R. Bass.

Figure 29.3  Effect of yaw in creating a larger surface area of effect. Source: Reproduced with permission of Robert R. Bass.

Figure 29.2  Examples of bullet shapes and deformity designed to inflict tissue damage. Source: Reproduced with permission of Robert R. Bass.

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Types of weapons Knives and Arrows Knives and arrows are considered to be low‐energy weapons. Although the projectile’s weight may be significantly higher, the velocity is generally much lower. Tissue damage is typically restricted to direct contact between the projectile and tissue. The extent of tissue damage can be extremely difficult to estimate because the projectile’s trajectory cannot be determined based on external injury appearance. The entrance wound will not predict whether the object moved around within the body or what organs it came into contact with. It is, however, useful to know the blade length; to a certain degree it can predict the maximum depth of penetration. Handguns Handguns are typically short barreled, medium‐energy weapons with small bullets. As a medium‐energy weapon, a handgun’s damage‐causing potential is more limited than that of higher energy firearms. Handgun bullets tend to have a blunter shape, causing early release of energy. Despite their shape and composition of softer metal (lead), handgun bullets tend not to deform due to their lower energy. As such, the bulk of the injury is caused in tissues damaged by the bullet’s passage. Rifles Rifles are named for the rifling in the barrel, which causes the bullet to spin. The spin of the bullet improves accuracy and range due to the conservation of angular momentum. Rifle bullets are larger, retain more kinetic energy, and travel much further with greater accuracy than do handgun projectiles. They are able to transfer significant energy with damage extending outside the bullet’s immediate track. Hunting ammunition is designed to expand dramatically (up to three times) on impact [4], increasing the speed of energy delivery and the wound pathway. Military ammunition is fully jacketed so it does not deform, which decreases the energy delivery rate [4].

Direct injury Direct injury is caused by a projectile’s impact, including crushing and lacerating tissues. Direct injury is based on the projectile size, although this may be modified by any deformation and bullet instability as it travels through the body. Crushing and laceration cause serious injury only if the bullet strikes organs or blood vessels [4].

Figure 29.4  Shotgun injuries to chest. Source: Reproduced with permission

of Robert R. Bass.

Shotguns While shotguns can fire single bullets (slugs), in general they fire a collection of spherical pellets, called shot, which radiate from the muzzle of the gun in a conical distribution. Typical muzzle velocity is 360 m/s [3]. Shot pellets have a high drag coefficient and lose velocity rapidly. At short range, they can be devastating; however, at longer range they lose much of their destructive potential (Figures 29.4 and 29.5).

High‐velocity projectile injury While low‐velocity projectiles inflict injury by direct cutting or tearing of tissues, higher‐velocity projectiles inflict injury in three ways: direct, pressure wave, and cavitation.

Figure 29.5  X‐ray of shotgun injuries to chest. Source: Reproduced with

permission of Robert R. Bass.

Penetrating trauma

Body armor protects the wearer by spreading the energy of impact over a larger area. Although this means that the projectile is prevented from hitting the body, the kinetic energy strikes a larger area, which can cause significant injury, such as fractured ribs and cardiac contusions. Pressure Wave When a high‐velocity projectile (greater than 750 m/s) hits human tissue, a high‐pressure wave moves outward from the missile track in all directions. Caused by the compression ahead of the bullet, the pressure wave moves faster than the bullet itself. The faster and blunter the projectile, the greater the effect. Pressure from higher velocity bullets can exceed 1,000 pounds per square inch. Pressure waves travel better through fluids, higher‐density tissues, and organs, causing tearing and crushing of tissues. Blood vessels and solid organs (e.g., liver or spleen) can be injured or in some cases fractured. Hollow organs (e.g., large bowel) can rupture, and bones can be broken by the pressure wave (see Figure 29.6) [4]. Cavitation A high‐velocity projectile create a temporary cavity behind the missile path as tissues move away from the track. Cavity size is dependent on energy transferred during the bullet’s journey and may be 30 to 40 times the diameter of the bullet [4]. The cavity will have a lower pressure than the air outside the body, causing air and, potentially, debris to be pulled in through the entrance and exit wounds. After the bullet has passed, the elasticity of the surrounding tissues tends to collapse the temporary cavity (Figure 29.6). Entry and exit wounds Bullets often have both entry and exit wounds. In general, the exit wound is the same size or larger than the entrance wound; however, this is not always the case. Although bullets typically follow the path of least resistance, they may not travel in a straight line. Projectiles may have an unpredictable path within body tissues, including rotation or ricochet and deflection off bony structures. Two injury sites do not always represent an

Permanent cavity

Temporary cavity

Sonic shock wave

Figure 29.6  Sonic wave and cavitation produced by a high‐velocity bullet

in tissue. Source: Reproduced with permission of Robert R. Bass.

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entry and an exit wound, but may instead represent two different entry wounds. Entrance wounds can be deceptively small. A very small entrance wound can hide a devastating injury, and EMS clinicians should not be lulled into a false sense of security by a small entrance wound.

Resuscitation and initial assessment Although the standard approach to patient assessment is described elsewhere, there are several unique considerations in the patient who has suffered a penetrating injury. Scene safety Although a thorough assessment of scene safety is always a priority, it takes on particular importance when dealing with penetrating trauma. Almost all potential causes of penetrating trauma harbor risks to the unwary EMS clinician, and these must be considered before scene entry. When penetrating trauma is a result of assault, the prehospital clinician must ensure the perpetrator is no longer in the immediate area or has been apprehended or restrained by police. On other scenes where penetrating trauma is a possibility, such as explosions or motor vehicle collisions, the EMS personnel must examine the scene before entry to ensure there is no undue risk. When the scene is unsafe, the clinician should withdraw to a safe distance and summon the appropriate assistance, such as police or fire services. Impaled objects In general, impaled objects are not removed in the field as the object may be providing tamponade to bleeding soft tissues and blood vessels, and removal could cause exsanguination. Because movement of the object may cause further injury, the object should be well stabilized with bulky dressings and tape. Occasionally this will require cutting the object to a shorter length on scene if it impedes extrication and transportation. Care should be taken to ensure minimal movement of the object during this process. The exceptions are removal of an object that impedes CPR in a pulseless patient or impedes airway management where airway control is required (Figure 29.7). Spinal motion restriction Spinal motion restriction (SMR) has little role in patients with isolated penetrating trauma. Numerous case series and a systematic review with meta‐analysis have found an association with increased mortality for SMR in penetrating trauma patients [5, 6, 7]. Penetrating trauma rarely leads to spinal cord injury, but when it does occur, it usually causes a direct, complete injury to the spinal cord (as opposed to an incomplete or secondary injury related to an unstable bony spine injury), and it is unlikely to be worsened or improved by prehospital SMR [8, 9, 10]. For this reason, the National Association of EMS

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Figure 29.7  Knife left in situ in the wound for removal in the operating

room. Source: Reproduced with permission of Robert R. Bass.

Physicians (NAEMSP), American College of Emergency Physicians (ACEP), American College of Surgeons Committee on Trauma (ACS‐COT), and Eastern Association for the Surgery of Trauma (EAST) all recommend that SMR not be used routinely in patients with penetrating trauma [11, 7]. It is well accepted that a cervical spine (c‐spine) rigid collar is not required for penetrating firearm injuries to the head [12]. Similarly, SMR for penetrating injuries to the neck and torso has limited value (less than 0.5% incidence of unstable injury) but could be considered when a neurologic deficit is apparent or when there is a high suspicion in an obtunded patient. However, even for these indications, rapid extrication and transport should take priority. External hemorrhage There are three main approaches to control of external hemorrhage: direct pressure, hemostatic dressings, and tourniquets. Most external bleeding, including arterial bleeding, can be controlled with direct pressure. When bleeding persists despite these maneuvers or massive hemorrhage is apparent, hemostatic dressings may quickly control life‐threatening hemorrhage. Hemostatic dressings and agents often incorporate inert minerals (e.g., kaolin) that activate the intrinsic coagulation cascade leading to fibrin clot formation. Very few clinical studies have been published and no randomized trials are available to provide guidance. However, observational evidence and animal studies on the ability of these agents to provide hemorrhage control has led to recommendations for use. The Committee on Tactical Combat Casualty Care (CoTCCC) guidelines recommend: “For compressible (external) hemorrhage not amenable to limb tourniquet use or as an adjunct to tourniquet removal, use Combat Gauze as the CoTCCC hemostatic dressing of choice [13].” If extremity bleeding is not controlled or for traumatic amputations or near amputations, application of a tourniquet may be lifesaving with minimal adverse events (less than 2%) (Figure  29.8 and 29.9) [14, 15]. Other indications that may

Figure 29.8  Tourniquet in place in a patient with extensive thigh injury.

Source: Photo courtesy of Matthew Sztajnkrycer, MD, PhD.

Figure 29.9  Tourniquet in place above knee in simulated lower leg

crush/near amputation. Source: Photo courtesy of Richard Kamin, MD.

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benefit from a tourniquet are when significant bleeding is apparent but constant direct pressure cannot be maintained due to additional injuries, multiple casualties, or tactical‐ or military‐casualty incidents. A retrospective before‐after comparison of the reintroduction of tourniquets for military use in 2007 found an association with a dramatic 85% reduction in mortality from extremity hemorrhage [16]. TCCC guidelines recommend a “CoTCCC‐recommended limb tourniquet to control life‐ threatening external hemorrhage that is anatomically amenable to tourniquet use for any traumatic amputation” [13]. Tourniquet use during the Boston Marathon bombing in 2013 allowed over 200 injured patients to be promptly treated and transported to area hospitals, likely leading to many lives saved [17]. The letters TK and the time the tourniquet was applied should be written on the patient’s limb or forehead. This is discussed more fully in Chapter 35, Hemorrhage Control. Permissive hypotensive resuscitation Intravenous crystalloid fluid therapy in trauma is controversial. Permissive hypotensive resuscitation advocates that only trauma patients without radial pulses or with SBP < 70 mmHg receive fluid resuscitation in the field [18]. In managing penetrating trauma patients, controlling hemorrhage is the priority. Replacing volume loss before the bleeding is controlled can lead to more bleeding, particularly concerning in the setting of penetrating trauma. Whole blood or red blood cell transfusion is preferred to crystalloid fluids, and if blood is not available in the field, then limiting fluid resuscitation until the hospital is preferred. Transport to hospital and definitive treatment should not be delayed; therefore, IV access should rarely be obtained on scene but rather delayed until en route. IV or IO access in the lower limbs is relatively contraindicated because abdominal vascular injuries may lead to direct extravasation and never reach the central circulation. A systematic review of permissive hypotension showed association with a significant reduction in mortality [19]. Tranexamic acid Tranexamic acid (TXA) is an important medication with antifibrinolytic activity that competitively inhibits the activation of plasminogen to plasmin. It has been shown to decrease bleeding in a number of surgical and spontaneous bleeding indications. Initial results of its use in hospital for the undifferentiated adult trauma in the international Clinical Randomization of an Antifibrinolytic in Significant Hemorrhage Study (CRASH‐2) showed a small 1.5% mortality benefit if given within 3 hours (a subgroup analysis showed greatest benefit within 1 hour, but greater mortality if given after 3 hours) and only 2% risk of complications [20, 21]. The complications/side effects are likely greater than that reported as their method for recognizing complications (thromboembolic events) were not ideal. Similarly, the main benefit may have been in patients with bleeding that could not be controlled by other means (areas where rapid access to surgery is not possible rather than in a North American trauma center). The MATTERs retrospective study of military use of TXA showed a positive correlation with increased survival in

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those patients needing massive transfusions but found a fourfold increase in thromboembolic events [22]. Subsequent trials of its use in traumatic brain injury (CRASH‐3) did not show benefit in the entire group but did show potentially higher risk of thromboembolism side effects [23]. A recent randomized controlled trial on the use of TXA by paramedics in North America was completed by the Resuscitation Outcomes Consortium (ROC‐TXA). That study had not yet been published in a peer‐reviewed journal by mid‐2020, but the raw outcomes were posted on clinicaltrials. gov and in abstracts and appear to show neutral benefits at most. Thus, any benefits for TXA use prior to arrival in hospital may be confined to only certain groups of patients: perhaps for military applications, and confirmed significant hemorrhage with prolonged time to a trauma center [24]. NAEMSP, ACEP, and ACS‐COT guidelines suggest that there is “insufficient evidence to support or refute the prehospital administration of TXA” [25].

Transport issues “Scoop and Run” versus “Stay and Play” An optimized and efficient trauma system is required to deliver a patient from injury location to definitive care through a coordinated system of public access (9‐1‐1), EMS care, trauma triage, and trauma center. The goal is to begin transport of the patient within 10 minutes of arrival on scene, barring extrication or other logistical issues that prevent prompt transport. This “scoop and run” approach is important in penetrating trauma patients who meet trauma triage criteria in which surgical management is likely. The term refers to the strategy of rapid assessment and transport. Interventions such as IV cannulation should be initiated en route to the hospital except in extenuating circumstances, such as a prolonged extrication. Conversely, the term “stay and play” refers to on‐scene stabilization and initial management, which is rarely indicated in penetrating trauma. In the hospital, use of thoracic or aortic occlusion can limit further distal hemorrhage and enhance cerebral and coronary perfusion in patients who are peri‐arrest or in arrest. This was traditionally accomplished via an open surgical approach (resuscitative or emergency department thoracotomy), but more recently endovascular aortic occlusion has also been shown to be beneficial for prearrest trauma patients. Resuscitative endovascular balloon occlusion of the aorta (REBOA) can be deployed via the femoral artery and placed in the thoracic or abdominal aorta and has been shown to reduce mortality compared to a resuscitative thoracotomy in patients who are prearrest [26]. A resuscitative thoracotomy may be useful if performed within 15 minutes of loss of circulation (especially in penetrating thoracic trauma) [27, 28]. EMS clinicians should focus on rapid transport and en route maintenance of the airway, correcting reversible causes of arrest, specifically hypoxia, tension pneumothorax, and hypovolemia, while transporting the patient to the hospital (with CPR ongoing, if applicable). Communication with the receiving ED or trauma center to notify them of the incoming patient, relevant injuries, and an estimated time of arrival is essential.

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Penetrating chest trauma

Penetrating abdominal trauma

The consequences of penetrating trauma depend on the mechanism and location of injury, the path of the projectile, and the underlying health of the patient. All patients with penetrating intrathoracic injury are at risk for intra‐abdominal or neck injury depending on the entry point and path of the projectile. It is also true that a penetrating traumatic injury to the neck or abdomen can have associated chest injuries. When patients have been stabbed, it is useful to know the approximate length of the blade to understand what structures may have been injured. In the setting of a gunshot wound, any entry wound that does not have an exit wound should be considered to have retained bullet fragments.

Gunshot wounds to the abdomen most commonly injure the small and large bowel because of the large space they occupy. A projectile passing through a gas‐filled bowel will often cause compression of that gas, which may limit the pressure wave and injury. However, a projectile passing through a solid organ, such as the liver and spleen, causes cavitation and more widespread injury. Penetrating abdominal trauma may cause devastating injury to the large vessels (i.e., aorta, inferior vena cava, iliac vessels), leading to immediate exsanguination and death. Due to the relative lack of skeletal protection and highly vascular structures, penetrating abdominal trauma has a high mortality. As opposed to blunt trauma, in which force is more diffuse, is transmitted across the abdomen, and leads to primarily solid organ injury, penetrating trauma is often a locally applied force affecting the hollow organs and mesentery. Solid organ injuries are less common with penetrating than blunt trauma, but they can occur, especially in stab wounds, with devastating consequences. Penetrating wounds should be covered to decrease infection, and observed for ongoing bleeding. Any intra‐abdominal organs visible (evisceration) should simply be covered with sterile saline‐soaked dressings and in turn covered with an occlusive dry or plastic dressing.

Lungs and bronchial tree Penetrating injury to lungs or bronchial tree can result in escape of air or blood into the thoracic cavity resulting in simple pneumothorax, tension pneumothorax, or hemothorax. Treatment for suspected simple pneumothorax or hemothorax should involve with rapid transport and supportive care en route. If a tension pneumothorax is suspected, chest decompression can be accomplished with a 10‐ to 14‐gauge 3.25‐inch needle/catheter thoracostomy in the fifth intercostal space anterior axillary line or second intercostal space midclavicular line (not medial to the nipple line). Heart and great vessels Penetrating injury to the “cardiac box” increases the likelihood of myocardial and great vessel injury. The cardiac box is a rectangular shaped area of the anterior chest bounded superiorly by the clavicles and sternal notch, laterally by the midclavicular lines/nipple lines, and inferiorly by the xiphoid and costal margins [29]. It should be noted that the cardiac box includes the epigastric area. Pericardial tamponade is a potentially rapidly life‐threatening condition resulting from accumulation of fluid in the pericardial sac. It occurs more frequently in stab than gunshot wounds: 60% to 80% of stab wounds involving the heart develop tamponade [29,30]. Only a small amount of blood (50–100 mL) is necessary for pericardial tamponade to develop. Signs and symptoms of pericardial tamponade are hypotension, tachycardia, muffled heart sounds (Beck’s triad); dyspnea; cyanosis; and distended jugular veins. These signs may be followed by cardiac arrest with pulseless electrical activity. The treatment for pericardial tamponade is primarily thoracotomy and surgical evacuation of the pericardium with repair of the cardiac wound. Occasionally, pericardiocentesis (potentially performed by the EMS physician in the field with ultrasound guidance) can be used as a temporizing measure until arrival at the trauma center. Diaphragm Any penetrating thoracic or abdominal trauma can result in a diaphragmatic injury. Because diaphragmatic injuries can result in significant respiratory compromise, respiratory distress associated with injuries to the chest or abdomen should prompt EMS personnel to consider the possibility of a diaphragmatic injury.

Penetrating neck trauma Penetrating neck wounds can be immediately fatal. Even the seemingly “innocuous” penetrating injuries to the neck should be treated with careful and expectant management as they can suddenly become life‐threatening. Injury to the major blood vessels of the neck may rapidly lead to exsanguination or delayed hemorrhage. Because of the thin overlying muscles and subcutaneous tissue, airway injuries to the larynx or trachea are common and may be devastating. Although somewhat protected by other structures, deeper injury can lead to pharyngeal and esophageal injuries. Neurologic injury can occur to the spinal cord posteriorly, the cranial nerves superiorly, or the brachial plexus inferiorly. Common carotid injuries occur in approximately 10% of all penetrating neck trauma. Significant carotid artery injuries are usually rapidly fatal but may occasionally tamponade briefly to allow transport and assessment. History of significant blood loss either at the scene or ongoing is evidence of a major vascular injury. Similarly, expanding hematomas may initially be subtle, but are signs of vascular injury and may lead to airway compromise from direct compression. Hematomas are often visible when the patient’s head is in a neutral position and the patient is examined from the feet. Jugular vein injuries may also be fatal, but they may be successfully managed with direct pressure in the field to allow transport to an operative setting. Venous injuries may be complicated by entrainment of air leading to air emboli, a potentially fatal complication.

Penetrating trauma

Neurologic deficits should be carefully documented and relayed to the receiving facility. Unilateral stroke symptoms may be related to carotid artery injury and subsequent brain ischemia. Additionally, unilateral cranial nerve and brachial plexus injuries may also be apparent as facial or arm weakness, respectively. Spinal cord injury may result in unilateral or bilateral motor deficits of the arms and legs. Penetrating neck trauma can lead to airway anatomy distortion due to either a primary direct airway injury or secondarily via compressing hematomas and bleeding. Signs of an expanding hematoma, hoarse voice, stridor, airway compromise, or blood in the airway are warning signs of impending airway compromise and require quick action. Airway compromise should be anticipated, intubation should occur early rather than late, and in most cases, rapid transport should be initiated to a trauma center with basic airway maneuvers if airway intervention is not immediately required. Although prehospital clinicians are accustomed to considering a potential spinal injury and providing SMR to most blunt trauma patients, this is not required or recommended in penetrating injury. As discussed above, isolated stab wounds to the neck are unlikely to cause unstable cervical spine injuries. Although gunshots can lead to cervical spine injury, most spinal cord injuries are complete and obvious on initial evaluation, prompting immobilization. The clinician should follow local directions regarding spinal immobilization with the understanding that if no spinal involvement is likely, the patient may be better managed without immobilization. Penetrating neck injuries should be covered with an occlusive dressing if possible, to reduce the chances of an air embolism if bleeding is minimal. If ongoing bleeding is present, direct manual pressure can be used on one side of the neck. Obvious brisk bleeding from the neck may be best controlled with direct pressure above and below the bleeding site with the clinician’s two thumbs. Gauze under each thumb may assist with traction on the skin. If this is required to control significant bleeding, care should be taken not to change clinicians or stop the pressure to inspect the wound until arrival at the trauma center. Bilateral compression and circumferential dressings should be avoided because this may lead to cerebral infarction from bilateral carotid artery compression. Lastly, intravenous cannulation, if performed, is preferentially performed on the upper limb that is opposite the side of neck injury. Because the subclavian vessels may be involved, it is best to avoid infusing fluid that will travel through an injured vessel leading to clot disruption, greater exsanguination, and local hematoma formation.

Penetrating head and facial trauma The prehospital approach and management of penetrating head trauma is similar to that for head injuries in general and is discussed in Chapter 30, Traumatic Brain Injury, except that a cervical collar is not indicated in isolated penetrating head

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injuries as discussed earlier. However, the airway management of facial trauma deserves special consideration. Facial wounds that are otherwise survivable may lead to death due to airway compromise. Penetrating wounds or impaled objects may lead to significantly distorted airway anatomy and blood and foreign bodies in the airway. If these patients are conscious, they are best managed sitting up and forward to help facilitate airway clearance from blood and secretions. Any patient with penetrating facial injuries should be carefully considered for airway control. In addition to oral airway and oral intubation, surgical airways, such as cricothyrotomy, may be required. Nasal airways should be avoided in patients with significant facial trauma.

Penetrating extremity trauma Penetrating injury to the extremity can disrupt blood vessels, bones, nerves, muscles, and other soft tissues. This section will focus primarily on vascular and bony injuries. Vascular injuries are either higher‐pressure arterial injuries or low‐pressure venous injuries, both of which can bleed profusely. Arterial injuries tend to be more serious and should be identified and acted on promptly to prevent further morbidity or mortality. Arterial bleeding is often a brighter red and spurts with each heartbeat. Venous bleeding tends to be darker and tends to flow as opposed to spurt. The majority of active bleeds, including arterial bleeding, can be managed with direct pressure. When these strategies fail, the application of a hemostatic dressing or a tourniquet can be considered. Details on indication and use of tourniquets and other modalities may be found in Chapter 35: Hemorrhage Control. Penetrating trauma can also cause bony injuries such as fractures or dislocations. These injuries should be considered open injuries because the penetrating object pathway will have exposed the injury to the outside. They should be treated as other fractures or dislocations by immobilization in the position found and by dressing open wounds.

Prevention and public health issues There were an estimated 2.1 million registered firearms for a total of 12.7 million civilian firearms in Canada in 2017, and 1.1 million registered for a total of 393.3 million firearms in the United States in 2017 [31]. Approximately 37%‐40% of U.S. households have access to firearms. EMS personnel face a high probability of responding to locations where firearms may be readily accessible to the occupants. This presents both a challenge and an opportunity. The challenge is that EMS clinicians must be aware of their surroundings and ensure that the scene is safe to enter before beginning patient care. EMS clinicians also have an opportunity to recognize safety concerns in the home that are not seen by traditional

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hospital‐based health care clinicians. An example of this would be a home where children are present and a firearm is seen within easy reach of the children. Although it may or may not be appropriate to educate the parents of the dangers of this circumstance at the time, it is an observation that can be relayed to hospital personnel or to the relevant child protection agency. Where children are felt to be at imminent risk, EMS clinicians may have a legal obligation to report this to the child protection agency (as do other health care clinicians).

Medicolegal issues Most jurisdictions require reporting of certain types of injuries. Many require hospitals to notify the police for all patients who present to the ED with gunshot wounds. The role of EMS will vary between jurisdictions. Clinicians should be familiar with the specific legislation in their jurisdictions and what (if any) requirements exist for reporting gunshot or stab wounds. EMS clinicians should carefully document historical or physical findings. Patient care records are legal documents and can be used as evidence in a court of law. Unless a criminal act is witnessed, EMS clinicians should document what is seen and heard as opposed to what they are told or what they perceive may have happened. Examples of this include: “The patient states he was shot by his father” rather than “The patient was shot by his father.” EMS clinicians should not make suppositions about which wound is the entrance versus exit, but simply document the locations and descriptions of the two penetrating wounds.

Forensic issues EMS often responds to crime scenes or to patients who are the victims or perpetrators of crime. As such, clinicians need some understanding of forensics and evidence preservation. Wherever possible, the clinician should ensure that neither the scene nor evidence is disturbed. • When a crime is suspected, notify the police immediately. When the police are already on scene, follow the instructions of the officer in charge, especially with respect to scene security and safety. When there is disagreement between law enforcement and EMS, the EMS clinician should notify the appropriate supervisor and document all discussions. • When arriving on scene, ambulances should be parked to allow safe and rapid access to the patient, where possible, without being on the immediate crime scene. • Gloves should be worn at all times. • Use the minimum number of clinicians needed. • Use the same route to get to and from the patient; avoid walking through fluids and other debris. • Try not to disturb physical evidence.

• Do not move or touch anything unless necessary to do so for patient care. • When it is necessary to move something, document it and notify law enforcement officials. • Do not cut through or near holes in patient clothing; they may be bullet or knife holes. • Any removed clothing and any personal articles should be left in the possession of law enforcement.

Prehospital termination of resuscitation in penetrating trauma Up to one third of all traumatic deaths occur before arrival at hospital, and prehospital traumatic cardiopulmonary arrest is associated with very poor survival (0%‐5%). Of patients who sustain traumatic cardiopulmonary arrest, isolated penetrating trauma (stab wound) to the thorax is the most salvageable subset of patients, and any signs of life at the time of EMS arrival may reflect a potential survivor if transport time to trauma center capable of resuscitative thoracotomy is less than 15 minutes. In these very specific circumstances, resuscitative thoracotomy may have up to a 25% survival rate [32]. The higher survival is seen in those patients who did not arrest until after arrival in the ED, but there can be survivors where the arrest occurred up to 15 minutes before arrival. Thus, this group of patients requires the most rapid transport with no delay on scene for additional procedures. “Futility” of prehospital medical resuscitation has been defined as a less than 1% chance of survival to hospital discharge and thus used to determine guidelines for ceasing resuscitation for nontraumatic cardiac arrest [33]. Using the literature, and a similar definition for futility, NAEMSP and ACS‐COT prepared joint guidelines for withholding resuscitation and termination of resuscitation in prehospital traumatic cardiopulmonary arrest [34]. For penetrating trauma, if the injuries are incompatible with life (decapitation, hemicorporectomy, rigor mortis, dependent lividity), or the patient is apneic, pulseless, and without organized electrocardiographic activity upon arrival of EMS, resuscitation may be withheld. Resuscitative measures can be terminated if CPR is provided up to 15 minutes

Summary Trauma is the leading cause of death between the ages of 1 and 34 years of age in North America. Those penetrating trauma patients who are alive on arrival of EMS clinicians have a better chance of survival if they are rapidly transported to a designated trauma center without interventions on scene. EMS clinicians should not be fooled by seemingly innocuous penetrating injuries. They can use their knowledge of anatomy and physiology to anticipate potential injuries and intervene en route before cardiovascular collapse or airway compromise.

Penetrating trauma

References 1 Statistics Canada. Deaths and Mortality Rate. 2017. Available at: www.statcan.gc.ca. Accessed August 3, 2020. 2 Centers for Disease Control and Prevention, National Center for Health Statistics. 2017. Available at: https://www.cdc.gov/nchs/ data/hus/hus17.pdf. Accessed August 3, 2020. 3 American College of Surgeons Committee on Trauma. Advanced Trauma Life Support For Doctors. 6th ed. Chicago: American College of Surgeons, 1997. 4 Ordog G, Wasserberger J, Balasubramanium S. Wound ballistics: theory and practice. Ann Emerg Med. 1984; 13:1113–22. 5 Vanderlan WB, Tew BE, McSwain NE. Increased risk of death with cervical spine immobilisation in penetrating cervical trauma. Injury. 2009; 40:880–3. 6 Haut ER, Kalish BT, Efron DT, et al. Spine immobilization in penetrating trauma: more harm than good? J Trauma. 2010; 68:115–20. 7 Velopulos CG, Shihab HM, Lottenberg L, et al. Prehospital spine immobilization/spinal motion restriction in penetrating trauma: a practice management guideline from the Eastern Association for the Surgery of Trauma (EAST). J Trauma Acute Care Surg. 2018; 84:736–44. 8 Brown JB, Bankey PE, Sangosanya AT, Cheng JD, Stassen NA, Gestring ML. Prehospital spinal immobilization does not appear to be beneficial and may complicate care following gunshot injury to the torso. J Trauma. 2009; 67:774–8. 9 Garcia A, Liu TH, Victorino GP. Cost‐utility analysis of prehospital spine immobilization recommendations for penetrating trauma. J Trauma Acute Care Surg. 2014; 76:534–41. 10 Rhee P, Kuncir EJ, Johnson L, et al. Cervical spine injury is highly dependent on the mechanism of injury following blunt and penetrating assault. J Trauma. 2006; 61:1166–70. 11 Fischer PE, Perina DG, Delbridge TR, et  al. Spinal motion restriction in the trauma –a joint position statement. Prehosp Emerg Care. 2018; 22:659–61. 12 Kaups KL, Davis JW. Patients with gunshot wounds to the head do not require cervical spine immobilization and evaluation. J Trauma. 1998; 44:865–7. 13 Committee of Tactical Combat Casualty Care Guidelines for Medical Personnel. [Internet]. USA Department of Defense, Joint Trauma System; 2018. [cited July 31, 2020]. Available from: https://www. deployedmedicine.com/market/11/content/40 14 Lee C, Porter K, Hodgetts T. Tourniquet use in the civilian prehospital setting. J Emerg Med. 2007; 24:584–7. 15 Beaucreux C, Vivien B, Miles E, Ausset S, Pasquier P. Application of tourniquet in civilian trauma: systematic review of the literature. Anaesth Crit Care Pain Med. 2018; 37:597–606. 16 Eastridge BJ, Mabry RL, Seguin P, et  al. Death on the battlefield (2001‐2011): implications for the future of combat casualty care. J Trauma Acute Care Surg. 2012; 73:S431–7. 17 Walls RM, Zinner MJ. The Boston Marathon response: why did it work so well? JAMA. 2013; 309:2441–42. 18 Bickell W, Wall M, Pepe P, et  al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med. 1994; 331:1105–9. 19 Tran A, Yates J, Lau A, Lampron J, Matar M. Permissive hypotension versus conventional resuscitation strategies in adult trauma

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patients with hemorrhagic shock: a systematic review and meta‐ analysis of randomized controlled trials. J Trauma Acute Care Surg. 2018; 84:802–8. 20 CRASH‐2 trial collaborators, Shakur H, Roberts I, et  al. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH‐2): a randomised, placebo‐controlled trial. Lancet. 2010; 376:23–32. 21 CRASH‐2 collaborators, Roberts I, Shakur H, et  al. The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH‐2 randomised controlled trial. Lancet. 2011; 377:1096–1101. 22 Morrison JJ, Dubose JJ, Rasmussen TE, Midwinter MJ. Military Application of Tranexamic Acid in Trauma Emergency Resuscitation (MATTERs) Study. Arch Surg. 2012; 147:113–9. 23 CRASH‐3 trial collaborators. Effects of tranexamic acid on death, disability, vascular occlusive events and other morbidities in patients with acute traumatic brain injury (CRASH‐3): a randomised, placebo‐controlled trial. Lancet. 2019; 394: 1713–23. 24 May S, Schreiber M. Prehospital tranexamic acid use for traumatic brain injury. Clinicaltrials.gov: NCT01990768. Available at: https:// clinicaltrials.gov/ct2/show/results/NCT01990768?view=results. Accessed November 10, 2020. 25 Fischer PE, Bulger EM, Perina DG, et al. Guidance document for the prehospital use of tranexamic acid in injured patients. Prehosp Emerg Care. 2016; 20:557–9. 26 Brenner M, Inaba K, Aiolfi A, et  al. Resuscitative endovascular balloon occlusion of the aorta and resuscitative thoracotomy in select patients with hemorrhagic shock. J Am Coll Surg. 2018; 226:730–40. 27 Seamon M, Fisher C, Gaughan J. Prehospital procedures before emergency department thoracotomy: “scoop and run” saves lives. J Trauma. 2007; 63:113–20. 28 Seamon MJ, Haut ER, Van Arendonk K, et al. An evidence‐based approach to patient selection for emergency department thoracotomy: a practice management guideline from the Eastern Association for the Surgery of Trauma. J Trauma Acute Care Surg. 2015; 79:159–73. 29 Nagy K, Lohmann C, Kim D, Barrett J. Role of echocardiography in the diagnosis of occult penetrating cardiac injury. J Trauma. 1995; 38:859–62. 30 Kim JS, Inaba K, de Leon LA, et al. Penetrating injury to the cardiac box. J Trauma Acute Care Surg. 2020; 89:482–7. 31 Small Arms Survey. Civilian Firearms Holdings, 2017. Available at: www.smallarmssurvey.org. Accessed August 3, 2020. 32 Owen JJ, Sne N, Coates A, Channan PK. Outcomes of emergency department thoracotomy in a tertiary care Canadian trauma centre. CJEM. 2015; 17:353–8. 33 Morrison L, Visentin L, Kiss A, et al. Validation of a rule for termination of resuscitation in out‐of‐hospital cardiac arrest. N Engl J Med. 2006; 355:478–87. 34 Millin MG, Galvagno SM, Khandker SR, et  al. Withholding and termination of resuscitation of adult cardiopulmonary arrest secondary to trauma: resource document to the joint NAEMSP‐ ACSCOT position statements. J Trauma Acute Care Surg. 2013; 75:459–67.

