Lessons Learned from OEF and OIF

Combat Casualty Care

Edited by

Eric Savitsky, MD

Colonel Brian Eastridge, MD

Pelagique, LLC 

Los Angeles, California

University of California at Los Angeles

Los Angeles, California

Office of The Surgeon General

United States Army, Falls Church, Virginia

AMEDD Center & School

Fort Sam Houston, Texas

Borden Institute

Fort Detrick, Maryland
Lessons Learned from OEF and OIF

Combat Casualty Care

Published by the

Office of the Surgeon General

Department of the Army, United States of America

Editor in Chief

Martha K. Lenhart, MD, PhD

Colonel, MC, US Army

Director, Borden Institute

Assistant Professor of Surgery

F. Edward Hébert School of Medicine

Uniformed Services University of the Health Sciences

Medical Content Editor

Eric Savitsky, MD

UCLA Professor of Emergency Medicine/Pediatric Emergency Medicine

Executive Director, UCLA Center for International Medicine

Director, UCLA EMC Trauma Services and Education

Military Editor

Brian Eastridge, MD, FACS 

Colonel, MC, US Army 

Trauma and Surgical Critical Care 

Director, Joint Trauma System Program

Trauma Consultant, US Army Surgeon General
Weapons Effects | iii

Office of The Surgeon General

United States Army

Falls Church, Virginia

AMEDD Center & School

Fort Sam Houston, Texas

Borden Institute

Fort Detrick, Maryland

2012

Editors

Eric Savitsky, MD

Colonel Brian Eastridge, MD

Associate Editors

Dan Katz, MD

Richelle Cooper, MD

Lessons Learned from OEF and OIF

Combat Casualty Care
iv | Combat Casualty Care

Editorial Staff: borden institute pelagique, llc

Vivian Mason Dan Katz, MD

Technical Editor Associate Medical Editor

Douglas Wise UCLA

Senior Layout Editor Richelle Cooper, MD

Research Methodology Editor

Bruce Maston pelagique, llc

Visual Information Specialist Nicole Durden, MPP 

Digital Media Editor

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Copy Editor

This volume was prepared for military medical educational use. The focus of the information is to foster discussion that may form 

the basis of doctrine and policy. The opinions or assertions contained herein are the private views of the authors and are not to be 

construed as official or as reflecting the views of the Department of the Army or the Department of Defense. 

Dosage Selection:

The authors and publisher have made every effort to ensure the accuracy of dosages cited herein. 

However, it is the responsibility of every practitioner to consult appropriate information sources to ascertain correct dosages for 

each clinical situation, especially for new or unfamiliar drugs and procedures. The authors, editors, publisher, and the Department 

of Defense cannot be held responsible for any errors found in this book. 

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Use of trade or brand names in this publication is for illustrative purposes only and does not imply endorsement by the Department 

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Published by the Office of The Surgeon General 

Borden Institute 

Fort Detrick, MD 21702-5000 

 Library of Congress Cataloging-in-Publication Data

Combat casualty care : lessons learned from OEF and OIF / editor-in-chief, Martha K. Lenhart; medical editor, Eric Savitsky; military editor, 

Brian Eastridge.

 p. ; cm.

 Includes bibliographical references and index.

 I. Lenhart, Martha K. II. Savitsky, Eric. III. Eastridge, Brian. IV. United States. Dept. of the Army. Office of the Surgeon General. V. Borden 

Institute (U.S.)

 [DNLM: 1. Military Medicine--methods. 2. Wounds and Injuries--surgery. 3. Afghan Campaign 2001-. 4. Iraq War, 2003-2011. 5. War. 

WO 800]

 616.9′8023--dc23

 2011032530

PRINTED IN THE UNITED STATES OF AMERICA 

19, 18, 17, 16, 15, 14, 13, 12 5 4 3 2 1
Weapons Effects | v

Contents

Contributors.............................................................................................................................................vii

Photo Contributors................................................................................................................................viii

Acknowledgments ....................................................................................................................................ix

Preface ........................................................................................................................................................xi

Prologue....................................................................................................................................................xiii

Chapter 1 Modern Warfare ....................................................................................................................1

Alec C. Beekley, Harold Bohman, and Danielle Schindler

Chapter 2 Weapons Effects ...................................................................................................................39

Sidney B. Brevard, Howard Champion, and Dan Katz

Chapter 3 Fundamentals of Combat Casualty Care ............................................................................85

Robert T. Gerhardt, Robert L. Mabry, Robert A. De Lorenzo, and Frank K. Butler

Chapter 4 Damage Control Resuscitation ..........................................................................................121

Jeremy G. Perkins and Alec C. Beekley

Chapter 5 Damage Control Surgery...................................................................................................165

Brian J. Eastridge, Lorne H. Blackbourne, Todd Rasmussen, Henry Cryer, and 

Alan Murdock

Chapter 6 Maxillofacial and Neck Trauma ........................................................................................225

Robert G. Hale, David K. Hayes, George Orloff, Kyle Peterson, David B. Powers, 

and Swaminatha Mahadevan

Chapter 7 Ocular Trauma ..................................................................................................................299

Raymond I. Cho and Eric Savitsky

Chapter 8 Traumatic Brain Injury......................................................................................................343

Scott A. Marshall, Randy Bell, Rocco A. Armonda, Eric Savitsky, and 

Geoffrey S. F. Ling

Chapter 9 Extremity Injury.................................................................................................................393

John F. Kragh, Jr., Jess M. Kirby, and James R. Ficke

Chapter 10 Spinal Trauma ...................................................................................................................485

Raymond F. Topp, Eric Savitsky, and William P. Cranston

Chapter 11 Pediatric Trauma ...............................................................................................................529

Philip C. Spinella, Jonathan Martin, and Kenneth S. Azarow

Contents | v
vi | Combat Casualty Care

Chapter 12 Acute Burn Care................................................................................................................593

Evan M. Renz and Leopoldo C. Cancio

Chapter 13 Critical Care.......................................................................................................................639

David Norton, Phillip Mason, and Jay Johannigman

Abbreviations and Acronyms ...............................................................................................................xv

Index..........................................................................................................................................................xxi

vi | Combat Casualty Care
Weapons Effects | vii

Contributors

Rocco A. Armonda, MD, LTC, MC, US Army

Kenneth S. Azarow, MD, FACS, FAAP, COL (Ret), MC, US Army

Alec C. Beekley, MD, FACS, LTC, MC, US Army

Randy Bell, MD

John Belperio, MD

Lorne H. Blackbourne, MD, COL, MC, US Army

Harold Bohman, MD, CAPT, MC, US Navy

Sidney B. Brevard, MD, MPH, FACS, COL, US Air Force

Frank K. Butler, MD, FACS, CAPT (Ret), US Navy

Leopoldo C. Cancio, MD, FACS, COL, MC, US Army

Howard Champion, MD, FRCS, FACS

Raymond I. Cho, MD, LTC, MC, US Army

William P. Cranston, PA, CPT, SP, US Army

Henry Cryer, MD

Robert A. De Lorenzo, MD, MSM, FACEP, COL, US Army

Brian J. Eastridge, MD, COL, MC, US Army

James R. Ficke, MD, COL, MC, US Army

Gelareh Gabayan, MD

Robert T. Gerhardt, MD, MPH, FACEP, FAAEM, LTC, US Army 

Robert G. Hale, DDS, COL, US Army

David K. Hayes, MD, COL, US Army

John Hiatt, MD

Jay Johannigman, MD, COL, US Air Force Reserve

Dan Katz, MD

Jess M. Kirby, MD, MAJ, MC, US Army

John F. Kragh, Jr., MD, COL, MC, US Army

Geoffrey S. F. Ling, MD, PhD, COL, US Army

Robert L. Mabry, MD, FACEP, MAJ(P), US Army

Swaminatha Mahadevan, MD

Scott A. Marshall, MD

Jonathan Martin, MD

Phillip Mason, MD, MAJ, US Air Force

Alan Murdock, MD, LTC, US Air Force

David Norton, MD, LTC, MC, US Air Force

George Orloff, MD

Jeremy G. Perkins, MD, FACP, LTC, MC, US Army

Kyle Peterson, DO, CDR, US Navy

David B. Powers, DMD, MD, COL, US Air Force

Todd Rasmussen, MD, LTC, US Air Force 

Evan M. Renz, MD, FACS, LTC(P), MC, US Army

Eric Savitsky, MD

Danielle Schindler, MD

Philip C. Spinella, MD

Areti Tillou, MD, MsED, FACS

Raymond F. Topp, MD, LTC, MC, US Army

Lee Ann Young, BSME, MA

Contributors | vii
viii | Combat Casualty Care

Joel Nichols, MD

North American Rescue, LLC

David Norton, MD, LTC, MC, US Air Force

Pelagique, LLC

Pelvic Binder, Inc.

David B. Powers, DMD, MD, COL, US Air Force

Rady Rahban, MD

Todd Rasmussen, MD, LTC, US Air Force

Reichert Technologies

Evan M. Renz, MD, FACS, LTC(P), MC, US Army

Jessica Shull, Illustrator

Philip C. Spinella, MD

Stryker Instruments

Raymond F. Topp, MD, LTC, MC, US Army

Trauma.org

UCLA Center for International Medicine

United Nations Mine Action Service

University of Michigan Kellogg Eye Center

Eric D. Weichel, MD

Wikimedia Commons

Photo Contributors

We thank the following individuals and organizations for providing some of the images used in this book.

American Academy of Neurology Practice Parameter on 

Management of Concussions

Applied Research Associates, Inc.

Harold Bohman, MD, CAPT, MC, US Navy

Borden Institute, Office of The Surgeon General, 

Washington, DC

David Burris, MD, COL, MC, US Army

Leopoldo C. Cancio, MD, FACS, COL, MC, US Army

David Carmack, MD

Center for Sustainment of Trauma and Readiness Skills 

(C-STARS)

Combat Medical SystemsTM

Composite Resources, Inc.

Subrato Deb, MD, CDR

Defense Imagery Management Operations Center (DIMOC)

Defense-Update.com

Delfi Medical Innovations, Inc.

Robert H. Demling, MD, Harvard Medical School

DJO, LLC

Brian J. Eastridge, MD, FACS, COL, US Army

Elsevier

James R. Ficke, MD, COL, MC, US Army

J. Christian Fox, MD, University of California–Irvine

Aletta Frazier, MD, Illustrator

GlobalSecurity.org

Mitchell Goff, MD

Tamer Goksel, DDS, MD, COL, US Army

Chris Gralapp, Illustrator 

Robert R. Granville, MD, COL, MC, US Army

Kurt W. Grathwohl, MD, COL, MC, US Army

Timothy Hain, MD, Northwestern University

Robert G. Hale, DDS, COL, US Army

John B. Holcomb, MD, COL (Ret), MC, US Army

iCasualties.org

Joint Combat Trauma Management Course, 2007

Joint Theater Trauma Registry

Joint Theater Trauma Systems Program, US Army Institute 

of Surgical Research

Dan Katz, MD

Glenn J. Kerr, MD, MAJ, MC, US Army

John F. Kragh, Jr., MD, COL, MC, US Army

Donald C. Kowalewski, LTC, MC, US Air Force

LearningRadiology.com

Gene Liu, MD, Cedars-Sinai Medical Center

Michael Shaun Machen, MD, COL, MC, US Army

Swaminatha V. Mahadevan, MD, Stanford University

Jonathan Martin, MD, Connecticut Children’s Medical 

Center

Massachusetts Medical Society

Bruce Maston, Illustrator

Alan Murdock, MD, LTC, US Air Force

Juan D. Nava, Medical Illustrator, Brooke Army Medical 

Center
Weapons Effects | ix

Acknowledgments

We extend our gratitude to Robert (Bob) Foster, Director of Biosystems (Ret), Office of the Director, Defense 

Research and Engineering; and Colonel (Ret) John Holcomb for their vision and guidance in support of this 

project.

This educational effort was made possible through the Defense Health Program Small Business Innovation 

Research (SBIR) Program and Telemedicine and Advanced Technology and Research Center (TATRC).

A special thanks to Colonel Lorne Blackbourne (USAISR), Colonel Karl Friedl (TATRC), and Jessica Kenyon 

(TATRC) for their support and guidance throughout this effort.

Acknowledgments | ix
x | Combat Casualty Care
Weapons Effects | xi

Preface

To enhance combat casualty care (CCC) pre-deployment education for all healthcare providers, this 

contemporary educational program was developed through the Small Business Innovative Research 

Program in partnership with civilian industry and the Office of the Secretary of Defense for Health Affairs. 

This military medicine textbook is designed to deliver CCC information that will facilitate transition from 

a continental United States (CONUS) or civilian practice to the combat care environment. Establishment 

of the Joint Theater Trauma System (JTTS) and the Joint Theater Trauma Registry (JTTR), coupled with 

the efforts of the authors, has resulted in the creation of the most comprehensive, evidence-based depiction 

of the latest advances in CCC. 

Lessons learned in Operation Enduring Freedom (OEF) and Operation Iraqi Freedom (OIF) have been 

fortified with evidence-based recommendations with the intent of improving casualty care. The chapters 

specifically discuss differences between CCC and civilian sector care, particularly in the scheme of 

“echelonized” care. Overall, the educational curriculum was designed to address the leading causes of 

preventable death and disability in OEF and OIF. Specifically, the generalist CCC provider is presented 

requisite information for optimal care of US combat casualties in the first 72 to 96 hours after injury. 

The specialist CCC provider is afforded similar information, which is supplemented by lessons learned for 

definitive care of host nation patients. 

These thirteen peer-reviewed and well-referenced chapters were authored by military subject matter experts 

with extensive hands-on experience providing CCC during the course of OEF and OIF, and were edited by 

an experienced team of physicians and research methodologists. Together they will provide readers with a 

solid understanding of the latest advances in OEF and OIF CCC. This information provides an excellent 

supplement to pre-deployment CCC training and education. Ideally, readers will aptly apply the newly 

acquired knowledge toward improving CCC. 

Eric Savitsky, MD 

UCLA Professor of Emergency Medicine/Pediatric Emergency Medicine

Executive Director, UCLA Center for International Medicine

Director, UCLA EMC Trauma Services and Education

Los Angeles, CA

June 2011

Preface | xi
xii | Combat Casualty Care
Weapons Effects | xiii

Prologue

“War is Hell.” — William Tecumseh Sherman

The battlefield will challenge your medical skills, knowledge, personal courage, and perseverance. However, 

in the end, you and the Wounded Warrior will be better for it. 

It is 0200. You are on a forward operating base in the high desert somewhere in southwest Asia. The radio 

in the TOC (Tactical Operations Center) crackles to life, breaking the silence of the night:

This is Whiskey ... Foxtrot ... Tango ... Niner. Inbound in six mikes with two urgent surgicals from an IED. 

Requesting a hot offload ... TIC in progress ... more casualties to pick up. ... Over. 

Outside of the resuscitation area, over the whisper of the cold wind, you hear the whir of the rotor blades of 

the approaching MEDEVAC Blackhawks. Setting down on the landing zone with a deafening roar, all you 

can see is the static electrical discharge from the spinning rotors. Appearing from the darkness are wheeled 

litter carriers bearing casualties and teams of attendants racing alongside. Now, it’s your turn. This is our 

calling, the reason we are here ... for the Warrior. The content of this book was composed for you by those 

who have “been in your boots.”

Similar situations have played out over 47,000 times for US military combat casualties. Survival from 

injury on the modern battlefield is unprecedented; the current case fatality rate is 11%. This is even more 

astonishing, considering the complexity of injury and evacuation of casualties through multiple levels of 

care across the globe. Throughout history, armed conflict has shaped advances in medicine and surgery. 

These conflicts are no different. However, with the progress of technology and communication, we are 

better able to potentiate and disseminate recent lessons learned. 

The paradigm of tactical combat casualty care has dramatically altered pre-hospital management of the 

combat casualty. Tourniquets have saved countless lives. The novel concept of damage control resuscitation 

was born on these battlefields and has reduced the mortality rate of casualties requiring massive transfusion 

from 40% to less than 20%. The Joint Theater Trauma System (JTTS) was implemented to enhance injury 

care performance and to improve provider communication and dissemination of lessons learned across 

the vast continuum of care. Efforts of the trauma system have lead to the development of more than 30 

evidence-based battlefield relevant clinical practice guidelines, and decreased morbidity and mortality from 

combat injury. 

The legacy of this conflict will not only be what we have learned, but also how rapidly we were able to 

disseminate, educate, and change practice on the battlefield in nearly “real-time,” and to translate many 

combat lessons learned into trauma care in the civilian environment. This text is a natural complement of 

our efforts contributing to evolution of casualty care on the battlefield.

Brian Eastridge, MD, FACS

Colonel, MC, US Army

Trauma Consultant, US Army Surgeon General

San Antonio, TX

June 2011

Prologue | xiii
xiv | Combat Casualty Care
Chapter 1

modern warfare

Contributing Authors

Alec C. Beekley, MD, FACS, LTC, MC, US Army

Harold Bohman, MD, CAPT, MC, US Navy

Danielle Schindler, MD
All figures and tables included in this chapter have been used with permission from Pelagique, LLC, the 

UCLA Center for International Medicine, and/or the authors, unless otherwise noted.

Use of imagery from the Defense Imagery Management Operations Center (DIMOC) does not imply or 

constitute Department of Defense (DOD) endorsement of this company, its products, or services.

Disclaimer

The opinions and views expressed herein belong solely to those of the authors. They are not nor should 

they be implied as being endorsed by the United States Uniformed Services University of the Health 

Sciences, Department of the Army, Department of the Navy, Department of the Air Force, Department of 

Defense, or any other branch of the federal government.
Modern Warfare | 3

Table of Contents

Introduction........................................................................................................... 4

Lessons Learned - Know Your Environment.......................................................................5

Joint Theater Trauma Registry (JTTR)....................................................................... 9

Combat Injury Patterns .....................................................................................................11

Causes of Preventable Death..............................................................................................11

Advances in Combat Casualty Care..........................................................................13

Advancements in Combat Casualty Care Training...........................................................13

Equipment Changes ...........................................................................................................15

Body Armor.........................................................................................................................15

Hemorrhage Control Adjuncts............................................................................................15

Organizational Innovations ...............................................................................................17

Echelons of Care .................................................................................................................17

Patient Evacuation and Transport .......................................................................................20

Damage Control Strategies.................................................................................................22

Damage Control Resuscitation ............................................................................................22

Permissive Hypotension......................................................................................................24

Blood Product Transfusion Ratios.......................................................................................24

Role of Fresh Whole Blood................................................................................................26

Role of Recombinant Factor VIIa.......................................................................................27

Damage Control Surgery.....................................................................................................27

Summary..............................................................................................................29

Case Study............................................................................................................29

References ............................................................................................................32
4 | Modern Warfare

Introduction

War has historically provided an opportunity for 

medical advancement and innovation. Military 

medical personnel face the challenge of managing a 

high volume of severe multisystem injuries, relative 

to what is encountered in civilian practice. Combat 

casualty care (CCC) providers face injury and illness 

in the context of an austere wartime environment, 

in which transport times may be unpredictable 

and supplies and staff limited. The frequency of 

multiple or mass casualties may overwhelm available 

resources. In addition, CCC providers not only care 

for injured members of the military, but for injuries 

and illnesses suffered by the local population and 

enemy combatants (Fig. 1). 

Such challenges have fostered innovation in all 

aspects of CCC. Since 2001, significant changes 

including the organization of medical teams, 

new resuscitation practices, new technologies, 

and changes in evacuation strategies have been 

implemented. The creation of a database of all 

military casualties from the current conflicts in 

Iraq and Afghanistan, known as the Joint Theater 

Trauma Registry (JTTR), has allowed for an 

unprecedented level of analysis of wartime injuries 

and deaths. Such analysis has been used to identify potentially preventable causes of death and paved the 

way for implementation of new technologies and practices targeted towards reduction of morbidity and 

mortality from combat.1,2

Combat casualty care providers face multiple challenges in wartime including an austere environment, 

limited supplies or staff, multiple-casualty-incidents, and caring for the local population or enemy 

combatants.

Comparing Operation Enduring Freedom (OEF) and Operation Iraqi Freedom (OIF) to Vietnam, the 

mortality rate of combat-sustained injury has decreased by nearly half.1 The survival rate in these conflicts 

exceeds 90 percent, which is higher than prior conflicts.3,4 Wounding patterns in OEF/OIF differ from 

that of previous conflicts (World War II, Korea, Vietnam, and the Persian Gulf War), which had a higher 

proportion of thoracic injuries and fewer head and neck injuries.5,6,7,8,9 There has been a decreased incidence 

of wounds to the abdomen since the Persian Gulf War.10 The percentage of blast-related injuries is now 

higher.9 

The resources and evacuation systems used to treat casualties have seen substantial improvements since the 

prior conflicts. A special emphasis has been placed upon identifying wounding patterns, adverse outcomes, 

Figure 1. Level III Combat Support Hospital. Image courtesy of the 

Borden Institute, Office of The Surgeon General, Washington, DC.
Modern Warfare | 5

and preventable deaths.9,11,12,13,14 Improvements in body armor, military tactics, and the ability to respond 

quickly and effectively to trauma in a combat environment has led to dramatic improvements in morbidity 

and mortality.1,13

Lessons Learned - Know Your Environment

The following is an experience of a general surgeon during an early deployment: 

I was assigned to a Forward Surgical Team (FST) that took us two hours driving south of Baghdad to reach 

by ground vehicle. It was my first time there; I was nervous about convoys, because we were driving through 

a heavily attacked route; and my intern classmate (a general surgeon) had been killed on an FST three weeks 

before I left for Iraq. Needless to say, my mind really wasn’t on how far we were from the nearest Combat 

Support Hospital (CSH), what the evacuation times were, or even how far we were actually driving (we were 

going very slowly, stopping and starting a lot). So when we arrived at our FST site, it felt like we had come 

a long way to get there. On my prior FST experience in Afghanistan, our FST was two and one-half hours 

by fixed-wing aircraft to the nearest CSH.

It turns out that we were only about 15 minutes by helicopter from the CSH. I assumed that we were much 

farther away. The proximity to more robust hospital support clearly makes a difference regarding how you 

triage multiple patients and what kind of operations you undertake. Nobody had oriented me to this, and 

at the time I didn’t think to ask. I was at the FST 17 days before our first casualties arrived. There were 

four wounded casualties from an improvised explosive device (IED) attack. So here I am, three years out of 

residency, used to taking calls two to four times a month at a relatively slow Level II trauma center. I had 

performed maybe four or five blunt trauma-related operations in that period, and only a few penetrating 

trauma cases from Afghanistan. Now I had to simultaneously care for four wounded, multisystem trauma 

patients with one other surgeon, who was less than a year out of residency. 

We actually thought we did okay. One guy had an abdominal fragment wound but was stable and had a 

negative focused assessment with sonography in trauma (FAST). Two of the guys had extremity wounds 

and fractures, but were able to be splinted and were not hemorrhaging. One guy, however, had a systolic blood 

pressure (SBP) of 70 mm Hg, an inadequate improvised tourniquet on his leg, and open femur, tibial, and 

fibular fractures. He also had an injury to his distal superficial femoral artery. We spent some time getting 

proximal control in the groin, then dissecting out his artery through his huge, hematoma-laden, torn and 

distorted thigh, and putting in a temporary vascular shunt. We transfused him most of our blood bank of 20 

units of red blood cells (RBCs). He was hemodynamically stabilized. He was cold, slightly acidemic, and 

coagulopathic when he left, but we had restored flow to his foot.

Sorting out all these casualties took us maybe one and one-half hours. We finally got them on a helicopter 

and on their way about two hours after they arrived to us. When they arrived to the CSH, the patient with 

the vascular injury had clotted off his shunt. He went back to the operating room (OR) at the CSH and was 

revascularized, but had too much ischemia time and ended up losing his leg. 

When the trauma consultant to the Surgeon General came to visit us at the FST a few weeks later, he noted 

that it took him 17 minutes by slow-flying helicopter to get there from the CSH. As I reviewed the case with 

him, we realized that rather than a vascular shunt, which ended up being harder than it sounded and cost us a 
6 | Modern Warfare

Upon arriving at your area of deployment, get to know your CCC environment and resources. Rapid 

evacuation to a higher level of care may be the best contribution you provide to a casualty (Fig. 2). In some 

Combat Support Hospitals, specialists from trauma surgery, orthopedics, vascular surgery, ophthalmology, 

and critical care are available. Knowing the approximate evacuation time to a higher level of care may 

change critical decisions of whether to operate on a critically injured patient who will ultimately need 

transfer, or whether to transport immediately. What is the nearest Combat Support Hospital? How can 

transport be arranged? What is the fastest method of transport and expected transport time? How many 

critically-injured patients is your unit prepared to handle? If this number is exceeded, casualties who would 

otherwise stay for operative intervention may instead need to be transferred.

Know your CCC environment and recognize your resources and limitations. 

The nature of war is that it is unpredictable. In civilian surgical practice, although the number and acuity of 

patients ebbs and flows, rarely is full capacity exceeded. In civilian urban settings, most injured patients are 

only 15 to 20 minutes from a Level I or II trauma center, and mass casualties are uncommon. In a combat 

environment, multiple-casualty-incidents are quite common (Fig. 3). The most common causes of injuries, 

explosions or exchanges of gunfire, are likely to create several casualties at once. Time to reach medical 

care may vary drastically not only by location, but by the tactical situation (i.e., ability to safely evacuate a 

casualty from a combat area without excessive endangerment of others).

lot of blood products and time, we could have simply applied secure tourniquets to this guy, resuscitated him, 

and sent him on his way to the CSH. He would have reached a facility with vascular surgery support, robust 

blood bank and critical care services, and everything else he needed within an hour.

 Dr. Alec Beekley, LTC 

 United States Army Medical Corps

Figure 2. Level II FRSS-6/STP-7 in Southern Iraq in March, 

2003.

Figure 3. Initial evaluation and resuscitation during a multiple-casualtyincident occurring at the Surgical Shock Trauma Platoon (SSTP) at 

Camp Taqaddum, Iraq 2006.
Modern Warfare | 7

Although Level III Combat Support Hospitals are well equipped with trauma specialists, blood banks, and 

multiple operating tables, many casualties first present to smaller, mobile medical and surgical units, such 

as Army Forward Surgical Teams (FSTs) or Marine Corps Forward Resuscitative Surgical System (FRSS) 

teams. Critical decisions on whether and when to intervene and when to transport critically ill casualties 

are made in these smaller mobile facilities (Table 1). These decisions will change with every new location, 

and even hour-by-hour with the availability of personnel, equipment, and transport. It is critical to know, 

to the best extent possible, what is occurring on the battlefield to prepare for the arrival of casualties. 

The chief surgeon or surgeon-of-the-day is usually the ultimate clinical decision maker and manages the 

clinical function of the unit and its resources. Attention to details, situational awareness of both internal and 

external conditions and good communication with the team are essential. 

All surgeons at forward surgical facilities need to have situational awareness that extends beyond taking care 

of patients in the operating room. The factors outlined in Table 2 are critical to optimal decision making.

Physicians in wartime are rarely fully prepared to treat combat-related injuries on their initial deployment. 

Explosive injuries comprise the majority of severe combat-related injuries (Fig. 4).9,13 In peacetime, even 

experienced surgeons rarely encounter injuries from explosions. Explosions combine primary blast, blunt, 

and penetrating mechanisms to create multisystem, high-energy injuries with extensive soft-tissue damage, 

wound contamination, and hemorrhage from multiple sites. In addition to encountering unfamiliar injury 

patterns, newly deployed physicians must also learn a new medical system, with policies and logistics far 

different from the civilian sector. While standards of medical care remain the same, physicians are challenged 

to meet these standards in a new and often stressful environment. 

Physicians in wartime are rarely fully prepared to treat combat-related injuries on their initial deployment. 

Unfamiliar injury patterns, such as explosive injuries, and a new medical system with policies and logistics 

differing from the civilian sector contribute to a unique and often stressful environment. Rehearsing 

scenarios of care may prove beneficial to newly deployed careproviders.

Because time and circumstance may not afford a thorough orientation, it is critical to ask questions, learn 

from those with experience, and become familiar with available resources before the arrival of your first 

critically-injured patient. Care of the severely-injured combat casualty requires a team effort, and with 

Service Level II Facilities

Air Force Mobile Field Surgical Team (MFST)

Expeditionary Medical Support (EMEDS)

Army Level II Medical Treatment Facility (MTF)

Forward Surgical Team (FST)

Marine Corps Forward Resuscitative Surgical System (FRSS)

Navy Casualty Receiving and Treatment Ships (CRTS)

Table 1. Level II treatment facilities with surgical capabilities according to military service branch. Adapted 

from Rasmussen, 2006.76
8 | Modern Warfare

every team there is a learning curve. An important lesson learned from Forward Surgical Teams has been 

that teams need to rehearse scenarios of caring for multiple casualties before the first true casualties arrive 

(Fig. 5). This is extremely critical to improving the skills of corpsman, medics, and nurses unfamiliar with 

the care of critically-injured patients, and in improving the efficiency of physicians and the team. An open, 

critical, and nonjudgmental review after every major casualty incident, a “hot wash,” has been found to 

improve the performance of Forward Surgical Teams.15

Figure 4. (Left) US serviceman injured by a large mortar round explosion, 

with traumatic amputation of the right hand, near amputation of the left 

leg, and extensive soft-tissue wounds to the right leg. Image courtesy of the 

Borden Institute, Office of The Surgeon General, Washington, DC.

Figure 5. (Below) FRSS patient care team at Forward Operating Base 

St. Michael outside Mahmudiyah, Iraq in March 2004.

Table 2. Forward Surgery - Lessons Learned.

Forward Surgery - Lessons Learned

Triage Issues

• Triage Officer responsible for:

• Clinical function of facility

-Ultimate clinical decision maker

-Status of all casualties

-Consider tactical situation

• Management of available resources

-Personnel, supplies, ORs, blood bank

-Control of walking blood bank

• Initial triage of arriving casualty groups

• Evacuation priorities

Situational Awareness

• Internal 

• Status personnel/supplies 

• Number and physiologic status of 

casualties 

• OR availability

• Blood products

• En-route-care capability

• External

• Evacuation assets

• Time/distance to facility with resources to 

provide appropriate care

• Weather conditions

• Tactical situation
Modern Warfare | 9

Joint Theater Trauma Registry (JTTR)

The civilian trauma systems and practice patterns in place today have emerged largely from the 

lessons learned during wartime. Military medicine has been the driving force behind many of the major 

advancements in trauma care. In the Civil War, the concept of a field hospital emerged, as did the link 

between treatment time and survival rates. In World War I, blood banks and the use of blood transfusions 

were developed. In World War II, antibiotics were put into widespread use, and the triage system was used 

to prioritize casualty evacuations.16 The Korean War brought the development of Mobile Army Surgical 

Hospital (MASH) units, and with Vietnam, improvements were made in rapid evacuation systems with 

helicopters.16,17

Combat casualty care providers must use the lessons learned from wartime to improve subsequent patient 

care. The military medical system is capable of adopting new changes more quickly and efficiently than is 

the civilian sector, and the large number of severe injuries seen in a relatively short span of time allows for 

rapid evaluation of new innovations. 

With the aim of improving CCC, the US Army established the Joint Theater Trauma System (JTTS) 

in 2004 to oversee the organization of medical facilities and resources as well as aeromedical evacuation 

systems.18 Among its many roles, the JTTS has established the Joint Theater Trauma Registry (JTTR), an 

extensive database of every United States (US) combat casualty.1 This comprehensive clinical database 

now contains over 40,000 entries.19 The JTTR allows for retrospective analysis of the type and severity 

of combat injuries and the identification of potentially survivable injuries. It is the cornerstone by which 

performance improvement measures can be developed, implemented, and analyzed. 

With over 40,000 entries, the JTTR has allowed retrospective analysis and actionable research of combat 

injuries.

Data from medical charts, hospital records, transport 

records, and elsewhere are gathered, reviewed, 

and coded by a team of nurses and coders (Figs. 6 

and 7). This allows for an unprecedented amount 

of medical data to be collected on US casualties. 

Important epidemiological questions, such as what 

is the rate of primary amputation or what is the 

percentage of thoracic injury with and without 

body armor, can now be answered. Moreover, the 

JTTR allows for analysis of changes that have been 

implemented, such as: are decreased transport 

times from the battlefield to medical aid associated 

with an improvement in survival, or does the rate 

of uncontrolled hemorrhage upon arrival to the 

hospital decrease with an increase in tourniquet use? Figure 6. An unprecedented amount of information is collected on US 

casualties allowing retrospective analysis and actionable research. Image 

courtesy of Defense Imagery Management Operations Center (DIMOC).
10 | Modern Warfare

Figure 7. Joint Theater Trauma Registry Treatment Record (front). Image courtesy of Joint Theater Trauma Systems Program, US Army Institute 

of Surgical Research.

DATE: VITAL SIGNS

 Immediate

 Minimal

INJURY DESCRIPTION R L L R Pulses Present: Assault/Fight Helo Crash

S= Strong Biological Hot Obj/Liquid

(AB)rasion W= Weak Blast/Explosion IED

(AMP)utation D= Doppler Blunt Trauma Knife/Edge

(AV)ulsion A=Absent Bomb Landmine

(BL)eeding Building Collapse Machinery

(B)urn %TBSA_____ Burn Mortar

(C)repitus Chemical Multi-frag

(D)eformity Crush MVC

(DG)Degloving Drowning Plane Crash

(E)cchymosis Fall Rad/Nuclear

(FX)Fracture Flying Debris Single Frag

(F)oreign Body Grenade UXO

(GSW)Gun Shot Wound GSW/Bullet Other _________

(H)ematoma CARE DONE PRIOR TO ARRIVAL

(LAC)eration Pre-hospital Airway: no yes 

(PW)Puncture Wound

(SS)Seatbelt Sign Pre-hosp. Tourniquet : no yes Type: ____ TIME On:____ Off:______

Pre-hosp. Chest Tube: no yes R L (circle as applicable)

HISTORY AND PRESENTING ILLNESS: __________________________________ Temp Control Measure: no yes Type: body bag other 

________________________________________________________________________________________

________________________________________________________________________________________

HISTORY & PHYSICAL INITIAL PROCEDURES / DIAGNOSTICS

Head & Neck: C-Collar

 Airway (oral/ nasal)

 Chest tube R L Output Blood: mls _____ Air

Chest: Needle decompression R L Output: Blood: mls ______ Air

 Thoracotomy

Abdomen: FAST

 DPL

 Gross Blood +/- NG/OG

Pelvis: Stable Unstable Pelvic Binder

 Foley

Upper Extremities:

Wound Washout

Lower extremities:

Wound washout

Neuro: GCS:______ Motor Deficit: R L Sedated HYPO / HYPERTHERMIA CONTROL MEASURES

E __/4 M __/6 V __/5 None Chemically Paralyzed Time/date

R UE/LE Ending Temp ______________ Time/date

C-Spine Tender L UE/LE Temperature Control Procedure

 Bair Hugger Fwd Resus Fluid Warmer

Skin: Burn: 1st 2nd 3rd %TBSA Light Perception Central Line Chill Buster Body Bag

No Light Perception A-Line Other __________________

____mm

CBC CHEMISTRY 7 LFT URINALYSIS ALLERGIES

Amylase: _____________________________ SpGr: _____________________ NKDA

Alk Phos: _____________________________ pH: _______________________ ASA

L LDH: _________________________________ Chem: _____________________ PCN

A Bili: __________________________________ Micro: _____________________ Sulfa

B SGOT: _______________________________ RBC: ______________________ Morphine

O SGPT: _______________________________ WBC: _____________________ Codeine

R Other: Bact: ______________________ Latex

A HCG: ______________________ Other

T ABG MEDICATIONS IV FLUIDS/BLOOD PRODUCTS PMH

O DT Unknown HTN

R Abx ____________________ Colloids None DM

Y Versed PRBC's _________ Cardiac Ulcer

 Morphine FFP ______________units Respiratory Other

 Fentanyl _____units Seizure

 Other: Cryo ______________units

PLT's ______________packs

Last: First MI MTF transferred from:

SSN/ID DOB/AGE

ASD(HA) September 2005 (March 2010 Interim Update) This Form is Subject to the Privacy Act of 1974 Page 1 of 2

(All shaded areas mandatory for Joint Theater Trauma Registry data collection)

TRIAGE CATEGORY 

TIME OF INJURY: _________________

TIME OF ARRIVAL: _____________ T_____ P____ R___ BP __/___ O2 Sat ___ Expectant

 Delayed

Patient NAME/ID: DATE: (dd,mm,yy)

 Splint

EXT Fixation

pH: ___________________ YES NO

 CRIC Cantholysis (circle L/R)

 Closed reduction

MECHANISM OF INJURY

POSTERIOR 

Intraosseous Access: no yes

 Tourniquet Type CAT / SOFTT / Oth Time On:_____ Time Off:_____

EXT Fixation

 Prostate_____

 Tone_____

PHYSICIAN TRAUMA ADMITTING RECORD (Theater Hospitalization Capability) - Previously Level 3

 Yes No

Clear R L

Blood R L 

 NR

ANTERIOR

 Intubate Canthotomy (circle L/R)

LOCATION OF PRE-HOSP. CARE: ________________________________

HISTORY & PHYSICAL

 Tourniquet Type CAT / SOFTT / Oth Time on:_____ Time off:_____

 Beginning Temp ______________

FiO2: ___________________ VENT:

 Seizure Protocol

Crystalloids ____________cc's NS LR

 Cooling Blanket

 Intraosseus

BE: _____________________

pCO2: _________________ ETT Size: ____

pO2: ____________________

HCO3: __________________

Sat: ____________________

______________cc's

________/_______/_________

 Sluggish

 Mannitol

Whole Bld _______

 Tymp Membranes

 Closed Reduction

Rectal Exam

Hand Motion

 Pericardiocentesis

Vision: Pupils

 Brisk

 GYN______

 Splint

PT/ INR/ PTT

 Size_____mm
Modern Warfare | 11

By understanding how deaths and injuries occur, investigators are best able to identify potential areas 

in which survival and other outcomes can be improved. Research by the JTTS and military healthcare 

providers remains ongoing, resulting in continued improvements in products, techniques, and systems-level 

aspects of medical care.

Combat Injury Patterns

Analysis of injury patterns and deaths during OEF and OIF indicates that most combat-related injuries 

occur as a result of injury from explosions, followed by gunshot wounds.9,11 Only a small percentage of 

injuries are related to motor vehicle accidents and other causes. Injury patterns demonstrate that the highest 

rate of injury is to the extremities, followed by the abdomen, face, and head.9,11 There is a low rate of 

thoracic injury, likely due to improvements in body armor.9, 10,12

Published data from the JTTR database from 2001 to 2005 demonstrated the following casualty data:9

• Mechanism of Injury – explosions (78 percent), gunshot wounds (18 percent)

• Injury Distribution – extremity (54 percent) 

 abdomen (11 percent)

 face (10 percent)

 head (8 percent) 

 thorax (6 percent) 

 eyes (6 percent)

 neck (3 percent) 

 ears (3 percent) 

With extremity injury, there is a high frequency of penetrating soft-tissue injury and associated fractures 

due to explosive fragments and gunshots (Fig. 8). Accordingly, there is a much higher proportion of open 

fractures in combat casualties compared to civilian practice.11,20

Causes of Preventable Death

Analysis of JTTR statistics and data from prior 

conflicts has demonstrated that hemorrhage is by 

far the leading cause of potentially preventable 

combat-related death.13,21 The case fatality rate 

has decreased significantly since Vietnam, from 

16.5 percent to 8.8 percent.1 The improvements 

in mortality are due not only to advancements in 

CCC, but improvements in body armor and rapid 

evacuation. A large part of the JTTS’s mission is 

to analyze casualties, both wounded and killed, 

for the purpose of identifying, implementing, and 

evaluating potential improvements at any point in 

the medical system from first response to long-term 

care and rehabilitation. Figure 8. Fragmentation wound with near complete traumatic amputation 

of the right arm. The injury was nonsalvageable and required a completion 

amputation. Image courtesy of CDR Subrato Deb.
12 | Modern Warfare

Hemorrhage, much of which is considered compressible or amenable to tourniquet placement, is the 

leading cause of preventable combat-related death.

In Vietnam, casualties were described in the Wound Data and Munitions Effectiveness Team (WDMET) 

database.22 From an analysis of the Vietnam casualties who ultimately died, but had survived until reaching 

medical care, a committee of surgeons deemed 8 to 17 percent of the deaths were potentially preventable 

with modern medical care.21 The causes of these deaths included severe hemorrhage, burns, pulmonary 

edema, and sepsis. Furthermore, review of Vietnam data attributes over 2,500 deaths to extremity 

hemorrhage, which is potentially preventable (Fig. 9).

In the early years of the OEF and OIF (2001 to 2004), up to 15 percent of deaths were deemed potentially 

survivable. By far, the leading cause of these deaths was uncontrolled hemorrhage (82 percent), much of 

which was considered compressible or amenable to tourniquet placement.13 Review of data has shown 

that over the past several wars (Korea, Vietnam, and the first Persian Gulf War), the killed in action (KIA) 

rate had not changed significantly.23,24 The KIA rate refers to the percentage of casualties who die before 

Figure 9. Injury caused by a rocket-propelled grenade (RPG) resulting in a large through-and-through wound to the left thigh and traumatic amputation 

of the lower right leg. Note the makeshift tourniquet applied in the field.
Modern Warfare | 13

reaching a medical facility out of all seriously injured casualties, and has been 20 to 25 percent since World 

War II.24 In OEF and OIF, the KIA rate has decreased to 13.8 percent. Additionally, the case fatality rate, 

the percentage of severely wounded casualties who die, has decreased by half since Vietnam.24 Of those 

KIA, the most common causes are severe head injury and severe thoracic trauma. However, 9 percent of 

those KIA die from hemorrhage from extremity wounds, 5 percent from tension pneumothorax, and 1 

percent of airway obstruction. This group comprises most of the deaths considered potentially preventable 

(15 percent of those KIA) and has become the focus of many of the improvements in the medical system. 

Since many of these fatalities occur within the first couple of hours after injury, large efforts have been made 

to improve the early medical access and response. 

Advances in Combat Casualty Care 

Since the recognition of hemorrhage as the major cause of potentially preventable death, a tremendous 

effort has been made to improve hemorrhage control and treatment of other survivable injuries. Rapid 

evacuation, expanded training, improved equipment, and a change in resuscitative and surgical techniques 

are some of the approaches discussed in greater detail below and in the chapters that follow.

Advancements in Combat Casualty Care Training

The golden hour and its associated platinum ten minutes of trauma response lies in the hands of first 

responders. On the battlefield, this is often another soldier, a combat lifesaver, or combat medic. In World 

War II, Vietnam, and OEF and OIF, the vast majority of combat deaths occur before the casualty reaches 

a medical facility. 24

Most medics, physicians and other medical personnel, and all Special Operations Forces (SOF) personnel 

undergo a Tactical Combat Casualty Care (TCCC) training course. The TCCC course was developed 

to teach deployed careproviders key elements of lifesaving prehospital medical care.25 Among the core 

curriculum, techniques in hemorrhage control, 

needle thoracostomy, casualty positioning, and even 

on-site cricothyroidotomy are taught.25 Tactical 

Combat Casualty Care was begun by the Naval 

Special Warfare Command in 1993 and later 

continued by the US Special Operations Command 

(USSOCOM). Much of its development came from 

a 1996 study outlining guidelines for combat care 

for Special Operations corpsmen and has since been 

expanded to all branches.25 

Injury care will often need to be delivered while an 

area is still under hostile fire, delaying the initial 

arrival of medical personnel and equipment (Fig. 

10). Prior to evacuation, available patient care 

equipment is limited to what can be carried by the 

first responder. Equipment such as stethoscopes and 

Figure 10. US soldiers run for cover after a simulated bomb explosion 

during a casualty evacuation exercise in the mock village of Medina Wasl 

at the National Training Center (NTC), Fort Irwin, California. Image 

courtesy of Defense Imagery Management Operations Center (DIMOC).
14 | Modern Warfare

blood pressure cuffs are not available, and would not often be useful in a noisy environment. First responders 

must rely on basic visual and physical examination findings to dictate treatment. Casualty evacuation times 

are widely variable, ranging from minutes to hours, depending on the tactical situation and resources. 

Given these constraints, TCCC training was designed to incorporate several principles that may depart 

from the standard approach to civilian trauma. These include:

• Cardiopulmonary resuscitation (CPR) is not attempted for a casualty with no signs of life

• Airway management and cervical spine immobilization are delayed until the casualty and 

rescuer are both removed from hostile fire

• Casualties found unconscious, but breathing, are given a nasopharyngeal airway and placed in 

the recovery position

• Only the minimal amount of clothing is removed to identify and treat injuries to minimize 

hypothermia

• Control of bleeding is paramount and takes precedence over all other efforts, including 

obtaining intravenous access and extrication from vehicles

• Early use of a tourniquet and hemostatic dressings are encouraged in the setting of hemorrhage

• Intravenous access is not attempted for casualties with superficial wounds, a strong radial pulse, 

and a normal Glasgow Coma Scale (GCS) motor score

Figure 12. Tension pneumothorax, a cause of potentially preventable 

battlefield death, may be treated by needle decompression.

Figure 11. US soldiers from Charlie Company, 4th Battalion, 23th 

Infantry Regiment conduct a foot patrol in the Helmand province of 

Afghanistan in January, 2010. Image courtesy of Defense Imagery 

Management Operations Center (DIMOC).
Modern Warfare | 15

Equipment Changes

Body Armor

Expansion in the use of body armor, improvements in its surface area coverage, and enhancement of 

the armor’s ability to deflect high-velocity projectiles are believed to explain the lower overall incidence 

of thoracic injury during OEF and OIF (Fig. 11).1,9 Early studies also suggest body armor decreases the 

incidence of abdominal injuries.10,26,27 Technological improvements in body armor are believed to contribute 

to the improvement in survival seen since Vietnam. Body armor came into widespread use during Operation 

Desert Storm, and its use further expanded during the current conflicts. In Vietnam, the rate of thoracic 

injury was 13 percent, in OEF and OIF, this rate has decreased to 5 percent.9 Moreover, an analysis of 

casualties in 2004 demonstrated a rate of thoracic injury of 18 percent in those without body armor, and 

less than 5 percent in those wearing armor.1 Despite the decrease in thoracic injuries, tension pneumothorax 

has been recognized as a potentially preventable cause of battlefield death (Fig. 12).13,21 This resulted in the 

training of most SOF in the technique of needle thoracostomy. First responders now carry a large-bore 

needle as part of their battlefield equipment.

Hemorrhage Control Adjuncts

Tourniquets, rarely used in the civilian sector, have become a standard part of every soldier’s equipment, 

and all medics and SOF personnel have been trained in their use (Fig. 13). In the past, tourniquets were 

avoided due to concerns regarding their misuse leading to limb ischemia and lack of adequate hemorrhage 

control. However, this scenario typically was associated with makeshift tourniquets, such as a bandage and 

a stick, which were often improperly applied. 

Figure 13. (Above) The Combat Application Tourniquet®. Liberal 

use is recommended for uncontrolled extremity hemorrhage in the tactical 

environment. Image courtesy of North American Rescue, LLC.

Figure 14. (Right) A casualty arrives at the SSTP at Camp Taqaddum, 

with Combat Application Tourniquets in place. Image courtesy of CDR 

Subrato Deb.
16 | Modern Warfare

Tourniquets save lives. Improved survival is associated with tourniquet placement before the onset of 

shock, while timely removal avoids complications.

Newly designed tourniquets combined with improved widespread training on tourniquet use have played a 

major role in improving hemorrhage control following combat injury.28 This is especially true in battlefield 

or other austere environments, when access to definitive care may be delayed. At the start of OEF and 

OIF, there was very little tourniquet use. However, tourniquets are now applied following nearly every 

severe extremity injury (Fig. 14).29 A 2008 study of severe extremity injury in an OIF Combat Support 

Hospital deemed that tourniquets are effective in controlling hemorrhage with no increased incidence of 

significant limb ischemia or early adverse outcomes.29 Kragh et al. conducted the first prospective study of 

2,838 casualties with major limb trauma admitted to a Level III Combat Support Hospital in Baghdad, and 

demonstrated survival benefit associated with tourniquet use.28 Improved survival was also associated with 

placement of tourniquets prior to the onset of clinical signs of shock. Of the 232 patients who received 428 

tourniquets (applied to 309 injured limbs), transient nerve palsy was the only adverse outcome attributed to 

their use.28,30 If removed within six hours of application, tourniquets save lives without causing limb damage 

or secondary amputation.

Topical hemostatic agents may be used as adjuncts in the treatment of noncompressible hemorrhage.

Figure 15. QuikClot® applied to a large penetrating fragmentation wound of the left shoulder.
Modern Warfare | 17

Hemostatic, clot-promoting agents, such as Combat GauzeTM, WoundStatTM granules, CeloxTM powder, 

QuikClot® and HemConTM dressings, have been used for bleeding not immediately controllable with direct 

pressure, pressure points, or tourniquet use (Fig. 15).31,32,33 These hemostatic agents were developed for use 

in conjunction with the standard techniques of hemorrhage control, including direct pressure, elevation, 

and pressure point use. Some form of hemostatic dressing is now given to every individual in a combat 

zone. Animal models and early studies from OEF and OIF demonstrate the superiority of many of these 

dressings over standard gauze dressings and describe safety considerations surrounding their use.31,32,33 A 

more detailed discussion of combat dressings is provided in the Damage Control Resuscitation chapter.

Organizational Innovations

Beyond new products and techniques, there has 

been improvement in the trauma and evacuation 

systems at organizational levels. Since 2003, the 

trauma system has been organized into levels of 

care designed to minimize the time from injury to 

treatment, and to provide a continuum of care. 

Forward Surgical Teams are small, mobile units 

capable of performing a limited number of lifesaving 

surgeries. These FSTs have been organized into 

rapidly responsive and efficient units. The process 

of casualty evacuation from the battlefield, to the 

initial level of surgical care, and then on to definitive 

care facilities in Germany and the United States, 

has dramatically improved in speed and capability. 

These rapid evacuation systems have enabled 

casualties to reach forward medical facilities in 

minutes rather than hours. The military is now able 

to transfer ventilated, critically ill patients from forward surgical sites near point-of-injury, over distances of 

thousands of miles while providing state-of-the-art critical care en-route (Fig. 16). 

Echelons of Care

To meet wartime needs, CCC and evacuation are organized by echelons of care. In this context, the word 

echelon refers to level of command and control. The medical care delivered at each echelon of the battlefield 

corresponds with respective levels of care (e.g., Level II care is delivered in Echelon II) (Fig. 17). 

Figure 16. An en-route-care nurse helps package a critically-injured 

casualty for transport in the operating room at Camp Taqaddum, Iraq.

Figure 17. Evacuation chain for combat casualties.

n

Echelon I Echelon II Echelon III Echelon IV Echelon V

Self-aid, 

buddy-aid, 

medic,

Battalion Aid 

Station

Forward 

Surgical Team

Combat 

Support 

Hospital

Landstuhl,

Germany

CONUS

Facility
18 | Modern Warfare

Trauma system activation in OEF and OIF occurs 

well before the combat casualty reaches the hospital. 

On the battlefield, the first medical responder to 

a casualty is usually another soldier or a combat 

medic, who in some instances will rapidly move the 

patient to a Battalion Aid Station. Care provided 

by the first responder through the Battalion Aid 

Station is considered Level I. The first response 

may occur when still under fire or in dangerous 

circumstances, and only limited equipment may 

be available. The combat medic assesses whether 

the casualty will require immediate evacuation and 

responds to immediately life-threatening injuries 

(Fig. 18). Most commonly, this includes control of 

hemorrhage using tourniquets as first-line therapy 

if care is being delivered under fire. Once the 

casualty and first responder are no longer under fire, 

hemorrhage control may be reassessed. Depending 

on the findings upon reassessment, hemorrhage 

control may either be augmented with additional 

tourniquets or hemostatic dressings, or controlled 

with a less stringent method (e.g., pressure dressing). 

Rapid evacuation systems have enabled combat casualties to reach forward medical facilities in minutes 

rather than hours. For patients requiring evacuation, the goal is to reach surgical care within one hour of 

injury.

For patients requiring evacuation, the goal is to reach surgical care within one hour of injury. Depending 

on the location, the casualty may initially reach either a Level II or Level III facility. Transport from pointof-injury or a Level I facility to a Level II or III facility is termed casualty evacuation (CASEVAC). A 

Level II facility is typically made up of a FST, capable of providing immediate, life-sustaining resuscitation 

and surgery until the patient can reach a higher-level facility for definitive treatment and longer-term 

care. Most FSTs consist of five to 20 personnel, including at least three surgeons, an orthopaedic surgeon, 

nurse anesthetists, critical care nurses, and technicians.34 Forward Surgical Team personnel are capable of 

rapid assembly and takedown of the facility. The facility comprises two operating tables and a blood bank 

supplying 20 to 50 units of packed RBCs. Most FST facilities now carry plasma and recombinant factor 

VIIa. These FST facilities logistically support up to 30 operations before needing to resupply. The FST 

facilities typically do not have plain radiography capacity, but most have portable ultrasound machines. 

Physicians should become proficient in the use of ultrasound for the evaluation of a combat casualty.

Forward surgical units offer a highly effective combination of proximity and capability for patients who 

cannot be evacuated rapidly to a Combat Surgical Hospital. Determining the ideal relationship between 

proximity to surgical care and the capability of the surgical unit, however, remains a challenge. In many 

cases, the tactical situation has permitted rapid helicopter casualty evacuation directly to a Level III facility, 

Figure 18. Combat medics evacuate a wounded casualty on a Black 

Hawk helicopter. Image courtesy of the Borden Institute, Office of The 

Surgeon General, Washington, DC.
Modern Warfare | 19

approaching that of transporting a civilian trauma patient to a regional Level-one trauma center in the 

United States. Inclement weather, the inability to land a casualty evacuation helicopter close to an active 

firefight, or a high volume of casualties arriving at the closest Level III facility may preclude this practice 

in theater. Similarly, remote combat operations may not allow timely transport of a surgical patient to 

a Combat Support Hospital. In these situations, the forward surgical unit’s mobility and sophisticated 

capabilities provide valuable resources. 

The physical and logistical resources required to provide life and limb-salvaging care to severely injured 

casualties are considerable. Managing several combat casualties over a relatively short timeframe (24 hours) 

can completely overwhelm a unit. The logistical support, communications, security, and ability to transfer 

postoperative patients are as essential to the success of these units as is their forward location. Thoughtful 

consideration of the tactical solution is needed to balance the benefits of enhanced proximity afforded by 

small and mobile forward surgical units against the disadvantages of dispersing resources and experience 

throughout the battlespace. Dispersion of small surgical units across the combat theater without including 

them in an integrated trauma system will not be effective. As noted by Dr. Ogilvie in commenting on the 

success of the Forward Surgical Teams used by the British 8th Army fighting the German Afrika Corps in 

the North African desert during World War II, “This point must be insisted on, because there is constant 

temptation on the part of keen medical administrative officers to push forward their surgeons beyond the 

point where they can do useful work, and for surgeons there to undertake more than lifesaving surgery with 

the splendid folly that prompted the charge of the Light Brigade.”35

Level III facilities include Combat Support Hospitals and are significantly larger, semi-permanent hospitals 

capable of providing immediate patient resuscitation, temporizing and definitive surgeries, medium-term 

intensive care unit (ICU), and postoperative care for hundreds of patients.1 At this level, surgical specialties 

including orthopedics, neurosurgery, maxillofacial surgery, urology and ophthalmology are available. All 

have plain radiography and fluoroscopy, and some have computed tomography (CT) capability. Level III 

facilities often treat host nation casualties in addition to military casualties (Fig. 19). As of 2005, there were 

three Army-based Combat Support Hospitals in Iraq and one in Afghanistan, as well as one Air Force 

Theater Hospital in Iraq. Most have five to 10 trauma bays, two to five operating rooms, and about 10 to 

20 ICU beds (Fig. 20). 

United States casualties requiring longer-term care 

are then evacuated to a Level IV facility. Nearly all 

US casualties in Iraq and Afghanistan are evacuated 

to Landstuhl Regional Medical Center in Germany, 

a large hospital offering all surgical specialties and 

rehabilitation. Finally, US casualties not expected to 

return to duty are ultimately evacuated back to the 

Continental United States (CONUS) to a Level V 

facility. These include Brooke Army Medical Center, 

Walter Reed Army Medical Center, National Naval 

Medical Center Bethesda, and almost all of the triservice major medical centers.

Figure 19. Outside the room of a 14-year-old host national patient who 

sustained blast-related injuries and was treated at a Level III facility in 

Balad AB, Iraq.
20 | Modern Warfare

Patient Evacuation and Transport

“The stated vision of the JTTS was to ensure that every soldier, marine, sailor, or airman injured on 

the battlefield has the optimal chance for survival and maximal potential for functional recovery. In other 

words, to get the right patient to the right place at the right time.”1 The rapid and efficient evacuation of 

a large number of casualties, including those with critical injuries, has been one of the major advances in 

OEF and OIF. Most severely injured casualties can be rapidly transported from the field by helicopter via 

casualty evacuation (CASEVAC), or between Level II and Level III care facilities as a medical evacuation 

(MEDEVAC) (Fig. 21). The CASEVAC system is designed for speed over medical capability. The helicopter 

may not contain medical equipment and the crew may have little or no medical training. Medical evacuation 

crews have medical training and fly in designated helicopters with some medical equipment.36 Helicopters 

are equipped with both a flight crew and medical team, and critically ill casualties are accompanied by an 

Figure 21. A pair of Army Black Hawk helicopters take off from Balad 

AB to perform a MEDEVAC. The MEDEVAC crews are a critical link 

in the chain of events to ensure casualties in Iraq are transported to the next 

level of care within one hour of being injured. Image courtesy of Defense 

Imagery Management Operations Center (DIMOC).

Figure 22. USAF Critical Care Air Transport Teams (CCATTs) have 

enabled the movement of critically ill patients, even in the midst of ongoing 

resuscitation.

Figure 20. Important considerations in casualty evacuation (CASEVAC). The prime objective is to stabilize and transport 

the wounded from the battlefield to the nearest appropriate medical facility available, in the most expedient fashion.

The Balance of Forward Surgery

?

Limited Capability

Dispersion of Resources

Potential for Stagnation

Slow Moving

Decreased Proximity

Proximity

Flexibility

Capability

Synergism

Experience

Forward Surgery Larger Units
Modern Warfare | 21

en-route-care nurse who manages the patient during transport from Level I or II to Level III. Casualties are 

transported from the battlefield to the nearest medical facility (usually a Level II facility) either by ground 

transport or helicopter. Distance, weather, ground conditions, availability, number of casualties and severity 

of injury are among the factors used to determine which mode of transport will be used.37

The US Marine Corps utilizes en-route-care (critical care nurses) to provide ongoing management of 

ventilated, critically ill patients during transport from a forward unit to Level III care. These nurses belong 

to the forward unit and are not part of the air transport unit. After completion of transfer to Level III 

facilities they return to their originating unit. En-route nursing care is an indispensable link as patients move 

from Level I through Level III facilities. During the three busiest periods of First Marine Expeditionary 

Force (I MEF) Operations in Iraq (2003, 2004, and 2006) more than 600 en-route-care missions, moving 

675 patients, were flown from Level II to Level III facilities. This accounted for 16 percent of all combat 

casualties during that time. Virtually all (99.5 percent) of the patients arrived safely at Level III. There 

were four patients who arrived unstable and all had severe injuries. All four were nonpreventable deaths on 

review (unpublished data, USMC 2008). Unfortunately, this was not always the case for patients transported 

without nursing care. Although further refinements and increased training for en-route-care between Level 

II and III units are necessary, this practice is an important step forward in CCC. 

An aeromedical evacuation system was developed during OEF and OIF for long-range transportation. 

This system has transported thousands of casualties by fixed-wing aircraft since its inception.38 In 

Vietnam, transporting an injured casualty back to the United States typically took well over a month. 

With the advancements in aeromedical transport in OEF and OIF, most casualties reach Germany or 

the United States within 36 hours of injury.4,36,38 This rapid transfer of care carries the risk of losing key 

information along the way. Communication between the transport team and receiving careproviders is 

critically important during such transfers. The medical capabilities of aeromedical aircraft and personnel 

have significantly advanced, and these aircraft function as a ‘mobile ICU’ (Fig. 22). 

With advancements in aeromedical transport during OEF and OIF, most casualties reach Germany or the 

United States within 36 hours of injury.

Transport of the most critically ill patients is conducted by Critical Care Air Transport Teams (CCATTs). 

Each CCATT is staffed with at least one physician and two critical care nurses, with the capability to 

transport critically ill ventilated patients for eight to 12 hours at a time, to a higher level of care. The 

CCATTs were developed in 1994 by the US Air Force and allow for postoperative transport of patients 

to Level IV and V hospitals where continuing intensive care, secondary operations, and rehabilitation can 

occur. Evacuation out of theater to Level IV and V facilities is termed air evacuation (AIREVAC). This 

enables Combat Support Hospitals in Iraq and Afghanistan to preserve their ICU and surgical resources. 

Since casualties with injuries not allowing them to return to duty will rapidly move through the system and 

rarely spend significant time at any specific level of care, communication of key information concerning 

their injuries and treatment is essential for optimal care. This is most problematic in an immature theater 

where communications and bandwidth are limited. Under these circumstances, multiple methods of 

transferring information have been utilized. These include paper records, writing on patients or dressings, 

and direct verbal transfer by accompanying medical personnel (Fig. 23). Additionally, items such as 
22 | Modern Warfare

handheld portable dictaphones and even memory 

sticks with downloaded photos of injuries and paper 

records have been tried with varying success. In a 

mature theater with established communication 

capability, availability of the Joint Patient Tracking 

Application (JPTA) – a web-based application that 

allows users to obtain real-time information, e-mail, 

and direct phone communication – have simplified 

transferring medical information and providing 

feedback to forward units on outcomes.1

Damage Control Strategies

Beyond new products and training, there has been 

a significant change in the management of critically 

injured patients reaching a medical facility, termed 

damage control resuscitation (DCR). Damage 

control resuscitation emphasizes resuscitation with 

hemostatic blood products and focuses on rapid control of bleeding and immediately life-threatening injuries. 

Its counterpart, damage control surgery (DCS) focuses only on immediately critical surgical interventions 

and delays more definitive care of injuries until the patient can be stabilized. In conjunction, these practices 

aim to prevent the lethal triad of acidosis, hypothermia, and coagulopathy. 

Damage Control Resuscitation 

The recognition of hemorrhage as the primary cause of preventable combat death led to significant changes 

in the initial resuscitation of severely injured patients.13,21 Most death due to hemorrhage occurs within six to 

24 hours of injury. This makes hemorrhage control, reversing coagulopathy, and restoring tissue perfusion 

critical. Advanced Trauma and Life Support (ATLS) curriculum recommends aggressive resuscitation with 

crystalloids both in the prehospital and hospital settings.39 Moreover, when a massive transfusion is required, 

conventional practice involves transfusion of packed RBCs first, with addition of platelets and clotting 

factors only after the transfusion of a full blood volume (e.g., five liters).39

Conventional resuscitation practices have been significantly influenced by recent CCC experiences in OEF 

and OIF. Upon arriving at a hospital setting, many severely injured casualties are already coagulopathic. 

One-third or more of combat casualties present with an international normalized ratio (INR) of 1.5 or 

greater.40 Aggressive resuscitation with crystalloid and packed red cells worsens coagulopathy through 

dilution, promotion of hypothermia, and worsening of acidosis.40 This lethal triad of acidosis, hypothermia, 

and coagulopathy has a downward spiral effect characterized by acidosis and hypothermia worsening 

coagulopathy, leading to progressive hemorrhaging, which itself worsens all three conditions (Fig. 24). Each 

of the three conditions has been shown to be an independent predictor of mortality in severely injured 

casualties.40

Figure 23. Improvised patient information communication strategy. 

Patient information is written directly onto the dressing of a patient 

emerging from a damage control laparotomy. Image courtesy of the Borden 

Institute, Office of The Surgeon General, Washington, DC.
Modern Warfare | 23

With conventional resuscitation practices, aggressive resuscitation with crystalloid solutions worsens 

coagulopathy through hemodilution, promotion of hypothermia, and worsening of acidosis. In contrast, 

DCR emphasizes resuscitation with hemostatic blood products, rapid control of bleeding and immediately 

life-threatening injuries, prevention of hypothermia, permissive hypotension, and minimal use of 

crystalloids.

Typical crystalloid fluids, including 0.9% normal saline and lactated Ringer’s solution, have a pH of 

5.5 and 6.6, respectively.41 They are often infused in large quantities through large peripheral intravenous 

catheters in prehospital and early resuscitative settings. These crystalloid fluids cause a lowering of blood 

pH and a dilutional effect on the platelets and clotting factors needed to control bleeding. Despite attempts 

at warming these crystalloid fluids prior to infusion, they are rarely administered at body temperature 

and frequently contribute to patient hypothermia. Prolonged transport times between initial injury and 

arrival to medical care further potentiate the risk for hypothermia in combat casualties. Acidosis results 

primarily from production of lactate and other metabolic byproducts due to anaerobic metabolism, a result 

of inadequate tissue perfusion during patient shock. While crystalloids lower pH, massive transfusion of 

blood products is thought to promote acidemia as well.42 Stored RBCs are thought to have a pH of 7.15 or 

lower.43 Transfusion of large quantities of stored RBCs may have a profound lowering effect on body pH.