CHAPTER 30

Traumatic Brain Injury Anjni Joiner

Introduction In 2014, an estimated 2.87 million people presented to an emergency department (ED), were hospitalized, or died as a result of a traumatic brain injury (TBI) in the United States [1]. TBI represents a significant health care burden. Hospitalizations for TBI tend to be 74% costlier, an average of 2 days longer, and carry an in‐hospital mortality rate four times higher than hospitalizations with non‐TBI diagnoses [2]. Unintentional falls comprise nearly half of all ED visits for TBI, followed by unintentional head trauma from an object (17.1%) and motor vehicle collisions (13.2%) [1]. Males represent a higher proportion of those affected by TBI in nearly all categories [2, 3]. Older adults represent the largest burden of TBI‐related ED visits and hospitalizations and are more likely to die from head injuries, with the highest rates of death in individuals greater than 75 years of age at 78.5 deaths per 100,000 persons, followed by those between 65 and 74 years of age at 24.7/100,000 [1]. Those who reside in low‐income communities tend to have disproportionately higher rates of ED visits for TBI [2]. TBI can be categorized into primary and secondary. Primary brain injury occurs with an initial insult from a direct impact, acceleration/deceleration injury, or penetrating wound resulting in bleeding, contusion, and ultimately cell death. Primary prevention focuses on efforts to prevent the initial injury. These can include policy changes and educational campaigns to increase the use of helmets, seatbelts, car seats for children, and efforts to reduce falls in the elderly [4, 5]. Once the primary brain injury has occurred, reversal of the insult is impossible. Prevention of secondary brain injury is the goal of therapeutic intervention. Secondary brain injury occurs over hours to days after the initial injury, with multiple cellular, vascular, and molecular changes resulting in further edema and cell death. Treatment must start with initial management on scene. Aggressive treatment of severe head injury patients has been

shown to be cost‐effective, with an increase in quality‐adjusted life years when all costs are considered [6]. Adherence to evidence‐based clinical practice guidelines addressing prehospital management of TBI should be considered. Statewide implementation of prehospital TBI clinical practice guidelines in Arizona demonstrated a doubling in adjusted survival to discharge in severe TBI patients and tripling in intubated severe TBI patients [7]. Hypotension, hypoxia, and hyperventilation are independently associated with increased mortality and poorer neurologic outcomes [6, 8–21]. When hypotension and hypoxia occur together, the combined effects result in worse outcomes than the sum of both individually [9]. Management of TBI is focused on transport to a trauma center while preventing secondary brain injury. A review of a few physiologic concepts is necessary for EMS clinicians to understand how to prevent secondary brain injury. Cerebral perfusion pressure (CPP) is equal to the mean arterial pressure (MAP) minus the intracranial pressure (ICP). Measuring an accurate MAP in the prehospital setting may be difficult, making the systolic blood pressure a surrogate that has been used in published guidelines and research [22]. In severe TBI, the normal autoregulatory processes are disrupted, resulting in inadequate compensation for changes in CPP. This can result in a rapid rise in ICP causing compression of the brain within an enclosed space (skull). This is known as the Monroe‐Kellie doctrine. As the pressure increases, the brain can be pushed downward, herniating in several possible directions. This herniation can cause compression of several critical areas of the brain, resulting in posturing, changes in respiration, paralysis, and sudden death. Additionally, changes in the partial pressure of oxygen (PaO2) and carbon dioxide (PaCO2) can cause constriction and dilation of cerebral blood vessels [23]. Thus, maintaining adequate MAP and prevention of hypotension, hypoxia, hypo‐ and hyperventilation are critical to preventing secondary brain injury.

Emergency Medical Services: Clinical Practice and Systems Oversight, Third Edition. Volume 1: Clinical Aspects of EMS. Edited by David C. Cone, Jane H. Brice, Theodore R. Delbridge, and J. Brent Myers. © 2021 NAEMSP. Published 2021 by John Wiley & Sons, Inc.

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Primary assessment The initial management of all injured patients should begin with assessment of airway, breathing, and circulation. Current consensus guidelines suggest that adult patients with a Glasgow Coma Scale (GCS) score ≤8, those unable to maintain an adequate airway, or those who remain hypoxic despite supplemental oxygen should have a secure airway placed [22]. Endotracheal intubation in pediatric TBI patients does not improve survival or neurologic outcomes compared to bag‐valve‐mask ventilation [24, 25]. All patients should undergo monitoring of oxygenation with continuous pulse oximetry, and supplemental oxygen should be applied to avoid hypoxemia (SpO2 < 90) [22]. Continuous capnography should be used to ensure adequate ventilation by maintaining an end‐tidal CO2 between 35 and 40 mmHg [22]. Hyperventilation (end‐tidal CO2 < 35 mmHg) should be avoided unless there are signs of cerebral herniation [10, 19, 22]. Maintaining adequate circulation is critical in the head‐injured patient. A single episode of hypotension, defined as a systolic blood pressure < 90 mmHg, has been associated with increased morbidity and a doubling in mortality [9]. Intravenous fluids should be administered to maintain a systolic blood pressure of at least 90 mmHg in adults [17, 18, 22]. Isotonic crystalloid is recommended in both adults and children [22]. For children, fluid resuscitation should be aimed at maintaining age‐appropriate blood pressure or for clinical signs of hypoperfusion [22]. Alterations in mental status due to hypoglycemia can easily be mistaken for those related to TBI. Patients with altered mental status should have a fingerstick glucose checked in the prehospital setting.

Secondary assessment Performing an efficient neurologic assessment is essential in the triage and management of brain‐injured patients. EMS clinicians will need to repeat and reassess a patient’s neurologic status frequently as it can change rapidly. The GCS was first introduced in 1974 by Teasdale and Jennett as a way to quickly assess the neurologic status of patients with a wide variety of neurologic and neurosurgical problems (Table 30.1) [26]. The GCS has been widely adopted as a reliable tool to categorize head injury severity [27]. Studies have also demonstrated the prognostic value of the scale to predict the need for trauma team activation, hospitalization, and outcomes [28, 29]. A GCS score of 14‐15 corresponds to a mild TBI, 9‐13 is classified as a moderate TBI, and 8 or less as severe (Table 30.2). The GCS should not be used as a static number, and prehospital clinicians must frequently reevaluate neurologic status for improvement or deterioration. A decrease of two or more points suggests significant neurologic deterioration. A recent National Trauma Data Bank study of 250,000 head‐injured patients found that 9% of these patients experienced prehospital neurologic deterioration, defined as a decrease in two or more points in

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Table 30.1  Glasgow Coma Scale Eye opening

Verbal response

4–spontaneous

5–oriented 4–confused

3–to speech 2–to pain

3–inappropriate 2–incomprehensible

1–none

1–none

Motor response 6–obeys commands 5–localizes pain 4–withdraws to pain 3–flexor posturing 2–extensor posturing 1–none

Table 30.2  Severity of head injury based on GCS Head injury severity

Glasgow Coma Scale

Mild Moderate Severe

14–15 9–13 3–8

GCS from EMS to the ED measurement [30]. This patient subgroup had higher in‐hospital mortality even after adjusting for type of injury and presence of intracranial hemorrhage. Patients with measurable decline in mental status represent high‐risk patients, and their initial care and evaluation should reflect the seriousness of this clinical finding [30]. Alternate scores measuring neurologic status in TBI include the pediatric GCS (pGCS) (Table 30.3), AVPU score, and Simplified Motor Scale (SMS). AVPU is a four‐point scale where the patient is assigned a letter corresponding to their level of alertness (A, Alert; V, responsive to Verbal stimuli; P, responsive to Painful stimuli; U, Unresponsive). The SMS gives only one score: 2 = obeys commands, 1 = localizes to pain, 0 = withdraws to pain or worse. AVPU and the SMS scale have been touted for their simplicity of use in comparison with the GCS and pGCS. Comparison of the interrater reliability between emergency physicians using GCS, AVPU, and SMS in adult trauma and nontrauma patients found that the SMS had the best interrater reliability [31]. A recent evaluation of AVPU in a prehospital pediatric population demonstrated correlation between pGCS scores of 15 and 3 with AVPU categories of A and U, respectively, and correlated a V score with a pGCS of 8 or above [32]. SMS in a prehospital setting has been shown to be similar to the traditional GCS in adult and pediatric TBI patients in predicting outcomes [33]. Current Brain Trauma Foundation guidelines recommend using the GCS in the prehospital setting [22]. Pupils must be evaluated for equality and reactivity to light after stabilization of the patient. Asymmetry is defined as a difference in diameter of greater than 1 mm, and a fixed pupil is defined as less than 1 mm response to bright light [22]. Unilateral pupillary dilatation with decreased reactivity is a sign of increased ICP and may indicate uncal herniation causing compression of the ipsilateral third cranial nerve or

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Table 30.3  Pediatric Glasgow Coma Scale (for nonverbal children) Eye opening

4–spontaneous 3–to speech 2–to pain 1–none

Verbal response

Motor response

5–coos, babbles 4–irritable crying 3–cries to pain 2–moans to pain 1–none

6–normal spontaneous movement 5–withdraws from touch 4–withdraws to pain 3–abnormal flexion 2–abnormal extension 1–none

brain stem ischemia. The eye and orbit should be assessed for signs of direct trauma. Bilateral pupillary dilatation is more likely to be due to a metabolic or toxic cause, but if secondary to trauma, is a poor predictor, with mortality reported at 60% [34, 35]. Other Assessment Considerations Drug and alcohol intoxication result in higher rates of traumatic injury, including head injuries. It is estimated that between 37% and 51% of adult patients who sustain TBI are intoxicated at the time of injury [36]. Intoxicated patients may be agitated or excessively sedated, making initial evaluation difficult. Alcohol intoxication can result in assigning an initial lower GCS score, which increases over time [37, 38]. Safety precautions may prompt the use of chemical sedation with benzodiazepines, opioids, or antipsychotics. It is preferable to over‐triage potentially intoxicated patients to higher levels of care and assume that their changes in consciousness are related to brain injury and not intoxicants alone. Only with time and serial examinations can alterations in mentation be ascribed solely to alcohol or drugs. Anticoagulant and antiplatelet therapies are commonly used for a variety of medical conditions. Medications that affect platelet function (aspirin), platelet aggregation (clopidogrel), coagulation (warfarin), thrombin (dabigatran), and factor Xa inhibition (apixaban, rivaroxaban) increase the risk of intracranial hemorrhage after trauma. EMS clinicians should inquire about the use of “blood thinners,” and these patients should be treated with a high degree of concern for intracranial bleeding, even in cases of mild head injury. Such a patient should be preferentially transported to a trauma center or a hospital capable of rapid evaluation and management [39]. Penetrating head injuries can be from missiles or impaled objects. Impaled objects should be left in place during transport as these objects will likely need to be removed in a surgical setting. A majority of TBI‐related deaths are due to self‐harm, with 86.9% of these deaths in males and 96.9% of those cases involving firearms [3]. The prognosis for penetrating head injuries is quite variable. Approximately two thirds of patients die prior to hospital arrival [40]. Poor prognostic indicators for those who arrive alive at the hospital include a low GCS on presentation, hypotension, ICP greater than 20 mmHg, bilateral hemisphere or posterior fossa involvement, and bilaterally nonreactive pupils [40, 41].

Prehospital intubation Endotracheal intubation helps prevent both hypoxia and aspiration in severely head‐injured patients. However, prehospital endotracheal intubation for TBI remains controversial, and supporting evidence in both adults and pediatrics is lacking. A randomized trial of bag‐valve‐mask ventilation versus intubation in all children requiring prehospital airway management in Los Angeles County showed no difference in survival or neurological outcomes [24]. When looking specifically at head‐ injured children, there was again no difference in outcome [24]. This remains the best clinical study to date; however, it was performed in children in an urban EMS system, making generalizability to adult or nonurban settings questionable. However, these findings are consistent in other studies and match current guideline recommendations [25, 42, 43]. The majority of studies in adult populations have also demonstrated increased mortality or poor outcomes in TBI patients intubated in prehospital settings, although often only those with the most severe injuries are intubated, thus likely resulting in some selection bias [42, 44–48]. Primary factors contributing to mortality are failed intubations and hyperventilation after successful intubation [49]. A Cochrane review article from 2008 suggests that there is no evidence for prehospital intubation in urban ground transport systems [50]. The Brain Trauma Foundation recommends that EMS systems develop specific protocols that include monitoring of oxygen saturation, blood pressure, and end‐tidal CO2 when possible, prior to EMS intubation [22]. Successful intubation is more likely to occur in systems with extensive training, close monitoring, and specialized paramedics [51]. For example, a randomized trial from Australia restricting intubation with end‐tidal CO2 monitoring to highly trained prehospital specialists when transport times were over 10 minutes reported a 97% intubation success rate, with no differences in the primary study outcome of extended Glasgow Outcome Scale at 6 months, but improved neurologic outcomes at 6 months and no increase in mortality [52]. An analysis of the Resuscitation Outcomes Consortium data of 1,555 trauma patients with GCS ≤ 8 demonstrated higher mortality for those in whom intubation was attempted; however, those participating sites that had higher rates of attempted intubation had lower adjusted mortality [48]. This suggests that increased clinician familiarity and experience may contribute to improved success rates of intubation and outcomes. The decision to include prehospital intubation for TBI should be determined at a local level after consideration of multiple factors, including transportation time, local infrastructure, and available training and resources. Routine hyperventilation to decrease intracranial pressure is no longer recommended for severely head‐injured patients after intubation. While hyperventilation does decrease intracranial pressure, it also decreases cerebral blood flow due to cerebral vasoconstriction, leading to decreased oxygenation of the brain. An end‐tidal CO2 of 35‐40 mmHg is recommended for intubated head‐injured patients [22]. Unfortunately, inadvertent hyperventilation occurs

Traumatic Brain Injury

in as many as 70% of cases, perhaps due to unintentional clinician actions or confusion over prior hyperventilation recommendations [53]. Continuous capnography is recommended and has been shown to reduce hyperventilation [19]. Hyperventilation for a goal end‐tidal CO2 of 30‐35 mmHg is indicated as a temporizing measure for signs of cerebral herniation, including dilated and unreactive pupils, asymmetric pupils, a motor exam that identifies either extensor posturing or no response, or decrease in GCS score by 2 points or more [22]. Prolonged hyperventilation can decrease cerebral perfusion and cause ischemia.

Additional treatments Mannitol is widely used in the hospital setting to reduce intracranial pressure, which may reduce relative risk of death. There is currently insufficient evidence to recommend the use of mannitol in the prehospital setting [22, 54]. In a randomized controlled study by Bulger et  al., prehospital use of hypertonic saline following severe TBI showed no improved neurologic outcomes at 6 months nor change in 28‐day survival in patients who were not in shock [55]. Current Brain Trauma Foundation recommendations include normal saline for volume resuscitation to maintain adequate blood pressure, defined as systolic blood pressure greater than 90 mmHg and hypertonic fluid as an “option” for patients with a GCS < 8 [22]. The administration of albumin has been shown to worsen outcome in patients with TBI, therefore its use is not recommended [56]. Steroids have been shown to increase the risk of death and are no longer recommended or widely used in head‐ injured patients [57]. Seizures resulting from brain injury place excessive metabolic strain on an already injured brain and should be treated quickly to prevent further hypoxic insult. The risk of post–head injury seizures is noted to be higher in younger children [58]. There does not appear to be any evidence to support the prophylactic treatment of seizures in head‐injured patients in the prehospital setting. The adoption of therapeutic hypothermia in the context of post–cardiac arrest care has led to research in the use of therapeutic hypothermia in severely brain‐injured patients [59]. To date, the effectiveness of therapeutic hypothermia for head injury has largely been inconclusive [60, 61]. Some have argued that hypothermia treatment has not been initiated early enough in prior trials, and that a difference in outcome may be noticeable if cooling is started closer in time to the injury [62]. There are no randomized controlled studies to support the use of prehospital therapeutic hypothermia in brain‐injured patients.

Concussion and Sports‐Related Head Injuries Concussions, a form of mild TBI, frequently occur at sports events. An estimated 1.6 to 3.8 million sports‐related concussions occur annually in the United States [63]. Football remains

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the high school sport with the highest rate of concussion, followed by girls’ soccer and boys’ ice hockey [64]. EMS clinicians often provide medical coverage at athletic events and are among the first to evaluate sports‐related head injuries. Concussions are not just limited to sports‐related injuries, and should be considered in all closed head injuries. Concussion is a self‐limited disruption of normal brain function. It is a clinical diagnosis based on presentation and symptoms and may or may not present with a loss of consciousness. Symptoms can include headaches, nausea, dizziness, fatigue, vision changes, irritability, and confusion [65]. Given the heterogeneity of case definitions for mild TBI, the World Health Organization Collaborating Center Task Force on mild TBI recommends a standardized case definition of “an acute brain injury resulting from mechanical energy to the head from external physical forces including 1) 1 or more of the following: confusion or disorientation, loss of consciousness for 30 minutes or less, post‐traumatic amnesia for less than 24 hours, and/or other transient neurological abnormalities such as focal signs, symptoms, or seizure; 2) Glasgow Coma Scale score of 13‐15 after 30 minutes post‐injury or later upon presentation for healthcare” [66, 67]. The diagnosis of concussion remains challenging due to delayed timing, the nonspecific nature of symptoms, and reliance on self‐reported symptoms [65]. The American Medical Society for Sports Medicine recommends a standardized approach to evaluating a possible sports‐related concussion [65]. The Concussion in Sport Group endorses the use of the Sport Concussion Assessment Tool 5 (SCAT5) and Child SCAT5 for use by health care professionals and the Concussion Recognition Tool 5 (CRT5) for use in nonmedically trained individuals [68–70]. The validity of these tools with EMS clinicians has not been evaluated and will require appropriate training prior to implementation. Additionally, comparison with baseline scores may not always be available and should be considered. All patients with suspected concussion should be removed from activities and undergo evaluation by trained medical professionals. Athletes who sustain head injuries should not return to play that day. Patients with symptoms such as altered mental status, concern for spinal cord injury, neurologic deficits, recurrent vomiting, retrograde amnesia, and prolonged loss of consciousness should be transported to an ED [65].

Pediatrics Prehospital concepts for pediatric TBI are similar to those in adults; however, there are some important physiological differences. Children’s heads are larger than adults, they have a smaller subarachnoid space compared to adults, and they have thinner skulls. Because of these factors, children are more susceptible to TBI. Pediatric patients are also more prone to brain edema, with more diffuse axonal injuries than primary bleeding or brain contusions [71]. Skull fractures have a significantly

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higher rate of intracranial pathology compared to adults, along with a much higher rate of seizures. Nonaccidental trauma must also be considered in pediatric head injuries, especially with injury patterns that do not match the history given by caregivers, or if there are other concerning injuries such as multiple bruises or old, unexplained fractures found on exam or imaging. The presence of TBI in infants should heighten suspicion for abusive head trauma as younger children are disproportionately affected [72]. Prevention The frequency and severity of TBI can be reduced through preventive efforts. EMS clinicians can identify potential hazards or risk‐taking behaviors as they are usually the only health care personnel to enter a patient’s living environment or witness the scene of a traumatic event. This allows the clinician to either directly educate the patient and family or relate appropriate observations to ED staff when the patient is transported to the hospital. Many EMS systems are involved in fall prevention programs for high‐risk populations. These programs typically involve a multifactorial approach in identifying the primary etiologies contributing to fall risk and include connecting participants with community or hospital‐based resources. Firearms in the home should be kept unloaded in secure, locked containers or cabinets, with ammunition stored in a different location. Appropriate protective equipment including a helmet should be worn whenever riding any wheeled device or when engaging in contact sports. Seatbelts should always be used by adults and appropriately sized child safety and booster seats should always be used by children riding in vehicles.

Transportation and Destination Decisions Appropriate transportation decisions are critical in ensuring that TBI patients receive the correct level of care. An evaluation of a statewide trauma database demonstrated a 50% increase in mortality for severe TBI patients who were indirectly transferred to Level I or Level II trauma centers [73]. Current Brain Trauma Foundation guidelines recommend: 1) the development of destination protocols for severe TBI patients; 2) transport of severe TBI patients to neurosurgical capable hospitals with CT scanners and the ability to monitor ICP; and 3) choosing the transport modality that will most likely reduce prehospital time [22]. These recommendations are also reflected in the CDC Guidelines for Field Triage of Injured Patients, which state that patients with moderate or severe TBI (GCS 13 or less) should be directly transported to trauma centers that are fully equipped and staffed to manage acute neurosurgical emergencies [39]. Patients classified as mild TBI (GCS 14 or 15) can generally be transported to other facilities based on established destination protocols, assuming other injuries do not require trauma center care [39].

Extremes of age and pregnancy should also be considered. If available, pediatric patients should preferentially be taken to pediatric trauma centers or Level I or Level II adult trauma centers capable of treating children [22]. A retrospective evaluation of trauma databases suggested that transporting elderly TBI patients (>70 years) with GCS 14 directly to trauma centers may reduce this group’s higher morbidity and mortality [74]. Older adults with low mechanism injuries are at higher risk of occult injuries, and transportation to trauma centers or hospitals capable of timely evaluation should be considered for these patients [39].

Summary TBI remains a leading cause of disability and death. Injury prevention through public health initiatives such as seatbelts and helmets are the mainstays of TBI prevention. Prehospital adherence to standardized clinical practice guidelines improves survival in severe TBI patients. Prehospital care is focused on prevention of secondary brain injury by optimizing delivery of blood and oxygen and avoiding further insult to the brain. Preventing hypotension and hypoxia and ensuring appropriate ventilation is critical. Crystalloid fluids should be used to maintain a systolic blood pressure of 90 mmHg. Supplemental oxygen should be given to maintain oxygen saturation greater than 90%. Prehospital intubation in both adults and pediatrics is controversial. When performed, it should be undertaken by experienced clinicians in systems that are well‐resourced. Any patient with an advanced airway should be monitored closely with continuous pulse oximetry and capnography with a goal end‐tidal CO2 of 35‐40 mmHg. ­Clinicians should avoid hyperventilation as this is associated with increased mortality. The GCS is the primary tool to assess neurologic status in TBI patients and can change rapidly in a patient with TBI. Mental status should be reassessed continually as those who have precipitous deteriorations in mental status have increased morbidity and mortality. Drug and alcohol intoxication result in higher rates of TBI and may falsely lower initial GCS. Over‐­ triage in these patients is appropriate as a head injury cannot be immediately ruled out. Concussion is a clinical diagnosis complicated by nonspecific and self‐reported symptoms. Suspected sports‐related concussions should be approached with a standardized assessment. Any athlete with a suspected concussion should be removed from play and evaluated by a trained physician. Appropriate transport decisions are critical in improving outcomes from TBI. Moderate and severe TBI patients should be preferentially transported to Level I or Level II trauma centers for adults, or pediatric trauma centers for children. Acknowledgments Prior contributions to this chapter from Dr. Kraigher O’Keefe are greatly appreciated.

Traumatic Brain Injury

References 1 Centers for Disease Control and Prevention. Surveillance Report of Traumatic Brain Injury‐Related Emergency Department Visits, Hospitalizations, and Deaths—United States, 2014. Centers for Disease Control and Prevention, U.S. Department of Health and Human Services; 2019. Available from: https://www.cdc.gov/ traumaticbraininjury/pdf/TBI‐Surveillance‐Report‐508.pdf 2 Reid LD, Fingar KR. Inpatient Stays and Emergency Department Visits Involving Traumatic Brain Injury, 2017. HCUP Statistical Brief #255 [Internet]. Rockville, MD: Agency for Healthcare Research and Quality; 2020 [cited September 12, 2020]. Available from: https://hcup‐us.ahrq.gov/reports/statbriefs/sb255‐Traumatic‐ Brain‐Injury‐Hospitalizations‐ED‐Visits‐2017.jsp. 3 Taylor CA, Bell JM, Breiding MJ, Xu L. Traumatic brain i­njury–related emergency department visits, hospitalizations, and deaths—United States, 2007 and 2013. MMWR. 2017; 66:1–16. 4 Park E, Bell JD, Baker AJ. Traumatic brain injury: can the consequences be stopped? CMAJ. 2008; 178:1163–70. 5 Centers for Disease Control and Prevention. Brain Injury Safety Tips and Prevention. Available at: cdc.gov/headsup/basics/concussion_prevention.html. Accessed Sept 12, 2020. 6 Whitmore RG, Thawani JP, Grady MS, Levine JM, Sanborn MR, Stein SC. Is aggressive treatment of traumatic brain injury cost‐ effective? J Neurosurg. 2012; 116:1106–13. 7 Spaite DW, Bobrow BJ, Keim SM, et  al. Association of statewide implementation of the prehospital traumatic brain injury treatment guidelines with patient survival following traumatic brain injury: the Excellence in Prehospital Injury Care (EPIC) study. JAMA Surg. 2019; 154:e191152. 8 Yeh DD, Velmahos GC. Prehospital intubation for traumatic brain injury: do it correctly, or not at all: Perspectives. ANZ J Surg. 2012; 82:484–5. 9 Chesnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma. 1993; 34:216–22. 10 Davis DP, Dunford JV, Poste JC, et al. The impact of hypoxia and hyperventilation on outcome after paramedic rapid sequence intubation of severely head‐injured patients. J Trauma. 2004; 57:1–8. 11 Fearnside MR, Cook RJ, McDougall P, McNeil RJ. The Westmead Head Injury Project outcome in severe head injury. A comparative analysis of pre‐hospital, clinical and CT variables. Br J Neurosurg. 1993; 7:267–79. 12 Ong L, Selladurai BM, Dhillon MK, Atan M, Lye MS. The prognostic value of the Glasgow Coma Scale, hypoxia and computerised tomography in outcome prediction of pediatric head injury. Pediatr Neurosurg. 1996; 24:285–91. 13 Manley G, Knudson MM, Morabito D, Damron S, Erickson V, Pitts L. Hypotension, hypoxia, and head injury: frequency, duration, and consequences. Arch Surg. 2001; 136:1118–23. 14 Pigula FA, Wald SL, Shackford SR, Vane DW. The effect of hypotension and hypoxia on children with severe head injuries. J Pediatr Surg. 1993; 28:310–4. 15 McHugh GS, Engel DC, Butcher I, et  al. Prognostic value of secondary insults in traumatic brain injury: results from the IMPACT study. J Neurotrauma. 2007; 24:287–93. 16 Miller JD, Sweet RC, Narayan R, Becker DP. Early insults to the injured brain. JAMA. 1978; 240:439–42. 17 Gentleman D. Causes and effects of systemic complications among severely head injured patients transferred to a neurosurgical unit. Int Surg. 1992; 77:297–302.

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18 Hill DA, Abraham KJ, West RH. Factors affecting outcome in the resuscitation of severely injured patients. Aust N Z J Surg. 1993; 63:604–9. 19 Davis DP, Dunford JV, Ochs M, Park K, Hoyt DB. The use of quantitative end‐tidal capnometry to avoid inadvertent severe hyperventilation in patients with head injury after paramedic rapid sequence intubation. J Trauma. 2004; 56:808–14. 20 Manley GT, Hemphill JC, Morabito D, et  al. Cerebral oxygenation during hemorrhagic shock: perils of hyperventilation and the therapeutic potential of hypoventilation. J Trauma. 2000; 48:1025–32. 21 Gaither JB, Spaite DW, Bobrow BJ, et  al. Balancing the potential risks and benefits of out‐of‐hospital intubation in traumatic brain injury: the intubation/hyperventilation effect. Ann Emerg Med. 2012; 60:732–6. 22 Badjatia N, Carney N, Crocco TJ, et al. Guidelines for prehospital management of traumatic brain injury 2nd edition. Prehosp Emerg Care. 2008; 12:S1–52. 23 American College of Surgeons Committee on Trauma. Advanced Trauma Life Support® Student Course Manual. 10th ed. Chicago, IL: American College of Surgeons, 2018. 24 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; 283:783–90. 25 Cooper A, DiScala C, Foltin G, Tunik M, Markenson D, Welborn C. Prehospital endotracheal intubation for severe head injury in children: a reappraisal. Semin Pediatr Surg. 2001; 10:3–6. 26 Teasdale G, Jennett B. Assessment of coma and impaired consciousness. Lancet. 1974; 304:81–4. 27 Menegazzi JJ, Davis EA, Sucov AN, Paris PM. Reliability of the Glasgow Coma Scale when used by emergency physicians and paramedics. J Trauma. 1993; 34:46–8. 28 Gómez PA, Lobato RD, Ortega JM, De La Cruz J. Mild head injury: differences in prognosis among patients with a Glasgow Coma Scale score of 13 to 15 and analysis of factors associated with abnormal CT findings. Br J Neurosurg. 1996; 10:453–60. 29 Norwood SH, McAuley CE, Berne JD, Vallina VL, Creath RG, McLarty J. A prehospital Glasgow Coma Scale score < or = 14 accurately predicts the need for full trauma team activation and patient hospitalization after motor vehicle collisions. J Trauma. 2002; 53:503–7. 30 Majidi S, Siddiq F, Qureshi AI. Prehospital neurologic deterioration is independent predictor of outcome in traumatic brain injury: analysis from National Trauma Data Bank. Am J Emerg Med. 2013; 31:1215–9. 31 Gill M, Martens K, Lynch EL, Salih A, Green SM. Interrater reliability of 3 simplified neurologic scales applied to adults presenting to the emergency department with altered levels of consciousness. Ann Emerg Med. 2007; 49:4037. 32 Hoffmann F, Schmalhofer M, Lehner M, Zimatschek S, Grote V, Reiter K. Comparison of the AVPU scale and the pediatric GCS in prehospital setting. Prehosp Emerg Care. 2016; 20:493–8. 33 Thompson DO, Hurtado TR, Liao MM, Byyny RL, Gravitz C, Haukoos JS. Validation of the Simplified Motor Score in the out‐of‐ hospital setting for the prediction of outcomes after traumatic brain injury. Ann Emerg Med. 2011; 58:417–25. 34 Signorini DF, Andrews PJ, Jones PA, Wardlaw JM, Miller JD. Predicting survival using simple clinical variables: a case study in traumatic brain injury. J Neurol Neurosurg Psychiatry. 1999; 66:20–5. 35 Jiang J‐Y, Gao G‐Y, Li W‐P, Yu M‐K, Zhu C. Early indicators of prognosis in 846 cases of severe traumatic brain injury. J Neurotrauma. 2002; 19:869–74. 36 Parry‐Jones BL, Vaughan FL, Miles Cox W. Traumatic brain injury and substance misuse: a systematic review of prevalence

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and outcomes research (1994–2004). Neuropsychol Rehabil. 2006; 16:537–60. 37 Shahin H, Gopinath SP, Robertson CS. Influence of alcohol on early Glasgow Coma Scale in head‐injured patients. J Trauma. 2010; 69:1176–81. 38 Uccella L, Bongetta D, Fumagalli L, Raffa G, Zoia C. Acute alcohol intoxication as a confounding factor for mild traumatic brain injury. Neurol Sci. 2020; 41:2127–34. 39 Sasser SM, Hunt RC, Faul M, et  al. Guidelines for field triage of injured patients: recommendations of the National Expert Panel on Field Triage, 2011. MMWR. 2012; 61:1–20. 40 Blissitt PA. Care of the critically ill patient with penetrating head injury. Crit Care Nurs Clin North Am. 2006; 18:321–32. 41 Gressot LV, Chamoun RB, Patel AJ, et  al. Predictors of outcome in civilians with gunshot wounds to the head upon presentation. J Neurosurg. 2014; 121:645–52. 42 Murray JA, Demetriades D, Berne TV, et  al. Prehospital intubation in patients with severe head injury. J Trauma. 2000; 49:1065–70. 43 Adelson PD, Bratton SL, Carney NA, et  al. Guidelines for the acute medical management of severe traumatic brain injury in infants, children, and adolescents. Chapter  3. Prehospital airway management. Pediatr Crit Care Med. 2003; 4:S9–11. 44 Davis DP, Hoyt DB, Ochs M, et al. The effect of paramedic rapid sequence intubation on outcome in patients with severe traumatic brain injury. J Trauma. 2003; 54:444–53. 45 Stockinger ZT, McSwain NE. Prehospital endotracheal intubation for trauma does not improve survival over bag‐valve‐mask ventilation. J Trauma. 2004; 56:531–6. 46 Wang HE, Peitzman AB, Cassidy LD, Adelson PD, Yealy DM. Out‐ of‐hospital endotracheal intubation and outcome after traumatic brain injury. Ann Emerg Med. 2004; 44:439–50. 47 Davis DP, Peay J, Sise MJ, et al. The impact of prehospital endotracheal intubation on outcome in moderate to severe traumatic brain injury. J Trauma. 2005; 58:933–9. 48 Davis DP, Koprowicz KM, Newgard CD, et  al. The relationship between out‐of‐hospital airway management and outcome among trauma patients with Glasgow Coma Scale scores of 8 or less. Prehosp Emerg Care. 2011; 15:184–92. 49 Davis DP, Stern J, Sise MJ, Hoyt DB. A follow‐up analysis of factors associated with head‐injury mortality after paramedic rapid sequence intubation. J Trauma. 2005; 59:486–90. 50 Lecky F, Bryden D, Little R, Tong N, Moulton C. Emergency intubation for acutely ill and injured patients. Cochrane Database Syst Rev. 2008; 2:CD001429. 51 Pepe PE, Roppolo LP, Fowler RL. Prehospital endotracheal intubation: elemental or detrimental? Crit Care. 2015; 19:121. 52 Bernard SA, Nguyen V, Cameron P, et al. Prehospital rapid sequence intubation improves functional outcome for patients with severe traumatic brain injury: a randomized controlled trial. Ann Surg. 2010; 252:959–65. 53 Thomas SH, Orf J, Wedel SK, Conn AK. Hyperventilation in traumatic brain injury patients: inconsistency between consensus guidelines and clinical practice. J Trauma. 2002; 52:47–52. 54 Wakai A, McCabe A, Roberts I, Schierhout G. Mannitol for acute traumatic brain injury. Cochrane Database Syst Rev. 2013; 8:CD001049. 55 Bulger EM, May S, Brasel KJ, et  al. Out‐of‐hospital hypertonic resuscitation following severe traumatic brain injury: a randomized controlled trial. JAMA. 2010; 304:1455–64.

56 SAFE Study Investigators, Australian and New Zealand Intensive Care Society Clinical Trials Group, Australian Red Cross Blood Service, et al. Saline or albumin for fluid resuscitation in patients with traumatic brain injury. N Engl J Med. 2007; 357:874–84. 57 Roberts I, Yates D, Sandercock P, et al. Effect of intravenous corticosteroids on death within 14 days in 10008 adults with clinically significant head injury (MRC CRASH trial): randomised placebo‐ controlled trial. Lancet. 2004; 364:1321–8. 58 Bennett KS, DeWitt PE, Harlaar N, Bennett TD. Seizures in children with severe traumatic brain injury. Pediatr Crit Care Med. 2017; 18:54–63. 59 Sagalyn E, Band RA, Gaieski DF, Abella BS. Therapeutic hypothermia after cardiac arrest in clinical practice: review and compilation of recent experiences. Crit Care Med. 2009; 37:S223–6. 60 Farag E, Manno EM, Kurz A. Use of hypothermia for traumatic brain injury: point of view. Minerva Anestesiol. 2011; 77:366–70. 61 Dunkley S, McLeod A. Therapeutic hypothermia in patients following traumatic brain injury: a systematic review. Nurs Crit Care. 2017; 22:150–60. 62 Boer C, Franschman G, Loer SA. Prehospital management of severe traumatic brain injury: concepts and ongoing controversies. Curr Opin Anaesthesiol. 2012; 25:556–62. 63 Langlois JA, Rutland‐Brown W, Wald MM. The epidemiology and impact of traumatic brain injury: a brief overview. J Head Trauma Rehabil. 2006; 21:375–8. 64 Kerr ZY, Chandran A, Nedimyer AK, Arakkal A, Pierpoint LA, Zuckerman SL. Concussion incidence and trends in 20 high school sports. Pediatrics. 2019; 144:e20192180. 65 Harmon KG, Clugston JR, Dec K, et al. American Medical Society for Sports Medicine position statement on concussion in sport. Br J Sports Med. 2019; 53:213–25. 66 Lumba‐Brown A, Yeates KO, Sarmiento K, et al. Centers for Disease Control and Prevention guideline on the diagnosis and management of mild traumatic brain injury among children. JAMA Pediatr. 2018; 172:e182853. 67 Carroll LJ, Cassidy JD, Holm L, Kraus J, Coronado VG, WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury. Methodological issues and research recommendations for mild traumatic brain injury: the WHO Collaborating Centre Task Force on Mild Traumatic Brain Injury. J Rehabil Med. 2004; 43:113–25. 68 Echemendia RJ, Meeuwisse W, McCrory P, et al. The Sport Concussion Assessment Tool, 5th Ed. (SCAT5): background and rationale. Br J Sports Med. 2017; 51:848–50. 69 Davis GA, Purcell L, Schneider KJ, et al. The Child Sport Concussion Assessment Tool, 5th Ed. (Child SCAT5): background and rationale. Br J Sports Med. 2017; 51:859–61. 70 Echemendia RJ, Meeuwisse W, McCrory P, et al. The Concussion Recognition Tool, 5th Ed. (CRT5): background and rationale. Br J Sports Med. 2017; 51:870–1. 71 Vavilala MonicaS, Kannan N, Ramaiah R. Pediatric neurotrauma. Int J Crit Illn Inj Sci. 2014; 4:130. 72 Keenan HT. A population‐based study of inflicted traumatic brain injury in young children. JAMA. 2003; 290:621. 73 Härtl R, Gerber LM, Iacono L, Ni Q, Lyons K, Ghajar J. Direct transport within an organized state trauma system reduces mortality in patients with severe traumatic brain injury. J Trauma. 2006; 60:1250–6. 74 Caterino JM, Raubenolt A, Cudnik MT. Modification of Glasgow Coma Scale criteria for injured elders. Acad Emerg Med. 2011; 18:1014–21.

CHAPTER 31

Electrical injuries Jeffrey Lubin

Introduction Injuries from electricity can vary widely from minor cutaneous burns to life‐threatening internal damage or death. Severe electrical injuries are thought to be relatively uncommon. However, because many electrical accidents go unreported, the true incidence is unknown. In addition, many electrocution victims fall from heights, present with arrhythmias, or are simply found dead, so the significance, and even the occurrence, of an electric shock may be unknown. The data that are available suggest that electrical injuries follow a bimodal age distribution. About 20% of all electrical injuries occur in children. Toddlers generally sustain electrical injuries from household electrical outlets and cords while adolescents tend to sustain high‐voltage injuries during outdoor risk‐taking behavior such as climbing electrical transformer towers [1]. The second peak occurs in adults who work with or around electricity for a living, such as miners, construction workers, and electrical utility workers [2]. Most estimates place the annual death rate from electrical injury at 1,000 to 1,500 per year, with more than 60% occurring in patients aged 15 to 40. Electrocutions at home account for more than 200 deaths per year and are mostly associated with malfunctioning or misused consumer products [3]. The National Electronic Injury Surveillance System from the Consumer Product Safety Commission estimates that U.S. EDs treated almost 102,000 patients for product‐related electrical shocks from 2000 to 2019 [4]. The majority of these incidents were minor, resulting in ED evaluation and subsequent discharge. According to data compiled by the Electrical Safety Foundation International using data from the U.S. Bureau of Labor Statistics, Census of Fatal Occupational Injuries, from 2003 through 2018 there were 2,948 workers who died on the job due to contact with or exposure to electrical current. Another 35,930 workers were nonfatally injured, but required

at least 1 day away from work. Electrocution is the third leading cause of construction worker death, following falls and being struck by an object. Contact with overhead power lines, failure to properly de‐energize electrical equipment prior to commencing work, contact with electrical components mistakenly thought to be de‐energized, and contact with buried underground power lines are the most common causes of electrocutions at construction sites [5].

Pathophysiology Electricity is a flow of electrons across a potential gradient from higher to lower concentration. It requires a complete path, a circuit, to create continuous flow. The potential gradient, measured in volts (V), is the difference between the high and low concentration of electrons and is required to drive the electrons through the circuit. The volume of electrons flowing along this gradient is the current (I), measured in amperes (A). Resistance (R) is the impedance to flow of the electrons and is measured in ohms (Ω). Using a plumbing analogy, amperage is the volume of water running through a pipe, voltage is the difference between the entrance and exit pressures of the pipe, and resistance is the diameter of the pipe. Per Ohm’s law, I = V/R, making current directly proportional to voltage and inversely proportional to resistance. There are two different types of current in widespread use today: direct current (DC) and alternating current (AC). In DC current, the electrons flow in one direction. Batteries are a common source of DC current, with electrons always flowing from the “negative” side to the “positive” side, with electrons traveling in one direction. High‐voltage DC current can be used as a means for the bulk transmission of electrical power over long distances. DC current is also commonly used in “third rail” mass transit systems. AC current pushes the electrons back and forth, changing the direction of the flow several times per

Emergency Medical Services: Clinical Practice and Systems Oversight, Third Edition. Volume 1: Clinical Aspects of EMS. Edited by David C. Cone, Jane H. Brice, Theodore R. Delbridge, and J. Brent Myers. © 2021 NAEMSP. Published 2021 by John Wiley & Sons, Inc.

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second. In the United States, standard household current is AC, flowing at 60 cycles per second (Hz) and 110 V. In much of the rest of the world the standard household current is 220–240 V, flowing at 50 Hz. Four main types of electrical injuries have been described: flash, flame, lightning, and true. Flash injuries, caused by a flashover of electric current leaving its intended path and traveling through the air from one conductor to another (an arc flash), are typically associated with superficial thermal burns since no electrical current travels through the skin. Flame injuries occur when an arc flash ignites an individual’s clothing; electrical current may or may not pass through the skin. Lightning injuries involve extremely short but very high‐voltage electrical energy that can be associated with an electrical current flowing through the victim’s entire body. True electrical injuries involve an individual becoming part of an electrical circuit; in these cases, entrance and exit sites are usually found [6]. There are three principal mechanisms by which electricity causes injury: direct effect of electrical current on body tissues, burns from the conversion of electrical energy into thermal energy, and blunt trauma from resultant muscle contractions or a related fall. Direct effects include cellular depolarization and electroporation. Electroporation, the creation of pores in cell membranes by means of electrical current, can be caused by electrical charges insufficient to produce thermal damage but strong enough to cause protein configuration changes that threaten cell wall integrity and cellular function [7, 8]. Six factors determine the outcome of human contact with electrical current: voltage, type of current, amount of current, resistance, pathway of current, and duration of contact [9]. In many cases, the magnitude of only a few of these factors is known. Voltage High voltage has been arbitrarily defined as greater than 1,000 V. As a rule, high voltage is associated with greater mortality, although fatal injury can occur with low voltage as well. High‐voltage electrical injuries are generally associated with greater morbidity in terms of a greater number of surgical procedures required, higher rates of medical complications, increased number of injuries due to falls, and more long‐term psychological and rehabilitative problems  [10]. High‐voltage electrical injuries are generally seen only in industrial settings or in relation to transmission lines. Type of current At the same voltage, AC exposure is about three times more dangerous than DC exposure. AC current is more likely to produce explosive exit wounds, while DC current tends to produce discrete exit wounds. DC current is less likely to cause muscular tetany than does AC current. However, high‐voltage contacts to both AC and DC current can produce a single violent skeletal muscle contraction, leading to the victim appearing to be “thrown” from a voltage source. These differences in the types of

current have practical significance only at low voltages; at high voltages both currents have similar effects. Amount of current The physical effects of different amounts of current vary. A narrow range exists between the threshold of current perception (0.2–0.4 mA) and the “let‐go current” (6–9 mA) [10]. The let‐go current is the level above which muscular tetany prevents release of the current source. When AC current flows through the arm, even at the standard household frequency of 50–60 Hz, flexor tetany of the fingers and forearm can overpower the extensors. If the hand and fingers are properly positioned, the hand will grasp the conductor more tightly, leading to extended contact with the power source [11]. However, current flow through the trunk and legs may cause opisthotonic postures and leg movements if the person has not grasped the contact tightly. Thoracic tetany is also possible and can occur at levels just above the let‐go current, usually at 20–50 mA, resulting in respiratory arrest. Ventricular fibrillation (VF) usually occurs at 50–100 mA. Resistance As electrical current is conducted through a material, resistance to that flow results in dissipation of both energy and heat, resulting in tissue damage from direct heating. The amount of heat produced during the flow of current can be predicted using Joule’s first law, Q = I2Rt, where Q is the amount of heat generated, I is the current flowing through a conductor, R is the amount of electrical resistance, and t is the time of exposure. This conversion of electrical energy to thermal energy can result in massive external and internal burns. Pathway of the current Because electricity requires a complete circuit for continuous flow, the path of electricity flow determines the tissues at risk, the type of injury, and the degree of conversion of electrical energy to heat. For example, current passing through the thorax might cause arrhythmias, direct myocardial damage, or respiratory arrest, whereas cerebral current could cause seizures or motor paralysis. Nerves, blood vessels, mucous membranes, and muscle tend to have the least resistance because of their high concentration of electrolytes [12]. The tissues that have the highest resistance to electricity tend to increase in temperature and coagulate. Bone, which has a very high resistance to electrical current, tends to generate a significant amount of heat and often causes damage to nearby muscles. Skin can have a wide range of resistance to electricity, with dry skin having a higher resistance than moist skin. As a result, a patient with dry skin may have extensive superficial tissue damage but more limited conduction of potentially harmful current to deeper structures. On the contrary, wet skin (e.g., electrocution of a person in a bathtub or in a swimming pool) offers almost no resistance at all, thus generating the maximal intensity of current that the voltage can generate [13].

Electrical injuries

Duration of contact Using Ohm’s Law, the relationship between voltage and heat generation can be derived as Q = V2t/R. Therefore, if resistance and other factors remain constant, the heat from current flow through tissue increases proportionately to the duration of current flow, the square of the current intensity, and the square of the voltage differential.

Evaluation and treatment Scene considerations Scene safety is of critical importance at the site of an electrical injury. It is generally wise for the EMS clinician to assume the victim is still in contact with the electrical source and may present a danger. Therefore, before approaching a victim, EMS personnel should ensure that the power source has been turned off. Some sources suggest using a nonconductive material, such as a broom handle, to attempt to remove a victim from electrical contact. This should be done only with extreme caution because when voltages are above approximately 600 V, even dry wood may conduct significant amounts of electric current, presenting danger to the rescuer. Electrical shock is not prevented by the rescuer wearing rubber gloves and boots unless they are specifically designed for the voltage present. The equipment must also have been recently tested for insulation integrity. A microscopic hole in a glove can result in an explosive injury to the hand because thousands of volts from the circuit can concentrate at the hole to enter the glove [14]. If there are downed power lines at a scene, the area must be isolated using apparatus and law enforcement. High‐voltage power lines are almost never insulated but may appear insulated from atmospheric contaminants deposited on the lines over time. These wires may arc and whip violently; even a wire that appears to be lying quietly can suddenly become very active when the insulation burns off or it becomes wet [15]. A rescuer standing on the ground touching any part of a vehicle that is in contact with a live power line is likely to be killed or seriously injured. In fact, electrocution can occur from ground current simply by walking too close to a downed power line. It is important to establish a safety perimeter that is adequate in size. The recommended isolation distance is one full span between the adjacent utility poles or towers in all directions from a break in the wire or from the point of contact with the ground. At a minimum, personnel should stay at least 3‐9 m (10‐30 ft) from downed power lines until the utility company unequivocally confirms that power to the lines is off [16, 17]. The EMS clinician must also be aware of other hazards at scenes of downed power lines. When voltage is reapplied to downed lines and circuit breakers reset, the lines may physically “jump” forcefully. In addition, although the metal cables that support telephone and power poles are normally grounded, they may become energized if they break or disconnect from an

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attachment and make contact with a nearby power line. Metal roadside guard rails may be energized for hundreds of meters if in contact with a downed, but live, power line.

Assessment and management Although serious cardiac complications from electrical injury are relatively uncommon, arrhythmias and cardiac arrest are the most common causes of death in electrocution. There are several established and theoretical mechanisms for this: • accommodation of the ventricular effective refractory period • asystole from direct current • direct induction of VF • induction of an intermediate ventricular tachycardia • induction of VF from long‐term high‐rate cardiac capture, ischemically lowering the VF threshold • respiratory arrest with secondary cardiac arrest • shock on the cardiac T‐wave It is classically taught that AC current is more likely to cause VF, whereas DC current is more likely to cause asystole. Evidence for this is lacking [18]. The incidence of arrhythmias after electrical injury, as compiled from several prospective and retrospective studies, has ranged from 4% to 17% [19–22]. All patients should undergo initial ECGs to assess for cardiac injury and arrhythmias. Continuous cardiac monitoring is indicated for any patient who has suffered significant electrical injuries unless an initial ECG is normal, there is no history of unconsciousness, and the injury is from a low‐voltage source [23]. Arrhythmias tend to occur in the first few hours after the injury, so prehospital monitoring can be particularly important. The most common ECG changes are sinus tachycardia and nonspecific ST‐T wave changes, which usually correct with time. If the patient’s overall clinical condition is good and he or she has a normal ECG at the time of admission to the ED, the probability of observing any delayed serious arrhythmia is low [24]. When arrhythmias are noted, they are usually transient and do not require therapeutic intervention. In fact, there is a growing body of literature that suggests that because most cardiac arrhythmias in patients presenting after electrical injury can be diagnosed by an initial ECG, routine cardiac monitoring may be unnecessary [25]. Sometimes an injury pattern mimicking infarction may be seen on the ECG; such patterns are generally due to direct myocardial injury and not coronary thrombosis [26]. The difficulty is identifying the existence of new myocardial damage and determining its physiological significance [27]. Cardiopulmonary resuscitation should be initiated as soon as safely possible for victims of electric shock‐induced arrest. For line workers, coworkers may be trained to begin rescue breathing even while still on utility power poles. As soon as the victim is lowered to the ground, chest compressions can be started if the patient is in cardiac as well as respiratory arrest.

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Because many victims are young and have no prior cardiovascular disease, resuscitative efforts should be aggressive. It is often not possible to predict the outcome of attempted resuscitation based on age and initial rhythm in electric shock‐ induced cardiac arrest [28]. Normal Basic Life Support (BLS) or Advanced Life Support (ALS) resuscitation protocols should be used, keeping in mind any necessary adjustments for rescuer safety and patient access. Respiratory arrest may result from electric shock due to tetanic contraction of the thoracic musculature, injury to the respiratory center in the central nervous system, or combined with cardiac arrest. Although cardiac function may recover spontaneously due to the heart’s automaticity, respiratory arrest can persist and lead to secondary hypoxia. In addition, establishing an airway can be challenging with patients who have suffered electric burns of the face, mouth, or anterior neck. This may be compounded by the rapid development of soft tissue edema. Therefore, rescuers should consider intubation early when caring for these patients [29]. Once cardiac arrhythmias and respiratory arrest are addressed, patients with electrical injuries should be evaluated as trauma patients, treating any blunt injuries and caring for burns. Rescuers should assume that victims of electrical injury may have multiple other traumatic injuries. Falls, being thrown from the electrical source by an intense muscular contraction, or blast effect from explosive forces that may occur with electric flashes can cause significant secondary blunt trauma. In addition, fractures and joint dislocations can be caused directly by forceful muscle contractions from an electric current [30]. Therefore, in addition to cardiac monitoring and measurement of oxygen saturation, intravenous access should be placed and in‐line stabilization of the spine should be considered after the primary survey is completed. The most common injuries associated with electrical injury are burns. Appropriate burn care should be instituted for external burns. Constricting rings and other jewelry should be removed from all extremities whether or not an injury is visualized. Patients with burns from high‐voltage electricity should be taken to trauma centers; they may have significant internal damage from internal current flow. A “kissing burn” is sometimes associated with electrical injury when a current arcs across two flexor surfaces, such as the antecubital fossa. It is important to recognize this type of injury because it is often associated with extensive underlying tissue damage [10]. Because visible cutaneous damage in electrical burns generally underestimates internal damage, fluid requirements may exceed prediction using standard thermal burn injury formulae such as the Parkland formula. Most sources advise that an initial fluid volume of 20 to 40 mL/kg over the first hour is appropriate for a typical patient with a significant electrical injury [17]. Further fluid administration should be guided by continued clinical and hemodynamic assessment.

Special circumstances Lightning injury Lightning is a unidirectional cloud‐to‐ground current resulting from static charges that develop when a cold high‐pressure front moves over a warm moist low‐pressure area [31–33]. It is neither a direct nor an alternating form of current [33, 34]. Although lightning can release greater than 1,000,000 V of energy, generate currents greater than 200,000 A, and reach temperatures as high as 50,000°F, the actual amount of energy delivered may be less than that typical of high‐voltage injuries because its duration is as short as a few milliseconds [13, 31, 35]. A comparison between lightning, high‐voltage, and low‐voltage electrical injuries is shown in Table 31.1. Although 70% of lightning strikes are not fatal, lightning kills approximately 80 to 90 people per year in the United States [36–39]. Thirty percent of lightning strikes involve more than one patient; people tend to seek shelter from lightning storms together [32]. Lightning strikes tend to result in five basic mechanisms of injury [33, 34, 38]: 1.  A direct strike is more likely to hit a person who is in the open and unable to find shelter. This type of lightning strike is usually fatal [38]. 2.  A splash injury occurs when lightning strikes an object, such as a tree or building, or another person, and the current “splashes” to a victim standing nearby. Current can also splash to a victim indoors via plumbing or telephone wires [33]. 3.  A contact injury occurs when the victim is in physical contact with an object or a person directly struck or splashed by lightning. 4.  A step voltage/ground current injury occurs when the current travels up through the body (e.g., up one leg and down the other) between the body’s two points of ground contact. This happens because when lightning hits the ground, the current spreads outward in a radial pattern and the human body offers less resistance to electrical current than does the ground. 5.  Blunt trauma can occur when victims of a lightning strike are thrown by the concussive forces of the shockwave created by the lightning. A lightning strike can also cause significant opisthotonic muscle contractions, which may lead to fractures, dislocations, or other trauma. Similar to other electrical incidents, the first priority in responding to a lightning strike is scene safety. Contrary to popular myth, lightning can—and often does—strike the same place twice. The most common cause of death from lightning is immediate cardiorespiratory arrest, from massive direct current shock or paralysis of the medullary respiratory center [33, 34, 38, 40, 41]. However, unlike the typical trauma arrest patient, lightning victims have significant resuscitation potential, which gives rise to the concept of “reverse triage.” Contrary to practice in most

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Table 31.1  Comparison between lightning, high‐voltage, and low‐voltage electrical injuries Lightning

High Voltage

Low Voltage

Voltage, V Current, A Duration Type of current Cardiac arrest (cause) Respiratory arrest (cause)

>30,000,000 200,000 Instantaneous Similar to DC Asystole Direct CNS injury

Muscle contraction

Single

20% TBSA) require IV access, preferably two large‐bore peripheral lines. Catheters may be placed through the burned tissue. Central venous access should be avoided because of its high complication rate in the early postburn period when vasospasm, low flow, and a hypercoagulable state contribute to complications. A urinary catheter and a nasogastric tube are recommended for long or delayed transport. Use of ice on a burn wound is absolutely contraindicated because of the risk of a cold injury superposed on the burn. Continual efforts must be made to keep the patient warm. Fluid resuscitation should continue. No burn debridement is required before transfer, and the burns should be wrapped in dry sterile or clean sheets or burn‐specific water‐ based gel dressings, and further covered with warm blankets.

Prevention The prehospital environment offers a unique “teachable moment” for clinicians to educate patients and their families about preventing burns in the future. Prevention programs

Box 33.2    American Burn Association Burn Center Referral Criteria

1  Partial‐thickness burns >10% total body surface area. 2  Burns that involve the face, hands, feet, genitalia, perineum, or major joints. 3  Third‐degree (full‐thickness) burns in any age group. 4  Electrical burns, including lightning injury. 5  Chemical burns. 6  Inhalation injury. 7  Burn injury in patients with preexisting medical disorders that could complicate management, prolong recovery, or affect mortality. 8  Any patients with burns and concomitant trauma (such as fractures) in which the burn injury poses the greatest risk of morbidity or mortality. In such cases, if the trauma poses the greater immediate risk, the patient may be stabilized initially in a trauma center before being transferred to a burn center. 9  Burned children in hospitals without qualified personnel or equipment for the care of children. 10  Burn injury in patients who will require special social, emotional, or rehabilitative intervention. Source: Based on Badulak JH, Schurr M, Sauaia A, Ivashchenko A, Peltz E. Defining the criteria for intubation of the patient with thermal burns. Burns. 2018; 44:531–8.

Box 33.3   Burn injury prevention

Flame burn prevention

Scald prevention

Test smoke detectors regularly. Create an escape plan for the home, and practice. Place safety device around fireplace and stoves. Keep matches, lighters away from children. Use splash guards on stove. Lower hot water heater maximum temperature to 2 years) 13  Inexpensive and cost‐effective Source: Kheirabadi, B. Evaluation of topical hemostatic agents for combat wound treatment. US Army Med Dep J. 2011 Apr‐Jun: 25–37.

and clotting factors at the wound site through rapid adsorption of water. The reaction generates a significant amount of heat ranging from 68°C to 140°C [49]. Initial studies demonstrated effectiveness in a large animal model with lethal groin injury; however, the injuries in these studies were different from those in follow‐on studies, and when compared against the more severe model (6 mm femoral arteriotomy) QuikClot failed to provide hemostasis [48]. QuikClot was initially fielded as a granular powder, but difficulty with application and the potential to be washed away by bleeding prompted a repackaging in gauze bags [50]. Concerns with heat generation have led to a newer product called QuickClot ACS+ that uses synthetic zeolite beads in a cotton bag that produces a minimal exothermic reaction [51]. Second generation: Celox Celox (Medtrade Biopolymers, Crewe, United Kingdom) is a chitosan‐based agent based on a proprietary granular mixture of different chitosan forms. Celox’s primary mechanism is similar to that of chitosan in that it is mediated by a mixture of chemical and mechanical (adherence) linkages to red blood cells and tissues that form a physical barrier around the severed vessels [50]. According to the manufacturer, this mechanism is not dependent on the coagulation factors of the patient. Celox is placed on top of a wound in a powder form, leading to the potential to be washed away if not secured to the wound. Attempts to place Celox in a gauze‐like bag have been unsuccessful [52]. In a comparison with other agents, it was shown to be inferior to Combat Gauze [53, 54].