The goal of DCR is to reverse the three components of the lethal triad and rapidly control hemorrhage. 

Damage control resuscitation applies to both initial resuscitative efforts as well as the first 24 to 48 hours of 

postoperative ICU care. Novel aspects of DCR include permissive hypotension, minimal use of crystalloids, 

rapid transfusion of blood products in an RBC-to-plasma-to-platelet ratio of 1:1:1, aggressive prevention 

of hypothermia with warm blankets and fluids, use of fresh whole blood (FWB) when available, and the use 

of new products, including hemostatic agents and recombinant factor VIIa, when appropriate for severe 

hemorrhage.44

An important aspect of DCR is early recognition of critically ill combat casualties who will require massive 

Figure 24. The lethal triad of acidosis, hypothermia, and coagulopathy. Acidosis and hypothermia worsen 

coagulopathy, leading to progressive hemorrhage and worsening of all three arms of the triad.

Coagulopathy

Hypothermia Metabolic

Acidosis
24 | Modern Warfare

transfusion and are susceptible to the aforementioned issues surrounding resuscitation. Limited blood 

product availability, lab capability, and personnel at forward resuscitative or surgical sites create the need for 

judicious utilization of resources. The rapid and precise recognition of casualties requiring DCR has been 

aided by injury pattern recognition. Casualties who present with any of the injury patterns shown in Table 

3 are likely to need massive transfusion and should be treated by DCR techniques.

Permissive Hypotension

Trauma patients suffering from severe injury, such as limb amputation, often arrive at medical care facilities 

with minimal bleeding. Once resuscitation is initiated, patients start rebleeding, often uncontrollably. Since 

rate of hemorrhage has a direct relationship with mean arterial pressure, it is postulated that lower blood 

pressures may slow the rate of hemorrhage, allow for clotting to occur, and help preserve blood volume.44

Thus, some degree of hypotension may be protective in preventing further hemorrhage in critically injured 

patients. This must be weighed against the effect of hypotension on end-organ perfusion leading to multiple 

organ dysfunction syndrome (MODS).45 

Traditional ATLS teaching calls for two large-bore intravenous catheter insertions in the prehospital setting 

with immediate aggressive crystalloid replacement.39 However, numerous animal-model studies suggest that 

this leads to poorer outcomes in both blunt and penetrating trauma, perhaps due to interference with normal 

physiologic responses to hemorrhage.46,47,48 In combat settings, casualties now receive minimal crystalloid 

or blood products in the field. Combat medics practice permissive hypotension, allowing for a mild degree 

of hypotension (systolic blood pressure of 90 mm Hg) in patients with a normal mental status.49,50 In the 

field, this translates to a palpable radial pulse in an alert patient. The goal is to prevent the conversion 

of controlled hemorrhagic shock to uncontrolled hemorrhagic shock in severely injured casualties before 

reaching definitive care. 

In a combat setting, patients without evidence of head injury who exhibit a normal mental status and a 

palpable radial pulse should not receive intravenous fluids.

Blood Product Transfusion Ratios

Although the definition of massive transfusion varies, the term is commonly applied to a transfusion of 10 

units of RBCs or greater within a 24-hour period (Figs. 25 and 26).51 Most combat and civilian casualties do 

Table 3. Injury patterns as predictors of massive transfusion.

Rapid Recognition Of Casualties Requiring DCR By Injury Pattern

• Truncal, axillary, neck, or groin bleeding not controlled by tourniquets or hemostatic 

dressings

• Major proximal traumatic amputations or mangled extremity

• Multiple long-bone or pelvic fractures

• Large soft-tissue injuries with uncontrolled bleeding

• Large hemothorax (greater than 1,000 milliliters)

• Large hemoperitoneum
Modern Warfare | 25

not require massive transfusion. In the civilian setting, it is required in only 1 to 3 percent of trauma cases. 

In a combat setting, the frequency is higher due to the increased incidence of penetrating trauma and blast 

injury. In OIF, the rate is 8 percent, compared with up to 16 percent during Vietnam.52

In a combat setting, the frequency of massive transfusion is higher due to the increased incidence of 

penetrating trauma and blast injury.

The aim of RBC transfusion is to restore the oxygen-carrying capacity of the blood, replace lost volume, 

and restore tissue perfusion. For patients requiring several units of RBCs, conventional teaching was that 

replacement of platelets and clotting factors due to dilution was not required until the patient had been 

transfused a full blood volume. Thus, most massive transfusions have been heavily weighted towards RBC 

transfusion before other blood products were added, resulting in low plasma-to-RBC and platelet-to-RBC 

ratios. Multiple retrospective studies of both civilian and combat trauma patients have shown an increase 

in mortality, particularly in death due to hemorrhage, associated with low plasma-to-RBC and plateletto-RBC ratios.53,54,55 In a 2008 study by Holcomb et al., a review of 466 civilian patients requiring massive 

transfusion demonstrated that patients receiving higher amounts of plasma and platelet transfusion in 

the context of massive transfusion had decreased truncal hemorrhage. This subset of patients also had 

increased six-hour, 24-hour, and 30-day survival, had less ICU and ventilator days, and spent fewer days in 

the hospital.55 

Blood product transfusion studies following combat-related injuries have shown the same trends. A 2008 

study by Spinella et al. reviewed 708 patients in Combat Support Hospitals who required at least one unit 

of RBC transfusion. Each unit of RBCs transfused was associated with increased mortality, while each unit 

of plasma transfused was associated with increased survival.56 Similarly, a 2007 study by Borgman et al. 

reviewed 246 patients at Combat Support Hospitals requiring massive transfusions and divided them into 

three groups based on the ratio of plasma-to-RBCs received. The three groups had the same median injury 

severity score of 18. The group with the lowest ratio (median 1 plasma: 8 RBC units) had significantly 

higher overall mortality (65 percent) and death due to hemorrhage (92.5 percent) compared to the high ratio 

Figure 25. Running tally of blood products administered, posted on the 

wall above a casualty’s bed. The casualty sustained injuries from multiple 

transabdominal gunshot wounds.

Figure 26. The need for massive transfusion should be determined early. 

Approximately 8 percent of combat casualties require massive transfusion. 

Image courtesy of the Borden Institute, Office of The Surgeon General, 

Washington, DC.
26 | Modern Warfare

group (median 1 plasma: 1.4 RBC units), which had a 19 percent mortality and 37 percent rate of death 

due to hemorrhage.53

Such studies have led to a paradigm shift in the provision of massive blood transfusion in combat casualties, 

with a low-ratio goal approaching 1:1:1 for RBCs, plasma, and platelets. This has led to significant changes 

in blood banking practices. For instance, since plasma is frozen, Combat Support Hospitals now pre-thaw 

fresh frozen plasma (FFP) daily to ensure rapid availability.

Role of Fresh Whole Blood 

With the advent of a low-ratio goal (e.g., 1:1:1) for massive blood product transfusion in combat casualties, 

the ideal blood replacement in the context of hemorrhage may be whole blood, rather than component 

transfusion.57,58,59 Whole blood contains the most physiologic ratio of red cells, platelets, clotting factors, 

and fibrinogen. Secondarily, one unit of whole blood contains overall less volume than the equivalent in 

blood components, which can be important in patients receiving massive transfusion who are at high risk of 

third-spacing fluids and developing pulmonary edema. A retrospective study of 354 patients with traumatic 

hemorrhagic shock receiving blood transfusion found both one-day and 30-day survivals were higher in the 

fresh whole blood cohort as compared to the component therapy group.57

In addition to the problems associated with dilutional effects when RBCs alone are transfused, the age of 

stored RBCs is also associated with an increase in mortality.60 The average lifespan of an RBC is 120 days, 

and this is traditionally the maximum storage time for a unit of frozen RBCs. As red cells age, an increasing 

number of cells will die or become damaged and release intracellular products. In animal models, transfusion 

of stored RBCs has been shown to cause release of inflammatory mediators and result in higher infection 

rates.61 In addition, as red cells age, their oxygen-carrying capacity per unit diminishes and the restoration 

of tissue perfusion decreases, which may have adverse clinical effects.62 

Recent investigation has given significant attention to the use of warm fresh whole blood (FWB) for massive 

transfusion required in a combat setting. The use of FWB started during World War I, initially out of necessity 

due to limited supplies of blood components in 

combat hospital settings. Transfusion practices have 

been revised during OEF and OIF to increase the 

safety and efficiency of the process.44 When the 

number and severity of casualties exceeded the 

ability of blood banks to keep up with transfusion 

requirements, walking blood banks were established 

to rapidly increase the supply of available blood in 

disaster scenarios (Fig. 27). Whole blood donated by 

military personnel, prescreened and blood-typed, 

can be rapidly cross-matched and available for use 

within hours without being divided into components. 

Though initially developed out of necessity, the 

use of warm FWB is now under investigation 

as a potentially superior approach compared to 

component therapy for massive transfusion.57,63

Figure 27. Military personnel donate blood at the Walking Blood Bank, 

Camp Taqaddum, Iraq in 2006.
Modern Warfare | 27

Whole blood donated by military personnel, prescreened and blood-typed, can be rapidly cross-matched 

and available for use within hours without being divided into components.

Role of Recombinant Factor VIIa

Recombinant factor VIIa has been under study for its use in severe hemorrhage.64,65 Currently, recombinant 

factor VIIa (rFVIIa) is Food and Drug Administration (FDA) approved for severe bleeding in patients with 

factor VII deficiency. It is, however, being used off-label for patients with normal coagulation systems with 

life-threatening hemorrhage. Its first use in trauma was reported in 1999, and it is now used in military 

and civilian settings for trauma patients and for intraoperative hemorrhage.64,65 Its off-label use has not yet 

been standardized and transfusion criteria, dosing, and redosing guidelines are still under investigation. 

Animal studies have indicated prolonged survival times and earlier control of hemorrhage associated with 

its use, and human case reports suggest that fewer blood products are required in hemorrhaging patients 

who receive rFVIIa.64,65,66 Early randomized control trials of rFVIIa for bleeding control during various 

surgical procedures and in coagulopathic populations did not show reduction in mortality or transfusion 

requirements.67,68,69 A 2005 randomized controlled trial of the use of rFVIIa versus placebo found rFVII 

demonstrated a reduction in the transfusion requirements for blunt trauma patients receiving rFVIIa, and 

a similar but nonsignificant trend in the penetrating trauma group.64 Other types of studies, such as case 

series, meta-analyses and post-hoc analyses of randomized controlled trials have demonstrated trends 

(albeit statistically insignificant) toward improved outcomes.70,71,72 Concerns regarding the use of rFVIIa are 

mainly related to the possibility of promoting thromboembolic complications. This was not observed in the 

2005 randomized controlled trial, but has been reported in retrospective reviews.73 Currently, in combat 

settings, rFVIIa is judiciously used in patients with life-threatening bleeding requiring massive transfusion. 

Damage Control Surgery

During the past 20 years, a new approach to trauma surgery known as damage control surgery (DCS) has 

been developed. Damage control surgery has been practiced in both civilian and combat settings, and is 

currently implemented in OEF and OIF. Traditional teaching advocates aiming for a single, definitive 

operation to repair traumatic injuries. Such an approach stems from the concern that an incomplete 

operation, or the need for multiple operations, could threaten a patient’s overall stability and recovery. 

However, some definitive repairs of complex injury patterns may take hours to complete. In casualties 

who arrive in hemorrhagic shock, the lethal triad of coagulopathy, acidosis, and hypothermia may not be 

completely reversed before and during operative repair of injury. In these patients, metabolic derangements 

may continue to worsen in the OR, even after control of hemorrhage is achieved. Such patients may have 

a poorer outcome if subjected to a long, complex operation before physiologic parameters are restored.74,75

The principle of DCS is to minimize initial operative time in critically injured casualties by focusing only 

on the immediately critical actions. These critical actions are: (1) control of hemorrhage; (2) prevention 

of contamination and gastrointestinal soilage; and (3) protection from further injury. Injuries to the bowel 

requiring primary anastomosis, or other time-consuming repairs, are left for the subsequent operation(s) 

(Figs. 28, 29, and 30). Packing is often left in the abdomen. The abdomen is left open and sealed at the 

skin with a vacuum-assisted dressing to prevent abdominal compartment syndrome. Orthopedic injuries 

are treated with splinting or external fixation, and vascular injuries may be temporized with temporary 

intralumenal vascular shunts.74,75,76
28 | Modern Warfare

In damage control surgery, an abbreviated operation is performed to control hemorrhage and contain 

gastrointestinal soilage. After a period of postoperative resuscitation in the ICU, patients may return to 

the operating room for a definitive procedure.

Following an abbreviated operation, patients are taken to the ICU to reverse the lethal triad through 

resuscitation and restoration of physiologic parameters. Here, crystalloids and transfusion are continued as 

needed to restore tissue perfusion and correct acidosis, and the patient is warmed and treated with vasoactive 

agents if needed. While the aim is to return to the OR in 24 to 48 hours, the definitive operation should 

not take place until the metabolic derangements are largely reversed. Several complications, including 

hemodynamic instability, organ failure, or acute respiratory distress syndrome (ARDS) may delay the 

timing of the second operation. In the definitive operation, abdominal packing and clots are removed and 

the abdomen is reexplored and washed out. Additional debridement, repair of shunted vascular injuries, 

anastomosis of bowel, and abdominal closure are performed at this subsequent operation.74,75 

The timing of definitive surgical repair and abdominal wall closure will often vary based on injury type, 

severity, status (military or civilian), and nationality of the patient. For example, many US service members 

will undergo definitive abdominal wall closure following AIREVAC to rearward Level IV or V facilities, 

Figure 28. (Top Left) This was a gunshot wound to the right back 

creating a large defect in the psoas muscle, laceration of the inferior vena 

cava (IVC) and destruction of the ascending colon and proximal transverse 

colon. The patient underwent control and repair of the IVC, packing of 

the retroperitoneal psoas defect (white pads seen in photo), and stapled 

resection of the right colon with blind ends left. Distal end of resected colon 

is seen under suction catheter tip. The proximal resected end was the distal 

ileum, which is being held in the foreground. 

Figure 29. (Top Right) Repaired inferior vena cava.

Figure 30. (Bottom Right) Completed temporary vacuum-assisted 

dressing abdominal closure. The bowel and abdominal cavity were 

irrigated and decontaminated before temporary abdominal closure. The 

casualty underwent damage control resuscitation – receiving PRBCs, 

FWB, and rFVIIa – and was transported to a Level III facility less than 

three hours after his arrival.
Modern Warfare | 29

while host nation patients typically receive definitive surgical care at the Combat Support Hospital.77 The 

combat trauma experience of the US Army 102nd FST in Afghanistan consisted of performing 112 surgeries 

on 90 patients over a seven-month period. Trauma accounted for 78 percent of surgical cases. Sixty-seven 

percent of these surgeries were performed on Afghan militia and civilians, 30 percent on US soldiers, and 

3 percent on other coalition forces. Mechanisms of injury included gunshot wounds (34 percent), blasts (18 

percent), motor vehicle crashes (14 percent), stab wounds (5 percent), and other trauma (7 percent).77

The three-step process of abbreviated operative repair, ICU resuscitation, and definitive operative repair 

of DCS follows the fundamental principle of treating the most immediate life-threats first. While DCR and 

DCS include several departures from classic ATLS teaching, the basic philosophy of prioritizing injury is 

the same.74,75 

Summary

 

The greatest honor we can pay to war casualties is to use their sacrifice to improve and optimize medical 

care. The lessons learned from OEF and OIF and prior conflicts have led to numerous advances in combat 

casualty and civilian trauma care. The CCC environment is vastly different from civilian trauma care 

settings. Thus, the approach to a combat casualty must take into account many additional logistical factors 

beyond the type and mechanism of injury. These include: what is the fastest way to reach a medical 

facility?, who is available to assist upon arrival?, is the area free of hostile fire?, will adequate personnel, 

blood products, and equipment be available for all those injured?, and, if not, how should casualties be 

prioritized? Awareness of local and support CCC capacity is as critical to improving patient survival rates 

as are initial airway, breathing, and circulation interventions. 

The recognition of hemorrhage as the major cause of preventable death has led to a paradigm shift in the 

approach to the bleeding patient. Hemorrhage must be immediately and aggressively addressed with direct 

pressure, tourniquets, hemostatic agents, and rapid evacuation to a CCC facility. Resuscitation must be 

geared toward preventing and treating the downward spiral of the lethal triad of acidosis, hypothermia, and 

coagulopathy. Surgical intervention is directed towards rapid control of hemorrhage and contamination, 

rather than definitive repair of injury. Combat casualty care continues to evolve. The JTTS and the 

promotion of peer-reviewed scientific research during the current conflicts is a relatively new phenomenon 

that fosters investigation and innovation. The many improvements developed from the lessons of prior wars 

are now saving lives, and the efforts to continue learning will offer the best chance of survival and recovery 

to those we care for in the future. 

Case Study 

The following is a copy of the Level II treatment summary from the record of a casualty from OIF that 

demonstrates most of the aspects of the prior discussions. It details the treatment from appropriate rapid 

initial care according to the TCCC guidelines, to utilization of DCR and DCS procedures on a critically 

injured casualty. The treatment summary illustrates how the continuum of care across the different levels of 

care leads to the survival of a casualty who in prior conflicts undoubtedly would have died. 
30 | Modern Warfare

Casualty # 0822

26-year-old male presented in class IV hemorrhagic shock about 25 minutes after wounding from a sniper 

round to abdomen. Treatment in field consisted of abdominal dressing over wound and single intravenous 

catheter access with limited fluid resuscitation. Initial evaluation in Shock Trauma Platoon (STP) revealed 

entrance wound to right flank with exit out anterior abdominal wall just to right of umbilicus with eviscerated 

omentum. Initial vital signs: blood pressure (BP) of 80/40, heart rate (HR) of 148, respiratory rate (RR) of 

26, and pulse oximeter oxygen saturation (SpO2) of 98 percent. Additional intravenous access was obtained, 

blood sent for labs, and antibiotics started and patient taken immediately to the operating room (less than 

five minutes). Walking blood bank (WBB) activated. 

Operative Findings: 

• 2,000 milliliters hemoperitoneum with gross fecal contamination

• Large central zone I and right zone II retroperitoneal hematoma with active bleeding 

• Abdominal cavity packed and aortic control at hiatus obtained (aortic cross clamp time of 55 minutes)

• Right medial visceral rotation performed

• Grade 5 (pulverized) right colon injury noted

• Multiple lacerations to inferior vena cava from confluence to just inferior to the right renal vein; the 

aorta is negative for injury

• Grade 3 laceration to third portion duodenum with ischemia

Initial Labs: 

pH = 7.1 Base Deficit = -16 Hematocrit = 28 percent

Procedures:

• Initial attempt at inferior vena cava venorraphy but multiple lacerations posteriorly (probable torn 

lumbars) quickly led to oversew and ligation 

• Simple whipstitch closure of duodenum to stop contamination and bleeding

• Stapled resection right colon with blind ends

• Packing right retroperitoneal psoas wound

• Washout peritoneum with rewarming

• Vacuum-pack closure abdominal dressing

• Bilateral lower extremity four compartment fasciotomies (for ligated inferior vena cava and one-hour 

ischemia time)

Resuscitation by Anesthesia:

• Three liters normal saline

• Six units PRBCs

• 24 units FWB

• 7.2 milligrams rFVIIa

Packaged for En-Route-Care: 

• VS: BP = 115/61 mm Hg HR=147 RR=12 (ventilated) SpO2=100 percent

• Departed to Level III facility less than four hours after arrival at STP

• En-route-care interventions: blood administration, sedation and paralytics, ventilator management; 

departing end-tidal carbon dioxide (EtCO2) = 52 mm Hg
Modern Warfare | 31

Notes from Joint Patient Tracking Application (JPTA) at Level III Facility:

Findings from original STP facility: Gunshot wound to right flank exited near navel. On exploratory 

laparotomy, patient had a long tear from the confluence of the inferior vena cava to just below the right renal 

vein. Inferior vena cava oversewn and ligated proximally and distally. Grade 3 injury to the third portion of 

the duodenum was oversewn. The aorta was cross-clamped at the hiatus (total aortic cross-clamp time was 

55 minutes). Right colon with grade 5 injury: colon was resected distal ileum to mid-transverse with blind 

ends. Gross fecal contamination in peritoneum. Two laparotomy pads packed in right retroperitoneum. 

One KerlexTM packing along anterior abdominal wall to exit wound. Vacuum-pack closure of abdomen, 

bilateral four compartment fasciotomies of lower extremities for ligated inferior vena cava and approximate 

one hour of ischemia time. Patient received six units of PRBCs, 24 units of FWB, 7.2 milligrams of rFVIIa.

Vital Signs Upon Arrival:

BP = 153/74 mm Hg HR=108 RR=15 SpO2=100 percent

Level III Facility Admit Note:

Patient was noted to be hemodynamically stable, sedated, and on the ventilator. His abdomen was dressed 

open and with a negative-pressure dressing (supplied by Jackson Pratts). The right lateral abdomen wound 

was noted. No other injuries were noted. The coagulation studies were normal and his hematocrit was 

normal. His base excess was +1. He appeared well-resuscitated. Given the large amount of blood loss at the 

original operation, will allow further time for hemostasis and he had just recently been taken from the OR. 

If he remains stable, will reexplore early this a.m.

Next Day Note:

Procedure Note: (1) Abdominal reexploration; (2) Segmental resection of proximal third portion of 

duodenum; (3) Side-to-side duodenoduodenostomy; (4) Pyloric exclusion; (5) Roux-en-Y gastrojejeunostomy; 

(6) Retrograde duodenostomy tube; (7) Jejeunostomy feeding tube; and (8) Stamm gastrostomy. 

Postoperative Day Three Note:

Patient stable and now off ventilator. Tolerating tube feeds. Fasciotomies closed today. Jackson Pratt (JP) 

with minimal drainage. Labs normal. Ready for transfer in a.m.
32 | Modern Warfare

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34 | Modern Warfare

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53. Borgman MA, Spinella PC, Perkins JG, et al. The ration of blood products transfused affects mortality 

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improves outcome in 466 massively transfused civilian trauma patients. Ann Surg 2008;248(3):447-458. 

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65. Spinella PC, Perkins JG, McLaughlin DF, et al. The effect of recombinant activated factor VII on 

mortality in combat-related casualties with severe trauma and massive transfusion. J Trauma 2008;64(2):286-

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66. Lynn M, Jerokhimov I, Jewelewicz D, et al. Early use of recombinant factor VIIa improves mean arterial 

pressure and may potentially decrease mortality in experimental hemorrhagic shock: a pilot study. J Trauma 

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67. Raobaikady R, Redman J, Ball JA, et al. Use of activated recombinant coagulation factor VII in patients 

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a randomized, placebo-controlled, double-blind clinical trial. Anesthesiology 2005;102(2):269–275.

69. Bosch J, Thabut D, Bendtsen F, et al. Recombinant factor VIIa for upper gastrointestinal bleeding in 

patients with cirrhosis: a randomized, double-blind trial. Gastroenterology 2004;127(4):1123-1130.

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bleeding control in severe trauma patients with coagulopathy: subgroup analysis from two randomized 

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Modern Warfare | 37

and traumatic hemorrhage. Am J Surg 2005;189(3):331-334. 

73. O’Connell KA, Wood JJ, Wise RP, et al. Thromboembolic adverse events after use of recombinant 

human coagulation factor VIIa. JAMA 2006;295(3):293-298.

74. Blackbourne LH. Combat damage control surgery. Crit Care Med 2008;36(7 Suppl):S304-310.

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76. Rasmussen TE, Clouse WD, Jenkins DH, et al. Echelons of care and the management of wartime 

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38 | Modern Warfare
Chapter 2

WEAPONS EFFECTS

Contributing Authors

Sidney B. Brevard, MD, MPH, FACS, COL, US Air Force

 Howard Champion, MD, FRCS, FACS

Dan Katz, MD
All figures and tables included in this chapter have been used with permission from Pelagique, LLC, the 

UCLA Center for International Medicine, and/or the authors, unless otherwise noted.

Disclaimer

The opinions and views expressed herein belong solely to those of the authors. They are not nor should 

they be implied as being endorsed by the United States Uniformed Services University of the Health 

Sciences, Department of the Army, Department of the Navy, Department of the Air Force, Department of 

Defense, or any other branch of the federal government.
Weapons Effects | 41

Table of Contents

Introduction..........................................................................................................43

Weapons ...............................................................................................................44

Small Arms ..........................................................................................................44

Explosives.............................................................................................................44

Physics ................................................................................................................................44

Low-Order ..........................................................................................................................45

High-Order .........................................................................................................................45

Devices ................................................................................................................................46

Antipersonnel Landmines and Unexploded Ordnances ....................................................46

Blast (Static) Landmines ......................................................................................................47

Fragmentation Landmines ..................................................................................................48

Directional Fragmentation Landmines ...............................................................................49

Rocket-Propelled Grenades ................................................................................................50

Improvised Explosive Devices .............................................................................................50

Antitank Munitions .............................................................................................................52

Shaped-Charge ................................................................................................................52

Kinetic Energy Rounds ......................................................................................................54

Antitank Landmines..........................................................................................................54

Explosion-Related Injury ........................................................................................54

Patterns...............................................................................................................................54

Military Casualties ...............................................................................................................54

Civilian Casualties................................................................................................................55

Potentiators.........................................................................................................................56

Categories ...........................................................................................................................58

Primary Blast Injury.............................................................................................................58

Ears ...............................................................................................................................58

Lungs ..............................................................................................................................60

Solid and Hollow Organs .................................................................................................63

Brain ..............................................................................................................................63

Eyes ................................................................................................................................65

Extremities ......................................................................................................................65

Secondary Blast Injury ........................................................................................................65

Primary and Secondary Fragments......................................................................................65

Fragment Physics..............................................................................................................66

Fragment Wounds.............................................................................................................66

Fragment Range................................................................................................................67

Tertiary Blast Injury.............................................................................................................68

Quaternary Blast Injury.......................................................................................................69

Quinary Blast Injury ............................................................................................................70

Management Considerations...............................................................................................72
42 | Weapons Effects

Embedded Unexploded Ordnance......................................................................................72

Conclusions ..........................................................................................................73

References ............................................................................................................74
Weapons Effects | 43

Introduction

Understanding modern warfare, including the types of weapons employed and the mechanisms and 

patterns of injury they cause, is critical to providing optimal combat casualty care (CCC). Certain types 

of weapons (e.g., improvised explosive devices) inflict patterns of injury that are repeatedly encountered 

by military careproviders. By recognizing these patterns and understanding the pathophysiology behind 

resultant injuries, CCC providers will be better prepared to treat the injured.

The Joint Theater Trauma Registry (JTTR) is a database used to track medical treatment information 

on troops injured in Operation Enduring Freedom (OEF) and Operation Iraqi Freedom (OIF). Data are 

collected at various points as injured troops receive medical treatment in-theater and at each medical 

facility overseas and in the United States (US). The information recorded is extensive and includes patient 

demographics, mechanism of injury, type of personal protective equipment (e.g., body armor, goggles, 

helmet) used, body regions injured, and more.1 

A query of the JTTR database for wounds sustained between October 2001 and January 2005 revealed 

the following distribution of injuries: extremities (54 percent), head and neck (29 percent), abdomen (11 

percent), and chest (6 percent).2 This injury pattern differs from that of previous conflicts, which had a 

higher proportion of thoracic injuries and fewer head and neck injuries.2,3,4,5,6 This shift is likely due to 

enhanced body armor that protects the chest and reduces mortality.2 Enhancements in personal protective 

equipment (PPE) and the shift from conventional warfare to “a complex mix of conventional, set-piece 

battles, and campaigns against shadowy insurgents and terrorists” contribute to current wounding patterns, 

which differ from those of previous conflicts (i.e., World War II, Korea, and Vietnam).7

The JTTR database for wounds sustained in OEF and OIF between October 2001 and January 2005 

reveals the following distribution of injuries: extremities (54 percent), head and neck (29 percent), abdomen 

(11 percent), and chest (6 percent).

The increase in explosion-related injuries and 

concomitant decrease in gunshot-related injuries 

in the past century and a half of US conflicts is 

summarized in Figure 1. This trend has accelerated 

substantially during recent years. This is illustrated 

by increases in explosion-related OEF and OIF 

casualties from 56 percent in 2003 to 2004 to 76 

percent in 2006 and in the number of surgeries for 

fragment wounds from 48 percent in OIF I (2003) to 

62 percent in OIF II (2004 to 2005) performed by 

US Navy/Marine Corps Forward Surgical Teams in 

OIF.8,9

Figure 1. Primary mechanisms of injury in United States wars.2 Data 

sources: Civil War,10 WWI and WWII,11 Korea,5 Vietnam,6 OEF/

OIF.2

0%

20%

100%

Civil War

40%

60%

80%

WWI WWII Korea

Percentage

Vietnam OEF/OIF

Gunshot Wound Explosion
44 | Weapons Effects

Weapons

The primary mechanisms of combat injury in OEF and OIF are small arms (pistols, shotguns, rifles, machine 

guns) and explosives (mortars, landmines, rocket-propelled grenades [RPGs], and improvised explosive 

devices [IEDs]). As of 2009, combat casualty statistics for hostile actions indicate that explosive devices 

are responsible for 80 percent of injuries and 81 percent of deaths in OEF, and for 86 percent of injuries 

and 90 percent of deaths in OIF.12 These mechanisms and their effects are discussed below, followed by an 

overview of blast injury.

Small Arms 

Current combat casualty statistics for hostile actions indicate that gunshot wounds are responsible for 22 

percent of injuries and 27 percent of deaths in OEF, and for 8 percent of injuries and 19 percent of deaths 

in OIF.12 Small arms are easily available in Iraq, which has an estimated combined military and civilian 

arsenal of seven to eight million firearms containing machine guns, submachine guns, sniper and assault 

rifles (including AK-47s and AK-47-style models such as the AKM), shotguns, pistols, and carbines.13

The degree of tissue damage resulting from small arms fire in OEF and OIF is highly variable. Combat 

casualty careproviders need to treat each patient’s wound(s) individually. Wide surgical exploration of all 

bullet wounds is no longer routinely recommended.14 Minimal tissue debridement is typically required for 

wounds resulting from small arms fire. As a bullet travels through tissue, a temporary cavity is created. Tissue 

damage in this temporary cavity is usually limited and may heal on its own without debridement.15 Inelastic 

tissues, such as the brain and liver, will exhibit the most damage resulting from temporary cavitation. Elastic 

soft-tissue, such as lung, skeletal muscle, nerves, and blood vessels, may show minimal damage.15 There may 

be cases when a bullet strikes bone or another structure and is deflected. In these cases, the damage could 

be more extensive and require larger debridement. Therefore, each case should be carefully evaluated and 

managed individually.14

The degree of tissue damage resulting from small arms fire is highly variable. Wide surgical exploration 

of all bullet wounds is no longer routinely recommended.

Explosives

Physics

With the prevalence of explosive weapons in use in Iraq and Afghanistan, it is important that CCC providers 

have a basic working knowledge of the physics behind explosions. Explosions are the result of chemical 

conversion of a liquid or solid into a gas with generation of energy. Explosives are classified as low- or 

high-order based on velocity of detonation (i.e., the interval between activation and release of the explosive 

energy). Knowing the type of explosive that caused a casualty’s injuries is important because low- and high-
Weapons Effects | 45

order explosives exhibit different patterns of injury and thus warrant different treatment considerations 

(Table 1).16,17

Low-Order 

Low-order explosives, which include gunpowder and dynamite, produce their effect through a relatively 

slow burning process called conflagration.18 The readily combustible substances in low-order explosives are 

used primarily for propelling projectiles, but also take the form of pipe bombs and petroleum-based bombs 

(e.g., Molotov cocktails). The blast wave generated by a low-order explosive typically has a speed of less than 

2,000 meters-per-second (m/sec). Low-order explosives have secondary, tertiary, quaternary, and sometimes 

quinary effects (see classifications described later). Importantly, they do not have the primary blast effects 

characteristic of high-order explosives.

High-Order 

Single-compound high-order explosives include ammonium nitrate, nitroglycerin, 2, 4, 6-trinitrotoluene 

(TNT), pentaerythritol tetranitrate (PETN), cyclotrimethylene trinitramine (RDX), cyclotetramethylene 

tetranitramine (HMX), and nitrocellulose. These compounds may be combined to form mixed-compound 

explosives, such as dynamite, composition C4, ammonium nitrate/fuel oil (ANFO), and sheet explosives.19

Commonly-used polymer-bonded high explosives (Gelignite, Semtex) have one and one-half times the 

power of TNT.

High-order explosives react very quickly and 

generate heat and energy almost instantaneously. 

Products of the explosive reaction occupy a greater 

volume than that filled by the original reactants. This 

results in a supersonic, superheated rise in pressure 

called a blast wave, which moves at speeds of 3,000 

to 8,000 m/sec.20 The blast front is the leading edge 

of the blast wave and has a shattering effect known 

as brisance. As the blast wave travels away from the 

site of detonation, it rapidly loses both pressure and 

velocity.18,21 The duration and magnitude of the blast 

wave’s peak depend on a host of factors, including 

Low-Order Explosives High-Order Explosives

• Dynamite

• Gunpowder

• Ammonium nitrate

• Nitroglycerin

• 2,4,6-trinitrotoluene (TNT)

• Pentaerythritol tetranitrate (PETN)

• Cyclotrimethylene trinitramine (RDX)

• Cyclotetramethylene tetranitramine (HMX)

• Nitrocellulose

Table 1. Examples of low- and high-order explosives.

Figure 2. As a blast wave travels away from the site of detonation, it 

rapidly loses both pressure and velocity. Combat blast injuries patterns 

often depend on the proximity of the individual to the site of detonation. 

Image courtesy of the Borden Institute, Office of The Surgeon General, 

Washington, DC.

Distance From Epicenter

Probability

Of

Injury

Ballistic

0

1.0

Blast

Thermal
46 | Weapons Effects

the type of explosive used and the conducting 

medium. 

The blast wave propels fragments with enormous 

force, generates environmental debris, and often 

causes intense thermal radiation. Its effects vary 

with distance from the detonation site (Figs. 2 

and 3). High-order explosives are often used in 

military ordnance and their characteristic brisance 

can crush soft-tissue and bone and propel debris 

at ballistic speeds (fragmentation). Unlike loworder explosives, high-order explosives create 

blast overpressure injuries (barotrauma). As the 

blast wave passes, a temporary relative vacuum 

is created as gases continue to expand from their 

point of origin, and a transient blast wind may 

travel immediately behind the blast front. In the 

vicinity adjacent to an explosion, this force can 

cause traumatic amputation, evisceration, or total 

disintegration of a body. The blast wind may also 

cause injury by accelerating the speed of debris and fragments that subsequently strike the victim, or by 

displacing the victim against a stationary object.19 These types of injuries are discussed in detail below.

Low-order explosives have secondary, tertiary, quaternary, and sometimes quinary effects. Importantly, 

they do not have the primary blast effects characteristic of high-order explosives. High-order explosives 

can create significant overpressure injuries, especially at close range.

Devices

Explosive devices, including artillery, mortars, rockets, grenades, and RPGs are responsible for more than 

3,600 deaths and almost 31,000 injuries of US troops in the current conflicts in Afghanistan and Iraq.12

Explosive devices are the weapon of choice of terrorists and insurgents, and are becoming ubiquitous in 

combat theaters and civilian venues alike. The major categories of explosives are landmines and unexploded 

ordnance, RPGs, and, most commonly, IEDs. 

Antipersonnel Landmines and Unexploded Ordnances 

Landmines and unexploded ordnances (UXOs) are often discussed together because it can sometimes be 

difficult to separate the injuries clinically. Landmines are a form of ordnance that are placed on or under 

ground and explode when triggered, generally by electromagnetic waves or direct pressure (e.g., being 

stepped upon).22 Unexploded ordnances include bombs, grenades, missiles, rockets, and mortar and artillery 

shells that were fired or dropped and did not explode.23

Injuries from landmines and UXOs are a risk for civilian and military personnel alike and are a worldwide 

problem. Landmines and UXOs are common in both Iraq and Afghanistan. Because it has been involved 

in intense conflict for decades, Iraq is considered one of the most heavily landmine and UXO-contaminated 

Figure 3. Idealized blast overpressure waveform. An explosion creates 

a nearly instantaneous expansion of gas that compresses the surrounding 

medium (air or water) generating a blast wave. As it travels away from 

the site of detonation, the blast wave rapidly loses its pressure and velocity 

with distance and time. PRESSURE

Peak overpressure

Positive phase

 overpressure duration

Atmospheric pressure

TIME
Weapons Effects | 47

countries in the world. Landmines and UXOs are particularly prevalent in the north along Iraq’s border 

with Iran and in the central and southern regions as well.24 In Afghanistan, the International Committee of 

the Red Cross reports that there are 10 million landmines and more than 50 different types of landmines, 

and that the most heavily mined areas are along the border with Pakistan and around the cities of Kabul 

and Kandahar.25 There are sections of Bagram Air Base, Afghanistan that are still not clear of landmines 

and are cordoned off to prevent troops from accidentally entering that area. Many of the landmine and 

UXO victims treated at US military medical facilities are civilians. 

A recent report from the US Centers for Disease Control and Prevention (CDC) compiled data from several 

sources to evaluate landmine and UXO injuries in Afghanistan over a six-year period.26 Major findings 

included the following: (1) almost all of the injuries were sustained by men; (2) more than half of the injured 

were under the age of 18 (one-third were between the ages of 10 and 14); (3) children were twice as likely to 

be injured by UXOs as adults, although the case-fatality rate (7 percent) was the same for both; and (4) adult 

males were more likely to be injured by landmines as they traveled for work or military activity, whereas 

children were more likely to be injured while playing with a newly found object that turned out to be an 

UXO.27 These trends were confirmed in later studies.23

Landmines and UXOs cause injury through the blast effects described below (i.e., primary blast effect, 

secondary fragments, tertiary [whole-body propulsion], and quaternary [burns]).28 The three main types 

of conventional antipersonnel landmines are blast or static, bounding fragmentation, and directional 

fragmentation; each has an associated pattern of injury (Table 2).

Blast (Static) Landmines 

Static landmines are small mines planted and designed to activate when a person steps on them (Fig. 4). 

Many of these devices are designed to injure but not kill an individual.30 However many are lethal, either due 

to the immediate injury or to subsequent uncontrolled hemorrhage. There are classically two patterns of 

Type of Mine How Concealed How Detonated Primary Areas of 

Wounding

Blast or static Buried just below 

ground surface

Pressure (e.g., being 

stepped upon)

Foot, upper leg, lower 

leg

Fragmentation

• Bounding

• Directional

Buried just below 

surface with fuse 

protruding, or laid on 

surface

Laid on surface

Fuse or tripwire 

Electrical charge, 

timed fuse, or tripwire

All

All

Table 2. Categories of Antipersonnel Landmines. Adapted from Bellamy, 199110 and the International Committee of the Red Cross.29
48 | Weapons Effects

injury: (1) complete or near-complete amputation of the foot (Fig. 5); and (2) random penetrating fragment 

injuries along the tissue and fascial planes of the lower leg (Fig. 6).31 When these types of mines explode, 

particles of the dirt in which they were buried, debris, clothing, bone, and mine fragments can be driven by 

the blast up the leg into the upper or mid-calf causing gross contamination.10,15

Fragmentation Landmines 

The two types of fragmentation landmines are bounding and directional fragmentation landmines (Fig. 7). 

The bounding type of antipersonnel mine is so named because it bounds upward and then explodes midair at approximately torso level. Upon detonation, this type of mine propels hundreds of fragments in all 

directions (as far as hundreds of meters), inflicts injuries higher in the body (e.g., torso, upper extremities, 

neck, or head) compared to static mines, and has the highest mortality of any landmine type.15 Perhaps the 

Figure 4. (Right) Example of static landmine. Image courtesy of the 

United Nations Mine Action Service.

Figure 5. (Below) Static landmines detonate when stepped on, resulting 

in partial or complete lower limb amputation, most commonly at the 

midfoot or distal tibia. Debris may be driven up along fascial planes with 

tissue stripped from the bone. Image courtesy of the Borden Institute, Office 

of The Surgeon General, Washington, DC. Illustrator: Bruce Maston.
Weapons Effects | 49

best-known type of bounding mine is the M16A2 or “Bouncing 

Betty,” which was developed in the 1930s and widely used 

during World War II.10,32

Directional Fragmentation Landmines 

Upon detonation, directional fragmentation landmines project 

fragments in a single direction to cause multiple wounds both 

high and low on the body.15 A commonly used directional 

fragmentation mine is the Claymore mine, which is placed 

above-ground and can spray 700 circular pellets over an arc 

Figure 6. (Above) A landmine blast leads to an umbrella effect in which the soft tissues, 

vessels, and nerves are stripped from the bone. This results in a more proximal injury 

than may be clinically apparent. Image courtesy of the Borden Institute, Office of The 

Surgeon General, Washington, DC.

Figure 7. (Right) When triggered, fragmentation mines project a lethal shower of 

metallic fragments in all directions. The bounding types are projected upwards, prior to 

exploding mid-air at approximately torso level. Image courtesy of the United Nations 

Mine Action Service.
50 | Weapons Effects

of 60 degrees (Fig. 8).15 Lethal injuries occur within 50 meters from the point of detonation, and nonlethal 

fragmentation injuries can occur as far as 300 meters away.10 

Rocket-Propelled Grenades 

Rocket-propelled grenades (RPGs) are muzzle-loaded, shoulder-fired weapons that are primarily used 

against armored vehicles and ground personnel (Fig. 9). The various types of RPGs can fire fragmentation 

and high-explosive (e.g., high-explosive antitank [HEAT]) rounds and have a lethal blast radius of four 

meters.33 Ground troops are sometimes injured when anti-vehicle rounds are aimed at adjacent structures, 

resulting in structural collapse and generation of multiple fragments. Because they are inexpensive and easy 

to transport and operate, RPGs are the weapon of choice for insurgents in many former Soviet-supported 

countries, including Iraq and Afghanistan. They can be found in almost 40 countries throughout the world.34

Although RPG effects vary case-by-case, they frequently cause devastating injuries.33

Improvised Explosive Devices 

Improvised explosive device (IED) attacks have become a mainstay in the current conflicts. IED attacks are most 

often used in insurgency and terrorist operations. They have been responsible for 40 to 60 percent of military 

casualties (wounded and killed) in Iraq between 2006 and mid-2009, and 50 to 75 percent in Afghanistan.35,36

The incidence of IED-related injuries will vary depending on the phase of military operations. The decline 

in IED-related casualties in Iraq has been partly attributed to the increase in mine-resistant ambush protected 

(MRAP) vehicles sent to Iraq.36 The sharp increase in IED-related casualties in Afghanistan has been attributed 

to “expanded military operations, a near-doubling of the number of troops since the beginning of the year 

and a Taliban offensive that has included a proliferation of roadside bombings.”37 Pentagon sources indicate 

that the number of IEDs in Afghanistan has increased 350 percent since 2007, with a subsequent increase 

in the number of IED-related combat injuries and deaths of more than 700 and 400 percent, respectively.38

IEDs are defined as devices that are placed or fabricated in an improvised manner incorporating destructive, 

lethal, noxious, pyrotechnic, or incendiary chemicals and are designed to destroy, incapacitate, harass, or 

distract (Fig. 10).39 They may incorporate military weapons, such as artillery shells or antitank mines, but 

Figure 8. Directional fragmentation landmines project fragments in a 

single direction to cause multiple wounds, both high and low on the body. 

Image courtesy of the United Nations Mine Action Service.

Figure 9. A rocket-propelled grenade (RPG). The high-explosive 

warhead is affixed to a rocket motor and stabilized in flight by fins. Image 

courtesy of the United Nations Mine Action Service.
Weapons Effects | 51

are usually devised from non-military components. 

IEDs vary in size, shape, form, and explosive power. 

They are easy to make and use, can be housed in 

almost any type of container, and can be hidden 

almost anywhere. The various types of IEDs use 

a range of explosive materials and are concealed, 

deployed, and detonated in different ways: 

 Casings, ranging in size from a cigarette 

pack to a large vehicle, are used to hide the 

IED and possibly provide fragmentation. 

Small or large packages, including 120-mm 

and larger artillery or mortar projectiles with 

armor-piercing capability, are often placed 

in potholes covered with dirt, behind cinder 

blocks or sand piles to direct the blast, hidden in garbage bags or animal carcasses, or 

thrown in front of vehicles. 

 Common hardware such as ball bearings, 

bolts, nuts, or nails can be used to enhance 

the fragmentation. Propane tanks, fuel cans, 

and battery acid have been added to IEDs to 

increase their blast and thermal effects. The 

damaging effects of IEDs can be maximized 

via coupling (linking one munition to another), boosting (stacking one munition upon 

another), and daisy-chaining (many munitions physically and temporally linked together length-wise).

 Triggers can be command-detonated by a remote device such as a cell phone, car alarm, toy car 

remote, or garage door opener, or with a time-delay device to allow the bomber to escape or to 

target military forces operating in a pattern. The initiator almost always includes a blasting cap and 

batteries as a power source for the detonator. 

 Person-borne or victim-actuated devices (suicide bombs), typically using a powerful explosive with 

enhanced fragmentary effects, are employed to kill or maim as many people as possible. These are 

concealed in clothing worn by the assailant and hand-detonated.

 Vehicle-borne devices can vary in size from 100 to 1,000 pounds, depending on the size of the vehicle. The explosive charge can include mortar and artillery rounds, rocket mortars, warheads, and 

PE4 explosives. These can be concealed in vehicles of all types (cars, trucks, donkey carts). They can 

be deployed singly or in multiple vehicles. A lead vehicle is used to slow traffic and is followed by the 

main explosive device to maximize casualties. Detonation is by a command firing system.

 IEDs can be engineered to overcome IED detection measures through rolling (i.e., a target vehicle 

rolls over an initial unfused munition and then triggers a second trailing munition, which in turn 

detonates the initial munition). This sequencing positions the second (and most damaging) explosion 

directly under the target vehicle.

Figure 10. IEDs are defined as devices that are placed or fabricated in an 

improvised manner incorporating destructive, lethal, noxious, pyrotechnic, 

or incendiary chemicals and are designed to destroy, incapacitate, harass, 

or distract. Image courtesy of the United Nations Mine Action Service. 
52 | Weapons Effects

Improvised explosive device (IED) attacks have become a mainstay in OEF and OIF. They have been 

responsible for 40 to 60 percent of military casualties (wounded and killed) in Iraq between 2006 and 

mid-2009, and 50 to 75 percent in Afghanistan.

Antitank Munitions 

In Iraq, there has been a trend away from small bombs (e.g., concealed in containers such as soft drink cans) 

to large rocket propellant or shaped-charges with armor-piercing capability.40 Heavily armored vehicles are 

less susceptible to smaller, home-made roadside IEDs, and newer vehicle designs such as the MRAP provide 

enhanced protection to occupants from even larger IEDs. Antitank munitions are categorized as: (1) shapedcharges; (2) kinetic energy rounds; and (3) antitank landmines.15

Shaped-Charge 

Shaped-charges have various degrees of armor-piercing capability (Fig. 11). High-explosive antitank (HEAT) 

rounds are composed of explosive charges packed around a reverse cone (this is the concept behind the 

anti-armor warhead of an RPG) (Fig. 12). If the charge is able to defeat the armor of the vehicle, injury 

to the occupants occurs via two methods. The initial potentially catastrophic injuries (including burns) are 

caused by the jet of the shaped-charge after it penetrates the vehicle’s armor. Next, as the weapon strikes 

the armor, small pieces of irregularly shaped debris (spall) break away from the interior of the vehicle and 

are propelled into the occupants. 

A commonly used shaped-charge variant is the explosively formed projectile (EFP) (Figs. 13 and 14). This 

IED variant consists of a cylindrical casing, such as a metal pipe. The side facing the target is closed with a 

concave-shaped metal plate facing inward, and the explosive charge is placed behind the metal plate.41 On 

detonation, the concave plate is propelled out of the casing, becoming a high-speed aerodynamic penetrator 

(velocity can exceed 1,500 m/sec). This bullet or rod-shaped projectile easily pierces vehicle armor, causing 

catastrophic damage to vehicle occupants and other personnel in its path.42

Figure 11. Shaped-charge round: (Left) Disruptive mechanisms of the shaped-charge warhead include the jet of the charge itself and the debris knocked 

off from the inside face of the armored plate. (Right) Diagram taken from photograph of an actual detonation of a shaped-charged warhead against the 

armor plate caused by antitank land mines. 

Image courtesy of the Borden Institute, Office of The Surgeon General, Washington, DC. 

Illustrator: Bruce Maston.

Spall Material

Jet

Explosive Melt Sheet Target Material

Fuse

Nose Cone

Armor

Exploding Charge

Gas and Fragments of

Melt Sheet
Weapons Effects | 53

The increased use and effects of EFPs are illustrated in a review of IED injuries seen in a British field 

hospital in 2006.42 All casualties had injuries from roadside bombs directed at Coalition vehicles. Almost 

all (91 percent) of the explosions were caused by an EFP, and EFPs were responsible for all deaths. Main 

findings included the following:

 Most casualties (87 percent in survivors and nonsurvivors) had extremity injuries

 Most casualties had injuries to several regions of the body (e.g., 2.6 mean areas injured in survivors 

and 4.7 in nonsurvivors)

 All casualties had open wounds

 More than half of casualties (53 percent) had fractures

 There was little primary blast injury; only two casualties were thought to have died directly from a 

primary blast mechanism (blast lung)

 Only 15 percent of casualties had burns; no burns covered more than five percent total body surface 

area (TBSA)

 Approximately half of the survivors required immediate operative intervention at the field hospital

Figure 12. Cross-section image of 

a high-explosive antitank (HEAT) 

round. Note the reverse cone of 

metal liner in the mid-section and 

the exploding charge at the base 

of the round. Image courtesy of 

Wikimedia Commons.

Figure 13. (Left) An explosively formed projectile is an IED variant consisting of a cylindrical casing, closed with a concave-shaped metal plate facing 

inward, and an internal explosive charge. On detonation, the concave plate is propelled out of the casing and can inflict catastrophic injury. Image courtesy 

of Defense-Update.com.

Figure 14. (Right) X-ray of explosively formed projectile (EFP) detonation. Image courtesy of Applied Research Associates, Inc.
54 | Weapons Effects

Explosively formed projectiles (EFPs) generate “all or nothing” wounding patterns whereby casualties 

experience either catastrophic injuries or relatively minor wounds.42 Significant EFP attacks cause multiple 

injuries in each survivor, including a high incidence of open wounds, extremity injuries, and fractures. 

Kinetic Energy Rounds

Kinetic energy rounds are shaped like darts and are made from hard metals such as depleted uranium. Like 

shaped-charges, these weapons inflict damage by direct penetration of the vehicle or by generating spall. 

Warfighters with wounds caused by depleted uranium fragments should undergo standard wound care. 

Although there is a potential long-term risk from chronic exposure to depleted uranium, it does not justify 

extensive procedures to remove the fragments.43 

Antitank Landmines

Antitank landmines are being modified and used as buried IEDs in OEF and OIF. Often, as described 

previously, more than one mine will be linked together to enhance the level of destruction.14

Explosion-Related Injury

Patterns

Explosive devices produce the ultimate polytrauma (i.e., a wide range of injury types to many body regions 

caused by the full range of injury mechanisms).44 Explosions produce patterns of injury that are distinct 

from those of other mechanisms.45 The simultaneous combination of different injury mechanisms (below) 

produces a complex array of injuries that must be understood to produce the best patient outcomes. In 

comparison with trauma patients whose injuries were not caused by explosions, bombing victims have lower 

states of consciousness as well as increased hypotension, injury severity, presence of multiple injuries, need 

for surgery, use of critical care services, length of hospital stay (LOS), and mortality.45

Explosive devices produce a complex array of injuries that must be understood to produce the best patient 

outcomes.

Military Casualties

A report that examined victims of close-proximity IED blasts of a variety of types (antipersonnel and 

antitank, including 105 to 120 mm mortars, 155 mm artillery-round IEDs, and a VS-1.6 antitank mine) 

revealed complex injuries in all cases and a 50 percent mortality rate despite the fact that all had been 

wearing Kevlar helmets, ballistic eye protection, and full body armor.46 Some were injured on foot patrol, and 

some were in vehicles. The aforementioned report demonstrates the complexity of IED-related injuries.42

The types of injuries produced by antitank weapons are shown in Figure 15 and include: 

A. Translational blast injury (tertiary blast injury) can occur as the vehicle and its occupants are suddenly 

propelled upward causing blunt injury to occupants. 

B. Toxic gases (a form of quaternary blast injury) can cause significant inhalation injury. 

C. Primary blast injury can cause injury to the ears, lung, bowel, brain, and other organs. 

D. Ballistic injury from the weapon and resultant debris fragments as the vehicle armor is defeated also 

occurs (secondary blast injury), as do thermal injuries resulting from flammable materials within the 

vehicle (quaternary blast injury). 
Weapons Effects | 55

Civilian Casualties

Following an explosion in the civilian sector (e.g., open market bombing), most patients with lethal injuries 

will die immediately. Although the majority of survivors do not have life-threatening injuries, approximately 

10 to 15 percent of casualties will have critical injuries and may be saved with appropriate management.47,48,49

Morbidity and mortality are generally dictated by the size of the explosive charge, whether the explosion 

occurs within a confined space, and whether it causes structural collapse.50 Patterns of injury unique to blast 

include the following:51

 Most injuries are noncritical soft-tissue or skeletal injuries

 Head injury predominates as a cause of death (50 to 70 percent)

 The incidence of head injuries is disproportionate to exposed total body surface area (TBSA) 

 Most blast lung injury kills immediately

Figure 15. Injuries sustained as a result of defeated armor: (A) translational blast injury, (B) toxic gases, (C) blast overpressure, 

and (D) penetrating missile wounds. 

Adapted image courtesy of the Borden Institute, Office of The Surgeon General, Washington, DC. 

Illustrator: Bruce Maston.

A B

Translational blast injury Blast overpressure

B Toxic gases Missiles

A

D

C

C

C

D
56 | Weapons Effects

In Israeli reviews, victims of terrorist bomb attacks, when compared to victims of non-terrorist trauma, 

have been shown to: (1) sustain more severe injuries, as measured by Injury Severity Score (ISS) (ISS greater 

than 16 in 74 percent versus 10 percent) and median intensive care unit (ICU) LOS (5 days versus 3 days);52

(2) commonly have a combination of blunt and penetrating injuries (85 percent versus 15 percent)53 and 

injuries to several areas of the body (three or more body regions injured in 28 percent versus 6 percent 

patients);52 and (3) have injuries that are more likely to be fatal (mortality 6 percent versus 2 to 3 percent).52,53

As demonstrated repeatedly among civilian populations that have been dealing with terrorism for years, 

terrorist bomb attacks produce injuries that are more complex, more severe, more lethal, and occur in a 

greater number of body regions than non-bomb-associated injuries.45,54

In civilian sector explosions, most patients with lethal injuries die immediately. Although the majority of 

survivors do not have life-threatening injuries, some 10 to15 percent of casualties with critical injuries may 

be saved with appropriate treatment.

Potentiators

A variety of strategies are used to increase the wounding and killing potential of explosives. These include: (1) 

increasing the size of the charge and amount of explosive; (2) increasing the number and type of secondary 

fragments (e.g., packing the devices with metal objects or pieces of concrete); (3) adding harmful substances 

such as chemicals, animal feces, or bacterial contaminants to produce infection; (4) planting explosives 

under vehicles to generate secondary fragments; and (5) adding incendiary substances such as petroleum 

products. Secondary explosions are often initiated by fuel-air explosives that disperse and ignite a spray of 

aerosol fuel, or by cluster bombs that distribute bomblets over a wide area.

The damage of the initial explosion is compounded by deploying snipers, subsequent bombs, or a remotelydetonated explosion to damage rescuers and first responders and vastly enhance the chaos. These tactics were used 

in Northern Ireland and are common in Iraq and Israel. Precise timing and location are also used to maximize the 

numbers of injured and dead.47 Responders at the scene must be aware of these tactics and their effects, especially 

as recent data show increased coordination of terrorist attacks, including secondary attacks on first responders 

at the scene of an explosion, and increased variability in IEDs, including the introduction of chemical IEDs.55

Perhaps one of the most effective potentiators is the planting of explosives in confined spaces. Explosions 

that take place in confined spaces (e.g., buses and buildings) have patterns of injury that differ from those in 

open spaces (e.g., markets). Confined-space (closed-space) explosions generally produce more primary blast 

injury (discussed below) and penetrating injuries than explosions in open areas (open-space). The pressure 

Open-Space Closed-Space

Deaths 8 percent 49 percent

Injuries

• Primary blast injury 34 percent 77 percent

• Burns, TBSA 18 percent 31 percent

• Injury severity: median

Injury Severity Score (ISS)

4 (minor) 18 (moderate/severe)

Table 5. Comparison of open- and closed-space bombing deaths and injuries. Adapted from Leibovici, 1996.58
Weapons Effects | 57

wave associated with high-order explosive detonation reflects off doors, ceilings, and walls in confined 

spaces, lasts longer, and comprises what is termed a “quasi-static” exposure to overpressure effects.56

In OEF and OIF, most explosions are open-space bombings, and most injuries and deaths are from 

explosive fragments (secondary blast injury).

Israeli studies show significantly increased morbidity and mortality among those in confined-space bombings 

compared to those in open-space attacks.57,58,59,60 In a 1996 study, an 8 percent mortality rate was observed 

among open-air (open-space) bombings versus 49 percent in bus bombings (Table 5).58 An earlier study 

showed high percentages of primary blast injuries in bus bombings. In this study, 76 percent of victims had 

tympanic membrane perforation, 38 percent had blast lung, and 14 percent had abdominal blast injury.57 

Blast Injury Effects Mechanism of Injury

Primary Injury caused by the effect of the blast wave on the body. Primary blast 

injury occurs principally in the gas-filled organs and results from extreme 

pressure differentials developed at body surfaces. Organs most susceptible 

include the middle ear, lung, brain, and bowel.

Secondary Injury caused by flying debris and fragments, propelled mostly by the blast 

winds generated by an explosion. Most commonly produces penetrating 

injury to the body. At very close distance to the explosion, debris and 

fragments may cause limb amputation or total body disruption. This is the 

most common mechanism of injury from blast.

Tertiary Injury results from victim being propelled through space by the blast wind 

and impacting a stationary object.

Quaternary Injury suffered as a result of other effects of bomb blasts, including crush 

injury from a collapsed structure, inhalation of toxic gases and debris, 

thermal burns, and exacerbation of prior medical illnesses.

Quinary Injury resulting from contamination via biological and chemical agents, 

radioactive materials, or contaminated tissue from attacker or other person 

at the scene.

Table 6. Categories of blast injury effects with corresponding mechanisms of injury.

When the confined space is a building, the force of the blast may break windows, producing thousands of 

glass shards, and buckle the walls, floor, and ceiling, resulting in partial or complete building collapse and 

subsequent crush injuries.61 Studies contrasting open-space bombings with bombings involving buildings 

(closed-space) show a much higher mortality rate in the latter. For example, all deaths and almost all (96 

percent) injuries in the 1996 Khobar Towers bombing in Saudi Arabia occurred inside the buildings; and 

in the 1995 Oklahoma City bombing, 87 percent of those in the collapsed section of the Murrah Building 

died, compared with 5 percent of those in the uncollapsed section.48,62 

In OEF and OIF, most explosions are open-space bombings and most injuries and deaths are from 

fragments.44,63
58 | Weapons Effects

Categories

Blast injuries are categorized as having primary, secondary, tertiary, quaternary, and quinary effects, each 

with its own mechanism of injury (Table 6). 

Primary Blast Injury

Primary blast injuries result when the pressure wave interacts with the body, especially the gas-containing 

organs, via spalling, implosion, acceleration-deceleration, or initiation of pressure differentials.31

 “Spalling, or spallation, occurs when particles from a more dense substance are thrown into a less 

dense substance at their interface.”31 Spall is a flake or small particles that are broken off a larger 

solid body and can be produced by a variety of mechanisms, including projectile impact (Fig. 16). 

 Implosion is the momentary contraction of gas pockets that occurs when the blast wave moves 

through the tissue. The pressure differential may force blood and fluid into the previously air-filled 

spaces, as seen with pulmonary contusion and hemorrhage in blast lung injury.31

 Acceleration-deceleration, or shear injury, occurs when movement of the body wall in the direction 

of the blast wave displaces the internal structures. Because the structures accelerate at different rates, 

shearing or disruption may occur. 

 The pressure differential between the inside and outside of the body induced by the blast wave 

produces injuries.31

Figure 16. Spall is debris generated when particles from a more dense substance are thrown into a less dense substance at their interface. In this illustration, 

the ball impacts a metallic plate and knocks off material from the inside surface into the air. Adapted image courtesy of Wikimedia Commons.

 

Survival after a primary blast injury is dependent on the energy of the blast, whether it occurred in an 

open or enclosed (closed) space, and the distance of the individual from the point of detonation (standoff 

distance).20 The main sites of primary blast injury are the ears, lungs, intestinal tract, and brain.64,65

Ears 

A powerful blast wave can overwhelm the extremely delicate structures within the ear, causing tympanic 

membrane rupture, fracture or dislocation of the ossicles, and permanent inner ear damage. Rupture of the 

tympanic membrane is a common injury following an explosive blast.66 Further, the tympanic membranes 

are the structures that are injured at the lowest pressure, and thus have been used as a sentinel for other, more 

serious injuries.64 Recent reports have disputed the reliability of tympanic membrane rupture as a sensitive 

screening tool for primary blast injury detection.21,66 The absence of tympanic membrane rupture does not 
Weapons Effects | 59

exclude other types of blast injury. An increase in pressure of as little as five pounds per square inch (psi) 

may cause eardrum rupture, 15 psi carries a 50 percent chance, and 30 to 40 psi will almost certainly rupture 

the eardrum.67 Recent data from OEF and OIF with explosion-related injuries indicated an approximate 15 

to 16 percent incidence of tympanic membrane rupture.21,66 The most common symptoms reported by the 

patients experiencing an audiovestibular injury are hearing loss (60 percent), tinnitus (49 percent), otalgia 

(26 percent), and dizziness (15 percent).68,69

Rupture of the tympanic membrane is a common injury following an explosive blast. Its absence may not 

be adequate to rule out primary blast injury and does not exclude other types of blast injury.

During the secondary survey in the initial evaluation of a blast victim, the tympanic membranes should be 

evaluated. Improvised explosive device detonations typically propel debris into the external auditory canal. 

The debris should be carefully removed to allow full visualization of the ear canal. The external auditory 

canal should not be blindly irrigated because this can result in pain and vertigo in patients with perforated 

tympanic membranes.70 If debris is noted in the external auditory canal or behind the ruptured tympanic 

membrane, topical antibiotic eardrops, such as a fluoroquinolone, are recommended to prevent infection.64,70

The presence of cerebrospinal fluid or blood in the external auditory canal or hemotympanum is suggestive 

of a basilar skull fracture.

Most (80 to 90 percent) tympanic membrane perforations heal spontaneously. The larger the perforation, 

however, the lower the probability that it will heal spontaneously.21 Perforations involving more than 30 

percent of the surface area of the tympanic membrane are significantly less likely to heal spontaneously 

than smaller perforations (Fig. 17).70 Spontaneous healing also varies with the location of the rupture. 

Central tympanic membrane ruptures have the least likelihood of healing spontaneously, whereas inferior 

perforations are the most likely.21 

Figure 17. Tympanic membrane perforation. Image courtesy of Gene 

Liu, MD, Cedars-Sinai Medical Center.