Second generation: Combat Gauze Created by Z‐medica, Combat Gauze is an FDA‐approved hemostatic agent consisting of ordinary cotton rolled gauze impregnated with kaolin, a fine claylike material used in some antidiarrheal preparations. Kaolin appears to be a potent activator of the intrinsic clotting pathway, inducing the patient’s own clotting factors, to produce a clot. In a comparison between several other hemostatic dressings, including HemeCon and Celox‐D, Combat Gauze proved to be the most effective and safest agent [52]. This led to Combat Gauze being recommended by the Tactical Combat Casualty Care Committee (the U.S. military’s lead agency in guidelines for treatment of wounded service members) as the solitary hemostatic agent in 2009 [53]. Combat Gauze also has other factors that make it desirable as a hemostatic agent, including low cost, ease of use, and strong safety profile. See Video Clip 35.3 for application of Combat Gauze to a wound. Third generation: Celox‐XG Celox‐XG Gauze (XG, SAM Medical Products, Wilsonville, OR) is also a chitosan‐based product; however, instead of a powder, Celox‐XG is a rolled fabric made with nonwoven chitosan‐derived hemostatic fibers. It works on the same principal

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Moderate and severe hypothermia (body temperature of less than 32°C) inhibit coagulation and contribute to ongoing hemorrhage. Hypothermia reduces the enzymatic activity of coagulation proteins and inhibits the activation of platelets. Dysfunction of the coagulation system is evident below temperatures of 35°C, and temperatures below 30°C result in a 50% reduction in platelet function [63]. Removing wet clothing, applying warm blankets, and increasing ambulance patient compartment ambient temperature are simple techniques for prevention of hypothermia. There are also several commercially available hypothermia prevention kits.

life support units compared to helicopter EMS required emergency department blood product administration, calling into question the utility of supplying ground units with blood products [65]. There are trials of using blood product transfusion (plasma and packed red cells) from point of injury care for the U.S. military in Afghanistan, and thus far there have been no known transfusion reactions [66]. Most prehospital clinicians resuscitate with uncrossmatched packed red blood cells, which lack platelets and clotting factors, which may support hemorrhage control. However, a recent prehospital randomized control trial demonstrated that administration of thawed fresh‐frozen plasma is safe and resulted in a lower 30‐day mortality rate in comparison to standard resuscitation that also included administration of packed red blood cells [67]. The physiological effect of plasma in hemorrhagic shock is volume expansion as well as mitigation of coagulopathy and the inflammatory response [68]. Fresh‐frozen plasma requires 20 minutes of thaw time, and after it is thawed, the shelf life is approximately 5 days [69]. Freeze‐dried plasma (commonly referred to as lyophilized plasma), on the other hand, can last up to 2 years. It was originally developed in the United States during World War II. Falling out of favor in the United States, it continued to be used successfully by the French military (with some interruption due to HIV transmission concerns) [70]. Use of lyophilized plasma in a prehospital setting would be advantageous in several scenarios, such as mass casualty incidents, long transports, or remote locations where access to other blood products might be difficult. Recent studies of patients requiring massive transfusions have demonstrated that transfusion of platelets and plasma in conjunction with packed cells leads to better hemostatic control, decreased transfusion volumes, and greater survival if maintained close to ratios of 1:1:1 [71]. Recently, fresh whole blood has been revisited as a resuscitation fluid in military and civilian populations. The advantages of fresh whole blood include reduction of dilution factors added to individual products and limiting exposure to multiple donors [72, 73]. However, it can only be stored at room temperature for up to 48 hours [74]. Patients with life‐threatening hemorrhage should be transfused before or during transport when blood products are available. Although cross‐matched blood products are preferable, uncrossmatched blood is often all that is available in emergent circumstances. The logistics of maintaining blood product supply prehospital continue to remain a challenge for EMS ­systems.

Transfusion

Medications

Treatment with blood products in the prehospital environment is largely limited to specialized teams and air medical clinicians, mainly due to the complexity of maintaining the supply [64]. One study recently found that only a small subset of trauma patients transported by ground advanced

Recombinant factor VIIA (Novoseven) Factor VIIa is part of the extrinsic pathway in the coagulation cascade and initiates thrombin generation (activated factor Xa). It is licensed for the treatment of hemophilia patients with antibodies to factor VIII but is also used for the treatment of

as Celox but is much easier to apply than is the powder form [54, 55]. It was the standard hemostatic agent for the United Kingdom military in Afghanistan. In one study, although outcomes were similar, Celox‐XG did have shorter clot time than did either Combat Gauze or standard gauze [56]. In a more recent study, a comparison of Combat Gauze, Celox‐XG, and standard gauze showed less secondary blood loss and faster packing times for Celox‐XG, but no differences in outcomes [57]. The benefits of Celox‐XG are comparable to Combat Gauze, including ease of use and a strong safety profile.

Adjunctive therapy Permissive hypotension Many studies suggest that limiting prehospital resuscitation protocols to achieve mean arterial pressures in the range 60–70 mmHg may improve outcomes over standard therapy designed to maintain systolic blood pressures of 100 mmHg [58, 59]. This “permissive hypotension” is thought to be sufficient to provide adequate perfusion to vital organs without exacerbating bleeding through clot dislodgement or dilution of clotting factors. Multiple studies have shown that that permissive hypotension is also beneficial by limiting exposure to crystalloids and fractionated blood products. Crystalloid fluids have been demonstrated to dilute clotting factors and induce inflammatory cascades, which may result in increased hemorrhage and decreased survival [60, 61]. One exception to permissive hypotension is concomitant traumatic brain injury, given that hypotension increases mortality in these patients [62].

Prevention of hypothermia

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trauma victims with life‐threatening hemorrhage [75]. Boffard demonstrated that administration of factor VIIa reduced the need for packed red blood cell transfusion and massive transfusion in severely bleeding blunt trauma patients [76]. Factor VIIa has not been shown to reduce mortality or critical complications. Furthermore, factor VIIa has been linked to complications including increased incidence of adult respiratory distress syndrome and is exceptionally expensive. In a more recent Cochrane review, the recommendation was that factor VIIa be used only in its FDA‐approved indications unless under a study protocol [77]. Tranexamic acid (TXA) Intravenous administration of TXA was approved by the FDA in 1986 for prevention or reduction of bleeding in hemophilia patients undergoing dental procedures. As an antifibrinolytic inhibiting both plasminogen activation and plasmin activity, TXA prevents clot breakdown rather than promoting new clot formation. In the CRASH‐2 study, trauma patients were given TXA or placebo with a small but significant reduction in all‐ cause and bleeding mortality in the TXA group. The highest improvements were in those given TXA in the first 3 hours and in the most severely injured subgroups. There was a very low incidence of harm [78, 79]. Studies in a combat environment showed similar benefits as well as improvement of clot stabilization [80, 81]. Given its low cost, low incidence of adverse events, and importance of early administration, TXA administration may become a useful prehospital intervention [79]. The Study of Tranexamic Acid During Air Medical Prehospital Transport (STAAMP) Trial, a recently published randomized control trial, did not demonstrate a 30-day mortality benefit in prehospital hemorrhagic shock patients who received TXA [82].

Antiplatelet and anticoagulation medications Ascertaining antiplatelet and anticoagulation use of prehospital patients, particularly in the elderly trauma or bleeding patient, is an important role for EMS clinicians. Knowledge of newer and less‐used antiplatelet and anticoagulant agents should be emphasized during continuing medical education [83]. Additionally, EMS clinicians should recognize platelet and coagulant deficiency and dysfunction syndromes such as hemophilia and Von Willebrand disease. Reversal agents, including platelets, plasma, four factor prothrombin complex concentrate, and protamine are largely reserved for in‐hospital and critical care transport use. Evidence for implementing these agents in the prehospital setting is lacking. For the patient with uncontrolled bleeding in the setting of antiplatelet and/or anticoagulant use, bleeding control measures such as direct pressure, tourniquet use, and other management strategies discussed should be prioritized.

Summary Uncontrolled hemorrhage is a leading cause of preventable death. Direct pressure remains the primary treatment for hemorrhage and is sufficient for most wounds. Patients who fail management with direct pressure require immediate hemorrhage control. Extremity wounds can be controlled with tourniquets, while advanced hemostatic agents or junctional tourniquets can treat wounds of the trunk and neck and those in body cavities. These agents are now capable of stopping even brisk arterial bleeding and have been shown to improve patient survival. Training laypersons in bleeding control is an important focus in the chain of survival. In situations of prolonged transport time or austere environments, consideration should be given to adjunctive therapies such as hypotensive resuscitation, maintenance of euthermia, and transfusion of blood and blood products to address coagulopathy. As has been proven in recent mass casualty incidents, EMS clinicians must be prepared to deal with exsanguinating hemorrhage on multiple patients that can parallel battlefield scenarios.

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50 Arnaud F, Tomori T, Saito R, et al. Comparative efficacy of granular and bagged formulations of the hemostatic agent QuickClot. J Trauma. 2007; 63: 775–83. 51 Arnaud F, Tomori T, Carr W, et al. Exothermic reaction in zeolite hemostatic dressings: QuikClot and ACS+. Ann Biomed Eng. 2008; 36:1708–13. 52 Kheirabadi BS, Scherer MR, Estep JS, et al. Determination of efficacy of new hemostatic dressings in a model of extremity arterial hemorrhage in swine. J Trauma. 2009; 67:450–9. 53 ITS Team. 2009 TCCC Guidelines. Available at: https://www. itstactical.com/medcom/tccc‐medcom/2009‐tccc‐guidelines/. Accessed on Aug 22, 2020. 54 Gerlach T, Grayson JK, Pichakron KO, et  al. Preliminary study of the effects of smectite granules (WoundStat) on vascular repair and wound healing in a swine survival model. J Trauma. 2010; 69:1203–9. 55 Johnson D, Johnson M. The effects of QuikClot Combat Gauze and Celox Rapid on hemorrhage control. Am J Disaster Med. 2019; 14:17–23. 56 Watters JM, Van PY, Hamilton GJ, et  al. Advanced hemostatic dressings are not superior to gauze for care under fire scenarios. J Trauma. 2011; 70:1413–9. 57 Kunio NR, Riha GM, Watson KM, et  al. Chitosan based advanced hemostatic dressing is associated with decreased blood loss in a swine uncontrolled hemorrhage model. Am J Surg. 2013; 205:505–10. 58 Duke MD, Guidry C, Guice J, et  al. Restrictive fluid resuscitation in combination with damage control resuscitation: time for adaptation. J Trauma Acute Care Surg. 2012; 73:674–8. 59 Bickell WH, Wall MJ Jr, Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med. 1994; 331:1105–9. 60 Hussmann B, Lefering R, Taeger G, et al. Influence of prehospital fluid resuscitation on patients with multiple injuries in hemorrhagic shock in patients from the DGU trauma registry. J Emerg Trauma Shock. 2011; 4:465–71. 61 Tran A, Yates J, Lau A, Lampron J, Matar M. Permissive hypotension versus conventional resuscitation strategies in adult trauma patients with hemorrhagic shock: a systematic review and meta‐ analysis of randomized controlled trials. J Trauma Acute Care Surg. 2018; 84:802–8. 62 Spaite DW, Hu C, Bobrow BJ, et al. Mortality and prehospital blood pressure in patients with major traumatic brain injury: implications for the hypotension threshold. JAMA Surg. 2017; 152:360–8. 63 DeLoughery T. Coagulation defects in trauma patients: etiology, recognition, and therapy. Crit Care Clin. 2004; 20:13–24. 64 Barkana Y, Stein M, Maor R, et al. Prehospital blood transfusion in prolonged evacuation. J Trauma 1999; 46:176–80. 65 Mix FM, Zielinski MD, Myers LA, et  al. Prehospital blood product administration opportunities in ground transport ALS EMS– a descriptive study. Prehosp Disaster Med. 2018; 33:230–6. 66 Malsby RF 3rd, Quesada J, Powell‐Dunford N, et  al. Prehospital blood product transfusion by U.S. Army MEDEVAC during combat operations in Afghanistan: a process improvement initiative. Mil Med. 2013; 178:785–91. 67 Sperry JL, Guyette FX, Brown JB, et al. Prehospital plasma during air medical transport in trauma patients at risk for hemorrhagic shock. N Engl J Med. 2018; 379:315–326.

68 Henriksen HH, Rahbar E, Baer LA, et al. Pre‐hospital transfusion of plasma in hemorrhaging trauma patients independently improves hemostatic competence and acidosis. Scand J Trauma Resusc Emerg Med. 2016; 24:145. 69 Downes KA, Wilson E, Yomtovian R, Sarode R. Serial measurement of clotting factors in thawed plasma stored for 5 days. Transfusion. 2001; 41:570. 70 Sailliol A, Martinaud C, Cap AP, et al. The evolving role of lyophilized plasma in remote damage control resuscitation in the French Armed Forces Health Service. Transfusion. 2013; 53:65S–71S. 71 Holcomb JB, Tilley BC, Baraniuk S, et  al. Transfusion of plasma, platelets, and red blood cells in a 1:1:1 vs a 1:1:2 ratio and mortality in patients with severe trauma: the PROPPR randomized clinical trial. JAMA. 2015;313:471–82. 72 Cotton BA, Podbielski J, Camp E, Early Whole Blood Investigators, et al. A randomized controlled pilot trial of modified whole blood versus component therapy in severely injured patients requiring large volume transfusions. Ann Surg. 2013; 258:527–32; discussion 532–3. 73 Chandler MH, Roberts M, Sawyer M, Myers G. The US military experience with fresh whole blood during the conflicts in Iraq and Afghanistan. Semin Cardiothorac Vasc Anesth. 2012; 16:153–9. 74 Spinella PC, Reddy HL, Jaffe JS, et  al. Fresh whole blood use for hemorrhagic shock: preserving benefit while avoiding complications. Anesth Analg. 2012; 115:751–8. 75 Barletta JF, Ahrens CL, Tyburski JG, Wilson RF. A review of recombinant factor VII for refractory bleeding in nonhemophilic trauma patients. J Trauma. 2005; 58:646–51. 76 Boffard KD, Riou B, Warren B, et al. Recombinant factor VIIa as adjunctive therapy for bleeding control in severely injured trauma patients: two parallel randomized, placebo‐controlled, double‐ blind clinical trials. J Trauma. 2005; 59:8–18. 77 Stanworth SJ, Birchall J, Doree CJ, Hyde C. Recombinant factor VIIa for the prevention and treatment of bleeding in patients without haemophilia. Cochrane Database Syst Rev. 2007 Apr 18:CD005011. 78 CRASH‐2 Collaborators. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH‐2): a randomised, placebo‐ controlled trial. Lancet. 2010; 376:23–32. 79 Neeki MM, Dong F, Toy J, et al. Efficacy and safety of tranexamic acid in prehospital traumatic hemorrhagic shock: outcomes of the Cal‐PAT Study. West J Emerg Med. 2017; 18:673–83. 80 Morrison JJ, Dubose JJ, Rasmussen TE, Midwinter, MJ. Military Application of Tranexamic acid in Trauma Emergency Resuscitation (MATTERs) Study. Arch Surg. 2012; 147:113–9. 81 Stein P, Studt JD, Albrecht R, et  al. The impact of prehospital tranexamic acid on blood coagulation in trauma patients. Anesth Analg. 2018; 126:522–9. 82 Guyette FX, Brown JB, Zenati MS, et al. Tranexamic acid during prehospital transport in patients at risk for hemorrhage after injury: a double-blind, placebo-controlled, randomized clinical trial. JAMA Surg. 2020; 156(1):11–20. doi: 10.1001/jamasurg.2020.4350. Online ahead of print. 83 Nishijima DK, Gaona S, Waechter T, et al. Do EMS providers accurately ascertain anticoagulant and antiplatelet use in older adults with head trauma? Prehosp Emerg Care. 2017; 21:209–15.

CHAPTER 36

Orthopedic injuries Mary P. Mercer

Introduction Epidemiology Trauma is a leading cause of death worldwide and in the United States [1]. Blunt trauma from motor vehicle accidents, falls, or other mechanisms can result in a range of orthopedic injuries. Recognition and management of orthopedic injuries is an essential component of any EMS system. General approach to management The prehospital management of suspected orthopedic injury begins with assessment of potential life threats. Obtaining a history that includes the mechanism of injury is important to develop an index of suspicion for associated injuries. Prehospital clinicians should first assess and address the airway, breathing, circulation, and disability of any injured patient. The only indication for addressing an orthopedic injury during the pri‑ mary survey is suspected hemodynamic compromise from an actively bleeding wound or suspected large‐volume hemorrhage from a long bone (femur) fracture. Once the primary survey is complete, an orthopedic evaluation is part of a comprehensive secondary survey. Open fractures and injuries with neurovascular compromise require special attention. Acute hemorrhage control is a pri‑ ority for open fractures and can generally be accomplished with direct pressure. Any exposed bone should be dressed with a sterile saline moistened dressing. The decision to reduce a frac‑ ture or dislocation in the field is situation dependent and should be based on presence of neurovascular compromise, anticipated extrication and transport duration, and clinician training and experience [2]. Pain management is an important component of the prehospital care for any orthopedic injury and should ideally be addressed prior to moving the patient to the ambulance. Pain management modalities include immobilization of the affected limb, application of ice if available, and a range of analgesic medications depending on injury severity, prehospital environ‑ ment, and patient factors. While opioids have been the historic

mainstay of medical management of pain control, additional modalities including ketamine, nonsteroidal anti‐inflammatory medications, and acetaminophen have emerging use and study  [3–7]. Awareness of the pharmacokinetics of different medications in special populations such as pediatric and geri‑ atric patients is important for effective prehospital management of orthopedic injuries [8, 9].

Anatomy, fractures, and dislocations Upper extremity

Upper extremity neurovascular exam

For all upper extremity injuries, both nerve function and vascular patency must be assessed early and repeated frequently, partic‑ ularly after any manipulation, splinting, or patient movement. The radial, ulnar, and median nerves should be assessed for both motor and sensory function in all injuries. The axillary and musculocutaneous nerves should be assessed in more proximal injuries (Table  36.1). The vascular exam consists of palpating both the radial and ulnar pulses and the brachial artery in more proximal injuries. For injuries distal to the wrist, nailbed capil‑ lary refill should be assessed.

Clavicle

Clavicular fractures are generally uncomplicated and can be managed in the field with sling and swathe placement. Assessment should include a complete neurovascular exam of the limb on the affected side as there is a risk of damage to the underlying subclavian vessels and brachial plexus as well as the possibility of pneumothorax. The clavicular articulations to the sternum (sternoclavicu‑ lar joint) and acromion (acromioclavicular joint) should be assessed as well. Acromioclavicular joint injury can be diag‑ nosed clinically and should be managed with a sling and swathe in the field. Sternoclavicular joint injuries most commonly occur because of vehicle accidents or sports injuries and are

Emergency Medical Services: Clinical Practice and Systems Oversight, Third Edition. Volume 1: Clinical Aspects of EMS. Edited by David C. Cone, Jane H. Brice, Theodore R. Delbridge, and J. Brent Myers. © 2021 NAEMSP. Published 2021 by John Wiley & Sons, Inc. 307

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Table 36.1  Upper extremity neurologic examination Nerve

Motor

Sensory

Radial

Wrist or finger extension

Ulnar Median

Index finger abduction Thumb and index finger opposition Deltoid Elbow flexion

First dorsal web space Pinky finger Index finger

Axillary Musculocutaneous

Lateral shoulder Lateral forearm

divided into less serious anterior dislocations and more serious posterior dislocations. While field treatment for both is immo‑ bilization, prehospital clinicians should have a heightened index of suspicion for serious intrathoracic injury with posterior dis‑ locations, in particular pneumothorax, great vessel injury, and tracheal injury [10].

Scapula

A patient with a scapular fracture will generally present with local tenderness and protecting the arm on the affected side. Management consists of sling and swathe placement and anal‑ gesia. Up to 75% of patients with scapular fractures will have additional injuries due to the significant mechanism of injury. Clinicians should carefully examine the patient for rib fractures, pneumothorax, or upper arm injuries [11].

Shoulder

Glenohumeral joint dislocations are the most common major joint dislocation encountered and are generally the result of an indirect blow with the arm in abduction, extension, and external rotation [12]. Anterior dislocations are the most common and can be identified clinically in the field with some reliability. In general, the patient will present guarding the affected arm with mild abduction and external rotation. Posterior dislocations are rare, usually the result of a mechanism of injury such as a sei‑ zure, electrical shock, or direct anterior blow to the shoulder, and while carrying a similar associated fracture rate, they are less likely to have neurovascular injury. Inferior and superior dislocations are even less common. When examining a suspected shoulder dislocation, close attention should be paid to the axillary nerve. Vascular injuries are rare, but when they do occur they will generally involve the axillary artery [13]. Associated fractures occur in 15% to 35% of shoulder dislocations and can include the humeral head (Hill‐Sachs lesion), anterior glenoid lip, and greater tuberosity. Although these fractures generally do not change management, prereduction x‐rays are recommended, and field reduction should typically not be attempted [14]. There are exceptions to this rule, in particular for patients with known recurrent dis‑ locations and athletes on the field with appropriately trained staff  [15, 16]. Clinicians should splint the extremity in the position found with a sling and swathe. A short board splint can be placed along the medial upper arm for extra stability,

particularly in the presence of a suspected humeral head frac‑ ture  [17]. In the event of a spontaneous reduction, clinicians should still splint and transport, as radiographs and follow‐up will be needed. Rotator cuff injuries may be associated with shoulder dislo‑ cations or may present independently. Complete evaluation of the rotator cuff could become more commonplace prehospital practice, particularly within a mobile integrated health care setting. However, no validated rules currently exist to exclude fracture or dislocation, and a patient with an acute shoulder injury would likely benefit from transport to the hospital [17].

Humerus

Fractures of the humerus can be divided into three categories: proximal, midshaft, and distal. Axillary nerve and artery injuries have been recognized in up to 50% of displaced humeral fractures. Humeral shaft injuries are most common in active young men and elderly osteoporotic patients and can be associ‑ ated with radial nerve injuries or vascular injuries to the brachial artery or vein [7, 18]. Field management is the same as for other shoulder injuries.

Elbow

The elbow joint is composed of the articulations of the distal humerus, proximal radius, and ulna. The brachial artery and the nerves of the forearm and hand travel in close proximity. It is the third most dislocated joint after the shoulder and knee. Supra‑ condylar fractures are among the most common fractures on children and can be associated with subsequent compartment syndrome  [17, 19]. The primary fracture patterns in adults include flexion and extension, the latter being more common. Most elbow dislocations (90%) are posterolateral, with the mechanism of injury being a fall on an outstretched hand. Com‑ monly associated neurovascular injuries include entrapment of the ulnar nerve and the brachial artery [18]. In the prehospital setting, it is difficult to differentiate an elbow fracture from a dislocation without x‐rays, and as such, it is recommended that EMS clinicians splint all suspected fractures or dislocations in the position found. Gentle reduction may be recommended in a severely angulated fracture or one with significant neurovascular compromise, particularly if transport time is significant. In the case that reduction is attempted, the elbow then should be splinted at 90 degrees with the forearm in supination with a posterior moldable splint and a sling and swathe placed.

Forearm

While the unique fracture and dislocation patterns of the forearm are of interest to the emergency physician in deter‑ mining definitive management, they are less important to the prehospital clinician. Field management involves splinting with a posterior mold or short boards in the position found. Indica‑ tions for attempted field reduction are similar to other fractures, although neurovascular compromise in these fractures is less

Orthopedic injuries

common than in injuries of the humerus or elbow. Fractures to the proximal ulnar, olecranon, and radius are treated similarly to other fractures and dislocations about the elbow.

Wrist

Fractures of the distal radius and ulna are the most common wrist fractures, followed by the carpal bones, notably the scaphoid and triquetrum [19]. Distal forearm fractures should be immobilized in the position of function, if tolerated, or the position found. Carpal fractures can be immobilized in either short boards or commercial wrist splints. Once splinted, the extremity may be placed in a sling and swathe to further reduce movement. Distal neurovascular assessment should be documented. EMS clinicians may be trained to assess for snuff box tenderness to assist in identifying potential scaphoid fractures  [20]. Carpal ligamentous injury frequently occurs in conjunction with bony injury and should be splinted similarly based on physical exam findings of tenderness.

Hand/fingers

Hand and finger injuries are rarely life threatening but can be emotionally disturbing to the patient and clinician. Once attention is appropriately turned to the hand injury, function of the median, radial, and ulnar nerves should be assessed as previ‑ ously outlined. Vascular status can be assessed through capillary refill, which should be less than 2 seconds. Flexor and extensor tendon function should be tested in each finger and compared between hands. Fractures and dislocations of the phalanx should be splinted as found, and buddy taping can be used to stabilize the finger itself prior to placing the affected hand in a wrist or short board splint. Field reduction may be appropriate in some situations. However, ideally, the patient can be trans‑ ported to the emergency department for a peripheral nerve block prior to reduction. Case reports do exist of successful paramedic performance of a digital block and subsequent reduction, and this is a potential future expansion of prac‑ tice [21]. While metacarpal fracture management and follow‐ up vary depending on radiographic findings and patient activity, field management is unchanged and involves splint‑ ing. One hand injury that deserves special mention is the high‐pressure injection injury, which always requires trans‑ port to the emergency department for evaluation and pos‑ sible surgical intervention [22]. Pelvis Although pelvic fractures are relatively rare among orthopedic injuries, they are associated with high mortality (10%‐15%) due to both the presence of concurrent severe traumatic injuries and the pathophysiology of unstable pelvic fractures [23]. The most common mechanisms associated with pelvic fractures involve the transmission of significant amounts of force such as through high‐speed motor vehicle collisions, pedestrians hit by automo‑ biles, or significant falls [24].

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Anterior‐posterior compressive forces are often associated with the highest degree of hemodynamic instability and mortality [19]. Such fractures cause significant disruption to the pelvic ring, resulting in widening of the pelvis, tearing of the iliac ligaments, and shear force injuries of the iliac vessels. The pre‑ dominantly venous hemorrhage spills into the retroperitoneum and expanded pelvic cylinder. If left uncontrolled, this hemor‑ rhage can be fatal due to the large potential space of the unstable pelvic vault. Pelvic injury should be suspected in any patient with significant traumatic injuries of the head, spine, thorax, abdomen, or mul‑ tiple extremities. Signs of shock should raise suspicion of an unstable pelvic fracture in patients without outward signs of frac‑ ture. Other signs and symptoms of pelvic fractures may include perineal or flank hematoma or blood at the penile meatus or vag‑ inal introitis. Obvious bony instability of the pelvis with light pal‑ pation is a clear finding of pelvic fracture. However, the absence of external findings does not exclude the presence of an unstable pelvic fracture  [25]. The examiner is discouraged from com‑ pressing the pelvis to test for stability, as this may exacerbate an unstable fracture or concomitant bleeding. Clinical management of the suspected pelvic fracture, as with other major trauma, includes immobilization and rapid trans‑ port to a trauma center. Given the risk of vascular and hemody‑ namic compromise, vital signs and distal neurovascular status should be monitored closely during transport. In addition to general immobilization techniques, use of a pelvic binder may be indicated. Whether it is a commercial product or an impro‑ vised sheet, the principle behind the use of a pelvic binder is to reduce the potential space of the pelvis and to tamponade the associated venous bleeding. Epidemiologic and biometric data suggest that the correct application of a pelvic binder reduces mortality  [26]. Although routinely used in prehospital care in the past, there is a theoretical concern for worsening of vascular injury and hemorrhage due to vessel laceration by bony frag‑ ments. Therefore, care should be taken when applying a binder. Lower extremity

Lower extremity neurovascular exam

Like the upper extremity, a thorough lower extremity neurovas‑ cular exam should be completed and documented before and after any intervention or patient movement. The tibial, sural, superficial peroneal, and deep peroneal nerves should be assessed for both motor and sensory function. The femoral and obturator nerves should be assessed when there is concern for pelvic and hip fractures (Table 36.2). The vascular exam involves palpation of the popliteal, dorsal pedal, and posterior tibial pulses.

Hip

Hip fractures are common, accounting for more than 300,000 hospitalizations per year in the United States [27]. Age and sex are major risk factors: 80% of hip fractures occur in patients aged 75 or over, and nearly three out of every four patients are female [28]. More than 90% of hip fractures are due to elderly

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Table 36.2  Lower extremity neurologic examination Nerve

Motor

Sensory

Tibial Sural Superficial peroneal Deep peroneal Femoral Obturator

Toe flexion N/A Ankle eversion Ankle dorsiflexion Knee extension Hip adduction

Plantar foot surface Posterolateral calf and foot Dorsal foot surface First dorsal web space Anterior thigh and knee Medial thigh

Table 36.3  Upper extremity immobilization approach Bone

Approach

Clavicle, scapula, shoulder Humerus Elbow

Sling and swathe Sling and swathe, short board Short board A‐splint (bent) or straight with short boards Short board with sling Short board or pillow in position of function with sling Malleable metal splint or tongue depressor with buddy splinting

Forearm Wrist, hand Finger

Short or long board splints are generally interchangeable with air or vacuum splints.

Table 36.4  Lower extremity immobilization approach Bone

Approach

Hip Femur Knee Tibia, fibula Ankle, foot Toe

Backboard or long board splints, pillows Traction splint Short board A‐splint (bent) or long board splints (straight) Long board splints Pillow splint Buddy taping

Short board or long board splints are generally interchangeable with air or vacuum splints.

falls, but they may also result from high‐energy trauma (such as from a motor vehicle collision) [29]. Classically, patients present with pain and shortening and external rotation of the affected limb [30]. However, these findings can be inconsistent depend‑ ing on the anatomical location of the fracture. Prehospital clinicians should rely on their standard trauma assessments to assess injuries to the hip. As a large amount of force is needed to fracture a hip in younger patients, concom‑ itant injuries are found in 40%–75% of cases [31]. Among the elderly, clinicians should evaluate for precipitating factors, other fall‐related injuries, and conditions related to delays in access‑ ing care. Depending on patient condition, further prehospital management could include general orthopedic trauma care, appropriate splinting, and aggressive analgesia as tolerated. While it is possible to provide skin traction using a commercial device for hip fractures, a 2011 Cochrane review found no benefit from preoperative traction of any sort [32].

Hip joints are inherently stable. Dislocations are gener‑ ally caused by high‐energy trauma, most often motor vehicle crashes. The force required to dislocate a hip is so great that 95% of these patients will have other major injuries as well [33]. Ninety percent of hip dislocations are posterior dislocations of the femoral head, while the remaining 10% are either anterior or medial (associated with acetabular fractures) [34]. Patients will most commonly complain of severe hip pain and limb defor‑ mity in the setting of a significant mechanism of injury. Due to the high rate of concomitant injuries, prehospital clinicians should generally approach those with suspected hip dislocations as major trauma patients. The focus of care should be on prompt packaging and transport, as these patients have significantly increased rates of serious neurovascular complica‑ tions if the dislocation is not reduced within 6 hours [35]. How‑ ever, appropriate splinting and analgesia should not be ignored.

Femur

As with hip dislocations, femoral shaft fractures are often seen in younger patients as a result of major trauma [29]. Of note, large‐volume hemorrhage can occur in the thigh, with poten‑ tial development of distal limb ischemia or clinically significant hypovolemia  [36]. Owing to the large size of the thigh, compartment syndrome is rare [37]. These fractures can be readily diagnosed in the field, as the thigh is generally painful, swollen, and deformed, while the affected limb appears shortened. Although there are limited data pertaining to their application in the prehospital setting, commercial traction splints have long been standard care in the field management of isolated femoral shaft fractures [25, 38, 39]. Their use is discussed later in this chapter.

Knee

Knee injuries include fractures, dislocations, and damage to the supporting structures of the joint, including all ligaments and menisci. When splinting knee injuries, it is often best to immobilize the limb in the position found or in the position of comfort  [33]. Care should be taken not to splint the leg fully extended, as this may compress the neurovascular bundle against the posterior tibia [40]. Although relatively uncommon, knee dislocations require additional care in the prehospital setting. Tibiofemoral dislo‑ cations can result from motor vehicle collision, sports injuries, and even falls [41]. These injuries have the potential to cause severe vascular damage at the site of the popliteal artery, leading to distal ischemia  [35]. Prompt treatment and trans‑ port are crucial to prevent long‐term damage to the affected limb. In extreme cases (such as severely delayed transport or other extenuating conditions significantly delaying definitive care), properly trained and authorized prehospital clinicians may consider attempting reduction in the field, if necessary, to restore distal circulation. Of note, up to 50% of knee dislo‑ cations spontaneously reduce prior to emergency department presentation [42].

Orthopedic injuries

Fractures of the tibial plateau can occur from both low‐ and high‐energy trauma and are seen in both young adults and the elderly  [43]. Those occurring at the medial plateau have the potential to damage the peroneal nerve and/or the popliteal artery, leading to distal neurovascular impairment [35]. Further complications can include the development of compartment syndrome, although this generally occurs 24‐48 hours after the time of injury [44].

Leg injuries

The tibia is the most commonly fractured of all long bones [45]. Eighty percent of the time there is an associated fibular frac‑ ture due to their adjacent positioning and attachment via the syndesmotic ligament [46]. This ligament can transmit energy between the bones such that they may be fractured at nonadja‑ cent sites [35]. The lower leg can be immobilized with a variety of devices, including cardboard, padded wood, and vacuum splints  [33]. Similar to the knee, it is best to immobilize the leg with a slight amount of flexion [35]. Care should be taken to also immobi‑ lize the ipsilateral knee and ankle, as the long bones of the leg play an important role in stabilizing the adjacent joints  [47]. Compartment syndrome is once again a concern, occurring in 8.1% of tibial shaft fractures [48].

Ankle and foot injuries

When splinting ankle or foot injuries, consider pillow splints, air splints, or any other method that avoids pressure on the boney prominences [33]. As with knee dislocations, if patient transport is to be significantly prolonged, properly trained and authorized prehospital personnel may consider reducing dislocated ankle joints that show signs of distal neurovascular compromise. Many foot and ankle injuries can be subtle and difficult to identify solely on clinical exam but may be at risk for long‐term complications if not evaluated early  [49]. To aid in triage of these patients, criteria such as the Ottawa decision rules have been developed to help emergency department clinicians deter‑ mine the need for radiographs [50, 51]. However, such methods have not been validated in the prehospital setting. Without a validated method to rule out severe injury in the field, every effort should be made to transport these patients for further evaluation. Spine Injuries of the bony spine and spinal column are of concern in patients with multiple system trauma. The cervical spine is the most injured area of the spine, followed by the thoracolumbar spine, lumbar, and thoracic spine, respectively  [52]. The inci‑ dence of cervical spine fractures in trauma has been estimated to be approximately 4% [53]. However, the incidence of cervical spine injuries is higher (5%‐10%) in patients with head trauma or trauma above the clavicles [54]. While the overall incidence of concomitant spinal cord injuries in all blunt trauma has been estimated to be less than 2%, it is the possibility of severe

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neurologic impairment, including paralysis, lasting disability, or death that raises the level of concern and caution in the prehos‑ pital and acute care environment [48]. Patients with vertebral spine or spinal cord injury can present with a variety of symptoms, from obvious paralysis to subtle neurologic deficits or simply neck or back pain. The primary trauma survey may reveal clues to high cervical spine trauma. For example, patients with high cervical injuries may have impairment of the phrenic nerve, presenting with abnormal breathing or respiratory failure that can rapidly progress to death. Neurogenic shock due to impairment of the autonomic pathways presents with hypotension refractory to fluids and often accompanied by bradycardia. Assessment of neurologic disability may further raise suspi‑ cion of severe vertebral column injury. Patients with diminished sensorium have higher potential for harboring occult spinal cord trauma. A careful secondary survey should include a more thorough assessment of neurologic status including motor and sensory testing. Furthermore, prehospital clinicians should be alert for neurologic symptoms indicative of central cord, ante‑ rior cord, and Brown‐Sequard syndromes. The most common of these, central cord syndrome, occurs frequently in the elderly and classically presents with bilateral weakness, most severe in the distal upper extremities. Spinal injury should be suspected in any patient with any of the following findings: • Evidence of multiple traumatic injuries • Focal neurologic symptoms such as weakness or numbness • Neck pain, back pain, or midline spine tenderness • Head injuries with significant mechanism AND altered mental status or evidence of significant intoxication • Distracting painful injuries in the setting of a suspicious mechanism • Torticollis in children Maintenance of neutral positioning of the spine through spinal motion restriction is the standard of care for any patient with suspected spinal injury. Previously referred to as “spinal immobilization,” the change in terminology to the term “spinal motion restriction” (SMR) acknowledges that true immobili‑ zation cannot be achieved. Two large, multicenter studies were conducted to explore predictors for safely clearing patients from SMR without radiographic imaging  [55, 56]. However, it is important to note that these studies were not conducted in the prehospital setting. Additionally, each study asked the question of whether or not to image the spine prior to clearing SMR, not whether to attempt motion restriction during initial assessment. The most common technique for SMR includes placing the patient in a hard cervical collar and on a backboard. Once SMR is initiated, the average amount of time patients spend on a backboard has been estimated to be over 1 hour [57]. Prolonged use of a rigid backboard is associated with several complications such as pain and pressure ulcers as well as respiratory compro‑ mise and aspiration events. Additionally, there are several cir‑ cumstances of prehospital care, such as wilderness or search

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and rescue settings, in which total spinal restriction places sub‑ stantial risks of injury to the first responders. Given the range of significant complications associated with full SMR, there has been much interest in the prehospital and trauma litera‑ ture regarding the utility of both full spine and cervical spine motion restriction [58]. There is increasing use of selective SMR policies among EMS systems (Chapter  40: Trauma Stabilizing Procedures) Some systems have examined the outcomes associ‑ ated with these policies, with promising results indicating that such policies could be implemented safely in the prehospital setting [59–61]. In 2018, the National Association of EMS Phy‑ sicians, the American College of Emergency Physicians, and the American College of Surgeons Committee on Trauma shared a joint position statement regarding consensus principles guiding the use and best practices for appropriate SMR in the prehos‑ pital setting. These principles highlighted the goals of identi‑ fying a cohort of the patients at highest risk for spinal injury, reducing motion (and morbidity) around potentially unstable spinal fractures, and minimizing harm induced by SMR devices and techniques [62].

Splinting Indications and basic technique Splinting is the mainstay of emergent immobilization of an injured extremity. Whether the injury is a fracture, dislocation, or sprain, immobilization in the position of comfort will help to reduce pain and chance of further injury. Other indications for splinting include reduction of hemorrhage and maintenance of alignment after reduction of a fracture or dislocation [33, 63]. The basic technique for splinting an injured extremity includes protecting the skin and soft tissue, applying a rigid material to immobilize the painful extremity, and securing the rigid material with a flexible material. While immobiliza‑ tion is essential, a splint should also not be applied tightly or circumferentially to the limb to avoid neurovascular compres‑ sion and compromise. The general rule of thumb is to leave at least one surface of a limb exposed in order to allow for continued swelling and to prevent complications [33]. Splinting materials There are many commercial materials made of fiberglass or other durable components. These are primarily used in the emergency department or wilderness settings for longer‐term splinting. In the prehospital setting, where transport time is limited to generally less than 1 hour, and patient function and mobility is also limited, temporary materials such as cardboard secured by tape will provide sufficient immobilization and pain control. In austere settings, such as the wilderness or during a disaster response, nontraditional items can easily be repurposed to create a variety of splints or slings. For example, a large sheet or piece of clothing can be tied tightly as a pelvic binder. Any large stick can be fastened to an extremity with tape or clothing

for immobilization  [64]. Even prefabricated extremity splints (e.g., fiberglass) can be fashioned into effective, temporary cervical collars  [65]. Additionally, larger water bottles or jugs, when filled with water and fastened with rope, can provide the weighted component for a makeshift traction splint [58]. Traction splints Prehospital use of traction devices for orthopedic trauma has been considered standard treatment of femoral shaft fractures [25, 33, 34]. Commercial traction splints are consid‑ ered required ambulance equipment [66]. These recommenda‑ tions posit that traction reduces pain and limits further blood loss, neurovascular damage, or soft tissue injury. However, there are downsides to prehospital traction splinting. Proper splint application requires two trained clini‑ cians approximately 5 to 6 minutes to perform, contributing to EMS on‐scene intervals [67]. Case studies have identified epi‑ sodes of transient peroneal nerve palsies, compartment syn‑ drome, urethral injury, pressure ulcers, and distal ischemia as a result of prolonged use of EMS traction devices [68]. Further research has demonstrated suboptimal rates of proper splint application, much of which is attributed to the infrequency of its usage  [69, 70]. Additionally, a recent Cochrane review found no benefit or significant analgesia related to preopera‑ tive hip traction [27]. Further research is needed to better guide prehospital usage of these devices.

Reductions with (and without) medications Field reduction versus definitive care While fracture and dislocation immobilization is a main‑ stay of prehospital trauma care, joint and fracture reduction are not included in the national EMT, AEMT, or paramedic scope of practice  [71]. Prehospital clinicians must be aware of local scope of practice authorizations before attempting a reduction, and if necessary, make appropriate direct medical oversight contact prior to attempting the procedure. System variations in protocol and expanded scope of practice should be considered for regions with large rural areas and extended transport times. Furthermore, programs that regularly staff large sporting events may provide additional training to their clinicians that could allow for more aggressive field reduction techniques. When considering implementation of such proto‑ cols, availability of both on‐scene supervisory personnel (e.g., EMS physician or sports medicine physician) and analgesia should be considered  [11]. Additionally, adequate training should be provided prior to implementing such protocols. A study performed in Europe examined differences in success rates for simple reductions among physicians working in the prehospital setting and found increased success among sur‑ geons compared to anesthesiologists and internists, which correlated most strongly with prior experience and skill level [72].

Orthopedic injuries

The decision to attempt a field reduction of an extremity fracture or dislocations is specific not only to the individual EMS system, but also to each clinical scenario. There are widely accepted indications for one attempt at gentle reduction, which includes distal neurovascular deficit or severe angulation [73]. However, even these should generally be deferred if anticipated transport time is minimal (e.g., less than 30 minutes). There are good reasons not to perform field reductions except for the most critical circumstances (e.g., pulse deficit), which include converting a dislocation to a fracture‐d­islocation, ca­using further neurovascular compromise, or converting a closed fracture to an open one. Without prereduction films, there is no proof that a fracture preceded a reduction attempt. If a reduction is performed, the extremity should be splinted immediately after in the position of function, distal neurovas‑ cular status reassessed, and the patient should always be trans‑ ported to the emergency department. Another reason to defer joint or fracture reduction until after arrival in the emergency department is lack of adequate analgesia. Many joint or frac‑ ture reductions that occur in the emergency department benefit from local or regional anesthetic, further pain medication administration, or even sedation. The quantity of medica‑ tions used, the time required for monitoring throughout the procedure, and the potential sequelae of medication interac‑ tions or oversedation are risks that should be considered before protocol creation and individual cases. Common field reductions without medications Despite the risks enumerated above regarding reductions of complex fractures or dislocations, there are several examples of simple reductions that can be performed without additional medication administration. Early performance of such reduc‑ tions, including in the prehospital setting, can ultimately improve the comfort and well‐being of the patient, the subsequent time spent in the ED, and the need for potentially sedating medica‑ tions such as opioids [74–76 ]. Examples of such potential reduc‑ tions include finger dislocations, anterior shoulder dislocations, and patellar dislocations. Nonmedicated or even patient‐led reductions of anterior shoulder dislocations have been among the most studied of these techniques in emergency medicine. Often, such dislocations are recurrent issues or nontraumatic in nature. Multiple studies have demonstrated the success of a variety of reduction techniques that do not need premedication, including scapular massage, the “Chair,” “FARES (FAst, REli‑ able and Safe),” and “Stimson” techniques  [77–79]. However, these studies have not been replicated in the prehospital setting or with nonphysician clinicians. Patients with recurrent dislo‑ cations may be knowledgeable of patient‐led techniques, and in such cases, a paramedic could assist or provide comfort to a patient in his or her attempt at self‐reduction. The best evidence for a prehospital protocol of an EMS‐performed patellar dislo‑ cation reduction examined outcomes following initiation of a formal patella reduction protocol in New York State. Implemen‑ tation of this protocol had a success rate of 92% and an average

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reduction in pain score from 10 to 2 (on a 1‐10 scale), with no reported complications [80].

Special considerations: partial or complete amputations and neurovascular injuries EMS clinicians are often the first medical personnel to encounter a patient suffering from a traumatic amputation and must be prepared to care for the amputated part as well as the patient. Once priorities such as bleeding control are addressed through either direct pressure or a tourniquet, attention should be turned to recovering and preserving the amputated part in addition to obtaining a thorough history that includes time of amputation, mechanism of injury, and the patient’s handed‑ ness and occupation. EMS clinicians should not prognosticate likelihood of replantation. The stump can be gently cleaned of debris and gross contamina‑ tion with sterile saline and then covered with sterile gauze moist‑ ened with saline. The blood vessels of the stump should not be clamped, nor should the stump be manually debrided. An under‑ lying fracture should be assumed, and the extremity should be splinted as such; this is particularly important in the setting of a partial amputation. Efforts should be taken by the EMS crew on scene to locate the amputated part, and if the patient is not stable enough to await locating it, then another responder should be instructed to locate, store, and transport it to the hospital urgently. The amputated part should be wrapped in a saline‐moist‑ ened gauze pad and placed in plastic bag, which then should be placed in a container of ice. The goal temperature is 4°C and care should be taken not to freeze the part. The part should not be placed directly on ice or be immersed in saline  [81]. The patient should be transferred urgently to a replantation capable hospital, if available. If the patient meets major trauma criteria and the trauma center is not a replantation center, the patient should preferentially go to the trauma center [66].

Conclusion Orthopedic injuries commonly present in the prehospital setting. EMS physicians, clinicians, and systems must be pre‑ pared to evaluate and treat these injuries appropriately. EMS physicians can provide a benefit to their systems by under‑ standing the current evidence and best practices.

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Science, Management and Reconstruction. 4th ed. Philadelphia, PA: Saunders Elsevier, 2009. 44 Chang YH, Tu YK, Yeh WL, Hsu RW. Tibial plateau fracture with compartment syndrome: a complication of higher incidence in Taiwan. Chang Gung Med J. 2000; 23:149–55. 45 Russell TA. Fractures of the tibial diaphysis. In: Levine AM, editor. Orthopedic Knowledge Update: Trauma. Rosemont, IL: American Academy of Orthopedic Surgeons, 1996:171–9. 46 Court‐Brown CM, McBirnie J. The epidemiology of tibial fractures. J Bone Joint Surg Br. 1995; 77:417–21. 47 Trafton PG. Tibial shaft fractures. In: Browner BD, Jupiter JB, Levine AM, et  al., editors. Skeletal trauma: basic science, management and reconstruction. 4th ed. Philadelphia, PA: Saun‑ ders Elsevier, 2009. 48 Park S, Ahn J, Gee AO, et  al. Compartment syndrome in tibial fractures. J Orthop Trauma. 2009; 23:514–8. 49 Abu‐Laban RB, Rose NG. Ankle and foot. In: Marx JA, Hockberger RS, Walls RM, et al. editors. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 8th ed. Philadelphia, PA: Saunders Elsevier, 2014. 50 Bachmann LM, Kolb E, Koller MT, et al. Accuracy of Ottawa ankle rules to exclude fractures of the ankle and mid‐foot: systemic review. BMJ. 2003; 326:417. 51 Dowling S, Spooner CH, Liang Y, et al. Accuracy of Ottawa Ankle Rules to exclude fractures of the ankle and midfoot in children: a meta‐analysis. Acad Emerg Med. 2009; 16:277–87. 52 Lin M, Mahadevan SV. Spine Trauma and Spinal Cord Injury. In: Adams JG, editors. Emergency Medicine. 1st ed. Philadelphia, PA: Saunders Elsevier, 2008. 53 Grossman MD, Reilly PM, Gillett T, et  al. National survey of the incidence of cervical spine injury and approach to cervical spine clearance in U.S. trauma centers. J Trauma. 1999; 47:684–90. 54 Marion DW. Head and spinal cord injury. Neurol Clin. 1998; 16:485–502. 55 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. National Emergency X‐Radiography Utilization Study Group. N Engl J Med. 2000; 343:94–9. 56 Stiell IG, Clement CM, McKnight RD, et al. The Canadian C‐spine rule versus the NEXUS low‐risk criteria in patients with trauma. N Engl J Med. 2003; 349:2510–8. 57 Cooney DR, Wallus H, Asaly M, et al. Backboard time for patients receiving spinal immobilization by emergency medical services. Int J Emerg Med. 2013; 20;6:17. 58 National Association of Emergency Medical Services Physicians. EMS spinal precautions and the use of the long backboard. Prehosp Emerg Care. 2013; 17:392–3. 59 Domeier RM, Frederiksen SM, Welch K. Prospective performance assessment of an out‐of‐hospital protocol for selective spine immo‑ bilization using clinical spine clearance criteria. Ann Emerg Med. 2005; 46:123–31. 60 Stroh G, Braude D. Can an out‐of‐hospital cervical spine clearance protocol identify all patients with injuries? An argument for selective immobilization. Ann Emerg Med. 2001; 37:609–15. 61 Burton JH, Dunn MG, Harmon NR, et al. A statewide, prehospital emergency medical service selective patient spine immobilization protocol. J Trauma. 2006; 61:161–7. 62 Fischer PE, Perina DG, Delbridge TR, et  al. Spinal motion restriction in the trauma patient–a joint position statement. Prehosp Emerg Care. 2018; 22:659–61. 63 Fitch MT, Nicks BA, Pariyadath M, et al. Videos in clinical medi‑ cine: basic splinting techniques. N Engl J Med. 2008; 359:e32.

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64 Kassel MR, Gianotti A. Splints and slings. In: Auerbach PS, editor. Wilderness Medicine. 6th ed. Philadelphia, PA: Elsevier Mosby, 2012. 65 McGrath T, Murphy C. Comparison of a SAM splint‐molded cervical collar with a Philadelphia cervical collar. Wilderness Environ Med. 2009; 20:166–8. 66 American College of Surgeons Committee on Trauma, American College of Emergency Physicians, National Association of EMS Physicians, Pediatric Equipment Guideline Committee— Emergency Medical Services for Children Partnership for Children Stakeholder Group, American Academy of Pediatrics. Equipment for ambulances. Prehosp Emerg Care. 2009; 13:364–9. 67 Hedges JR, Feero S, Moore B, et al. Factors contributing to para‑ medic on scene time during evaluation and management of blunt trauma. Am J Emerg Med. 1988; 6:443–8. 68 Agrawal Y, Karwa J, Shah N, et al. Traction splint: to use or not to use. J Perioper Pract. 2009; 19:295–8. 69 Abarbanell NR. Prehospital midthigh trauma and traction splint use: recommendations for treatment protocols. Am J Emerg Med. 2001; 19:137–40. 70 Daugherty MC, Mehlman CT, Moody S, et  al. Significant rate of misuse of the hare traction splint for children with femoral shaft fractures. J Emerg Nurs. 2013; 39:97–103. 71 NHTS. National EMS Scope of Practice Model. Available at: https://www.ems.gov/education/EMSScope.pdf. Accessed July 27, 2020. 72 Siebenbürger G, Zeckey C, Fürmetz J, Böcker W, Helfen T. Med‑ ical speciality, medication or skills: key factors of prehospital joint reduction. A prospective, multicenter cohort study. Eur J Trauma Emerg Surg. 2018; 44:637–42. 73 Limmer DJ, O’Keefe MF, Grant HT, et al. Emergency Care. 12th ed. Upper Saddle River NJ: Prentice Hall, 2011. 74 Connor DR, Schwarze D, Perdomo M, Fragomen AT. Painless reduction of acute anterior shoulder dislocations without anes‑ thesia. Orthopedics. 2006; 29:528–32. 75 Jaques K, Beard D, Dewar A, et al. Procedural sedation and anal‑ gesia in the emergency department: what are the factors associated with complications? Proceedings of the 5th European Congress on emergency medicine. Munich, Germany; 2008 September 15‐18th. Eur J Emerg Med. 2008; 15:293–4. 76 Sacchetti A, Senula G, Strickland J, et al. Procedural sedation in the community emergency department: initial results of the ProSCED registry. Acad Emerg Med. 2007; 14:41–6. 77 Alkaduhimi H, van der Linde JA, Willigenburg NW, van Deurzen DFP, van den Bekerom MPJ. A systematic comparison of the closed shoulder reduction techniques. Arch Orthop Trauma Surg. 2017: 137,589–99. 78 Guler O, Ekinci S, Akyildiz F, et  al. Comparison of four differ‑ ent reduction methods for anterior dislocation of the shoulder. J Orthop Surg Res. 2015; 10:80. 79 Smith SLF. An investigation comparing the Oxford chair tech‑ nique with the traditional methods of glenohumeral disloca‑ tion reduction currently implemented. Int Emerg Nurs. 2009; 17:38–46. 80 Lord S, Brodell J, Lenhardt H, Dailey M, Cushman J. Implementa‑ tion of a prehospital patella dislocation reduction protocol. Prehosp Emerg Care. 2020; 29:1–4. 81 Moorell D. Management of amputations. In: Roberts JR, Custalow CB, Thomsen TW, et al., editors. Roberts & Hedges’ Clinical Procedures in Emergency Medicine. 6th ed. Philadelphia, PA: Saunders Elsevier, 2014.

CHAPTER 37

Ocular trauma Eric Hawkins and Joseph Blackwell

Introduction Traumatic eye injuries are extremely common in the prehospital setting and range from the minor to the sight‐threatening. They may occur as isolated injuries or as part of more extensive maxillofacial or multisystem trauma. EMS physicians must be prepared to rapidly identify serious problems that could result in permanent blindness or further complications. Once significant eye injuries are recognized, the patient should be stabilized, appropriately treated, and evaluated by a hospital or physician with adequate access to full ophthalmologic services to provide definitive care.

Epidemiology In the United States, an estimated 2‐3 million people seek medical attention for eye injuries each year [1, 2]. Among many risk factors, the most significant seem to be male sex and age under 30 [3]. Many minor eye problems require no treatment [2]. Of patients with more serious injuries, 16% have ocular or orbital damage, and over 50% of patients with significant facial trauma have associated sight‐threatening eye injuries [4]. Trauma is the second most common cause of monocular blindness, trailing only cataracts. Each year, eye injuries are the number one cause of ophthalmologic hospital admissions in the United States, and eye trauma is considered the most common cause of enucleation in children over 3 years of age [5].

Evaluation Initial assessment and treatment should focus on the ABCs of trauma resuscitation, and any life‐threatening injuries should be addressed first [6, 7]. Eye injuries can be distracting; it is important not to divert attention from other sources of serious injury

early in the trauma survey process. Associated facial trauma and swelling may affect airway patency, thus the airway may need to be secured before further examination of the orbit. After initial stabilization and primary survey, a thorough evaluation of ocular injuries should be performed. In the case of known or suspected chemical contact to the face and eye, immediate irrigation with normal saline or clean water should be performed during this evaluation process. The key evaluation components for traumatic eye injuries are a thorough history and careful eye examination. The history focuses on key points surrounding the event and should note the type of injury, the time of onset, and any specific symptoms reported by the patient  [6]. Mechanism of injury is also recorded and may include blunt or penetrating trauma and thermal or chemical burns to the eye or periorbital areas of the face. Other important points include the patient’s visual acuity before the injury, if known, the presence or absence of contact lenses, any past medical history of eye disorders, and any history of ophthalmologic surgical or medical treatment [7]. The physical examination of the eye begins with evaluation of visual acuity, establishing a baseline level of function, and providing functional assessment of possible damage to the eye [7, 8]. In the field, this can be performed using a handheld Snellen chart to document the smallest objects or letters identifiable at a specific distance from the eye. Visual acuity is recorded for each eye individually and then using both eyes simultaneously [7]. If no chart is available, a newspaper or other source of small print is useful to estimate visual acuity. Patients should wear their usual prescription glasses for reading this examination, but contact lens wearers should not place them for this examination (if they are not already in). If the patient’s glasses are unavailable, it is possible to use a piece of paper with a small pin‐sized hole through which the patient can view the chart and complete the examination  [6, 7]. This “pinhole test” corrects for the refractive error of the patient’s eyes and should allow completion of the examination. For those who cannot read the

Emergency Medical Services: Clinical Practice and Systems Oversight, Third Edition. Volume 1: Clinical Aspects of EMS. Edited by David C. Cone, Jane H. Brice, Theodore R. Delbridge, and J. Brent Myers. © 2021 NAEMSP. Published 2021 by John Wiley & Sons, Inc.

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Snellen chart due to injury or underlying ocular disease, other options include assessing the patient’s ability to count fingers, detect hand motions, or perceive the presence or movement of light [6]. The method of testing and patient performance should be documented for each eye. After rapid evaluation of visual acuity, the external eye and surrounding structures should be examined. Each globe is examined for protrusion or proptosis and for external signs of penetration or damage from a foreign body. (Figures  37.1 to 37.3) Ocular movement in the cardinal directions of gaze (vertical up‐down, horizontal right‐to‐left, and diagonal left‐to‐ right and right‐to‐left) is tested and any deficit or entrapment recorded. The pupil and iris are inspected for size, shape, and reaction to light. Results should be compared between eyes. The presence or absence of a hyphema (blood in the anterior chamber that may obscure the iris or pupil) is especially important (Figure  37.4). Finally, the conjunctivae are inspected for erythema, subconjunctival hemorrhage, chemosis, conjunctival swelling, or subconjunctival emphysema. If the patient reports

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a foreign body sensation in the eyelid (Figure 37.5) or if there is any concern for an intraocular foreign body or a punctured globe (such as teardrop shaped pupil or vitreous extrusion) (Figure  37.6), the examination should conclude at this point. The affected eye should be covered with an eye shield or improvised protective device (such as a cup or shield) to protect the globe from external pressure before transport for more definitive evaluation and care  [7]. The EMS physician should not remove a protruding foreign body (such as a nail) lodged in the globe, and any foreign body should be stabilized in place. Finally, examination of the surrounding structures of the eye focuses on associated maxillofacial trauma or related complications. The eyelids and periorbital soft tissues are inspected for lacerations, ecchymosis, edema, foreign bodies, and cutaneous evidence of thermal or chemical burns. The orbital rims are similarly inspected and palpated for signs of crepitus or obvious bony deformities. If injuries are unilateral, comparisons

Figure 37.3  Intraocular foreign body on slit lamp. Source: Michael Mills.

Reproduced with permission of Michael Mills.

Figure 37.1  Intraocular foreign body x‐ray (lateral view). Source: Michael

Mills. Reproduced with permission of Michael Mills.

Figure 37.2  Intraocular foreign body x‐ray (anterior‐posterior view). Source: Michael Mills. Reproduced with permission of Michael Mills.

Figure 37.4  Hyphema from air bag injury. Source: Michael Mills.

R­eproduced with permission of Michael Mills.

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Figure 37.5  Foreign body in eyelid. Source: Michael Mills. Reproduced

with permission of Michael Mills.

Figure 37.6  Ruptured globe. Source: Michael Mills. Reproduced with

p­ermission of Michael Mills.

are made between the eyes because normal foramina of the surrounding eye rim may be mistaken for fractures. If the patient has obvious periorbital trauma, an orbital blowout fracture with associated diplopia or inability to move the eye superiorly is concerning. Finally, the patient should have a sensory examination of the skin around the eye. Any numbness or paresthesias could indicate damage to the infraorbital nerve.

Specific eye injuries Ocular burns Ocular chemical burns are true ophthalmic emergencies and are best treated in the field with copious irrigation with water or normal saline. Delays in irrigation have been associated with increased risks to visual acuity and higher rates of subsequent complications when compared with immediate irrigation of the eye [9]. Tap water and normal saline work equally well initially, with the keys being the volume and duration of irrigation

rather than the type of fluid. Patients with chemical burns will present with tearing, photophobia, conjunctival redness, pain, and, in the case of severe alkali burns, the eye may appear white secondary to ischemia of the conjunctival and scleral vessels  [10]. Irrigation should continue during transport for a minimum of 30 minutes or until hospital arrival for significant exposures. Important historical information to obtain includes the duration of exposure, type of chemical, and the pH of the substance if known. If the chemical is an industrial source, a Safety Data Sheet is particularly helpful to identify and categorize the substance in question [10]. Injuries from acid exposures tend to be less serious than alkali substances [11], but this varies by the chemical involved. Common household products that contain alkali materials include cleaning solutions containing sodium hydroxide, ammonia, and calcium hydroxide [12]. In addition to irrigation, proper prehospital management includes pain control and transport to an appropriate center for immediate ophthalmologic consultation and evaluation. Globe injuries Open globe injuries have full thickness defects in the ocular wall and include lacerations, intraocular foreign bodies, and globe rupture from blunt trauma  [13]. These high‐energy mechanisms of injury are frequently associated with other ocular or periorbital injuries. Symptoms include decreased visual acuity, difficulty with ocular motility, and abnormal or absent pupillary reflexes. On examination, open globe injuries may be evident on gross inspection, as with a visible foreign body, a large scleral laceration with clear penetration, or an obvious deformity of the eye or pupil (teardrop pupil). However, penetrating injuries may cause negligible external damage to the sclera or globe, and a small intraocular foreign body may cause minimal pain after the initial event [14]. The key point for the EMS physician is to consider an open globe, especially if there is associated significant head injury, periorbital damage, or hyphema. Once an open globe is suspected, all further evaluation of the eye should be postponed until definitive care is available [7]. The eye should be protected with a hard eye shield, and the patient should be transported for further emergency evaluation and potential surgical repair by an ophthalmologist. Other appropriate prehospital care includes pain control, elevation of the head of the bed to 30 to 45 degrees, and antiemetic medication to reduce potential increased intraocular pressure during vomiting. Closed globe injuries occur when there is partial penetration of the eye and include hyphema, damage to the retina, superficial abrasions and lacerations, and nonpenetrating foreign bodies. These can cause significant eye pain, loss of visual acuity, and decreased ocular function, but vary by the type and location of injury. Traumatic hyphema A traumatic hyphema is a collection of blood in the anterior chamber of the eye caused by blunt or penetrating injury. The highly vascular ciliary body or iris is usually the

Ocular trauma

Grade 1: less than 33% filled with layered blood

Grade 2: 33-50% filled with layered blood

Grade 3: 50% to less than the entire anterior chamber filled with layered blood

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Grade 4: complete filling of the anterior chamber with layered blood

Figure 37.7  Grading of traumatic hyphema. Source: Courtesy of Dr. Joseph Blackwell.

source of bleeding for a hyphema and is often associated with head trauma or other eye injuries to the cornea, iris, lens, or globe [15–17]. Signs include direct visualization of blood in the anterior chamber, poor visual acuity, and decreased pupil reactivity. Hyphema severity is graded on a scale of 1 to 4 based on the amount of blood in the anterior chamber when the patient is in a upright position, ranging from a minimal layering (grade 1) to a complete filling of the anterior chamber with blood (grade 4) [15, 17] (Figure 37.7). This classification is important because higher‐grade (grade 3 or 4) hyphemas have an increased risk of complications and are a threat to permanent damage or loss of visual acuity [18]. Complications include rebleeding, corneal blood staining, and damage of the optic nerve or retina from increased intraocular pressure [16–18]. Prehospital care focuses on pain management, elevation of the head of the bed from 30 to 45 degrees if possible, covering of the eye with a protective shield, and prompt transport to a medical facility for further ophthalmologic evaluation and management [16, 17]. Medical history is also very important as patients with certain medical conditions (e.g., sickle cell disease, hemophilia, or other bleeding disorders) are at a significantly increased risk for complications [19]. Corneal injuries Corneal injuries are common and may present with ocular pain, foreign body sensations, blepharospasm, or tearing [18]. Decreased visual acuity, blurred vision, and photophobia are also common initial symptoms. Corneal abrasions often result from a direct blow to the eye or a foreign body under the eyelid that irritates the corneal surface. These may be visible on gross examination, but often the lesion can only be seen on slit lamp or Woods lamp examination after staining with fluorescein dye, which is not commonly performed in the prehospital setting  [20]. Similarly, corneal foreign bodies may be seen on visual inspection of the eye and should be suspected in any patient with eye pain associated with high‐risk activities like use of power tools, grinding, hammering, or sanding objects with or without use of protective eyewear  [11]. If an object is

visualized in the eye it should be flushed with saline or removed by a skilled practitioner unless there is concern that it has penetrated the globe, in which case the eye should be covered or patched and the object left in place until appropriate evaluation by a physician. Prehospital care of corneal injuries focuses on a thorough history, pain management, and transport to a center with appropriate specialty care. Most superficial corneal injuries heal within 24 to 72 hours, but the prognosis and potential for further complications depend on the depth and overall size of the lesion [18]. Retinal injuries Trauma of the retina and posterior segments of the eye is less common than injuries to anterior eye structures, but carries a higher risk of blindness and irreversible loss of vision  [21]. Common presentations include decreased visual acuity or a report of “flashing lights” or “floaters” in the visual field of the affected eye  [22]. Retinal injuries require a complete fundus examination for definitive diagnosis, and these techniques are beyond the scope of this review and the scope of prehospital practice. For the EMS physician, it is important to remember the signs of retinal and posterior segment injury and to obtain a focused eye history and examination, including visual acuity, before transporting the patient for ophthalmologic evaluation and treatment.