Figure 18. Blast effect can cause inner ear injuries, such as the 

perilymphatic fistula shown here, and ruptures of the saccule, utricle, 

and basilar membrane. In the middle ear, the ossicles may fracture or 

disarticulate, independent of a tympanic membrane perforation. Image 

courtesy of Timothy Hain, MD, Northwestern University.
60 | Weapons Effects

Besides rupturing the tympanic membrane, the blast can also cause middle ear damage, such as fracture 

of the ossicles or disarticulation of the ossicular chain.68 Although these usually occur in conjunction 

with tympanic membrane perforation, they can occur independently. Injury to the inner ear, such as 

perilymphatic fistulae in the oval window and ruptures of the saccule, utricle, and basilar membrane, may 

also occur (Fig. 18). Sensorineural hearing loss may be seen with loss of hair cell integrity. Similarly, damage 

to the vestibular apparatus may occur and manifest as vertigo.19

Consultation with the otolaryngology service should be performed when greater than 50 percent tympanic 

membrane perforation occurs or if other audiovestibular symptoms are noted. All blast injury patients 

requiring inpatient care should have audiometric testing when possible.21,71 The management guidelines 

used at Balad Air Base in Iraq are presented in Table 7. Hearing protection has been shown to significantly 

reduce the incidence of tympanic membrane rupture, and its use should be encouraged in combatants who 

are deployed in high-risk environments.72

Lungs

The lungs are also vulnerable to primary blast effects. Explosions can cause a variety of thoracic injuries 

including pulmonary contusion, pneumothorax, pneumomediastinum, air emboli, hemothorax, and 

subcutaneous emphysema (Fig. 19).64 An external force acting on the chest wall may compress the lungs 

slowly enough to allow air contained in the alveoli to be expelled through the trachea. However, when a 

significant blast wave impacts the chest wall, there is little time for pressure equilibration. The pressure 

Consultation

Indications

Absolute Relative

Otolaryngology Vertigo lasting greater than three days Tympanic membrane rupture greater 

than 50 percent

Presence of clear otorrhea Debris in the external auditory canal 

that does not resolve with topical 

antibiotics

Discolored otorrhea that persists 

despite seven days of topical antibiotic 

therapy

Inability to visualize the tympanic 

membrane despite removal of debris 

from the external auditory canal

Audiology An average hearing threshold greater 

than 30dB at frequencies of 500, 

1000, and 2000Hz

Significant communication problems

A hearing threshold greater than 

35dB at frequencies of 500, 1000, or 

2000Hz

Tinnitus significantly affecting quality 

of life

A hearing threshold greater than 55dB 

at frequencies of 3000 or 4000Hz

New-onset asymmetrical hearing loss

Table 7. Management guidelines for otolaryngology and audiology consultations used at Balad Air Base, Iraq. Adapted from Depenbrock, 2008.70
Weapons Effects | 61

differentials that develop at the interface between media of different densities tear the alveolar walls, disrupt 

the alveolar–capillary interface, and cause the emphysematous spaces to fill with blood,resulting in primary 

blast injury to the lung (blast lung).19 Pressures of 30 to 40 psi are associated with possible lung injury, and 

at 80 psi, a 50 percent chance of lung injury exists.67 As a point of reference, pressures in the 100 to 200 psi 

range may be lethal, and when psi exceeds 200 to 250, death is almost certain.67 

Lungs are vulnerable to primary blast effects. Explosions can cause a variety of intrathoracic injuries 

including pulmonary contusion, pneumothorax, pneumomediastinum, air emboli, hemothorax, and 

subcutaneous emphysema.

Pulmonary manifestations vary greatly depending on the size of the blast wave. The mildest form of this 

tissue disruption was noted to be pleural and subpleural petechiae in animal studies.73,74 The classic chest 

radiograph demonstrates bilateral central infiltrates and has been described as a butterfly or batwing pattern 

(Fig. 20). This pattern is probably caused by reflection of the blast wave off of the mediastinal structures 

within the thoracic cavity. Additionally, the central location of the infiltrates helps differentiate this from the 

more classic lateral infiltrates seen with pulmonary contusion (Fig. 21).75

Figure 19. (Top Right) Chest radiograph demonstrating pneumothorax, 

hemothorax, and a penetrating fragment, following an IED explosion.

Figure 20. (Top Left) The classic chest radiograph seen with primary 

blast injury to the lung demonstrates a butterfly or batwing pattern.

Figure 21 (Bottom Left) Chest radiograph demonstrating a peripherally 

located pulmonary contusion resulting from blast injury. 
62 | Weapons Effects

The incidence of blast lung in OEF and OIF has been low because open-space explosions predominate. When 

blast lung occurs in patients, it has high associated morbidity and its treatment is resource-intensive.76,77,78 

Primary blast injury to the lung may not be immediately obvious upon external examination.79 Symptoms 

of blast lung can manifest within the first few minutes following a blast or can develop and evolve over a 

period of hours to days.21,57,75,80,81 Blast lung has been shown to have the following characteristics:

 Symptoms include dyspnea, chest pain, hemoptysis, and cough19

 Clinical signs include cyanosis, tachypnea, rapid or shallow breathing, crackles, diminished breath 

sounds, dullness to percussion, increased resonance, retrosternal crunch, subcutaneous crepitus, and 

tracheal deviation19

 Hypoxemia and hypercarbia81

 Rapid respiratory deterioration with progressive hypoxia58

 Progressive need for ventilation with high FiO2

58

 Progressive haziness in serial chest radiographs58

 Hemodynamic instability58

 Pulmonary edema with frothing at the mouth, frequently lethal64

Enclosed-space (closed-space) bombings should raise the index of suspicion for blast lung and other primary 

blast injuries.53 Patients with blast lung require supportive care with special emphasis on ensuring adequate 

oxygenation and ventilation. Standard ventilator management with initial use of positive end-expiratory 

pressure of 10 centimeters (cm) water is acceptable.18 However, advanced ventilatory methods, such as 

independent lung ventilation, high-frequency jet ventilation, nitric oxide inhalation, and extracorporeal 

membrane oxygenation, may also be of value.47,80,82 Intravenous fluids should be administered judiciously 

to minimize capillary leak and pulmonary edema. Patients should be monitored closely for development 

of pneumothorax. The clinical efficacy of prophylactic antibiotics and steroids in blast lung injury is 

undetermined.64 Published blast lung injury severity categories, based on radiographic appearance, oxygen 

requirement, and the presence of bronchopleural fistula, may be helpful in determining which patients 

Indications & Requirements Blast Lung Injury Categories

Mild Moderate Severe

Indications

Radiographic infiltrates Unilateral Asymmetrical and 

bilateral

Diffuse

PaO2 to FiO2 Ratio (mm Hg) >200 60 to 200 <60

Bronchopleural fistula No Yes Yes

Requirements

Positive pressure ventiliation (PPV) 

requirement

Unlikely for 

respiratory problem

Highly likely but 

usually conventional 

methods

Universal and 

unconventional 

methods common

Positive end-expiratory pressure 

(PEEP) requirement (cm H2O)

<5 if PPV needed 5 to 10 usually 

needed

>10 commonly 

needed

Table 8. Severity categories for blast lung injury based upon radiographic appearance, oxygen requirement, and the presence of bronchopleural fistula.

Adapted from Pizov, 1999.80
Weapons Effects | 63

require positive pressure mechanical ventilation and positive end-expiratory pressure (Table 8).80 While 

ear protection has been shown to offer some protection of the tympanic membrane against primary blast 

injury, thoracic body armor may not have the same protective effect on the lungs.64,83

Solid and Hollow Organs 

A blast wave can cause rapid compression and expansion of air in gas-filled organs, which often results 

in contusions, perforations, or intramural hemorrhage. When air emboli fill the pulmonary and coronary 

vessels, early death often occurs.54 Delayed rupture of the intestinal tract can occur secondary to significant 

ischemia and infarction within the mesentery.64 While the gastrointestinal tract is particularly susceptible to 

primary blast injury, especially the colon, primary blast injury of hollow organs in OEF and OIF is rarely 

encountered.84,85,86,87

Solid organs, principally the liver, spleen, and kidney, have a relatively uniform liquid density. When a 

blast wave impacts these organs, little compression occurs, and significant injury to the tissue is less likely 

to occur.19,88 Solid intraabdominal organs are more likely to be injured through secondary or tertiary 

mechanisms. However, blast waves can cause shear forces to develop at points of attachments of organs or 

at the surfaces of the organs. In the former case, an organ may tear off of its point of attachment, while in 

the latter case, subcapsular petechiae, contusions, lacerations, or rupture may occur.19

Patients may present with a variety of abdominal signs and symptoms including pain, nausea, vomiting, 

hematemesis, melena, and signs of peritoneal irritation.21 Patients with overt hemodynamic instability should 

undergo immediate exploratory laparotomy for presumed active hemorrhage from the intestinal mesentery 

or a solid organ injury.89 More stable patients can be evaluated using computed tomography (CT) imaging. 

Ritenour noted that “CT evidence of blast injury includes pneumoperitoneum, free intraperitoneal fluid 

not consistent with blood, and a sentinel clot seen on bowel wall or mesentery.”21 Intestinal contusion, 

submucosal hematoma, and mesenteric hematoma can also be seen on CT imaging following blast injury.89

The gastrointestinal tract is particularly susceptible to primary blast injury, especially the colon. Significant 

ischemia and infarction within the mesentery following primary blast injury can lead to delayed rupture 

of the intestinal tract.

Brain 

The prevalence of traumatic brain injury (TBI) among combat casualties is higher in the current conflicts 

than in previous wars. This is primarily because many patients with previously lethal injuries are now 

surviving, largely due to enhanced helmets that prevent or reduce penetrating head trauma, advances in 

battlefield medicine, and rapid evacuation to a well-honed system of care.90 Thus, TBI has become the current 

signature injury of combat, much as shell shock was the signature injury of World War I.65,91 Traumatic brain 

injury potentially affects up to one-third of OEF and OIF combatants and approximately 320,000 reported 

experiencing symptoms that may be related to TBI during deployment.92 Of patients admitted to Walter 

Reed Army Medical Center (WRAMC) between 2003 and 2005 who had been exposed to explosive blasts, 

59 percent were found to have symptoms that may relate to TBI. Of these, 56 percent had moderate/severe 

TBI and 44 percent had mild TBI.93,94 In contrast, only 20 percent of civilian TBIs are moderate/severe.95

It is difficult to determine which explosion-related TBIs can be attributed to primary blast effects alone,

even in cases where no fragment injuries are present.96 In a recent study of 2003 to 2008 OIF casualties 

with head trauma, 48 percent had closed head injury that was attributed to primary and/or tertiary blast 
64 | Weapons Effects

injury mechanisms.97 Kinetic energy following blasts causes shearing in the central nervous system, resulting 

in both focal and diffuse axonal injury, air embolism, and cranial fractures with associated sinus cavity 

involvement.64,89,98 Cognitive and biochemical changes occur in animals exposed to blasts (oxidative stress in 

the hippocampus), and electroencephalographic changes, punctuate hemorrhages, and chromatolysis have 

been seen in the brains of human blast victims.21,88,99,100 The authors of the aforementioned studies could 

not reliably differentiate between injury mechanisms due to lack of specifics about the individual explosions 

and/or coexistence of blunt trauma mechanisms (e.g., vehicle incidents). The exact mechanism(s) of brain 

injury from blast overpressure remains unclear.44,101,102,103,104,105

Traumatic brain injury has become the current signature injury of combat. It is difficult to determine 

which explosion-related TBI-type symptoms can be attributed to primary blast alone, as opposed to 

other blunt trauma-related TBI. The exact mechanism(s) of brain injury from blast overpressure remains 

unclear. 

Patients can present with a variety of signs and symptoms ranging from a headache to coma. Clinical 

findings may include fatigue, headache, back or generalized pain, vertigo, paralysis (transient or persistent), 

and altered mental status.21,99 Psychological symptoms include excitability, irrationality, amnesia, apathy, 

lethargy, poor concentration, insomnia, psychomotor agitation, depression, or anxiety.21,104 

Cumulative and long-term effects of mild TBI on US troops are beginning to be a cause for concern. In one 

study, 44 percent of soldiers suffering mild TBI with loss of consciousness (LOC) met the criteria for posttraumatic stress disorder (PTSD) on evaluation three to four months after returning home.65 Twenty-seven 

percent of soldiers who were simply dazed after a blast subsequently reported PTSD symptoms. Many 

soldiers reported significant problems with their general health, poor work habits, and a variety of symptoms. 

A study by Hoge “concluded that PTSD and depression were mediators of the relationship between mild 

TBI and physical health problems.”65 The Defense and Veterans Brain Injury Center (DVBIC), the lead 

agency in investigating TBI in the military, publishes updated data on military TBI. Their recommendations 

have included pre-deployment neurocognitive testing and the use of the Brief TBI Screen (BTBIS) in the 

post-deployment process. 

Clinical Practice Guidelines (CPGs) published by the Joint Theater Trauma System (JTTS) provide 

algorithms for TBI evaluation at Level I (medic at point of wounding), Level II (Forward Surgical Team 

[FST]), and Level III (Combat Support Hospital [CSH]).106,107 For mild TBI (GCS score of 13 to 15), Level 

I and II facility careproviders should perform the standard physical examination and use the Military Acute 

Concussion Evaluation (MACE) for assessment (MACE form available through the Defense and Veterans 

Brain Injury Center). Level III facility evaluation is often more comprehensive and may involve further 

neurocognitive testing following MACE performance.108 Patients with a head injury and a GCS score of 

nine to 12 are classified as having moderate head injuries, and patients with GCS scores lower than nine are 

considered to have severe TBI. The lower the GCS score within this range, the higher the chance of death 

and the lower the chance that the patient will return to independent living (Fig. 22).

Blast effects to the brain can result in neurocognitive changes that may not manifest as obvious physical 

symptoms requiring treatment. Possible injury to the brain may be manifested in other ways, which can 

be assessed using the MACE scale. Individuals who have “seen stars” or are “just not themselves” may 
Weapons Effects | 65

have suffered a mild TBI. In an effort to decrease 

the possibility of exposure to sequential concussive 

brain injury, warfighters who have been exposed 

to explosive blasts should be tested using MACE. 

Scores lower than 25 warrant further evaluation 

and treatment. As a preventive measure, it is 

recommended that these individuals only return to 

light duty in an effort to decrease the possibility of a 

subsequent exposure to a blast or vehicle crash while 

their brains recover.106

Eyes

Although primary blast injury to the eye is rare 

because of the uniform density of the eye, it 

occasionally occurs in the form of globe rupture, 

retinitis, and hyphema.64 The most common sign of 

primary blast injury to the eye is subconjunctival hemorrhage.74 Injuries to the eye are more commonly 

caused by secondary blast fragments (e.g., splinters of glass and other debris), many of which are preventable 

with simple eye protection equipment. 

Extremities 

Primary blast injury resulting in amputation is rare and often part of a pattern of lethal injuries.109 As the 

blast wave impacts an extremity, tremendous pressure differentials may shatter the bone, and the nearsimultaneous blast wind may subsequently avulse the extremity. On the whole, avulsions are observed 

mainly along the shaft of long bones and are most common among dead or dying victims. In one study, 

traumatic amputations due to primary blast primarily occurred in the upper third of the tibia.110 These 

amputation injuries have a high risk for exsanguination, and the limbs are rarely reattachable.19

Secondary Blast Injury 

The overpressurization wave created by the primary blast is followed by a negative-pressure phase. This 

generates a blast wind that propels debris and objects with ballistic speed and force to create multiple 

penetrating injuries.31 Although they are termed secondary blast injuries, these are the predominant 

explosion-related injuries in survivors.63,111

The greatest diagnostic challenges for clinicians at all levels of care in the aftermath of explosions are the 

large numbers of casualties and multiple penetrating injuries.44

Primary and Secondary Fragments

Flying fragments and debris from the explosive and its surrounding environment are differentiated as 

primary and secondary fragments. In conventional military ordnance, primary fragments typically consist 

of bits of the exploding weapon. In IEDs, primary fragments include the shell casing as well as items packed 

into the explosive to increase wounding potential, such as nails, bolts, ball bearings, or other small, sharp 

items (Fig. 23). The effectiveness of this technique has been demonstrated. For example, following a suicide 

bomb attack in Israel, the bodies of all those who died immediately after the blast and all with severe injury 

(ISS greater than 16) were “saturated with steel spheres.”112

Figure 22. Prognosis for OEF/OIF combatants with severe TBI 

(GCS score less than 9). Data source: Joint Theater Trauma Registry 

(JTTR).

0%

10%

50%

20%

30%

40%

Percentage

GCS 3 to 5

Death

60%

70%

Return to Independent Living

GCS 6 to 8
66 | Weapons Effects

All explosives generate secondary fragments that 

consist of debris from manufactured (e.g., metal from 

vehicle interiors, shattered furniture, splinters of 

window glass) and natural environments (e.g., rocks, 

dirt).113 Dust and tiny grains of dirt can become 

embedded in the skin, causing a characteristic, 

dusky, tattooed effect.114 Among all fragment types, 

glass causes a disproportionate amount of secondary 

injury. Of the 95 percent of survivors of the 1996 

Khobar Towers bombing with fragment injuries, 

88 percent were injured by glass (primarily from 

windows).62

Fragment Physics

Fragment projectiles differ from bullet projectiles 

in that they are scattered (not channeled through a 

barrel), are irregularly shaped, and have different velocities upon impact.31 After detonation, aerodynamic 

drag is exerted on the fragments, which then strike the body as both high- and low-velocity projectiles.31

Initial velocities of primary fragments can be as high as 1800 m/sec, but under 600 m/sec appears to be the 

upper limit of survivability.15,115 Low-velocity fragments may tumble or shimmy, crush large areas of tissue, 

and fragment further to exacerbate the injuries.116,117,118 This is counter to the previously held notion that the 

higher the velocity of a missile, the more tissue damage there will be.15 In addition, fragments contaminate 

wounds with environmental debris. All of these factors likely account for the differences in fragment and 

bullet injuries, even though both are caused by small missiles propelled at great speeds.31

Fragment Wounds

The distinguishing feature of most explosion-related injuries is the presence of multiple penetrating fragment 

injuries to several regions of the body (Fig. 24).44,119Because fragment wounds can be so numerous (e.g., 30 

to 40 in a single patient), CCC providers can find it difficult to determine which wound(s) requires highpriority evaluation. The body region involved and associated clinical findings determine clinical impact and 

treatment priorities.119

Because of the protection offered by body armor, military personnel have a high incidence of fragment injuries 

to the head, extremities, and the junctions between the torso, arms, neck, and legs. These should be managed 

in the same way as other penetrating injuries. Meticulous wound inspection and debridement are important in 

the management of such injuries. Secondary blast injury also frequently results in facial and ocular injuries.21,64

The eyes are particularly vulnerable to secondary blast injuries largely caused by minute bits of shattered 

glass or metal. As many as 10 percent of all blast injury survivors have significant eye injuries from projectiles, 

with signs and symptoms that include pain, irritation, sensation of a foreign body, changes in visual acuity, 

swelling, and contusions.17 Most such eye injuries are preventable with appropriate eye protection. Among 

survivors of the September 11, 2001 attacks on the World Trade Center, 26 percent had ocular injuries.120

The distinguishing feature of most explosion-related injuries is the presence of multiple penetrating 

fragment injuries, or fragment wounds, to several regions of the body. Injuries and deaths from fragments 

occur much further from the point of detonation than do those associated with the primary blast.

Figure 23. A combat casualty undergoing removal of metallic shrapnel 

embedded in his right periorbital region following an IED blast. 
Weapons Effects | 67

Although prior literature advocated extensive debridement of fragment wound tracts, recent experience 

shows that this is no longer required. This is because: (1) high-velocity projectiles often do not cause 

temporary cavitation; (2) elastic soft-tissue generally heals without excision if the blood supply is intact; 

and (3) antibiotics play a larger role in mitigating infection.121 In cases involving multiple fragments, it is not 

recommended to attempt to extract every fragment, but instead to remove those that pose a threat to life 

or health. The potential damage that could be caused by removing a fragment or through extensive wound 

exploration or debridement must be weighed against the damage that might result from not removing it. For 

example, in casualties with low-velocity penetrating head injury, debridement was limited to minimize risk 

of causing additional neurologic injury, with no apparent adverse affects on outcome.122

Fragment Range

Risk of fragment injury occurs over a much wider radius than blast overpressure. Thus, in an open-space 

explosion, the primary mechanism of injury is fragment penetration.119 The safe standoff distance for 

fragments has been noted to exceed that for blast overpressure by a factor of 100. Injuries and deaths from 

fragments occur much further from the point of detonation than do those associated with the primary blast 

Figure 24. A casualty seen at Camp Taqaddum, Iraq in 2004, with fragmentation wounds from an IED blast. The distinguishing feature of most 

explosion-related injuries is the presence of multiple individual injuries in several regions of the body. Image courtesy of Harold Bohman, MD, CAPT, 

MC, US Navy.
68 | Weapons Effects

(Table 9).47,119 Following the 1998 terrorist bombing of the US Embassy in Nairobi, fragment injuries were 

sustained by people as far as two kilometers from the point of detonation.18 Secondary injury is largely 

penetrating, but victims can experience nonpenetrating injuries as well. For example, the low-velocity 

fragments responsible for all Khobar Towers bombing injuries caused penetrating, blunt, and crush injuries.62

A large proportion of blunt injuries, however, are caused by tertiary blast effects. 

In an open-space explosion, the primary mechanism of injury is fragment penetration. 

Injuries and deaths from fragments occur much further from the point of detonation than do those 

associated with the primary blast.119

Tertiary Blast Injury

Tertiary blast injuries are caused by propulsion and displacement of the blast victim, of large fragments, or 

of surrounding structures such as a building or vehicle. The subsequent impact of victims upon structures 

or structures upon victims causes blunt and penetrating injuries that include crush, impalement, and other 

injuries whose severities vary with the degree of fragmentation and structural collapse.64

Although most tertiary blast injuries comprise soft-tissue wounds or fractures that are not immediately 

life-threatening, complete structural collapse is rarely survivable.123 This was illustrated in the examples of 

the Khobar Towers and Oklahoma City bombings.16 Individuals inside vehicles sustaining an IED blast 

can also experience tertiary blast injuries as the vehicle is propelled upward against the occupants or as 

the occupants are projected within the vehicle. In blast injury tests on vehicles, the vast majority of the 

injuries were tertiary. For undercarriage blasts, lower limbs were crushed, and in roadside blasts, occupants 

sustained severe head and side-thoracic impacts. These results are not dissimilar from those observed in data 

from OEF/OIF.

Crush syndrome, or traumatic rhabdomyolysis, often follows structural collapse and entrapment causing 

crush injury. Severe muscle damage, prolonged ischemia, and cell death can result in release of myoglobin, 

urates, and potassium. Myoglobinuria produces dark amber urine that will test positive for hemoglobin on 

urine dipstick analysis. Significant rhabdomyolysis can cause hypovolemia, metabolic acidosis, hyperkalemia, 

hypocalcemia, and coagulopathy.124 Early and aggressive fluid resuscitation to ensure adequate renal 

perfusion and urinary output is vital in preventing renal failure.124,125

Crush syndrome, or traumatic rhabdomyolysis, often follows structural collapse and body entrapment.

Morbidity and mortality

Distance From Blast Primary Blast Injury Secondary Blast Injury

0 to 50 feet Death, eardrum rupture Death 

50 to 80 feet Eardrum rupture Death 

80 to 130 feet Temporary hearing threshold shift Injury 

130 to 1800 feet None Injury 

Table 9. Blast injury effects based on distance from open-space blast explosion (155-mm shell). 

Adapted from Champion, 2009.44
Weapons Effects | 69

Myoglobinuria produces dark amber urine that will test positive for hemoglobin on urine dipstick analysis. 

Significant rhabdomyolysis can cause the following:

 hypovolemia,

 metabolic acidosis,

 hyperkalemia,

 hypocalcemia, and

 coagulopathy.

Osmotic diuretics (mannitol) and intravenous sodium bicarbonate are commonly advocated as adjuncts 

to prevent renal failure.124 Alkalinization of the urine with intravenous sodium bicarbonate is thought to 

decrease intratubular precipitation of myoglobin in the kidneys.124 Mannitol has been suggested to minimize 

intratubular pigment deposition, act as a renal vasodilator, and act as a free-radical scavenger.124,126,127,128 It is 

worth noting that some authors feel that there is no clear clinical data showing benefit with either of these 

agents over simple fluid resuscitation.124,129 Compartment syndromes can also develop in association with a 

crush injury or over-resuscitation and are discussed in later chapters.

Alkalinization of the urine with intravenous sodium bicarbonate is thought to decrease intratubular 

precipitation of myoglobin in the kidneys. Mannitol has been suggested to

 minimize intratubular pigment deposition,

 act as a renal vasodilator, and

 act as a free-radical scavenger.

Quaternary Blast Injury

Quaternary blast injury encompasses blast sequelae that include, but are not limited to, burns, inhalation 

injury, and asphyxiation.119 Burns are a form of quaternary blast injury in OEF and OIF and more frequently 

occur when victims are trapped in a burning vehicle or building than because of the blast fireball (which 

lasts for milliseconds). Burns that immediately follow an explosion result from exposure to the intense heat 

of the blast and indicate close proximity to the point of detonation.123

An analysis of OEF and OIF casualties with significant burns treated at the US Army Institute of Surgical 

Research (USAISR) between 2003 and 2005 revealed increases in burn frequency, extent, and severity.130

Findings included:

 Burns caused by explosions increased from 18 percent to 69 percent

 Total body surface area burned increased from 15 percent (± 12 percent) to 21 percent (± 23 percent)

 Injury severity scores (ISS) increased from minor (8 ±11) to moderate/severe (17 ±18)130

Inhalation injury is especially prevalent with building collapse.

As illustrated in the 1993 World Trade Center bombing, 93 percent of victims suffered acute and chronic 

inhalation injuries

Burns were caused primarily by IEDs (55 percent), car bombs (16 percent), and RPGs (15 percent) and were 

largely sustained in unprotected areas of the body. The hands and face were the most frequently burned 

areas, and only one-third (36 percent) of burned patients resumed full military duty. The study also revealed 

an increase in the frequency of inhalation injury in the current conflicts from 5 percent to 26 percent.130
70 | Weapons Effects

Inhalation injury is especially prevalent with building collapse, as illustrated in the 1993 World Trade Center 

bombing, in which 93 percent of victims suffered acute and chronic inhalation injuries.113 

Burns are a form of quaternary blast injury and occur more frequently when victims are trapped in a 

burning vehicle or building, rather than due to a blast fireball.

Quinary Blast Injury

Quinary effects largely refer to contamination of tissues resulting from the release of chemical, biological 

agents, or radioactive materials upon detonation of an explosive device. A unique type of quinary injury 

encountered in OEF and OIF is that inflicted by human-remains-shrapnel, or pieces of bone from suicide 

bombers or other victims that cause penetrating injuries and increase the risk of transmission of bloodborne diseases such as hepatitis or human immunodeficiency virus (HIV).87,131,132,133

These agents are classified as

 nerve

 blister (vesicant), and

 choking agents. 

Indications of nerve agent exposure include a variety of autonomic and neuromuscular signs and 

symptoms, for example.

 pinpoint pupils,

 muscular twitching,

 unexplained nasal secretion,

 hypersalivation,

 tightness of the chest,

 shortness of breath,

 nausea,

 abdominal cramps,

 seizures,

 paralysis, and

 respiratory failure.

Chemical agents may be inhaled or absorbed through the skin, and can induce coughing, itching, skin, and 

eye inflammation.119 These agents are classified as nerve, blister (vesicant), and choking agents. Indications of 

nerve agent exposure include a variety of autonomic and neuromuscular signs and symptoms (e.g., pinpoint 

pupils, muscular twitching, unexplained nasal secretion, hypersalivation, tightness of the chest, shortness 

of breath, nausea, abdominal cramps, seizures, paralysis, and respiratory failure). Immediate intramuscular 

injection of atropine, combined if possible with pralidoxime chloride (2-PAM), is recommended.134 Blister 

agents cause a spectrum of injury to exposed surfaces (e.g., skin, eyes, and mucous membranes) and result 

in symptoms over varying timeframes (minutes to several hours). Immediate decontamination by removal 

of contaminated clothing and irrigation of exposed surfaces with large amounts of water is first-line therapy.134,135,136 Choking agents cause coughing, tightness in the chest, vomiting, headache, and lacrimation.134

Treatment consists of removing the patient from the offending agent and providing supportive care. All of 

these effects can exacerbate preexisting conditions.64 Exposure to radiation released in an explosion will 

result in a variety of effects that are largely determined by the size and type of explosion, which radioactive 

elements are involved, length of exposure, and other factors.137 While discussion of chemical and biological 
Weapons Effects | 71

Figure 25. (Above) Unexploded ordnance tenting 

the subcutaneous tissue of the right thigh, having 

traversed the pelvis in a left-to-right trajectory. The 

extruding tail of the rocket is demarcated by the 

arrow. Image courtesy of the Borden Institute, Office 

of The Surgeon General, Washington, DC. 

Figure 26. (Right) A radiograph of the UXO 

embedded in the pelvis and femur confirms the 

warhead is not attached to the rocket. Image courtesy 

of the Borden Institute, Office of The Surgeon 

General, Washington, DC. 
72 | Weapons Effects

agents and radiation threats is beyond the scope of this chapter, CCC providers should have a decontamination plan in place to avoid secondary contamination of their combat care facility and themselves.

Know your environment, and have a decontamination plan in place to avoid secondary contamination of 

yourself and your combat care facility.

Management Considerations

While damage-control practices will need to be applied to explosion-related injury management by CCC 

providers, the polytrauma that ensues in bomb explosions creates management challenges.79 Patients 

with concurrent brain and hemorrhaging solid organ injuries often need to undergo immediate damage 

control surgery prior to delineation of a brain injury via CT imaging.79 Advanced ventilatory strategies 

(e.g., permissive hypercapnia, high-frequency oscillatory ventilation) may often be required to manage 

lung overpressure injuries.79 The coagulopathy that often accompanies blast injury will need to be rapidly 

recognized and appropriately managed.79 Finally, the crystalloid and blood product requirements in patients 

with multiple injuries that include burns, head, and pulmonary injuries must be balanced against the risks 

(among others) of dilutional coagulopathy and compartment syndromes.45,138

Embedded Unexploded Ordnance

The management of intracorporeal unexploded ordnances (UXOs) represents a unique challenge for CCC 

providers. Mortars, rockets, and grenades that fail to trigger may become embedded in a casualty without 

exploding (Figs. 25 and 26). Due to the extensive time and resources needed to appropriately manage these 

casualties and the potential for collateral damage from premature detonation, military recommendations include 

initially triaging such patients as nonemergent, isolating them from others, and operating on them last.15,139

Military recommendations include:

 initially triaging such patients as nonemergent,

 isolating them from others, and

 operating on them last.

According to Lien, “the fuse is the key to understanding unexploded ordnance.”139 A fuse serves as a trigger 

for an explosive device and may be set off by impact, electromagnetically, or as a function of time or 

distance traveled. Care should be taken to minimize manipulation or movement of the UXO and casualty. 

If helicopter transport is necessary, the patient should be flown independent of other patients, and the 

flight crew should be kept to a minimum and protected with body armor.140 Diagnostic and therapeutic

Electrical equipment, such as:

 electrocautery, 

 surgical saws or drills,

 blood warmers,

 monitors,

 defibrillators,

 ultrasound, or

 computed tomography imaging,

should be avoided until the unexploded ordinance is removed.
Weapons Effects | 73

medical equipment can trigger a fuse and inadvertently cause an explosion. Electrical equipment, such 

as electrocautery, surgical saws or drills, blood warmers, monitors, defibrillators, ultrasound, or computed 

tomography imaging should be avoided until the UXO is removed.15 Some of these diagnostic and treatment 

adjuncts may radiate electrical fields, cause severe vibration, or result in elevated temperatures that may 

arm the fusing mechanism.139 

Plain radiography is considered safe and is used to identify the type of munition and fuse, as well as 

to define the surgical approach to embedded UXOs.139 As part of preoperative planning, the explosive 

ordnance disposal (EOD) team should be notified and present to assist in the proper handling and disposal 

of the UXO.

Traditional recommendations for removal of UXOs include the use of regional or spinal anesthesia and 

departure of operating room personnel except for the operating surgeon.15 Recent case reports from OEF 

and OIF have suggested that general anesthesia allows for a more controlled environment, and that having 

the appropriate, rather than minimal, number of assistants in the operating room can lead to the most 

successful outcomes.140 Operating room staff should wear protective gear, including body armor, ballistic 

eye protection, and a helmet. Sandbags should be positioned around the patient. Gentle technique and 

en-bloc resection of the UXO minimizes manipulation and the inherent risk of detonating the device. If 

embedded in an extremity, amputation should be considered.15,140

Conclusions

Understanding modern warfare, including the types of weapons employed and the mechanisms and 

patterns of injury they cause, is critical to providing optimal CCC. The primary mechanisms of combat 

injury in OEF and OIF are small arms and explosives. Explosion-related injuries account for a majority of 

the injuries and deaths in OEF and OIF. Improvised explosive device attacks have become a mainstay in the 

current conflicts. Explosive devices produce the ultimate polytrauma (i.e., a wide range of injury types to 

many body regions caused by the full range of injury mechanisms). Explosions produce patterns of injury

Understanding modern warfare, including the types of weapons employed and the mechanisms and 

patterns of injury they cause, is critical to providing optimal combat casualty care.

that are distinct from those of other mechanisms. In an open-space explosion, the primary mechanism of 

injury is fragment penetration. Injuries and deaths from fragments occur much further from the point of 

detonation than do those associated with the primary blast. The simultaneous combination of different 

blast injury mechanisms produces a complex array of injuries. Combat casualty care providers must fully 

understand these complex injuries and their management to ensure optimal patient outcomes. 
74 | Weapons Effects

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84 | Weapons Effects
FUNDAMENTALS OF 

COMBAT CASUALTY CARE

Contributing Authors

Robert T. Gerhardt, MD, MPH, FACEP, FAAEM, LTC, US Army

 Robert L. Mabry, MD, FACEP, MAJ(P), US Army

 Robert A. De Lorenzo, MD, MSM, FACEP, COL, US Army

 Frank K. Butler, MD, FACS, CAPT, US Navy (Ret)

Chapter 3
All figures and tables included in this chapter have been used with permission from Pelagique, LLC, the 

UCLA Center for International Medicine, and/or the authors, unless otherwise noted.

Use of imagery from the Defense Imagery Management Operations Center (DIMOC) does not imply or 

constitute Department of Defense (DOD) endorsement of this company, its products, or services.

Disclaimer

The opinions and views expressed herein belong solely to those of the authors. They are not nor should 

they be implied as being endorsed by the United States Uniformed Services University of the Health 

Sciences, Department of the Army, Department of the Navy, Department of the Air Force, Department of 

Defense, or any other branch of the federal government.
Fundamentals of Combat Casualty Care | 87

Table of Contents

Introduction..........................................................................................................88

Leading Causes of Preventable Death ......................................................................88

Case Study: Out-of-Hospital Care ............................................................................89

Combat Versus Civil Sector Out-of-Hospital Care ......................................................91

Tactical Combat Casualty Care (TCCC)....................................................................92

Care-Under-Fire Issues.......................................................................................................93

Tactical Field Care..............................................................................................................95

Hemorrhage Control and Tourniquet Use..........................................................................95

Hemostatic Agents...............................................................................................................95

Vascular Access and Fluid Resuscitation .............................................................................96

Acute Airway Obstruction and Ventilatory Support ...........................................................97

Tension Pneumothorax.......................................................................................................98

Spinal Injury Precautions.....................................................................................................99

Traumatic Brain Injury........................................................................................................99

Hypothermia Prevention and Management......................................................................101

Infection Prophylaxis..........................................................................................................102

Pain Management..............................................................................................................102

Air Medical Evacuation Considerations............................................................................103

Tactical Evacuation Care .................................................................................................103

Health Services Support (HSS): Echelons, Levels, and Roles of Care .......................... 107

Mass-Casualty-Incident Management .................................................................... 109

US and NATO Military Mass-Casualty Triage Systems..................................................109

Alternative Mass-Casualty Triage Systems.....................................................................111

Reprise and Conclusion of Case Study ................................................................... 111

Future Directions................................................................................................. 112

References .......................................................................................................... 113
88 | Fundamentals of Combat Casualty Care

Introduction

Over the past century, an evolution in combat casualty care (CCC) has occurred. As the current century 

unfolds, we expect even more remarkable advances as increasing resources are focused on the out-ofhospital phases of emergency care. In addition to the development of new resuscitation strategies, surgical 

techniques, pharmaceuticals and other adjuncts, the military and emergency medicine communities 

continue to champion innovation in first responder and combat medic training and seek the means to provide 

effective medical direction to the incipient “Combat Emergency Medical Services (EMS) system.”1

From its earliest days, the process of evacuating the sick and wounded from the battlefield resulted in displays 

of great sacrifice, bravery, and all too often, tragic errors of both omission and commission. In most cases, 

current practices have evolved from the on-the-job experiences of CCC providers. Clinical and treatment 

data in the out-of-hospital arena remain sparse, with minimal granularity consisting of occasional afteraction reports bolstered by sporadic field medical records. Civilian sector solutions and training paradigms 

are often extrapolated and applied to the tactical setting, but translate into suboptimal tactical and clinical 

outcomes.2 

Leading Causes of Preventable Death

The Wound Data and Munitions Effectiveness Team (WDMET) study provided one of the first objective 

databases from which inferences regarding evacuation and en-route-care were drawn.3 Building on the 

WDMET concept, the Joint Theater Trauma Registry (JTTR) was developed by the United States (US) 

Army Institute of Surgical Research in partnership with the US Air Force and US Navy, in response to a 

Department of Defense directive to capture and report battlefield injury.4 The JTTR is designed to facilitate 

the collection, analysis, and reporting of CCC data along the continuum of care and to make this data 

accessible to healthcare providers engaged in the care of individual patients, as well as for system analysis 

and quality improvement. While implementation of the JTTR has been successful from the point of initial 

surgical intervention back to rehabilitative care, success in collection of the out-of-hospital components of 

the registry has been more elusive. Factors limiting consistent, systematically standardized and complete 

out-of-hospital data collection include: (1) legacy data collection methods (handwritten documents and 

antiquated field medical treatment cards); (2) lack of a complementary out-of-hospital component of the 

Joint Theater Trauma System; and (3) lack of a standard requirement for reporting out-of-hospital casualty 

care clinical records. 

Recent studies confirm many of the WDMET findings, with evidence that compressible hemorrhage, 

tension pneumothorax, and airway and ventilatory compromise, are the leading causes of preventable 

death in Operation Enduring Freedom (OEF) and Operation Iraqi Freedom (OIF).5,6 The WDMET study 

identified the following three conditions as primary causes of preventable death on the battlefield: (1) airway 

obstruction (6 percent), (2) tension pneumothorax (33 percent), and (3) hemorrhage from extremity wounds 

(60 percent). Analysis of autopsy records from OIF indicated a frequency of preventable battlefield death 

between 10 to 15 percent from airway obstruction and 33 percent for extremity hemorrhage thought to 

be preventable by tourniquet application.6 In a smaller study describing 12 potentially preventable deaths 

in special operations forces, Holcomb et al. reported the following six conditions as potential contributors 
Fundamentals of Combat Casualty Care | 89

to death: noncompressible hemorrhage (eight deaths), tourniquet-amenable hemorrhage (three deaths), 

“non-tourniquetable” hemorrhage (two deaths), tension pneumothorax (one death), airway obstruction 

(one death), and sepsis (one death).5 One death was deemed due to dual conditions. To affect survival, it 

is critical to recognize and treat most of these conditions within the first minutes after wounding.7 Only 

combatant first responders, combat medics, and other far-forward clinicians can deliver this timely care.

Compressible hemorrhage, tension pneumothorax, and airway and ventilatory compromise are the 

leading causes of preventable death in OEF and OIF. 

Despite the relative simplicity of the maneuvers required to treat these conditions, they remain a significant 

cause of mortality. This underscores the need to ensure clinical competence among CCC providers, 

including combatant first responders, medics, corpsmen, physicians, physician assistants and nurses, 

as well as an effective means of capturing clinical data in the out-of-hospital setting.8 Gerhardt et al. 

recently studied the impact of deploying emergency medicine specialty-trained CCC providers including 

an emergency physician, an emergency medicine physician assistant, and advanced-scope-of-practice 

combat medics. The study demonstrated a 7.1 percent case fatality rate as compared to the concurrent 

theater aggregate US case fatality rate of 10.5 percent. This occurred despite a battle casualty rate nearly 

three times that of the contemporaneous combat theater-wide rate, an out-of-theater evacuation rate 

over twice that of the theater aggregate rate, and an equivalent injury severity score (ISS) to that of the 

theater aggregate. No deaths were attributed to airway obstruction or tension pneumothorax. One case of 

potentially compressible hemorrhage following traumatic lower extremity amputation resulting in death 

was reported.9 

The Defense Health Board’s Committee on Tactical Combat Casualty Care (TCCC) recently developed 

and promulgated coherent guidelines for those who engage in out-of-hospital CCC.10 To the extent possible, 

the guidelines were created using literature-based evidence, rather than solely relying upon expert consensus. 

The importance of fully understanding TCCC principles and guidelines is underscored by the following 

case study.

Case Study: Out-of-Hospital Care 

A combat engineer section with attached civil affairs and medical personnel mounted in up-armored HighMobility Multipurpose Wheeled Vehicles (HMMWVs) is conducting civil-military operational activities 

in a semipermissive section of a large urban center in US Central Command (CENTCOM) Area of 

Responsibility. The three-vehicle patrol halts along an alternate supply route after visually identifying an 

unexploded artillery shell. Several soldiers dismount. Moments later, the convoy comes under effective fire 

from a four-man team of insurgents armed with a light machine gun, a rocket-propelled grenade (RPG) 

launcher, and two assault rifles. One vehicle is disabled by an RPG. A second RPG is launched and strikes 

the unit’s combat medic at an oblique angle, ricocheting off his individual body armor small arms protective 

insert and detonating after striking the ground near his feet. The medic sustains shrapnel wounds to the 

right medial thigh and right forearm, in addition to blunt chest trauma. A combat engineer is also wounded 

with shrapnel in his right forearm. Both casualties have brisk bleeding from their forearm wound sites. As 
90 | Fundamentals of Combat Casualty Care

the medical officer and other soldiers approach the wounded, the RPG gunner rises again, preparing to fire 

at them.

What actions should be taken in this vignette? Combatants are often faced with similar scenarios. Rapid 

action, decision making, and technical performance of interventions are critical. In this scenario, the 

appropriate immediate response would be to return effective fire to suppress or neutralize the threat (i.e., 

enemy combatant RPG gunner). Once the tactical situation allows, hasty (rapidly applied) tourniquets 

should be placed proximal to both respective forearm wounds. The tourniquets should be rapidly applied 

over casualties’ clothing in care-under-fire scenarios. Additional casualties who are unable to ambulate 

independently should be extricated and moved to an area of cover.

Upon reaching the relative safety of cover, the CCC provider should assess casualties for airway patency, 

adequate ventilation, type and severity of chest trauma, and tourniquet efficacy. A brief survey of 

the casualties for additional (undiscovered) wounds should be quickly performed. Suspected tension 

pneumothorax is treated by needle thoracostomy. If tactical conditions permit, previously applied 

tourniquets should be reassessed for efficacy. Such tourniquets should be more deliberately positioned 

Figure 1. TCCC casualty treatment card (DA 7656).
Fundamentals of Combat Casualty Care | 91

directly proximal to the wound over bare skin. If, upon further examination of the casualty, a tourniquet is 

believed unnecessary, extremity wounds can be treated with standard or hemostatic wound dressings. This 

is followed by administration of prophylactic antibiotics and analgesics. During the ongoing process of 

assessment and tactical field care, appropriate tactical evacuation should be arranged. The CCC provider 

should continue to monitor and treat casualties during casualty evacuation. A TCCC casualty treatment 

card (DA 7656) should be completed at the earliest possible juncture, and it should be submitted to the 

appropriate authority (Fig. 1). Lastly, upon arrival at the receiving facility or upon transfer to the evacuation 

conveyance, the CCC provider should verbally sign over care (e.g., briefly summarize injuries and care) of 

casualties to receiving medical personnel.

Combat Versus Civil Sector Out-of-Hospital Care 

While some similarities exist, out-of-hospital care in combat settings often radically differs from civil 

sector practice in the US. Beyond the challenges of individual patient care, harsh weather conditions, and 

austere settings, out-of-hospital careproviders face unique tactical challenges. For example, in civilian sector 

emergency medical services (EMS), a typical motor vehicle collision scene might include an ambulance crew 

routinely consisting of two or even three emergency medical technicians (EMTs), with at least one being an 

EMT-Paramedic. Often, firefighters will be present, providing additional capabilities. Ambulances will be 

stocked with a wide array of basic and advanced life support devices, monitors, and pharmaceuticals. First 

responders will have telecommunication capacity and some form of medical direction for decision support 

and destination guidance. In the majority of cases, significant resources will be brought to bear upon one 

or two patients. In addition, civilian sector out-of-hospital careproviders do not typically face hostile gunfire 

and are able to fully focus on patient care.

Though some similarities exist, out-of-hospital care in combat settings often differs radically from civil 

sector practice in the US.

In contrast to the aforementioned scenario, one 

may envision a combat medic or other careprovider 

responding to casualties after a roadside bomb 

detonates adjacent to their convoy. After exiting his 

or her vehicle, the first responder proceeds on foot to 

the scene. Usually, all available medical equipment 

is carried by the medics themselves in a rucksack or 

otherwise harnessed to them. There is likely to be 

only one medic assisting casualties that were injured 

by a combination of high-explosive ordnance, 

vehicle fires, or small-arms fire. The medic is 

appropriately focused on patient care but must also 

be cognizant that the overarching priorities are the 

combat unit’s integrity and mission. While working, 

the medic may become the target of hostile fire and 

may have to return fire. 

Figure 2. Medical evacuation (MEDEVAC) of an injured soldier onto 

a UH-60 Black Hawk helicopter in Afghanistan. Evacuations tend to 

be longer in distance, duration, and complexity as compared to civilian 

settings. Image courtesy of Defense Imagery Management Operations 

Center (DIMOC).
92 | Fundamentals of Combat Casualty Care

As highlighted previously, TCCC poses additional unique challenges compared to civilian practice. Combat 

casualty careproviders are more likely to encounter mass- and multiple-casualty-incidents and patients 

with catastrophic wounds. The epidemiology of wounding in OEF and OIF reveals a high incidence of 

penetrating trauma and blast-related mechanisms of injury.11,12 Casualty evacuations tend to be longer in 

distance, duration, and complexity as compared to civilian settings. Such conditions combine to make CCC 

extremely challenging (Fig. 2). 

As compared to civilian practice, TCCC providers are more likely to encounter penetrating trauma, 

blast-related mechanisms of injury, and mass- and multiple-casualty-incidents while facing more complex 

casualty evacuation scenarios.

In addition to the individual challenges of CCC, several systemic issues pose significant obstacles to the 

optimization of CCC in the modern battlespace. The most pressing of these issues is a lack of effective 

clinical data collection in the forward setting and the need for adaptation of clinical operating guidelines 

(COG) and scope of practice for out-of-hospital practitioners. Outcomes research in EMS is sparse in both 

the civilian sector and combat settings. Randomized, controlled, prospective trials are the exception rather 

than the rule.13 Much of what is available comes in the form of case reports or series focusing on single 

aspects of out-of-hospital CCC or case series resulting from individual engagements.14 A primary challenge 

facing military medical leaders is the development and implementation of an effective, sustainable, and 

physically hardy system for documenting and sharing the equivalent of what would be a routine patient care 

report (PCR). Until the advent of such a system, critical elements of out-of-hospital CCC will lag behind 

civil sector EMS. This lack of out-of-hospital clinical data presents a formidable obstacle to implementing 

a civilian sector EMS-style medical direction model with its component process improvement mechanisms, 

including field medical treatment record review. 

Future steps include: (1) organizing and training the military’s out-of-hospital enlisted CCC providers to a 

level approaching that of special operations advanced tactical practitioners; (2) optimally utilizing military 

emergency medicine-trained practitioners (including emergency physicians and specialty-trained physician 

assistants, and certified emergency nurses); and (3) developing true emergency medical direction capability. 

Reflecting the success of civil sector EMS and trauma systems, the future military EMS medical direction 

capability should encompass retrospective process improvement program management as well as online 

decision support to far-forward practitioners.7 In the interim, it is incumbent on individual CCC providers 

to make the best effort possible to document and forward clinical data pertaining to the casualties they treat, 

the interventions they performed, and the resulting outcomes.

Tactical Combat Casualty Care (TCCC) 

The inadequacy of applying a civilian trauma model to tactical situations has long been recognized.15,16,17

The TCCC program was initiated by the Naval Special Warfare Command in 1993, and later continued by 

the US Special Operations Command (USSOCOM). This effort developed a set of tactically appropriate 

battlefield trauma care guidelines that provide CCC providers with trauma management strategies that 

combine good medicine with good small-unit tactics.15 Tactical Combat Casualty Care guidelines recognize 

that trauma care in the tactical environment has three goals: (1) treat the casualty; (2) prevent additional 

casualties; and (3) complete the mission. 
Fundamentals of Combat Casualty Care | 93

The first TCCC course was taught in 1996 in the Undersea Medical Officer course sponsored by the Navy 

Bureau of Medicine and Surgery (BUMED). Shortly thereafter, this training was mandated for all US 

Navy Sea-Air-Land (SEAL) naval special warfare corpsmen.15 Since that time, TCCC has gradually gained 

acceptance in US and foreign military forces.15,16,17,18,19,20,21,22,23 It has also found acceptance in the civilian 

law enforcement medical community.24 Preliminary evidence from the current conflicts in Afghanistan and 

Iraq supports the contention that in the hands of clinically and tactically competent CCC providers, TCCC 

contributes to casualty survival.25

Tactical Combat Casualty Care is divided into three phases: (1) care-under-fire, (2) tactical field care, and 

(3) tactical evacuation care.

Trauma care measures proposed in the original TCCC guidelines are outlined in Table 1. The overarching 

goal of the TCCC initiative is the combination of good tactics with good medicine. As the name implies, 

TCCC is practiced during combat missions. TCCC is divided into three phases: (1) care-under-fire, (2) 

tactical field care, and (3) tactical evacuation care. In care-under-fire, CCC providers and their units are 

presumed to be under effective hostile fire, and the care they are capable of providing is very limited. In 

the tactical field care phase, CCC providers and their patients are no longer under effective hostile fire, and 

more extensive care can be provided. In the tactical evacuation care phase, casualties are transported to a 

medical facility by an aircraft, ground vehicle, or boat, and there is an opportunity to provide a higher level 

of care.

Care-Under-Fire Issues

The first phase of the TCCC paradigm is composed of two verbs: care and fire. This implies the unpleasant 

realities that one’s unit has come under attack by hostile personnel who have made the unit the target of 

effective fire by one or more lethal weapon systems, and, as a result, someone has been wounded. The 

essential initial action is to return effective fire toward the threat with the specific intent of neutralizing or 

otherwise preventing hostile personnel from continuing to place effective fire on the CCC provider or their 

unit. Until this is accomplished, the CCC provider will be unable to render effective medical care, and the 

careprovider, fellow warfighters, or existing casualties could be further wounded or killed. A summary of 

Original Tactical Combat Casualty Care Treatment Measures

1. Early use of tourniquets to control clinically important extremity hemorrhage

2. Systemic antibiotic prophylaxis near point of injury 

3. Tactically appropriate intravenous or intraosseous access and fluid resuscitation

4. Improved battlefield analgesia (intravenous or intramuscular opiates) 

5. Nasopharyngeal airways as first-line airway devices

6. Surgical airways for maxillofacial trauma with an obstructed airway 

7. Aggressive diagnosis and treatment of tension pneumothorax via needle decompression 

8. Incorporation of input from CCC providers into TCCC guidelines 

9. Employment of tactically and clinically-relevant scenarios into TCCC training

Table 1. Original Tactical Combat Casualty Care treatment measures.
94 | Fundamentals of Combat Casualty Care

actions conducted during the care-under-fire phase includes: (1) returning effective fire toward the source 

of hostile engagement; (2) tactical movement of the casualty and careprovider to an area of cover and 

concealment; (3) and the rapid assessment for sources of massive extremity hemorrhage amenable to 

placement of a tourniquet, followed by rapid tourniquet placement if practicable. Once these tasks have 

been accomplished and the unit is no longer under effective hostile fire, this phase of TCCC is complete 

(Fig. 3).

In care-under-fire situations, the CCC provider should return effective fire, move the casualty to a safe 

area, rapidly assess the casualty for sources of massive extremity hemorrhage, and apply a tourniquet if 

necessary.

The care-under-fire phase of TCCC is often difficult for careproviders transitioning from civilian 

healthcare backgrounds. It is imperative that all CCC providers develop and maintain, at a minimum, basic 

proficiency in fundamental soldier skills prior to tactical deployment. Basic tactical warfighting skills include 

four fundamental components: shooting, moving, communicating, and surviving. It is important to: (1) 

understand how small units (squads, platoons, and companies) operate in combat; (2) know how to employ 

cover and concealment when moving tactically (both in vehicles and while dismounted on foot); (3) possess 

basic firearm marksmanship culminating in true proficiency with one’s primary weapon and familiarity 

with other weapons used by one’s unit or organization; and (4) have a working knowledge of how to locate 

and use the unit’s radio and other available communications systems. A CCC provider should not presume 

the aforementioned skills will be provided by one’s gaining unit. Rather, one should actively seek training 

and mentoring in these essential tasks prior to and during deployment. 

Figure 3. (Above) After returning effective fire, casualties should be moved 

to an area of cover and concealment and assessed for massive extremity 

hemorrhage amenable to placement of a tourniquet. Image courtesy of 

Defense Imagery Management Operations Center (DIMOC).

Figure 4. (Right) Hemorrhage control is a priority in all phases of 

TCCC. Tourniquets or hemostatic dressings combined with direct pressure 

should be applied early, when indicated. Image courtesy of Defense Imagery 

Management Operations Center (DIMOC).
Fundamentals of Combat Casualty Care | 95

Tactical Field Care

Hemorrhage Control and Tourniquet Use

Uncontrolled hemorrhage remains the largest single cause of combat deaths, accounting for over 80 percent 

of combat deaths.6 Moreover, compressible hemorrhage remains a significant cause of preventable battlefield 

deaths.5,6 As such, the control of hemorrhage remains a priority in all phases of TCCC and includes the 

employment of hasty (rapidly applied) tourniquets as the primary means of controlling significant extremity 

hemorrhage (Fig. 4). After the casualty is extracted from effective hostile fire, hemostatic dressings may be 

placed with direct pressure applied to extremity bleeding sites, distal to tourniquets. Similarly, hemostatic 

dressings and direct pressure are applied to sources of bleeding on the torso and other sites that are not 

amenable to tourniquet application.

Uncontrolled hemorrhage remains the largest single cause of combat deaths, accounting for over 80 

percent of combat deaths.

Extremity wounds that require continued tourniquet use for hemostasis should have hasty (rapidly applied) 

tourniquets converted to definitive (deliberate) tourniquets. This is accomplished by removing overlying 

clothing and armor and applying definitive tourniquets immediately proximal (two to three inches above the 

wound) to the hemorrhage site (e.g., mangled or amputated extremity). If required, additional tourniquets 

may be placed (in sequence longitudinally) proximal to the source of bleeding to reinforce the hemostatic 

effect. In situations where hasty tourniquets were placed in a care-under-fire scenario, reassessment of the 

injured extremity can now be performed in the tactical field care phase. In a hemodynamically stable patient, 

a tourniquet can be removed if the extremity injury was not as severe as originally judged, or hemostasis 

is maintained with hemostatic dressings and direct pressure. Additional information on tourniquets can be 

found in the Extremity Injury chapter.

Hemostatic Agents 

Operation Enduring Freedom and OIF have supported important research, development, and acquisition 

efforts focused on creating effective hemostatic agents for out-of-hospital setting use. The use of parenteral 

hemostatic agents, such as recombinant factor VIIa, has been met with controversy and conflicting clinical 

data, resulting in limited use.26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41 Likewise, there is little definitive clinical data 

supporting the use of hemostatic dressings, despite their ubiquitous presence on the battlefield.42,43,44,45,46,47

First-generation agents such as Zeolite (QuikClot®) and Chitosan-impregnated semi-rigid dressings 

(HemCon®) have given way to hemostatic-impregnated gauze (e.g., Kaolin Combat GauzeTM, HemCon 

ChitoFlexTM, CELOX Chitosan GauzeTM). The current TCCC guidelines recommend Combat GauzeTM 

as the hemostatic agent of choice for compressible hemorrhage not amenable to tourniquet use.10 These 

hemostatic agents may offer incremental benefits, particularly in cases of junctional hemorrhage (inguinal or 

axillary wounds) or in cavitary wound applications. At present, there is insufficient evidence to recommend 

specific products over others in out-of-hospital care. It should be emphasized that proper dressing and 

bandaging techniques and the early and appropriate use of tourniquets are the most critical elements of 

out-of-hospital hemorrhage control.
96 | Fundamentals of Combat Casualty Care

Vascular Access and Fluid Resuscitation 

Casualties with controlled sources of hemorrhage who have a palpable radial pulse and a normal mental 

status do not require immediate vascular access and resuscitative fluids in the out-of-hospital phase of care 

(Fig. 5).48 Vascular access should be obtained for casualties with uncontrolled hemorrhage or in cases of 

presumed significant head injury (e.g., altered mental status) and significant blood loss. While peripheral 

intravenous access remains the criterion standard, the emergence of intraosseous devices has provided a 

viable alternative.49 Requiring minimal training to achieve and maintain proficiency, common intraosseous 

devices in current military use employ the sternal manubrium, tibial tuberosity, lateral humeral head, 

or iliac crest as access sites and permit administration of resuscitation fluids, blood products, and many 

pharmaceuticals (Fig. 6).50,51,52,53

Casualties with controlled sources of hemorrhage who have a palpable radial pulse and a normal mental 

status do not require immediate vascular access and resuscitative fluids in the out-of-hospital phase of 

care.

The optimal type and volume of intravenous solution to employ in acute hemorrhagic shock in the 

out-of-hospital tactical setting is still a subject for debate. Described by Beecher as a result of combat 

surgical experience in World War II and resurfacing with the work of Bickell et al. in 1994, the concept 

of hypotensive resuscitation has regained traction in the military CCC community.49,54,55 The evidence 

in support of specific volumes and types of intravenous resuscitation fluids for use in combat is limited. 

Existing data does support logistical arguments favoring a hypotensive resuscitation scheme including the 

use of colloids due to decreased carrying weight and space requirements.56 Hetastarch 6% in lactated 

electrolyte solution and 7% hypertonic saline (HTS) have been studied as fluid resuscitation solutions.48,57

These resuscitation solutions effectively restore intravascular volume, minimize inappropriate immune 

response and cellular injury, and improve overall survival in the absence of blood products.57 Of note, 

colloids such as hydroxyethyl starch have been known to increase coagulopathy (in vitro) by impairing von 

Willebrand factor activity in plasma.58 The only trauma clinical trial involving Hextend® to date uncovered 

Figure 5. Casualties with controlled sources of hemorrhage who have a 

palpable radial pulse and a normal mental status do not require immediate 

vascular access and resuscitative fluids in the out-of-hospital phase of 

care. Image courtesy of Defense Imagery Management Operations Center 

(DIMOC).

Figure 6. If immediate vascular access is needed and a standard 

intravenous line cannot be established, intraosseous access should be 

obtained. All resuscitative medications and blood products can be infused 

via an intraosseous needle.
Fundamentals of Combat Casualty Care | 97

no clinical signs of coagulopathy in the Hextend®-resuscitated group as compared to the control group.59

As a practical matter, hypertonic saline solutions are not readily available commercially for use as 

intravascular volume replacement, whole blood and fresh frozen plasma are currently impractical in 

tactical settings, and hemoglobin-based oxygen carriers are still under development. As of this printing, 

the current TCCC recommendation for intravascular fluid resuscitation is the use of Hextend® (6% 

Hetastarch in Lactated Electrolyte Injection) in 500 milliliter aliquots, with a maximum administration of 

1,000 milliliters.10 Similarly, the recommended resuscitation endpoints for combat casualties are evolving. 

Reasonable endpoints include a palpable radial pulse or a systolic blood pressure of 90 mm Hg and 

improved mental status in non-head-injured patients.49

Acute Airway Obstruction and Ventilatory Support

Recent analyses of preventable deaths in OEF and OIF revealed 10 to 15 percent of casualties were 

deemed to have acute airway obstruction or ventilatory failure as a proximate cause of death.6,60,61 To 

further underscore the need for out-of-hospital phase early airway support, a subanalysis of the Registry of 

Emergency Airways at Combat Hospitals (REACH) study by Adams et al. reported that 76 of 1,622 subjects 

(5 percent) arrived at a Combat Support Hospital (CSH) without a definitive airway, despite needing one.62 

Ten to 15 percent of preventable deaths in OEF and OIF were attributed to acute airway obstruction or 

ventilatory failure.60,61

The CCC provider must be able to provide basic and advanced airway support and control. This includes 

use of basic airway adjuncts (oral and nasopharyngeal airways), providing bag-valve-mask ventilatory 

support, establishing definitive airways (endotracheal intubation and cricothyroidotomy), and using a 

portable mechanical ventilator. While rapid sequence direct laryngoscopic orotracheal intubation remains 

the criterion standard for advanced airway management in the civil sector, its efficacy and continued role 

in the out-of-hospital setting remains the subject of debate.63,64,65,66 Furthermore, this intervention does 

not translate well into the tactical environment, unless performed by practitioners who are proficient in 

its execution.9,62 According to TCCC guidelines, surgical cricothyroidotomy (provided careproviders are 

trained in its performance) is the preferred method for establishing a definitive airway during tactical field 

care or the tactical evacuation phase.1,9,10,17 This recommendation assumes careproviders in the field lack the 

necessary equipment, pharmaceutical agents, or training to perform rapid-sequence orotracheal intubation.

Alternative methods of securing a definitive airway in the tactical environment include standard laryngoscopic 

orotracheal intubation, blind insertion airway devices, such as laryngeal tube devices, or esophageal gastric 

tube airways. Laryngeal-mask airways (LMA) are considered a temporizing airway measure as opposed 

to a definitive airway. While they are among the easiest-to-use, they are limited by their inability to be 

firmly secured in place and provide definitive airway protection. Lastly, the recent advent of video-based 

laryngoscopic devices (such as Glidescope® and RES-Q-SCOPE®) may offer a viable option for orotracheal 

intubation in field and transport settings; however, data confirming efficacy in this setting is lacking.67,68,69 

Ensuring combat casualties have a secure and patent airway is strongly recommended during the tactical 

field care phase prior to tactical evacuation. In circumstances where this is impossible or impractical, the 

practitioner’s goal will shift toward attempting to prevent airway compromise en route, as the environment 
98 | Fundamentals of Combat Casualty Care

in most evacuation conveyances is suboptimal at best for advanced airway placement. In the event that 

unanticipated airway compromise occurs during evacuation, the practitioner must rapidly assess the 

likely cause and attempt to mitigate it. Simple suctioning and jaw-thrust maneuvers may suffice. If these 

initial interventions fail, the practitioner may be forced to perform an advanced airway maneuver. Under 

such circumstances, the decision whether to perform surgical cricothyroidotomy or to employ alternative 

methods of securing an airway will have to be made, taking into consideration the patient’s unique anatomy, 

conditions in the vehicle (vibration, kinetics, visibility, maneuver room), available airway supplies, and skill 

of the CCC provider. 

Tension Pneumothorax 

Traumatic pneumothorax is a potentially life-threatening condition and may rapidly progress to tension 

pneumothorax, an immediate life-threat. Likewise, an accumulating hemothorax or hemopneumothorax 

may cause similar cardiovascular collapse due to both ongoing hemorrhage, as well as the introduction of 

tension physiology. 

Tension pneumothorax, hemodynamically significant hemothorax, or tension hemopneumothorax should 

be suspected in the setting of blunt or penetrating thoracic trauma when a combination of the following 

Figure 7. Immediate needle thoracentesis should be performed in cases of suspected tension pneumothorax.
Fundamentals of Combat Casualty Care | 99

clinical findings are present: progressive respiratory distress, hypotension, contralateral tracheal deviation, 

hyperresonance or dullness on percussion of the affected hemithorax, asymmetric chest wall rise with 

inhalation, or ipsilateral or bilateral decreased breath sounds upon auscultation. Under such conditions a 

needle thoracentesis should be performed. A 14-gauge intravenous catheter with a minimum length of eight 

centimeters (3.25 inch needle/catheter unit) is placed in the second intercostal space along the midclavicular 

line.10,70,71 The recently revised recommendation to use a longer needle is based on data indicating a larger 

chest wall thickness in military personnel.71 Tube thoracostomy should follow needle thoracentesis at the 

earliest possible juncture. Chest tube insertion in the setting of a pneumothorax is strongly recommended in 

advance of tactical evacuation, particularly if casualties will be transported by air. If this is not practicable, 

placement of a three-way stopcock for serial decompression or repeated needle thoracentesis may be 

required. The casualty should be closely monitored for recurrence of tension pneumothorax (Fig. 7). 

Spinal Injury Precautions

In the current conflicts in Afghanistan and Iraq, spinal trauma is an increasing source of morbidity often 

leading to spinal cord injury and paralysis.72 Cervical, thoracic, and lumbar spinal injuries (along with 

multiple spinal level injuries) are encountered in combat casualties injured by gunfire, explosions, motor 

vehicle accidents, and falls.73,74,75,76

Although recently challenged in cases of penetrating spinal trauma, spinal immobilization is a fundamental 

tenet of out-of-hospital EMS practice in the civil sector.77 The employment, methods, and point of 

initiation of spinal immobilization in combat settings differ by necessity from civil sector practice. Factors 

influencing this phenomenon include tactical considerations, the effect of individual body armor on both 

spinal immobilization and alignment, and the logistical challenges associated with the movement of a 

properly immobilized patient through the tactical evacuation chain. 

By necessity, the employment, methods, and point of initiation of spinal immobilization in combat settings 

differ from civil sector practice.

There is insufficient literature to provide definitive guidelines on spinal immobilization in tactical settings.78

First responders will need to use their best judgment in such settings. When a CCC provider suspects 

spinal trauma, tactically sound attempts at maintaining the casualty’s spinal column in as near-neutral a 

position as possible should be attempted during care-under-fire and initial extrication. Individual body 

armor, though in itself a potential source of spinal misalignment, should remain on the casualty for as 

long as there continues to be a realistic threat of further engagement by hostile ordnance (Fig. 8). When 

tactical conditions allow, individual body armor should be removed or loosened to facilitate further casualty 

examination. If suspicion for spinal injury persists after secondary survey, and tactical conditions permit, 

individual body armor should be removed and spinal immobilization measures instituted. Spinal injury 

precautions should then be maintained throughout tactical evacuation (Fig. 9).

Spinal immobilization techniques used in a combat setting mirror those found in the civilian sector. 

Traumatic Brain Injury 

Blunt and penetrating head injuries are common occurrences in OEF and OIF, despite the advent of 

Kevlar-based helmets.6 The continued use of roadside bombs by enemy combatants has accelerated efforts 
100 | Fundamentals of Combat Casualty Care

to improve both diagnostic and therapeutic approaches to traumatic brain injury. Civilian research studies 

have established that patients suffering severe head injuries complicated by episodes of transient hypoxia or 

hypotension in the prehospital phase of care have worse outcomes.79 As such, out-of-hospital careproviders 

should attempt to prevent episodes of hypoxemia and hypotension in patients with traumatic brain injuries. 

Casualties with head injuries who manifest signs of hemorrhagic shock should undergo interventions 

directed towards hemorrhage control, optimization of airway and ventilatory status, and restoration of 

adequate tissue perfusion. The goal of airway and ventilatory support in the tactical setting is to maintain 

adequate tissue oxygenation and normal ventilation. Patients should have their partial pressure of oxygen 

in arterial blood (PaO2) maintained at or above 60 mm Hg (pulse oximeter reading greater than 90 percent 

oxygen saturation) and partial pressure of carbon dioxide (PCO2) values in the normal range of 35 to 40 

mm Hg.79 While endpoints of fluid resuscitation in the tactical setting include a palpable radial pulse or 

improved mental status in non-head-injured patients, alternative strategies may be indicated in patients 

with suspected traumatic brain injury. More aggressive fluid resuscitation may be required to minimize 

secondary brain injury from hypotension (defined as systolic blood pressure less than 90 mm Hg). The 

ability to meet these parameters in a tactical field care setting is complicated by numerous factors. 

In patients with suspected head injury, more aggressive fluid resuscitation strategies may be necessary to 

minimize secondary brain injury from cerebral hypoperfusion resulting from systemic hypotension.

Patients with blunt head injuries are at risk for coexisting cervical spine injury.80,81,82 Hence, spinal 

immobilization or at least maintenance of neutral spinal alignment is recommended at the earliest possible 

juncture during the tactical field care phase. Similar to casualties with other causes for potential closedspace gas collection, patients with suspected intracranial injury should be transported with the minimal 

possible increase in altitude and should be positioned in a neutral supine position.83 Early post-traumatic 

seizures have been observed in 5 to 30 percent of severe head injury patients and may exacerbate secondary 

brain injury.84,85 Seizures occurring in the tactical setting may be controlled initially with benzodiazepines 

administered via intramuscular, intravenous, intraosseous, or rectal routes. Airway control and breathing 

Figure 8. An injured US Army soldier aboard a UH-60 Black Hawk 

MEDEVAC helicopter as he is airlifted to a Level III facility. Individual 

body armor should remain on the casualty for as long as there continues 

to be a realistic threat of further engagement by hostile ordnance. Image 

courtesy of Defense Imagery Management Operations Center (DIMOC).

Figure 9. Spinal immobilization applied during a training drill. Image 

courtesy of Defense Imagery Management Operations Center (DIMOC).
Fundamentals of Combat Casualty Care | 101

support in the setting of head trauma and seizures are important because the administration of 

benzodiazepines may hasten or exacerbate hypotension and ventilatory insufficiency. 

A final consideration in the tactical care of head injury patients is the potential need for neurosurgical 

intervention and the availability of such services within range of evacuation assets. The determination of 

whether to seek the nearest resuscitative surgical care versus overflight to more comprehensive medical 

treatment facilities is a complex decision. These decisions can be made by communicating with Level III 

careproviders, ideally prior to evacuation of the combat casualty. 

Hypothermia Prevention and Management

Hypothermia is recognized as an independent factor contributing to increased morbidity and mortality 

in trauma patients.86 In the combat casualty, hypothermia may occur due to prolonged prehospital time, 

cold fluid administration, environmental factors, and trauma-related bleeding and hypoperfusion. Arthurs 

et al. found that 18 percent of casualties presenting to a CSH in OIF were hypothermic (temperature 

less than 36 ̊C).87 Keeping a patient warm, especially early in tactical field care, will minimize subsequent 

hypothermia and resultant cold coagulopathy. This may be accomplished using passive external means, 

such as blankets, vehicle heating systems, hats and hoods to minimize heat loss from the head and scalp, and 

by ensuring that wet clothing or dressings are replaced. The recent fielding of the Hypothermia Prevention 

and Management Kit (HPMK®), which is composed of a disposable weather-resistant bag, insulating 

liner, chemical heat packet, and a heat-radiant cap, has capitalized on several effective field-expedient 

Figure 10. A US casualty being loaded onto a UH-60Q Black Hawk helicopter in Afghanistan. Note casualty is covered in a solar blanket. Image 

courtesy of Defense Imagery Management Operations Center (DIMOC).
102 | Fundamentals of Combat Casualty Care

treatments developed by tactical practitioners (Fig. 10). Many alternative hypothermia prevention devices 

exist (e.g.,Thermal Angel®, ChillBuster®, Blizzard Survival Blanket). 

The CCC provider should be cognizant of the relative temperatures of intravenous fluids being administered 

to casualties. Ideally, intravenous fluids are delivered at body temperature. Infusing cold fluids will hasten 

hypothermia and initiate cold coagulopathy. Potential tactical countermeasures include storage of small 

volume intravenous fluids on the body (in the axilla against the torso), field-expedient insulation of 

intravenous tubing using rolled paper or cloth, and placement of the intravenous infusion set along with the 

casualty in a sleeping bag or similar cover.

Infection Prophylaxis

It is a widely held belief in military medical circles that combat wounds are more likely to become infected 

than corresponding wounds occurring in the civilian sector setting. Gerhardt et al. presented data that both 

lent credence to this notion and also provided evidence in support of copious wound irrigation and systemic 

antibiotic prophylaxis of combat wounds in a population of subjects not requiring surgical intervention.88

In this study, infections developed within 48 hours in 7 percent of subjects receiving systemic antibiotic 

prophylaxis versus 40 percent without antibiotic prophylaxis. Infections developed within 48 hours in 4.5 

percent of cases undergoing wound irrigation versus 55 percent of cases that did not undergo irrigation. 

Further analysis demonstrated that the lowest infection rates were associated with the combination of 

systemic antibiotic prophylaxis and irrigation. The high frequency of complex combat wounds, delays in 

evacuation to definitive care, and the logistical difficulty associated with irrigation at the point of injury 

support the current TCCC guideline encouraging early systemic antibiotic prophylaxis after wounding 

through the use of combat pill packs on the battlefield.10

Evidence supports the use of systemic antibiotic prophylaxis and copious wound irrigation in the 

management of combat wounds.

Tactical Combat Casualty Care recommendations for systemic antibiotic prophylaxis include moxifloxacin 

(400 milligrams by mouth once daily) for patients who are able to tolerate oral administration, or intravenous 

cefotetan (2 grams every 12 hours) or ertapenam (1 gram intravenously or intramuscularly once daily).10

Of note, the author (RG) has utilized oral levofloxacin or intramuscular/intravenous ceftriaxone to good 

effect. An additional factor in favor of these latter antibiotics is the widespread availability of these agents 

throughout the current battlespace. 

Pain Management

Despite decades of dogma to the contrary, numerous studies have demonstrated that the judicious use of 

analgesic agents does not significantly alter the physical examination or impede medical diagnosis.89 The 

timely and adequate relief of pain is both humane and often the only effective treatment that may be 

offered to a casualty.83 In addition, recent evidence supports the contention that the failure to address acute 

pain in the setting of combat wounds may increase the incidence of both post-traumatic stress disorder and 

chronic regional pain syndromes.90,91 

Use of analgesics does not significantly alter physical examination or medical diagnosis.
Fundamentals of Combat Casualty Care | 103

In the setting of mild, particularly musculoskeletal injuries, a nonsteroidal antiinflammatory drug 

(NSAID) may be administered. For more severe wounds, or if a NSAID fails to provide adequate relief, 

opioid analgesics (e.g., morphine sulfate) provide potent acute analgesia. Intramuscular use of opiates is 

discouraged, due to unpredictability of absorption and bioavailability. Oral or intravenous preparations 

are recommended. As of this writing, oral transmucosal fentanyl citrate (OTFC) is emerging as a potential 

solution for tactical analgesia (800 micrograms transbuccally). Although this is an off-label use of this 

medication and the Food and Drug Administration (FDA) has issued a black box warning that states that 

oral transmucosal fentanyl citrate should not be used except for breakthrough pain in opioid-tolerant 

patients, this medication has been used safely in combat.92 Current TCCC recommendations for combat 

pill packs include meloxicam (15 milligrams by mouth once daily). Meloxicam was selected due to its lack 

of a sulfa moiety, which could prove hazardous in cases of sulfa-allergic casualties.10

Air Medical Evacuation Considerations

Air medical transport can adversely affect medical conditions characterized by gas trapped in a fixed space 

such as untreated pneumothorax. Lower ambient atmospheric pressures at altitude cause intrapleural gas 

to expand with a resultant increased compression of the heart and contralateral lung. The practical effect 

of Boyle’s law (P1V1=P2V2 ; P denotes the pressure of the system, and V denotes the volume of the gas) 

on a casualty with an untreated simple pneumothorax undergoing air evacuation via an unpressurized 

compartment is development of a tension pneumothorax after ascent to altitude. The same may be said 

for other trapped-gas clinical conditions. As a result, it is recommended that patients suspected or known 

to have a pneumothorax receive decompression of the affected anatomical space prior to transport.83 If 

decompression is not performed, evacuation should be conducted via routes that minimize elevation within 

the confines of the tactical situation. Although little scientific evidence exists for such cases, avoiding ascent 

to altitudes in excess of 5,000 feet above mean sea level has been recommended.93 In cases where a unit is 

operating in alpine terrain (routinely above 5,000 feet mean sea level), the authors’ recommend minimizing 

further ascent, to the extent possible. Air medical transport-related barometric complications also include 

pneumocephalus, pneumoperitoneum, and overexpansion of endotracheal and Foley catheter tube cuffs 

filled with air.83 Endotracheal tube and Foley catheter cuffs should be filled with crystalloid solutions or 

sterile water prior to evacuation, mitigating the risk of cuff overexpansion. Occlusive dressings covering 

thoracic puncture wounds should be checked periodically while en route and should be vented as clinically 

indicated. 

Tactical Evacuation Care

Once casualties arrive at a company combat casualty collection point or equivalent element, evacuation 

becomes the responsibility of the gaining medical unit. As such, each Battalion Aid Station is equipped 

with an ambulance squad and charged with transport of casualties from casualty collection point to 

Battalion Aid Station. Likewise, each Brigade Support Medical Company (BSMC) possesses ambulance 

platoons to transport patients from the Battalion Aid Station to the Brigade Support Medical Company 

and to coordinate ambulance exchange points in settings where distances or terrain separating medical 

treatment facilities are prohibitive. In addition to these unit-level assets, combat divisions possess Medical 

Companies (Air Ambulance), more commonly known as MEDEVAC units. These units are often allocated 

to subordinate medical units, or staged at Level III facilities such as CSHs. 

There will be circumstances when the evacuation capabilities of maneuver units are temporarily 
104 | Fundamentals of Combat Casualty Care

overwhelmed. It is under these circumstances that nonstandard vehicles may be employed for casualty 

evacuation. While often necessary in mass-casualty-incidents, this form of transportation should be 

considered a last resort. This is because of the relative difficulty involved in adequately securing patients 

for transport and the probable lack of en-route-care resulting from the absence of medics assigned to the 

casualty evacuation (CASEVAC) vehicles.

After initial triage and stabilization, casualties in 

the tactical setting are categorized for evacuation.83

Traditionally, the primary objectives of air 

medical evacuation have been speed and access. 

While quantitative data are lacking, the transport 

time interval between point of injury to damage 

control resuscitation and damage control surgery is 

perceived as critical to the survival of combat 

casualties in OEF and OIF. Designated MEDEVAC 

precedence categories (urgent, urgent surgical, 

priority, routine, and convenience) are used to 

determine evacuation priorities and should not 

be confused with US/NATO mass casualty triage 

categories (immediate, delayed, minimal, expectant, 

and urgent surgical) (Fig. 11).

The transport time interval between point of injury to damage control resuscitation and damage control 

surgery is critical to the survival of combat casualties in OEF and OIF.

The urgent evacuation category is reserved primarily for casualties requiring immediate care who should be 

evacuated within a maximum time interval of one hour. An urgent surgical subcategory exists for casualties 

deemed to be at the greatest severity who require rapid evacuation for lifesaving surgical interventions to 

prevent death. Under current US and Coalition doctrine, urgent patients receive MEDEVAC if weather and 

tactical conditions allow. Priority evacuation is conducted mainly for delayed category casualties requiring 

transport to higher level care within four hours in order to avoid deterioration to an urgent condition or to 

avoid undue pain or disability. This category usually is transported via ground assets, although air transport 

may be used under some conditions. Routine evacuation is reserved for casualties triaged as minimally 

injured, and generally is performed by standard ground or waterborne assets within 24 hours of the initial 

event. Convenience denotes cases where medical evacuation is performed for convenience rather than 

necessity. It is worth noting that a recent requirement placed by the Office of the Secretary of Defense now 

mandates a one-hour evacuation for urgent casualties.

Figure 11. A severely wounded service member aboard an HC-130P 

Hercules aircraft flying over Afghanistan en route to a CSH. Image 

courtesy of Defense Imagery Management Operations Center (DIMOC).

Figure 12. Evacuation chain for combat casualties.

Echelon I Echelon II Echelon III Echelon IV Echelon V

Self-aid, 

buddy-aid, 

medic,

Battalion Aid 

Station

Forward 

Surgical Team

Combat

Support 

Hospital

Landstuhl,

Germany

CONUS

Facility
Fundamentals of Combat Casualty Care | 105

Another challenge to the evacuation system is the 

ability to deliver effective, advanced en-route-care 

(Fig. 12). Traditionally, MEDEVAC platforms have 

been staffed with combat medics or their sisterservice counterparts. Training and experience 

levels vary widely, as does the capability to provide 

or continue advanced lifesaving interventions such 

as ventilatory, circulatory, or pharmacological 

support.94,95 Given the limited scope of practice of 

Army flight medics who staff MEDEVAC aircraft, 

the need to augment the MEDEVAC crew with an 

advanced practice medic or credentialed provider 

should be anticipated if critically injured patients 

will be transported.94,95

The US military refers collectively to the effects 

of the operational milieu as mission, equipment, 

terrain and weather, time, troops (both US and 

enemy combatants), and civilians (METT-TC) 

on the battlefield.96 All of these factors possess the 

potential to impact, either positively or negatively, 

an evacuation plan. Combat casualty careproviders 

must be aware of these issues as they affect both tactical and medical operations. Operational areas may 

be broad and deep, resulting in significantly greater distances required for evacuation. These conditions 

compound the standard risks inherent in tactical evacuation and en-route-care. As a result, evacuation 

planning and coordination among first responders, destination facilities, evacuation assets, and maneuver 

elements become critical for mission success and casualty survival.

Important time-distance considerations in casualty evacuation and en-route-care include:

1. Location, number, and type of elements supported 

2. Their internal (organic) medical support and evacuation assets 

3. Location of echelon II and III combat health support units in your respective Area of Responsibility 

(AOR)

4. Terrain features affecting potential evacuation routes

5. Analysis of adversary locations, capabilities and limitations, and prior conduct toward noncombatant 

medical units

6. US or Coalition maneuver and support elements available to escort or otherwise assist the evacuation 

mission

7. Friendly evacuation assets available to you, including dedicated medical evacuation vehicles and aircraft, 

nonstandard vehicles, potential crew members, and nonmedical attendants

8. Your source of launch authority

The METT-TC information forthcoming from the requesting unit is most readily obtained by receipt 

of a standard MEDEVAC request, usually composed in a nine-line format. An example of a standard 

MEDEVAC request appears in Table 2. 

Figure 13. A US casualty with a neck injury is loaded onto a UH-60 

Black Hawk MEDEVAC helicopter at a landing zone in Camp Victory, 

Iraq. Image courtesy of Defense Imagery Management Operations Center 

(DIMOC).
106 | Fundamentals of Combat Casualty Care

Nato Nine-Line Medevac Request

1. Location of landing zone (LZ) for casualty collection (eight digit MGRS grid coordinates) 

2. Radiofrequency, call sign, and suffix of requesting element

3. Number of patients by precedence: 

A - Urgent

B - Urgent surgical

C - Priority

D - Routine

E - Convenience

4. Special equipment required:

A - None

B - Hoist

C - Extrication equipment

D - Ventilator

E - Other (specify)

5. Number of casualties by type

A - Litter

B - Ambulatory

C - Escort

6. Security at LZ / pick-up site

N - No enemy troops in area

P - Possible enemy troops – approach with caution

E - Enemy troops in area

X - Enemy troops in area – armed escort required

7. Method of marking LZ* / pick-up site

A - Panels (VS-17 or similar)

B - Pyrotechnic

C - Smoke

D - None

E - Other (specify)

*Methods may be listed by local tactical standard operating procedures

8. Casualty nationality and status

A - Coalition military

B - Coalition civilian

C - Non-Coalition forces

D - Non-Coalition civilian

E - Opposing forces detainee

F - Child

9. Pick-up zone terrain obstacles

Table 2. NATO nine-line MEDEVAC request.
Fundamentals of Combat Casualty Care | 107

Air medical evacuation is the primary method for urgent and urgent surgical casualties, and may be 

appropriate for priority casualties (Fig. 13). The decision to employ MEDEVAC support is complicated by 

many variables and must take into account the vulnerability of rotary wing aircraft to virtually any modern 

weapons system.83 This risk is amplified in urban terrain or mountains where flight paths and landing 

zones often intersect closely with terrain features of similar or greater elevation, providing optimal battle 

positions to engage the aircraft with hostile fire. A sobering thought to be considered by anyone requesting 

MEDEVAC is the possibility that both the casualty and the MEDEVAC crew might perish as the result 

of hostile fire or marginal flight conditions.83 As such, these resources should be used carefully, and the 

decision to employ MEDEVAC should be made with input by competent clinical and tactical operators 

with a minimum of emotion. Appropriate indications for air medical evacuation are outlined in Table 3.

Health Services Support (HSS): Echelons, Levels, and Roles of Care

Nearly two decades after the end of the Cold War the US and its Allies are facing new and emerging 

threats. Military operations are often conducted in an expeditionary fashion employing minimal permanent 

footprints in host or target nations and often involve nonpermissive or forced initial entry operations. The 

physical environment for most current conflicts has shifted from remote to urban. Emphasis has also shifted 

from major theater wars to full-spectrum operations, including simultaneous combat and stability and 

peacekeeping operations. Retired Marine Corps General Charles Krulak summarized this concept as “the 

Three Block War.” 97,98 New paradigms have been developed for defining, identifying, and mitigating threats 

to the US and its Allies.98

Traditionally, the US Army divided CCC and evacuation into five levels corresponding to the command 

and control echelons of the battlespace (Fig. 12). Echelons I to III compose the combat zone, while echelon 

IV consists of the communications zone, and echelon V is the zone of the interior, or US Homeland. The 

medical care delivered at each echelon of the battlefield is referred to as respective levels of care. Thus, 

at echelon I (unit level), one would encounter Level I medical care, comprising self- and buddy-aid, initial 

treatment by a combat lifesaver, and emergency medical treatment by a healthcare specialist (known more 

commonly as a combat medic). In most cases, Level I care also encompasses company casualty collection 

points and Battalion Aid Station care. Doctrinally, the evacuation of casualties from the Battlefield Aid 

Stations would progress to echelon II (division level), with its corresponding Level II care, which focuses 

primarily at the Brigade Support Medical Company. Level II care includes advanced trauma management 

Indications for Air Medical Evacuation

1. Casualties meeting criteria for urgent evacuation (loss of life, limb, or eyesight within two hours)

2. Casualties meeting priority evacuation criteria, but for whom other means of evacuation will cause 

deterioration

3. Circumstances in which the organic (internal) medical capabilities of the supported unit have been 

rendered ineffective (e.g., mass-casualty-incident, medical element neutralized by hostile action)

4. Risk of loss of evacuation aircraft and air crew is considered manageable by launch authority

Table 3. Indications for air medical evacuation.
108 | Fundamentals of Combat Casualty Care

by physicians and physician assistants. Level II facilities are equipped with limited plain radiography and 

laboratory services and, in some instances, may be supplied with blood products for emergency transfusion. In 

addition, the Brigade Support Medical Company is also the primary site of attachment for Forward Surgical 

Teams (FSTs), which are capable of conducting forward resuscitative surgical interventions aimed primarily 

at hemostasis of non-compressible hemorrhage, such as intraabdominal or intrathoracic wounds. 

Traditionally, the US Army divided CCC and evacuation into five levels corresponding to the command 

and control echelons of the battlespace. The medical care delivered at each echelon of the battlefield is 

referred to as respective levels of care.

While the traditional system describes Army CCC 

doctrine, the Navy and Marine Corps possess 

additional out-of-hospital units. These include 

Forward Surgical Companies, Forward Resuscitative 

Surgical Systems (FRSS), and Shock Trauma 

Platoons (STP) (Fig. 14). The Forward Resuscitative 

Surgical Systems share some similarities with the 

Army Forward Surgical Teams but have several 

notable differences, including self-sustainability 

and the assignment of an emergency physician to 

the unit. The Shock Trauma Platoons consist of 

two emergency physicians, physician assistants, an 

emergency nurse, and several medical corpsmen 

(the Navy equivalent of the combat medic). Both 

the Forward Resuscitative Surgical Systems and 

Shock Trauma Platoons are capable of augmenting 

a Battalion Aid Station or Brigade Support Medical Company in mass-casualty circumstances, such as 

might be expected during an amphibious assault or vertical envelopment (helicopter or Vertical Take-Off 

and Landing [VTOL]) entry operation.99 The Forward Resuscitative Surgical Systems and Shock Trauma 

Platoons may also be combined into a hybrid entity known as a Surgical Shock Trauma Platoon (SSTP), 

representing perhaps the most robust forward medical capability within the Department of Defense. Lastly, 

the Air Force maintains Mobile Field Surgical Teams (MFST) as part of its modular Expeditionary Medical 

System (EMEDS), possessing resuscitative surgical capability, emergency care, and a preventive medicine 

cell (Fig. 15).100

If required, evacuation continues to echelon III (corps level), where the Level III Army CSHs, Navy 

Expeditionary Medical Facilities (EMF), and Air Force Theater Hospitals (AFTH) conduct both resuscitative 

and definitive surgery to save life, limb, and eyesight. If more complex surgical intervention or prolonged 

convalescence is required, casualties may be evacuated to echelon IV (communications zone level), where 

regional medical centers provide Level IV tertiary care and convalescence for up to two weeks. These 

facilities are currently located in Germany and Hawaii. The most severely injured, requiring extensive 

rehabilitation and convalescent care, are evacuated to echelon V (zone of interior or continental US). 

Here they receive Level V care at Army, Navy, and Air Force medical centers, and in the event of medical 

discharge, at Department of Veterans Affairs medical facilities.

Figure 14. Medical care at a Forward Resuscitative Surgical System.

Image courtesy of Harold Bohman, MD, CAPT, MC, US Navy.
Fundamentals of Combat Casualty Care | 109

This complex description of echelons of the battlefield and levels of health care has recently undergone 

further revision in order to meet North Atlantic Treaty Organization (NATO) standards.101 Utilizing Roles 

of Care, the NATO system simplifies the levels of care based upon the availability and sophistication of 

surgical intervention. Under the NATO system, Role I medical treatment encompasses out-of-hospital 

and presurgical care analogous to Level I and Level II (absent forward surgical attachments). Role II also 

encompasses out-of-hospital care but incorporates forward resuscitative surgical capability and advanced 

resuscitative techniques, thus requiring the presence of a Forward Surgical Team, Forward Resuscitative 

Surgical System, or Mobile Field Surgical Team. Role III represents theater hospitalization, correlating 

directly to Level III. Finally, in the NATO system, Levels IV and V are combined into Role IV, representing 

continued surgical, recuperative, and rehabilitative care outside of the combat zone.

Mass-Casualty-Incident Management

US and NATO Military Mass-Casualty Triage Systems

In US military parlance, a mass-casualty-incident is defined as a casualty-producing event that overwhelms 

the existing medical capacity of the receiving facility or of the unit providing medical support in the outFigure 15. Attributes of Echelon I/II combat health support (CHS) units in branches of the US military.
110 | Fundamentals of Combat Casualty Care

of-hospital setting. After initial collection, sorties of casualties who arrive in numbers sufficient to initially 

overwhelm the treatment and evacuation resources are triaged for priority of treatment (Fig. 16). The 

US military mass-casualty triage process comprises immediate, delayed, minimal, expectant, and urgent 

surgical categories. This is similar to the NATO triage system, which is partly based upon Medical 

Emergency Triage Tags (METTAG) methodology. Unlike METTAG, the US/NATO system adds a fifth 

urgent surgical category, which has been used to describe surgical patients who need an operation but can 

wait a few hours. It is important to note that urgent surgical patients who receive the appropriate initial 

categorization (e.g., urgent surgical) and intervention may be sufficiently stabilized and retriaged to a lower 

subsequent category (e.g., delayed). This US/NATO triage categorization should not be confused with 

MEDEVAC precedence categories (urgent, urgent surgical, priority, routine, and convenience) that are 

used to determine evacuation priorities.102

Similar to the NATO triage system, the US military mass-casualty triage process comprises immediate, 

delayed, minimal, expectant, and urgent surgical categories.

Beekley et al. recorded a series of “lessons learned” in mass-casualty triage conducted at surgical facilities 

in Iraq, which may have some application in the out-of-hospital setting.103 They included the observation 

that the requirement to perform triage in close proximity to the medical treatment facility can complicate 

the process. Likewise, the type of evacuation platform upon which casualties arrive may adversely affect 

the triage process. While Beekley et al. may have been referring to variation in numbers of casualties-persortie, what is of equal import is that the arrival of large sorties of casualties in high-capacity conveyances 

(such as flatbed trucks and buses) generally equates to a relative lack of en-route-care and minimal casualty 

triage. Beekley et al. also emphasized the importance of retriaging at progressive treatment sites as well 

as after time elapses, particularly in situations where significant delays in access to surgical intervention 

may occur. Lastly, Beekley et al.’s observations regarding the utility of focused abdominal sonography 

in trauma (FAST) as a triage tool resonated with similar anecdotal experiences by forward practitioners. 

While ultrasound use near point of injury is logistically and tactically undesirable, it has been successfully 

employed at Battalion Aid Stations, casualty collection points, and MEDEVAC landing zones, particularly 

in cases of prolonged delays in evacuation. In addition to traditional FAST applications, McNeil et 

al.104 employed ultrasound for assessment of long-bone fractures. Potential additional uses include ocular 

assessment for intracranial pressure elevation, thoracic ultrasound for pneumothorax, and vascular 

assessments for diagnosis and access (Fig. 17).

Figure 16. Multiple-casualty-incident at a Level III facility. Figure 17. Use of portable ultrasonography at a Level III facility. 
Fundamentals of Combat Casualty Care | 111

The authors’ practical experience with current NATO triage methodology has been satisfactory, but 

its effectiveness is dependent upon the practitioner being facile with the common types of injuries and 

associated respective triage categories. Anecdotal reports from the field indicate that many CCC providers, 

and in particular those with less clinical experience, tend to overtriage patients. Alternatively, overtriage 

may arise from the desire to not underestimate a casualty’s injuries or from personal motivation to secure 

expeditious evacuation for patients who are acquaintances or close personal friends. While laudable, this 

practice should be avoided as it poses the potential to deplete limited MEDEVAC resources and may place 

MEDEVAC crews and aircraft in excessive danger for what might amount to relatively minor and otherwise 

survivable injuries.

Alternative Mass-Casualty Triage Systems

Alternatives to the US/ NATO and METTAG systems include but are not limited to the Simple Triage And 

Rapid Treatment (START®) triage system, the International Committee for the Red Cross (ICRC) method, 

and the Sort, Assess, Lifesaving Interventions, Triage/Treat/Transport (SALT) system. The START® 

methodology incorporates a very brief assessment (spontaneous respiration, presence of peripheral pulses, level 

of consciousness) and simple interventions (noninvasive airway maneuvers, tourniquets) to triage casualties 

into one of five color-coded categories: immediate (red), delayed (yellow), minimal (green), expectant/

salvageable (blue), and expectant/unsalvageable (black). The blue category represents casualties who might be 

saved, but who require such intense resource allocation that they would likely cause the death of other more 

salvageable casualties due to neglect. It is theorized that this additional category may provide a better means 

of staging expectant patients for care once resources become available; in addition, it may ease the process of 

triaging casualties to expectant status, as at least semantically, the blue category differs from the black category.

The ICRC system reflects the austerity and remoteness often encountered by ICRC personnel, as well as the 

limitations of healthcare systems in many developing countries. While the ICRC recognizes and references 

a METTAG variant (immediate, delayed, minimal, expectant), they have also employed a simpler, twotiered system for settings where no surgical care is available locally. This methodology simply divides 

casualties by the determination of whether they require surgical intervention. Those needing surgery and 

who are anticipated to survive a journey are transported to the nearest available surgical facility, while 

nonsurgical and expectant casualties are provided care by existing local resources. 

Most recently, the US Centers for Disease Control and Prevention convened an expert consensus panel to 

develop an optimized mass-casualty triage scheme.105 The resulting product, referred to as the SALT system 

(Sort, Assess, Lifesaving Interventions, Triage/Treat/Transport), provides a model for a standardized, allhazards model for triage. The model also integrates adult, child, and special populations into the single 

protocol. If implemented widely, it possesses the potential to improve interoperability and standardization 

of triage. Trials of relative efficacy and accuracy, along with the international community’s response to 

this method, remain to be observed before recommendations regarding adoption of the SALT system for 

tactical medical use may be offered.

Reprise and Conclusion of Case Study 

While the team is packaging the casualties for tactical evacuation, the medical officer observes, acquires, 
112 | Fundamentals of Combat Casualty Care

and engages the RPG gunner with small-arms fire, neutralizing him. The remaining insurgents disengage 

after receiving fire from the convoy’s crew-served weapons (M-2 heavy machine guns). Hasty tourniquets 

are applied to bleeding extremity wounds on both casualties, followed by performance of rapid secondary 

surveys. Both casualties possess patent airways and are conscious. The casualty with blunt thoracic trauma 

has clinical signs of multiple rib fractures, but no flail segment is present, there is no jugular venous 

distention, the trachea is midline, and the affected hemithorax is resonant upon percussion. The casualties 

are loaded into an operating HMMWV escorted by the medical officer. After hastily attaching the disabled 

HMMWV to an operating vehicle via a tow rope, the convoy proceeds at top speed to the nearest forward 

operating base where the casualties are further stabilized. On arrival at the Battalion Aid Station, the staff 

radios a nine-line MEDEVAC request. The casualty with the isolated penetrating wound to the forearm 

receives a hemostatic dressing and direct pressure, which provides adequate hemostasis. The other casualty 

receives a tube thoracostomy, with approximately 30 milliliters of blood drained after placement. Both 

receive intravenous morphine and ceftriaxone, and both are packaged on stretchers with warm blankets. 

Tactical Combat Casualty Care casualty cards (DA Form 7656) are prepared and appended with clinical 

and treatment data. Subsequently, they undergo air MEDEVAC to a CSH. Both survive, are evacuated to 

the continental US, and eventually return to duty with their unit prior to rotation home.

Future Directions

The practice of out-of-hospital CCC is poised for dramatic change. Senior military leadership, military 

medical thought leaders, and combat casualty researchers have arrived at a collective agreement that the 

out-of-hospital phase of care (Roles I and II) is the place where the next “great leap” in casualty survival 

will be realized. Innovations in technology, training, medical direction, and communications will occur. 

Future solutions may include field-deployable blood components and procoagulants designed to prevent 

or mitigate traumatic coagulopathy and improve tissue oxygenation. These first steps toward a system 

of remote damage control resuscitation hold great promise and may decrease prehospital mortality and 

postoperative multiorgan system failure. The development of tactical medical information systems is an 

area of intense focus. The eventual goal is reliably capturing out-of-hospital physiologic and therapeutic 

data. This data will improve training and support of CCC providers, as well as help to define future 

research agendas. Perhaps most exciting is the potential for developing integrated and graduated out-ofhospital CCC. This would combine professional medical oversight and real-time decision support with 

skilled resuscitation teams and critical care air transport capability for MEDEVAC units. While integration 

and implementation of this “Combat EMS System” will prove challenging, the successes of past and 

current CCC providers – coupled with the aforementioned research and development foci – may set the 

conditions for this “next great leap.”
Fundamentals of Combat Casualty Care | 113

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1):S25-34. 
Chapter 4

DAMAGE CONTROL

RESUSCITATION

Contributing Authors

Jeremy G. Perkins, MD, FACP, LTC, MC, US Army

 Alec C. Beekley, MD, FACS, LTC, MC, US Army
All figures and tables included in this chapter have been used with permission from Pelagique, LLC, the 

UCLA Center for International Medicine, and/or the authors, unless otherwise noted.

Disclaimer

The opinions and views expressed herein belong solely to those of the authors. They are not nor should 

they be implied as being endorsed by the United States Uniformed Services University of the Health 

Sciences, Department of the Army, Department of the Navy, Department of the Air Force, Department of 

Defense, or any other branch of the federal government.
Damage Control Resuscitation | 123

Table of Contents

Introduction........................................................................................................ 124

Damage Control Resuscitation: Lessons Learned .................................................... 126

Preventing the Need for Massive Transfusion .......................................................... 126

Hemorrhage Control Techniques.....................................................................................126

Tourniquets and Hemostatic Dressings ..........................................................................127

Preventing Hypothermia..................................................................................................130

Predicting the Need for Massive Transfusion .......................................................... 132

Mechanism of Injury........................................................................................................132

Bedside Clinical Findings.................................................................................................133

Laboratory Testing ...........................................................................................................134

Newer Technologies for Predicting the Need for Massive Transfusion..........................134

Transfusion of Blood Products .............................................................................. 135

Massive Blood Transfusion..............................................................................................135

Red Blood Cells.................................................................................................................135

Fresh Frozen Plasma ......................................................................................................136

Platelets.............................................................................................................................137

Fibrinogen ........................................................................................................................137

Fresh Whole Blood ..........................................................................................................137

Massive Transfusion-Associated Complications ...................................................... 138

Electrolyte Disorders........................................................................................................138

Massive Transfusion-Associated Coagulopathy..............................................................138

Damage Control Resuscitation Adjunctive Measures................................................ 140

Hypotensive Resuscitation .............................................................................................140

Optimal Use of Crystalloid and Colloid Solutions ..........................................................142

Vasoactive Agents .............................................................................................................143

Nonsurgical Hemostatic Agents .......................................................................................143

Topical Sealants ...............................................................................................................143

Recombinant Factor VIIa ................................................................................................143

Antifibrinolytics..................................................................................................................144

Conclusions ........................................................................................................ 144

References .......................................................................................................... 145
124 | Damage Control Resuscitation

Introduction

Hemorrhage accounts for 30 to 40 percent of all fatalities, second only to traumatic brain injury as a 

cause of death following trauma.1,2,3 Hemorrhagic death is the leading preventable cause of mortality 

in combat casualties and typically occurs within six to 24 hours of injury.4,5,6,7,8,9,10 Patients who die from 

hemorrhage enter a “vicious bloody cycle” characterized by the lethal triad of hypothermia, acidosis, and 

coagulopathy.11 

Hemorrhagic death is the leading preventable cause of mortality in combat casualties and typically occurs 

within six to 24 hours of injury. Causes of death from massive hemorrhage include compressible extremity 

hemorrhage (due to amputation or vascular injury), noncompressible proximal extremity hemorrhage 

(axillary or groin vascular injuries), and truncal hemorrhage (from solid organ, pelvic fracture, and thoracic 

injuries).

Damage control resuscitation (DCR) is a strategy that seeks to prevent or mitigate hypothermia, acidosis, 

and coagulopathy through combined treatment paradigms. Damage control resuscitation comprises 

early hemorrhage control, hypotensive resuscitation (permissive hypotension), hemostatic resuscitation 

(minimization of crystalloid fluids and fixed ratio blood product transfusion), prevention or alleviation 

of hypothermia (through warming measures), and amelioration of acidosis through judicious use of 

blood products and hemodynamic resuscitation endpoints.12,13,14,15,16 In short, the goal of DCR is to stop 

hemorrhage and prevent or reverse the three components of the lethal triad. 

The majority of trauma patients arriving at hospitals in both civilian and military settings will not require 

transfusion and are not coagulopathic on arrival. However, an important subset of severely injured casualties 

will manifest coagulopathy on arrival.17,18 These patients are more likely to require massive transfusion, 

defined as infusion of 10 or greater units of red blood cells (RBCs), in the first 24 hours following injury. 

Traumatic coagulopathy exacerbates bleeding from injury, and aggressive resuscitation can cause patients 

to spiral into the “bloody vicious cycle” in which coagulopathy leads to further hemorrhage and worsening 

Figure 1. The lethal triad.

Coagulopathy

Hypothermia

Metabolic

Acidosis
Damage Control Resuscitation | 125

acidosis, in turn prompting additional fluid resuscitation and transfusion (Fig. 1). Such resuscitation can 

then contribute to more profound coagulopathy resulting from hemodilution and hypothermia. When 

such coagulopathy is present, it is associated with increased mortality.17,18 Acidosis, hypothermia, and 

coagulopathy have been collectively termed the “lethal triad.”19

Massive transfusion is defined as infusion of 10 or greater units of RBCs in the first 24 hours after injury. 

Massive blood transfusion is infrequent in civilian trauma, occurring in only 2 to 13 percent of trauma 

admissions. Due to a higher rate of penetrating injury in combat casualties, massive transfusion occurred 

in approximately 8 percent of OIF casualties.

Causes of death from massive hemorrhage include compressible extremity hemorrhage (due to amputation 

or vascular injury), noncompressible proximal extremity hemorrhage (axillary or groin vascular injuries), 

and truncal hemorrhage (from solid organ, pelvic fracture, and thoracic injuries).5

 Patients with the 

aforementioned injuries may benefit from DCR in parallel with damage control surgical management.5 Both 

damage control strategies are used to treat the acute traumatic problems of hemorrhage and coagulopathy. 

They are intended to prevent the complications that can occur following extensive operations and infusion 

of large volumes of fluids and blood products. 

DCR Lessons Learned in OEF and OIF as of 2010

• Rapid control of compressible hemorrhage should be initiated with direct pressure, tourniquets, or 

hemostatic dressings.

• There should be rapid identification and surgical control of noncompressible and major vascular 

hemorrhage sites.

• The use of crystalloid and colloid solutions should be minimized in hemodynamically stable 

patients.

• Patients requiring DCR should be identified early using rapid bedside measures or tests. 

• The early delivery of plasma and platelet transfusion in fixed ratios to red blood cells approaching 

1:1:1 should be considered.

• Until surgical control of bleeding has been achieved, continued transfusion should be based primarily 

on the clinical condition of the patient rather than on laboratory values. 

• Advanced bedside coagulation studies (e.g., thromboelastography) are available at some Level III care 

facilities and may provide better guides to a patient’s blood product needs than standard laboratory 

values such as prothrombin time (PT) and activated partial thromboplastin time (aPTT).

• The use of low-dose vasopressin and other vasopressors as an adjunct to DCR is a treatment option 

that requires further validation.

• Adjuncts for control of nonsurgical bleeding (e.g., recombinant factor VIIa or antifibrinolytics) can be 

considered but remain controversial.

• Damage control resuscitation can be terminated once clinical hemorrhage is controlled and validated 

endpoints of resuscitation, such as clearance of serum lactate or base deficit, have been achieved. 

Table 1. DCR lessons learned in OEF and OIF.
126 | Damage Control Resuscitation

Damage Control Resuscitation: Lessons Learned

This chapter will address the key components of DCR, including: (1) preventing the need for massive 

transfusion through external hemorrhage control to prevent exsanguination; (2) predicting the need 

for massive transfusion of blood products; (3) current recommendations for massive transfusion and 

management of the anticipated complications; and (4) adjuncts to resuscitation and transfusion that are 

frequently employed in damage control settings. An overview of DCR lessons learned over the course of 

Operation Enduring Freedom (OEF) and Operation Iraqi Freedom (OIF) is provided in Table 1.

Preventing the Need for Massive Transfusion

Ideally, traumatic hemorrhage is controlled prior to hemodynamic compromise resulting from 

exsanguination. A series of preventive measures and prehospital treatment techniques have been instituted 

in both military and civilian trauma settings to rapidly control hemorrhage. The tools and techniques 

discussed below may prevent or slow ongoing blood loss, decrease the number of blood products required, 

and ultimately prevent unnecessary deaths.

Hemorrhage Control Techniques

Hemorrhage sites are either anatomically compressible and amenable to tourniquet control, compressible but 

not amenable to tourniquet control (e.g., axillary or groin vascular injuries), or completely noncompressible 

(e.g., truncal injuries) (Fig. 2). Patients with noncompressible hemorrhage sources should receive the 

highest priority for evacuation to a hospital, as there are few tools available to prehospital careproviders 

to manage such bleeding. Compressible hemorrhage sites are amenable to direct digital pressure, which 

can be instituted by first responders as the initial hemorrhage control intervention. Attempts to reinforce 

saturated dressings with large stacks of gauze or additional dressings (in lieu of manual compression) 

should be avoided, as this technique dissipates the pressure applied directly to the bleeding site and may 

delay identification of ongoing bleeding (Fig. 3).

Hemorrhage sites are either anatomically compressible and amenable to tourniquet control, compressible 

but not amenable to tourniquet control (e.g., axillary or groin vascular injuries), or completely 

noncompressible (e.g., truncal injuries). Tourniquet application, direct pressure, or hemostatic dressings 

applied to the wound site should be favored over pressure point control and extremity elevation for the 

initial control of hemorrhage. 

Direct pressure to arteries proximal to bleeding sites and elevation of the affected extremity above the level 

of the heart should be considered as second-line adjunctive hemorrhage control interventions, and they are 

not currently recommended for use by the Committee on Tactical Combat Casualty Care for any phases 

of care.20 Applying direct pressure to arteries proximal to the bleeding site may control arterial inflow, 

but it will not control venous hemorrhage. Associated injuries (e.g., fractures) and patient transportation 

considerations often make extremity elevation problematic. Hence, tourniquet application, direct pressure, 

or hemostatic dressings applied to the wound site should be favored over pressure point control and extremity 

elevation for the initial control of hemorrhage.21 
Damage Control Resuscitation | 127

Tourniquets and Hemostatic 

Dressings

The use of direct pressure to control hemorrhage is only a temporizing measure until a more secure and 

durable form of hemorrhage control can be employed. First responders often find it necessary to perform 

other tasks or treat other casualties; hence, modular tourniquets and hemostatic dressings have been 

developed to provide the first responder with alternative methods for hemorrhage control.

Historically, extremity tourniquets were a controversial method of last resort for extremity hemorrhage 

control.22,23 Extremity tourniquets are now used as a first-line therapy for the prehospital control of extremity 

hemorrhage for care-under-fire scenarios (Fig. 4).20 Expanded guidelines for tourniquet use, combined with 

a rapid evacuation system in OEF and OIF, have resulted in significant numbers of casualties arriving to 

surgical care with extremity tourniquets in place (Fig. 5). Multiple reports in the literature of tourniquet use in 

OEF and OIF have defined the characteristics and advantages of tourniquet use.16, 24,25,26,27,28 These include: 

(1) an average prehospital tourniquet time under six hours; (2) improved hemorrhage control upon patient 

arrival; (3) decreased incidence of shock in those casualties treated with tourniquets; (4) improved survival; 

and (5) acceptably low tourniquet-related complications. Tourniquets should be applied to exsanguinating 

extremities as soon as possible in care-under-fire scenarios.29 Additional information on tourniquets can be 

found in the Extremity Injury chapter. 

Figure 2. (Left) Potential sites for pressure point control of hemorrhage.

Figure 3. (Below) A combat casualty arriving at a Level III facility 

following a fragmentation injury from a blast. Note the saturated layers of 

gauze on this limb where no tourniquet or hemostatic agents was applied.

Wound of lower face (below eyes)

Wound of

lower arm

Wound

of thigh

Wound of

lower leg

Wound

of foot

Wound

of hand

Wound of lower part of

upper arm and elbow

Wound

of neck

Hemorrhage Pressure Points
128 | Damage Control Resuscitation

Figure 4. (Right) The Combat Application Tourniquet® is a onehanded tourniquet that uses a self-adhering band to fit a wide range of 

extremities. It incorporates a windlass system that locks into place. Image 

courtesy of North American Rescue, LLC.

Figure 5. (Below) A combat casualty who sustained bilateral lower 

extremity injuries from an improvised explosive device (IED) blast with 

right-sided tourniquet in place.
Damage Control Resuscitation | 129

Extremity tourniquets are used as a first-line therapy for the prehospital control of extremity hemorrhage 

in care-under-fire scenarios. If used before onset of shock, there is 90 percent improved survival relative 

to use after onset of shock. Hemostatic dressings and agents are used with increased frequency, as both 

primary hemorrhage control measures for wounds not amenable to tourniquet control or as adjuncts to 

tourniquet use.

Similarly, hemostatic dressings and agents are now deployed and used with increasing frequency as both 

primary hemorrhage control measures for wounds not amenable to tourniquet control or as adjuncts to 

tourniquet use.20,21 Animal research demonstrates the superiority of dressings such as the fibrin-impregnated 

bandage (produced by the American Red Cross) and chitosan dressings over standard gauze.30 Another 

agent, granular zeolite [QuikClot® (Z-Medica; Wallingford, CT)], a microporous crystalline aluminosilicate 

hemostatic agent, is Food and Drug Administration (FDA) approved for hemostasis of external wounds 

(Fig. 6). Granular zeolite has been fielded by the United States (US) Marine Corps and US Army during 

OEF and OIF with some success.31,32 Limitations of granular zeolite include an exothermic reaction that 

can cause burns, and the time-consuming removal of granules from wounds. The potential utility of these 

dressings has been supported by early clinical reports from OEF and OIF.31,33 

Figure 6. This Iraqi civilian was injured by a blast fragment. The blast fragment caused a through-and-through injury to the proximal left arm causing 

hemorrhage that was not amenable to tourniquet use. Hemorrhage was controlled with QuikClot®. Image courtesy of Harold Bohman, MD, CAPT, 

MC, US Navy.
130 | Damage Control Resuscitation

The challenge of developing and fielding newer 

generations of bandages is illustrated by the recall 

of a granular combination of a smectite mineral 

and polymer in 2008 (WoundStatTM [TraumaCure, 

Inc; Bethesda, MD]) due to concerns over the risk 

of thrombosis and endothelial injury when applied 

to arteries. This agent had been tested by the US 

Army Institute of Surgical Research (USAISR) and 

had been shown to be more efficacious in treating 

animal models of arterial hemorrhage than currently 

deployed products.34 Combat GauzeTM (Z-Medica, 

Wallingford, CT) is composed of surgical gauze 

impregnated with kaolin (Fig. 7). This dressing has 

been shown to be extremely safe and effective in a 

lethal animal hemorrhage model.35 Combat GauzeTM 

is the current hemostatic dressing of choice for the 

military as recommended by the Committee on 

Tactical Combat Casualty Care.20 It is important to 

note that clinical experience with Combat GauzeTM 

is limited, and there are currently no publications on 

its use in humans. Further clinical experience with 

hemostatic agents and dressings will be required to 

fully define their clinical benefits and risks.

Preventing Hypothermia

Hypothermia is defined as mild when the core body temperature is 32°C to 35°C, moderate when the 

core body temperature is 28°C to 32°C, and severe when the core body temperature is below 28°C.36

Hypothermia is associated with an increased risk of uncontrolled bleeding and mortality in trauma 

patients.36,37 Severe trauma-related hypothermia has been associated with 100 percent mortality.38 Trauma 

patients in hemorrhagic shock have uncoupling of normal metabolic pathways, resulting in the loss of the 

ability to maintain temperature homeostasis. Factors such as cold or wet weather, prolonged extrication or 

scene time, intoxication, infusion of cold or room temperature fluids, and convective heat losses (e.g., open 

helicopter door during flight) can worsen hypothermia. Both civilian and military trauma centers have 

linked the presence of hypothermia on arrival to increased mortality.39,40,41 

Hypothermia in combat casualties was identified as a theater-wide trauma system challenge in OIF.42,43

Simple hypothermia prevention measures were disseminated to the combat medics on the battlefield. These 

measures included emphasis on external hemorrhage control as the first priority, limiting removal of clothing 

to areas of the body requiring treatment, wrapping casualties in wool or solar blankets, and using in-line 

fluid warmers such as the Thermal Angel® (Estill Medical Technologies, Inc., Dallas, Texas) (Fig. 8).

Figure 7. Combat GauzeTM, a kaolin-impregnated surgical gauze, is 

the current hemostatic dressing of choice. The gauze is tightly packed into 

the wound, then pressure is held directly over the bleeding source until 

hemorrhage stops. Image courtesy of Combat Medical SystemsTM.
Damage Control Resuscitation | 131

Prevention and treatment of hypothermia at initial care facilities include the use of standardized heat-loss 

prevention kits, forced-air warming blankets, fluid warmers and rapid infusers, maintenance of warmed 

trauma suites and operating rooms, and warm humidified ventilator circuits.

Measures to prevent and treat hypothermia at initial care facilities have included the use of standardized 

heat-loss prevention kits (e.g., solar blankets, heated blankets, and body bags), the use of forced-air warming 

blankets, the use of fluid warmers and rapid infusers, the maintenance of warmed trauma suites and 

operating rooms, and the use of warm humidified ventilator circuits (Fig. 9).15,44,45,46,47,48,49 Since institution 

of these performance improvement measures, the incidence of hypothermia in patients arriving at Combat 

Support Hospitals (CSHs) has fallen from 7 percent to below 1 percent.43 Since severe hypothermia has 

become a rarity in OEF and OIF, active core body rewarming measures, such as continuous arteriovenous 

rewarming and body cavity lavage of warmed fluids, are less frequently needed.50,51 While cardiopulmonary 

bypass may be used in extreme cases of hypothermia for controlled active rewarming in some civilian 

trauma centers, it is not available in Level III care facilities in Iraq or Afghanistan.

Figure 8. (Above) A combat casualty arriving at a Level III facility. 

Hypothermia prevention measures include wrapping the casualty in wool 

and solar blankets, and limited removal of clothing.

Figure 9. (Right) Active rewarming and stabilization of the patient in 

an intensive care unit (ICU) using a solar blanket, warmed fluids, and a 

warm humidified ventilator circuit. Image courtesy of the Borden Institute, 

Office of The Surgeon General, Washington, DC.
132 | Damage Control Resuscitation

Predicting the Need for Massive Transfusion

Despite marked advances in the prehospital management of hemorrhage, patients with noncompressible 

sources of bleeding will still arrive in the trauma bay with uncontrolled hemorrhage. Effective DCR often 

requires the early delivery of coagulation factors, soon after patient arrival to the resuscitation area.4 Since 

coagulation factor replacement is needed by only a small fraction of trauma patients, rapid identification 

of such patients is critical.4,52 Clinical and laboratory parameters are used to predict the need for massive 

transfusion in such patients.53 

Penetrating mechanisms of injury, particularly involving the trunk, predict the need for massive 

transfusion in combat casualties. Systemic hypotension is a useful and validated predictor for the need 

for both emergent intervention and transfusion in the arriving trauma patient.

Mechanism of Injury

Penetrating mechanisms, particularly involving the trunk, predict the need for massive transfusion in 

Figure 10. This host national was admitted to a CSH with hypotension and multiple fragment entry wounds to his chest and abdomen. This patient is 

at elevated risk for requiring massive transfusion. Image courtesy of the Borden Institute, Office of The Surgeon General, Washington, DC.
Damage Control Resuscitation | 133

combat casualties and for emergent intervention in civilian trauma patients (Fig. 10).52,54 This contrasts 

with blunt mechanisms of injury, which are poor predictors of the need for trauma team activation or 

emergent intervention.54,55 The presence of penetrating wounds in combat casualties is frequently obvious 

and dramatic, as with high-velocity penetrating abdominal wounds with associated evisceration, multiple 

proximal limb amputations, and penetrating buttock or pelvic wounds (Fig. 11). Combat casualty care (CCC) 

providers are usually able to visually appreciate the extent of tissue destruction and anticipate associated 

anatomic and physiologic derangements in such casualties. 

Bedside Clinical Findings

Heart rate alone is an insufficient predictor of the need for emergency interventions for management of 

hemorrhage.56 A core body temperature below 36°C (96°F) on arrival has been shown in both civilian and 

military trauma patients to be associated with worse outcomes.39,41,57 Furthermore, several investigators 

have correlated the presence of hypothermia with injury severity and the requirement for blood 

transfusion.58,59,60 

Systemic hypotension is a useful and validated predictor of the need for both emergent intervention and 

Figure 11. Host national who sustained a blast injury to his flank with traumatic evisceration. Image courtesy of the Borden Institute, Office of The 

Surgeon General, Washington, DC.
134 | Damage Control Resuscitation

transfusion in the arriving trauma patient.54,61,62,63 Systolic blood pressure has been combined with other 

variables to create trauma scores, such as the Revised Trauma Score (RTS).64,65,66,67 Although not perfect, 

these scores are superior to any single test alone and have emerged as useful and accurate predictors of 

mortality and the requirement for massive transfusion.68 Rapid manual bedside tests such as the radial 

pulse character and Glasgow Coma Scale (GCS) motor score have also been shown to predict the need for 

lifesaving interventions.69 In Holcomb’s study, trauma patients with a weak or absent radial pulse combined 

with an abnormal GCS verbal or motor score on arrival had an 88 percent probability of requiring a 

lifesaving intervention.69 On the basis of simplicity, rapidity, and relative accuracy, these techniques are 

helpful in both the prehospital and initial hospital management of trauma patients.69,70 

While hypotension historically has been defined as a systolic blood pressure (SBP) below 90 mm Hg, recently 

this value has been challenged. Eastridge and colleagues recently evaluated data from the National Trauma 

Data Bank and found that an admission SBP value below 110 mm Hg was associated with higher mortality 

rates.71 Every 10 mm Hg drop in SBP below 110 mm Hg was associated with a 4.8 percent increase in 

mortality, up to a maximum of 26 percent mortality at a systolic blood pressure of 60 mm Hg. The authors 

also noted that base deficits began to rise below a SBP of 118 mm Hg. These findings imply that some 

trauma patients may have systemic tissue hypoperfusion despite systolic blood pressures well above 90 mm 

Hg. 

Laboratory Testing

The role of clinical laboratory testing in predicting the need for massive transfusion remains in evolution. 

Admission labs associated with the need for massive transfusion include a base deficit greater than six,

an international normalized ratio (INR) of 1.5 or greater, and a hemoglobin value of less than 11 grams 

(g) per deciliter.52,72,73 In a more recent study, McLaughlin et al. found that a heart rate greater than 105 

beats per minute, a SBP less than 110 mm Hg, a pH value less than 7.25, and a hematocrit value of 

less than 32 percent were all independent predictors of massive transfusion in combat casualties.74 This 

preliminary study awaits further validation. Patients with any of these values, particularly in combination 

with hypotension, diminished GCS score, or obvious physical exam findings, should be considered for 

immediate transition from a standard resuscitation mode to a damage control resuscitation mode.63

Admission labs associated with the need for massive transfusion include a base deficit greater than six, an 

international normalized ratio of 1.5 or greater, and a hemoglobin value of less than 11 g per deciliter. 

Such laboratory tests are generally available at Level II facilities.

Laboratory tests generally available at Level II facilities (Forward Surgical Teams and Forward Resuscitative 

Surgical Systems) include arterial blood gas, complete blood count analysis, PT and INR. At Level III 

facilities, PT and INR are routinely available, and even thromboelastography is available at some CSHs 

in Iraq and Afghanistan. Thromboelastography provides real-time graphic evidence of clot formation in 

whole blood and may be a better method of detecting coagulopathy in trauma patients.75,76 

Newer Technologies for Predicting the Need for Massive Transfusion

The utility of novel applications of continuous, noninvasive monitors linked to computer software are 

under study as tools to provide an early warning of systemic hypoperfusion. These technologies include 

the measure of heart rate complexity, arterial pulse pressure, and tissue oxygenation as measured by near-
Damage Control Resuscitation | 135

infrared spectroscopy.77,78,79,80,81,82,83,84 Loss of heart rate variability has predicted the need for lifesaving 

interventions and increased mortality in trauma patients.85,86,87 Decreased tissue oxygen saturation detected 

by continuous near-infrared spectroscopy has predicted the development of multiple organ failure and the 

need for massive transfusion.88 While these technologies will not replace clinical judgment, they may add 

objective data to help careproviders maximize patient outcomes while minimizing resource utilization.

Transfusion of Blood Products

For most casualties, current resuscitation guidelines published in the American College of Surgeons 

Advanced Trauma Life Support (ATLS) course and elsewhere are sufficient for managing blood and fluid 

losses. However, the frequent need for massive transfusion of blood products in OEF and OIF has prompted 

critical reassessment of the appropriateness of these standard resuscitation and transfusion practices for 

this subset of casualties with exsanguinating hemorrhage. Military careproviders have found that massively 

bleeding patients may actually be harmed by standard approaches (Beekley A, MD, FACS, LTC, MC, US 

Army, personal communication, January 13, 2010). There is mounting evidence that these patients require 

an approach that begins treating all the physiologic derangements of massive blood loss as soon as possible 

after injury (Beekley A, MD, FACS, LTC, MC, US Army, personal communication, January 13, 2010). This 

realization has strongly influenced current damage control resuscitation practices, which are described in 

detail below.

Military careproviders have found that massively bleeding patients may be harmed by standard approaches 

to resuscitation. Such casualties require an approach that immediately treats all physiologic derangements 

associated with massive blood loss.

Massive Blood Transfusion

Massive blood transfusion requires extensive blood banking resources and is associated with high 

mortality.89,90,91,92,93,94 The most frequently used definition of massive transfusion is replacement of a patient’s 

entire blood volume or 10 or more units of blood transfused in 24 hours.95,96 Massive blood transfusion is 

infrequent in civilian trauma, occurring in only 2 to 13 percent of trauma admissions.93,97 Due to a higher 

rate of penetrating injury in combat casualties, massive transfusion occurred in approximately 8 percent of 

OIF admissions and in as many as 16 percent during the Vietnam War.98,99 

Resuscitation of exsanguinating patients is a challenging problem that is exacerbated when clear massive 

transfusion protocols have not been developed.100 Although many institutions have massive transfusion 

protocols in place, adherence to such guidelines requires strong collaboration and effective communication 

between providers in the emergency department, operating room, ICU, and blood bank.101 A study by 

Dente et al. demonstrated that the institution of a massive transfusion protocol in a civilian trauma center 

reduced early coagulopathy and decreased mortality in blunt trauma patients.102

Red Blood Cells

Patients requiring blood can safely receive uncrossmatched Type O blood until type-specific products are 

available.103,104,105 Although type-specific uncrossmatched blood has also been used successfully for massive 

transfusion, acute hemolytic reactions have been reported.106,107,108 
136 | Damage Control Resuscitation

Fresh Frozen Plasma 

Fresh frozen plasma (FFP) has been recognized as an important component in preventing and treating 

coagulopathy in trauma.14,109,110,111 A donor unit of whole blood (approximately 450 milliliters) is separated 

into several components, with the plasma comprising approximately 250 milliliters (ml) of the liquid 

portion of blood containing water, electrolytes, and proteins (and lacking red blood cells, leukocytes, 

and platelets) (Fig. 12). The plasma proteins include the major 

clotting factors and intrinsic anticoagulants. In addition to the 

coagulation factors, the plasma found in one unit of whole blood 

also contains approximately 500 milligrams (mg) of fibrinogen 

(approximately equal to the amount of fibrinogen found in two 

units of cryoprecipitate).112 While most clotting factors are stable 

at normal concentrations in plasma, some factors including 

factor V and factor VIII, termed labile factors, degrade over 

time; this degradation accelerates while plasma is stored in the 

liquid state (hence, why plasma is stored in a frozen state).

Transfusion of fixed ratios of FFP to RBCs has been proposed 

as a strategy to manage coagulopathy, particularly with rapid 

exsanguination and absent lab testing. Data from combat 

casualties in OIF support the use of plasma transfusion, showing 

a 65 percent mortality for patients who receive less than one unit 

of FFP for every four units of RBCs compared to a 19 percent 

mortality with more than one unit of FFP for every two units 

of RBCs.113 While the optimal FFP to RBC ratio is unknown, 

mathematical models for FFP transfusion have been developed 

that support clinical data, suggesting that a ratio of 2:3 to as high 

as 1:1 (units of FFP to RBC) would be appropriate.114,115 

The optimal FFP to RBC ratio is unknown. Both mathematical models and clinical data for FFP 

transfusion favor a ratio of 2:3 to as high as 1:1 (units of FFP to RBC).

It has been suggested that FFP should be transfused early in the resuscitation to prevent dilutional 

coagulopathy.73,94,96 Unfortunately, thawing of FFP is time-consuming, and patients often receive more blood 

or crystalloids in place of FFP, further exacerbating coagulopathy. Once patients have been stabilized, fixed 

FFP to RBC ratios are less critical, and standard transfusion strategies for plasma may be more appropriate. 

Standard transfusion criteria for plasma products include an INR greater than or equal to 1.5 or prolonged 

R-time on thromboelastography in the presence of active bleeding, or in a patient at high-risk for recurrent 

bleeding.75

All studies to date examining plasma, as well as other products including whole blood, platelets, and 

fibrinogen, have been retrospective and cannot be used to make definitive conclusions about the best care for 

trauma casualties. With retrospective analyses, there is the influence of survival bias that excludes patients 

dying quickly before being able to receive products such as plasma or platelets. It remains possible that 

patients received products such as plasma or platelets because they survived as opposed to surviving because 

Figure 12. Blood may be transfused as whole blood, 

or separated into its components via centrifugation.

Plasma

White blood cells

Platelets

Red blood cells
Damage Control Resuscitation | 137

they received the products.116 A recent study by Watson et al. even linked administration of FFP with a 

higher subsequent risk of developing multiple organ failure and acute respiratory distress syndrome.117

Further prospective study evaluating the use of blood products in fixed ratios is warranted prior to drawing 

any definitive conclusions.

Platelets

Retrospective civilian data have supported the use of platelets in patients requiring massive transfusion.92,109,118 

Apheresis platelets (aPLT) have been available in Iraq since November 2004. Apheresis is the process 

of removing select components such as platelets from blood and returning remaining components to the 

blood. Emerging data from OIF have shown an improved survival at 24 hours in patients receiving a high 

platelet ratio greater than or equal to 1:8 apheresis platelet unit per stored red blood cell unit (aPLT to 

RBC) as compared to patients receiving a medium ratio (less than 1:8 to 1:16 aPLT to RBC), and patients 

receiving the lowest ratio of platelets (less than 1:16 aPLT to RBC) (24-hour survival 95 percent, 87 percent, 

and 64 percent, respectively).116 The survival benefit for the high and medium ratio groups persisted at 30 

days as compared to the lowest ratio group (75 percent and 60 percent versus 43 percent). On multivariate 

regression, the aPLT to RBC ratio was independently associated with improved survival at 24 hours and 

at 30 days.116 A single unit of apheresis platelets is approximately equal to six units of pooled platelets. 

To simplify massive transfusion protocol strategies, the current Joint Theater Trauma System guidelines 

recommend transfusion of 1:1:1 pooled platelets to FFP to RBC (or 1:6:6 apheresis platelets to FFP to RBC) 

for patients requiring or anticipated to require massive transfusion.