Summary Ocular trauma, while rare, remains an important aspect of prehospital care as the risk of unrecognized or mismanaged injuries can lead to irreversible loss of vision. Initial evaluation is centered around the same principles as any other traumatic injury. After initial stabilization and thorough history and physical, the key components of the exam include visual acuity, extraocular movements, and other signs of trauma to the facial structures. Specific injuries are broken into the categories of open versus closed globe injuries. Open globe injuries present with

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decreased visual acuity, difficulty with extraocular movements, and abnormal pupillary reflexes. Prehospital management focuses on preventing further injury with an eye shield or stabilization of any penetrating injury or foreign body and transport to an appropriate facility. Closed globe injuries include traumatic hyphemas, corneal injuries, retinal injuries, and ocular burns. Management of these injuries is largely the same as with open globe injuries: prevention of further injury and transport for evaluation. Management of ocular burns involves the a­forementioned therapies as well as copious irrigation.

References 1 McGwin G Jr, Hall TA, Xie A, Owsley C. Trends in eye injury in the United States, 1992–2001. Invest Ophthalmol Vis Sci. 2006; 47:521–7. 2 McGwin G Jr, Xie A, Owsley C. Rate of eye injury in the United States. Arch Ophthalmol. 2005; 123:970–6. 3 Kuhn F, Morris R, Mester V, et  al. Epidemiology and socioeconomics. Ophthalmol Clin North Am. 2002; 15:145–51. 4 Poon A, McCluskey PJ, Hill DA. Eye injuries in patients with major trauma. J Trauma. 1999; 46:494–9. 5 U.S. Eye Injury Registry. Eye trauma epidemiology and prevention. Available https://useir.org/epidemiology/. Accessed September 6, 2020. 6 Harlan JB Jr, Pieramici DJ. Evaluation of patients with ocular trauma. Ophthalmol Clin North Am. 2002; 15:153–61. 7 Juang PS, Rosen P. Ocular examination techniques for the emergency department. J Emerg Med. 1997; 15:793–810. 8 Khaw PT, Shah P, Elkington AR. Injury to the eye. BMJ. 2004; 328:36–8.

9 Schrage NF, Langefeld S, Zschocke J, et al. Eye burns: an emergency and continuing problem. Burns. 2000; 26:689–99. 10 Bhattacharya SK, Hom GG, Fernandez C, Hom LG. Ocular effects of exposure to industrial chemicals: clinical management and proteomic approaches to damage assessment. Cutan Ocul Toxicol. 2007; 26:203–25. 11 Peate WF. Work‐related eye injuries and illnesses. Am Fam Physician. 2007; 75:1017–22. 12 Hemmati H, Colby KA. Treating acute chemical injuries of the cornea. American Academy of Ophthalmology. 2012. Available at: www.aao.org/eyenet/article/treating‐acute‐chemical‐injuries‐of‐ cornea. Accessed September 6, 2020. 13 Colby K. Management of open globe injuries. Int Ophthalmol Clin. 1999; 39:59–69. 14 Mester V, Kuhn F. Intraocular foreign bodies. Ophthalmol Clin North Am. 2002; 15:235–42. 15 Sankar PS, Chen TC, Grosskreutz CL, Pasquale LR. Traumatic hyphema. Ophthalmol Clin. 2002; 42:57–68. 16 Walton W, Von Hagen S, Grigorian R, Zarbin M. Management of traumatic hyphema. Surv Ophthalmol. 2002; 47:297–334. 17 Brandt MT, Haug RH. Traumatic hyphema: a comprehensive review. J Oral Maxillofac Surg. 2001; 59:1462–70. 18 Wilson FM. Traumatic hyphema—pathogenesis and management. Ophthalmology. 1980; 87:910–9. 19 Walton W, Von Hagen S, Grigorian R, Zarbin M. Management of traumatic hyphema. Surv Ophthalmology. 2002; 47:297–334. 20 Wilson SA, Last A. Management of corneal abrasions. Am Fam Physician. 2004; 70:123–8. 21 Pieramici DJ. Vitreoretinal trauma. Ophthalmol Clin North Am. 2002; 15:225–34. 22 Pokhrel PK, Loftus SA. Ocular emergencies. Am Fam Physician. 2007; 76:829–36.

CHAPTER 38

Bites, stings, and envenomations Adam Frisch, Andrew King, and Stephanie O. Frisch

Introduction Animal bites are estimated to account for one million physi‑ cian visits each year and 1% of emergency department (ED) visits [1]. The actual number of animal‐related injuries is impossible to calculate because many injuries go unreported [1, 2]. The infrequent nature of animal‐related calls, coupled with the excitement and emotion often found on scene, can lead to poor clinician judgment or errors in care. This chapter focuses on prehospital management of animal bites, stings, and envenomations and reviews injuries likely to be encoun‑ tered, with specific prehospital treatments and interventions where appropriate.

Animal bites General

Scene safety and planning

As with any EMS response, scene safety is a primary con‑ cern. When responding to a call involving animals, all per‑ sonnel should prevent or avoid interaction with the offending animal. Prehospital clinicians and medical directors should be aware of animal control resources available in their coverage areas. Protocols for responding to animal‐related calls should include these resources when appropriate and available. The primary responsibility of EMS personnel is their own safety and the safety of the patient. Clinicians should not be primarily responsible for dealing with the animals. While identification of the offending animal may be helpful for treatment, attempt‑ ing to catch, kill, photograph, collect, or quarantine the animal exposes the EMS clinician to undue risk [3]. For related rea‑ sons, transportation of animals, dead or alive, to the hospital for identification is not advised.

Refusal concerns

As many animal‐related injuries initially appear benign, both patients and clinicians often underestimate their potential seriousness, resulting in inappropriate refusal of treatment or transport. Agencies should consider mandatory medical over‑ sight contact for refusal of care in animal encounter situations, as serious risks exist.

Animal‐specific concerns Mammals Domesticated animals account for the vast majority of mam‑ malian bite wounds, with dogs and cats representing 93% to 96% of mammalian bites [2]. Bites by both types of animals occur most frequently to the upper extremity, followed by the lower extremity, and finally the face and neck [1]. Acutely lethal wounds tend to occur in young children [1]. Children are often familiar with the offending animal and are more prone to attacks to the face and neck [1, 4]. In both cats and dogs, unique oral flora contributes to considerable infection risk. While most wounds do not become infected, those that do often require in‐hospital therapy and potential operative management. Two thirds of infected hand bites in one study required hospitaliza‑ tion for IV antibiotics, and one third required at least one sur‑ gical procedure [5]. Systemic infections, including endocarditis, meningitis, brain abscess, and sepsis, are potential complica‑ tions of recent animal bites and must also be considered by cli‑ nicians and medical directors when determining protocols and transport decisions [6]. Human bites carry risks of complications like those of other mammalian bites. Hand wounds involving the metacarpal‐ phalangeal joint and overlying extensor tendons are often “fight bites” (injuries to the hand from striking teeth during an

Emergency Medical Services: Clinical Practice and Systems Oversight, Third Edition. Volume 1: Clinical Aspects of EMS. Edited by David C. Cone, Jane H. Brice, Theodore R. Delbridge, and J. Brent Myers. © 2021 NAEMSP. Published 2021 by John Wiley & Sons, Inc.

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altercation) and are especially prone to infection. More than 30% of fight bites become infected, resulting in decreased functional capacity. Fight bites often coincide with intoxication or criminal activity that may act as a barrier to prehospital care through reluctance to disclose the true mechanism, patient refusal, or law enforcement custody. Very few poisonous mammals exist in North America. Only the short‐tailed shrew, found in central and eastern sections of North America, poses a toxic threat. Several nonindigenous mammals have poisonous reputations. The shrew‐like solenodon, found in Central America, induces toxins in its saliva through grooved incisors. The platypus, found in Australia, has venomous glands introduced by spurs at the base of its hind feet. In all these ani‑ mals, the toxins serve to kill prey and defend from predators [7]. Bites to humans result in unusually painful wounds with local edema, but typically lack serious or systemic effects. Accounting for less than 10% of animal bites [2], attacks by wild or undomesticated mammals are rare and usually require only supportive care and basic wound management in the pre‑ hospital setting. In general, most bite victims should be trans‑ ported to the ED for wound evaluation, tetanus shots, rabies risk assessment (see below), and possibly antibiotics.

Rabies

Mammalian bites carry the unique risk of rabies virus trans‑ mission, which is almost universally fatal [8, 9]. Current Cen‑ ters for Disease Control and Prevention guidelines recommend postexposure prophylaxis (PEP) including immunoglobulin administration and vaccination series for high‐risk bites in vaccine‐naive individuals and a modified vaccination series for those previously vaccinated [10]. Bites from skunks, foxes, raccoons, bats, and some other carnivorous animals are con‑ sidered at risk and should receive PEP promptly. For domestic animals that appear healthy and can be quarantined for 10 days, PEP can be withheld pending development of symptoms. Patients with bites from other animals should be transported to the hospital so that the need for PEP can be determined [10]. Bats require special consideration because rabies transmis‑ sion has occurred outside of recognized bites. Although data are conflicting and perhaps viewed as controversial [10], PEP “can be considered for persons who were in the same room as the bat and who might be unaware that a bite or direct contact had occurred (e.g., a sleeping person awakens to find a bat in the room or an adult witnesses a bat in the room with a pre‑ viously unattended child, mentally disabled person, or intoxi‑ cated person) and rabies cannot be ruled out by testing the bat” [10]. Thus, EMS clinicians should have a very low threshold to transport potential victims to the ED for evaluation whether an obvious bite exists or not [10]. Reptiles

Venomous Snakes

Of the estimated 45,000 annual snakebites in the United States, roughly 8,000 are reportedly from venomous snakes. There

are 25 venomous species of snakes in the United States. The majority of these are in the subfamily of Crotalids (rattlesnakes, cottonmouths, and copperheads), and the remainder in the Elapid subfamily (coral snake) [11]. This division also repre‑ sents a difference in their respective toxins and clinical manifes‑ tations of envenomation. Crotalid venom is a primarily a hemotoxin (with some cytotoxic and neurotoxic properties) and produces symptoms ranging from local swelling and ecchymosis to systemic coagu‑ lopathy, altered consciousness, and shock. The constellation of effects begins within minutes to hours and steadily progresses to its maximal extent over several hours (up to 24 hours with leg bites). Elapid envenomations can remain relatively asymptomatic for up to 12 hours and then manifest neurotoxicity ranging in severity from paresthesias to complete paralysis requiring ven‑ tilatory support. In either case, it is important to avoid underestimating bite severity based on initial patient assessment at the scene. Although “dry bites” occur with relative frequency, the lack of clinical swelling should not lead the clinician to assume that no envenomation has occurred. A period of observation of varying lengths depending on the bite site, the suspected offending snake species, age of the individual, and medical comorbidities is recommended by toxicologists and should prompt any and all patients with suspected bites to be transported to the ED for evaluation. Much of EMS clinician education about snakebites should focus on dispelling common myths. Clinicians may encounter well‐meaning citizens attempting to render “first aid” to snake bite victims. Cold therapy, arterial tourniquets, electricity (from TASERs or car batteries), incision of the wound, and suction (via commercially available device or oral) are popular lay therapies for snakebites that are without scientific backing and may lead to more local tissue damage and infec‑ tion [3, 11–14]. While some of the literature has suggested treatments such as compression immobilization [12–14], all the major toxicolog‑ ical societies of North America advocate against this technique for U.S. crotalid envenomations [15]. Keeping the patient calm and immobilizing the affected extremity in a neutral position is the best course of action in the prehospital setting. Insufficient evidence exists for compression immobilization in hemodynamically unstable patients. Effectiveness of pressure immobilization has been suggested in the setting of Australian Elapid snakebites, and thus, as a corollary, compression immo‑ bilization for confirmed North American Elapid envenomation may be considered for those with anticipated long transport times [16, 17]. Furthermore, if longer transport times are antic‑ ipated after Elapid envenomation, EMS should be prepared to intervene on the airway and assist with ventilation. Routine use of antivenin therapy is not generally recommended in the pre‑ hospital setting, as it requires a significant amount of time and resources to prepare and administer [3].

Bites, stings, and envenomations

Adequate analgesia is a significant concern after crota‑ lid envenomation. In the acute phase, toxicologists recom‑ mend the use of intravenous fentanyl as opposed to other opioids so as not to confuse the crotalid envenomation symptoms with morphine‐induced histamine release, both of which can cause anaphylaxis, hypotension, and local swelling [16]. There are two FDA‐approved commercially available antivenins to treat U.S. crotalid envenomations: Crofab® and Anavip®. Crotalidae Polyvalent Immune Fab (ovine) (Crofab®) has been a mainstay of treatment of moderate to severe snake envenomations since 2000. It is derived from sheep serum after inoculation with venom from four North American Crotalide snakes: western diamondback rattle‑ snake (Crotalus atrox), eastern diamondback rattlesnake (Crotalus adamanteus), Mojave rattlesnake (Crotalus scutulatus), and cottonmouth/water moccasin (Agkistrodon piscivorus). Crotalidae immune F(ab′)2 antivenom (Anavip®) was FDA approved in 2015 and is derived from horse serum after inoculation with venom from two Crotalidae snakes not endemic to the United States: fer‐de‐lance/lancehead (Bothrops asper) and tropical rattlesnake (Crotalus durissus). While both antivenins treat Crotalidae snake enven‑ omations, they have different pharmacokinetic parameters that lead to differences in dosing. Studies evaluating relative clinical benefits are ongoing.

Nonvenomous Snakes

Most snakebites in the United States are from nonvenomous species in the Colubrid family and include the garter snake, hognose snake, banded water snake, rat snake, and parrot snake. Morbidity from these snakes is extremely rare. Trans‑ port to a hospital for observation and wound evaluation is recommended. Bites should be considered contaminated since they may contain broken teeth. Antibiotics are generally not necessary except for retained teeth or significant soft tissue injury. Constrictors and pythons are commonly kept as pets and can have very forceful bites. Their teeth are brittle and prone to fracture with attempted extrication. X‐rays to assess for retained teeth and tetanus prophylaxis should be considered, and thus EMS should recommend transport to the ED for radiographic evaluation of these bites [18].

Other Reptiles

Gila monsters and bearded lizards have venom in their saliva injected through grooved teeth and a strong and tenacious bite. Envenomation, however, is usually not lethal and most often causes only local inflammation and pain. Although rare, there have been reports of anaphylactic reactions as well as angio‑ edema, hypotension, myocardial infarction, and coagulopathy [19–21]. Other reptiles have been involved in fatal bite attacks, and appropriate trauma care should be used for these wounds. Transport should be advised as these bites are prone to infection with uncommon forms of bacteria.

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Marine animals Marine animals that sting can cause serious pain and tissue damage. North American venomous marine vertebrates (i.e., stonefish, scorpionfish, lionfish, catfish, stingrays) carry heat‐ labile toxins that generally respond to heat therapy for toxin neutralization and pain reduction [3, 14, 22–24]. Invertebrate marine animals (i.e., jellyfish) use tentacles or nematocysts to deploy their toxins. Previous recommendations include flood‑ ing the area with acetic acid (vinegar) and then scraping off the tentacles [14, 23, 24]. More recent literature suggests that hot water and topical lidocaine may be more effective for symptom control, and acetic acid may be more efficacious for bluebottle jellyfish stings [25]. Gloves or forceps should be used to man‑ ually remove visible tentacle remnants. Other therapies are sourced in folklore, including the use of urine, sand, or meat tenderizer, all of which are inappropriate. Often, reimmersion in salt water improves pain. Prehospital personnel should not routinely remove impaled foreign bodies, such as sea urchin spines or stingray barbs, as the spines easily fracture and may require surgical debridement. Insect bites and stings

Butterflies, moths, and caterpillars

The order Lepidoptera encompasses the families of butter‑ flies, moths, and their larvae, caterpillars. In the United States, the puss caterpillar, hairy tussock caterpillar, flannel moth caterpillar, Io moth, and saddleback caterpillar can have toxic effects. The venom is transmitted via hollow spines, and clinical manifestations may include local pain, burning, swelling, vesicle formation, and less commonly, nausea, vomiting, seizures, and regional adenopathy [26, 27]. Ingested or partially ingested cat‑ erpillars can cause airway swelling and respiratory compromise. Treatment is symptomatic and supportive, with antiemetics for nausea and vomiting and benzodiazepines for seizures. Severe airway swelling may respond to epinephrine, diphenhydramine, and steroids and may require upper airway and esophageal eval‑ uation by an otolaryngologist to remove retained urticating hairs/spines.

Hymenoptera

Hymenoptera account for most severe allergic responses and anaphylaxis in comparison with other insects. There are three families of Hymenoptera: Apidae (honeybees and bumblebees), Vespidae (yellow jackets, hornets, and wasps), and Formicidae (fire ants). About 1% of children and 3% of adults report severe systemic allergic reactions to Hymenoptera venom, and ana‑ phylaxis does not require a previous exposure (or sting) [28, 29]. Furthermore, if a person is allergic to one type of Hymenoptera, he or she is likely to be allergic to the others as well [30]. Clinical manifestations of Hymenoptera envenomation range from local reaction to hypersensitivity reactions (including anaphylaxis), fever, rhabdomyolysis, acute renal failure, and death [31, 32]. Apis mellifera scutellata or “killer bees” are an aggressive hybrid

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of the honeybee and have the same venom, but they are prone to mass attack, thus increasing the risk of a severe reaction [33, 34]. Fire ants are named after the burning pain and necrosis vic‑ tims experience after exposure. Grabbing the skin with its man‑ dibles, the fire ant injects venom from a stinger on its abdomen in a circular pattern an average of seven or eight times. Large areas of swelling develop that later turn into sterile pustules. Anaphylaxis is relatively common and occurs in up to 6% of those envenomated [35]. Allergic reactions should be treated with antihistamines, albuterol, and/or intramuscular epinephrine depending on the severity. Angioedema, stridor, and signs of upper airway obstruction are of concern and should be moni‑ tored closely. Cool compresses may help with local pain. Emesis and abdominal pain can be additional symptoms of anaphylaxis. and EMS should have a low threshold to transport any of these patients to the hospital and admin‑ ister epinephrine [18].

Spiders

Three species of spiders found in North America are clinically significant: the widow, the brown recluse, and the hobo spider. Black widow spider bites are often painless but may be expe‑ rienced as a pinprick sensation that quickly resolves. Calcium channel–mediated neurotransmitter release of acetylcholine and other excitatory neurotransmitters can result in extremely painful muscle spasm, hypertension, and diaphoresis in the hours following envenomation. Fatalities are rare, and therapy should be supportive. Opioids for pain and benzodiazepines to aid in muscle relaxation and minimize hypertension may be considered in the field [3, 18]. Some controversy exists among experts about the use of black widow antivenin. EMS should transfer all suspected cases of widow bites to the ED for possible antivenin administration. Brown recluse and other recluse species are found in the Mis‑ sissippi River Valley and the surrounding states, the Southeast, and the Southwest. The bite has been associated with an evolv‑ ing necrotic lesion; however, more severe systemic manifesta‑ tions have been reported, termed “systemic loxoscelism.” Signs and symptoms of loxoscelism include fever, vomiting, rhab‑ domyolysis, hemolysis, disseminated intravascular coagula‑ tion, renal failure, and death. Appropriate clinical skepticism should be exercised given the frequency of misdiagnosis and conflicting reports of loxoscelism in areas where recluses are not endemic and the attribution of more common skin lesions, including folliculitis and abscess formation, to a “spider bite” [36]. Regardless, transport to the ED for wound evaluation is recommended, and intravenous fluids and antiemetics should be administered. The hobo spider, a European native, is found in the north‑ western United States. It is reported to cause dermonecrotic lesions as well. These lesions can be associated with headache, visual impairment, nausea, vomiting, weakness, and lethargy [37, 38]. Regardless, as with the brown recluse, treatment is

supportive, and there are no specific prehospital therapies ­recommended. Fifty‐four species of tarantulas are known to habit the desert Southwest. Despite their size, their toxicity is relatively minor. New World tarantulas are equipped with urticating hairs they release in self‐defense. Depending on the species and type of hairs, clinical manifestations range from local inflammation to severe respiratory inflammation and significant eye injury. Pre‑ hospital management includes removal of hairs with cellophane tape and irrigation of the eyes. Antihistamines and corticoste‑ roids may be considered. Any patient with ocular complaints requires transport to the hospital for ophthalmological evalu‑ ation.

Scorpions

The only scorpion of toxicological importance endemic to the United States is Centruroides exilicauda (the bark scorpion). Scorpions envenomate by stinging with their tails and can cause significant morbidity, especially in children. The venom is a neurotoxin that opens sodium channels causing catecholamine and acetylcholine release. A scorpion antivenom exists and is used for those with systemic neurotoxic symptoms. Prehospital treatment may consist of symptomatic treatment with opioids and benzodiazepines [39].

Ticks

Ticks are eight‐legged arthropods that live off the blood of various animals. Accordingly, they are vectors for viral, bacte‑ rial, and parasitic diseases including Rocky Mountain spotted fever, typhus, tularemia, Lyme disease, babesiosis, ehrlichio‑ sis, Colorado tick fever, and tick‐borne encephalitis [40]. Certain North American species, namely the Lone Star tick, the American dog tick, and the Rocky Mountain wood tick, secrete venom capable of causing paralysis in a manner similar to botulinum toxin. Discussion of each of the various tick‐borne illnesses is outside the scope of this chapter; however, prehos‑ pital clinicians should be aware that prophylactic therapy may be offered to patients with known tick bites, and that the cura‑ tive therapy for tick paralysis is removal of the tick. Supportive therapy, including close attention to airway and breathing, is paramount in any patient with ascending motor paralysis from possible tick‐related disease [41, 42]. Nonindigenous animals This chapter has focused on species found in North America. EMS physicians and clinicians should take the time to learn about nonindigenous animals in their area. There is not enough room to cover all harmful animals in this chapter, and clini‑ cians should look to other toxicological texts for more in‐depth information. Exposure to nonindigenous animals can occur not only in zoos or known refuges, but also in private collections or simply as pets. In the case of private collectors, the owner often is aware of the species as well as its clinical effects but may be resistant to seeking medical care for fear of legal persecution or

Bites, stings, and envenomations

confiscation of his or her collection. Poison centers and zoos are the best resources to help find appropriate antivenoms. High‐ quality supportive care should be the standard, with local public health and poison control authorities guiding specific therapy.

Transport EMS clinicians should encourage transport to the hospital. Transport preference should be a facility with a toxicology ser‑ vice or access to a toxicology consultant. If this is not possible within a reasonable time frame, patients should be transported to a local tertiary care facility that has emergency, trauma, and surgical specialties readily available. Prehospital protocols should specify when to contact medical oversight about the use of aircraft for transport of patients to an appropriate facility.

Summary Our environment presents unpredictable encounters with animal bites, stings, and envenomations. Education on animals found locally may help EMS clinicians feel more comfortable during a response. Clinicians and medical directors should remember that most care is supportive and symptomatic. Transport to an appropriate facility will give the patient the best chance of a good outcome.

References 1 Ball V, Younggren BN. Emergency management of difficult wounds: part I. Emerg Med Clin North Am. 2007; 25:101–21. 2 Freer L. North American wild mammalian injuries. Emerg Med Clin North Am. 2004; 22: 445–73. 3 Singletary EM, Rochman AS, Bodmer JC, Holstege CP. Envenom‑ ations. Med Clin North Am. 2005; 89:1195–224. 4 Hon KL, Fu CC, Chor CM, et  al. Issues associated with dog bite injuries in children and adolescents assessed at the emergency department. Pediatr Emerg Care. 2007; 23:445–9. 5 Benson LS, Edwards SL, Schiff AP, et al. Dog and cat bites to the hand: treatment and cost assessment. J Hand Surg [AM]. 2006; 31:468–73. 6 Brook I. Management of human and animal bite wounds: an over‑ view. Adv Skin Wound Care. 2005; 18:197–203. 7 Fox RC, Scott CS. First evidence of a venom delivery apparatus in extinct mammals. Nature. 2005; 435:1091–3. 8 Jackson AC. Recovery from rabies. N Engl J Med. 2005; 352:2549–50. 9 Willoughby RE Jr, Tieves KS, Hoffman GM, et  al. Survival after treatment of rabies with induction of coma. N Engl J Med. 2005; 352:2508–14. 10 Human rabies prevention—United States, 1999. Recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. 1999; 48:1–21. 11 Gold BS, Barish RA, Dart RC. North American snake envenom‑ ation: diagnosis, treatment, and management. Emerg Med Clin North Am. 2004; 22:423–43.

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12 McKinney PE. Out‐of‐hospital and interhospital management of crotaline snakebite. Ann Emerg Med. 2001; 37:168–74. 13 Pizon AF. Snakebites: prehospital assessment & treatment of enven‑ omations. JEMS. 2007; 32:76–81, 83, 85–8. 14 Powers DW. Stings and bites: what to do about envenomation injuries. Emerg Med Serv. 2005; 34:67, 69–75. 15 American College of Medical Toxicology, American Academy of Clinical Toxicology, American Association of Poison Control Cen‑ ters, European Association of Poison Control Centres, International Society of Toxinology, Asia Pacific Association of Medical Toxicology. Position statement: pressure immobilization after North American Crotalinae snake envenomation. J Med Toxicol. 2011; 7:322–3. 16 American Pain Society. Principles of Analgesic Use in the Treatment of Acute Pain and Cancer Pain. 5th ed. Glenview, IL: American Pain Society; 2003. 17 Sutherland SK, Coulter AR, Harris RD. Rationalisation of first‐aid measures for elapid snakebite. Lancet. 1979; 1:183‑5. 18 Nelson L, Lewin N, Howland MA, et  al. Goldfrank’s Toxicologic Emergencies.9th ed. New York, NY: McGraw Hill Education; 2011. 19 Piacentine J, Curry SC, Ryan PJ. Life‐threatening anaphylaxis fol‑ lowing gila monster bite. Ann Emerg Med. 1986; 15:959–61. 20 Preston CA. Hypotension, myocardial infarction, and coagulopa‑ thy following gila monster bite. J Emerg Med. 1989; 7:37–40. 21 Bou‐Abboud CF, Kardassakis DG. Acute myocardial infarction fol‑ lowing a gila monster (Heloderma suspectum cinctum) bite. West J Med. 1988; 148:577–9. 22 Atkinson PR, Boyle A, Hartin D, McAuley D. Is hot water immersion an effective treatment for marine envenomation? Emerg Med J. 2006; 23:503–8. 23 Hertelendy A. Aquatic emergencies: pathophysiology of and treatment for underwater stings. JEMS. 2004; 29:86–92, 94, 96, 98, 100. 24 Perkins RA, Morgan SS. Poisoning, envenomation, and trauma from marine creatures. Am Fam Physician. 2004; 69:885–90. 25 Ward NT, Darracq MA, Tomaszewski C, Clark RF. Evidence‐based treatment of jellyfish stings in North America and Hawaii. Ann Emerg Med. 2012; 60:399–414. 26 Norris R. Caterpillar envenomations. 2013. Available at http:// emedicine.medscape.com/article/769448‐overview. Accessed Sept 13, 2020. 27 Norris R. Millipede envenomations, 2012. Available at: http:// emedicine.medscape.com/article/772881‐overview. Accessed Sept 13, 2020. 28 Klotz JH, Klotz SA, Pinnas JL. Animal bites and stings with anaphylactic potential. J Emerg Med. 2009; 36:148–56. 29 Yates AB, Moffitt JE, deShazo RD. Anaphylaxis to arthropod bites and stings. Immunol Allergy Clin North Am. 2001: 21:635–51. 30 Graft DF. Insect sting allergy. Med Clin N Am. 2006; 90:211–32. 31 Betten DP, Richardson WH, Tong TC, Clark RF. Massive honey bee envenomation‐induced rhabdomyolysis in an adolescent. Pediatrics. 2006; 117:231–5. 32 França FO, Benvenuti LA, Fan HW, et  al. Severe and fatal mass attacks by ‘killer’ bees (Africanized honey bees‑Apis mellifera scu‑ tellata) in Brazil: clinicopathological studies with measurement of serum venom concentrations. Q J Med. 1994; 87:269–2. 33 Lovecchio F, Cannon RD, Algier J, et al. Bee swarmings in children. Am J Emerg Med. 2007; 25:931–3. 34 Bresolin NL, Carvalho LC, Goes EC, et al. Acute renal failure fol‑ lowing massive attack by Africanized bee stings. Pediatr Nephrol. 2002; 17:625–7.