As with plasma, once patients have been stabilized, platelet transfusion in a fixed ratio with RBCs may 

be less critical, and standard transfusion strategies for platelets may be more appropriate. The commonly 

recommended platelet transfusion threshold is a platelet count below 50,000/μL in patients with active 

bleeding.119 In cases of high-energy multisystem trauma or central nervous system bleeding frequently seen 

in combat casualties, a higher platelet transfusion threshold of 100,000/μL has been recommended.120

Fibrinogen 

Fibrinogen depletion develops earlier than other coagulation factor deficiencies.121 Fibrinogen ratios 

examined in OIF casualties, and fibrinogen to RBC ratios of less than 0.2 g fibrinogen per RBC unit 

were associated with a higher mortality.122 Given that there are 0.4 g of fibrinogen in one unit of FFP, 

administration of FFP in appropriate ratios (1:2 to 1:1) exceeds this fibrinogen ratio. Most deployed medical 

units do not have the capability to check fibrinogen in the laboratory, although thromboelastography 

is available at some Level III CSHs and can detect hypofibrinoginemia. Clot strength, as measured by 

the maximum amplitude on thromboelastography, is influenced by both platelet function and fibrinogen 

concentration. In cases where the platelet count is adequate, a decreased maximum amplitude would 

indicate hypofibrinoginemia.123

Fresh Whole Blood 

Fresh whole blood (FWB), defined as blood collected and maintained at 22°C for a maximum of 24 hours, 

is rarely used in civilian practice.124 However, the military has relied upon the use of FWB in circumstances 

when stored blood products are unavailable.125 As FWB contains red blood cells, plasma, and platelets in 

physiologic ratios and contains less total preservative solution – compared to a mixture of separate RBC, 

FFP, and platelet components – some have advocated that FWB is a superior resuscitation product.126,127 In a 
138 | Damage Control Resuscitation

retrospective study of 354 patients with traumatic hemorrhagic shock receiving blood transfusion, both 24-

hour and 30-day survival were higher in the FWB cohort as compared to a component therapy group.128 An 

increased amount (825 ml) of additives and anticoagulants were administered to the component therapy as 

compared to the FWB group. More recent data on combat casualties has tempered this conclusion, showing 

equivalence of 24-hour and 30-day survival between massively transfused patients receiving apheresis 

platelets compared to those receiving FWB.276

In patients with hemorrhagic shock, when standard blood components such as apheresis platelets or 

plasma are unavailable, FWB is a lifesaving alternative. 

Massive Transfusion-Associated Complications

Electrolyte Disorders

Hyperkalemia is a common complication with rapid or large-volume transfusion of red blood cells. 

Increased levels of extracellular potassium develop during the storage of red blood cells with concentrations 

averaging 12 milliequivalents (mEq) per liter at seven days and increasing to 32 mEq per liter after 21 

days of storage.129 Massive transfusion of senescent red blood cells could produce ventricular arrhythmia 

and cardiac standstill.130,131 Some authors have theorized that effects of hyperkalemia may be mitigated 

by infusing blood into lines farther away from the right atrium to permit greater mixture of blood before 

arrival to the heart.125 Fresher blood may also be requested from the blood bank or may be considered as 

an institutional policy for massively transfused patients. Once massive transfusion-associated hyperkalemia 

develops, it is treated in a conventional manner based on the clinical scenario (e.g., intravenous calcium, 

dialysis, dextrose and insulin infusion, bicarbonate, and diuretics).

Hyperkalemia, due to extracellular potassium build-up in stored red blood cells, and hypocalemia, due 

to the binding of ionized calcium by citrate, may cause cardiovascular toxicity following large-volume 

transfusions.

Massive transfusion-associated hypocalcemia results from the presence of citrate as an anticoagulant in 

blood products (and subsequent citrate binding of serum ionized calcium), particularly in those with high 

plasma content such as FFP and platelets.132,133 Citrate metabolism may be dramatically impaired in patients 

with hypoperfusion states, hypothermia, and advanced liver disease. This can produce citrate toxicity 

with resultant hypocalcemic tetany, prolonged QT interval on electrocardiogram, decreased myocardial 

contractility, hypotension, narrowed pulse pressure, and elevated end-diastolic left ventricular and central 

venous pressures.134 If hypocalcemia is anticipated based on the clinical features, electrocardiographic 

changes, or ionized calcium levels, it may be managed with intravenous calcium chloride or calcium 

gluconate. 

Massive Transfusion-Associated Coagulopathy

Coagulopathy is frequently present on admission in severely injured patients, particularly with brain or 

penetrating trauma injuries, and is associated with increased mortality.17,52,94,135,136,137Coagulopathy leads 

to further hemorrhage and worsening physiologic derangements, in turn prompting additional fluid 
Damage Control Resuscitation | 139

resuscitation and transfusion that can exacerbate 

coagulopathy, particularly if not appropriately 

managed, leading to the “bloody vicious cycle.”11 

Absent laboratory testing, clinical factors such as 

severe injury, shock, and hypothermia can predict 

coagulopathic bleeding.118 Coagulopathy may be 

clinically recognized as abnormal microvascular 

bleeding of uninjured mucosal or serosal surfaces, or 

by prolonged bleeding at sites of vascular access and 

wound tissue surfaces following control of vascular 

bleeding.138 At times, coagulopathy may not be 

recognized immediately and can be further obscured 

by standard clinical laboratory tests that fail to reflect 

clinically observed (in vivo) coagulopathy.139 The 

laboratory values that are most frequently abnormal 

in the setting of coagulopathy are the PT time (97 

percent), platelet count (72 percent), and aPTT (70 

percent).140 Notably, abnormal coagulation tests 

have been associated with increased mortality.141

Thromboelastography, while less widely available 

at medical centers, is a method of measuring whole 

blood coagulation and has been proposed as a more 

accurate marker of coagulopathy and predictor of 

transfusion requirements than standard coagulation 

tests (Fig. 13).75,142 More studies are needed to better 

define the potential role of thromboelastography as 

a diagnostic test and its ability to guide subsequent 

transfusion practices.128

Factors contributing to coagulopathy in patients undergoing massive transfusion include systemic acidosis, 

hypothermia, and consumptive and dilutional coagulopathy. Acidemia, largely due to lactate production 

by hypoperfused tissues utilizing anaerobic metabolism, can develop during hemorrhagic shock.143,144,145

Acidosis may both exacerbate and cause coagulopathy.118,146,147 Clotting factors and platelet aggregation are 

impaired by acidosis.148,149 There is also evidence of natural anticoagulant activation through protein C and 

enhanced fibrinolysis through increased tissue plasminogen activator release and plasminogen-activator 

inhibitor-type 1 (PAI-1) depletion in shock and acidosis.150,151 

Coagulopathy may be present on admission in severely injured patients and is associated with increased 

mortality. Factors contributing to coagulopathy in patients undergoing massive transfusion include 

systemic acidosis, hypothermia, and consumptive and dilutional coagulopathy. Though standard 

coagulation tests (INR, aPTT, and platelets) are relied upon, thromboelastography may be a more 

accurate marker of coagulopathy and predictor of transfusion requirements.

Figure 13. Illustration of thromboelastography patterns. This method of 

measuring whole blood coagulation has been proposed as a more accurate 

marker of coagulopathy and predictor of transfusion requirements than 

standard coagulation tests.

Normal

Anticoagulants/Hemophilia

Platelet Blockers

Fibrinolysis

Hypercoagulation

DIC

Stage 1

Stage 2
140 | Damage Control Resuscitation

Hypothermia impairs the coagulation system in multiple ways.36,39,152,153,154 Hypothermia has a modest effect 

on coagulation factor activity with a reduction of 10 percent of clotting factor activity for each 1°C decrease 

in temperature.13 It also results in a marked effect on platelet function.13,155,156 Platelet dysfunction develops 

due to defects in platelet activation, adhesion, and aggregation. Normalization of body temperature has 

been found to reverse inhibition of thrombin generation on platelets.157,158,159 

Consumption of factors with disseminated intravascular coagulation (DIC) has been noted in early trauma, 

particularly in association with extensive endothelial injury, massive soft-tissue damage,fat embolization from 

long-bone fractures, and brain injury.160,161 In addition to consumption of clotting factors, there is dysregulation 

of coagulation through consumption of antithrombin III, acquired platelet defects, and through increased 

fibrinolysis from increased tissue plasminogen activator and decreased α-2 antiplasmin.162,163,164,165,166,167

Dilutional coagulopathy develops during DCR as a consequence of the replacement of lost whole blood 

with coagulation factor-poor and platelet-poor fluids like crystalloids, colloids, and stored packed red 

blood cells.126,168 In addition to coagulation factor and platelet deficiencies, a lowered hematocrit may 

further contribute to coagulopathy as erythrocytes marginalize platelets toward the capillary wall and 

endothelium.169 Local platelet concentrations along the endothelium are nearly seven times higher than the 

average blood concentration due to this effect.170 Studies have shown that anemia has been correlated with 

increased bleeding times that are reversible with RBC transfusion.171,172 While clotting factors and platelets 

can be transfused during DCR, preservatives in these solutions of stored blood products may further worsen 

the dilutional coagulopathy. 126 

Damage Control Resuscitation Adjunctive Measures

Hypotensive Resuscitation 

The practice of hypotensive resuscitation (permissive hypotension) has been traced back to Walter Cannon, 

who in 1918 proposed hypotension as a method for reducing uncontrolled internal hemorrhage.173

Hypotensive resuscitation has been described as a method to improve patient outcomes by simultaneously 

limiting active hemorrhage and dilutional coagulopathy by tolerating lower than normal blood pressures 

(e.g., systolic pressure of less than 90 mm Hg) in trauma patients.12 The combined effect of the natural 

coagulation cascade, hypotension, and vessel spasm is thought to temporarily arrest traumatic hemorrhage 

and serves as the underlying foundation for hypotensive resuscitation.4,12,174,175,176,177 The direct effects of 

hypotensive resuscitation, or the failure to employ hypotensive resuscitation, are most readily apparent 

in traumatic amputation patients (Fig. 14). These patients often arrive without apparent bleeding from 

traumatically amputated limbs, only to have rapid arterial bleeding resume once resuscitation begins and 

hypotension is corrected to normal systolic pressures. This bleeding can sometimes overwhelm tourniquet 

control.178 This rebleeding phenomenon was well-known and previously described by World War I and II 

era surgeons.179
Damage Control Resuscitation | 141

Current military doctrine and training emphasize minimizing fluid and blood product delivery in 

prehospital settings for combat casualties who have a palpable radial pulse and normal mental status. 

The combined effect of the natural coagulation cascade, hypotension, and vessel spasm is thought 

to temporarily arrest traumatic hemorrhage and serves as the underlying foundation for hypotensive 

resuscitation. Such strategies are inappropriate with central nervous system injury or when cardiovascular 

collapse is imminent.

Several terms have been used to describe the strategy of tolerating relative hypotension in trauma victims 

prior to surgical hemorrhage control. These terms include hypotensive resuscitation, deliberate hypotension, 

and permissive hypotension. Although mixed results have been noted in studies, both animal and human 

clinical trials have supported the concept.12,176,180,181,182,183,184,185,186,187,188 Current military doctrine and training 

emphasize minimizing fluid and blood product delivery in prehospital settings for combat casualties who 

have a palpable radial pulse and normal mental status.189,190 This approach is also employed in the trauma 

bays with Forward Surgical Teams and CSHs to prevent unnecessary blood loss before surgical control is 

achieved.190 

Figure 14. Overly aggressive fluid resuscitation of patients with traumatically amputated limbs may cause nonbleeding wounds to hemorrhage profusely. 

Image courtesy of the Borden Institute, Office of The Surgeon General, Washington, DC.
142 | Damage Control Resuscitation

The challenge to providers using hypotensive resuscitation as part of their strategy is recognizing when to 

withhold additional fluid, but also knowing when such strategies are inappropriate, such as with central 

nervous system injury or when cardiovascular collapse is imminent.191 Tissue ischemia followed by 

reperfusion is associated with biochemical and cellular changes resulting in complement activation and 

inflammatory responses.192,193 These inflammatory responses are responsible for the development of acute 

lung injury and multiple organ failure, and are potentially exacerbated by the choice of resuscitation 

fluid.194,195 The understanding of these processes is incomplete and an area of active research.

Patients with active hemorrhage may deteriorate quickly, and currently there are few data available to 

guide the hypotensive resuscitation strategy. As a general recommendation, patients are permitted to 

remain mildly hypotensive in two clinical circumstances. The first is the patient who is being rapidly 

transported to an operating room with the anticipation that surgical control of hemorrhage will be 

obtained quickly. Volume administration prior to hemorrhage control has the potential to raise the SBP 

sufficiently to overcome the natural hemostatic mechanisms. The second circumstance is for the patient 

with noncompressible hemorrhage who is a great distance from an operating room, either geographically 

or temporally. These patients may reach a temporary stable state where natural hemostatic mechanisms 

have slowed or stopped ongoing hemorrhage. Large volumes may overwhelm this natural hemostasis and 

cause exsanguination during transport. In both cases, the goal should be transfer to an operating room at 

the earliest possible time. 

Optimal Use of Crystalloid and Colloid Solutions

Crystalloids and colloids greatly intensify dilutional effects if given in significant quantities (greater than 

20 ml per kilogram). In addition to dilutional effects, colloids such as hydroxyethyl starch (HES) are also 

known to increase coagulopathy by impairing von Willebrand factor activity in plasma.196,197 Moreover, a 

preventable cause of iatrogenic acidemia involves the choice of resuscitation fluid. The two most commonly 

used isotonic crystalloid solutions in emergency departments and prehospital settings are lactated Ringer’s 

solution and normal saline. Both of these fluids possess pH ranges as low as 4.5 for normal saline (NS) and 

6.0 for lactated Ringer’s (LR) solution. 

Crystalloids and colloids greatly intensify hemodilutional effects if given in significant quantities (greater 

than 20 ml per kilogram). The low pH values of normal saline and lactated Ringer’s solution contribute 

to iatrogenic acidemia when administered in large volumes. 

In a fairly extensive review of animal research, case reports, case series, and clinical studies, Ho and 

colleagues demonstrated that use of large amounts of normal saline in trauma patients with shock 

contributes to metabolic acidosis, which also can significantly worsen coagulopathy.198 This effect was 

not demonstrated with lactated Ringer’s solution. Several other recent animal studies have demonstrated 

superiority of lactated Ringer’s solution over normal saline as a resuscitation fluid in hemorrhagic 

shock.199,200,201 Nevertheless, the choice of lactated Ringer’s solution as a resuscitation fluid, particularly for 

severely injured patients undergoing damage control surgery and massive transfusion, has other drawbacks. 

Lactated Ringer’s solution in large volumes provides little or no direct contribution to improve coagulation 

or oxygen-carrying capacity, relative to early use of blood products. More recently, lactated Ringer’s 

solution has also been found to dramatically activate the immune system and potentially contribute to 

secondary cellular injury.190,202,203,204,205 Use of this fluid may be detrimental in patients with uncontrolled 

hemorrhage.176,180,181
Damage Control Resuscitation | 143

Vasoactive Agents 

Exogenous catecholamines and other vasopressor agents (e.g., vasopressin) are used frequently as adjuncts 

to the resuscitation of patients with severe hemorrhagic shock. Although previous data on the employment 

of vasopressors in hemorrhagic shock are mixed,recent animal studies reveal potentially favorable results 

with the use of low-dose vasopressin in resuscitation after brain injury or hemorrhage and blunt pulmonary 

contusion or hemorrhage.206,207,208,209,210,211,212,213,214,215,216,217,218,219,220,221 Other investigators have shown that 

vasopressin becomes deficient in advanced stages of hemorrhagic and vasodilatory shock and hence is an 

appropriate target for replacement.222 A recent review article by Cohn suggests that low-dose vasopressin 

in severe hemorrhagic shock can lower resuscitation volumes and potentially improve morbidity and 

mortality.223 Overall, the multiple publications analyzing the effects of low-dose vasopressin in various clinical 

settings have resulted in conflicting results.217,218,219,224,225,226,227,228,229,230,231 Further well-designed clinical trials 

in trauma patients are necessary to better define the role of vasoactive agents (e.g., vasopressin) as adjuncts 

to resuscitation.

While exogenous catecholamines and other vasopressor agents are frequently used during resuscitation of 

patients with severe hemorrhagic shock, further studies are necessary to establish their efficacy.

Nonsurgical Hemostatic Agents

Topical Sealants 

Topical hemostatic sealants are used as adjuncts for local hemostasis in cases where conventional measures for 

bleeding control fail. Agents such as FloSealTM, Gelfoam®, and Surgicel® are useful adjuncts to 

standard hemorrhage control techniques in patients undergoing cardiac, vascular, and spinal surgery.232,233,234

Recombinant Factor VIIa 

While recombinant factor VIIa (rFVIIa) is currently only approved for the management of bleeding in 

patients with congenital Factor VII deficiency and hemophilia A or B with inhibitors, this agent has been 

extensively used off-label in trauma. Further interest was spurred following a series of experimental animal 

liver trauma studies that showed prolongations in survival and decreased blood loss with its use.235,236,237,238,239

These studies coincided with a number of subsequent case reports and case series of rFVIIa use in trauma 

and uncontrolled hemorrhage suggesting decreased blood loss or decreased transfusion requirements for 

patients.98,240,241,242,243,244,245,246,247,248,249,250,251,252,253,254,255,256,257,258,259,260 

As of 2009, there is no evidence of improved major clinical outcomes (e.g., decreased mortality) as a direct 

result of using rFVIIa in the management of trauma patients.

The only randomized trial of rFVIIa in trauma patients (published in 2005) randomized 301 patients with 

blunt or penetrating injuries to receive placebo or rFVIIa after the eighth unit of blood.261 This trial showed 

a reduction of 2.6 units of RBC transfusions for the blunt trauma subgroup and a similar though nonsignificant trend in the penetrating injury subgroup receiving factor rVIIA. While trends toward reductions 

in mortality and critical complications were seen, no statistically significant results were documented.261

The CONTROL study, a randomized double-blind trial whose purpose was to evaluate the safety and 

effectiveness of rFVIIa in severely injured trauma patients, was discontinued at Phase III because a 

preplanned futility analysis predicted a very low likelihood of reaching a successful outcome on the primary 
144 | Damage Control Resuscitation

efficacy endpoints.262 As of 2010, there is no evidence of improved major clinical outcomes (e.g., decreased 

mortality) as a direct result of using rFVIIa in the management of trauma patients.

The potential for thromboembolic complications associated with rFVIIa has received considerable 

attention. Meta-analyses of randomized, controlled trials have shown mixed results while multiple studies 

have suggested that thromboemboli are an apparent complication.263,264,265,266,267,268,269 

Antifibrinolytics

As hyperfibrinolysis is a contributor to the coagulopathy of trauma, antifibrinolytics have the potential to 

reduce blood loss and improve outcomes in traumatic bleeding. Antifibrinolytic agents have been noted to 

reduce blood loss in patients with both normal and exaggerated fibrinolytic responses to surgery.270 The 

most extensively evaluated agents are aprotinin, epsilon aminocaproic acid, and tranexamic acid. The Food 

and Drug Administration suspended marketing of aprotinin in November 2007 due to reports of increased 

mortality in coronary bypass surgery.271 While aminocaproic acid is approved by the FDA for enhancing 

hemostasis in states of hyperfibrinolysis, and tranexamic acid is approved for hemophilia patients undergoing 

tooth extraction, a Cochrane Review of antifibrinolytic drugs in acute traumatic injury revealed no studies 

of sufficient quality to assess the benefits in this population.272,273,274 There is currently a major ongoing 

international trial, CRASH-2: Clinical Randomization of an Antifibrinolytic in Significant Hemorrhage 

(NCT00375258), to evaluate the use of tranexamic acid compared to placebo in trauma patients.275 Until 

these results are available, there is little role for the prophylactic or empiric use of antifibrinolytics in acute 

trauma.

Conclusions

The resuscitation of severely injured trauma patients will continue to remain a complex and multifaceted 

problem. The recent large numbers of combat casualties requiring massive transfusion, an unfortunate by 

product of modern war, has enabled both the military and civilian trauma communities to formulate an 

evolving DCR strategy. Ongoing and future research are needed to further refine and validate: (1) novel 

prehospital therapies for the treatment of noncompressible hemorrhage; (2) technologies to rapidly assess 

the physiologic status of injured patients; (3) methods to select patients for damage control approaches; 

(4) the optimal content and proper sequence of administration of resuscitation products; and (5) novel 

approaches to managing patients at or near the limits of physiologic reserve. 
Damage Control Resuscitation | 145

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269. Levy JH, Fingerhut A, Brott T, Recombinant factor VIIa in patients with coagulopathy secondary 

to anticoagulant therapy, cirrhosis, or severe traumatic injury: review of safety profile. Transfusion 

2006;46(6):919-933.

270. Porte RJ, Leebeek FW. Pharmacological strategies to decrease transfusion requirements in patients 

undergoing surgery. Drugs 2002;62(15):2193-2211.

271. FDA Requests Marketing Suspension of Trasylol®. U.S. Food and Drug Administration Website, U.S. 

Food and Drug Administration, 2007. (Accessed January 13, 2010, at http://www.fda.gov/NewsEvents/

Newsroom/PressAnnouncements/2007/ucm109021.htm.)

272. Amicar® (aminocaproic acid), package insert, 2008a.

273. Cyclokapron® (tranexamic acid), package insert, 2008c.

274. Coats T, Roberts I, Shakur H. Antifibrinolytic drugs for acute traumatic injury. Cochrane Database 

Syst Rev 2004;(4):CD004896.

275. Roberts I. Clinical Randomisation of an Antifibrinolytic in Significant Haemorrhage, 2009. (Accessed 

January 12, 2010, at http://clinicaltrials.gov/ct2/show/NCT00375258.)

276. Perkins JG, Cap AP, Spinella PC, et al. Comparison of platelet transfusion as fresh whole blood versus 

apheresis platelets for massively transfused combat trauma patients. Transfusion, 2011;51(2):242-252.
164 | Damage Control Resuscitation
DAMAGE CONTROL 

SURGERY

Contributing Authors

Brian J. Eastridge, MD, COL, MC, US Army

 Lorne H. Blackbourne, MD, COL, MC, US Army

 Todd Rasmussen, MD, LTC, US Air Force

 Henry Cryer, MD

 Alan Murdock, MD, LTC, US Air Force

Chapter 5
All figures and tables included in this chapter have been used with permission from Pelagique, LLC, the 

UCLA Center for International Medicine, and/or the authors, unless otherwise noted.

Use of imagery from the Defense Imagery Management Operations Center (DIMOC) does not imply or 

constitute Department of Defense (DOD) endorsement of this company, its products, or services.

Disclaimer

The opinions and views expressed herein belong solely to those of the authors. They are not nor should 

they be implied as being endorsed by the United States Uniformed Services University of the Health 

Sciences, Department of the Army, Department of the Navy, Department of the Air Force, Department of 

Defense, or any other branch of the federal government.
Damage Control Surgery | 167

Table of Contents

Introduction to Damage Control............................................................................ 169

General Principles of Damage Control................................................................... 169

Thoracic Injury Damage Control ........................................................................... 173

Emergency Thoracotomy.................................................................................................173

Intrathoracic Vascular Injury .........................................................................................175

Pulmonary and Tracheobronchial Injuries.....................................................................178

Esophageal Injury.............................................................................................................180

Neck Injury Damage Control................................................................................. 181

Abdominal Injury Damage Control ........................................................................ 184

Damage Control Laparotomy ..........................................................................................184

Retrohepatic Hematoma....................................................................................................186

Perihepatic Vascular Injury................................................................................................186

Hepatic Parenchymal Injury..............................................................................................186

Pancreatic and Duodenal Injuries......................................................................................187

Renal Injury .......................................................................................................................188

Ureteral Injury ...................................................................................................................190

Splenic Injury.....................................................................................................................190

Large Soft-Tissue and Retroperitoneal Wounds................................................................192

Intestinal (Enteric) Injuries ..............................................................................................192

Rectal Injury .....................................................................................................................193

Abdominal Wall Closure ..................................................................................................194

Peripheral Vascular Injury Damage Control............................................................ 195

Arterial Injury and Temporary Vascular Shunts ............................................................195

Role of Temporary Vascular Shunts in Afghanistan and Iraq ..........................................196

Complications ....................................................................................................................198

Conclusions........................................................................................................................199

Venous Injury....................................................................................................................200

Proximity to Great Vessel Injury.....................................................................................200

Extremity Tourniquets.....................................................................................................200

Upper Extremity Arterial Injury......................................................................................201

Femoral Vasculature Injury .............................................................................................201

Popliteal and Tibial Vasculature Injuries........................................................................201

Pelvic Injury Damage Control ............................................................................... 202

Background.......................................................................................................................202

Physical Examination ...............................................................................................................203

Radiographic Evaluation..................................................................................................203

Plain Radiography .............................................................................................................204

Computed Tomography Imaging ......................................................................................204
168 | Damage Control Surgery

Angiography.......................................................................................................................205

Acute Management...........................................................................................................205

Open Pelvic Fractures ......................................................................................................207

Bladder and Urethral Injuries..........................................................................................208

Management of Bladder Injuries ......................................................................................209

Management of Urethral Injuries ....................................................................................209

Genitalia Injuries .............................................................................................................210

Damage Control Summary ................................................................................... 211

References .......................................................................................................... 212
Damage Control Surgery | 169

Introduction to Damage Control

Damage control surgery techniques have evolved 

within the continuum of military and civilian 

trauma care since the Napoleonic Wars. Though 

civilian trauma surgeons now uniformly embrace 

the relatively contemporary label “damage control,” 

the techniques have firm foundation within the 

history of military medicine.1 In the later part of 

the 18th century during the Napoleonic campaign, 

the French surgeon Larrey succinctly alluded to 

the rationale for expedited battlefield procedures: 

“When a limb is so much injured by a gunshot wound 

that it cannot be saved, it should be amputated 

immediately. The first 24 hours is the only period 

during which the system remains tranquil, and we 

should hasten during this time, as in all dangerous 

diseases, to adopt the necessary remedy.”2

 Military 

historical references to the techniques of damage 

control surgery in the United States (US) appear 

around the time of the Civil War (Fig. 1).3 In 

World War II, the Second Auxiliary Surgery Group 

treated over 22,000 combat wounded soldiers, 

including 8,800 “severely wounded,” during a twoyear interval from 1943 to 1945.4

 The ensuing 912-

page report and scientific publications that were 

consequent to the operation yielded insight into the 

surgical treatment of thoracic injury; the reactive 

lung injury associated with severe trauma denoted “the wet lung of trauma,” which we now know as acute 

respiratory distress syndrome (ARDS); and the utility of techniques aimed at the “correction of profound 

physiologic disturbances which immediately endanger life” is now described by the moniker, damage 

control. In the Vietnam War, it was recognized in several case series that temporizing surgical procedures 

often demonstrated a survival advantage when compared to definitive surgical therapy.5

 Though apparently 

temporarily forgotten after the Vietnam War, the technique reappeared in the hallmark publication by 

Stone in 1983, which advocated abbreviated celiotomy in patients with abdominal injury with associated 

coagulopathy and hypothermia.6 Since that time, many reported successes with similar salvage techniques 

have been cited.7,8,9,10 Within the last decade, a number of authors have also described the expansion of this 

lifesaving surgical practice to include thoracic, vascular, orthopedic, and neurosurgical procedures.11,12,13,14

General Principles of Damage Control 

Modern day concepts of damage control have been honed in the civilian sector resulting in survival rates 

of 50 percent in severely injured patients in hemorrhagic shock.15,16,17,18,19,20,21,22 Damage control as it is 

Figure 1. Damage control surgery at a Level III facility. This lifesaving 

surgical paradigm now includes thoracic, vascular, orthopedic, and 

neurosurgical procedures.
170 | Damage Control Surgery

currently practiced is simply defined as the rapid initial control of hemorrhage and contamination with 

packing and a temporary closure, followed by physiologic resuscitation in the intensive care unit (ICU), and 

subsequent reexploration and definitive repair once normal physiology has been restored (Fig. 2). From a 

military perspective, damage control concepts apply to all body regions, with an emphasis on abbreviated 

and focused surgery on patients expected to survive, thus conserving resources and allowing definitive care 

at the next level of care. 

Rapidly achieving these objectives in severely injured trauma patients is crucial to mitigating the trauma 

“lethal triad” of hypothermia, acidosis, and coagulopathy.23 The acidosis results from hypovolemic shock and 

inadequate tissue perfusion. Hypothermia results from exsanguination and loss of intrinsic thermoregulation. 

Coagulopathy results from hypothermia, acidemia, platelet and clotting factors consumption, and blood 

loss. Coagulopathy, in turn, causes more hemorrhage and thus causes more acidosis and hypothermia; so 

the “bloody vicious cycle” continues. Once established, this vicious cycle is almost uniformly fatal and must 

be prevented using damage control principles rather than attempting to treat it once it has occurred.

Damage control surgery is defined as the rapid initial control of hemorrhage and contamination with 

packing and temporary closure, followed by resuscitation in the ICU, and subsequent reexploration and 

definitive repair once normal physiology has been restored.

While the current principles of damage control in well-equipped trauma centers have led to improved 

survival, the combat environment offers challenges and adds complexity to the practice of damage control. 

Nonetheless, descriptions of military applications of damage control procedures have recently emerged 

in the trauma literature. Although these publications comprise a small series of patients, they suggest that 

damage control in the combat environment is as effective as it is in civilian trauma care.24,25,26,27

As currently configured, the military process involves the simultaneous and coordinated operation, 

resuscitation, and serial evacuation of the casualty, via both rotary-wing and fixed-wing aircraft, through 

several levels of military medical care across continents (Fig. 3). The feasibility of damage control in 

combat casualty care (CCC) settings is dependent upon: (1) the availability of resources to prevent and 

treat hypothermia, coagulopathy, and acidosis; and (2) the ability to provide supportive care pending staged 

reoperation or evacuation from theater with subsequent staged operation in Germany, future Level IV 

facilities, or the US. Central to CCC that takes place in the relatively resource-constrained environment 

of a theater of war is the capability of military Level II and Level III care facilities to supply blood 

components, including packed red blood cells, plasma, and platelets commensurate with demand

Figure 2. Damage control procedures are defined by an abbreviated surgery, followed by resuscitation in the ICU, with subsequent reexploration and 

definitive repair once normal physiology has been restored. This approach has led to improved patient survival.

ER OR DEATH

Time

ER OR ICU OR ICU
Damage Control Surgery | 171

The military CCC process involves the simultaneous and coordinated operation, resuscitation, and serial 

evacuation of the casualty, via both rotary-wing and fixed-wing aircraft, through several levels of military 

medical care across continents.

Recent advances in the concept of damage control resuscitation (DCR) have resulted in the transfusion of 

one unit of plasma for each unit of packed red blood cells in the massive transfusion setting.28 This novel 

paradigm of resuscitation is thought to be largely responsible for the substantially decreased mortality from 

coagulopathy in the most severely injured casualties.29 Another novel concept developed by the military has 

been the use of the walking blood bank using fresh whole blood donated by soldiers on site, when large 

stores of fresh frozen plasma and packed red blood cells are in short supply (Fig. 4).30 

Damage control resuscitation is a strategy that seeks to prevent or mitigate hypothermia, acidosis, 

and coagulopathy through combined treatment paradigms. Damage control resuscitation comprises 

early hemorrhage control, hypotensive resuscitation (permissive hypotension), hemostatic resuscitation 

(minimization of crystalloid fluids and fixed ratio blood product transfusion), prevention or alleviation of 

hypothermia (through warming measures), and amelioration of acidosis through judicious use of blood 

products and hemodynamic resuscitation endpoints. 

Figure 3. (Above) Improvised patient information communication 

written directly onto a dressing following damage control surgery. The 

current military process involves simultaneous and coordinated operation, 

resuscitation, and serial evacuation of casualties through several levels of 

combat casualty care across continents, making accurate communication 

exceedingly important.

Figure 4. (Right) The walking blood bank can rapidly collect fresh 

whole blood when other blood products are in short supply. Image courtesy 

of Defense Imagery Management Operations Center (DIMOC).
172 | Damage Control Surgery

Given the battlefield constraints of multiple-casualty-incidents, the need for rapid turnover of operating 

rooms, and the limited number of critical care beds, it is more advantageous to resource allocation and 

utilization to perform damage control procedures early. Intensive care units at Level III facilities are robustly 

staffed and resourced such that care received on the battlefield of Iraq and Afghanistan is akin to care at any 

Level I trauma center in the US (Fig. 5). However, operational tempo limits the combat casualty’s ability to 

occupy an ICU bed for an extended length of time. 

One of the most substantial advances in recent military medicine, the Critical Care Aeromedical Transport 

Team (CCATT), has been instrumental in circumventing this problem. These teams provide en-route 

intensive care to patients requiring evacuation. Most US and coalition casualties spend less than 48 

hours in-theater and many times in high-acuity cases, less than 24 hours (Figs. 6 and 7).31,32,33 With such 

advanced surgical and critical care capacity, it is feasible to care for the high-acuity patient requiring 

damage control surgery within the combat theater during the acute surgical, postoperative intensive care 

stabilization, reoperation, and evacuation phases. As such, the philosophy of damage control continues 

to be appealing within the realm of CCC, since encompassed within the contingencies of the modern 

battlefield are a finite pool of manpower and therapeutic resources, a nonlinear battlefield with a highly 

mobile force, a multiplicity of casualties, and highly destructive mechanisms of injury.

Figure 5. (Top Right) Intensive care units at Level III facilities are 

robustly resourced such that care received on the battlefield is akin to care 

at any Level I trauma center in the US. 

Figure 6. (Bottom Left) All US and coalition casualties with critical 

care requirements in the current conflicts in Iraq and Afghanistan are 

flown out-of-theater to Germany with the assistance of a CCATT. Image 

courtesy of Donald C. Kowalewski, LTC, MC, USAF.

Figure 7. (Bottom Right) The CCATT teams facilitate the rapid 

evacuation of severely ill patients, which translates into better patient 

care as well as a significantly decreased forward medical footprint. Image 

courtesy of Donald C. Kowalewski, LTC, MC, USAF.
Damage Control Surgery | 173

Thoracic Injury Damage Control 

Emergency Thoracotomy

Thoracic damage control surgery can be stratified into two domains: procedures that occur in the emergency 

department (ED) and those that take place in the operating room. Thoracic procedures that are undertaken 

in the ED are reserved for those patients who present in extremis with signs and symptoms suggestive of 

thoracic injury. Collective reviews in the literature have demonstrated survival rates of 8.8 to 11.1 percent 

for penetrating injury and 1.4 to 1.6 percent for blunt injury after resuscitative thoracotomy for civilian 

injury.34,35 In a related combat-environment setting analysis, 12 of 94 patients undergoing resuscitative 

thoracotomy for penetrating injuries survived, while none of the seven patients with blunt injury survived. 

Of note, this military study expanded the indication for resuscitative thoracotomy for patients in extremis 

with injuries to the abdomen (30 percent) and extremities (22 percent).36

The objectives of a thoracotomy are to: (1) confirm ventilatory support by observing expansion of the 

left lung; (2) open the pericardium to relieve pericardial tamponade; (3) apply occlusive pressure and 

clamp the descending aorta to restore central perfusion to the brain and heart; (4) provide direct cardiac 

compression to circulate blood; and (5) control visible hemorrhage.

The basic conduct of resuscitative thoracotomy includes simultaneous left-sided anterolateral thoracotomy 

with establishment of an airway and ventilatory support, chest tube placement in the contralateral chest 

cavity, large-bore intravenous access, and initiation of a massive transfusion protocol with a 1:1 ratio of 

fresh frozen plasma to packed red blood cells or the use of fresh whole blood. The thoracotomy is initiated 

with an expeditious and generous left anterolateral chest incision in the fifth intercostal space (i.e., below 

the nipple at the inframammary fold) carried down to the chest wall sharply (Fig. 8). At this point, one 

blade of a pair of heavy Mayo scissors is inserted into the pleural space on the cephalad edge of the sixth 

rib, and with a pushing stroke the intercostal musculature is opened both posteriorly and anteriorly to the 

sternal edge. Care must be taken to incise along the curvature of the ribs to avoid accidentally transecting 

ribs. This will minimize injury to the intercostal neurovascular bundle and avoid creating sharp bone 

margins capable of creating iatrogenic injury to careproviders. A rib-spreading retractor is placed within 

the thoracotomy incision with the handle positioned downward toward the bed and opened to expose the 

left thoracic cavity. Once the thoracic cavity has been exposed, the objectives of the procedure are to: (1) 

confirm ventilatory support by observing expansion of the left lung; (2) open the pericardium anterior to 

the phrenic nerve to relieve pericardial tamponade; (3) apply occlusive pressure and clamp the descending 

aorta to restore central perfusion to the brain and heart; (4) provide direct cardiac compression to circulate 

blood; and (5) control visible hemorrhage. Although most careproviders perform cardiac compressions by 

holding the heart between their hands (mostly fingers due to space constraints), compressions are generally 

more efficient with placement of the palm of one hand on the posterior heart and pressing upward towards 

the sternum (Fig. 9). 

The pericardium is grasped with DeBakey forceps anterior to the phrenic nerve, and the pericardial 

sac is opened completely with Metzenbaum scissors in a craniocaudal direction so as not to injure the 

phrenic nerve. Once the pericardium is incised, the tamponade is relieved and the heart can be delivered 

into the left chest. If obvious ongoing hemorrhage from the heart is noted, it is initially controlled with 

digital pressure. The descending aorta can either be compressed manually against the spine or clamped 
174 | Damage Control Surgery

with a vascular clamp. Lifting the lung anteriorly 

helps to visualize the posterior mediastinum and 

facilitates direct access to the aorta. Once the 

posterior mediastinum is visualized, the parietal 

pleura is incised, and the opening extended bluntly 

anteriorly as well as posteriorly along the spine to 

allow insertion of a large vascular clamp across the 

aorta. Direct visualization is also useful so that the 

clamp is not inadvertently placed on the esophagus 

or below the level of an aortic injury, thereby 

exacerbating hemorrhage. Adjunctive measures to 

attain visualization and vascular control include a 

surgical assistant compressing the lung anteriorly, 

temporarily disconnecting the patient from positiveFigure 8. (Left) Emergency thoracotomy is reserved for patients presenting 

in extremis with signs and symptoms suggestive of thoracic injury. Image 

courtesy of J. Christian Fox, MD, University of California, Irvine.

Figure 9. (Below) Although many careproviders perform cardiac 

compressions by holding the heart between their hands, compressions may 

be more efficient by placing the palm of one hand on the posterior heart and 

pressing upward towards the sternum. Image courtesy of J. Christian Fox, 

MD, University of California, Irvine.
Damage Control Surgery | 175

pressure ventilation, or performing a right mainstem bronchus intubation if the patient’s cardiopulmonary 

status can tolerate single-lung ventilation. The inferior pulmonary ligament must be released from the 

diaphragm via sharp dissection to allow full exposure of the mediastinal structures. 

Hemorrhage from penetrating cardiac wounds can often initially be controlled through digital pressure or 

occlusion. Atrial hemorrhage can also be temporized with a tangential vascular clamp and subsequently 

undergo a simple 3-0 ProleneTM running suture repair. If digital pressure is not sufficient to control 

ventricular bleeding, hemorrhage can be temporized with Foley catheter or Fogarty balloon tamponade, 

suture repair, or stapling (which is quick and effective for small lacerations).37,38,39,40 If a Foley catheter 

is used, it is important to completely flush the catheter with crystalloid solution to avoid subsequent air 

embolism upon introduction of the catheter into the injured heart. While controlling hemorrhage through 

suture repair of the ventricles, it is paramount to spare the coronary arteries (i.e., avoid accidentally 

ligating them). This can be performed by tying pledgeted suture bolsters on opposing sides of the 

coronary artery at-risk using vertical mattress sutures, while at the same time approximating the cardiac 

wound (Fig. 10). 

If digital pressure or occlusion is not sufficient to control ventricular bleeding, hemorrhage can be 

temporized with Foley catheter or Fogarty balloon tamponade, suture repair, or stapling. 

Control of hemorrhage from major thoracic vascular structures can be obtained by clamping or compressing 

affected vessels under direct visualization. In the circumstance where additional exposure to the right heart 

or right hemithorax is required, a left-sided anterolateral thoracotomy can be converted into a clamshell 

thoracotomy. This is done by extending the incision through the right fifth intercostal space after transecting 

the sternum with either a Gigli saw, Lebsche knife, heavy bone cutter, or electric sternal saw (Fig. 11). This 

incision provides the best exposure to the entire anterior and superior mediastinum and both pleural spaces 

by extending the incision to right chest above the nipple in a gentle S-shaped configuration. Vascular control 

of the internal mammary arteries following thoracotomy is important to prevent further blood loss and can 

be obtained by clamping or suture ligation. 

Once a cardiac rhythm has been restored and bleeding temporarily controlled, the patient is expeditiously 

taken to the operating room. Such patients are at significant risk for the lethal triad of coagulopathy, acidosis, 

and hypothermia, so efforts to prevent and treat these conditions must be made during the resuscitative 

process. Once in the operating room, the patient is prepped and draped. Cardiac wounds can now be 

definitively repaired. When suturing ventricular cardiac wounds, it is important to use pledgets fashioned 

from Teflon® strips or pericardium to prevent suture shearing through the myocardium upon tying. 

Coronary vascular injuries occurring in combat typically require ligation, as coronary revascularization 

requires a cardiac bypass technician, bypass pump, and cardiac surgeon.

When suturing ventricular cardiac wounds, it is important to use pledgets fashioned from Teflon® strips or 

pericardium to prevent suture shearing through the myocardium upon tying. Additionally, it is paramount 

to avoid ligation of the coronary arteries when performing suture repair of the heart.

Intrathoracic Vascular Injury 

Vascular injuries to the thorax (aorta and proximal arterial and venous branch vessels) are treated with basic 
176 | Damage Control Surgery

Figure 10. Bleeding from penetrating trauma to the heart may be temporized with digital pressure (occlusion), Foley catheter or Fogarty balloon 

tamponade, suture repair, or stapling. When suturing or stapling, it is vital to avoid occlusion of a coronary artery. Images courtesy of J. Christian Fox, 

MD, University of California, Irvine and the Borden Institute, Office of The Surgeon General, Washington, DC.
Damage Control Surgery | 177

proximal and distal vascular control and reconstitution of flow principles. Injuries to the aorta require repair. 

Lateral aortorrhaphy or primary tension-free repair are preferable, although in the authors’ experience, in 

extreme circumstances the aorta can be transiently shunted with a large-bore chest tube tied into position 

above and below the injury site with large suture or umbilical tape. 

Control of the descending thoracic aorta is easily obtainable through a left-sided anterolateral thoracotomy. 

Exposure of the proximal left subclavian and proximal left common carotid artery is limited from a true 

left-sided anterolateral thoracotomy and would be better obtained via a more traditional posterolateral 

thoracotomy. A “book” or “trapdoor” incision would provide better exposure of a long segment of the left 

common carotid and left subclavian artery. This surgical approach is seldom used due to lack of familiarity, 

as well as complications related to stretch on the brachial plexus and upper posterior costal junctions, 

resulting in neurologic and upper back pain syndromes.41 It should be only used when control and repair 

are absolutely necessary. A better approach to specifically control subclavian artery hemorrhage would be 

an anterolateral thoracotomy via a third intercostal space incision combined with a separate infraclavicular 

incision for definitive repair.42 Visualization of the subclavian artery and vein, particularly more distally, can 

be facilitated by resection of the clavicle. 

Figure 11. If additional exposure to the right heart or right hemithorax is required, a left-sided anterolateral thoracotomy can be converted into a clamshell 

thoracotomy. Image courtesy of J. Christian Fox, MD, University of California, Irvine.
178 | Damage Control Surgery

Injuries to the aortic arch vessels and definitive repairs usually require a median sternotomy. As a general 

principle, dissection into mediastinal hematomas can be disorienting, so it is often useful to open the 

pericardium and trace vessels upward. The left innominate vein can be divided in order to identify the 

innominate artery, and the dissection can then continue cephalad. Due to relatively large vessel caliber, the 

best management method for injuries to thoracic outlet arteries is usually bypass using a synthetic conduit. 

However, in a damage control scenario, this may not be possible. In extreme circumstances, most aortic 

arch arteries can be singly ligated since the vigorous collateral flow of the cervical and thoracoacromial 

region will usually sustain acceptable perfusion. Ligation of cervical vessels carries the risk of stroke, and 

subclavian and innominate artery ligations carry the risk of limb ischemia. Except for the superior vena 

cava, injuries to the thoracic venous system can be repaired with lateral venorraphy or ligated. Injuries to 

the superior vena cava should be repaired.

In extreme circumstances, most aortic arch arteries can be singly ligated since the collateral flow of the 

cervical and thoracoacromial region will usually sustain acceptable perfusion.

Pulmonary and Tracheobronchial Injuries

Pulmonary and tracheobronchial damage control procedures are performed to control hemorrhage or air 

leak. With respect to pulmonary injury, the three main damage control procedures are: (1) nonanatomic 

pulmonary resection; (2) pulmonary tractotomy; and (3) pneumonectomy (Figs. 12 and 13). Nonanatomic 

resections using a GIATM or TATM stapler are generally preferred for peripheral injuries with ongoing 

hemorrhage or air leak. The advantage of the nonanatomic resection over anatomic resection is the reduction 

in time associated with not having to develop formal lobar surgical planes. However, if deeper bleeding 

persists after pneumorraphy or nonanatomic pulmonary resection, this must be addressed with further 

exposure and repair or ligation. When this occurs or when there is profuse hemorrhage from deeper within 

Figure 12. Illustration of pulmonary tractotomy. Image courtesy of the Borden Institute, Office of The Surgeon General, Washington, DC. Illustrator: 

Aletta Frazier, MD.
Damage Control Surgery | 179

the lung parenchyma from penetrating injury, a pulmonary tractotomy can be performed. This procedure 

involves placing two long vascular clamps through the pulmonary wound tract, clamping them, and incising 

between the two. The lung edges can then be stapled with a TATM stapler. Alternatively, a GIATM stapler can 

be advanced through the tract and fired, creating a linear passage to the source of hemorrhage. The focus 

of hemorrhage will lie at the base of the tract and can be sutured with 4-0 or 5-0 vascular suture. 

Pulmonary and tracheobronchial damage control procedures that are performed to control hemorrhage 

or air leak may include: (1) nonanatomic pulmonary resection; (2) pulmonary tractotomy; and (3) 

pneumonectomy.

Figure 13. (Above) Patient with penetrating right chest injury from a 

mortar round. A posterolateral thoracotomy was perfomed, demonstrating 

intact lower lobe and stapled upper and middle lobe structures. (Right) 

Resected right upper and middle lobes of the lung. Images courtesy of the 

Borden Institute, Office of The Surgeon General, Washington, DC.
180 | Damage Control Surgery

In patients with global or hilar parenchymal lung injury, pneumonectomy is an option of last resort. There 

is a stepwise increase in mortality with more extensive lung resections that is independent of injury severity.43

The mortality of trauma patients undergoing pneumonectomy is over 50 percent.43,44,45 Large air leaks from 

the bronchial tree or major pulmonary hemorrhage can temporarily be controlled by incising the inferior 

pulmonary ligament and clamping the pulmonary hilum, or by twisting the lung 180 degrees around its 

hilar axis (Figs. 14 and 15).46 Should pneumonectomy or hilar clamping be necessary, the hilum of the lung 

should be clamped slowly. This will give the other lung a chance to accommodate, and volume resuscitation 

should be minimized to avoid acute right heart failure, which inevitably occurs. Ligation of hilar vascular 

and bronchial structures should be performed by isolation, stapling, or suture ligation and buttressed with 

pleural or other easily mobile soft-tissue such as intercostal muscle. 

Esophageal Injury

The incidence of esophageal injuries is low, and injuries are most often the result of penetrating trauma.47

The cervical esophagus represents the most common site of injury. Injuries involving less than 50 percent 

of the circumference of the esophagus can be closed in layers after debridement. Esophageal repairs need 

to be buttressed with pleural or intercostal muscles due to the tenuous nature of these types of repairs. 

If the injury encompasses more than 50 percent of the circumference of the esophagus, or the patient 

remains physiologically compromised, the esophageal injury is locally resected and the esophagus is stapled 

in discontinuity. The proximal esophagus should be drained via nasogastric tube. Consideration should be 

given to concurrently performing gastric decompression (i.e., gastrostomy tube) and feeding jejeunostomy; 

however, both could be performed during definitive repair. The hemithorax must be widely drained with 

Figure 14. Hilar clamping or “hilar twist.” Image courtesy of the Borden Institute, Office of The Surgeon General, Washington, DC. Illustrator: 

Aletta Frazier, MD.
Damage Control Surgery | 181

a large-bore (32 French or larger) chest tube. Subsequently, definitive restitution of continuity or cervical 

esophagostomy can be performed once the patient has stabilized.48,49

The incidence of esophageal injuries is low. Esophageal injuries are most often the result of penetrating 

trauma, and the cervical esophagus represents the most common site of injury.

Neck Injury Damage Control

Vascular injury is noted in 20 percent of cases of penetrating neck trauma, and exsanguinating hemorrhage 

is the primary cause of death.50 The neck is traditionally divided into three zones to aid decision making and 

management (Fig. 16). A more detailed discussion of damage control surgery in the neck is provided in the 

Maxillofacial and Neck Trauma chapter. 

Zone II neck injuries with hard signs of vascular injury require immediate exploration (Fig. 17). These hard 

Figure 15. A patient with penetrating injuries to the right chest. This image demonstrates the right lung after it has been mobilized and twisted around 

the hilum to achieve hemorrhage control. Image courtesy of the Borden Institute, Office of The Surgeon General, Washington, DC.
182 | Damage Control Surgery

signs include uncontrollable hemorrhage, rapidly expanding hematoma, pulsatile hemorrhage, palpable 

thrill or audible bruit, or signs of neurovascular compromise (Table 1).51,52 As a general principle, the groin 

and upper thigh should be prepped to allow for saphenous vein interposition graft harvesting prior to 

vascular exploration. A standard neck incision is made from the mastoid to the sternal notch on the anterior 

border of the sternocleidomastoid muscle. The facial vein should be identified and ligated and the internal 

jugular vein retracted posteriorly using a self-retaining retractor. Injuries to the internal jugular vein can be 

repaired with lateral venorraphy or ligated (Fig. 18). After repairing vascular injuries in this zone, one must 

have a high index of suspicion and assess for esophageal and tracheal injuries. 

After repairing vascular injuries in Zone II, one must have a high index of suspicion and assess for 

esophageal and tracheal injuries.

The common carotid artery can be explored from the thoracic inlet to the base of the skull. Suspected 

proximal (Zone I) carotid injury requires partial sternotomy for proximal vascular control. Injuries to the 

common or internal carotid arteries may be repaired using lateral arteriorrhaphy, patch angioplasty, endto-end anastomosis, or bypass.53 If the patient is in extremis, the common or internal carotid vessels could 

be ligated. This approach leads to dismal outcomes, with stroke rates exceeding 20 percent and mortality 

approaching 50 percent.54 Recent studies suggest patients fare better when the internal carotid artery is 

repaired rather than ligated.53 Therefore, it is advisable to repair the injury as long as the patient remains 

Figure 16. The neck is commonly divided into three anatomic zones for 

purposes of initial assessment and management.

Figure 17. Penetrating neck trauma with expanding hematoma 

mandating immediate surgical exploration. Image courtesy of David B. 

Powers, DMD, MD, COL, US Air Force.

Hard Signs Mandating Immediate Exploration of the Neck

• Uncontrollable hemorrhage

• Rapidly expanding hematoma

• Pulsatile hemorrhage

• Palpable thrill or audible bruit

• Focal neurologic compromise

• Absent or decreased pulses in the neck or arms

Table 1. Hard signs mandating immediate exploration of the neck.

Mandible

Cricoid

III

II

I
Damage Control Surgery | 183

Figure 18. Penetrating neck injury (initial point of entry was anatomicright side of neck; Zone II). (Top Left) Preoperative radiograph 

demonstrates a fragment from a 40-millimeter grenade overlying the 

left sternoclavicular joint. (Top Right) Upon median sternotomy and 

exploration, the fragment was noted in the innominate vein, digital pressure 

was applied, and vascular control was obtained. (Bottom Right) A 

venorrhaphy was performed. After repairing vascular injuries in this zone, 

one must have a high index of suspicion and assess for esophageal and 

tracheal injuries. Images courtesy of the Borden Institute, Office of The 

Surgeon General, Washington DC.

clinically stable. An alternative approach to ligation would be placement of a temporary shunt between the two 

ends tied in place with 2-0 silk suture. 

In the case of a distal (Zone III) internal carotid artery injury that is too high for reconstruction, ligation is 

appropriate if the distal end can be ligated. In the case of a distal carotid lesion that is within the skull base, a size 

3 Fogarty embolectomy catheter can be inserted into the distal end of the internal carotid artery, placing two clips 

just below the balloon to keep it expanded and cutting the shunt to leave the balloon in the internal carotid artery 

to tamponade it and allowing it to thrombose.53 Lastly, injuries to the external carotid artery may be repaired 

using standard techniques or ligated. Transposition of the external carotid artery to the internal carotid artery 

is particularly useful when the internal carotid artery cannot be primarily repaired. This technique is used as an 

alternate to ligation.55

Transposition of the external carotid artery to the internal carotid artery is particularly useful when the 

internal carotid artery cannot be primarily repaired.
184 | Damage Control Surgery

Abdominal Injury Damage Control

The battlefield environment presents two discrete conditions in which damage control abdominal surgery 

is indicated: first and foremost is abdominal injury with severe physiologic derangement and second are the 

resource constraints of the austere environment. Examples of the former include casualties with penetrating 

abdominal injury with shock, high-velocity gunshot or abdominal penetrating injury from a secondary blast 

injury mechanism, or multisystem trauma with major abdominal injury (Fig. 19). An example of the latter 

is a mass-casualty-incident; each casualty presents with discrete surgical requirements that temporarily 

overwhelm the capacity of the system. This necessitates performing abbreviated operations (i.e., not 

definitive repairs) to accommodate all patients in an expedient manner (Fig. 20). In a recent military analysis, 

the presence of shock and penetrating torso injury was an independent risk factor for the requirement for 

damage control resuscitation and expedited operative intervention.29,56

Damage Control Laparotomy

Early anticipation of the necessity for damage control resuscitation and surgery improves outcomes in this 

severely injured population.

Adequate patient preparation is essential. Once in the operating room, the patient is placed in the supine 

position and prepped from chest to groin. A generous midline incision is made and carried down through 

the midline fascia. Once the peritoneum is opened, the aorta may be manually compressed at the hiatus of 

the diaphragm if severe arterial hemorrhage is noted, and intraperitoneal blood can be quickly evacuated. 

This can be rapidly accomplished by pressing the sides of the abdomen together, expressing most of the 

blood and clot out onto the drapes, and subsequently packing any areas of ongoing hemorrhage. If control 

Figure 19. (Left) Abdominal damage control surgery is indicated for 

abdominal injury with severe physiologic derangement. This patient was 

injured by an M16 round. Image courtesy of the Borden Institute, Office 

of The Surgeon General, Washington, DC.

Figure 20. (Below) Resource constraints in a battlefield environment 

(e.g., mass-casualty-incident) may mandate an abbreviated operation. 

Image courtesy of Harold Bohman, MD, CAPT, MC, US Navy.
Damage Control Surgery | 185

of hemorrhage is adequate, time is given to the 

anesthesiologist to restore intravascular volume in 

response to any decrease in blood pressure caused 

by releasing the peritoneal tamponade. 

In patients with persistent hemorrhage from 

abdominal great vessel injury not amenable to 

packing, priority is given to inflow and outflow 

control of the injured vessel. Temporary aortic 

control can be gained at the diaphragmatic hiatus 

by posterior compression with a Richardson 

retractor or clamping of the aorta, which can 

be accessed through the gastrohepatic ligament. 

Likewise, control of the aorta can be obtained 

through the left chest via left-sided anterolateral 

thoracotomy if more proximal control is necessary. 

Once aortic inflow is controlled, exposure is the key 

to abdominal vascular control. The entire abdominal aorta and the common iliac vessels can be visualized 

through a left medial visceral rotation. Conversely, a right medial visceral rotation with a Catell-Braasch 

maneuver will allow visualization of the infrarenal inferior vena cava and the aorta up to the level of the 

superior mesenteric artery axis (Fig. 21). Adding a Kocher maneuver will expose the inferior vena cava to 

the subhepatic level as well as fully mobilize the duodenum and head of the pancreas. 

In patients with persistent hemorrhage from abdominal great vessel injury not amenable to packing, 

priority is given to inflow and outflow control of the injured vessel.

Once the injury is identified, a damage control therapeutic plan can be better developed. With injuries 

to the suprarenal aorta, lateral arteriorrhaphy should be strongly considered since protracted clamping 

of the aorta at this level during repair will result in visceral ischemia and exacerbation of physiologic 

anomalies.57 For an infrarenal aortic injury, an attempt should be made at local repair, and at this point 

aortic clamping should be reassessed and either removed or repositioned to the most distal portion of the 

aorta. If not feasible, an interposition tube graft is a better option than patch angioplasty. It should be 

remembered that in young adults, the aorta is quite small and rarely will accommodate a graft larger than 

16 millimeters (mm). Repair in young or thin patients should be buttressed with omentum due to the thin 

retroperitoneum. In dire circumstances, a temporary chest tube shunt can be considered. The iliac arteries 

can likewise be shunted in the damage control setting. In select circumstances, the surgeon may need to 

transect the overlying right common iliac artery to expose and control an injury to the confluence of the 

common iliac veins for hemorrhage control. 

With injuries to the suprarenal aorta, lateral arteriorrhaphy should be strongly considered since protracted 

clamping of the aorta at this level during repair will result in visceral ischemia, and exacerbation of 

physiologic anomalies. For an infrarenal aortic injury, an attempt should be made at local repair.

Figure 21. A right medial visceral rotation with a Catell-Braasch 

maneuver will allow visualization of the infrarenal inferior vena cava and 

the aorta up to the level of the superior mesenteric artery axis.
186 | Damage Control Surgery

Retrohepatic Hematoma

A retrohepatic hematoma controlled with packing should not be explored. If vigorous hemorrhage is 

emanating from the posterior aspect of the liver, a Pringle maneuver should be performed to control 

hepatic arterioportal vascular inflow. If this maneuver controls the hemorrhage, then the hemorrhagic 

source is intrahepatic. If this maneuver does not control the hemorrhage, then there is a high likelihood 

that the patient has a retrohepatic vena cava injury.58 Upon identifying a retrohepatic vena cava injury 

that is not amenable to tamponade by packing, an immediate decision needs to be made to approach the 

injury via total hepatic vascular isolation. Anesthesia must be forewarned that the isolation procedure will 

restrict preload from the lower half of the body so large-bore upper central venous access is mandatory. 

The hepatic arterioportal inflow occlusion is maintained. Then, control of the inferior vena cava above 

the renal veins is developed.59 At this point, control of the suprahepatic inferior vena cava is obtained in 

order to minimize manipulation of the retrohepatic hematoma. This can be done most easily by gaining 

control within the pericardium. Pericardial access can be developed through the diaphragm or via median 

sternotomy and pericardiotomy. 

A retrohepatic hematoma controlled with packing should not be explored.

An alternate approach to the suprahepatic inferior vena cava would be to extend the abdominal incision 

via a right thoracoabdominal incision, which would also offer better exposure to the right and superior 

portions of the liver. In either approach, it is important to mobilize the right triangular ligament of the liver 

first. Once the injury is identified, it can be repaired using monofilament suture. Penetrating injuries with 

suspicion of injury to the subhepatic inferior vena cava require exploration. These juxtarenal caval injuries 

also require repair. If hemorrhage stops with repair of the anterior hole, it is not necessary and even may be 

counterproductive to expose the posterior wall of the vena cava looking for a posterior hole in the damage 

control setting. Infrarenal inferior vena cava injuries can be ligated if patient acuity dictates. Infrarenal 

inferior vena cava ligation is fairly well tolerated in younger patients.60 However, ligation of the suprarenal 

inferior vena cava is usually associated with renal failure and massive lower extremity edema.61,62

Infrarenal inferior vena cava injuries can be ligated if patient acuity dictates. However, ligation of 

the suprarenal inferior vena cava is usually associated with renal failure and massive lower extremity 

edema.

Perihepatic Vascular Injury

Perihepatic vascular injuries require special consideration. Once again, packing is the damage control 

mainstay, provided it controls hemorrhage. Hepatic artery ligation may be useful in controlling 

hemorrhage if packing is not successful.63,64 The supraduodenal portal vein may be ligated for damage 

control. When both the portal vein and hepatic artery are damaged, at least one of the vessels must be 

salvaged.

Hepatic Parenchymal Injury

Bleeding from within the hepatic parenchyma can often be controlled initially with manual compression, 

with placement of hands on either side of the major laceration(s) and pressing together. This will allow 

the anesthesia team to restore intravascular volume via blood component transfusions before proceeding. 

The decision at this point should be whether packing (superiorly, anteriorly, and posteriorly) is adequate to 

maintain hemostasis. 
Damage Control Surgery | 187

Adjunctive measures like topical hemostatic agents (e.g., fibrin sealants) in conjunction with packing may be 

useful with large hepatic lacerations. Topical hemostatic agents may not be readily accessible and are often 

time-consuming to prepare. Direct suturing is one of the oldest techniques to control deep parenchymal 

bleeding using large blunt-tipped 0-chromic sutures.65 The sutures may be placed in a continuous or 

mattress configuration. Suturing should be limited to lacerations less than three centimeters in size to 

prevent blind suturing leading to significant bile duct injuries.66,67 More complex lacerations often involve 

larger hepatic artery or portal branch vessels, which usually do not respond to packing. Gentle finger 

fracturing may be used to identify specific bleeding vessels and facilitate ligation.68 One must be careful not 

to create excessive additional parenchymal bleeding using this finger-fracturing technique.

Bleeding from within the hepatic parenchyma can often be initially controlled with manual compression. 

Suturing should be limited to lacerations less than three centimeters in size, as blind suturing may lead to 

significant bile duct injuries.

Omental packing has been successfully used for tamponading dead spaces with live-tissue, as well as for 

achieving hemostasis following hepatic hemorrhage. The omentum is first mobilized from the transverse 

mesocolon in the avascular plane and then off the greater curvature of the stomach. In general, this 

technique is superior to most direct techniques of hemorrhage control.68,69 In civilian study populations, 

severe and complex liver lacerations treated with formal hepatic resections are associated with low mortality 

and liver-related morbidity.70 The authors in these studies achieved 9 percent liver-related mortality and 

17.8 percent liver-related morbidity with senior surgeon support (often a surgeon specifically from the liver 

service). A similar level of surgical expertise (i.e., liver specialists) is not available in a combat theater, hence 

such surgical interventions are generally avoided in a deployed setting.

Pancreatic and Duodenal Injuries

The surgical management of duodenal and pancreatic (particular head region) injuries can be challenging 

and complex. Pancreatic injuries (other than distal injuries) should be treated with hemorrhage control, 

modest debridement of devitalized tissue, and wide closed-suction drainage.71,72 Placement of a feeding 

jejeunostomy tube, assessment for pancreatic ductal continuity, and further definitive care should be 

performed at the next rearward level-of-care. Pancreatic injuries distal to the superior mesenteric artery 

can be managed with distal pancreatectomy and closed-suction drainage.73

Pancreatic injuries (other than distal injuries) should be treated with hemorrhage control, modest 

debridement of devitalized tissue, and wide closed-suction drainage. Pancreatic injuries distal to the 

superior mesenteric artery can be managed with distal pancreatectomy and closed-suction drainage.

Duodenal injuries can be primarily repaired when there is no risk of lumenal compromise.71 The duodenum 

should be debrided and closed transversely if the injury involves less than 50 percent of the circumference 

of the duodenal wall (Fig. 22). If tissue destruction is extensive, the repair will necessitate pyloric exclusion 

with triple-tube placement: gastrostomy tube, retrograde jejeunostomy (to decompress the duodenum), 

and antegrade feeding jejeunostomy.74 With complete duodenal transection, it would be best to perform 

closure of the proximal and distal duodenum with definitive repair at the next rearward level-of-care with 

either Roux-en-Y jejeunostomy or duodenojejeunostomy.75 In uncommon cases of destructive combined 

injuries to the duodenum and pancreatic head, a pancreaticoduodenectomy (Whipple procedure) is a 

surgical option.72 This should only be performed by experienced personnel in well-resourced facilities. 
188 | Damage Control Surgery

A pancreaticoduodenectomy should not be performed in an austere environment. In a damage control 

surgery setting, destructive injury to the pancreatic head should be treated with drainage.

Renal Injury

Renal injuries will often respond to compressive tamponade in the damage control setting provided that 

Gerota’s fascia has not been violated. Nonexpanding hematomas within Gerota’s fascia need not be 

explored during a damage control celiotomy. Subsequent management can be determined after the patient 

is stable.76,77

Although the dictum for renal vascular injuries has been proximal and distal control prior to opening 

Gerota’s fascia, vascular control of the renal hilum has been shown to have no impact on nephrectomy 

rates, transfusion requirements, or blood loss.

Absolute indications for renal exploration during damage control laparotomy include hemodynamic 

instability, expanding pulsatile renal hematoma, suspected renal pedicle avulsion, and ureteropelvic junction 

disruption (Figs. 23 and 24).76,77 Although the dictum for renal vascular injuries has been proximal and 

distal control prior to opening Gerota’s fascia, vascular control of the renal hilum has been shown to have 

Figure 22. Duodenal injuries can be primarily repaired when there is no 

risk of lumenal compromise. (Top Left) Kocher maneuver demonstrating 

through-and-through injury to the duodenum. (Top Right) Repair 

of injury with two-layer closure. (Bottom Right) Closed duodenum.

Images courtesy of the Borden Institute, Office of The Surgeon General, 

Washington, DC.
Damage Control Surgery | 189

Figure 23. (Top Right) Penetrating renal injury. A nephrectomy should 

be performed following complex renal injuries in an unstable patient. 

Image courtesy of the Borden Institute, Office of The Surgeon General, 

Washington, DC.

Figure 24. (Middle) A renal injury may be locally debrided and closed 

if operative conditions allow or (Bottom) excised in the course of partial 

nephrectomy. Images courtesy of the Borden Institute, Office of The 

Surgeon General, Washington, DC. Illustrator: Jessica Shull.
190 | Damage Control Surgery

no impact on nephrectomy rates, transfusion requirements, or blood loss.78 In fact, operative time may be 

increased with such vascular control techniques. Based on this study and the fact that most surgeons are 

not experienced in renal hilum isolation, it is recommended to forego renal hilar vascular control prior 

to entering Gerota’s fascia. With complex injuries and/or an unstable patient, a nephrectomy should be 

performed rather than attempting repair. If nephrectomy is considered, the presence of a contralateral 

kidney should be confirmed. 

A nephrectomy should be performed following complex renal injuries in an unstable patient, rather than 

attempting repair.

Ureteral Injury 

Ureteral injuries are uncommon and account for only 1 to 3 percent of penetrating urologic trauma.79,80,81

They are often overlooked when not appropriately considered and are more likely to be associated with 

retroperitoneal hematoma and injuries of the fixed portions of the colon, duodenum, and spleen.82,83,84

Management of ureteral injuries depend on location, severity of injury, and hemodynamic stability of the 

patient. 

Primary ureteral repair is not recommended in patients who present in shock or in those with severe 

colonic injury requiring colostomy.83 Ureteral repair in these patients necessitates exteriorization of the 

ureter via tube or cutaneous ureterostomy, ureteral ligation and nephrostomy, or even ligation and primary 

nephrectomy.83 Short proximal and midureteral injuries in hemodynamically stable patients are best 

managed by end-to-end spatulated anastomosis over a stent. Longer segment injuries may require ureteral 

exteriorization or ligation with nephrostomy (Fig. 25).82

Short ureteral injuries may be managed by anastomosis over a stent, while longer ureteral injuries may 

require cutaneous ureterostomy with stent placement or ureteral ligation with tube nephrostomy.

Distal ureteral injuries are best managed by ureteroneocystostomy. This is performed by a transverse 

cystotomy, which elongates the bladder to the location and fixation of the bladder to the psoas fascia. 

Both maneuvers facilitate the construction of a tension-free anastomosis.82 Some have advocated against 

ureteral reimplantation following distal ureteral injuries associated with rectal injuries due to concerns 

about wound dehiscence.82,83 Successful ureteroneocystostomy following distal ureteral injuries complicated 

by rectal injuries has been reported.85 Meticulous debridement of all necrotic tissues, urinary and fecal 

diversion, tension-free wound closure with well-vascularized tissue, and adequate drainage and separation 

of injured sites with well-vascularized tissue (such as omentum) are integral to reducing the incidence of 

fistulae formation following combined ureteral and rectal injuries.85 

Splenic Injury

Severely injured combat casualties undergoing damage control surgery with active hemorrhage from 

the spleen should undergo immediate splenectomy (Fig. 26). Observational management or packing of 

the spleen following injury is not feasible in most injured US service members. Such patients rapidly 

undergo aeromedical evacuation and are cared for by multiple careproviders as they are moved to more 

rearward facilities for definitive care. These factors make observational (nonoperative) management of 

significant splenic injuries impractical. This approach differs significantly from civilian trauma care where 
Damage Control Surgery | 191

Figure 25. Ureteral injuries: (Top Right) Short proximal and 

midureteral injuries in hemodynamically stable patients are best managed 

by end-to-end spatulated anastomosis over a stent. Longer segment injuries 

may require ureteral exteriorization or ligation with nephrostomy. (Bottom 

Left and Bottom Right) Distal ureteral injuries are best managed by 

ureteroneocystostomy. This is performed by a cystotomy, which elongates 

the bladder to the location and fixation of the bladder to the psoas fascia. 

Images courtesy of the Borden Institute, Office of The Surgeon General, 

Washington, DC. Illustrator: Jessica Shull.
192 | Damage Control Surgery

nonoperative management of blunt splenic injury is the treatment of choice for a hemodynamically stable 

patient, regardless of grade of injury.86 Angiographic embolization is a useful adjunct in the nonoperative 

management of a hemodynamically stable patient with continued bleeding from a splenic injury.87

Unfortunately, this interventional technology is not readily available in Level III facilities in Iraq and 

Afghanistan.

Severely injured combat casualties undergoing damage control surgery with active hemorrhage from the 

spleen should undergo immediate splenectomy.

Large Soft-Tissue and Retroperitoneal Wounds

Large abdominal soft-tissue and retroperitoneal wounds are not uncommon in the combat environment, 

particularly with explosion-related injuries (Fig. 27). These wounds present the vexing challenge of controlling 

a large area of soft-tissue hemorrhage in an often coagulopathic casualty. Temporizing hemorrhage control 

can be achieved with the combination of topical hemostatic agents such as Surgicel® Nu-Knit® 

(Ethicon, Inc.) or Gelfoam® tightly compressed into the wound with laparotomy pads.88

Intestinal (Enteric) Injuries

Once control of hemorrhage is obtained, attention is turned to control of contamination. In the damage 

control laparotomy, all enteric injuries that cannot be repaired by simple suture repair are resected locally, 

or en bloc if multiple injuries in close proximity are noted (Fig. 28). The bowel is then stapled with a GIATM 

stapler and left in discontinuity. No attempt should be made to do a primary enteric anastomosis in the 

damage control setting.89 Likewise, enteric diversion should be postponed and not performed during the 

initial damage control procedure.90 Abdominal wounds associated with colonic injuries (particularly leftsided) need to be monitored closely, and serial local debridement should be strongly considered since these 

injuries are often complicated by infections.

Figure 26. Splenic laceration due to gunshot wound (GSW). Severely 

injured combat casualties with active hemorrhage from the spleen should 

undergo immediate splenectomy. Images courtesy of the Borden Institute, 

Office of The Surgeon General, Washington, DC. 

Figure 27. Large abdominal soft-tissue and retroperitoneal wounds, seen 

with explosion-related injuries, will have difficult to control hemorrhage. 

Image courtesy of David Burris, MD, COL, MC, US Army.
Damage Control Surgery | 193

During damage control laparotomy, all enteric injuries that cannot be repaired by simple suture repair 

should be resected locally, or en bloc if multiple injuries in close proximity are noted. Primary enteric 

anastomosis should not be attempted during the initial damage control laparotomy.

Rectal Injury

Injuries to the rectum should be defined as either intraperitoneal or extraperitoneal. Intraperitoneal rectal 

injuries follow the same concepts outlined previously with enteric injuries. However, extraperitoneal rectal 

injuries should be treated with end colostomy or loop colostomy. If the rectal defect is not readily identifiable 

for closure, one should not perform extensive dissection and mobilization of the rectum. Although civilian 

data suggest that presacral drains and distal stump washout are of limited benefit, military doctrine remains 

to place presacral drains and consider a distal washout for massive injuries.91,92,93

Extraperitoneal rectal injuries should be treated with end colostomy or loop colostomy.

Figure 28. Suture repair of small bowel perforations following penetrating abdominal injury.
194 | Damage Control Surgery

Abdominal Wall Closure

Once hemorrhage is controlled and the contamination contained, the abdomen is covered with a sterile 

dressing and a negative-pressure suction device applied. The open abdomen accommodates abdominal 

visceral swelling, which is a consequence of reperfusion injury, and minimizes the risk of postoperative 

abdominal compartment syndrome (Fig. 29).94,95,96,97 Abdominal compartment syndrome (intraabdominal 

hypertension) is a potentially lethal disorder caused by conditions that elevate intraabdominal pressure to 

the point of impairing end-organ function. Excessive fluid resuscitation, reperfusion injury, burn injury, 

abdominal cavity packing, and intraperitoneal hemorrhage are examples of factors that can lead to 

abdominal compartment syndrome in the combat casualty.98,99

The fascia is left open following damage control surgery, and the abdomen is temporarily sealed with a 

sterile dressing and negative-pressure suction device. Skin closure may lead to abdominal compartment 

syndrome.

The physiologic effects of abdominal compartment syndrome affect many organs.99,100,101,102 Clinical 

manifestations result from diminished preload (decreased venous return) and elevated systemic vascular 

resistance leading to a decrease in end-organ perfusion. Patients will also exhibit evidence of respiratory 

insufficiency due to diminished lung volumes (due to impeded diaphragmatic excursion). Patients undergoing 

mechanical ventilation will exhibit high peak airway pressures and decreased urine output caused by 

falling renal perfusion pressures, despite adequate volume resuscitation. Elevated intracranial pressures 

and adverse effects on cerebral perfusion pressures have also been linked to abdominal compartment 

syndrome in patients with severe head injuries. 99,102

Abdominal compartment syndrome was noted in 33 percent of patients in one case series of patients 

undergoing a damage control surgery in a civilian setting.97 The diagnosis of abdominal compartment 

syndrome is made by indirectly assessing intraabdominal pressures via Foley catheter bladder pressure 

measurements. A partially filled bladder is very compliant and has been used as an accurate method to 

assess surrounding intraperitoneal pressures.98 Abdominal compartment syndrome has been defined by 

Figure 29. Temporary abdominal wall closure. Leaving the abdominal wall open accommodates abdominal visceral swelling and minimizes the risk of 

postoperative abdominal compartment syndrome. (Left) A sterile dressing with negative-pressure suction device. (Right) A sterile three-liter crystalloid 

solution bag used for closure. Right-sided image courtesy of the Borden Institute, Office of The Surgeon General, Washington, DC. 
Damage Control Surgery | 195

intraabdominal pressures greater than 20 mm Hg, abdominal perfusion pressure less than 60 mm Hg 

(mean arterial pressure minus intraabdominal pressure), and single or multisystem organ failure.98,100,103 

It is important to remember that an abdominal compartment syndrome can develop even with an open 

abdomen, and it is imperative that serial evaluation for this contingency occurs with revision of the 

closure if necessary. The exact intraabdominal pressure that warrants an intervention remains unclear. 

There appears to be consensus agreement that intraabdominal pressures greater than 30 mm Hg require 

an intervention.98,99,100,104 Decompressive laparotomy, or an alternative intervention (e.g., loosening of 

abdominal dressings), to relieve intraabdominal pressures in patients with an open abdomen is indicated 

when abdominal compartment syndrome is suspected. If left untreated, abdominal compartment syndrome 

can lead to death.

Peripheral Vascular Injury Damage Control

The concept of successful damage control surgery for peripheral vascular injury had not been fully realized 

until the recent implementation of temporary vascular shunts in Afghanistan and Iraq.105,106 During 

World War I, German surgeons reported repair of over 100 arterial injuries and pioneered autogenous 

reconstruction of injured vessels.105 However, the proclivity for mass casualties, significant soft-tissue injury, 

and protracted transport times made routine vascular reconstruction impractical, and subsequently, ligation 

of vessels became standard practice.105,106,107 DeBakey reported 2,471 arterial injuries treated by ligation 

in World War II with a 49 percent amputation rate.108 With these dismal results, the standard of practice 

became definitive arterial repair in the Korean War with a dramatic reduction in amputation rate to 13 

percent.109 Similar successes were documented during the Vietnam conflict.105,106,107 Therefore, leading up 

to the conflicts in Afghanistan and Iraq, damage control with ligation was abandoned in favor of definitive 

vascular repair with greatly improved results.

Arterial Injury and Temporary Vascular Shunts

Improvements in the paradigm of casualty resuscitation during Operation Enduring Freedom (OEF) and 

Operation Iraqi Freedom (OIF) have provided greater opportunities for deployed surgeons to successfully 

perform vascular repair after injury on the battlefield. The use of temporary vascular shunts allowed 

the extension of this damage control paradigm to the treatment of peripheral vascular injuries. In one 

report, 57 percent of casualties with peripheral arterial injuries had shunts placed at forward surgical 

facilities, and 86 percent of these shunts were patent when the patient arrived at the Combat Support 

Hospital (CSH). In two separate analyses of data from the Joint Trauma Theater Registry (JTTR), damage 

control resuscitation and damage control surgery techniques applied in the context of vascular injury using 

temporary shunts allowed for delayed prolonged complex limb revascularizations with limb salvage rates 

of 95 percent.110,111 Clouse and Sohn independently demonstrated similar in-theater acute limb salvage 

rates for revascularization of 92 to 95 percent.112,113 The successful use of temporary vascular shunts allows 

for ongoing patient resuscitation and transport to definitive care with a perfused extremity.114

Temporary vascular shunts are an effective tool in the management of extremity vascular injury and allow 

for ongoing patient resuscitation and extremity perfusion during transport to definitive care.

An important difference between combat and civilian practice is the role of arteriographic study to rule out 

vascular injury for proximity wounds. Civilian practice has evolved to expectant management of wounds in 
196 | Damage Control Surgery

proximity to critical blood vessels if there are no hard signs of vascular injury. Studies have demonstrated 

no increase of vascular lesions requiring surgical therapy under these circumstances.115,116,117 However, the 

high-energy nature of combat wounds led military investigators to reevaluate this management paradigm 

in combat casualties (Fig. 30). In a study of 99 patients who underwent angiography after evacuation for 

wound proximity, 47 percent had vascular abnormalities noted on angiography. Two-thirds of this group 

had a normal physical examination. Importantly, 52 percent of the patients with an abnormal arteriogram 

required operative intervention.118 In an analysis of combat-related penetrating neck trauma by Fox et 

al., 30 percent of patients undergoing computerized tomographic angiography had occult injury and 50 

percent of these required interventional or surgical management.119

Role of Temporary Vascular Shunts in Afghanistan and Iraq

Experience from nearly a decade of war in Afghanistan and Iraq suggests that temporary vascular shunts 

are a feasible and effective tool in the management of extremity vascular injury. 114,120,121,122 The use of 

temporary vascular shunts is particularly germane in modern combat where the rate of vascular injury (5 to 

7 percent) is much higher than reported in previous wars.112,120 The increased use of body armor and other 

force protection measures as well as tourniquets may increase the survivability of wounds that were deadly 

in previous wars.123 As such, injured service members who in the past may have succumbed to torso wounds 

or exsanguination from extremity injuries now survive to have vascular injuries recorded and treated.120

In this context, temporary vascular shunts are part of a management triad of: (1) vascular injury exploration; 

(2) thrombectomy and restoration of flow; and (3) fasciotomy. Following injury exploration, vascular shunts 

are inserted in both ends (proximal and distal) of the disrupted vessel to bridge and provide flow distal to 

the defect, and maintain limb viability (Fig. 31). Shunts can typically be placed in an expeditious manner 

and require less time and technical expertise than formal vascular repair. Data from the Balad Vascular 

Figure 30. Proximity wounds. (Left) Due to the greater energy imparted by military ballistic projectiles, injury in proximity to critical blood vessels, 

particularly in the cervical region, should be evaluated by angiography to mitigate the risk of occult vascular injury. (Right) The subsequent carotid 

angiogram revealed a vascular injury requiring coil repair. Images courtesy of David B. Powers, DMD, MD, COL, US Air Force.
Damage Control Surgery | 197

Figure 31. Vascular repair: (Top Left) Level III facility care of a 

casualty with a GSW to the right upper arm with an open comminuted 

humeral fracture and transected right brachial artery and median nerve. 

The casualty was initially treated at a Level II facility and underwent 

vascular injury exploration, placement of a JavidTM temporary vascular 

shunt in the right brachial artery, and forearm fasciotomy. An external 

fixator was applied. (Top Right) A radiograph obtained at the Level III 

ED five hours following injury reveals the presence of an indwelling shunt.

(Center Left) A patent shunt with excellent Doppler signal was noted 

during surgical exploration. (Center Right) The shunt was removed and 

an interposition vein graft repair of the brachial artery was performed.

(Bottom Left) A negative-pressure suction device was applied and the 

patient was transported to a Level IV facility. 
198 | Damage Control Surgery

Registry reveals that a majority of temporary vascular shunts are placed during Level II damage control 

surgical care, prior to the medical evacuation of casualties to Level III facilities.112,114 A review of in-theater 

evacuation data reveals an average time from loading on a helicopter to arrival at a Level III facility of 46 

minutes.120

Temporary vascular shunts are part of a management triad of: (1) vascular injury exploration; (2) 

thrombectomy and restoration of flow; and (3) fasciotomy.

Once placed, shunts maintain perfusion to the extremity (distal to the site of injury) during medical 

evacuation (MEDEVAC) or treatment of other life-threatening torso or head injuries. In this sense, 

shunts are amenable to use in forward surgical units where damage control or abbreviated operations (less 

than one hour) are the goal.114,121,122 The alternative to initiating the previously mentioned management 

triad is deferring vascular injury treatment during MEDEVAC and/or management of other injuries. 

If restoration of flow to the extremity is delayed in these instances, warm-ischemia time compounds 

increasing neuromuscular damage and decreases the likelihood of limb recovery and salvage. 

Data from a large-animal model of hind-limb ischemia and reperfusion demonstrated that early restoration 

of flow using temporary vascular shunts reduced circulating markers of injury and resulted in improved 

flow in the injured extremity.124 Specifically, this study showed that restoration of flow following one hour 

of ischemia resulted in an 18-hour reperfusion profile that was the same as controls (i.e., no ischemia). In 

contrast, restoration of extremity flow with a temporary vascular shunt after three to six hours resulted in 

reperfusion profiles that were incrementally adverse. The conclusion of this study was that early (one hour) 

versus delayed (greater than three hours) restoration of flow was associated with measurably improved 

responses.124 The presence of shock or other soft-tissue or bony injury may even further reduce this ischemic 

threshold to less than three hours, after which recovery of the limb should not be expected. Results from 

these large-animal experiments inform surgeons that the critical warm-ischemia time for an extremity in 

the combat setting (i.e., with hemorrhage and soft-tissue injury) is likely less than three hours and may be 

as short as one hour.

Results from large-animal experiments suggest that the critical warm-ischemia time for an extremity in a 

combat setting (i.e., with hemorrhage and soft-tissue injury) is likely less than three hours and may be as 

short as one hour.

Early reports from Iraq indicated that shunts were being used effectively at forward Level II facilities.114,121,122

Specifically, JavidTM, ArgylTM, and SundtTM shunts have been extensively used. Shunts remained in 

place during MEDEVAC to higher levels of in-theater care where they were then removed and definitive 

reconstruction performed.114,121,122 During times of high casualty rates in Iraq, shunts were used in up to 50 

percent of femoral/popliteal injuries, a frequency that is similar to that currently encountered in Afghanistan 

by the author (TR).125

Complications

Early temporary vascular shunt-related complications have been rare, and shunt patency, when placed in 

larger, more proximal arteries of the extremities, approaches 90 percent at four to six hours.114,121,122 Data 

from the JTTR, Balad Vascular Registry, and the Walter Reed Vascular Registry demonstrate that use of 
Damage Control Surgery | 199

temporary vascular shunts as an adjunct in damage control surgery did not result in worse outcomes. In 

fact, the use of shunts extended the window of opportunity for limb salvage in the most severely injured 

limbs. However, demonstration of definitive benefit was not shown.126 Late complications associated 

with revascularization do occur and include thrombosis, infection, and compartment syndrome.110,127

Interestingly, the factor most significantly associated with post-revascularization morbidity was the use of 

prosthetic graft implants. Unlike the results of civilian vascular injury, when a prosthetic graft was used 

with combat vascular injuries, the incidence of graft loss was 80 percent.110,120,127 Hence, a primary goal 

of vascular surgeons at Level III facilities is to ensure no temporary vascular shunt or prosthetic conduit be 

sent out of theater. Definitive repair of vascular injuries with primary or autologous vein repair is a priority.

Vascular surgeons at Level III facilities should perform definitive repair of vascular injuries that have been 

previously treated with a temporary vascular shunt or prosthetic conduit prior to transport to a Level IV 

or Level V facility.

Reperfusion injury often results in extremity compartment syndrome following restoration of perfusion 

to injured limbs. Hence, prophylactic fasciotomy following definitive vascular repair of an injured limb 

is recommended.128 Prophylactic fasciotomy should also be considered (especially if prolonged medical 

evacuation times are anticipated) concurrent with the placement of temporary vascular shunts, for similar 

reasons.

Recent increased operational activity in the Afghanistan Theater has provided the opportunity to assess the 

effectiveness of temporary vascular shunts in an environment with unique casualty evacuation (CASEVAC) 

and MEDEVAC characteristics. In contrast to OIF, CASEVAC and MEDEVAC in Afghanistan are 

challenged by mountain passes, which hinder direct rotary-wing transport in many cases. Additionally, the 

multinational nature of combat casualty care in OEF results in instances of intratheater transport of injured 

casualties to nation-specific air hubs for preparation for transcontinental air evacuation (AIREVAC). These 

realities have given rise to a form of MEDEVAC which includes intratheater use of fixed-wing casualty 

movement referred to as tactical evacuation (TACEVAC). In this setting, vascular injury management has 

been challenged by instances of longer times between injury and definitive vascular repair. The generally 

longer TACEVAC times in OEF have given rise to observations by the author (TR) of longer indwell times 

of temporary shunts (up to 12 to 24 hours) without complication. Although not tested because of rapid 

and consistent MEDEVAC during OIF, these observations are consistent with experiments demonstrating 

up to 24-hour patency of shunts without the use of heparin.124,129 In the author’s (TR) experience, the 

use of temporary vascular shunts in Afghanistan is nearly uniform in extremity vascular injuries, and 

complications remain uncommon. As in Iraq, even if temporary vascular shunts occlude or clot, it does not 

preclude removal of the shunt and restoration of flow with formal vascular repair at Level III facilities. 

Conclusions

In aggregate, this data, combined with a decade’s experience in OEF/OIF, lead to the conclusions that 

early restoration of flow (within one hour) using temporary vascular shunts is advantageous. Specifically, 

when formal vascular repair is not possible, shunts should be used as part of the management triad of: 

(1) extremity vascular injury exploration; (2) thrombectomy and restoration of flow; and (3) fasciotomy. 

The application of this management triad should occur as soon as feasible after injury, in the context of 

tactical considerations and other concomitant life-threatening head and torso injuries. Whether this triad 
200 | Damage Control Surgery

is undertaken at a Level II or III facility is a matter of semantics and is more dependent upon the time 

from injury to point of surgical care. Temporary vascular shunts are part of the management triad of 

injury exploration, restoration of flow, and fasciotomy. Ideally, their use reduces warm-ischemia time 

and extends the window of opportunity for limb salvage. Experienced vascular surgeons, cardiothoracic 

surgeons, or trauma surgeons are usually only located at Level III facilities. Vascular injuries sustained in the 

combat environment must undergo arterial reconstruction with autogenous material at Level III facilities, 

since prosthetic grafts have a much higher rate of infection. 

Venous Injury

In the context of battlefield venous injury, ligation is a safe and effective option. Venous ligation is an 

expedient solution that allows the surgeon to address other injuries in critically ill patients. A review of 

the management of 103 venous injuries from the Global War on Terror indicates ligation (63 percent) is 

more common then repair (37 percent).130 All patients, regardless of management, developed postoperative 

edema. While thrombosis of the repair was demonstrated in 16 percent of the repaired veins, there was no 

acute limb loss or venous graft failure associated with venous ligation.130 Pulmonary embolus developed in 

three cases, one in a patient with open repair, and two in cases managed with ligation. Long-term outcomes 

and follow-up data are needed to determine what the best approach to management should be.

Ligation is a safe and effective option for combat-related venous injury.

Proximity to Great Vessel Injury

Contrary to civilian trauma literature recommendations, penetrating extremity injury in proximity to critical 

blood vessels, particularly in the cervical region, should be evaluated by angiography to mitigate the risk of 

occult vascular injury due to the greater energy imparted by military ballistic projectiles.119 It is important 

to know the patient’s total trauma burden and physiology when deciding how to manage that patient’s 

vascular injury. The treatment of vascular injuries in combat casualties can be a challenging endeavor in a 

resource-limited environment. Optimal care depends upon technical expertise on the part of the operating 

surgeon and solid judgment regarding when to perform temporizing maneuvers versus definitive repairs. 

Surgeons at all Level II and III facilities need to be intimately familiar with the use of vascular shunts as a 

means to stabilize a critically wounded casualty and then move them along the continuum of care.

Penetrating extremity injury in proximity to critical blood vessels, particularly in the cervical region, 

should be evaluated by angiography to identify occult vascular injury.

Extremity Tourniquets

Control of life-threatening hemorrhage following extremity injury has been greatly improved through 

the field application of the extremity tourniquet.131,132 Patients requiring damage control procedures 

for presumed extremity vascular hemorrhage should have the prehospital tourniquet prepped into the 

operative field or replaced by a sterile tourniquet in the operating room (Fig. 32). Basic vascular surgery 

principles of proximal and distal control are employed to access extremity vessel injury (Fig. 33). The 

majority of injuries in patients with penetrating extremity trauma can be explored directly with no need 

for preoperative arteriography. However, in patients with diffuse or multiple extremity injuries associated 

with vascular compromise, arteriography is often useful if the patient’s physiologic status will tolerate the 

procedure.118,133
Damage Control Surgery | 201

Upper Extremity Arterial Injury

The axillary artery can be exposed through an infraclavicular incision from midclavicle to the deltopectoral 

groove through the clavipectoral fascia. The brachial artery is accessed by incising the medial aspect of 

the upper arm between biceps and triceps. When gaining control of the brachial vessel, care should be 

taken to avoid injury to the basilic vein and median nerve. An S-shaped incision is required if the incision 

crosses antecubital fossa. If the vascular injury is below the profunda brachii, the patient will usually tolerate 

ligation. The radial and ulnar arteries can generally be singly ligated.134 However, an Allen test is required 

to assess the vascular integrity of the hand prior to vessel ligation.

Femoral Vasculature Injury

In the lower extremity, the femoral artery can be accessed proximally via a standard femoral cutdown. For 

superficial femoral arteries, acute occlusion in young healthy patients without established collateral flow 

is not well-tolerated.135 In the damage control setting, the superficial femoral vessels are easily shunted by 

standard shunting techniques. This vessel can be definitively repaired or an autogenous interposition graft 

placed once the patient has been adequately resuscitated. The majority of venous injuries can be ligated, 

especially if the patient is in extremis.130 After performing a deep venous ligation in the lower extremity, it is 

incumbent upon the surgeon to be aware of the subsequent lower extremity venous hypertension and risk 

for the development of a lower extremity compartment syndrome. As such, liberal use of four compartment 

fasciotomies through extended incisions should be considered.

 

Popliteal and Tibial Vasculature Injuries

The popliteal artery behind the knee requires an extended medial approach, dividing tendinous muscular 

attachments of the hamstring complex and the soleus. Again, depending upon the acuity of the patient 

and available resources, the therapeutic options include shunting, repair, or bypass. If the popliteal vein is 

injured, it should be repaired if the patient’s condition allows. This will reduce subsequent lower extremity 

venous hypertension and the risk for compartment syndrome. Tibial arteries are uniformly ligated in the 

damage control paradigm.136

Figure 32. Control of life-threatening hemorrhage following extremity 

injury has been greatly improved through the field application of 

the extremity tourniquet. Image courtesy of Joint Combat Trauma 

Management Course, 2007.

Figure 33. Basic vascular surgical principles of proximal and distal 

vessel control are a cornerstone of extremity injury management.
202 | Damage Control Surgery

Pelvic Injury Damage Control

Background

Pelvic fracture is a marker of severe injury and is 

classically associated with a substantial rate of 

morbidity and mortality. Although pelvic fractures 

account for only 3 percent of all acute fractures, 

mortality in this patient population varies from 10 to 

50 percent depending upon fracture pattern.137,138,139

Morbidity and mortality in this patient population are 

multifactorial and often associated with concomitant 

injury to the brain, thorax, and abdomen since the 

force imparted to fracture the pelvis is also imparted 

to other regions of the body.137,138,139 Pelvic fractures 

can be associated with considerable hemorrhage, 

especially when the posterior elements of the pelvis 

are significantly disrupted.137,138,139 The resultant 

pelvic hemorrhage can be both arterial and venous 

and may emanate from the major vasculature or its 

truncal branches, the presacral venous plexus, the 

soft-tissue, or the large bulk of open cancellous bone in the region (Fig. 34). Survival of patients with pelvic 

fracture is optimized by prompt diagnosis of the pelvic fracture, vigorous resuscitation, pelvic stabilization, 

and definitive control of hemorrhage.137,138,139

Pelvic fractures can be associated with considerable hemorrhage, especially when the posterior elements 

of the pelvis are significantly disrupted.

The effective management of pelvic fractures and associated hemorrhage, especially in the deployed 

military environment, requires multidisciplinary cooperation of the emergency physician, trauma surgeon, 

and the orthopedic surgeon. While the use of interventional angiographic embolization has dramatically 

improved outcomes in the civilian management of severe pelvic fracture hemorrhage, interventional 

radiology is not typically available on the battlefield. To date, this has meant that damage control maneuvers 

such as pelvic wrapping and external fixation have become the primary means for temporizing hemorrhage 

control. Unfortunately, these maneuvers cannot reliably control pelvic arterial hemorrhage. The relatively 

recent adoption of extraperitoneal pelvic packing through the space of Retzius has offered a potentially 

effective damage control procedure for pelvic fracture-associated hemorrhage that may temporarily arrest 

or abrogate hemorrhage, to allow transport to a facility capable of angiographic embolization.140

Extraperitoneal pelvic packing through the space of Retzius is a potentially effective damage control 

procedure for pelvic fracture-associated hemorrhage. It may temporize bleeding until angiographic 

embolization can be performed.

Figure 34. Pelvic fractures can be associated with considerable hemorrhage, 

especially when the posterior elements of the pelvis are significantly 

disrupted as depicted in this radiograph.
Damage Control Surgery | 203

Physical Examination

Pelvic fracture should be suspected in all patients with appropriate mechanisms of injury. Evidence of 

systemic hypoperfusion in combination with a pelvic fracture suggests fracture-associated hemorrhage and 

requires prompt resuscitative and therapeutic interventions.139 The objectives of the pelvis examination 

are to estimate the likelihood of fracture, assess pelvic ring stability, and identify injuries to the adjacent 

structures. The examination begins with visual inspection of the pelvis for signs of injury. Look for 

abrasions, contusions, and lacerations. The presence of progressive flank, scrotal, perineal ecchymosis, 

or edema suggests pelvic injury with significant bleeding. Destot’s sign is a hematoma above the inguinal 

ligament. Grey-Turner’s sign is a flank ecchymosis secondary to retroperitoneal hemorrhage. Wounds in 

the pelvic area should be assessed carefully to exclude an open pelvic fracture. Lacerations involving the 

perineum, vagina, rectum, or scrotum are highly suggestive of an open pelvic fracture. Failure to thoroughly 

examine the gluteal cleft, buttock fold, rectum, and vagina for open wounds may lead to missed injuries. 

All patients with pelvic fractures should undergo a rectal exam with special attention to the rectal tone, the 

presence of rectal bleeding, and the position of the prostate. Diminished rectal tone could result from a 

pelvic fracture with accompanying lumbosacral nerve plexus injury. Gross blood or stool that tests guaiacpositive could represent a possible open pelvic fracture.141 A high-riding or free-floating prostate suggests 

membranous prostatic urethral injury.142 In patients with a concomitant pelvic hematoma, the outline of 

the prostate may be indistinct to palpation despite a normal position. A positive Earle’s sign is the presence 

of a bony prominence, palpable hematoma, or tender fracture line on rectal exam. The genitourinary 

system should be carefully examined. Scrotal swelling or ecchymosis and the presence of bleeding from 

the urethral meatus are signs of urethral disruption (Fig. 35). A vaginal examination should be performed 

in female patients to assess for palpable fractures, vaginal lacerations, and blood within the vaginal vault. 

Pelvic fractures in association with vaginal or rectal lacerations are considered open fractures.143

Examination of the lower extremities begins with visual inspection. Discrepancies in leg length, gross 

rotational deformities, or asymmetry of the hips should be noted. In the absence of a lower extremity 

fracture, these findings suggest a pelvic fracture or hip dislocation. A patient with a posterior hip dislocation 

will have a shortened extremity held in an internally rotated position. Range of motion at each hip should 

be assessed. A study by Ham et al. found that the inability to actively flex the hip was the maneuver 

most reliably predictive of a pelvic fracture. It had a 90 percent sensitivity and 95 percent specificity for 

detecting a pelvic fracture.144 The stability of the pelvis may be assessed by applying lateral-to-medial 

compression and anterior-posterior compression over the anterior-superior iliac crests. Many clinicians 

advocate foregoing any forceful manipulation of a potentially injured pelvis for fear of dislodging clots 

from injured vessels and precipitating renewed pelvic hemorrhage. Neurologic examination should be 

thorough, as many patients have significant neurological disability, especially when the pelvic fracture 

extends into or through the sacral foramina. Particular attention should be paid to the lumbar (L5) and 

sacral (S1) nerve roots to detect an injury to the lumbosacral nerve plexus or its nerve roots. The L5 

nerve root may be tested by assessing dorsiflexion of the great toe against resistance and sensation over 

the dorsum of the foot. The S1 nerve root is tested by evaluating plantar flexion of the great toe against 

resistance, sensation along the lateral aspect of the foot, and the Achilles tendon reflex. 

Radiographic Evaluation

Contingent upon resources, radiographic evaluation should be performed to allow the surgeon to determine 

the morphology of the pelvic fracture.
204 | Damage Control Surgery

Plain Radiography

An anteroposterior (AP) plain radiograph of the pelvis will identify the vast majority of pelvic fractures 

(Fig. 36). It allows for early identification of serious pelvic injuries that may be a source of blood loss. It 

may also detect proximal femur fractures and hip dislocations. When the patient is in a supine position, 

the AP pelvis radiograph actually provides an oblique view of the pelvic brim. This is because the pelvis 

lies 45 to 60 degrees oblique to the long axis of the skeleton. Many acetabular fractures are not visible on 

the AP pelvic radiographs. Plain radiography is not as accurate as computed tomography (CT) imaging 

for evaluation of pelvic fractures.145,146 When compared with CT imaging, plain films missed 57 percent of 

acetabular rim fractures, 50 percent of femoral head fractures, 40 percent of intraarticular fragments, 34 

percent of vertical shear fractures, and 29 percent of sacroiliac diastasis injuries.147

Computed Tomography Imaging

Computed tomography imaging is extremely valuable in the diagnosis and characterization of pelvic 

injuries. Computed tomography may be utilized to identify or exclude a pelvic injury in equivocal cases 

or to further delineate a known pelvic fracture. When compared with plain pelvis radiographs, CT is 

more sensitive in the detection of pelvic fractures and allows better characterization of the fractures and 

adjacent soft-tissues.146 The primary advantage of CT imaging is the ability to simultaneously screen for 

associated injuries (e.g., visceral injuries). In most trauma victims, the bony pelvis is scanned as part of a 

combined abdomen and pelvis CT study. If a fracture is detected, further imaging with thinner axial sections 

may be obtained of the area of interest. An important aspect of CT imaging is the use of reformatted 

images. Multiplanar reconstruction is the reformatting of data to produce images along the sagittal and 

coronal planes. Inlet and tangential views may be created, eliminating the need for additional plain 

films. In addition to multiplanar reconstruction, three-dimensional images may also be constructed 

using three-dimensional image rendering software. Three-dimensional spiral CT images may detect subtle 

fractures (specifically those in the axial plane), demonstrate spatial relationships of fracture fragments, and 

guide management (Fig. 37).

Figure 35. The presence of urethral meatal bleeding and scrotal swelling 

or ecchymosis are signs of potential urethral disruption.

Figure 36. An anteroposterior (AP) plain radiograph of the pelvis will 

identify the vast majority of significant pelvic fractures.
Damage Control Surgery | 205

Angiography

The use of intravenous contrast allows simultaneous evaluation of both osseous and vascular structures. 

Contrast-enhanced CT imaging can demonstrate active arterial bleeding. This is usually from branches 

of the internal iliac artery or internal pudendal artery. Nonarterial bleeding may also be detected. These 

hematomas typically originate from disruption of the posterior pelvic veins or the surfaces of fractured 

bones. The gold standard test for detecting arterial bleeding associated with pelvic fractures is traditional 

angiography (Fig. 38). Spiral CT angiography of the pelvis has been shown to be moderately sensitive 

(84 percent) and specific (85 percent) for the detection of acute pelvic bleeding in trauma.148 Standard 

angiography has the important advantage of serving as an excellent diagnostic and therapeutic modality 

(e.g., embolization).149,150,151

Acute Management

The acute management of the patient with pelvic fracture and hemorrhage involves three basic tenets: 

(1) stabilization of the pelvis; (2) control of pelvic hemorrhage; and (3) identification and control of 

extrapelvic hemorrhage sources. Pelvic stabilization limits radial expansion of the pelvis and protects 

against increases in pelvic volume and additional hemorrhage. It is hypothesized that stabilization affects 

hemostasis via tamponade and clot maintenance.137,152 Emergent stabilization of the pelvis is almost 

exclusively temporizing in nature, from the point of view of fracture fixation and serves as a bridge to later 

definitive internal fixation once the patient is physiologically stable. Potential stabilizing methods include 

the pelvic sheet sling, pelvic binder, and external fixation (Fig. 39).153,154

The acute management of the patient with pelvic fracture(s) and hemorrhage involves three tenets: (1) 

stabilization of the pelvis; (2) control of pelvic hemorrhage; and (3) identification and control of extrapelvic 

hemorrhage sources.

When placing the sheet sling, the boundaries of the wrap should be the anterior-superior iliac spine 

(cephalad) and the greater trochanter (caudad). After wrapping the pelvis, twist the wrap in front and clip 

Figure 37. Three-dimensional CT images may detect subtle fractures, demonstrate spatial relationships of fracture fragments, and guide management.

Images courtesy of Swaminatha V. Mahadevan, MD, Stanford University.
206 | Damage Control Surgery

or tie the wrap back to itself to maintain the stabilization.155 The pelvic binder is a useful adjunct in the 

battlefield environment because it is light, adaptable to any body size, and easy to apply. 

External fixation can be applied within minutes by an orthopedic surgeon or a specially trained general 

surgeon in more remote environments. When the external fixator is placed, crossmembers should be placed, 

with thought given to potential future therapeutic adjuncts (Fig. 40). A substantial percentage of pelvic 

hemorrhage is venous and can be controlled through efforts to effect pelvic ring stabilization in conjunction 

with blood resuscitation to replace volume loss.153,156 This ongoing resuscitation often requires upwards of 

10 units of packed red blood cells and additional blood component therapy to accomplish, and the patient 

must be cared for in the ICU. In general, pelvic hemorrhage is not approached operatively via celiotomy. 

The primary reason is that once the hematoma has been released into the peritoneal cavity and tamponadeeffect lost, bleeding will increase. It is difficult, if not impossible, to locate and ligate the bleeding vessels. 

Furthermore, packing the pelvis once the retroperitoneal hematoma has been disrupted into the peritoneal 

cavity is not effective since there is nothing to pack against. This scenario often results in exsanguination. 

Early pelvic stabilization can control hemorrhage and reduce mortality. Potential stabilizing methods for 

pelvic fractures include the pelvic sheet sling, pelvic binder, and external fixation.

Recent evidence from the civilian literature suggests that an alternative preperitoneal approach and packing 

Figure 38. The gold standard test for detecting arterial bleeding associated 

with pelvic fractures is traditional angiography.

Figure 39. Pelvic stability may be improved with application of a 

pelvic binder or bed sheet around the patient’s hips. Image courtesy of 

Swaminatha V. Mahadevan, MD, Stanford University.
Damage Control Surgery | 207

of the pelvis through the space of Retzius may be more effective. Such an approach controlled pelvic 

bleeding and significantly reduced blood product transfusions and mortality in a selected high-risk group 

of patients.157,158 Preperitoneal and pelvic packing may prove to be an important intervention in the austere 

deployed environment where resources and therapeutic options are limited. In this scenario, if a patient does 

not respond to initial resuscitation, they are taken to the operating room where an initial small laparotomy 

incision is made above the umbilicus. If the source of hemorrhage is in the abdomen, the incision is extended. 

On the other hand, if there is a large pelvic retroperitoneal hematoma, a separate lower midline incision 

is made to enter the extraperitoneal space of Retzius. The pelvic hematoma is evacuated, the bladder 

displaced, and packs are placed on both sides of the bladder deep into the pelvis. If an unstable pelvic 

fracture is present, it is necessary to apply a pelvic fixator to provide something to pack against. The patient 

can then be resuscitated and transported to a rearward facility with angiographic embolization capabilities. 

Interventional angiography (e.g., embolization) is often only available at Level IV and V care facilities.

Open Pelvic Fractures

Open pelvic fractures present a unique management challenge to the surgeon (Fig. 41). The same basic 

management principles apply with some notable additions. Efforts must be made to directly control or 

tamponade external hemorrhage. Soft-tissue injury must be vigorously debrided. Fecal diversion must be 

Figure 40. Early pelvic stabilization can control hemorrhage and reduce 

mortality. External fixator placement in the iliac crests is often used to 

stabilize the pelvis. Image courtesy of the Borden Institute, Office of The 

Surgeon General, Washington, DC. 

Figure 41. Open pelvic fractures require hemorrhage control, aggressive 

debridement, and fecal diversion if significant perineal soft-tissue or 

anorectal disruption exists. Image courtesy of Leopoldo C. Cancio, MD, 

FACS, COL, MC, US Army.
208 | Damage Control Surgery

strongly considered in patients with significant perineal soft-tissue or anorectal injuries, though this may 

be done at subsequent reoperation.143,159 As with all combat wounds, the early administration (ideally 

within three hours of injury) of broad-spectrum prophylactic antibiotics is recommended.160 Exclusive 

of associated injury, the prognosis of patients with pelvic fractures is directly correlated with severity of 

injury and prompt institution of therapeutic strategies for temporizing pelvic stabilization and hemorrhage 

control. Morbidity and mortality of open pelvic fractures are higher than their closed counterparts.159 This 

is secondary to difficulty controlling external pelvic hemorrhage and sepsis associated with soft-tissue and 

enteric injuries.143,159

Management of open pelvic fractures includes hemorrhage control, aggressive debridement of softtissues, pelvic stabilization, and fecal diversion through a colostomy.

Bladder and Urethral Injuries

The incidence of genitourinary injuries associated with pelvic fractures is reported to be as high as 25 

percent and includes bladder injuries, urethral injuries, and combined injuries.141,142 The posterior urethra 

is firmly attached to the pubis (in males), making it prone to injuries with anterior pelvic ring fractures. 

Urethral injury associated with pelvic fractures is much less common in females due to the female urethra’s 

short length, mobility, and lack of attachments to the pelvis.161 The bladder is most commonly injured in 

association with pubic ramus fractures. Injuries to the vagina or rectum may occur in association with pelvic 

fractures. Most result from the penetration of a bone fragment but may also occur with pubic symphysis 

diastasis. 

Genitourinary tract injuries should be assumed in all patients with pelvic fractures until proven 

otherwise.

All pelvic fractures should be assumed to have accompanying genitourinary tract injuries until proven 

otherwise.141,142 A retrograde urethrogram may diagnose urethral injuries in patients who have characteristic 

physical exam findings (Fig. 42). These include blood at the urethral meatus, a high-riding prostate, scrotal 

Figure 42. Retrograde urethrogram demonstrating proximal urethral 

injury and extraperitoneal extravasation of contrast.

Figure 43. Retrograde cystogram demonstrating extravasation of contrast 

from an injured bladder.
Damage Control Surgery | 209

hematoma, an inability to urinate, or difficulty with insertion of a urinary catheter.141,142 Physical signs may 

be absent in some patients with urethral injuries. A retrograde cystogram may help to identify bladder 

ruptures, which often occur in association with pelvic ring injuries (Fig. 43). Evidence of gross hematuria is an 

indication for performing a retrograde cystogram. The cystogram may be performed using plain radiography 

or with CT imaging. The latter is often more convenient and provides more accurate imaging.

Management of Bladder Injuries 

Bladder injuries are categorized as intraperitoneal or extraperitoneal. Intraperitoneal injuries are repaired 

surgically in two-layer fashion with absorbable suture and transurethral catheter drainage. Previous 

standards included the use of a large-bore suprapubic catheter either alone or in combination with 

transurethral catheter, but this is no longer recommended due to greater association with complications 

regardless of degree of bladder injury. In addition, the previous average duration of indwelling suprapubic 

catheters was 42 days, which with modern treatment standards is now reduced to only 13 days duration of 

transurethral catheter insertion.162,163 These advances along with primary bladder repair approaches have 

improved outcomes.162,163

The mainstay treatment of extraperitoneal bladder injuries remains nonoperative management with 

transurethral catheter drainage for 10 to 14 days with follow-up cystogram prior to removal.164,165,166

Relative contraindications to nonoperative management of extraperitoneal bladder injuries include bone 

fragments projecting into the bladder, open pelvic fractures, and bladder injuries associated with rectal 

perforations.167

Management of Urethral Injuries 

Urethral injury in civilian settings is secondary to blunt trauma, occurring in 10 percent of pelvic 

fractures.141 However, in combat situations, urethral injury may be associated with pelvic fractures or 

penetrating gunshot or fragment wounds (Fig. 44). Diagnosis and extent of injury are assessed by retrograde 

urethrogram. Options for management for partial or complete disruption both include delayed operative 

reconstruction or primary stenting of injury with a urethral catheter. Either approach appears to have 

similar complications, impotency rates, and incontinence rates.168,169,170,171,172 Consequently, in most cases, 

bladder drainage, either via retrograde urethral catheter or suprapubic catheter alone, is adequate. 

If urethral injury is clinically suspected, urethral integrity can be confirmed by a retrograde urethrogram. 

Alternatively, a Foley catheter can be gently passed into the urethra. If minimal resistance is encountered 

the catheter is fully advanced into the bladder and the cuff inflated. If there is difficulty passing the 

catheter, no further attempts should be made, and a suprapubic tube cystostomy should be performed.

Delayed operative reconstruction requires expertise, which may not be available for host nationals. In 

these instances, immediate realignment may offer the best chance to reestablish continuity. In the author’s 

experience (AM), based on reports of successful realignment using antegrade cystoscopy, if retrograde 

urethral catheter placement is unsuccessful, consideration should be given to antegrade urethral catheter 

placement, particularly if the patient is undergoing laparotomy.173,174,175 This procedure is performed by 

opening the dome of the bladder and passing a Foley catheter antegrade into the urethra. A sterile largebore Foley catheter is sutured to the antegrade catheter and pulled retrograde into the bladder. The bladder 

is closed in standard two-layer fashion, and the retrograde urethral catheter can be secured to the foreskin 
210 | Damage Control Surgery

of the penis to reduce unintentional removal. The catheter should remain in place for a minimum of three 

weeks with retrograde urethrogram prior to permanent removal of the catheter to ensure continuity is 

reestablished. 

Genitalia Injuries 

The management of combat wounds to the penis, scrotum, testes, and spermatic cord comprises 

hemorrhage control, debridement, and early penile repair to prevent deformity.82 Disruption of Buck’s 

fascia in penile injuries requires suture repair to prevent bleeding and long-term penile deformity.

Figure 44. (Left) External genital trauma. There is significant injury 

to the glans penis and the transected corpus cavernosum is evident. The 

proximal urethral opening is visible at the base of the wound. A left-sided 

orchiectomy was performed while the right testicle was repaired.

Figure 45. (Bottom Left) Penetrating scrotal injuries require exploration 

to examine the testicles and spermatic cords for injury.

Figure 46. (Bottom Right) Orchiectomy should not be performed unless 

the testicle is irreparably damaged or its vascular supply is destroyed.
Damage Control Surgery | 211

The management of combat wounds to the penis, scrotum, testes, and spermatic cord comprises 

hemorrhage control, debridement, and early repair to prevent subsequent complications.

The scrotum is very vascular, and extensive scrotal debridement is unnecessary.82 Penetrating scrotal 

injuries require exploration to examine the testes for injury and minimize the risk of hematoma 

formation (Fig. 45). Management of testicular injuries should be directed toward conservation of tissue 

with debridement of herniated parenchymal tissue and closure of the tunica albuginea with mattress 

sutures.176,177 Orchiectomy should not be performed unless the testicle is irreparably damaged or its 

vascular supply is destroyed.178 The testicle should be replaced in the scrotum, which can be closed 

primarily within eight hours of injury or closed over a Penrose drain, if longer delays to operative care 

occur (Fig. 46). If scrotal closure is not possible due to extensive tissue loss, the testicle should be placed 

in available subcutaneous tissue (e.g., thigh soft-tissue). 

Damage Control Summary

Damage control surgery is defined as the rapid initial control of hemorrhage and contamination with 

packing and temporary closure, followed by resuscitation in the ICU, and subsequent reexploration and 

definitive repair once normal physiology has been restored. Patients requiring damage control procedures 

are a higher acuity patient population in whom temporizing procedures to control hemorrhage and 

contamination improve survival. Damage control techniques are both feasible and effective on the battlefield. 

This damage control paradigm challenges surgeons in resource-constrained combat environments to have 

a low threshold to perform damage control procedures in order to mitigate the deleterious consequences 

of the challenging lethal triad of hypothermia, coagulopathy, and acidosis. 
212 | Damage Control Surgery

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154. Eastridge BJ. Butt binder. J Trauma 2007;62(6 Suppl):S32.

155. Simpson T, Krieg JC, Heuer F, et al. Stabilization of pelvic ring disruptions with a circumferential 

sheet. J Trauma 2002;52(1):158-161.

156. Tucker MC, Nork SE, Simonian PT, et al. Simple anterior pelvic external fixation. J Trauma 

2000;49(6):989-994.

157. Cothren CC, Osborn PM, Moore EE, et al. Preperitonal pelvic packing for hemodynamically unstable 

pelvic fractures: a paradigm shift. J Trauma 2007;62(4):834-839; discussion 839-842. 

158. Osborn PM, Smith WR, Moore EE, et al. Direct retroperitoneal pelvic packing versus pelvic 

angiography: a comparison of two management protocols for haemodynamically unstable pelvic fractures. 

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159. Grotz MR, Allami MK, Harwood P, et al. Open pelvic fractures: epidemiology, current concepts of 

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160. Gerhardt RT, Matthews JM, Sullivan SG. The effect of systemic antibiotic prophylaxis and 

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161. Venn SN, Greenwell TJ, Mundy AR. Pelvic fracture injuries of the female urethra. BJU International 

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Damage Control Surgery | 223

165. Cass AS, Luxenberg M. Features of 164 bladder ruptures. J Urol 1987;138(4):743-745.

166. Corriere JN Jr, Sandler CM. Mechanisms of injury, patterns of extravasation and management of 

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167. Cass AS, Luxenberg M. Management of extraperitoneal ruptures of bladder caused by external 

trauma. Urology 1989;33(3):179-183.

168. Morehouse DD, Mackinnon KJ. Management of prostatomembranous urethral disruption: 13-year 

experience. J Urol 1980;123(2):173-174.

169. Follis HW, Koch MO, McDougal WS. Immediate management of prostatomembranous urethral 

disruptions. J Urol 1992;147(5):1259-1262.

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172. Elliott DS, Barrett DM. Long-term followup and evaluation of primary realignment of posterior 

urethral disruptions. J Urol 1997;157(3):814-816.

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Urol 1996;156(4):1288-1291.

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urethral disruption. Urology 2001;57(4):628-632.

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2004;93(9):1195-1202.

176. Brandes SB, Buckman RF, Chelsky MJ, et al. External genitalia gunshot wounds: a ten-year experience 

with fifty-six cases. J Trauma 1995;39(2):266-271; discussion 271-272.

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224 | Damage Control Surgery
Chapter 6

MAXILLOFACIAL 

 AND NECK TRAUMA

Contributing Authors

Robert G. Hale, DDS, COL, US Army

 David K. Hayes, MD, COL, US Army

 George Orloff, MD

 Kyle Peterson, DO, CDR, US Navy

 David B. Powers, DMD, MD, COL, US Air Force

Swaminatha Mahadevan, MD
All figures and tables included in this chapter have been used with permission from Pelagique, LLC, the 

UCLA Center for International Medicine, and/or the authors, unless otherwise noted.

Use of imagery from the Defense Imagery Management Operations Center (DIMOC) does not imply or 

constitute Department of Defense (DOD) endorsement of this company, its products, or services.

Disclaimer

The opinions and views expressed herein belong solely to those of the authors. They are not nor should 

they be implied as being endorsed by the United States Uniformed Services University of the Health 

Sciences, Department of the Army, Department of the Navy, Department of the Air Force, Department of 

Defense, or any other branch of the federal government.
Maxillofacial and Neck Trauma | 227

Table of Contents

Introduction........................................................................................................ 229

Overview ............................................................................................................ 229

Lessons Learned - Maxillofacial Injuries ................................................................ 234

Information for the Generalist - Maxillofacial Injuries ............................................. 236

Airway Control and Breathing Support...........................................................................237

Airway and Breathing Assessment ....................................................................................237

Initial Airway Control........................................................................................................240

Oral and Nasal Airways..................................................................................................241

Cervical Spine Protection and Control ............................................................................242

Definitive Airway Control and Breathing Support..........................................................243

Preparation for Endotracheal Intubation ..........................................................................243

Endotracheal Intubation Technique ..................................................................................244

Rapid Sequence Intubation...............................................................................................245

Awake Endotracheal Intubation........................................................................................245

Crash Endotracheal Intubation .........................................................................................246

Confirmation of Endotracheal Tube Placement...................................................................246

Surgical Airway Management ...........................................................................................247

Cricothyroidotomy ...........................................................................................................247

Percutaneous Transtracheal Ventilation (Needle Cricothyroidotomy).......................................250

The Difficult Airway .........................................................................................................250

Initial Management Considerations ................................................................................251

Mandible Fractures ............................................................................................................251

Dental Injury......................................................................................................................253

Facial Injury .......................................................................................................................254

Parotid and Facial Nerve Injuries......................................................................................254

Facial Lacerations...........................................................................................................255

Information for the Specialist - Maxillofacial Injuries .............................................. 256

Overview...........................................................................................................................256

Initial Management..........................................................................................................257

Maxillofacial Wound Care ...............................................................................................257

Infection Prevention and Management ...........................................................................258

War Wounds.......................................................................................................................258

Epidemiology of Wound Infection.....................................................................................260

Prevention of Infection: Surgical Management....................................................................260

Diagnosis of Infection .....................................................................................................260

Management of Infection .................................................................................................261

Definitive Management .....................................................................................................261

Evaluation and Treatment Planning..................................................................................262

Radiographic Imaging .....................................................................................................262

Fracture Stabilization ......................................................................................................262
228 | Maxillofacial and Neck Trauma

Definitive Repair................................................................................................................263

Informed Consent............................................................................................................263

Timing of Surgery ..........................................................................................................263

Surgical Principles ..........................................................................................................264

Facial Soft-Tissue Injuries..................................................................................................266

Facial Burns........................................................................................................................267

Upper and Midface Injuries...............................................................................................268

Ocular Assessment...........................................................................................................268

Frontal Sinus Fractures....................................................................................................269

Naso-Orbito-Ethmoid (NOE) Region Fractures.................................................................270

Zygoma Fractures............................................................................................................273

Orbit Fractures ...............................................................................................................274

LeFort Fractures..............................................................................................................274

Lower Face Injuries............................................................................................................274

Evaluation .....................................................................................................................275

Treatment.......................................................................................................................275

Panfacial Fractures.............................................................................................................277

Summary ..........................................................................................................................277

Penetrating Neck Wounds ..................................................................................... 278

Introduction......................................................................................................................278

Anatomy............................................................................................................................279

Neck Zones........................................................................................................................279

Information for the Generalist - Neck Wounds......................................................... 281

Initial Assessment and Management...............................................................................281

Airway................................................................................................................................281

Bleeding..............................................................................................................................281

Considerations for the Specialist .....................................................................................283

Operative Indications.........................................................................................................283

Role of Imaging .................................................................................................................283

Immediate Hemorrhage Control.......................................................................................283

Penetrating Neck Injury Management...............................................................................284

Zone I ...........................................................................................................................284

Zone II..........................................................................................................................284

Zone III.........................................................................................................................285

Esophageal Injury ..............................................................................................................286

Laryngotracheal Injury ......................................................................................................287

Summary ..........................................................................................................................288

References .......................................................................................................... 289
Maxillofacial and Neck Trauma | 229

Introduction

This chapter will review maxillofacial and neck 

injuries combat casualty care (CCC) providers 

will likely encounter at Level II and III care 

facilities. The chapter is intended to convey lessons 

learned in Operation Enduring Freedom (OEF) 

and Operation Iraqi Freedom (OIF). Pertinent 

anatomy, injury patterns, treatment of battle 

injuries, and differences between civilian trauma 

management in the United States (US) versus CCC 

are presented. The generalist CCC provider will be 

presented with the information required to assess 

and stabilize maxillofacial and neck injuries. Special 

consideration is given to airway management since 

significant trauma to the maxillofacial and neck 

areas greatly influences airway management (Fig. 

1). Evidence-based recommendations to prevent 

and manage infections of combat-related injuries 

of the head and neck are provided. Additionally, 

information is provided to prepare the specialist 

CCC provider, deployed for the first time, to both 

stabilize and definitively manage (typically in host 

nation patients) maxillofacial and neck battle 

injuries. 

Overview

The combat theater will produce varying combinations of blunt and penetrating injuries to the head 

and neck. Blunt trauma can result from motor vehicle accidents, blast injury (tertiary effect), falls, heavy 

equipment injuries, sport injuries, and altercations. Many of these blunt trauma injury mechanisms are 

similar to those experienced in the US. The majority of these blunt trauma-related maxillofacial injuries 

are closed fractures and lacerations. Management of these injuries involves: (1) airway management, (2) 

prevention of disability from central nervous system injuries, and (3) systematic reconstruction of facial 

structures (Figs. 2 and 3).

Combat (gunshot wounds and blast injuries) often results in penetrating maxillofacial and neck injuries. 

Penetrating trauma results in a combination of complex lacerations, open fractures, and wounds 

complicated by tissue avulsions and burns (Fig. 4).1 There is an increased frequency of maxillofacial 

injuries in OEF/OIF compared to previous American wars in the past century. The incidence of head 

and neck region injuries in World War II and the Korean War was 21 percent, in the Vietnam War it was 

16 percent, and in OEF/OIF is 30 percent.2 Recent advances in body armor and cranial vault protection 

have led to the increase in the percentage of head and neck casualties that survive initial injuries (Fig. 5).3

The high incidence of blast injuries caused by improvised explosive devices (IEDs) is likely an additional 

factor contributing to the higher frequency of head and neck injuries in OEF/OIF.4

Figure 1. The first consideration in this casualty with significant head 

and neck trauma is securing the airway. Image courtesy of Tamer Goksel, 

DDS, MD, COL, US Army.
230 | Maxillofacial and Neck Trauma

Figure 2. Relative distribution of battlefield facial fractures. Most battlefield injury facial fractures are open. Data source: Joint 

Theater Trauma Registry (unpublished).

Figure 3. Relative distribution of battlefield versus non-battlefield open fractures. Data source: Joint Theater Trauma Registry 

(unpublished).

0

100

200

300

400

Total Open

50

450

150

250

350

Nasal Mandibular Maxillary Orbital

Closed

500

Relative distribution of battlefield facial fracture

s

0

100

200

300

400

Total Battlefield

50

450

150

250

350

Nasal Mandibular Maxillary Orbital

Non-Battlefield

Relative distribution of battlefield

versus non-battlefield open fracture

s
Maxillofacial and Neck Trauma | 231

Figure 4. (Above) Explosive blast trauma can result in a combination 

of complex facial lacerations, open fractures, tissue avulsion, and burns. 

Image courtesy of Tamer Goksel, DDS, MD, COL, US Army.

Figure 5. (Right) Recent advances in body armor and cranial vault 

protection have led to an increase in the percentage of head and neck 

casualties that survive initial injuries. Defense Imagery Management 

Operations Center (DIMOC).
232 | Maxillofacial and Neck Trauma

Combat injuries often cause complex penetrating maxillofacial and neck wounds, including lacerations, 

open fractures, tissue avulsions, and burns.

Lew et al. analyzed the Joint Theatre Trauma Registry (JTTR) database to describe the type, distribution, 

and mechanism of injury of maxillofacial injuries experienced by US service members in OEF/OIF 

(Tables 1, 2 and 3).1 The JTTR is a military healthcare database, started at the beginning of military 

operations in Afghanistan (October 19, 2001), of all US military service members injured and treated at 

any medical facility throughout the evacuation system and spanning all military services at all levels of 

care.5 During the six-year study period there were 7,770 injured service members entered into the JTTR. 

Approximately 26 percent of injured service members (2,014/7,770) had maxillofacial injuries.1 There 

were 4,783 maxillofacial injuries among the 2,014 injured service members (average 2.4 injuries per 

service member with range of 1 to 8). The majority of patients were male (98 percent) and the average age 

was 26-years-old, with a range of 18 to 57 years of age. The relative distribution of maxillofacial injuries 

stratified by branch of military service was 72 percent (Army), 24 percent (Marines), 2 percent (Navy), and 

1 percent (Air Force). 

Craniomaxillofacial Wound Types Number Percent

Total Soft-Tissue 2788 58

 Complicated Penetrating Soft-Tissue 660 14

 Simple Penetrating Soft-Tissue 2128 44

Fractures 1280 27

Abrasions 231 5

Dental 204 4

Contusions 111 2

Dislocations 6 <1

Skull 15 <1

Unknown 148 3

Table 1. Percent distribution of wounds by body region. Adapted from Lew, 2010.1

Table 2. Characterization of craniofacial injuries sustained in battle by US service members in OEF and OIF. Adapted from Lew, 2010.1

Body Region

Body 

Surface Area 

(Percent)

WWII Korea Vietnam OEF/OIF

Head/Neck 12 21 21.4 16.0 30.0

Thorax 16 13 10 13.4 5.9

Abdomen 11 8 8.4 9.4 9.4

Extremities 61 58 60.2 61.1 54.5
Maxillofacial and Neck Trauma | 233

Mechanism of Injury Number of 

Injuries Percent

Explosive 4061 84

 IED 3228 67

 Grenade/Rocket-propelled grenade (RPG) 428 9

 Mortar 263 5

 Landmine 142 3

 Bomb 26 <1

Gunshot Wound 400 8

Motor Vehicle Accident 77 2

Other / Not Documented 81 2

Fragment / Shrapnel 43 1

Helicopter / Plane Crash 40 1

Miscellaneous 55 1

Table 3. Mechanism of injury of combat-related craniomaxillofacial injuries in OEF and OIF. Adapted from Lew, 2010.1

Figure 6. Distribution of combat facial fractures in OEF and OIF. Adapted from Lew, 2010.1

100%

80%

60%

40%

20%

0%

Percentage

Type of Fracture

Nasal Mandible Maxillary Orbital Facial
234 | Maxillofacial and Neck Trauma

Based on analysis of the JTTR, the majority of maxillofacial combat injuries were penetrating soft-tissue 

injuries and fractures. A majority of the fractures were open. The primary mechanism of injury to the 

maxillofacial region was explosive devices.

The majority of maxillofacial combat injuries were penetrating soft-tissue injuries (58 percent) and 

fractures (27 percent). A majority of the fractures (76 percent) were open. Amongst the facial fractures, the 

mandible (36 percent) most frequently involved bone, followed by the maxilla and zygoma (19 percent), 

nasal bone (14 percent), and orbital wall (11 percent). The remaining fractures (20 percent) were not 

otherwise specified facial fractures (Fig. 6).1 The primary mechanism of injury to the maxillofacial region 

was explosive devices (84 to 88 percent); this injury mechanism is much higher than previous wars.1,2

Improvised explosive device wounds are the consequence of high-energy projectiles and are characterized 

by tissues grossly contaminated with dirt, rocks, plastic, glass, animal or human remains, and other 

materials.6 Gunshot wounds (GSWs) accounted for just 8 percent of maxillofacial combat injuries. 

Burns traditionally account for 5 percent of all evacuated combat casualties. Explosions were the primary 

cause of combat burns (86 percent), which involved the face in 77 percent of cases.7

Lessons Learned - Maxillofacial Injuries

Maxillofacial battle injuries are present in 26 percent of casualties evacuated from Combat Support 

Hospitals (CSHs).1 These highly visible injuries, although bloody, are rarely the sole cause of shock. 