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35 DeSchazo RD, Butcher BT, Banks WA. Reactions to the stings of the imported fire ant. N Engl J Med. 1990; 323:462–6. 36 Saucier JR. Arachnid envenomation. Emerg Med ClinNorth Am 2004; 22:405–22. 37 Vetter RS. The distribution of brown recluse spiders in the south‑ eastern quadrant of the United States in relation to loxoscelism diagnoses. South Med J. 2009; 102:518–22. 38 Centers for Disease Control. Necrotic arachnidism–Pacific Northwest, 1988‐1996. MMWR Morb Mortal Wkly Rep. 1996; 45:433–6.

39 Vest DK. Necrotic arachnidism in the northwest United States and its probable relationship to Tegenaria agrestis (Walckenaer) spi‑ ders. Toxicon. 1987; 25:175–84. 40 Skolnik AB, Ewald MB Pediatric scorpion envenomation in the United States: morbidity, mortality, and therapeutic innovations. Pediatr Emerg Care. 2013; 29:98–103. 41 Aurebach PS. Wilderness Medicine. 6th ed. Philadelphia, PA: Mosby; 2012. 42 Diaz JH. A 60‐year meta‐analysis of tick paralysis in the United States: a predictable, preventable, and often misdiagnosed ­poisoning. J Med Toxicol. 2010; 6:15–21.

CHAPTER 39

Field trauma triage Matthew Cobb and Aaron Dix

Background In the United States, unintentional injury is the leading cause of death for persons aged 1‐44 years [1]. In 2017, injuries accounted for approximately 243,039 deaths in the United States, and approximately 43.2 million injuries were serious enough to require the injured persons to visit hospital emergency departments (EDs) [2]. In an analysis of 2010 data from the National Emergency Medical Services Information Systems, Wang et al. reported between 17.1 and 28.1 million EMS responses annually, with trauma representing the largest percentage (25.2%) of EMS personnel impressions [3]. Ensuring that severely injured trauma patients are treated at trauma centers has a profound effect on their survival [4]. Ideally, all persons with severe, life‐threatening injuries would be transported to Level I or Level II trauma centers, and all persons with less serious injuries would be transported to lower‐level trauma centers or community EDs. The National Study on the Costs and Outcomes of Trauma identified a 25% reduction in mortality for severely injured adult patients who received care at Level I trauma centers rather than at nontrauma centers [5]. However, patient differences, occult injuries, and the complexities of patient assessment in the field can affect triage decisions.

History of the field triage decision schemes In 1976, the American College of Surgeons Committee on Trauma (ACS‐COT) published resource documents to provide guidance for designation of facilities as trauma centers and appropriate care of acutely injured patients [6–11]. Before this guidance appeared, the typical trauma victim was transported to the nearest hospital, regardless of the capabilities of that hospital, and often with little prehospital intervention [6]. ACS‐COT regularly revised the resource document, which included a decision scheme to provide guidance for the field

triage of injured patients. During each revision, the decision scheme was evaluated by a subcommittee of ACS‐COT, which analyzed the available literature, considered expert opinion, and developed recommendations regarding additions and deletions to the decision scheme. Final approval of the recommendations rested with the ACS‐COT Executive Committee. Following its initial publication in 1986, the decision scheme was updated and revised four times: in 1990, 1993, and 1999 [6]. In 2005, the Centers for Disease Control and Prevention (CDC), with financial support from the National Highway Traffic Safety Administration, collaborated with ACS‐COT to convene the initial meetings of the National Expert Panel on Field Triage. The panel comprises persons with expertise in acute injury care, including EMS clinicians and medical directors, state EMS directors, hospital administrators, adult and pediatric emergency physicians, nurses, adult and pediatric trauma surgeons, persons in the automotive industry, public health personnel, and representatives of federal agencies. During 2005 and 2006, the panel met to revise the decision scheme, and the end product of that comprehensive revision process was published by ACS‐COT in 2006 [11]. In 2009, CDC published a comprehensive review of the revision process and the detailed rationale for the triage criteria underlying the 2006 version of the decisions scheme as the Guidelines for Field Triage of Injured Patients: Recommendations of the National Expert Panel on Field Triage (Guidelines) [12]. In 2011, the panel reconvened to review the guidelines in the context of recently published literature as well as the experience of states and local communities working to implement the guidelines and to make recommendations regarding any changes or modifications to the guidelines. A major outcome of the panel’s meetings was the revision of the guidelines (Figure 39.1). In 2012, CDC published an update to the guidelines, including the rationale for modifications [13]; this update was endorsed by multiple national organizations.

Emergency Medical Services: Clinical Practice and Systems Oversight, Third Edition. Volume 1: Clinical Aspects of EMS. Edited by David C. Cone, Jane H. Brice, Theodore R. Delbridge, and J. Brent Myers. © 2021 NAEMSP. Published 2021 by John Wiley & Sons, Inc.

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Measure of vital signs and level of consciousness Step one

≤ 13 < 90 mmHg < 10 or > 29 Breaths per minute (< 20 in infant aged < 1 year) or need for ventilator support

Glasgow coma scale Systolic blood pressure (mmHg) Respiratory rate

Yes

Transport to a trauma center. Step one and two attempt to identify the most seriously injured patients. These patients should be transported preferentially to the highest level of care within the defined trauma system.

Yes

Transport to a trauma center, which, depending upon the defined trauma system, need not be the highest level of trauma system

Yes

Transport to trauma center or hospital capable of timely and thorough evaluation and initial management of potentially serious Injuries. Consider consultation with medical control.

No Assess anatomy of injury.

Step two’

• All penetrating injuries to head, neck, torso, and extremities proximal to elbow or knee. • Chest wall instability or deformity (e.g.: Flail chest) • Two or more proximal long-bone fractures • Crushed, degloved, mangled, or pulseless extremity. • Pelvic fractures. • Open or depressed skull fracture. • Paralysis. No Assess mechanism of injury and evidence of high-energy impact.

Step three’

• Falls –Adults: > 20 feet (one story is equal to 10 feet). –Children: > 10 feet or two or three times the height of the child. • High-risk auto crash –Intrusion, including roof: > 12 inches occupant site; > 18 inches any site. –Ejection (partial or complete) from automobile. –Death in same passenger compartment. –Vehicle telemetry data consistent with a high risk for injury; • Auto vs pedestrian/bicyclist thrown, run over, or with significant (>20 mph) impact; or • Motorcycle crash > 20 mph. No Assess special patient or system considerations.

Step four

• Older adults −Risk for injury/death increases after age 55 years. –SBP < 110 might represent shock after age 65 years. −Low impact mechanisms (e.g., ground-level falls) might result in severe injury. • Children −Should be triaged preferentially to pediatric-capable trauma center. • Anticoagulants and bleeding disorders −Patients with head injury are at high risk for rapid deterioration • Burns −Without other trauma mechanism: triage to burn facility*** –With trauma mechanism: triage to trauma center*** • Pregnancy ≥ 20 weeks. • EMS provider judgment.

No Transport according to protocol.

Abbreviations: EMS-emergency medical services. * The upper age limit of respiratory rate in infants is >>29 breaths per minute to maintain a higher level of overtriage for infants. † Trauma centers are designated level I –IV. A level I center has the greatest amount of resources and personnel for care of the Injured patient and provides regional leadership in education, research and prevention programs. A level II facility offer similar resources to a level I facility, possibly differing only in continuous availability of certain subspecialties or sufficient prevention, education, and research activities for level I designations; level II facilities are not required to be resident or fellow education centers. A level III center is capable of assessment, resuscitation, and emergency surgery, with severely injured patients being transferred to a level I or II facility. A level IV trauma center is capable of providing 24-hour physician coverage, resuscitation, and stabilization to injured patients before transfer to a facility that provides a higher level of trauma care. § Any injury noted in step two or mechanism identified in step three triggers a ”yes” response. ¶ Age < 15 years ** Intrusion refers to interior compartment intrusion, as opposed to deformation, which refers to exterior damage. †† Includes pedestrians or bicyclist thrown or run over by a motor vehicle or those with estimated impact > 20 mph with a motor vehicle. §§ Local or regional protocols should be used to determine the most appropriate level of trauma center within the defined trauma system; need not be the highest level trauma center. ¶¶ Age> 55 years *** Patients with both burns and concomitant trauma for whom the burn injury poses the greatest risk for morbidity and mortality should be transferred to a burn center. If the nonburn trauma presents a greater immediate risk, the patient may be stabilized in a trauma center and then transferred to a burn center. ††† Patients who do not meet any of the triage criteria in steps one through four should be transported to the most appropriate medical facility as outlined in local EMS protocols.

Figure 39.1  Guidelines for field triage of injured patients–United States, 2011. Source: Sasser SM. Guidelines for field triage of injured patients, ­recommendations of the National Expert Panel on Field Triage. MMWR Recomm Rep. 2012; 61:1–20.

Field trauma triage

Accuracy of field triage The accuracy of field triage can be thought of as the degree of match between the severity of injury and the level of care. Sensitivity and specificity of screening tests are useful indicators of accuracy (Figure 39.2). Maximally sensitive triage would mean that all patients with injuries appropriate for Level I or Level II trauma centers would be sent to such centers. Maximally specific triage would mean that no patients who could be treated at Level III or Level IV centers or community EDs would be transported to Level I or Level II centers. Triage that succeeded in transporting only patients with high injury severity to Level I or Level II centers would maximize the positive predictive value (PPV) of the process, and triage that succeeded in transporting only patients with low injury severity to Level III, IV, or community EDs would maximize the negative predictive value (NPV). Patient differences, occult injuries, and the complexities of patient assessment in the field preclude perfect accuracy in triage decisions. Inaccurate triage that results in a patient who requires higher‐level care not being transported to a Level I or Level II trauma center is termed under‐triage. The result of under‐triage is that a patient does not receive the specialized trauma care required. Over‐triage occurs when a patient who does not require care in a higher‐level trauma center nevertheless is transported to such a center, thereby unnecessarily consuming scarce resources. In the triage research literature, all these measures (sensitivity, specificity, PPV, NPV, under‐­ triage, and over‐triage; see Figure 39.2) are used together with

Destination decision

Injury severity Severe Not severe (Requires level I or II) (Requires level III or IV)

Level I or II TC†

a

b

Level III or IV TC

c

d

Sensitivity = a/(a + c) Specificity = d/(b + d) Rate of undertriage = c/(a + c) Rate of overtriage = b/(b + d) Positive predictive value = a/(a + b) Negative predictive value = d/(c + d) * In this figure, “a”, “b“, “c“, and “d“ represent injured patients, categorized by severity of injury and destination. † Trauma center.

Figure 39.2  Measures of field triage accuracy. Source: Sasser SM. Guidelines for field triage of injured patients, recommendations of the National Expert Panel on Field Triage. MMWR Recomm Rep. 2009; 58:1–35.

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measures of association (e.g., odds ratios) to assess the effectiveness of field triage. As with sensitivity and specificity applied to screening tests, reductions in under‐triage usually are accompanied by increases in over‐triage, and reductions in over‐triage are accompanied by increases in under‐triage. Because the potential harm associated with under‐triage (i.e., causing a patient in need of trauma center care not to receive appropriate care) is high and could result in death or substantial morbidity and disability, trauma systems frequently err on the side of minimizing under‐triage rather than minimizing over‐triage. Target levels for under‐­triage rates within a trauma system range from 0% to 5% of patients requiring Level I or Level II trauma center care, depending on the criteria used to determine the under‐triage rate (e.g., death and Injury Severity Score [ISS]) [11]. Target levels of over‐triage vary (approximate range: 25%–50%) [11]. As field triage continues to evolve based on new research findings, over‐triage rates might be reduced while maintaining low under‐triage rates.

Field triage decision scheme This information is based upon the 2011 Guidelines for Field Triage of Injured Patients published by the Centers for Disease Control and Prevention, with additional updates from the literature for discussion. Step one: physiological criteria Step one of the decision scheme seeks to guide EMS personnel in identifying critically injured patients rapidly through vital signs level of consciousness measurement. The instruction “measure vital signs and level of consciousness” has been included since the 1986 version of the ACS Field Triage Decision Protocol [7]. Multiple peer‐reviewed articles continue to support the use of physiological criteria [14–17]. The sensitivity of physiological criteria to identify severely injured patients has been reported to range from 55.6% to 64.8%, with PPV of 41.8% and specificity of 85.7% [18, 19]. A study of 333 patients transported by helicopter to a Level I trauma center during 1993 and 1994 indicated that physiological criteria alone were specific (0.9) but not sensitive (0.6) for identifying ISS >15 [18]. An evaluation of data in the South Carolina EMS registry, conducted to determine under‐triage and over‐triage rates when EMS personnel used the 1990 version of the ACS Field Triage Guidelines, determined that physiological criteria alone had a sensitivity of 0.65 and PPV of 42% for severe injury (ISS of >15) for 753 trauma patients transported to a Level I trauma center in Charleston [19]. Adults meeting such physiological criteria treated at Level I trauma centers had reduced odds of mortality compared with patients treated at lower‐level trauma centers and nontrauma center hospitals (OR: 0.7; CI = 0.6–0.9). In 2020, a pair of analyses representing 155 studies reviewed respiratory and circulatory parameters for the identification

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serious injury in the prehospital environment and found that both respiratory and circulatory were less sensitive, with greater specificity [20, 21]. Additionally, Pearson et  al. examined data from 51,952 traumatic brain injury patients from the National Trauma Data Bank and noted that these patients who met physiological criteria had greater odds of death. Specifically, those presenting with GCS scores ≤ 13 were found to have higher odds of death (OR 17.4; 95% CI, 10.7‐28.3) [22]. Under the current guidelines, transport is recommended to a facility that provides the highest level of care within the defined trauma system if any of the following are identified: • GCS ≤ 13, or • SBP 15 in those patients meeting no other criteria. Intrusion greater than 12 inches had a PPV of 10.4%. Death in the vehicle had a PPV of 21.4%, while ejection from the vehicle had a PPV of 9.8%. The highest PPV was found in incidents of steering wheel collapse (25.7%) [27]. Transport is recommended to a trauma center if any of the following are identified: • falls ○○ adults: >20 feet (one story = 10 feet) ○○ children: >10 feet or two to three times the height of the child • high‐risk auto crash ○○ intrusion, including roof: >12 inches occupant site; >18 inches any site ○○ ejection (partial or complete) from automobile ○○ death in same passenger compartment ○○ vehicle telemetry data consistent with a high risk for injury; • automobile versus pedestrian/bicyclist thrown, run over, or with significant (>20 mph) impact; or • motorcycle crash >20 mph Step four: special considerations In step four, EMS personnel must determine whether persons who have not met physiological, anatomical, or mechanism criteria have underlying conditions or comorbid factors that place them at higher risk of injury or that aid in identifying the seriously injured patient. Persons who meet step four criteria might require trauma center care. A retrospective study of approximately 1 million trauma patients indicated that using physiological and anatomical criteria alone for triage of patients resulted in a high degree of under‐triage, implying that using special considerations for determining trauma center need helped reduce the problem of under‐triage [24]. Among

Field trauma triage

89,441 injured patients evaluated by EMS clinicians at six sites, physiological, anatomical, and MOI criteria identified 4,049 (70.8%) patients with ISS >15; step four identified another 956 (16.7%) seriously injured patients, with an increase in over‐­ triage from 25.3% to 37.3% [26]. In a population‐based retrospective cohort study, EMS clinician judgment was found to be the most commonly used triage criterion at 40%. It was the sole criterion in 21.4%. It was independently associated with a serious injury. The odds ratio of ISS >16 based on EMS clinician judgment was 1.23 (95% CI, 1.03‐1.47). The PPV varied based on sites, however [28]. Transport to a trauma center or hospital capable of timely and thorough evaluation and initial management of potentially serious injuries is recommended for patients who meet the following criteria: • older adults ○○ risk for injury/death increases after age 55 years—SBP 20 weeks • EMS clinician judgment

Pediatric concerns To our knowledge, no published data suggest that injured children, in the absence of physiological, anatomical, or MOI triage criteria, are at risk for negative outcomes solely on the basis of their age. The criteria in steps one, two, and three of the 2006 decision scheme are expected to identify nearly all seriously injured children. Therefore, the panel identified no specific age below which all injured children should be transported to trauma centers. In 2018, van der Sluijs et  al. performed an assessment of five studies (1,222 patients) examining three distinct protocols (the Pediatric Trauma Triage Checklist, the Trauma Scorecard, and the 2011 Field Triage Guidelines) used for prehospital identification of pediatric patients who need specialized care. The authors reported a sensitivity of 84.1% to 87.3% with the Field Triage Guidelines, a sensitivity of 86.2% with the Pediatric Trauma Triage Checklist, and a sensitivity of 66.7% with the Trauma Scorecard [29]. In a 2016 study, Lerner et al. studied 5,610 injured pediatric patients regarding the Field Triage Guidelines and found that physiological criteria were a moderate predictor for the need of trauma center care [30]. A subsequent

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study compared over‐triage and under‐triage rates for children of the 2011 guidelines to prior versions and found an 8.2% increase in under‐triage and a 4.6% decrease in over‐triage with use of the 2011 guidelines [31]. Lerner et al. in a 2020 examination of 62 children ≤ 15 years of age, who were identified as needing trauma center care but did not meet physiological or anatomical criteria, found an under‐triage rate of 77% using the MOI criteria in the triage decision scheme [32]. Children meeting the revised field triage criteria for transport to trauma centers in steps one through three of the decision scheme should be transported preferentially to pediatric‐capable trauma centers. Recent studies indicate that organized systems for trauma care contribute to improved outcomes for children [33] and that seriously injured children fare better in pediatric‐ capable trauma centers. Multiple reports document improved survival in pediatric‐capable trauma centers [34–38], including data from the Pennsylvania Trauma Outcome Study registry that demonstrate absolute reductions in injury mortality ranging from 3.8% to 9.7% [38] and improved functional outcomes (e.g., feeding and locomotion) [40] when children aged 15 are treated at pediatric trauma centers or at adult trauma centers that have acquired additional qualifications to treat children. The charts of 175,585 injured children were retrospectively reviewed following presentation to 252 trauma centers in a 3‐year period. Mortality rates decreased from 2.3% in adult trauma centers to 1.8% in mixed‐trauma centers to 0.6% in pediatric trauma centers. The study subsequently age‐stratified mortality rates based on trauma center type. A significant difference in the odds of death was found only in younger children (≤5 years old) treated at adult trauma centers. There was no association between mortality and trauma center type for older children (6–11 years old) and adolescents (12–18 years old) [41]. What appears to matter most is the availability of pediatric‐ specific resources, particularly the availability of a pediatric ICU, not the designation as a pediatric trauma center per se [42, 43]. Although some earlier studies concluded that injured children treated in adult trauma centers had outcomes comparable to those of children treated in pediatric trauma centers, those investigations were conducted in hospitals with comprehensive pediatric services, including pediatric emergency medicine, critical care medicine, and nursing [44–50]. Older adults Under‐triage of the older adult population is a substantial problem, and the evidence reviewed suggests that the physiological parameters used in younger patients might not apply to older adults. Occult injury is likely to be greater among older adults, low‐energy transfers (e.g., ground‐level falls) might result in serious injuries in this population, and field identification of serious injury among older adults must be more proactive. In a 5‐year review of Medicare claims data, Uribe et al. evaluated the under‐triage (treatment of patients with an ISS score of ≥16 at a nontrauma center) of older adults (≥65 years) [51]. Forty‐six

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percent of the patients reviewed were found to have been under‐ triaged, and under‐triage increased with age, distance to trauma center, and location [51]. A study of adults age ≥65 years found that the existing field triage guidance had low sensitivity for identification of those at higher risk for severe injury, and noted that the addition of comorbidity and geriatric‐specific vital signs improved the recognition of older adults at high risk [52]. Newgard et al. noted improvement in sensitivity (92.1% vs. 75.9%) and lower specificity (41.5% vs. 77.8%) of the triage guidelines for higher risk older adults by adding older adult–specific criteria (GCS ≤ 14, SBP ≤ 110 or ≥ 200 mmHg, respirations ≤ 10 or ≥ 24/ min, or HR ≤ 60 or ≥ 110/min) to the current Field Triage Guidelines if a patient did not meet any current criteria [53]. International trauma triage models Field triage methodology has also been evaluated internationally. In a 2018 prospective evaluation of 4,950 adult trauma patients transported as high priority to ten hospitals in the Netherlands, the authors noted an under‐triage rate of 63.8% and an over‐triage rate of 7.4% using the Dutch protocol, which is based on the Field Triage Guidelines [54]. van Rein et al. proposed a new model that included age, physiological criteria, anatomical criteria, AIS scoring, and MOI, with a predicted under‐triage rate of 11.2% and over‐triage rate of 50% [55]. In a 2016 observational study of 1,160 patients from Paris, France, the authors proposed a decision tree algorithm that focuses on determining patient need for trauma center resources (e.g., physiological changes, spinal cord injury, age) and found that their algorithm had a sensitivity of 0.94 and specificity of 0.48 [56]. Future research for field triage In its 2011 analysis, the panel noted an increase in the peer‐ reviewed published literature regarding field triage from the 2006 guidelines to the 2012 update. The 2011–2012 revision process identified and reviewed 289 articles published during 2006–2011 (approximately 48 articles/year) directly relevant to field triage, 24 times the annual number of articles during 1966–2005 (approximately 2/year) cited in the 2006 guidelines [12]. Shortly after the publication of the National Field Triage Guidelines in 2011, a prospective cohort study was completed in an effort to validate the guidelines. In 2011, 17,633 patients were enrolled from Oregon and Washington. The Field Triage Guidelines were found to be 66.2% (95% CI, 60.2%‐71.7%) sensitive and 87.8% (95% CI, 87.7%‐88.0%) specific for ISS >16. It was also found to be 80.1% (95% CI, 65.8%‐89.4%) sensitive and 87.3% (95% CI, 87.1%‐87.4%) specific for use of early critical care resources, identified as airway intervention in the ED, or if any of the following occurred in the first 24 hours: nonorthopedic operation, blood transfusion >6 units, any blood transfusion in pediatric patients, or death. They noted a decrease in guideline sensitivity with age, 87.4% in children as compared to 51.8% in adults [57]. As evidenced in this chapter, the research base focusing on field triage to determine the best methodology to identify severely

injured patients in the prehospital environment continues to expand. Future research and revisions of the guidelines must ensure that the guidelines are based on the best clinical evidence, and must continue to address outcomes measures in field triage, under‐triage, and the effect of field triage on the cost of trauma care. Recognizing that a substantive portion of the U.S. population lives >60 minutes from the closest major trauma center and that 28% of U.S. residents are only able to access specialized trauma care within this time window by helicopter [58], research must enable a better understanding of field triage in nonurban environments. To the latter point, in a secondary analysis of 53,487 patients transported by EMS in Washington, the authors found that 29.4% of rural patients needing critical resources were cared for in trauma centers versus 88.7% of those injured in urban settings; there was no difference in mortality [59]. Ongoing collaboration among local, state, and regional EMS agencies with governmental, nongovernmental, academic, and public health agencies and institutions will allow the continuing analysis and evaluation of the Field Triage Guidelines and their effect on the care of acutely injured patients. Statewide EMS and trauma databases provide opportunities for statewide quality improvement of field triage, research, and adaptation of the guidelines to meet state‐specific circumstances. Large, nationally representative databases could be used for future triage research if advances are made to link these data files across phases of care (e.g., prehospital to in‐hospital). Finally, uniform definitions of prehospital variables (including triage criteria) with a standardized data dictionary and data standards (e.g., HL7 messaging) could provide comparable data across study sites and assist with linking data files from the prehospital to the hospital setting.

Conclusion The current field trauma triage guidelines are based on current medical literature, the experience of multiple states and communities working to improve field triage, and the expert opinions of the panel members. This guidance is intended to assist EMS and trauma systems, medical directors, and EMS physicians and clinicians with the information necessary to make critical decisions that have been demonstrated to increase the likelihood of improved outcomes in severely injured trauma patients [8]. The guidelines must be continually evaluated in the context of current literature and updated as needed and appropriate. Improved field triage of injured patients can have a profound effect on the structure, organization, and use of EMS and trauma systems, the costs associated with trauma care, and most importantly, on the lives of the millions of persons injured every year in the United States. As is noted throughout this chapter, improved research is needed to assess the effect of field triage on resource allocation, health care financing and funding, and, most importantly, patient outcomes.

Field trauma triage

References 1 Centers for Disease Control and Prevention. National Vital Statistics System, National Center for Health Statistics. 10 Leading Causes of Death by Age Group, United States–2018. Available at: https://www. cdc.gov/injury/wisqars/pdf/leading_causes_of_death_by_age_ group_2018‐508.pdf. Accessed September 1, 2020. 2 Centers for Disease Control and Prevention. National Center for Health Statistics. All Injuries. Available at: https://www.cdc.gov/ nchs/fastats/injury.htm. Accessed September 1, 2020. 3 Wang HE, Mann NC, Jacobson KE, et al. National characteristics of emergency medical services responses in the United States. Prehosp Emerg Care. 2013; 17:8–14. 4 Sasser S, Varghese M, Kellermann A, Lormand JD, editors. Prehospital trauma care systems. Geneva, Switzerland: World Health Organization; 2005. 5 MacKenzie EJ, Rivara FP, Jurkovich GJ, et al. A national evaluation of the effect of trauma center care on mortality. N Engl J Med. 2006; 354:366–78. 6 Mackersie RC. History of trauma field triage development and the American College of Surgeons criteria. Prehosp Emerg Care. 2006; 10:287–94. 7 American College of Surgeons. Hospital and Prehospital Resources for the Optimal Care of the Injured Patient: Appendices A Through J. Chicago, IL: American College of Surgeons; 1986. 8 American College of Surgeons. Resources for the Optimal Care of the Injured Patient: 1999. Chicago, IL: American College of Surgeons; 1999. 9 American College of Surgeons. Resources for the Optimal Care of the Injured Patient: 1990. Chicago, IL: American College of Surgeons; 1990. 10 American College of Surgeons. Resources for the Optimal Care of the Injured Patient: 1993. Chicago, IL: American College of Surgeons; 1993. 11 American College of Surgeons. Resources for the Optimal Care of the Injured Patient: 2006. Chicago, IL: American College of Surgeons; 2006. 12 CDC. Guidelines for field triage of injured patients: recommendations of the National Expert Panel on Field Triage. MMWR. 2009; 58:1–35. 13 CDC. Guidelines for field triage of injured patients. MMWR. 2012; 61:1–20. 14 Cherry RA, King TS, Carney DE, Bryant P, Cooney RN. Trauma team activation and the impact on mortality. J Trauma. 2007; 63:326–30. 15 Edelman DA, White MT, Tyburski JG, Wilson RF. Post‐traumatic hypotension: should systolic blood pressure of 90–109 mmHg be included? Shock. 2007; 27:134–8. 16 Codner P, Obaid A, Porral D, Lush S, Cinat M. Is field hypotension a reliable indicator of significant injury in trauma patients who are normotensive on arrival to the emergency department? Am Surg. 2005; 71:768–71. 17 Lipsky AM, Gausche‐Hill M, Henneman PL, et  al. Prehospital hypotension is a predictor of the need for an emergent, therapeutic operation in trauma patients with normal systolic blood pressure in the emergency department. J Trauma. 2006; 61:1228–33. 18 Wuerz R, Taylor J, Smith JS. Accuracy of trauma triage in patients transported by helicopter. Air Med J. 1996; 15:168–70.

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19 Norcross ED, Ford DW, Cooper ME, Zone‐Smith L, Byrne TK, Yarbrough DR. Application of American College of Surgeons’ field triage guidelines by pre‐hospital personnel. J Am Coll Surg. 1995; 181:539–44. 20 Daya MR, Cheney TP, Chou R, et  al. Out‐of‐hospital respiratory measures to identify patients with serious injury: a systematic review. Acad Emerg Med. Published online ahead of print June 22, 2020. doi: 10.1111/acem.14055. 21 Newgard CD, Cheney TP, Chou R, et al. Out‐of‐hospital circulatory measures to identify patients with serious injury: a systematic review. Acad Emerg Med. Published online ahead of print. June 22, 2020. doi: 10.1111/acem.14056. 22 Pearson WS, Ovalle F Jr, Faul M, Sasser SM. A review of traumatic brain injury trauma center visits meeting physiologic criteria from The American College of Surgeons Committee on Trauma/Centers for Disease Control and Prevention Field Triage Guidelines. Prehosp Emerg Care. 2012; 16:323–8. 23 Esposito TJ, Offner PJ, Jurkovich GJ, Griffith J, Maier RV. Do prehospital trauma center triage criteria identify major trauma victims? Arch Surg. 1995; 130:171–6. 24 Brown JB, Stassen NA, Bankey PE, Sangosanya AT, Cheng JD, Gestring ML. Mechanism of injury and special consideration criteria still matter: an evaluation of the National Trauma Triage Protocol. J Trauma. 2011; 70:38–44. 25 Haider AH, Chang DC, Haut ER, Cornwell EE, Efron DT. Mechanism of injury predicts patient mortality and impairment after blunt trauma. J Surg Res. 2009; 153:138–42. 26 Newgard CD, Zive D, Holmes JF, et al. A multisite assessment of the American College of Surgeons Committee on Trauma field triage decision scheme for identifying seriously injured children and adults. J Am Coll Surg. 2011; 213:709–21. 27 Davidson GH, Rivara FP, Mack CD, et al. Validation of prehospital trauma triage criteria for motor vehicle collisions. J Trauma Acute Care Surg. 2014; 76:755–61. 28 Newgard CD, Kampp M, Nelson M, et al. Deciphering the use and predictive value of “emergency medical services provider judgment” in out‐of‐hospital trauma triage: a multisite, mixed methods assessment. J Trauma Acute Care Surg. 2012; 72:1239–48. 29 van der Sluijs R, van Rein EAJ, Wijnand JGJ, Leenen LPH, van Heijl M. Accuracy of pediatric trauma field triage: a systematic review. JAMA Surg. 2018; 153:671–6. 30 Lerner EB, Drendel AL, Cushman JT, et al. Ability of the physiologic criteria of the field triage guidelines to identify children who need the resources of a trauma center. Prehosp Emerg Care. 2017; 21:180–4. 31 Lerner EB, Cushman JT, Drendel AL, et al. Effect of the 2011 revisions to the field triage guidelines on under‐ and over‐triage rates for pediatric trauma patients. Prehosp Emerg Care. 2017; 21:456–60. 32 Lerner EB, Badawy M, Cushman JT, Drendel AL, et al. Does mechanism of injury predict trauma center need for children? Prehosp Emerg Care. 2020; 24:1–8. 33 Hulka F, Mullins RJ, Mann NC, et  al. Influence of a statewide trauma system on pediatric hospitalization and outcome. J Trauma. 1997; 42:514–9. 34 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; 19:150–9.