Death resulting from airway loss following maxillofacial injury is the primary concern. Establishing a 

secure airway is paramount for casualties with severe head and neck injuries. Direct laryngoscopy with 

endotracheal intubation and surgical cricothyroidotomy are commonly used techniques to secure an airway 

in combat casualties. 

Although they are often bloody, maxillofacial injuries are rarely the source of shock. The critical, 

immediate life-threat following maxillofacial injury is airway compromise due to oropharyngeal 

bleeding, swelling, and loss of mandibular structural integrity.

During direct laryngoscopy, exposure of the glottis is highly dependent on displacement of the tongue 

with a laryngoscope blade against an intact mandibular arch. Once mandibular body integrity is disrupted 

by fracture or avulsion, anterior displacement of the tongue is easier, but blood, soft-tissue swelling, and 

debris may continue to obscure the glottis. A maneuver to consider if the glottis is obscured despite 

aggressive suctioning is to push air through the glottis by compressing the chest; bubbles will localize the 

glottis for intubation. If this fails, and bag-valve-mask ventilation is not feasible, the CCC provider needs 

to perform an immediate cricothyroidotomy.

Once the casualty has a secured airway, in the authors’ experience, direct pressure and aggressive 

packing of open bleeding wounds or bleeding nasal and oropharyngeal cavities will control all but the 

most catastrophic hemorrhages (Figs. 7 and 8). Flail mandible fractures may compromise a patient’s 

airway and, if left untreated, cause considerable pain and morbidity. Early tracheotomy and external 

pin fixation to stabilize mandible fractures prior to air evacuation should be considered. An orthopedic 

pin fixator, such as the Hoffman® II device, works well to obtain gross alignment and fixation of the 

fractured mandible (Fig. 9). 
Maxillofacial and Neck Trauma | 235

For uncontrolled hemorrhage from open wounds and nasal or oropharyngeal cavities, the airway should 

be secured and the wounds or cavities aggressively packed.

Head and neck wounds should be copiously irrigated, wound contaminants should be removed, and 

clearly nonviable tissue fragments should be debrided. Judicious initial debridement of facial wounds 

will provide the face surgeon with a subsequent opportunity to assess viability of critical structures. Facial 

Figure 7. (Left) With the airway secure, a compression dressing has been 

applied to control bleeding in the oropharyngeal cavity.

Figure 8. (Below) A casualty with explosive blast-related penetrating 

fragmentation wounds to the torso and head. Note the secured airway and 

compression dressings applied to the head and face. Image courtesy of Kurt 

W. Grathwohl, MD, COL, MC, US Army.
236 | Maxillofacial and Neck Trauma

lacerations that can be explored and debrided effectively should be closed primarily unless underlying 

fractures are present.8 Facial fractures are frequently accessed through existing lacerations. Packing the 

wound open (temporarily), rather than closing the wound, will prevent open facial fractures from being 

overlooked in later evacuation phases. Wound packing should be changed at least every 24 hours. Definitive 

facial fracture repair can be delayed up to two weeks without significantly affecting the outcome in most 

cases.8

With the exception of fractures that significantly alter normal dental occlusion or compromise the airway, 

definitive facial fracture repair can be delayed up to two weeks.

Information for the Generalist - Maxillofacial Injuries

Improvised explosive devices cause a majority of injuries in OEF/OIF.2 The face of combat casualties 

is particularly vulnerable to explosive injuries. Explosions cause a high incidence of ocular injuries, 

facial fractures, and complex soft-tissue wounds and burns.1,7 The critical, immediate problem following 

maxillofacial injury is airway compromise due to oropharyngeal bleeding, swelling, and loss of 

mandibular structural integrity. Initial treatment of oromaxillofacial injury involves securing the 

patient’s airway and controlling bleeding, while simultaneously protecting the brain, cervical spine, and 

eyes from further injury. Once the airway is stabilized, efforts can be focused upon hemorrhage control 

and treatment of additional injuries identified in the secondary survey. 

Figure 9. (Left) An orthopedic pin fixator, such as the Hoffman® II 

device, works well to obtain gross alignment and fixation of a fractured 

mandible prior to transport. Image courtesy of Tamer Goksel, DDS, MD, 

COL, US Army.

Figure 10. (Below) The maxillofacial region corresponds to head 

structures not protected by a Kevlar® helmet. Image courtesy of Defense 

Imagery Management Operations Center (DIMOC).
Maxillofacial and Neck Trauma | 237

Maxillofacial anatomy comprises the bony and soft-tissue structures anterior and inferior to the base 

of the skull, from the ears forward and from the brow down to the chin. This region corresponds to 

head structures not protected by a Kevlar® helmet (Fig. 10). The tongue is attached to the forward 

projecting mandible, which supports the patency of the upper airway. Beneath the skin, critical structures 

at risk from penetrating trauma are the parotid glands, parotid ducts, and major facial nerve branches. 

Unrecognized injuries to these structures may result in high morbidity.9

The midface is the area between the eyebrows and base of the nose. The midface contains pneumatized 

(air-filled) paranasal sinuses. The bones encasing the sinus cavities are thin and lined by mucosa. Projectiles 

can easily perforate and traverse the midface and lead to subsequent infections. Globe injuries, vascular 

injuries, and intracranial penetration are critical associated injuries following penetrating trauma to the 

midface.10,11 

The lower face is the area from the base of the nose to the chin, including the tooth-bearing parts of the 

maxilla and the entire mandible. The lower face skeleton is composed of thick cortical bone and dense 

dental structures. The tongue, surrounded by these hard structures, is at risk for severe injury leading to 

airway obstruction when high-speed projectiles fragment surrounding structures and produce secondary 

projectiles. 

Airway Control and Breathing Support

Airway management is arguably the single most important skill taught to and possessed by emergency 

careproviders. Effective airway management in the combat casualty often makes the difference between 

life and death and takes initial precedence over most other clinical considerations. 

There are fundamental differences in the management of casualties arriving to treatment facilities with 

blunt trauma to the face versus penetrating injury. Patients with isolated blunt force trauma to the face 

and neck typically undergo standard spinal immobilization measures (e.g., in-line traction) during initial 

airway management (when the tactical setting allows). Combat casualties with penetrating injuries to the 

face and neck often pose significant airway visualization challenges (Fig. 11). The primary priority in such 

patients (at immediate risk for airway obstruction) is securing a stable airway. This often results in more 

liberal initial manipulation of the head and neck to enable lifesaving airway interventions. Fortunately, 

studies performed in civilian and combat settings suggest that most patients with normal neurological 

motor exams following isolated penetrating trauma to the neck will not have a mechanically destabilized 

spinal column.12,13 Of note, blast injury management is complicated by the fact that combined blunt force 

and penetrating injuries to the face and neck often occur.

Studies performed in civilian and combat settings suggest that following isolated penetrating trauma to 

the neck, most patients with normal neurological motor exams will not have a mechanically destabilized 

spinal column.

Airway and Breathing Assessment 

The initial casualty assessment determines whether the airway is open and protected and if breathing 

is present and adequate. This is achieved through inspection, auscultation, and palpation (look, listen, 

and feel). Start by observing the patient for objective signs of airway compromise. Note the presence 
238 | Maxillofacial and Neck Trauma

or absence and quality of speech. A normal voice suggests that the airway is adequate for the moment. 

Gurgling is a consequence of obstruction of the upper airway by liquids, such as blood or vomit, pooling 

in the oral cavity or hypopharynx. Snoring usually indicates partial airway obstruction at the pharyngeal 

level, while hoarseness suggests a laryngeal process. Snoring is classically due to obstruction of the upper 

airway by the tongue. This can occur due to loss of muscle tone secondary to loss of consciousness or as 

a result of loss of structural integrity of the mandible, as is seen in explosive or ballistic trauma. Stridor, a 

high-pitched sound, may be associated with partial airway obstruction at the level of the larynx (inspiratory 

stridor) or at the level of the trachea (expiratory stridor). Wheezing is usually secondary to narrowing of 

the lower airways. This can result from exacerbation of preexisting disease (e.g., reactive airway disease) 

or due to compression of the airway by soft-tissue edema, a foreign object, or an expanding hematoma. 

Aphonia in the conscious patient is an extremely worrisome sign. A patient who is too short of breath to 

speak is in grave danger of impending respiratory compromise. 

Feel for air movement at the mouth and nose. Open the mouth and inspect the upper airway, taking 

care not to extend or rotate the neck. Look for and remove any vomitus, blood, or other foreign bodies. 

Identify swelling of the tongue or uvula, any sites of bleeding, or any other visible abnormalities of the 

Figure 11. Penetrating trauma to the maxillofacial region can make visualization of the airway extremely challenging. Image courtesy of Tamer Goksel, 

DDS, MD, COL, US Army.
Maxillofacial and Neck Trauma | 239

oropharynx. The gentle use of a tongue blade may facilitate this task. The patient’s ability to spontaneously 

swallow and handle secretions indicates airway protective mechanisms are intact. In the unconscious patient, 

the absence of a gag reflex has traditionally been equated to a loss of protective airway reflexes. 

The midface and mandible should be inspected and palpated for structural integrity. Injuries to these 

structures may lead to distortion and loss of airway patency. Mandible fractures can lead to a loss of 

structural support and subsequent airway obstruction. Patients with these injuries may refuse to lie down 

in an attempt to maintain airway patency. The anterior neck should be carefully inspected for penetrating 

wounds. Asymmetry or swelling (i.e., from a vascular injury) of the neck may herald impending airway 

compromise. The detection of crepitus upon palpation of the neck suggests injury to the airway or a 

communicating pneumomediastinum. Auscultation should demonstrate clear and equal breath sounds. 

Diminished breath sounds may result from respiratory splinting causing atelectasis, pneumothorax, 

hemothorax, or pleural effusion. Wheezing and dyspnea imply lower airway obstruction. Patient agitation 

may represent hypoxia. Obtundation suggests hypercarbia. Cyanosis indicates hypoxemia. Hypoxia 

represents low oxygen at the cellular level, whereas hypoxemia is low oxygen solely with reference to 

arterial blood. In essence, each relates to low oxygen levels. Note the patient’s respiratory rate and pattern. 

Figure 12. (Top Left) A jaw-thrust maneuver is an effective way to open 

the airway in a patient with potential cervical spine injury. Illustrator: 

Chris Gralapp.

Figure 13. (Top Right) The oropharyngeal airway is a C-shaped 

device designed to hold the tongue off the posterior pharyngeal wall while 

providing an air channel through the mouth. Illustrator: Chris Gralapp.

Figure 14. (Bottom Right) Example of oropharyngeal airway (top) 

and nasopharyngeal airway (below).
240 | Maxillofacial and Neck Trauma

Bradypnea or tachypnea may be a sign of respiratory compromise. Respiratory muscle fatigue may result 

in the recruitment of accessory muscles of respiration. This is clinically manifested as suprasternal, 

supraclavicular, or intercostal muscle retractions. Look for a symmetrical rise and fall of the chest. 

Significant chest trauma may result in paradoxical or discordant chest wall movement (e.g., flail chest). 

Initial Airway Control

Ensuring airway patency is essential for adequate oxygenation and ventilation and is the first priority in 

airway control. The conscious patient uses the musculature of his/her upper airway and protective 

reflexes to maintain a patent airway and protect against aspiration of foreign substances (e.g., vomitus). 

In the severely ill or unconscious trauma patient, protective airway mechanisms may be impaired or lost, 

predisposing the patient to aspiration of secretions, blood, and gastric contents. 

Opening the airway is the first step in airway management. Upper airway obstruction in the unconscious 

Figure 15. (Top Left) Nasopharyngeal airways inserted in a combat 

casualty. A nasopharyngeal airway can establish a temporary, nonsurgical 

airway in a spontaneously breathing patient. (Top Right, Bottom 

Right) Though it does not provide definitive airway protection, these CT 

images clearly demonstrate the effectiveness of the nasopharyngeal airway 

as an adjunct in maintaining airway patency.
Maxillofacial and Neck Trauma | 241

patient is most commonly the result of posterior displacement of the tongue and epiglottis. Simple 

bedside maneuvers can remove this occlusion and reestablish airway patency and airflow. Carefully 

remove a casualty’s helmet or any headgear while maintaining manual in-line stabilization of the cervical 

spine. The chin-lift with head-tilt maneuver is a simple, effective technique for opening the airway but 

should be avoided in any patient with a potentially unstable cervical spine. The jaw thrust without headtilt maneuver can be performed while maintaining cervical spine alignment (Fig. 12). Between 2 to 4 

percent of patients with facial fractures from blunt trauma (in civilian studies) have concomitant cervical 

spinal fractures, and approximately 10 to 12 percent have cervical ligamentous injury.14,15 Although these 

techniques work well, they require the continuous involvement of several careproviders to maintain 

airway patency and cervical spine alignment.

Although effective in opening the airway, the chin-lift with head-tilt maneuver should be avoided in 

any patient with a potential cervical spine injury.

Oral and Nasal Airways

Oral and nasal adjunctive airway aids can establish a nonsurgical airway in a spontaneously breathing 

patient (Fig. 13). Though an oropharyngeal or nasopharyngeal airway may help establish a temporary 

airway, they do not provide definitive airway protection (e.g., protect against aspiration of vomitus). 

Nasal airways should not be placed in the setting of midface craniofacial injuries, as they can 

inadvertently be introduced into the cranial vault in cases of concomitant midface and skull base 

fractures.

The oropharyngeal airway is a C-shaped device designed to hold the tongue off the posterior pharyngeal 

wall while providing an air channel and suction conduit through the mouth (Fig. 14). An oropharyngeal 

airway is most effective in patients who are 

spontaneously breathing and lack a gag or cough 

reflex. The use of an oropharyngeal airway in a 

patient with a gag or cough reflex is contraindicated 

as it may stimulate vomiting or laryngospasm. 

Oral airways can cause complications; when used 

in conscious or semiconscious casualties, they 

may stimulate vomiting, laryngospasm, or patient 

agitation. Hence, inappropriate use of oral airways 

may worsen airway problems (e.g., potentially 

exacerbate cervical spinal injuries). They are 

also useful in assisting bag-valve-mask ventilation 

efforts in patients with respiratory failure. The 

oropharyngeal airway comes in various sizes to 

accommodate children to large adults. Proper 

oropharyngeal airway size is estimated by placing 

the oropharyngeal airway flange at the corner of 

the mouth. The distal tip of the airway should 

then reach the angle of the jaw.

Figure 16. The nasopharyngeal airway is an uncuffed curved tube made 

of soft rubber or plastic that provides a conduit for airflow between the 

nares and pharynx. Nasal airways should not be used in the setting of 

midface craniofacial injuries. Illustrator: Chris Gralapp.
242 | Maxillofacial and Neck Trauma

The nasopharyngeal airway is an uncuffed, curved tube made of soft rubber or plastic that provides a 

conduit for airflow between the nares and pharynx (Fig. 15). Nasopharyngeal airways are commonly 

used in intoxicated or semiconscious patients who do not tolerate an oropharyngeal airway. They are 

also effective when trauma, trismus (i.e., clenched teeth), or another obstacle (i.e., wiring of the teeth) 

preclude the placement of an oropharyngeal airway. Proper nasopharyngeal airway length is determined 

by measuring the distance from the tip of the nose to the tragus of the ear. Nasal airways may induce 

bleeding from the nose. Nasal airways should not be placed in the setting of midface craniofacial injuries, 

as they potentially can be introduced into the cranial vault in cases of concomitant midface and skull 

base fractures (Fig. 16).16

Cervical Spine Protection and Control 

All patients with significant blunt trauma to the head or face are at risk for cervical spine injury. The 

amount of force required to fracture the facial bones ranges from 275 to 1800 pounds per square inch, 

and careful consideration for unstable cervical spinal injury must be maintained throughout the process 

of securing the airway.17 Inadvertent movement of the neck of a patient with an unstable cervical spine 

injury can lead to permanent neurologic disability or death. Accordingly, many combat casualties are 

transported to the CSH with spinal immobilization.

An effective approach to airway management in patients with possible cervical spine injuries is rapid 

sequence intubation with in-line spinal immobilization. Pharmacologically paralyzing the patient reduces 

the risk of the patient moving during intubation attempts, improves airway visualization, and facilitates 

subsequent endotracheal intubation. A second individual maintaining immobilization of the head and 

neck in the neutral position throughout the procedure prevents inadvertent movement of the cervical 

spine by the laryngoscopist (Fig. 17). Careproviders need to ensure the patient can be effectively bagvalve-mask ventilated or that an alternative rescue airway intervention is planned (e.g., surgical airway) 

prior to pharmacologically paralyzing the patient, in the event endotracheal intubation is not possible.

As previously noted, combat casualties with penetrating injuries to the face and neck often pose significant 

Figure 17. In-line cervical spine immobilization in a casualty with 

penetrating maxillofacial injury.

Figure 18. A combat casualty with a definitive airway. A secured 

endotracheal tube is positioned in the trachea with its cuff inflated, attached 

to an oxygen-rich ventilation device.
Maxillofacial and Neck Trauma | 243

airway visualization challenges, which often result in more liberal manipulation of the head and neck 

to enable lifesaving airway interventions. Studies suggest that most patients with normal neurological 

motor exams following penetrating trauma to the neck will not have a mechanically destabilized spinal 

column.12,13

Definitive Airway Control and Breathing Support

A definitive airway ensures airway patency and protection. It requires an endotracheal tube (ETT) or 

tracheostomy tube in the trachea with the cuff inflated, secured in place, and attached to an oxygenrich ventilation device (Fig. 18). Failure to secure a definitive airway in a timely manner can have adverse 

consequences for the combat casualty. The decision to intubate a combat casualty is often complicated 

and may depend on a variety of clinical factors. There are several fundamental reasons for securing a 

definitive airway in such patients. These include: (1) failure of ventilation or oxygenation; (2) inability to 

maintain or protect an airway; (3) potential for deterioration based on the patient’s clinical presentation; 

and (4) facilitation of patient management (e.g., combative head injury patient who needs a neuroimaging 

or aeromedical evacuation). At this stage, intubation should be attempted with one of the following 

modalities:

• Standard oral or nasal endotracheal intubation

- Adjuncts include the GlideScope®, Light Wand® or fiberoptic scope

- Extreme caution should be used with nasal endotracheal intubation in patients with known midface 

fractures due to potential violation of the anterior cranial vault.

• Laryngeal mask airway (LMATM)

• Esophageal tracheal Combitube®

The benefit of endotracheal intubation or a Combitube® is that the casualty can be transported with 

either of these devices after they are properly secured. Should an LMATM be used and patient transport 

remains an issue, the patient should be considered to only have a temporary airway since the LMATM 

does not actually enter the trachea and dislodgement or movement is a potential complication. In 

addition, the LMATM has limitations associated with decreased ability to ventilate at increased airway 

pressures, contraindications in penetrating upper airway trauma or central airway obstruction with 

foreign body, and potential aspiration risks.18 In a Level III or higher care facility where immediate 

patient movement is not a tactical concern, the LMATM serves as an appropriate adjunct to facilitate 

ventilation prior to performing endotracheal intubation or a surgical airway. 

Extreme caution should be used with nasal endotracheal intubation in patients with known midface 

fractures due to potential violation of the anterior cranial vault.

Preparation for Endotracheal Intubation 

Careful preparation prior to attempting endotracheal intubation is essential to achieving success. This 

point cannot be emphasized enough. Careproviders need to ensure adequate suction, oxygen flow, airway 

equipment, pharmacologic agents, and monitoring equipment are present. This includes airway adjuncts 

and alternative airway devices, including a cricothyroidotomy tray in case initial methods are unsuccessful. 

Suction systems should be tested and readily available at the bedside for removal of blood, vomitus, and 

foreign bodies. A high-flow oxygen mask and bag-valve-mask ventilation device should be ready for 
244 | Maxillofacial and Neck Trauma

use. Ideally, patients should be preoxygenated with 100 percent high-flow oxygen to enable several 

attempts at intubation without the need for bag-valve-mask ventilation (which causes gastric distention 

and increases the risk of passive regurgitation of gastric contents). At least two functioning laryngoscope 

handles and appropriately sized and shaped laryngoscope blades should be obtained. The anticipated 

blade of choice should be clicked into position to ensure that the light functions properly. An ETT should 

be chosen based on the patient’s anatomy and one smaller size should be prepared as well. The average 

adult male will require a 7.5- or 8.0-millimeter (internal diameter) ETT, the average adult female requires 

a 7.0- or 7.5-millimeter ETT. In children, the ETT size may be estimated by the formula: ETT size = 4 + 

(age in years /4). The ETT cuff should be inflated to test for an air leak. A stylet should be inserted within 

the ETT to shape it into a configuration that will facilitate insertion into the airway. Care must be taken to 

ensure that the tip of the stylet does not protrude from the end of the ETT or through the small distal side 

port (Murphy’s eye). The patient should have at least one intravenous (IV) catheter inserted, and patency 

of the line should be verified and ensured. The specific rapid sequence intubation medications, proper 

dosing, and sequence of administration should be determined. These pharmacological agents should be 

drawn up and syringes labeled. Cardiac monitoring, blood pressure monitoring, and pulse oximetry are 

mandatory for all patients. If available, an end-tidal CO2 monitor should be readied as well. 

In children, the ETT size may be estimated by the formula: ETT size = 4 + (age in years /4).

Endotracheal Intubation Technique

With the laryngoscope in the left hand (assuming a right-hand-dominant laryngoscopist), the mouth is 

gently opened with the right hand. The laryngoscope is gently inserted into the right side of the patient’s 

mouth, and the tongue is displaced to the left (Fig. 19). The curved (Macintosh) blade is slid into the 

vallecula and the straight (Miller) blade is positioned below the epiglottis (Fig. 20). The handle is pushed 

along the axis of the handle at a 45-degree angle to the patient’s body. Avoid the tendency to leverage (i.e., 

crowbar) the laryngoscope blade against the teeth, as this may fracture the teeth.

Figure 19. Insertion of laryngoscope and application of cricoid pressure 

during intubation. Illustrator: Chris Gralapp.

Figure 20. The straight (Miller) blade is positioned below the epiglottis 

whereas the curved (Macintosh) blade is placed in the vallecula during 

endotracheal intubation.
Maxillofacial and Neck Trauma | 245

With a clear view of the glottis, the right hand gently inserts the ETT until the cuff is about two to three 

centimeters past the vocal cords. Blind intubation (i.e., passing the ETT without visualization of the vocal 

cords) increases the likelihood of esophageal intubation. In the average-size adult male, the 23-centimeter 

mark of the ETT will be located at the corner of the mouth (21 centimeters in women). Once the ETT 

is in place, the stylet should be removed and the cuff inflated until there is no audible air leak with bag 

ventilation. The ETT cuff pressure should be kept below 25 cm H2O pressure. This will minimize the 

risk of tracheal mucosal injury attributable to excessive cuff pressures.19 Adequate preoxygenation should 

allow the laryngoscopist multiple attempts at intubation before arterial oxygen desaturation occurs. A 

dedicated team member should be focused on the patient’s cardiac rhythm, blood pressure, and oxygen 

saturation during laryngoscopy and should alert the endoscopist to any abnormalities. 

Endotracheal tube cuff pressure should be kept below 25 cm H2O to minimize the risk of tracheal mucosal 

injury.

After any unsuccessful attempt, always recheck the patient’s position, and make the necessary adjustments. 

It is important to attempt to improve your chance of successfully intubating the patient with each 

successive attempt. This is often done by changing the size or type of laryngoscope blade, repositioning 

the patient, or by utilizing additional techniques (e.g., fiberoptic intubation). 

Rapid Sequence Intubation 

Rapid sequence intubation is a series of defined steps intended to allow for rapid endotracheal intubation 

of a patient with minimal bag-valve-mask ventilation. Given that most patients requiring emergent 

intubation have not fasted and may have full stomachs, bag-valve-mask ventilation may inadvertently 

lead to gastric distention and passive regurgitation and increase the risk of aspiration. To perform rapid 

sequence intubation and avoid this complication, the patient is first preoxygenated to provide adequate 

blood oxygentation despite a period of apnea without interposed assisted ventilation. This is followed by 

the sequential administration of an induction agent and a rapidly acting neuromuscular blocking agent to 

induce a state of unconsciousness and paralysis, respectively. An assistant should apply Sellick’s maneuver 

(cricoid pressure), just as the patient is noted to lose consciousness (Fig. 19). This application of firm 

pressure to the cricoid cartilage is intended to compress the esophagus (although recent studies suggest 

the postcricoid hypopharynx is the site of compression) and prevent passive regurgitation of gastric 

contents.20 Sellick’s maneuver should be maintained until the ETT has been placed, its position verified, 

and the cuff inflated. Cricoid pressure can occasionally hinder airway visualization; hence, pressure should 

be reduced to facilitate vocal cord visualization as indicated.21 Sellick’s maneuver should be discontinued 

in patients who are actively vomiting (versus passive regurgitation). Esophageal compression in a patient 

who is actively vomiting risks esophageal rupture. 

Awake Endotracheal Intubation 

Performing oral intubation on a patient who is awake is an intervention that will require liberal topical 

airway anesthesia and patient sedation prior to inspection or intubation of the patient’s airway. This 

approach allows for the preservation of the patient’s airway reflexes and spontaneous breathing while the 

laryngoscopist takes a quick look at the glottis, vocal cords, and internal airway anatomy. The classic 

scenario for employing such a technique is the patient with distorted upper airway anatomy (Fig. 16). 

Under these circumstances, intubation by rapid sequence intubation is often unsuccessful. Subsequent 

bag-valve-mask ventilation may be ineffective due to loss of normal architecture and inability to create 
246 | Maxillofacial and Neck Trauma

an adequate mask-to-mouth seal (e.g., displaced mandible fractures and soft-tissue loss) or can cause 

air to dissect into the tissue planes of the neck (e.g., following penetrating oropharyngeal injuries), 

further distorting airway anatomy. Disadvantages of oral intubation of a patient who is awake include 

oversedation, discomfort and stress, deleterious effects in patients with cardiac disorders, or increased 

intracranial pressure. Fiberoptic laryngoscopy assessment of the airway (when available) and subsequent 

ETT placement are alternatives and very valuable methods of performing an awake oral intubation.

Crash Endotracheal Intubation 

A crash intubation is the immediate endotracheal intubation of a patient without the use of any medications. 

It is indicated in patients with respiratory arrest, agonal respirations, or deep unresponsiveness. The 

advantages of this approach often include technical ease and rapidity. Disadvantages include the potential 

for increased intracranial pressure from the stress of intubation as well as emesis and aspiration. 

Confirmation of Endotracheal Tube Placement 

As inadvertent intubation of the esophagus can occur during airway management, proper positioning 

of the ETT within the trachea needs to be confirmed after every intubation. Failure to recognize an 

esophageal intubation can result in patient death. Methods used to detect ETT placement include 

clinical assessment, pulse oximetry, end-tidal carbon dioxide (ETCO2) detection, suction bulb or syringe 

aspiration techniques, and ultrasonography.22 Chest radiography can be used to assess ETT position 

but does not confirm ETT placement within the trachea. Since the esophagus lies directly behind the 

trachea, an ETT placed incorrectly in the esophagus may appear to be within the trachea on an anteriorposterior chest radiograph. 

Failure to recognize an esophageal intubation can result in patient death. Clinical observations, end-tidal 

CO2 colorimetry, and continuous noninvasive pulse oximetry can be used to help confirm appropriate 

positioning of the ETT within the trachea.

Classically, a combination of clinical observations has been used to confirm correct ETT placement. 

These include (1) direct visualization of the ETT passing through the vocal cords during intubation; (2) 

auscultation of clear and equal breath sounds over 

both lung fields; (3) absence of breath sounds when 

auscultating over the epigastrium; (4) observation 

of symmetrical chest rise during ventilation; and (5) 

observation of condensation (fogging) of the ETT 

during ventilation. Though these clinical findings 

should be assessed in every intubated patient, they 

are subject to failure as the sole means for confirming 

ETT placement. 

Continuous noninvasive pulse oximetry should be 

standard for every patient being intubated. A drop in 

oxygen saturation following intubation is suggestive 

of an esophageal intubation. However, this drop 

may be delayed for several minutes if the patient 

was adequately preoxygenated. In certain patients 

Figure 21. A colorimetric end-tidal CO2 detector can be placed between the 

ETT and bag following intubation, with a (depending on brand) blue- or 

purple-to-yellow color change indicating a correctly placed ETT.
Maxillofacial and Neck Trauma | 247

(i.e., hypotensive), oxygen saturation measurements may be unreliable or difficult to detect. Detection and 

measurement of exhaled carbon dioxide is a highly reliable method for detecting proper placement of 

the ETT within the trachea.23 A colorimetric end-tidal CO2 detector is a small disposable device that 

connects between the bag and the ETT. When the device detects end-tidal volume CO2, its colorimetric 

indicator (depending on brand) changes from blue or purple to yellow (Fig. 21). The absence of this 

color change usually indicates the tube is incorrectly placed in the esophagus. An important exception is 

that the colorimetric indicator will remain purple even with correct ETT placement within the trachea 

in patients with prolonged cardiac arrest. These patients are not circulating carbon dioxide to their 

pulmonary circulation and into their airways. The recovery prognosis for such patients is dismal.23

Aspiration devices may also be used for confirmation of ETT placement and work based on the principle 

that the trachea is a rigid air-filled structure, whereas the esophagus is soft-walled.22 Attempts to draw 

air through an ETT placed in the esophagus will meet resistance from collapse of the esophageal wall 

around the distal ETT, whereas air will freely flow when drawn through an ETT in the trachea. Two 

commonly used aspiration appliances are a bulb suction device and a large-volume syringe. 

Surgical Airway Management

Despite active bleeding and gaping facial wounds, the fastest and most direct technique to establish a 

definitive airway is often direct laryngoscopy and oral endotracheal intubation. If direct laryngoscopy 

fails, a cricothyroidotomy is an expedient technique to establish a definitive airway. Even in the hands 

of experienced careproviders, alternative surgical airways (e.g., tracheotomy) require a formal surgical 

setting, proper patient positioning, surgical assistance, and good lighting. The degree of skill required 

to surgically create such alternative airways coupled with the required resources conspire to make such 

surgical interventions challenging for generalists providing CCC.

If attempts at direct laryngoscopy and endotracheal intubation fail, a cricothyroidotomy is an expedient 

technique to establish a definitive airway.

Cricothyroidotomy

Surgical airway management entails the creation of an opening into the trachea to provide oxygenation and 

ventilation. Proficiency with surgical airway techniques can mean the difference between life and death. 

Should difficulty arise in obtaining a secure airway via endotracheal intubation (and bag-valve-mask 

ventilation is not feasible), there should be no hesitation to proceed directly to a surgical cricothyroidotomy. 

In an emergency, a surgical cricothyroidotomy is preferred to a tracheotomy, as the distance from the 

skin to the cricothyroid membrane in most adults is approximately 10 millimeters (mm), compared to the 

average distance from the skin to the trachea being approximately 20 to 30 mm.24 In addition, at the level 

of the second and third tracheal rings, the potential exists for violating the highly vascular thyroid isthmus.

The resultant hemorrhage can complicate visualization of the trachea. 

A cricothyroidotomy is preferred to a tracheotomy as an emergency surgical airway.

A cricothyroidotomy creates an immediate surgical opening through the cricothyroid membrane to allow 

the placement of an ETT or cuffed tracheostomy tube. The primary indication for a cricothyroidotomy 

is the immediate need for an airway when oral endotracheal intubation is not achievable and bag-valve-
248 | Maxillofacial and Neck Trauma

Figure 22. A cricothyroidotomy creates an immediate surgical opening through the cricothyroid membrane to allow the placement of an ETT or cuffed 

tracheostomy tube. It requires decisive action and a coordinated team effort.

Figure 23. Landmarks for cricothyroidotomy. Image courtesy of the Borden Institute, Office of The Surgeon General, Washington, DC. Illustrator: 

Bruce Maston.
Maxillofacial and Neck Trauma | 249

mask ventilation is not feasible (Figs. 22 and 23). A classic example is the patient with severe facial trauma 

in whom conventional airway management might be extremely complicated or impossible (Fig. 11). The 

steps of surgical cricothyroidotomy are outlined in Table 4.

A CCC provider inexperienced in performing cricothyroidotomy should not attempt a smaller stab 

incision of only the cricothyroid membrane in an emergency situation unless the patient has a thin softtissue profile with readily apparent thyroid and cricoid cartilages. The characteristic thick, muscular 

neck of many US service members makes correct performance of an isolated stab incision into the 

cricothyroid membrane extremely difficult.

Contraindications to cricothyroidotomy include: (1) the ability to secure an orotracheal intubation; 

and (2) complete tracheal transection with retraction of distal trachea into the mediastinum. Relative 

Table 4. Steps of surgical cricothyroidotomy.

Steps of Surgical Cricothyroidotomy

1. Identify the cricothyroid membrane, which is positioned between the cricoid ring and thyroid 

cartilage 

2. Prepare and sterilize the skin widely to allow for increased visualization of the operative field

3. Anesthetize the site if time or circumstances allow

4. Grasp and secure the thyroid cartilage with your nondominant hand, placing digits one and three

along the outer contour of the thyroid cartilage, and use your second digit to identify the cricothyroid 

membrane

5. Make a one- to two-centimeter vertical skin incision* placed just inferior to the thyroid cartilage past

the level of cricothyroid membrane through the following structures:

 a. Skin

 b. Subcutaneous tissues

 c. Cervical fascia

* The author prefers vertical incisions, as the potential is decreased for injuring the anterior jugular 

veins or superior thyroid arteries that lay lateral to the cricothyroid membrane25

6. Bluntly dissect the tissues to expose the cricothyroid membrane

7. Make a horizontal incision through the lower half of the cricothyroid membrane and pass a tracheal

hook under the inferior surface of the thyroid cartilage and retract upward with the tracheal hook

8. Open the membrane with dilator forceps or the back of a scalpel handle 

9. Insert a lubricated, small-cuffed endotracheal tube (6.0 to 7.0 mm internal diameter tube works well

in adults) until you see the balloon of the tube disappear below the level of the membrane

10. Confirm tracheal intubation:

a. End-tidal CO2 colorimetry

b. Chest rise

c. Bilateral breath sounds

11. Secure the endotracheal tube with sutures to the skin
250 | Maxillofacial and Neck Trauma

contraindications include the presence of injuries or infections of the larynx and children under the 

age of 12 years. In children of this age, poorly defined anatomic landmarks and an extremely small 

cricothyroid membrane make the procedure difficult, if not impossible to perform. These age-based 

guidelines are variable. If a younger child is large for his or her age and has well-developed anatomy, the 

procedure may be successful. A surgical tracheotomy is the preferred method for airway stabilization in 

children under the age of 12, if conditions allow. Complications of cricothyroidotomy include incorrect 

location of tube placement, hemorrhage (and tube obstruction), tracheal or laryngeal injury, infection, 

pneumomediastinum, subglottic stenosis, and voice change.26,27

Percutaneous Transtracheal Ventilation (Needle Cricothyroidotomy)

An important (particularly in young children) surgical airway procedure is needle cricothyroidotomy 

with percutaneous transtracheal ventilation (PTTV) (Fig. 24). Percutaneous transtracheal ventilation 

involves inserting a 14-gauge transtracheal 

catheter into the cricothyroid membrane with the 

catheter connected to a ventilation system; lungs 

are insufflated with 15 liters per minute oxygen 

flow, one second on and four seconds off.28,29

Advantages of this technique include its simplicity, 

safety, and speed. There is typically less bleeding 

when compared with cricothyroidotomy, and age is 

not a contraindication, making it a valuable airway 

management adjunct in children younger than age 

12. During PTTV, the upper airway must be free 

of obstruction to allow for complete exhalation; 

otherwise, the patient is at risk for barotrauma 

from air stacking. All patients receiving PTTV 

should have oral and nasal airways placed. Unlike 

cricothyroidotomy, PTTV does not provide airway 

protection. Therefore, it should be thought of as a 

temporizing measure until a definitive airway can 

be established.

The Difficult Airway

A recurring difficult-to-manage scenario in OEF/OIF is a casualty with avulsion of the lower face. 

Despite injury severity, such casualties often present conscious, sitting up in an air-hungry position, and 

drooling a combination of saliva and blood. Attempts to place these patients in a supine position is 

resisted by the patient because the airway becomes immediately impaired. In addition, such patients are 

not easy to bag-valve-mask ventilate, as creating a tight mask seal is impeded by missing anatomy and 

active bleeding. The inability to bag-valve-mask ventilate a patient is a contraindication to administering 

a muscle paralytic medication (rapid sequence induction). 

There are several approaches to such a scenario. One approach involves the use of a nonparalytic 

medication such as ketamine (1 to 2 milligrams [mg] per kilogram intravenous bolus infusion) and an 

antisialogogue like atropine (0.01 mg per kilogram) to facilitate direct laryngoscopy. This often provides 

Figure 24. Percutaneous transtracheal ventilation (PTTV). Illustrator: 

Chris Gralapp.
Maxillofacial and Neck Trauma | 251

the endoscopist with the ability to visualize the vocal cords and perform intubation or gain confidence 

that intubation is achievable if a paralytic medication is subsequently administered. A surgical 

cricothyroidotomy is another airway intervention that can be performed under ketamine anesthesia (1 

to 2 mg per kilogram intravenous bolus infusion), which preserves a patient’s ability to maintain airway 

tonicity and respiratory drive. Alternatively, if equipment and trained careproviders are available, fiberoptic 

laryngoscopy can be attempted. However, fiberoptic laryngoscopy efforts are often unsuccessful due to 

active bleeding obscuring airway visualization or the unavailability of instruments and trained personnel.

An additional approach involves preoxygenating such patients with 100 percent high-flow oxygen for 

several minutes and then initiating rapid sequence induction while the patient is still sitting upright. 

Once the patient is unconscious and supine, direct laryngoscopy is immediately attempted. Exposure 

of the glottis is highly dependent on displacement of the tongue with a laryngoscope blade against an 

intact mandibular arch. Once mandibular body integrity is disrupted by fracture or avulsion, anterior 

displacement of the tongue is easier; but blood, soft-tissue swelling, and debris may continue to obscure 

the glottis. To aid exposure of the glottis in these situations, traction on a suture passed through the tip of 

the tongue can assist in opening the airway for intubation. If the glottis is still obscured despite aggressive 

suctioning, pressing on the chest to push air through the glottis may produce bubbles that will help 

localize the glottis for intubation. If this fails, a surgical cricothyroidotomy is rapidly performed. 

When mandibular body integrity is disrupted, traction on a suture passed through the tip of the tongue 

can assist in exposure of the glottis and in opening the airway for intubation.

Initial Management Considerations

Once a definitive airway is established, active bleeding is controlled with nasal packs, oropharyngeal 

packs, and pressure dressings that are applied by wrapping the head with KerlixTM gauze. The goal is 

to at least slow blood loss to a level that can be replaced by blood products and allow the patient to 

be fully assessed and stabilized before transfer to the operating room. Patients with suspected ocular 

globe injuries should not have compression dressings applied, pending exclusion of globe rupture. After 

primary survey and stabilization of other injuries, secondary survey of severely injured maxillofacial 

structures is performed along with appropriate imaging.

Computed tomography (CT) imaging of the maxillofacial region and cervical spine (to screen for spinal 

injury) is often required prior to maxillofacial reconstruction. The sequence of treatment steps includes 

fracture management and soft-tissue repair. In the combat theater, time and resource-consuming 

maxillofacial reconstruction is avoided in casualties eligible for evacuation. The administration of an 

initial course of broad-spectrum prophylactic antibiotics should be considered following head and 

neck combat-related injuries (especially open fractures). A comprehensive review of the literature fails 

to support prophylactic antibiotic coverage beyond 24 hours of initial surgical intervention.8 Hence, 

perioperative antibiotics should be terminated 24 hours after primary repair of maxillofacial wounds.

Mandible Fractures

Definitive management of maxillofacial fractures is best deferred to face specialists. A Barton bandage is 

an effective measure a generalist may use to stabilize a flail mandible fracture. This temporizing measure 

incorporates an extension of the head wrap bandage under the chin to stabilize the mandible against the 
252 | Maxillofacial and Neck Trauma

Figure 25. Casualty arrives at a Field Hospital with a pressure 

dressing in place. An AK-47 bullet entrance wound is adjacent to the nose 

(anatomical left side of patient).

Figure 26. Rapid sequence induction is immediately performed with oral 

endotracheal intubation. Note exit wound on anatomical right side of face.

Figures 27 and 28. Two axial CT images demonstrating the bullet’s path from the base of the nose (anatomical left side of face) traversing the face 

and causing fragmented dentition and extensive soft-tissue injury to the anatomical right side of the face. 

Figures 29 and 30. Definitive care on this nontransferable host nation casualty occurred in one step. This included tracheotomy, debridement of 

hopelessly comminuted fragments and debris, fracture repair with open reduction and internal fixation, and parotidectomy and facial nerve repair with 

greater auricular nerve graft to the upper division, followed by oral and skin flaps for closure.
Maxillofacial and Neck Trauma | 253

maxilla to control pain. This intervention should be delayed until the airway is secured or deemed safe 

and uncompromised (Figs. 25 to 30). Application of dental wires and arch bar techniques requires dental 

expertise; these techniques can effectively stabilize fractures and control pain (Fig. 31). Wiring the teeth 

together, however, compromises the airway and should be avoided in most cases of severe maxillofacial 

trauma treated in-theater. Elastic intermaxillary fixation with lightly applied rubber band ligatures is 

an excellent substitute to wire fixation for the ambulatory patient.

Wiring the teeth together compromises the airway and should be avoided in most cases of severe 

maxillofacial trauma treated in-theater.

Dental Injury

Teeth avulsed on the battlefield should be 

discarded. Even under the most ideal conditions of 

immediate root canal therapy and dental fixation, 

reimplanted teeth activate a chronic inflammatory 

response that causes irreversible root resorption. 

An exception is if the avulsion time for an anterior 

maxillary root is less than 30 minutes, and dental 

expertise is readily available for reimplantation as a 

temporizing measure to preserve alveolar bone until 

a dental implant is placed.30 Likewise, dentoalveolar 

fragments suspended in the airway from a scant 

soft-tissue pedicle should be removed to prevent 

aspiration of loose dentition. Lost dentoalveolar 

structures can be replaced by tissue grafting 

techniques and dental implants once the casualty is 

evacuated to the US.

Figure 31. Intermaxillary fixation is used judiciously in the combat 

theater and only on ambulatory patients with no airway compromise. 

Elastic bands between the dental arches instead of wire ligatures are 

highly recommended for transport. Image courtesy of the Borden Institute, 

Office of The Surgeon General, Washington, DC.

Figure 32. Near complete avulsion of the ear. (Left) Prior to surgical intervention, note small soft-tissue pedicle. (Right) Following repair, venous 

congestion threatens tissue survival. Medical leeches can be beneficial in such cases.
254 | Maxillofacial and Neck Trauma

Teeth avulsed on the battlefield should be discarded. The primary exception is an anterior maxillary 

tooth with an avulsion time of less than 30 minutes. 

Facial Injury

Facial features such as the ears, nose, and lips are at risk for avulsion on the battlefield. Following complete 

avulsion, very little can be done to reattach the body part without immediate microvascular surgical 

resources. Partially avulsed structures should be assessed by a face specialist before debridement. Even a 

small soft-tissue pedicle can perfuse an ear or nose, and the consequence of failure is no worse than not 

trying at all. Venous congestion of reattached tissue can be treated with leeches (Fig. 32).31,32,33 Access to 

leeches for such interventions is limited in OEF/OIF. In the authors’ experience, the resourcefulness of 

host nationals (e.g., obtaining leeches from a nearby riverbank) should be not be underestimated.

Even a small soft-tissue pedicle can perfuse a partially avulsed ear or nose, and the consequence of 

failure is no worse than not trying at all.

Parotid and Facial Nerve Injuries

Penetrating injuries to the face can disrupt the parotid capsule, sever parotid ducts, and injure major 

branches of the facial nerve. Careful evaluation and inspection are necessary to rule out these injuries 

prior to wound closure because significant morbidity occurs when these injuries go unrecognized.34 A 

reference line dropped vertically from the lateral canthus helps identify the parotid duct as posterior to 

the line, just below the nasal base, and lying over the masseter (Figs. 33 and 34). If there is any doubt 

regarding parotid duct integrity, the laceration should be cleaned, packed open, dressed wet-to-dry, 

and referred for treatment by a specialist. The same reference line is used to establish reparability of 

Figure 33. Branches of the facial nerve and a parotid duct injury. Parotid 

duct injuries and severed facial nerve branches posterior to a vertical line 

drawn down from the lateral canthus of the eye should be cleaned, packed 

open, and referred for treatment by a specialist. Image courtesy of the 

Borden Institute, Office of The Surgeon General, Washington, DC.

Figure 34. Repair of the parotid duct should be completed by a face 

specialist. Image courtesy of the Borden Institute, Office of The Surgeon 

General, Washington, DC.
Maxillofacial and Neck Trauma | 255

facial nerve branches. Wounds posterior to this reference line are packed open for specialist care if nerve 

dysfunction is clinically evident. Parotid capsule disruption requires special closure, pressure bandages, 

and possibly botulinum (toxin) injections (Fig. 35). These injections minimize saliva secretion as the 

wound heals and are intended to prevent cutaneous fistula formation. 

Parotid duct injuries and severed facial nerve branches posterior to a vertical line drawn down from the 

lateral canthus of the eye should be cleaned, packed open, and referred for treatment by a specialist. 

Facial Lacerations

Facial lacerations are anesthetized by subcutaneous injection of 1 percent lidocaine with epinephrine 

through the wound edges (the addition of 0.25 percent bupivacaine will add hours of postoperative pain 

relief), followed by careful cleansing and inspection of the wound. After hemostasis is achieved, deep 

lacerations are closed in layers with absorbable 4-0 polyglycolic interrupted sutures starting with the 

deep subcutaneous layer, then the dermis to approximate the wound edges. Finally, 4-0 to 6-0 (depending 

on exact location) nylon skin sutures are used to create a tension-free closure of the skin. Petroleum gel 

coverage of the wound maintains a physiologic environment for favorable healing. Facial sutures should 

be removed within three to five days to prevent track scars, and adhesive skin closure interventions (e.g., 

Steri-StripsTM or cyanoacrylate tissue glue) are applied for an additional two weeks. 

Figure 35. Through-and-through cheek laceration. (Top Left) Penetrating 

injuries to the face can disrupt the parotid capsule, sever parotid ducts, 

and injure major branches of the facial nerve. (Top Right) Parotid duct 

and branches of marginal mandibular nerve were identified and repaired, 

followed by watertight closure of the mucosa and (Bottom Right) repair 

of deep layers and dermis.
256 | Maxillofacial and Neck Trauma

Facial lacerations that can be explored and debrided effectively should be closed primarily unless 

underlying fractures are present.8 In the authors’ experience, simple lacerations can be packed open 

and closed in a delayed fashion (up to four days later) without significant cosmetic compromise, whereas 

complex lacerations should be definitively treated within two days to achieve the best possible repair. 

Macerated or abraded facial soft-tissue should be cleaned and covered with petroleum gel (ophthalmic 

petroleum gel if wounds are near eyes). Closing facial wounds with advanced flaps should be deferred 

(when possible) until arrival at Level IV and V facilities. 

Facial lacerations that can be explored and debrided effectively should be closed primarily unless 

underlying fractures are present.

Information for the Specialist - Maxillofacial Injuries

Overview

According to a study of a six-year period of battle injuries recorded in the JTTR, penetrating trauma is 

the mechanism of injury in 92 percent of US service members evacuated from theater with maxillofacial 

injuries.1 Face burns occur in 77 percent of service members evacuated from theater with combat-related 

burns.7 Maxillofacial blast injury is characterized in the JTTR database as a combination of complex 

lacerations and open comminuted fractures, complicated by avulsions and burns.1 This is in sharp contrast 

to maxillofacial injuries encountered in the civilian setting, which are predominately caused by blunt 

trauma. While most injured US service members are stabilized for evacuation to a Level IV or V medical 

facility for definitive care, the deployed surgeon will be expected to provide definitive care to injured host 

Figure 36. Casualties with complex facial wounds that can be transferred to higher levels of care should have their wounds cleaned, stabilized, and 

packed wet-to-dry.
Maxillofacial and Neck Trauma | 257

nation patients, security forces, and detainees. This is especially true in Afghanistan, where transfer to 

local surgical facilities is rarely possible. Since severe blast injury is uncommon in the US, the nature of 

injuries the deployed face surgeon will likely encounter will be outside his/her usual scope of practice. 

This section will help bridge this experience gap for the newly deployed face surgeon by addressing 

penetrating maxillofacial battle injuries.

As severe blast injury is uncommon in the US, the nature of injuries the deployed face surgeon will 

encounter will likely be outside his/her usual scope of practice.

Initial Management

The high incidence of airway compromise following severe maxillofacial trauma requires immediate 

interventions to stabilize and secure a patient’s airway. Endotracheal intubation (when feasible) and 

surgical cricothyroidotomy are well established first-line interventions for securing a casualty’s airway. 

Face specialists may also need to reduce fractured and displaced facial bones that are encroaching on a 

patient’s airway. Severe hemorrhage from fractured bony segments may necessitate immediate surgery to 

ligate injured vessels or reduce fragments to control hemorrhage (covered later in this chapter). 

Once the airway is secured and active bleeding controlled with application of pressure bandages, 

damage control resuscitation and, when indicated, damage control surgery are immediate priorities. 

Initial maxillofacial fracture stabilization and soft-tissue repair can be delayed for several days until the 

casualty is deemed stable from the trauma surgeon’s perspective (Fig. 36).

Maxillofacial Wound Care

“The maxillofacial region is anatomically complex with skin and mucosa lining structures that support 

the upper airway, deglutition apparatus, and specialized sensory organs of sight, smell, hearing, taste, 

and touch.”8 Although the integrity of the mucosal lining is often disrupted by penetrating maxillofacial 

battle injuries, the rich blood supply allows for early primary closure after appropriate debridement.8

The risk of cavitation necrosis to the head and neck following gunshot wounds is low. This is because 

the head and neck lack large muscle masses, the investing tissues are highly vascular, and the potential 

space for disruption is limited in depth prior to encountering the hard tissues of the mandible.8

Primary closure of penetrating maxillofacial injuries may be performed following judicious wound 

debridement.

Maxillofacial wounds suffered in combat will often require serial debridement and irrigation to remove 

gross debris and foreign bodies. Such interventions can be scheduled in coordination with the multiple 

trips to the operating room casualties undergo during damage control surgery for concurrent injuries. 

The surgeon should consider early lateral canthotomies for maxillofacial wounds complicated by 

burns involving the periorbita to prevent orbital compartment syndrome and loss of vision (Fig. 37). 

Tracheotomy should also be considered at this early phase. Frost sutures (intermarginal sutures placed 

between the eyelids to protect the cornea) and bolster dressings will help protect against corneal injury 

and ectropion formation (Fig. 38). 

Application of arch bars and external pin fixation (Hoffman® II orthopedic devices) are expedient 
258 | Maxillofacial and Neck Trauma

techniques to stabilize flail mandible fractures (Fig. 39). Nasal packs should be removed at three days. 

Facial pressure dressings should be removed and replaced, wet-to-dry, daily. Standard ear-nose-throat 

(ENT) textbooks routinely recommend prophylactic antibiotic administration while the nose is packed to 

prevent complications associated with Staphylococcus aureus dissemination.35

Infection Prevention and Management

Infection prevention and management are integral components of all phases of CCC. In 2007, the 

US Army Surgeon General commissioned a group of researchers to review the literature and publish 

evidence-based recommendations for the prevention and treatment of combat-related infections.36

A team consisting of an infectious disease specialist, a head and neck surgeon, an ophthalmologist, 

and an oral and maxillofacial surgeon focused on infections of maxillofacial and neck combat-related 

injuries.8

War Wounds

War wounds are traditionally considered contaminated. Animal studies have demonstrated that animals 

become rapidly colonized with bacteria found in the immediate environment in which projectile-related 

wounding occurs.37 The integrity of the mucosal lining (especially the oral cavity) is an important factor

Figure 37. Second-degree face burns involving the periorbita. Lateral 

canthotomies are performed to prevent orbital compartment syndrome. 

Using tape or Velcro® straps to secure the endotracheal tube interferes with 

wound healing and risks accidental extubation. A better technique is to 

wire the tube to the lower teeth.

Figure 38. Bolster dressings and Frost sutures will help prevent ectropion 

in the acute phase of burn recovery. Likewise, a plastic lip retractor will 

help prevent microstomia.
Maxillofacial and Neck Trauma | 259

following injuries to the maxillofacial region. Wounds characterized by disruption of the integrity of the 

mucosal lining within the oral cavity are prone to infection by bacteria found within saliva. Despite these 

characteristics, the rich vascular supply of the face (among other factors) does allow for early primary 

wound closure of face wounds following wound irrigation and debridement.8

Early definitive treatment with debridement, irrigation, early repair of soft- and hard-tissues, and 

early administration of broad-spectrum prophylactic antibiotics are interventions that decrease war 

infections.8,38,39,40 All war wounds to the head and neck should be treated with 24 hours of prophylactic 

antibiotic therapy. There is no evidence to indicate that longer courses of antibiotics are of any benefit, 

provided war wounds are repaired in less than 12 hours, and prophylactic antibiotics are administered 

within six hours of initial head and neck injury.41,42,43 Third-generation cephalosporin antibiotics provide 

adequate perioperative prophylaxis for maxillofacial, head, and neck injury surgical interventions.44

Current US Army recommendations are that maxillofacial war injuries not repaired in less than or equal 

to 12 hours, or without prophylactic antibiotics greater than or equal to six hours following injury, have 

a high risk of infection and require a treatment course of 10 to 14 days of antibiotics.15 Combat casualty 

care data supporting these recommendations are limited. However, similar recommendations are widely 

published in civilian oral and maxillofacial textbooks.39,40 High-risk maxillofacial wound characteristics 

include those with comminuted fractures or avulsed mandible defects, wounds with compromised blood 

supply, wounds closed under tension, and tissue flap or skin graft closures. Such wounds may benefit 

from a more prolonged course of prophylactic antibiotic therapy.8

Early definitive treatment with debridement, irrigation, repair of soft- and hard-tissues, administration 

of broad-spectrum prophylactic antibiotics, minimal introduction of foreign surgical material during 

initial surgery, and coverage of bone with tension-free closure are all interventions that decrease war 

infections.

Figure 39. Flail mandible. (Above) Avulsed dentate mandible was 

stabilized with a wrist external pin fixator and the lower lip wound 

temporarily closed. (Right) Once sutures were released at a Level V 

facility, the preexisting two-thirds avulsion of the lower lip, chin, and oral 

vestibule become apparent.
260 | Maxillofacial and Neck Trauma

Epidemiology of Wound Infection

Infection rates following war-related maxillofacial injuries are outlined in Table 5. The actual pathogens 

that cause infections following war-related maxillofacial injury are poorly characterized.45,46 Civilian 

studies in non-trauma patient populations have found that the cause of infection was polymicrobial in 88 

to 96 percent of patients who develop infections following head and neck surgery.47,48 Aerobic organisms 

were found in 54 to 91 percent of infections and anaerobic organisms were found in 54 to 74 percent 

of infections.47,48 The specific pathogens cultured in the aforementioned studies were highly variable 

and included Staphylococcus aureus, Pseudomonas aeruginosa, Klebsiella species, Escherichia coli, Proteus mirabilis, 

Bacteroides fragilis, Peptococcus, Fusobacterium species, Peptostreptococcus, and fungi (among others). Osteomyelitis 

is a notable infectious complication in several civilian gunshot wound injury studies.49,50,51 Inadequate 

wound exploration, debridement, foreign body removal, and closure of pharyngoesophageal injuries 

were cited as reasons for developing osteomyelitis.

Prevention of Infection: Surgical Management

Early repair of soft- and hard-tissues following irrigation, conservative wound debridement, early 

administration of broad-spectrum prophylactic antibiotics, minimal introduction of foreign surgical 

material during initial surgery, and coverage of bone with tension-free closure have been cited as 

interventions that decrease war infections.39,40,55,56,57 The inner mucosal lining of maxillofacial structures 

should be maximally preserved during debridement efforts. Avulsion defects of the mandible are best 

treated by early stabilization of existing bone fragments, primary soft-tissue closure, wound drainage, 

repeated debridements, and delayed bone reconstruction (e.g., eight weeks following injury).8 Bone grafting 

of mandibular injuries is best deferred to Level IV and V care facilities and performed in a delayed 

fashion. Bone grafting of mandibular defects is best performed on infection-free and well-perfused wound 

beds.58,59 Further studies are required to determine whether rigid internal fixation of maxillofacial war 

wounds (as is often practiced in the course of host national care in OEF/OIF) has favorable outcomes 

(e.g., decreasing wound infection rates).

Avulsion defects of the mandible are best treated by early stabilization of existing bone fragments, 

primary soft-tissue closure, wound drainage, repeated debridements, and delayed bone reconstruction.

Diagnosis of Infection

Signs of a head and neck infection include erythema, edema, warmth, lymphadenopathy, drainage, or 

fluctuance at the wound site. Patients may complain of fever, increased pain at the site of injury, malaise, 

fevers, or difficulty tolerating oral intake. Laboratory testing may reveal evidence of inflammation (e.g., 

elevated white blood cell count). Radiographic imaging such as ultrasonography and CT or magnetic 

resonance imaging (MRI) can be used to help define the infection. Radionuclide scanning and MRI 

War-Related Maxillofacial Injury Infection Rates

Vietnam: 7 percent rate of infection52 

Iran-Iraq War: 11 percent rate of infection53 

Balkan conflict: 19 percent rate of infection54

Table 5. War-related maxillofacial injury infection rates.
Maxillofacial and Neck Trauma | 261

can be used to screen for evidence of early osteomyelitis. Of note, the ferromagnetic characteristics of 

embedded projectiles need to be assessed prior to MRI. Plain radiograph findings of osteomyelitis occur 

late in the disease course, following significant destruction of cortical bone.60

Management of Infection

The following interventions are helpful in treating wound infections: (1) incision and drainage of 

accumulated purulent collections; (2) debridement of foreign bodies or necrotic material; (3) stabilization 

of fracture fragments; and (4) broad-spectrum antibiotic therapy.45,54 There are no definitive studies in 

war settings to determine optimal choice or duration of antibiotic therapy for established infections. 

Standard expert-based recommendations include a 10 to 14 day course (or two to three days following 

wound closure and no evidence of infection) of broad-spectrum antibiotic therapy.36 Osteomyelitis 

typically requires a minimum of six weeks of antibiotic therapy.8 Ampicillin/sulbactam, clindamycin 

and a quinolone, and piperacillin/tazobactam have all been described as reasonable first-line agents 

for treatment of established infections of the head and neck in war settings.8 Complications of wound 

infections of the head and neck include delayed healing, scarring/deformity, sinus tracts, nonunion of 

bone fragments, ocular infections, osteomyelitis, venous and cerebral sinus thrombosis, and necrotizing 

fasciitis.40,45,50,51

Although no definitive studies exist, standard recommendations for treatment of established combat 

wound infections include 10 to 14 days of broad-spectrum antibiotic therapy.36

Definitive Management 

Over the past 25 years, the development of modern craniomaxillofacial surgical principles and 

techniques has resulted in dramatic improvements in facial fracture surgery. However, these 

principles and techniques are primarily based on the experience of civilian patients with blunt trauma. 

The preponderance of penetrating maxillofacial battle injuries (complicated by tissue avulsions and 

burns) caused by explosive devices in OEF/OIF has increased treatment requirements, including the 

application of microvascular composite tissue transfer, a technology driven by oncologic surgery. Even the 

combination of these technologies falls short of reconstructing the face to a natural form and function, 

because transferred tissues lack both the delicate contours and features of the face and neuromuscular 

integration. 

Research in regenerative medicine and composite tissue allotransplantation over the next five to 10 years 

holds promise to improve reconstruction results for severely wounded service members. For now, the 

deployed face surgeon needs to stabilize US casualties with severe maxillofacial wounds for transfer 

to Level IV and V facilities for definitive care. Face specialists need to apply time-honored techniques 

to close severe facial wounds on casualties not eligible for evacuation, which, in the experience of the 

authors, make up the largest surgical patient load. Basic principles are reviewed in this section with 

emphasis placed on management of unique wounds the face specialist will most likely encounter in the 

combat zone versus within the US. Unless otherwise noted, the following recommendations are based on 

the training and experience of the authors. 

Severe maxillofacial wounds in US casualties should be stabilized and transferred to Level IV and V 

facilities for definitive care.
262 | Maxillofacial and Neck Trauma

Evaluation and Treatment Planning

Beyond the primary and secondary surveys and initial resuscitation of a combat casualty, maxillofacial 

examination begins with an overall inspection of the face for asymmetry, contusions, swellings, and 

lacerations. Palpate the entire facial skeleton for areas of irregularity or instability. The canthal 

attachments should be tested for stability, especially in cases of midface trauma. The nose should be 

palpated and inspected for signs of fracture. Mandibular range of motion should be assessed and jaw 

joints palpated. Evaluate for malocclusion, signs of dental trauma, intraoral lacerations, through-andthrough lacerations, embedded debris, disruption of salivary ducts, and cranial nerve dysfunction. 

Evaluation of visual acuity, inspection of the anterior and posterior chambers, pupillary reflexes, and 

extraocular movements may be difficult to perform on the traumatized patient, and ophthalmology 

consultation is desirable. A detailed discussion of the ocular exam is provided in the Ocular Trauma 

chapter.

Radiographic Imaging

Three-dimensional reconstruction of CT scans is the imaging procedure of choice for facial injuries. 

Computed tomography scans can be extended to the cervical spine and cranium to define trauma to 

these areas. Panoramic tomography (Panorex) provides additional information on the dentition of an 

ambulatory patient should this modality be available in the deployed setting. Preinjury photographs and 

identification cards are also helpful during the evaluation phase. 

Fracture Stabilization

After thorough maxillofacial evaluation and specialty consultations, a list of injuries is developed in order 

to plan definitive treatment. Clinical judgment is a critical factor in determining the indication, scope, and 

timing of surgery. As noted earlier, if the severely injured casualty can be evacuated to a higher level of 

care, the focus should then be on stabilizing the maxillofacial wounds for transfer. Often two to three days 

of damage control surgery in-theater will allow the face specialist the opportunity to secure a definitive 

surgical airway, serially debride and irrigate wounds and remove foreign material and necrotic tissue, 

address grossly unstable fractures, and apply wound dressings. 

A small bone (Hoffman® II) or specific craniomaxillofacial external pin fixation device is an expedient 

technique to temporarily stabilize flail mandible fractures. Arch bars and bridle wires for intra-arch 

stabilization are also helpful, but wire intermaxillary fixation should be avoided (Figs. 40 and 41). Wiring 

the teeth together compromises the airway and should be avoided in most cases of severe maxillofacial 

trauma treated in-theater. Elastic intermaxillary fixation with lightly applied rubber band ligatures is an 

excellent substitute to wire fixation for the ambulatory patient.

Figure 40. Bridle wires may be used for intra-arch stabilization.
Maxillofacial and Neck Trauma | 263

For transferable patients, a small bone (Hoffman® II) or specific craniomaxillofacial external pin 

fixation device is an expedient technique to temporarily stabilize flail mandible fractures. Wiring the 

teeth together compromises the airway and should be avoided in most all cases of severe maxillofacial 

trauma treated in-theater.

Definitive Repair

Definitive treatment of the nontransferable casualty requires preoperative analysis of incisions to expose 

the skeleton for fracture mobilization and reduction, methods of bony fixation, need for primary bone 

grafting, and repair of soft-tissues. The presence of tissue avulsions and burns obviously complicates 

planning. In those situations, wound closure may require local and regional flaps or, in the case of burns, 

stabilization of fractures through external pin fixation and interdental fixation techniques. Incisions may 

involve the use of existing lacerations, scalp incisions, periorbital incisions, cervical incisions, and incisions 

in the oral cavity (Fig. 42). Rigid internal fixation is desirable, but if the soft-tissue envelope is compromised, 

external pin and/or dental fixation may be required. Airway management, both during and after the 

operation, should be collaboratively performed with input from the anesthesiologist and trauma surgeon. 

Oral or nasal intubations are airway options, but if access to the surgical field or associated injuries (e.g., 

unstable cervical spine or basilar skull fractures) prevents their use, an elective tracheotomy should be 

considered. 

Informed Consent 

Even in the combat theater, informed consent for an elective operation is a feature of comprehensive 

care. If the patient is not able to make an informed consent, review the potential risks with the patient’s 

family. The concerned parties should be aware that despite your best efforts, preinjury appearance will 

unlikely be achieved. The possibility of revision or staged surgeries to achieve the best results cannot be 

realistically determined or promised in the combat theater. The consent process with the potential for loss 

of vision, intracranial injury, and even death, although rare, needs to be accepted and documented.