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35 Nakayama DK, Copes WS, Sacco WJ. Differences in pediatric trauma care among pediatric and nonpediatric centers. J Pediatr Surg. 1992; 27:427–31. 36 Hall JR, Reyes HM, Meller JL, et al. Traumatic death in urban children, revisited. Am J Dis Child. 1993; 147:102–7. 37 Cooper A, Barlow B, DiScala C, et al. Efficacy of pediatric trauma care: results of a population‐based study. J Pediatr Surg. 1993; 28:299–305. 38 Hall JR, Reyes HM, Meller JT, et al. Outcome for blunt trauma is best at a pediatric trauma center. J Pediatr Surg. 1996; 31:72–7. 39 Potoka DA, Schall LC, Gardner MJ, Stafford PW, Peitzman AB, Ford HR. Impact of pediatric trauma centers on mortality in a statewide system. J Trauma. 2000; 49:237–45. 40 Potoka DA, Schall LC, Ford HR. Improved functional outcome for severely injured children treated at pediatric trauma centers. J Trauma. 2001; 51:824–34. 41 Sathya C, Alali AS, Wales PW, et al. Mortality among injured children treated at different trauma center types. JAMA Surg. 2015; 150:874–81. 42 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; 50:96–101. 43 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. 2004; 5:5–9. 44 Knudson MM, Shagoury C, Lewis FR. Can adult trauma surgeons care for injured children? J Trauma. 1992; 32:729–39. 45 Fortune JM, Sanchez J, Graca L, et  al. A pediatric trauma center without a pediatric surgeon: a four year outcome analysis. J Trauma. 1992; 33:130–9. 46 Rhodes M, Smith S, Boorse D. Pediatric trauma patients in an “adult” trauma center. J Trauma. 1993; 35:384–93. 47 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; 29:11–8.

48 Partrick DA, Moore EE, Bensard DD, et al. Operative management of injured children at an adult level I trauma center. J Trauma. 2000; 48:894–901. 49 Sherman HF, Landry VL, Jones LM. Should level I trauma centers be rated NC‐17? J Trauma. 2001; 50:784–91. 50 D’Amelio 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; 61:968–74. 51 Uribe‐Leitz T, Jarman MP, Sturgeon DJ, et al. National study of triage and access to trauma centers for older adults. Ann Emerg Med. 2020; 75:125–35. 52 Newgard CD, Lin A, Eckstrom E, et al. Comorbidities, anticoagulants, and geriatric‐specific physiology for the field triage of injured older adults. J Trauma Acute Care Surg. 2019; 86:829–37. 53 Newgard CD, Holmes JF, Haukoos JS, et  al. Improving early identification of the high‐risk elderly trauma patient by emergency medical services. Injury. 2016; 47:19–25. 54 Voskens FJ, van Rein EAJ, van der Sluijs R, et al. Accuracy of prehospital triage in selecting severely injured trauma patients. JAMA Surg. 2018; 153:322–7. 55 van Rein EAJ, van der Sluijs R, Voskens FJ, et al. Development and validation of a prediction model for prehospital triage of trauma patients. JAMA Surg. 2019; 154:421–9. 56 Follin A, Jacqmin S, Chhor V, et  al. Tree‐based algorithm for prehospital triage of polytrauma patients. Injury. 2016; 47:1555–1. 57 Newgard CD, Fu R, Zive D, et al. Prospective VALIDATION of the National Field Triage Guidelines for Identifying Seriously Injured Persons. J Am Coll Surg. 2016; 222:146–58. 58 Branas CC, MacKenzie EJ, Williams JC, et al. Access to trauma centers in the United States. JAMA. 2005; 293:2626–33. 59 Newgard CD, Fu R, Bulger E, et  al. Evaluation of rural vs urban trauma patients served by 9‐1‐1 emergency medical services. JAMA Surg. 2017; 152:11–18.

CHAPTER 40

Trauma‐stabilizing procedures Benjamin A. Smith

Introduction Stabilization of traumatically injured patients relies primarily upon mitigating ongoing hemorrhage, preventing further physiological insults, and treating any reversible causes of hypotension or hypoxia. Hemorrhage mitigation, via hemorrhage control, blood products, and tranexamic acid, as well as stabilization of orthopedic injuries, is covered elsewhere. Prevention of further physiological insults by airway management and ventilation is also covered in detail in other chapters. This chapter will cover decompression of hemo/pneumothoraces via needle, finger, and tube thoracostomies, pericardiocentesis for cardiac tamponade, and spinal motion restriction to prevent secondary spinal cord injury. EMS physicians must possess a significant level of expertise in the use of these noninvasive and invasive procedures for prehospital stabilization of trauma patients. The nature of care and the procedures appropriate for different levels of clinicians are based on the education, training, and legal scope of EMS clinician practice. An EMS medical director must be skilled in these procedures, maintain active educational programs, and engage in continuous quality improvement activities to ensure procedures are correctly performed under the correct circumstances. In some cases, it may be appropriate that only an EMS physician perform a procedure, either due to special circumstances or due to the clinician’s ability or scope. Appropriate hands‐on and didactic training, as well as verification of procedural proficiency, should occur prior to implementing any procedural skill.

Needle thoracostomy A pneumothorax occurs when air leaks into the pleural space. Traumatic pneumothoraces often result from penetrating chest trauma as the pleural space communicates to the external world via the wound (termed an open pneumothorax). In blunt chest

trauma, a pneumothorax can occur if the lung is injured from a rib fracture, but it may also occur from blunt injury alone if there is a structural predisposition to pneumothorax such as in patients with chronic obstructive pulmonary disease or if the energy of the trauma is high enough. Occasionally, the anatomy of the lung injury is such that air enters the pleural space on inspiration but little air leaves the pleural space on expiration. In this scenario, pressure can develop in the pleural space, resulting in hemodynamic compromise from decreased preload due pressure on the vena cava. This is the definition of a tension pneumothorax. The placement of a needle to relieve tension pneumothorax is often used in ground EMS systems. Some air medical (and critical care) services have also authorized finger thoracostomy or even the placement of formal chest tubes by their crews. The placement of a needle into the pleural space can produce dramatic results in a patient with tension pneumothorax by converting it to an open pneumothorax and relieving the intrathoracic pressure. Indication A needle thoracostomy is indicated when tension pneumothorax is suspected. Diagnosis of a tension pneumothorax requires suspicion of pneumothorax based on exam combined with hypotension. However, this procedure should be considered in any patient who suffers from rapid cardiopulmonary decompensation in an appropriate clinical setting. Although tracheal deviation and decreased breath sounds are commonly accepted signs of tension pneumothorax, they may not always be present and may not be appreciated in some prehospital environments [1]. Clinicians should be encouraged to perform this procedure in any blunt chest trauma patient who has a precipitously decreasing course, especially if there is a history of chronic obstructive pulmonary disease or asthma. Trauma patients with obvious subcutaneous emphysema may also benefit from the early application of this technique.

Emergency Medical Services: Clinical Practice and Systems Oversight, Third Edition. Volume 1: Clinical Aspects of EMS. Edited by David C. Cone, Jane H. Brice, Theodore R. Delbridge, and J. Brent Myers. © 2021 NAEMSP. Published 2021 by John Wiley & Sons, Inc.

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Technique First, locate the second intercostal space, located in the midclavicular line on the anterior chest wall of the affected side. An alternative site is the midaxillary line at the level of the nipple, similar to the usual chest tube site. Next, prep the area with sterile antiseptic solution. Direct the needle with a loaded catheter perpendicular to the skin and just superior to the inferior rib of the selected interspace, to avoid injury to the neurovascular bundle. Several commercial devices exist with various mechanisms to verify entry into the pleural space, such as a spring‐loaded indicator. If the device does not include such a mechanism, a syringe can be connected to the needle, and if the plunger is withdrawn as the needle is advanced, air (or blood) will flow freely into the syringe once the pleural space is entered. The plastic catheter should then be advanced off of the needle and into the chest. The syringe (frequently a larger syringe) may be used in conjunction with a stopcock to aspirate the air from the pneumothorax until resistance is noted on the plunger. If the patient is intubated, the thoracostomy catheter may be placed and left open to the air. If the patient is spontaneously breathing, a one‐way valve must be created to prevent reentry of air during inspiration. One‐way valves, such as the Heimlich valve, are available with tubing that will connect with a standard venous catheter. Other commercially available devices have built‐in one‐way valves. Other solutions that have been used include puncturing a condom with the catheter and then unrolling it after the catheter has been placed in the patient. Surgical gloves have also been used, but when compared with condoms, they may produce unacceptable air leakage. A definitive thoracostomy tube will need to be placed after acute decompression with needle thoracostomy (typically in the hospital setting or in critical care transport situations). Complications The rate of significant complications is thought to be low. Eckstein and Suyehara reviewed their experience in a series of over 6,000 trauma patients [2]. They concluded, based on the 108 patients who received needle decompression, that needle thoracostomy was a potentially life‐saving intervention with a low complication rate. If the catheter is placed into the lung parenchyma, the puncture will be small and should heal rapidly. The resultant pneumothorax is an open one, and therefore the patient should suffer little further compromise. It is possible to puncture the subclavian vein and/or artery if the second interspace technique is performed improperly and the needle is placed too high in the chest. If the lateral approach is used, abdominal organ injury may result from a needle placed too caudad. Laceration of the internal mammary artery and the risk of infection are two other complications to consider. Care is needed to avoid these complications by providing the best available level of preprocedural cleaning and use of landmarks when placing the needle. While not truly a complication, studies suggest many decompression needles may not be long enough to reach the pleural space, particularly in obese individuals [3, 4]. If the

procedure does not produce clinical improvement, the clinician must consider whether this is due to the lack of a tension pneumothorax or due to inadequate catheter placement. If the latter is felt to be more likely, then the clinician should consider placement in an alternative location (i.e., attempt in the midaxillary line if the first attempt was in the second intercostal space at the midclavicular line). Additionally, if the procedure was successful, the catheter can occasionally migrate out of the plural space and a tension pneumothorax may reaccumulate if the clinician is not vigilant.

Tube and finger thoracostomy Thoracostomy, mostly limited to air medical services or military situations, is used to evacuate air or blood from the pleural space. Following an incision in the skin, the pleural space is punctured with a hemostat or Kelly clamp. As the soft tissue is bluntly dissected, the pleural space becomes open to the environment and elevated intrathoracic pressure is relieved. A finger is then inserted through the tract to verify entry into the pleural space. At this point, a finger thoracostomy has been performed, and the pneumothorax has been converted into an open pneumothorax. Some services use finger thoracostomies in lieu of needle decompression as it allows for verification of successful entry into the pleural space. If a formal tube thoracostomy is to be performed, a chest tube is then placed through this tract. Tube thoracostomy is particularly useful when transport times are sufficiently long. Once the tube has been secured, one must decide what to do with the free end of the tube. If the patient is intubated, the tube may theoretically be left open, creating an open pneumothorax, though this is rarely performed. For a patient who is not intubated, a one‐way valve must be created to prevent entry of air into the thorax during inspiration. The Heimlich valve, essentially a rubber flapper valve in a tube, is the most practical device for the prehospital clinician. The chest tube may be connected to suction or, if there is a large amount of drainage, a urinary catheter bag or formal chest tube collection system may be attached to collect the drainage. Indication The indication for a finger thoracostomy is the same for a needle thoracostomy as its intent is to relieve pressure in the pleural space. The purpose of tube thoracostomy is to rapidly evacuate a large amount of blood or air from the trauma patient’s pleural space to provide relief of a tension hemothorax or tension pneumothorax, or to improve respiratory function in the case of a large hemo/pneumothorax causing poor oxygenation or ventilation. If placed for a large hemo/pneumothorax, the benefit for prehospital clinicians typically comes when there are extended transport times. Other potential advantages of tube thoracostomy over needle thoracostomy are the lower likelihood of kinking, clotting, and dislodgement of the tube when compared to a catheter.

Trauma‐stabilizing procedures

Technique First, abduct and externally rotate the arm on the affected side so that it is up and out of the way. Locate the fifth intercostal space, in the midaxillary line on the chest wall of the affected side. The tube should not be placed any more caudad than the fifth intercostal space as it is possible to puncture into the abdominal cavity. The placement site should be lateral to the pectoralis muscle. Prep the area with sterile antiseptic solution. Locally inject the site with anesthetic. Using a no. 10 blade scalpel, make a 3‐4 cm transverse incision over the fifth or sixth rib at the midaxillary line. With a large Kelly clamp or hemostat, bluntly dissect over top of the rib into the intercostal space. Some force may be required to enter pleural space and the operator should feel a definitive pop upon entering pleural cavity. At this point, there may be a rush of air or blood. Spread the tips of the Kelly clamp in the pleural cavity to widen access, then turn the clamp 90 degrees and spread again. Insert a gloved finger into the pleural space to verify proper position. If the intent was simply to perform a finger thoracostomy, then the procedure is complete, and the incision can be covered with an occlusive dressing taped on three sides or with a formal chest seal device to create a one‐way valve. To complete a tube thoracostomy, an appropriately sized chest tube is then inserted through the tract, typically using a Kelly clamp to guide the tube. The tube should be inserted along the tract and into the pleural cavity, while directing it posteriorly and superiorly. The tube should slide smoothly without significant resistance and all of the fenestrations must be inside the chest wall to allow for suction. Once the tube is in position, secure the chest tube to the chest wall with silk suture. Petroleum gauze with a single cut half‐way across the middle of the gauze can then be placed around the tube to create a seal. Dry gauze, with the same cut, is then placed over the petroleum gauze and the elastic adhesive tape is used to hold the dry gauze in position. The tube is then bolstered and taped to the chest wall. The end of the tube should then be connected to the chest tube drainage apparatus or a Heimlich (one‐way flutter) valve should be placed on the end.

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pulseless electrical activity (PEA) due to cardiac tamponade, pericardiocentesis may theoretically restore a perfusing rhythm. Medical directors may wish to include pericardiocentesis in a traumatic PEA protocol; however, use should be reserved for patients in whom fluid challenge and needle or finger thoracostomy have not resulted in palpable pulses. Additionally, point of care ultrasonography, when available, can be used to identify cardiac tamponade and guide the periocardiocentesis. Indication Pericardiocentesis is indicated for patients with hypotension or cardiac arrest secondary to traumatic cardiac tamponade. Beck’s triad (muffled heart sounds, jugular venous distention, and hypotension) and Kussmaul’s signs (pulsus paradoxus, a drop of >10 mmHg during inspiration, and paradoxical increase in jugular vein distention, as a sign of increased jugulovenous pressure) are indications of cardiac tamponade. Point of care ultrasonography can identify cardiac tamponade when a pericardial effusion is seen with right ventricular collapse or hypotension. Cardiac tamponade is present in up to 90% of penetrating injuries to the heart [5]. Pericardiocentesis is also potentially indicated for resuscitation of a patient in PEA when other causes have been ruled out and the patient remains pulseless. Pericardiocentesis has been successful even in cases of cardiac tamponade from blunt trauma [6].

Pericardiocentesis

Technique without ECG or ultrasound guidance Expose the subxyphoid region and prep the area with sterile antiseptic solution. Position an 18‐gauge (either 3.5 or 6 inch) spinal needle so that it will enter the skin directly below or adjacent to the xiphoid process. The needle should be held at a 45° angle to the skin, aiming at the left shoulder (assuming normal anatomy) to minimize the likelihood of injuring other important structures. The needle is advanced, maintaining angle and direction, while withdrawing on the plunger. The operator stops advancing when blood returns. After removal of up to 50 mL of blood, vital signs are reassessed. In cases of acute tamponade, removal of as little as 25‐30 mL can lead to immediate improvement [6]. If hemodynamic status does not improve, perform additional aspiration of blood in 25 mL increments until condition improves. A stopcock may be placed on the Luer lock end of the spinal needle and may be used for subsequent drainage (either through tubing into a bag or into a syringe with aspiration). If the needle is left in place, it must be stabilized. If removed, the operator should consider drainage of pericardial blood until little to no blood returns, and then check for reaccumulation prior to removal. A sterile dressing should be placed over the site. At this point, if equipped, the operator may choose to use Seldinger guidewire technique and place a flexible plastic catheter instead of leaving the metal spinal needle. If available, a kit that includes a flexible catheter loaded onto a needle can be used instead of a spinal needle.

Pericardiocentesis is classically taught as the procedure of choice for treating cardiac tamponade but use in the prehospital setting has not been fully investigated. In the patient with

Technique with ECG guidance Pericardiocentesis may be performed under ECG guidance. Prior to initiating the procedure described above, the operator

Complications The tube should be placed under sterile conditions. However, this may be difficult or impossible in the prehospital environment. Infection may lead to an empyema, should the patient survive. Placement in the wrong interspace can result in injury to the abdominal organs, the heart, or great vessels, and the use of trocars or Kelly clamps to place the tube may cause injury to the lung parenchyma or other thoracic structures.

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uses an alligator clip jumper cable to bridge from the ECG lead (V1 in the case of a 12‐lead monitor, lead II for a 3‐lead monitor) to the proximal metal portion of the spinal needle. The same procedure may be used, and advancement of the needle is now additionally guided by blood returned and the change on the ECG lead to ST elevation on the monitor. The rest of the procedure is the same as above. Technique with ultrasound guidance Prehospital ultrasound may be used to guide needle placement into the pericardium. The operator will identify the point of maximal effusion in order to guide site selection. The site should represent a superficial access to the effusion and will not likely be the subxyphoid site, due to the ability of the ultrasound to visualize both the effusion and the needle during the procedure. Angle and depth will be guided by the ultrasound. The operator should use the probe before (to identify the site), during (to guide the needle to the effusion), and after (to check for reaccumulation). The rest of the procedure is the same as the blind technique above. Complications Classically, the use of this technique has been discouraged in the patient with traumatic tamponade as it may delay the implementation of thoracotomy. Thoracotomy is not usually available in the prehospital setting unless a properly trained and equipped EMS physician is present [7]. Theoretically, the needle could also cause injury to the myocardium or puncture or lacerate a coronary vessel.

Spinal motion restriction Before the advent of organized EMS services and paramedic training, motor vehicle crash victims were often extricated and transported by lay bystanders without concern for spinal cord injury. Occasionally these patients presented to the hospital with completed spinal cord injuries [8]. Spinal motion restriction has since become one of the most fundamental interventions provided by prehospital clinicians. Changes in automotive design since the 1960s have led some to question the need for universal spinal motion restriction of motor vehicle crash victims. In light of recent studies exposing the lack of evidence for cervical collar and long spine board effectiveness in the maintenance of spinal alignment, coupled with detrimental effects of routine spinal motion restriction, protocol design and quality‐assurance processes must be carefully crafted to limit the adverse effects of this now ubiquitous but not evidence‐ based practice [9–22]. The theoretical reason to restrict motion of the spine is to prevent any injury to the spinal cord that may result from undesired movement if an unstable fracture or dislocation pattern exists. The term “spinal immobilization” has been historically used to describe these techniques; however, further studies have

shown that these techniques do not truly immobilize the spine but are effective in limiting motion of the spine [23]. Since the techniques do not truly immobilize the spine, the term “spinal motion restriction” has become preferred terminology [24]. Traditional teaching of spinal immobilization has been that patients must be secured to rigid devices until the patient arrives at the hospital to truly “immobilize” the patient. As discussed below, this may result in patient harm, while the motion of patients’ spines can be adequately restricted by other means. Indications Spinal motion restriction is generally indicated when there is concern for spinal column injury based upon clinical exam and symptomology or due to mechanism when spinal injury cannot be reliably excluded due to altered mental status, intoxication, or a distracting injury. A 2018 joint position statement by the National Association of EMS Physicians, American College of Emergency Physicians, and the American College of Surgeons Committee on Trauma summarizes these factors [24]. In this position statement, the indications for spinal motion restriction following blunt trauma include: 1.  Acutely altered level of consciousness (e.g., GCS 20 weeks should be avoided in the prehospital setting and preferably until an ultrasound has been performed to rule out placenta previa. Airway Airway management is among the most critical skills for the EMS clinician to master. Failure to appropriately manage a compromised airway increases the risk of hypoxemic cardiopulmonary arrest or pulmonary aspiration, resulting in high maternal morbidity and mortality  [2]. Several airway anatomical changes

during pregnancy can complicate airway management in the prehospital setting including capillary engorgement of the respiratory mucosa causing swelling of the pharynx, larynx, and trachea  [3]. Mucosal edema associated with elevated estrogen levels and an increase in extracellular fluid volume may lead to more profound airway obstruction, especially if exacerbated by an upper respiratory tract infection, fluid overload, or preeclampsia. These airway anatomical changes may cause difficult airway management (Box 41.1). EMS clinicians must anticipate difficult airway issues and be hypervigilant when using basic airway techniques and airway adjuncts such as oral or nasal airways. Suctioning devices must always be ready and available to address vomiting, for which there is increased risk due to delayed gastric emptying in pregnancy. For advanced airway interventions, clinicians should perform an airway assessment by evaluating mouth opening, using standardized Mallampati scoring to predict a difficult airway, atlanto‐occipital extension, and ability to protrude the mandible. A smaller sized endotracheal tube and gum elastic bougie should be kept on hand in case of difficulty passing the tube through the glottic opening. Standard monitoring such as oxygen saturation and end tidal CO2 waveform capnography are critical. Breathing As the gravid uterus enlarges, significant respiratory challenges result, including upward displacement of the diaphragm, decreased functional residual capacity, increased oxygen consumption of 30%‐60%, and decreased venous return due to inferior vena cava compression. These physiologic variations may lead to rapid desaturation with any medical or traumatic insult. In the pregnant patient with respiratory distress, the mother should be positioned as upright as feasible to decrease abdominal pressure on the thorax and maximize oxygen delivery with a nonrebreather or BiPAP to ensure the fetus is receiving adequate oxygenation. Clinicians should be prepared for impending difficult airway issues before deciding to intubate.

Emergency Medical Services: Clinical Practice and Systems Oversight, Third Edition. Volume 1: Clinical Aspects of EMS. Edited by David C. Cone, Jane H. Brice, Theodore R. Delbridge, and J. Brent Myers. © 2021 NAEMSP. Published 2021 by John Wiley & Sons, Inc.

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Box 41.1  Anatomical and physiological considerations affecting the obstetric airway

Box 41.2  Indications for hyperbaric oxygen therapy in the pregnant patient

Increased upper airway edema Breast enlargement Excessive weight gain Upward displacement of diaphragm Increased risk of regurgitation and aspiration Increased risk of bleeding due to capillary engorgement Decreased functional residual capacity (20%) Increased oxygen consumption (30%‐60%)

COHb level ≥ 20% Syncope Coma Altered mental status/confusion Seizures Metabolic acidosis Fetal distress, i.e., fetal tachycardia, decreased beat‐to‐beat variability, decelerations Cardiotoxicity Any neurologic findings in the mother (especially cerebellar)

Circulation During pregnancy, increased maternal blood volume may allow for initial compensation of major blood loss followed by rapid deterioration. Accordingly, pregnant patients should be treated aggressively with fluid resuscitation to prevent hypotension and hypovolemic states. EMS clinicians should closely observe for signs of pulmonary edema and third spacing with crystalloid infusions due to lower oncotic pressure. Insufficient data exist to support a permissive hypotension resuscitation approach for traumatic pregnant patients. Given the relative anemia of pregnancy, blood transfusion may be necessary earlier in resuscitative efforts. EMS clinicians should place the hypotensive pregnant patients in the left lateral decubitus position (tilted to the left 15‐30 degrees using sandbags or pillows) to prevent the gravid uterus from compressing the inferior vena cava and to improve venous return to the heart. Vasopressors may be used if necessary, to correct shock.

Source: Shannon MW, Borron SW, Burns MJ. Shannon: Haddad and Winchester’s Clinical Management of Poisoning and Drug Overdose. 4th ed. Philadelphia, PA: Saunders Elsevier, 2007. © 2007 Elsevier.

Box 41.3  Physiology changes in pregnancy

Increases Blood volume by 40 – 50% Baseline heart rate by 10 – 15% Cardiac output by 30 – 50% Minute ventilation by 10 – 15%

Decreases Functional residual capacity by 20% due to upward displacement of diaphragm Venous return due to inferior vena cava compression pCO2

Oxygen consumption Hematocrit

Toxicology Carbon monoxide is one of the most relevant toxicologic exposures for EMS clinicians. Carbon monoxide exposure deserves particular attention as the fetus is at higher risk of adverse effects than the mother  [4]. Pregnant patients are more susceptible to carbon monoxide due to increased minute ventilation along with increased endogenous production of carbon monoxide from the fetus [5]. Treatment includes removing the patient from the source of exposure, initiating high‐flow 100% oxygen, and consideration for hyperbaric oxygen, which rapidly increases the arterial O2 content and quickly reduces the carbon monoxide level by increasing the carbon monoxide dissociation rate from hemoglobin [6]. EMS clinicians should consider transport to a specialty hyperbaric center if indicated according to local protocols (Box 41.2).

Pregnancy Effects by System (Box 41.3) Cardiovascular Early in the first trimester, maternal total blood volume and cardiac output increase secondary to production of hormones by the fetus and placenta as well as the uteroplacental circulation acting as an arteriovenous shunt [7]. Blood volume reaches a maximum of 40%‐50% above baseline by 32  weeks’

Glomerular filtration rate Gastric emptying

Blood pressure (or can be normal)

gestation  [8]. Because plasma volume increases more than red blood cell mass, hematocrit falls, leading to physiological “anemia of pregnancy.” Cardiac output rises in the first trimester to 30%‐50% above baseline, peaking at 20‐32 weeks of gestation. Systemic and pulmonary vascular decrease accordingly [9]. Initially, cardiac output rises due increased stroke volume; later, stroke volumes fall, but cardiac output remains elevated due to increased heart rate [10]. Resting heart rate in pregnant women increases by approximately 10 beats/min, and blood pressure gradually decreases due to lower systemic vascular resistance induced by progesterone and the expansion of the low‐pressure placenta [11]. Pregnancy is associated with characteristic ECG changes (Q waves in leads II, III, and aVF and flat or inverted T waves in leads III, V1‐V3) with the most common being slight left‐axis deviation due to an altered heart position as the diaphragm is increasingly elevated  [12]. Dependent edema is common in the third trimester due to decreased systemic vascular resistance and pressure on the inferior vena cava from the growing uterus.

Physiology of pregnancy

Respiratory Pregnant women commonly experience dyspnea, even at rest, from increased respiratory effort and work of breathing. Maternal oxygenation is preserved, and PO2 is generally higher than in a nonpregnant woman secondary to pregnancy‐related hyperventilation. Several changes during pregnancy result in a compensated respiratory alkalosis with a higher PO2 and lower PCO2 than in a nonpregnant state. During pregnancy, a mother’s lung capacity changes as the diaphragm rises up to 4 cm above its usual resting position, and the chest diameter increases 2 cm or more. The chest wall enlarges due to a progressively expanding uterus and outward flaring of ribs, which may be related to hormone‐induced relaxation of ligamentous attachments to the lower ribs [13]. Functional residual capacity decreases by 20% during the second and third trimesters because of decreased expiratory reserve volume and residual volume [14]. One of the most striking changes to the respiratory system is an increase in resting minute ventilation by nearly 50% in the third trimester caused by a larger tidal volume (increases up to 40%) and relatively unchanged respiratory rate  [15]. Arterial pCO2 falls to a plateau of 27 to 32 mmHg during pregnancy, resulting in respiratory alkalosis followed by compensatory renal excretion of bicarbonate allowing for a normal to slightly alkalotic resultant arterial pH (usually between 7.4 and 7.45) [16]. Hematologic Pregnancy leads to a hypercoagulable state by increasing clotting factors I, II, VII, VIII, IX, and XII; decreasing fibrinolysis; and decreasing anticoagulant activity (fall in protein S and activated protein C levels). The most likely evolutionary reason for these coagulation alterations is protection against hemorrhage at birth. However, these changes also increase a mother’s risk for venous thromboembolism. Pregnant women are four to five times more likely to develop deep venous thrombi or pulmonary emboli and have increased risk of venous thromboembolism immediately post partum and then up to 12  weeks thereafter. The prevalence of venous thromboembolism in pregnancy is 0.5‐3 per 1,000 pregnancies and of death is 1.1 per 100,000 pregnancies, becoming the leading cause of maternal mortality in the United States [17]. Gastrointestinal The most common gastrointestinal issues associated with pregnancy are hyperemesis gravidarum, constipation, and heartburn. Many mothers will have some degree of nausea and vomiting during pregnancy, most commonly in the first trimester. Hyperemesis gravidarum is a more severe form of nausea and vomiting that leads to weight loss, dehydration, and electrolyte abnormalities (e.g., hypokalemia)  [18]. In the prehospital environment, treatment consists of antiemetics and IV fluids. Two surgical emergencies that should be highlighted for pregnant women are appendicitis and cholecystitis. Compared to a nonpregnant patient, the clinical assessment, diagnosis, and treatment of these illnesses present a challenging management

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dilemma, and a missed diagnosis may have dire, unfavorable outcomes. Acute appendicitis is the most common nonobstetric indication for surgery during pregnancy with an incidence of 0.5 to 1 per 1000 pregnancies, and most commonly occurs during the second trimester  [19]. The clinical presentation of appendicitis in a pregnant patient is complicated by the normal physiologic changes of pregnancy, including anatomic displacement of the appendix superiorly and posteriorly by the uterus, leukocytosis, and gastrointestinal symptoms such as abdominal pain, decreased appetite, nausea, and vomiting  [20]. This atypical presentation of acute appendicitis during pregnancy may lead to a higher incidence of complications including preterm labor, miscarriage, appendix perforation, surgical wound infections, peritonitis, septic shock, bowel obstruction, pneumonia, and longer hospital stays  [21]. EMS clinicians should consider the diagnosis of appendicitis in any pregnant patient presenting with right‐sided abdominal pain, whether it is in the right lower quadrant, right upper quadrant, or right flank area. Gallbladder disease is the second most common cause of right‐sided abdominal pain in pregnancy. Pregnancy is a known risk factor for biliary disease due to increased levels of estrogen and progesterone leading to cholestasis and supersaturation of bile with cholesterol [22]. Cholecystitis occurs in 1 in 1,600 to 1 in 10,000 pregnancies and is the second most common nonobstetric surgical emergency in pregnancy. Clinical presentation may consist of postprandial pain due to biliary colic, fever, nausea, vomiting, and mid and right upper‐quadrant pain. The classic Murphy’s sign on physical exam may not be present in pregnant patients depending on gestational age and maternal body habitus. EMS clinicians should take abdominal pain seriously in the prehospital setting, recommending transport for mothers for further evaluation. Renal Pregnant women commonly report symptoms of urinary frequency and nocturia. Renal plasma flow increases by 60%‐80% due to arterial vasodilation and increased cardiac output. Urinary frequency is due to hormonal changes and uterus growth affecting renal function leading to hypervolemia and bladder compression. Pyelonephritis is the most common cause of serious bacterial infection in pregnant women, and results in a higher risk of premature delivery (180 in a child deserves prompt action. While this may be due to sinus tachycardia, it is also important to determine if this is supraventricular tachycardia. A slow heart rate (