Timing of Surgery

It is prudent to delay surgery on unstable patients with intracranial injuries. Once intracranial injuries 

Figure 41. Bridle wire placement (red line denotes fracture line).
264 | Maxillofacial and Neck Trauma

stabilize, early repair of facial fractures in these patients should be considered with input from neurosurgical 

consultants. It is difficult to predict when an unconscious patient will neurologically improve. If 

maxillofacial surgery is delayed beyond two to three weeks, subsequent attempts at repair are exceedingly 

difficult, if not impossible, because of soft-tissue envelope contracture and fibrous unions.61

It is prudent to delay facial reconstruction in unstable patients with intracranial injuries. However, delayed 

maxillofacial repair is more difficult after two to three weeks due to soft-tissue envelope contracture and 

fibrous unions.

Surgical Principles

The overall plan to treat hard- and soft-tissue injuries to the maxillofacial region is to reconstruct facial 

fractures before definitively closing the soft-tissue wounds. The goal of fracture repair is to reconstruct 

preinjury facial projection, proportions, and form and function, and to support subsequent soft-tissue 

Figure 42. (Top Left) Improvised explosive device injury to lower face resulting in lower lip and chin avulsion and avulsion of entire dentate mandible.

(Top Right) Three-dimensional CT imaging is the modality of choice for facial injuries. (Bottom Left) A fibular microvascular flap is grafted and

restores soft-tissue and bone continuity. (Bottom Right) The flap will remain insensate, adynamic, different in color and texture, and hairless.
Maxillofacial and Neck Trauma | 265

Figure 43. (Top Left and Top Right) An explosive device caused third- and fourth-degree burns and comminuted fractures to the midface. The 

mandible fracture was reconstructed primarily through cervical incisions. Burn closure took precedence over midface bony reconstruction. (Bottom Left) 

After one to two weeks, the burns on the face will demarcate tissue requiring debridement. The resultant soft-tissue bed is dressed until healthy enough to 

receive split-thickness skin grafts. (Bottom Right) Multiple secondary procedures are expected in cases of burns and soft-tissue avulsion.
266 | Maxillofacial and Neck Trauma

reconstruction. The soft-tissue wounds can then be redraped over a rigid and correct facial framework. 

In cases of severe facial burns and avulsions, soft-tissue care often precedes definitive fracture care, and 

extensive revisions are expected (Fig. 43). 

The goal of facial fracture repair is to restore preinjury facial projection, proportions, and form and 

function, and to support subsequent soft-tissue reconstruction.

Facial Soft-Tissue Injuries

Penetrating trauma on the battlefield tends to injure both hard- and soft-tissues. This section will initially 

address soft-tissue injuries, but composite tissue injuries are discussed later by region (upper face, midface, 

and lower face) because penetrating battle injuries are manifested differently in those regions. Blunt trauma 

injury patterns and treatment to the maxillofacial area will not be discussed in detail since it is expected 

that the deployed face specialist is competent in this injury pattern (commonly seen in the US civilian 

setting). The deployed face surgeon should ensure access to reference sources that cover maxillofacial 

trauma, orbital trauma, soft-tissue management, and pedicle and rotational flap management. Beyond 

book references, the deployed face surgeon should develop online communication with rear echelon 

experts in their respective fields. This online connection, more than any collection of books, will give 

the face specialist access to expert consultation and provide a forum to discuss difficult management 

decisions.

Penetrating trauma to the face causes a variety of soft-tissue defects. This section will outline facial 

wound closure and surgery to reconstruct the lips and nose, features that remain extremely challenging to 

reconstruct. Ear avulsions are seen with combat injuries. The face surgeon may have the opportunity to 

salvage avulsed ear cartilage in a postauricular skin pouch. The avulsed ear is prepared by removing or 

dermabrading the skin but leaving perichondrium intact over the cartilage. In general, cheek defects from 

penetrating trauma are closed by wide undermining of wound edges, or development of a rhomboid 

or cervicofacial flap. Buccal, tongue, or floor of mouth flaps will close the mucosal lining of most fullthickness cheek defects. Severed parotid ducts should be cannulated and repaired primarily. Repair of at 

least the severed temporal nerve or upper division of the facial nerve is critical to restore the protective 

function of the eyelid. 

As a general rule, lip defects with less than 33 percent vermillion-lip-length loss can be closed primarily 

by modifying the defect to a “V” or “M” and advancing the skin-muscle flaps.62 The blood supply to 

even macerated facial skin and mucosa is surprisingly robust, and no tissue should be discarded until 

defect closure is carefully planned. Defects measuring 33 to 67 percent of vermillion-lip-length can be 

closed with staged lip switch flaps, such as Abbe-Estlander flaps.62,63 Larger lip defects can be treated by 

dissection of perioral skin-muscle flaps and advancing flaps circumferentially to provide orbicularis oris 

function using classic procedures of Karapandzic and Giles.63 All of these flaps cause microstomia, but 

lip function is preserved. Loss of over 67 percent of vermillion-lip-length will require lateral sliding cheek 

flaps or nasolabial flaps to close the wound, along with buccal mucosa advancement or pedicle ventral 

tongue flaps to replace the vermillion.62 Total lip avulsion in a nontransferable patient will require multiple 

staged tissue transfers (i.e., temporoparietal or cervicofacial flaps). Staged flap reconstruction is necessary 

to reconstruct commissure defects. Patients, families, and command need to make the commitment for 

host nation patients to return for staged procedures.
Maxillofacial and Neck Trauma | 267

As a general rule, lip defects with less than 33 percent vermillion-lip-length loss can be closed primarily by 

modifying the defect to a “V” or “M” and advancing the skin-muscle flaps.

Staged forehead flaps based on supraorbital, supratrochlear, infratrochlear, and superficial temporal 

vessels are robust flaps useful for immediate reconstruction of the avulsed nose (Fig. 44). Full-thickness 

nasal avulsion with loss of mucosal lining can lead to synechiae and chronic nasal airway obstruction 

unless the lining is replaced. The author (RGH) prefers a separate broad-based pericranial flap to replace 

intranasal lining.64 Loss of septal support is reconstructed with a cantilever cranial bone graft. Melolabial 

flaps are useful to reconstruct alar defects.

Facial Burns

The immediate concern for significant facial burns (second- and third-degree) is to evaluate the patient 

for airway burns and secure the airway accordingly. After irrigating the wounds, sterile dry dressings 

should be applied to wounds. The choice of topical burn dressings and when to apply them are often 

based on provider preference, available supplies, and transport times between successive medical facilities. 

Providers in the field should simply cover burns with a clean, dry dressing and avoid applying any topical 

ointments, including burn creams, to the wounds.65

This approach eliminates the need for careproviders to later have to remove creams when patients present at 

Figure 44. Gunshot wound to the nose in a host nation male. (Left) A median forehead flap was fashioned. (Right) Rotation of the flap onto the defect. 

Image courtesy of the Borden Institute, Office of The Surgeon General, Washington, DC.
268 | Maxillofacial and Neck Trauma

the next facility in the evacuation chain. The use 

of silver-impregnated dressing such as Silverlon®, 

Acticoat®, or SilverSeal® as the initial dressing 

is an alternative option. These materials are easy 

to apply, provide topical antimicrobial protection, 

and do not impede the subsequent wound 

evaluation and care. A more detailed discussion of 

burn management is found in the Acute Burn Care 

chapter.

Oral ETTs are best secured by keeping tape and 

straps off the face and affixing the tube to several 

lower anterior teeth. Significant burn involvement 

of the periorbita puts the patient at risk for orbital 

compartment syndrome, which is prophylactically 

treated by lateral canthotomies (discussed in 

detail in the Ocular Trauma chapter). Corneal 

protection and ectropion prevention are achieved 

by bolstering eyelids together or performing a Frost 

suture. Intercommissure lip distance is maintained 

by a plastic oral prosthesis for perioral burns. Sepsis 

is not risked by delaying face debridement until 

burn margins fully demarcate, typically by seven to 

10 days. Debridement of deep second- and thirddegree burns is followed by dressing changes until 

the wound bed is ready for closure with skin grafts. 

Split-thickness skin grafts are used in areas where 

contracture will minimally harm function (i.e., 

contracture can be tolerated). Full-thickness skin 

grafts are preferred in areas such as the perioral 

region and lower eyelid. Use sutures, XeroformTM 

bolsters, and face dressings to secure grafts on the 

face.

Upper and Midface Injuries

Ocular Assessment

Management of maxillofacial blast injuries requires the face surgeon to diagnose and treat conditions that 

threaten vision following trauma or surgery. This is a difficult but important task, especially when treating 

foreign-speaking, uncooperative, sedated, or obtunded patients. In these situations, an objective clinical 

method to assess for an afferent pupillary defect (Marcus Gunn pupil) indicates optic nerve dysfunction is 

helpful (Fig. 45). A field expedient test is the swinging flashlight test. The test is performed in a dark room 

by methodically swinging a flashlight from one eye to the other. An abnormal exam that indicates optic 

nerve dysfunction-related vision loss will demonstrate that both pupils will dilate symmetrically when 

Figure 45. Swinging flashlight test reveals an afferent pupillary defect in 

the left eye (anatomical left).

Right Left

Room Light

Flashlight to Right Eye

Flashlight to Left Eye
Maxillofacial and Neck Trauma | 269

the light is directed into the affected eye, and both pupils will constrict symmetrically when the light is 

directed into the normal eye. 

Frontal Sinus Fractures

The frontal sinus is a paranasal cavity lined by mucosa located between the anterior cranial fossa and the 

naso-orbito-ethmoidal (NOE) region of the frontal bone. Sinus drainage is through ducts located in the 

anterosuperior part of the anterior ethmoid complex into the middle meatus. Thin bone separates this 

sinus from the cranium, which puts the brain at risk from penetrating trauma. Additionally, injury to the 

frontonasal ducts prevents drainage of mucosal secretions, which can lead to intracranial complications 

(Fig. 46).66 Frontal sinus and NOE fractures that extend intracranially can cause a cerebrospinal fluid leak 

manifested as rhinorrhea (Fig. 47). Significantly displaced posterior wall fractures are usually associated 

with torn dura.67 An indication for surgery is the presence of a foreign body in the frontal sinus. Bloody 

nasal drainage can be field tested at bedside for cerebrospinal fluid by placing the fluid on a linen sheet. 

Cerebrospinal fluid diffuses faster than blood and creates a clear halo around a bloodstain.68 Of note, 

this test is not very accurate and maintaining a high index of suspicion for these injuries is prudent 

irrespective of test results. The definitive laboratory diagnosis for the presence of cerebrospinal fluid is 

beta-2 transferrin, which is not routinely available in the combat theater.69,70,71 

Frontal sinus and NOE fractures that extend intracranially can cause a cerebrospinal fluid leak 

manifested as rhinorrhea. 

The frontal sinus can be approached through an existing skin laceration, but a coronal incision provides 

the best exposure. The sinus should be explored, irrigated, and all foreign bodies and devitalized tissue 

removed. If a nasofrontal outflow tract (frontonasal duct) injury is absent, the anterior sinus wall is 

anatomically reduced and fixated. If significant bone loss is present or if the fragments are comminuted 

Figure 46. Schematic of facial sinuses.

Frontal

sinus

Maxillary

sinus

Ethmoid

sinus

Sphenoid

sinus

SAGITTAL VIEW CORONAL VIEW

Ethmoid sinus

Sphenoid

sinus

Frontal sinus

Maxillary

sinus
270 | Maxillofacial and Neck Trauma

beyond repair, fixated cranial bone grafts are useful 

to fill the defects. Fractures involving the nasofrontal 

outflow tract (frontonasal duct) may produce 

obstruction and infection. Treatment designed 

to prevent infection involves sinus membrane 

ablation and frontonasal duct obliteration.72 This 

is performed through a frontal bone flap with 

removal of all mucosa from the sinus with a rotary 

diamond burr. A pericranial flap elevated from the 

coronal flap and placed over bone grafts to plug the 

duct system is useful to isolate the nasal cavity from 

the cranium.73 Obliteration of the sinus with fat 

or muscle-free grafts is frequently recommended in 

the literature, but the operated sinus can also be left 

empty for spontaneous osteogenesis.74,75,76,77

Significantly displaced frontal bone fractures 

associated with a cerebrospinal fluid leak require 

a cranialization procedure in consultation 

with neurosurgery, if available (Figs. 48 to 55). 

Cranialization is the removal of the posterior wall of the frontal sinus to repair torn dura and allow 

anterior displacement of the brain into the prepared sinus cavity. Care must be taken to avoid injury 

to the dura and superior sagittal sinus during the flap osteotomy. The author (RGH) uses a powered 

perforator to develop burr holes in the frontotemporal areas, followed by a craniotome with a guarded 

side-cutting burr to cut and remove two parasagittal frontal bone flaps, leaving a two-centimeter wide 

bone strut in the midline. The dura over the superior sagittal sinus can then be elevated from the frontal 

crest and protected during removal of the midline bone strut. This technique adds several minutes to the 

cranialization procedure but helps avoid tremendous blood loss from violation of the superior sagittal 

sinus; avoiding neurosurgical complications in a CSH is important because consultation may only be 

available by Internet. After the posterior wall of the frontal sinus is removed, the dura injury can be 

repaired. Complete mucosal ablation of the remaining sinus walls is followed by obliteration of the 

frontonasal ducts. A pericranial flap dissected from the coronal flap can be advanced over the ducts 

to provide a vascularized brain–nose barrier. It is important to note that performing a cranialization 

procedure on US service members in a deployed setting without neurosurgical support is not advised. 

Ideally, such an intervention should be deferred until service members are evacuated to Level IV or 

V care facilities due to the potential for a catastrophic bleed from the superior sagittal sinus. The face 

specialist may be forced to perform such an intervention on host nationals, as they typically do not have 

access to higher levels of care. 

Naso-Orbito-Ethmoid (NOE) Region Fractures

The NOE region is beneath the frontal bone and is located below the floor of the anterior cranial 

fossa and between the medial orbital walls. Besides involving issues relating to nasofrontal outflow tract 

drainage described above, fractures and penetrating trauma can also cause displacement of the medial 

canthal ligaments. Instability of the medial canthal ligaments can be assessed by palpating the medial 

canthus while applying traction on the lateral canthus (bowstring test). A bimanual exam is performed 

Figure 47. An axial CT image of a posteriorly displaced frontal sinus 

fracture. Fracture displacement of the posterior wall of the frontal sinus 

with cerebrospinal fluid leakage or a foreign body lodged in the frontal sinus 

is an indication for surgery.
Maxillofacial and Neck Trauma | 271

by inserting an instrument intranasally into the area of the medial canthus while placing the index finger 

externally on the medial canthus. All displaced or unstable NOE fractures require surgery to reconstruct 

intercanthal distance and nasal projection. 

Figure 48. A 16-year-old Afghan male with an avulsed nose and 

penetrating injury to the frontal sinus and anterior cranial fossa and left 

eye from an explosive device. Cranialization of frontal sinus and repair of 

dura were indicated.

Figure 49. CT image demonstrating frontal sinus and anterior cranial 

fossa injury.

Figure 50. A guarded craniotome connected the burr holes and the bone 

flap was carefully elevated to avoid damaging the superior sagittal sinus.

Figure 51. The frontal flap and fragments are replaced and fixated 

rigidly.
272 | Maxillofacial and Neck Trauma

Figure 52. Skin flap reapproximation. Figure 53. Occipital view of scalp wound closure.

Figure 54. Patient at one week following injury. Figure 55. Patient at three months following injury after flap division 

and minor revision.
Maxillofacial and Neck Trauma | 273

Type I NOE fractures involve a large bone fragment with the medial canthi attached. This fracture 

can be reduced and managed by rigidly fixating the fragment to stable bones superiorly and inferiorly. 

Type II is a comminuted fracture with the medial canthi attached to operable central bone fragments.78

Type III NOE fractures involve avulsion of the medial canthus from bone. Type II and III fractures 

are difficult to treat and require wide exposure through multiple incisions or reflection of a coronal flap 

beyond the level of the nasofrontal junction with placement of transnasal wires to restore intercanthal 

distance. Reconstruction of comminuted NOE fractures may require a cantilever cranial bone graft to 

support nasal projection. The cantilever bone graft engages the area between the upper lateral cartilages 

and fixates superiorly with miniplates and screws. 

Battle injuries to the maxilla, zygomas, orbits, and nose make up at least 44 percent of the injuries to 

the maxillofacial area.1 The maxilla occupies the mid-aspect of the face between the cranial base and 

dentition. Three bony struts support the maxilla: the nasomaxillary, the zygomaticomaxillary, and the 

pterygomaxillary buttresses. The zygoma articulates with the frontal bone, maxilla, temporal bone, and 

greater wing of the sphenoid bone. The orbital floor extends back 35 to 40 mm from the rim to the 

posterior wall of the maxillary sinus. Exploding debris easily penetrates the thin walls of the orbits and 

paranasal sinuses. The fracture pattern from penetrating trauma varies from typical LeFort to comminuted 

fractures with avulsed bony fragments. Fractures with no displacement require only observation. Blast 

debris in the sinuses and airway should be removed. If the fracture is displaced, exploration with anatomic 

reduction and fixation is indicated. The experience and clinical judgment of the surgeon will dictate the 

exposure and methods of fixation. 

 

Naso-orbito-ethmoid fractures without displacement require observation only, whereas displaced 

fractures necessitate exploration with anatomic reduction and fixation.

Zygoma Fractures

Reconstruction of a significantly displaced zygoma fracture requires multiple exposure sites in areas 

of fracture: the zygomaticofrontal suture, the infraorbital rim, the zygomaticomaxillary buttress, and 

occasionally the zygomatic arch. The zygomatic arch is an important consideration in aligning significantly 

displaced or comminuted zygoma fractures because the arch defines midface width and projection. The 

zygomatic arch should be reduced and fixated as a relatively straight structure. A maxillary vestibule 

incision provides exposure of the zygomaticomaxillary buttress and infraorbital area. The choice of 

lower eyelid incision depends on the surgeon’s training and experience, but the transconjunctival incision, 

with or without a canthotomy, has the least risk for lower lid retraction. The zygomaticofrontal suture is 

exposed by a separate incision in the lateral aspect of the supratarsal fold of the upper eyelid. 

For comminuted or severely displaced zygoma fractures, a coronal incision is performed to reconstruct 

the facial width and projection by exposing the zygomatic arch. In front of the ear and above the arch, 

the superficial layer of the deep temporal fascia is identified and then incised to the fatty space (superficial 

temporal fat pad); dissection is carried out in this layer to the arch to avoid injury to the frontal branch 

of the facial nerve. The zygomatic arch is reduced and fixated, followed by figure-of-eight wire ligature 

to the zygomaticofrontal fracture and a microplate to the rim. The fractured zygoma can then be rotated 

into proper position and fixated at the zygomaticomaxillary buttress after confirming intraorbitally that 

the zygomaticosphenoid (greater wing) articulation is aligned. Cranial bone grafts should be used in areas 

of avulsion or severe comminution. 
274 | Maxillofacial and Neck Trauma

Orbit Fractures

Orbital floor fractures are reconstructed in the usual fashion by identifying the residual floor ledge of 

the posterior orbit through a lid incision with dissection beneath periorbita. If available, an endoscope 

inserted into the maxillary sinus can visualize the posterior ledge and confirm adequacy of reduction and 

reconstruction. Large floor defects are reconstructed with a variety of materials, but in the combat theater 

choices are limited. To avoid late complications of infection and extrusion, the author (RGH) prefers 

cranial bone graft shavings harvested from the temporoparietal area with the pericranium attached. These 

grafts are harvested using a wide, short, and sharp osteotome angled at a low profile and engaged by a 

heavy mallet. The resultant bone shaving, slightly curled and attached to pericranium, is placed over 

floor defects. Several stacked shavings may be necessary to correct orbital volume defects; fixation is not 

necessary.

LeFort Fractures

LeFort fractures present with malocclusion, midface instability, nasal bleeding, and periorbital edema. 

Penetrating trauma of the maxilla above the dentition can cause a LeFort fracture or penetrate the thin 

bony walls and lodge debris into paranasal sinuses (Fig. 56). Caldwell Luc access may be necessary to 

remove debris from the sinus followed by nasal antrostomy (endoscopic equipment is not necessarily 

available in Level III care facilities). LeFort fractures are manipulated through vestibule incisions and 

reduction performed to reconstruct facial height, projection, and occlusion. Typically, 1.5 to 2.0 mm 

bone plates are used to fixate the fracture at the nasomaxillary and zygomaticomaxillary buttresses, and 

bone grafts are placed in defect areas.

Lower Face Injuries

Penetrating trauma to the lower face by explosive debris can fragment and avulse the thick cortical bones 

of the mandible and dentoalveolar structures. Fragmentation of the mandible and dentoalveolar structures 

places the tongue and surrounding areas at risk of laceration with subsequent airway compromise (Fig. 

57). Securing a definitive airway is an important consideration for penetrating trauma to the lower face.

Figure 56. (Left) A piece of shrapnel removed from a combat casualty suffering penetrating fragmentation injuries to the face. (Right) Axial CT image 

revealing shrapnel that has perforated and comminuted the thin bones of the midface.
Maxillofacial and Neck Trauma | 275

The U-shaped mandible has a dentate portion 

and an articular portion. The dentate portion 

has a thick, compact, inferior border and a dense 

dentoalveolar process superiorly. The ascending 

ramus ends as the condylar process that articulates 

with the cranium to form the temporomandibular 

joint. Blood supply to the mandible varies with 

anatomical area: the ramus, condyles, and 

symphysis have large muscular attachments to 

nourish the bone; however the mandibular body 

receives the majority of blood supply centrally 

from the inferior alveolar vessels.79

Evaluation

Evaluation of the lower face begins with inspection 

and palpation of the face along the inferior border 

and joints to reveal point tenderness, instability, 

or step-off deformities. Orally, evaluate for 

malocclusion and disruptions of the soft-tissue envelope, teeth, and dental arch. Anterior traction on the 

mandible by grasping the mandibular incisors and chin will often cause pain at the fracture sites. Likewise, 

pushing inward at the angles of the mandible will also reveal fracture sites. Radiographic evaluation of 

the mandible is best done with a CT scan. 

Treatment

The goal of mandibular reconstruction is restoration of the lower facial height, chin projection, arch form, 

and occlusion. The location and condition of the fracture dictates the surgical approach. Nondisplaced 

fractures without occlusal disturbances are treated with a soft diet. Closed reduction is used when a 

fracture is displaced with minimal occlusal disturbances. Grossly displaced fractures usually require open 

reduction with internal or external fixation. 

The goal of mandibular reconstruction is restoration of lower facial height, chin projection, arch form, 

and occlusion.

Uncorrectable or irreparably comminuted open mandibular fractures should be debrided of small, 

devitalized fragments. Larger, viable fragments should be reduced and fixated as soon as possible to 

minimize pain, soft-tissue injury, and risk of infection. Reduction of the fractured mandible is aided 

by dental knowledge and intraoperative intermaxillary fixation to align major dentoalveolar fragments 

(Fig. 58). The decision to debride or retain a fragment rests with the surgeon’s clinical judgment and 

experience. Any retained fragment needs to be large enough to be fixated and yet remain attached or covered 

with an adequate soft-tissue envelope for healing. Keep in mind, the soft-tissue envelope of a severely 

comminuted mandibular body fracture is not only torn and compromised, but also contaminated by 

bacteria-laden saliva in a nondependent wound bed. The prudent face surgeon chooses the least risky 

course of action for the situation. An overly limited debridement puts the polytrauma casualty at risk 

for complications of mandibular infection, while an overly aggressive debridement adds multiple major 

future interventions to an already complicated treatment course. Of the two extremes, mandibular 

Figure 57. An axial CT image demonstrating a comminuted mandibular 

fracture. Fragmentation of the lower face can result in loss of mandibular 

tongue support and supraglottic edema leading to airway compromise.
276 | Maxillofacial and Neck Trauma

infection will likely delay other surgical services from performing critical and timely procedures, whereas 

complex mandibular reconstruction for a continuity defect can be electively delayed for months until the 

casualty is sufficiently recovered from multiple other wounds. Likewise, overly limited debridement of a 

complicated mandible fracture on host nation patients risks infection with the possibility of not having 

access to timely or sufficient care. Overly aggressive treatment may leave a mandibular continuity defect 

unrepaired. The treatment decision in a combat zone is difficult; but, in the case of the US service 

member, the decision can be deferred to a higher level of care. In the case of the injured host nation 

patient in the combat zone, decision making should involve the patient, family, and command.

Immediate bone grafting of mandibular body defects is not recommended because the wound bed is 

compromised by injury, contaminated by saliva, and is essentially a nondependent wound of the floor 

of the mouth.80 Late grafting of bone defects requires adequate soft-tissue bed and in cases of avulsion, 

regional soft-tissue flaps (pectoralis) are often needed to prepare the recipient site. Mandibular body 

continuity defects greater than six centimeters, especially central, are problematic to reconstruct without 

the advantage of microvascular surgery to perform osseous free flaps.81,82,83 Consultation with the host 

nation patient and family, along with command input, will lessen the burden of decision-making since 

long-term follow-up by the same face surgeon is unlikely.

Figure 58. (Top Left) An explosion caused avulsions of 40 percent of 

the upper lip and 80 percent of the lower lip in this casualty. Shrapnel 

perforated through the posterior face to cause a LeFort fracture and 

comminuted bilateral mandible fractures. (Bottom Left) Six weeks 

after bone reconstruction, a series of soft-tissue procedures attempt lip 

reconstruction (rhomboid, lateral sliding cheek, buccal mucosa flaps, 

bilateral cervicofacial flap, and ventral tongue flap) with limited success.

(Bottom Center and Bottom Right) Reconstruction replaced facial 

features, but microstomia and lip incompetence persisted. This soldier chose 

to redeploy to Iraq after lip reconstruction.
Maxillofacial and Neck Trauma | 277

Immediate bone grafting of mandibular body defects is not recommended because the wound bed is 

compromised by injury, contaminated by saliva, and is a nondependent wound of the floor of mouth.

Panfacial Fractures

The two basic approaches to panfacial fractures 

have traditionally been from bottom-to-top or from 

top-to-bottom.84,85 The bottom-to-top approach 

is based on the premise that the mandible can be 

anatomically reconstructed to provide an intact 

relationship for positioning of the maxilla. Facial 

width reconstruction in this technique is based on 

correct anatomical reduction of the mandibular 

body, ramus, and condyles. Positioning of the 

fractured maxilla to the cranium is then based 

on seating the condyles into the glenoid fossae, 

as dictated by intermaxillary fixation, followed 

by zygoma and frontonasal reconstruction. The 

bottom-to-top approach is preferred in cases of 

blunt trauma when mandibular continuity can be 

assured through anatomic alignment and fixation 

of large fragments. 

In cases of severe mandibular comminution from 

a maxillofacial blast injury, anatomical reduction 

of the mandible may be impossible (Fig. 59). In 

the top-to-bottom approach, midface projection is 

defined initially by reconstructing the outer facial 

frame to include the zygomatic arch, zygoma, and 

frontal areas. Second, the inner facial frame – including the nasoethmoid complex and infraorbital rims – 

is reconstructed. Third, the maxilla is repositioned and reconstructed by plating the zygomaticomaxillary 

and nasomaxillary buttresses. Lastly, temporary intermaxillary fixation followed by open reduction and 

fixation of the mandible is performed using interdental relationships to dictate mandibular projection. 

Mandibular continuity defects are reconstructed with reconstruction plates and bone grafted secondarily.

Summary

Management of maxillofacial battle injuries ranges from the simple to the highly complex. Penetrating 

trauma on the battlefield is the predominant mechanism of maxillofacial injuries. Injuries include 

multiple complex soft-tissue wounds and open fractures, occasionally complicated by tissue avulsions and 

burns. Infection of combat-related wounds remains a problem. Broad-spectrum prophylactic antibiotic 

therapy, administered one hour prior to surgical intervention and continued for a 24-hour period, is 

recommended. An important consideration to prevent infections is early wound care, early stabilization, 

preservation of soft-tissue, and early evacuation. 

Figure 59. Complex right orbit, zygoma, maxilla, and mandible fractures 

due to an IED. Partial avulsion of the maxilla and mandible will challenge 

the surgeon’s ability to symmetrically reconstruct facial width and height. 

Computer reconstruction of image from a live patient. Stereolithographic 

resin models and computer imaging are useful reconstruction tools (used 

at Level V care facilities) when avulsion of key anatomical parts occurs.
278 | Maxillofacial and Neck Trauma

Following patient stabilization, including securing a definitive airway, US service members with severe 

maxillofacial wounds should undergo conservative wound debridement and be transported to higher 

levels of care. Difficulty arises in the appropriate planning and execution of definitive repair in host 

nation civilians, local forces, and detained personnel. In such cases, complex battle injuries are best 

approached with interventions that have the least risk of postoperative complications but are consistent 

with predictable and favorable outcomes. Before surgery, it is critical to communicate the operative plan 

and the possibility of deviation depending on operative findings or postoperative complications. The 

patient, family, and military command need to be aware of the severity of the injury and the high 

likelihood that further future reconstructive surgeries and treatment will be needed.

Penetrating Neck Wounds

Introduction

Three percent of wounds sustained in OEF and OIF from October 2001 through January 2005 were neck 

wounds. Seventy-eight percent of wounds were sustained from explosions.2 The patterns of injury created 

by high-energy explosive devices (e.g., IEDs), the weapon of choice of insurgents in Iraq and Afghanistan, 

are more variable, less predictable, and not as well understood as those seen in previous conflicts or at 

civilian US trauma centers. Several studies are in the data collection phase, but comprehensive data on 

battle injuries to the neck and outcomes of treatment have not yet been compiled and published. With 

that understood, historical studies of trauma management remain a useful starting point for making 

clinical decisions. In particular, the Advanced Trauma Life Support (ATLS) protocols developed by the 

American College of Surgeons are largely based on civilian trauma experience, but are the basis of a 

logical approach to trauma casualties that has stood the test of time.86

The patterns of injury created by high-energy explosive devices are more variable, less predictable, and 

not as well understood as those seen in previous conflicts or at civilian US trauma centers. 

During the 50 years prior to the widespread use of IEDs, injury patterns and treatment outcomes following 

penetrating neck wounds were fairly consistent. In 1963, Stone et al. reported that vascular injuries in 

the neck accounted for 50 percent of deaths following penetrating neck trauma.87 Thirty years later, in 

a multi-institutional review of penetrating neck injuries from 16 US medical centers, McConnell et al. 

also reported the number one leading cause of death from penetrating neck trauma was exsanguinating 

hemorrhage.88 In that study, the following incidence of injury to structures of the neck was reported: 

larynx and trachea (10 percent), internal jugular vein (9 percent), common and internal carotid arteries 

(7 percent), subclavian artery (2 percent), external carotid artery (2 percent), and vertebral artery (1 

percent). Other relevant observations in the study include: (1) that one-third of initially asymptomatic 

patients with Zone I neck trauma were ultimately diagnosed with significant Zone I neck injuries; and (2) 

25 percent of initially asymptomatic patients with neck Zone III trauma were diagnosed with an arterial 

injury. Penetrating trauma to Zone II managed by mandatory neck exploration was negative 30 to 50 

percent of the time. A major cause of late mortality was missed esophageal injuries because esophageal 

and pharyngeal injuries were often asymptomatic on presentation. When surgical repair or drainage 

was performed less than 24 hours after the injury, the survival rate was greater than 90 percent; when 

performed more than 24 hours after the injury, survival dropped to 65 percent.88,89
Maxillofacial and Neck Trauma | 279

Anatomy

It is useful to divide structures of the neck into five major functional groups to ensure a comprehensive 

assessment is performed and as a map for focusing a secondary survey and surgical approaches (Table 

6). Two muscles of the neck serve as key landmarks and their importance must be understood. The 

platysma defines superficial from deep structures of the neck. If a wound does not penetrate deep 

to the level of the platysma, it is not classified as a penetrating neck wound. Although the transverse 

cervical veins, running superficial to the platysma, may be large and can bleed profusely when 

severed, they are easily controlled with direct pressure and can be managed with simple ligature. The 

sternocleidomastoid muscle further divides the neck into the anterior triangle and posterior triangle 

(Fig. 60). Generally speaking, the posterior triangle contains the spine and muscles, whereas the anterior 

triangle contains the vasculature, nerves, airway, esophagus, and glands. 

If a wound does not penetrate the platysma, it is not classified as a significant penetrating neck wound.

Neck Zones

When evaluating penetrating injuries, the neck is commonly divided into three anatomic zones for purposes 

of initial assessment and management planning (Fig. 61). The utility of this division is based upon two 

concepts: injury patterns and surgical management approaches. As discussed above, injury patterns from 

high-energy explosives are variable, lowering the predictive value of observing a penetrating wound in a 

particular zone. However, the limitations associated with surgical exploration and control of hemorrhage 

in each zone still make the concept useful. The boundaries and major contents of each zone are reviewed 

here. The impact of injuries on management planning is discussed by zone in a later section.

Zone I is the horizontal area between the clavicle/suprasternal notch and the cricoid cartilage (including 

the thoracic inlet). Surgical access to this zone may require thoracotomy or sternotomy, management of 

vascular injuries here is challenging, and injury mortality is high.90 The proximal common carotid, vertebral 

and subclavian arteries, subclavian, innominate and jugular veins, proximal trachea, recurrent laryngeal 

nerves, esophagus, thoracic duct, lower thyroid and parathyroid glands, and thymus are located in this 

zone. Zone II is the area between horizontal lines drawn at the level of the cricoid cartilage and the 

angle of the mandible. Surgical access to this zone is straightforward, via a standard neck exploration 

incision. Zone II contains the internal and external carotid arteries, jugular veins, pharynx, larynx, 

esophagus, recurrent laryngeal nerves, spinal cord, trachea, upper thyroid, and parathyroid glands. Zone 

III lies between the angle of the mandible and the base of the skull. Surgical access to this zone often 

Neck Anatomy

• Airway (pharynx, larynx, trachea, lung)

• Major Vessels (carotid arteries, innominate artery, aortic arch vessels, jugular veins, subclavian 

veins)

• Gastrointestinal Tract (pharynx, esophagus)

• Nerves (spinal cord, brachial plexus, peripheral nerves, cranial nerves)

• Bones (mandibular angles, styloid processes, spine)

Table 6. Neck anatomy.
280 | Maxillofacial and Neck Trauma

requires mandibulotomy or maneuvers to anteriorly displace the mandible, and may require craniotomy. 

Management of vascular injuries here is difficult, and injury mortality is high.91,92 Zone III contains the 

extracranial carotid and vertebral arteries, the jugular veins, cranial nerves IX through XII, and the 

sympathetic nerve trunk. 

Figure 60. Triangles of the neck. The sternocleidomastoid muscle divides the neck into the anterior triangle and posterior triangle.

Figure 61. The neck is commonly divided into three anatomic zones for purposes of initial assessment and management.

Occipital triangle

Supraclavicular triangle

Submandibular triangle

Carotid triangle

Muscular triangle

Sternocleidomastoid muscle

Mandible

Cricoid

III

II

I
Maxillofacial and Neck Trauma | 281

Information for the Generalist - Neck Wounds

Initial Assessment and Management 

Casualties with signs of significant neck injury, including active pulsatile hemorrhage, expanding 

hematoma, bruit, pulse deficit, subcutaneous emphysema, hoarseness, stridor, respiratory distress, 

or hemiparesis, have indications for immediate operative management and require urgent surgical 

consultation.93

Airway

The first priority in penetrating neck trauma is to assess and secure the airway, keeping in mind the 

potential for concomitant cervical spine injury. It may be difficult to fully assess the cervical spine until 

the airway is controlled, and rigorous spinal precautions should not be maintained at the expense of 

managing life-threatening airway or vascular injuries. Orotracheal intubation is the initial method of 

choice for securing the airway under most circumstances in Level III care facilities. Nasal intubation and 

fiberoptic intubation techniques are technically more difficult, require special equipment, and should be 

reserved for elective airway management. Use of a LMATM to ventilate a casualty may serve as a bridge 

to buy time but is not a secure airway. A pharynx filled with blood or distortion of laryngeal landmarks 

can make endotracheal intubation difficult, and repeated blind intubation attempts risk enlarging a 

penetrating injury of the pharynx. 

As discussed earlier in the chapter, cricothyroidotomy is the preferred method for establishing an 

immediate airway if rapid endotracheal intubation is not possible or is contraindicated. In casualties 

with large penetrating anterior neck wounds that require an urgent airway, consider extending the 

wound as necessary and intubating through the wound by isolating the trachea between two fingers and 

completing an incision into the anterior trachea. An emergency tracheotomy is the preferred method 

of establishing a definitive airway in cases of suspected tracheal disruption. Attempts at endotracheal 

intubation could convert a partial tracheal disruption into a complete transection, while attempts at a 

cricothyroidotomy would be futile, as the injured segment lies distal to the incision site.

The airway should be considered at-risk in any casualty that presents with a penetrating neck wound. 

An unremarkable physical exam in a soldier with well-developed cervical musculature who presents 

with a small penetrating wound(s) to the neck can be deceiving (Fig. 62). Casualties who appear to have a 

minor neck wound may still have a significant injury. Stridor, hoarseness or dysphonia, hemoptysis, and 

subcutaneous air should be specifically looked for and indicate potentially significant injury to deeper 

structures. Fiberoptic laryngoscopy (when available) is a helpful adjunct for identifying airway injuries.

In difficult to intubate casualties with large penetrating anterior neck wounds that require an urgent 

airway, consider extending the wound as necessary and intubating through the wound by isolating the 

trachea between two fingers and completing an incision into the anterior trachea.

Bleeding

Do not blindly clamp bleeding vessels in the neck. Most survivable hemorrhage from neck wounds can 
282 | Maxillofacial and Neck Trauma

be controlled with directed pressure above and/or below the wound (compressing a bleeding vessel 

against the vertebrae), application of pressure directly over the wound, or by packing the wound with 

gauze. Vaginal tampons inserted into wounds (one- to two-centimeter size bleeding lacerations) caused 

by shrapnel can be effective at controlling hemorrhage. Pharyngeal packing after an airway has been 

secured is effective at controlling severe oral bleeding but must be under pressure and may require a 

full KerlixTM roll or more to tamponade bleeding. Do not probe open neck wounds. This may lead to 

clot dislodgement and vigorous bleeding can occur. Injuries that do not penetrate the platysma do not 

cause significant injuries.94 If violation of the platysma is uncertain, gently spread wound edges without 

probing. Stop as soon as platysma violation is recognized and call a surgeon. Suspect subclavian artery 

or vein injury in casualties with Zone I penetrating neck injuries. Intravenous access should be attained 

on the side of the body opposite the site of injury or in the lower torso/extremities to avoid potential 

extravasation of fluids.

Figure 62. (Top Left and Top Right) These images illustrate a gunshot wound to the neck with an expanding hematoma. Casualties who appear to 

have a minor neck wound may still have a significant injury. (Bottom Left) Proximal and distal ligature control. (Bottom Right) Primary repair of 

a common carotid injury with saphenous vein graft. Images courtesy of Joel Nichols, MD.
Maxillofacial and Neck Trauma | 283

Do not blindly clamp bleeding vessels in the neck. Most survivable hemorrhage from neck wounds can 

be controlled through application of pressure directly over the wound or by packing the wound with 

gauze.

Considerations for the Specialist

Operative Indications

It is useful to triage patients with penetrating neck injuries as either symptomatic or asymptomatic. 

Symptomatic injuries require immediate surgical exploration. Evidence of significant injury includes 

active pulsatile hemorrhage, expanding hematoma, bruit, pulse deficit, hoarseness, stridor, respiratory 

distress, or hemiparesis. Asymptomatic patients may be observed pending completion of appropriate 

studies. Choice of studies is guided by the location of the wound and often dictated by availability of 

resources. 

Role of Imaging

Improvements in imaging technology, particularly computed tomographic angiography (CTA), are 

changing the management of patients with penetrating injuries of the neck in combat zones. In many 

Level III CSHs, CTA for examination of the vasculature has become the preferred method of evaluation 

due to the possibility of retained projectiles and occult injuries to the great vessels of the neck.95 This 

reflects civilian trauma center experience. In a five-year retrospective study from 2000 to 2005 evaluating 

the role of CTA in clinical decision-making in the management of penetrating injuries to the neck, 

Osborn et al. reported that the use of CTA eliminated the performance of negative neck explorations 

without increasing adjunctive studies (esophagography, angiography, and various endoscopic procedures). 

No difference in morbidity or mortality was reported between their two study groups.96 

Immediate Hemorrhage Control

In the authors’ experience, external carotid artery injuries are easily managed by suture ligation. All 

veins in the neck can be safely ligated to control hemorrhage. Casualties with large venous injuries should 

have their wounds covered with tightly adherent dressing (e.g., Vaseline® gauze dressing) and should 

be placed in the Trendelenburg position if there is any concern about internal jugular vein injury and 

possible air embolus. If both internal jugular veins are interrupted by the injury, an attempt to repair 

one is appropriate. Exsanguinating oropharyngeal hemorrhage should be controlled by obtaining an 

immediate surgical airway (cricothyroidotomy or tracheotomy) followed by packing the pharynx. The 

casualty is then taken to the operating room, where a wide apron-incision is made from the mastoid tip 

to the midline of the neck at the cricoid level for definitive exploration. Although studies have shown that 

it is safe to close uncontaminated penetrating neck wounds primarily within six hours of injury, there is 

insufficient evidence to make a recommendation regarding primary closure of neck wounds caused by 

IEDs.97

Exsanguinating oropharyngeal hemorrhage should be controlled by obtaining an immediate surgical 

airway followed by packing the pharynx.
284 | Maxillofacial and Neck Trauma

Penetrating Neck Injury Management

Zone I

Zone I injuries are reported to have a mortality rate as high as 12 percent.90 The bony thorax and clavicle 

make surgical exploration of the root of the neck challenging. Stable casualties with Zone I injuries 

should be further evaluated by arteriography, laryngoscopy, and esophagoscopy. Unstable casualties with 

Zone I injuries require a median sternotomy or left anterior thoracotomy to control hemorrhage. Surgical 

repair is preferred unless the patient has already developed neurological changes consistent with coma 

and arteriogram confirms absence of antegrade flow. The decision to explore a Zone I injury should be 

reserved for surgeons with experience with these approaches.

Unstable casualties with Zone I injuries require a median sternotomy or left anterior thoracotomy to 

control hemorrhage.

Zone II

Management of Zone II injuries continues to be debated. Multiple civilian studies have documented 

the safety of selective exploration of neck wounds that penetrate the platysma, and the management 

of casualties without significant symptoms is changing as technology advances. The most recent 

thorough review published on this subject was performed by Tisherman et al. in 2008.98 These authors 

evaluated 112 articles examining the issue of mandatory exploration of all patients with penetrating 

neck wounds versus selective exploration based on physical examination with or without use of current 

imaging technologies and summarized their conclusions as clinical practice guidelines. They found strong 

evidence that selective operative management and mandatory exploration of penetrating injuries to Zone 

II of the neck have equivalent diagnostic accuracy and recommended selective exploration to minimize 

unnecessary surgery. They identified multiple studies that showed selective operative management of 

these injuries by experienced surgeons was safe in both community hospital and trauma center settings, 

with no difference in morbidity or mortality.99,100,101 Tisherman et al. cited studies demonstrating CTA 

can safely reduce the number of negative neck explorations and that CTA or duplex ultrasound can be 

used in lieu of arteriography to rule out Zone II arterial injury following penetrating trauma to Zone II 

of the neck.102,103,104,105 Based on the strength of evidence cited, the authors recommended high-resolution 

CTA as the initial diagnostic study of choice for Zone II penetrating injury to the neck. They also 

found evidence that careful serial physical examination, including auscultation of the carotid artery, is 

greater than 95 percent sensitive for detecting arterial or aerodigestive tract injuries requiring repair, but 

cautioned that clinicians should have a low threshold for obtaining imaging studies.106,107

The review by Tisherman et al. is thorough and timely, but caution must be exercised in extrapolating 

conclusions drawn from civilian experience to current combat environments.98 In the authors’ 

experience, the following management practices have been successfully employed in OEF and OIF. 

Symptomatic casualties (e.g., active pulsatile hemorrhage, audible bruit, rapidly expanding hematoma, 

airway or neurovascular compromise) with penetrating Zone II neck wounds undergo neck exploration. 

Asymptomatic casualties with penetrating Zone II neck wounds may be observed with frequent monitoring 

while being further evaluated for injury to the great vessels, trachea, or aerodigestive tract. Computed 

tomographic angiography or conventional arteriography, laryngoscopy and esophagoscopy are performed 

if the wounds are not surgically explored. If CTA or conventional arteriography, laryngoscopy, and 
Maxillofacial and Neck Trauma | 285

esophagoscopy are not available, asymptomatic casualties with penetrating Zone II neck wounds are 

monitored continuously until transfer to a facility with advanced capabilities, or the wounds are surgically 

explored.

Although there is strong evidence that selective operative management and mandatory exploration of 

penetrating injuries to Zone II of the neck have equivalent diagnostic accuracy, caution must be exercised 

in extrapolating conclusions drawn from civilian experience to current combat environments.

A low threshold for proceeding to surgical exploration is suggested for casualties with multiple penetrating 

Zone II neck wounds such as shrapnel injuries from a high-energy explosive device. Further studies of 

high-energy blast wounds are necessary to determine whether CTA is sufficiently sensitive for detecting 

injuries that require surgical intervention and whether CTA may be relied upon to guide patient 

management. Based on the authors’ experience, strict observation of casualties with penetrating Zone II 

neck wounds from blast injuries without concurrent radiographic evaluation of the great vessels, trachea, 

and esophagus (observation alone) is not recommended (Fig. 63).

Zone III

Zone III injuries are also associated with a high mortality rate.91,92 The skull base, styloid process, and 

Figure 63. (Top Left) Shrapnel injuries to the face and neck. This 

image demonstrates a patient with a secure surgical airway. (Top Right) 

Exposure of the great vessels of the neck during surgical exploration of 

Zone II neck injury. (Bottom Right) Closure of the wound.
286 | Maxillofacial and Neck Trauma

mandible make surgical exposure in this area difficult. The mandible may need to be divided or displaced 

anteriorly by dividing the stylomandibular ligament. Craniotomy may be required to control a highcarotid injury in this location. Stable casualties with Zone III should be further evaluated by arteriography 

to exclude carotid/vertebral artery injuries and a Gastrografin® contrast swallow imaging study should 

be considered if there is any suspicion of esophageal injury.89, 93,108 When arteriography is not available, 

frequent intraoral examination should be performed to observe for edema or expanding hematoma 

within the parapharyngeal or retropharyngeal spaces. Nerves exiting the skull base are in close proximity 

to the great vessels, thus neurological deficits in a casualty with a Zone III injury are suggestive of injury 

to the great vessels.91 

The decision to explore a Zone III injury should be reserved for surgeons with experience performing 

these approaches.

Bleeding from the internal carotid artery in Zone III may be controlled by passing a small-diameter (e.g., 

4 French size) Fogarty catheter proximal to the injury and inflating the balloon to occlude the lumen. 

Alternatively, the internal carotid artery may be ligated through an incision parallel to the anterior 

border of the sternocleidomastoid muscle. If the internal carotid artery is ligated, the distal injury may 

continue to bleed from collateral circulation through the Circle of Willis and require packing as the 

artery enters the skull base. Achieving hemorrhage control of penetrating vertebral artery injuries can 

be very challenging and is associated with high morbidity and mortality rates.92 The decision to explore 

a Zone III injury should be reserved for surgeons with experience performing these approaches.

Esophageal Injury

Esophageal injuries may be clinically silent initially. Signs of esophageal injury include subcutaneous 

air, crepitus, dysphagia, odynophagia, drooling, and hematemesis. Missed esophageal injuries are 

the cause of the majority of delayed complications seen with penetrating neck injuries.89,108 When an 

esophageal leak progresses to mediastinitis, morbidity and mortality are significant.89,107,109 Either contrast 

esophagography or esophagoscopy should be used to rule out an esophageal perforation that requires 

operative repair. Diagnostic workup should be expeditious as management delayed by more than 24 

hours increases morbidity and mortality.89,108 Early diagnosis may allow primary repair to be performed 

and generally results in superior outcomes.109

If esophageal injury is suspected, either contrast esophagography or esophagoscopy should be used to rule 

out an esophageal perforation that requires operative repair. Diagnostic workup should be expeditious as 

management delayed by more than 24 hours increases morbidity and mortality.

The accuracy of the evaluation for esophageal injury is dependent on the skills of the careproviders 

and the availability of diagnostic equipment. The sensitivity of esophagography to detect an esophageal 

injury is 62 percent to 100 percent, and the sensitivity of esophagoscopy is 43 percent to 100 percent.110,111

In cases in which the cervical spine has not been cleared, flexible endoscopy is helpful in evaluating 

injuries of the pharynx and esophagus.112,113 There have been reports of missed perforations near the 

cricopharyngeus muscle or in the hypopharynx, where flexible endoscopy is less effective because of 

mucosal redundancy.114,115,116 Studies utilizing a combination of flexible endoscopy and rigid esophagoscopy 

to examine the entire cervical and upper thoracic esophagus generally demonstrate the best results. No 

perforations were missed in those series that used both techniques to evaluate all patients.117 Gastrografin® 
Maxillofacial and Neck Trauma | 287

is recommended as a first-line contrast study agent for evaluation of esophageal injury.118 Barium is used 

as a second-line agent because barium extravasation radiographically distorts soft-tissue planes for future 

studies, and it is more toxic to the peritoneal cavity. Care must be exercised to ensure patients do not 

aspirate Gastrografin®, which can cause significant pulmonary toxicity.119

If suspicion of a pharyngeal perforation remains despite an initial negative examination or exploration, 

the casualty should be kept nil per os (NPO), observed for seven days, and a swallow study should be 

repeated prior to advancing the diet to clear liquids. Fever, tachycardia, or widening of the mediastinum 

on serial chest radiographs or CT indicates the need for repeat endoscopy or neck exploration. When an 

esophageal injury is found early, surgical management should include copious wound irrigation, cautious 

debridement, a two-layer closure, and adequate drainage.116 After repair of the mucosal perforation, 

a muscle flap should be placed over the esophageal suture line for further protection. If an extensive 

esophageal injury is present, a lateral cervical esophagostomy should be created and definitive repair 

performed later.116

If an extensive esophageal injury is present, a lateral cervical esophagostomy should be created and 

definitive repair performed later.

Laryngotracheal Injury

When a wound involves the larynx or upper trachea, a tracheotomy should be established below the 

level of the injury. After a definitive airway is established, laryngotracheal injuries are not life-threatening, 

and definitive management may be delayed while treating more acute injuries. Laryngeal injuries may 

be evaluated with flexible endoscopy to differentiate between wounds that need only observation (small 

or shallow lacerations, nondisplaced fractures) and those that require a thyrotomy for open fracture 

reduction and mucosal approximation. If rigid endoscopy is performed, care must be taken to avoid 

extending lacerations. 

When a wound involves the larynx or upper trachea, a tracheotomy should be established below the level 

of the injury. Definitive tracheal repair may be delayed while treating more acute injuries.

Multiple authors recommend repair of laryngeal mucosal lacerations from a penetrating injury as soon 

as possible and have found an increase in debilitating long-term sequelae, including airway stenosis and 

poor voice quality associated with delayed repair. 51,120 Danic reported that even extensive laryngotracheal 

injuries may be safely repaired early.97 When the inner laryngeal mucosa in an adult patient is badly 

macerated, a soft laryngeal stent fashioned from a six-centimeter segment of a 7.0 mm ETT, which has 

been permanently crimped in the middle by clamping it while heated, should be inserted. The crimp 

should be at the level of the vocal cords and fixed in place with through-and-through 1-0 Prolene® suture 

secured to the skin of the neck. An appropriately sized ETT should be selected and fashioned accordingly 

in smaller adults and children. In the authors’ experience, tracheal lacerations extending less than 50 

percent of the tracheal circumference do not require repair or tracheotomy. Longer lacerations without 

significant disruption of the tracheal mucosa may be reapproximated with interrupted 5-0 Prolene® 

sutures spaced two to three millimeters apart, without the need for a tracheotomy. More severe disruptions 

are initially treated by placing a tracheotomy either below or through the injury. 
288 | Maxillofacial and Neck Trauma

Summary

As with all trauma patients, initial management priorities include airway protection, breathing, and 

circulatory support. Casualties who present with signs and symptoms of shock and continuous hemorrhage 

from a neck wound should undergo immediate surgical exploration. After life-threatening injuries 

are stabilized, a more focused evaluation of the penetrating neck wound is undertaken. Upon wound 

exploration, if the platysma is not violated, surgical exploration is not indicated. Symptomatic casualties 

(e.g., active pulsatile hemorrhage, audible bruit, rapidly expanding hematoma, airway, or neurovascular 

compromise) with penetrating Zone II neck wounds should undergo neck exploration. Asymptomatic 

casualties with Zone II injuries that penetrate the platysma should be evaluated to rule out significant 

injury to the great vessels, trachea, or esophagus. The evaluation of stable casualties may be delayed if 

they are carefully monitored at frequent intervals. Casualties with Zone I and III penetrating injuries and 

penetrating esophageal and laryngotracheal injuries should be transferred to a Level IV or V facility for 

definitive management as soon as possible. 
Maxillofacial and Neck Trauma | 289

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298 | Maxillofacial and Neck Trauma
Chapter 7

ocular trauma

Contributing Authors

Raymond I. Cho, MD, LTC, MC, US Army

Eric Savitsky, MD
All figures and tables included in this chapter have been used with permission from Pelagique, LLC, the 

UCLA Center for International Medicine, and/or the authors, unless otherwise noted.

Disclaimer

The opinions and views expressed herein belong solely to those of the authors. They are not nor should 

they be implied as being endorsed by the United States Uniformed Services University of the Health 

Sciences, Department of the Army, Department of the Navy, Department of the Air Force, Department of 

Defense, or any other branch of the federal government.
Ocular Trauma | 301

Table of Contents

Introduction........................................................................................................ 303

Levels of Ophthalmic Combat Casualty Care (CCC).......................................................304

Levels I and II ....................................................................................................................304

Level III .............................................................................................................................306

Levels IV and V .................................................................................................................307

Evaluation of the Ocular Trauma Patient ............................................................... 307

History ..............................................................................................................................307

Visual Acuity.....................................................................................................................308

Pupil Examination ...........................................................................................................309

Ocular Motility .................................................................................................................309

Visual Field Testing ..........................................................................................................310

Intraocular Pressure Measurement.................................................................................310

External Ocular Examination..........................................................................................310

Anterior Segment Examination .......................................................................................311

Posterior Segment Examination......................................................................................313

Ocular Imaging Techniques.............................................................................................314

Closed Globe Injuries........................................................................................... 315

Corneal Abrasion..............................................................................................................315

Corneal Foreign Bodies ....................................................................................................315

Hyphema...........................................................................................................................316

Traumatic Iritis ................................................................................................................317

Lens Subluxation / Dislocation ........................................................................................317

Vitreous Hemorrhage .......................................................................................................317

Retinal / Choroidal Injuries .............................................................................................318

Open-Globe Injuries ............................................................................................ 318

Overview...........................................................................................................................318

Initial Management of Open-Globe Injuries ...................................................................319

Open-Globe Injury Repair................................................................................................320

Sympathetic Ophthalmia.................................................................................................323

Globe Repair versus Enucleation.....................................................................................323

Enucleation .......................................................................................................................324

Intraocular Foreign Body (IOFB)......................................................................................325

Ocular Adnexal Trauma ....................................................................................... 326

Eyelid Lacerations ............................................................................................................326

Conjunctival Lacerations .................................................................................................328

Orbital Trauma................................................................................................... 329

Retrobulbar Hemorrhage.................................................................................................329

Orbital Foreign Bodies......................................................................................................330

Orbital Fractures ..............................................................................................................331
302 | Ocular Trauma

Miscellaneous Ocular Injuries............................................................................... 331

Chemical Eye Injuries ......................................................................................................331

Traumatic Optic Neuropathy...........................................................................................332

Summary............................................................................................................ 333

Case Studies ....................................................................................................... 333

Case 1 ................................................................................................................................333

Case 2 ................................................................................................................................336

References .......................................................................................................... 339
Ocular Trauma | 303

Introduction

Trauma to the eye and its associated structures 

accounts for a significant number of combatrelated injuries. Despite the fact that the eyes 

cover less than 1 percent of the total body surface 

area, the proportion of combat injuries involving 

ocular structures has exceeded 10 percent in recent 

conflicts, with an increasing trend over the past 

century of warfare. Ocular injuries accounted for 

2 percent of all combat injuries during the First 

and Second World Wars, compared to 13 percent 

during Operation Desert Storm (Fig. 1).1 Although 

combat-related ocular injuries in the United States 

(US) military have decreased somewhat over the past 

several years due to the widespread implementation 

of combat eye protection, these injuries remain a 

significant cause of disability and suffering among 

wounded combat veterans (Fig. 2). 

Penetrating projectile injuries have had a significant effect on the nature of modern combat ocular 

trauma, most commonly causing open-globe injuries (55 percent), eyelid injuries (33 percent), orbital 

fractures (13 percent), orbital foreign bodies (12 percent), corneal/conjunctival foreign bodies (11 

percent), and traumatic optic neuropathy/optic nerve avulsion (3 percent).

Many valuable lessons have been learned through the experience of caring for thousands of ocular 

combat casualties during Operation Enduring Freedom (OEF) and Operation Iraqi Freedom (OIF). As has 

been noted by combat casualty care (CCC) providers throughout the history of warfare, combat injuries 

tend to be much more severe and extensive than those seen as a result of civilian trauma. These conflicts 

have also demonstrated that, in counterterrorism 

and counterinsurgency operations, blast injuries 

tend to account for a higher proportion (78 

percent) of trauma when compared to conventional 

battlefields of the past.2

 These penetrating projectile 

injuries have had a significant effect on the nature 

of modern combat ocular trauma. There has also 

been a high incidence (62 percent) of concomitant 

head, face, and neck trauma in ocular trauma 

patients.3 This finding in large part has led to the 

establishment of integrated multispecialty head 

and neck surgical teams that have been successfully 

deployed by the US Army in Iraq. Finally, the large 

number of host national injuries treated by coalition 

medical personnel has required a rethinking of many 

Figure 1. Ocular injury incidence as a percentage of combat 

injuries, American Civil War through Operation Desert Storm. 

Adapted from Wong, 1997.1

Figure 2. Open-globe injury with large corneoscleral laceration and uveal 

prolapse following gunshot wound.

0%

5%

10%

15%

Civil War WWI WW2 Korea Vietnam Desert

Storm

0.6%

2.3%

3.4%

8%

9%

13%

Ocular Injury Incidence
304 | Ocular Trauma

trauma management patterns that are commonly practiced in the US, but have questionable applicability 

in resource-limited countries. For example, open-globe repair versus primary enucleation following openglobe injury is addressed later in this chapter.

The most common types of ocular injury requiring specialized ophthalmic care during OIF from 2003 

to 2005 were open-globe injuries (55 percent), eyelid injuries (33 percent), orbital fractures (13 percent), 

orbital foreign bodies (12 percent), corneal/conjunctival foreign bodies (11 percent), and traumatic optic 

neuropathy/optic nerve avulsion (3 percent) (Table 1).4 A separate study during OIF from 2005 to 2006 

also reported that 20 percent of patients with combat ocular trauma were treated for orbital compartment 

syndrome.5 The prevalence of less serious injuries such as corneal abrasion or hyphema has not been 

recently reported, although during the Vietnam War, hyphemas were seen in 15 percent of ocular combat 

casualties.6

Levels of Ophthalmic Combat Casualty Care (CCC)

Levels I and II

The resources available for treating ocular injuries at Level I and II facilities are limited, but certain actions 

taken at these levels may prove critical to optimizing ultimate outcomes. It is of utmost importance for 

providers at this level to recognize when an ocular injury is severe enough to warrant evacuation to the 

next level of care, and this requires an appropriately thorough ophthalmic examination. It is often difficult 

to examine an injured eye due to the frequent presence of eyelid edema, hemorrhage, tissue damage, or 

pain. However, it is possible in most cases to open the eyelids long enough to obtain at the very least a 

cursory glance at the globe and a gross assessment of visual acuity. If necessary, Desmarres retractors, a 

lid speculum, or even a bent paper clip can be used to carefully retract the eyelids while avoiding pressure 

on the globe (Fig. 3). A topical anesthetic (e.g., 0.5 percent proparacaine or tetracaine drops) may be used 

to decrease the discomfort caused by examination. However, excessive manipulation of the eyelids in 

the presence of a ruptured globe can increase the risk of intraocular content extrusion. The moment the 

examiner notes findings suggestive of globe rupture, the examination should be terminated and the injured 

globe should be protected from further manipulation. The specific exam findings suggestive of an openglobe injury are discussed later in this chapter.

Injury Type Percent

Open-globe injuries 55

Eyelid injuries 33

Orbital fractures 13

Orbital foreign bodies 12

Corneal / conjunctival foreign bodies 11

Traumatic optic neuropathy/optic nerve avulsion 3

Table 1. Most common types of ocular injury requiring specialized ophthalmic care during OIF 

2003 to 2005. Adapted from Thatch, 2008.4
Figure 3. (Right) Desmarres 

retractors or a bent paper clip 

can be used to retract the eyelids 

during the assessment of the 

acutely injured eye.

Figure 4. (Far Right)

Placement of Fox eye shield 

(right eye) and truncated 

disposable drinking cup (left eye) 

for eye protection. The rim of 

the device rests on the frontal and 

maxillary bones.

Ocular Trauma | 305

Patients with ocular injuries should undergo as complete an ophthalmic examination as possible. A detailed 

description of this exam is provided below, although some aspects, such as the slit-lamp exam, are 

not feasible at this level. At a minimum, visual acuity, pupils, extraocular motility, and visual fields by 

confrontation should be assessed. Gross examination of the eyelids, conjunctiva, sclera, cornea, and anterior 

chamber structures may reveal lacerations, anatomic disruption, hemorrhage, or foreign bodies.

Combat casualty care providers at Level I and II facilities must perform thorough ophthalmic 

examinations and recognize when an ocular injury is severe enough to warrant evacuation to the next 

level of care. If globe rupture is suspected, the eye examination should be terminated and the eye 

protected from further injury. Foreign bodies protruding from the eye or orbit should be left in place 

unless they are too large to safely immobilize during evacuation. Patients with severe vision loss, pupillary 

abnormalities, gross proptosis, or limited ocular motility should be evacuated whenever possible.

The most important action medical personnel at Level I or II facilities can perform for a patient with an 

ocular injury requiring evacuation is to protect the eye from further injury. To this end, Fox eye shields 

have been recently added as a standard item to the combat medic bag. This eye shield is designed to rest 

on the bony support of the face and vault over the ocular structures and can be secured with one or more 

strips of tape spanning the forehead and cheek. In the absence of a Fox eye shield, any item that can 

effectively perform the same function, such as a specimen cup or truncated disposable drinking cup, can 

be substituted (Fig. 4). It is important to make the distinction between shielding, as described above, and 

patching, (i.e., placing a pressure dressing on the eye). Patching of the eye should never be performed by 

nonophthalmic personnel on a suspected ocular injury. Similarly, the application of solutions or ointments 

to a suspected open-globe is not recommended. As a rule, foreign bodies protruding from the eye or orbit 

should be left in place unless they are too large to safely immobilize during evacuation (Figs. 5 and 6). 

The decision to evacuate a patient to a Level III facility for ophthalmologic evaluation is not always clear-
306 | Ocular Trauma

cut and must take into account many nonclinical variables such as operational security, the availability 

of evacuation assets, and the impact of evacuation on the unit’s mission. In general terms, patients with 

severe vision loss, pupillary abnormalities, gross proptosis, or limited ocular motility should be evacuated 

whenever possible. More specific indications for evacuation include suspected open-globe injuries, corneal 

infections, large hyphemas, retinal detachments, full-thickness eyelid lacerations, orbital compartment 

syndromes, and orbital fractures. As discussed below, suspected orbital compartment syndrome must be 

immediately treated by the first qualified CCC provider prior to evacuating the patient to the next level 

of care. This list is by no means all-inclusive, and additional guidelines for evacuation are provided later 

in this chapter. If telephonic or electronic consultation with an ophthalmologist is available in-theater, it 

should be utilized in cases where doubt exists about the severity of an ocular injury.

Level III 

Under current doctrine, specialized ophthalmic care is first available in the combat zone at Level III 

(Fig. 7). As stated above, ophthalmologists at Level III care facilities are typically deployed as part of 

multidisciplinary head and neck teams that include neurosurgery, otolaryngology, and oral maxillofacial 

surgery. Facilities and equipment vary, but the bare minimum should include a slit-lamp biomicroscope, 

Tono-Pen®, indirect ophthalmoscope, and an operating room with a surgical microscope and complete 

sets of ophthalmic surgical instruments. Surgical loupes can also be very useful, particularly when treating 

periocular and orbital injuries. Essential supplies include balanced salt solution (BSS), viscoelastics, 

microsurgical sponges, orbital implants, and other medications and surgical devices unique to ophthalmic 

surgery. Individual surgeons should ensure that their preferred sutures are available. Some of the 

more commonly employed sutures include: 8-0, 9-0, and 10-0 nylon; 4-0, 5-0, and 6-0 polyglactin; 5-0 

polydiaxanone; 4-0 and 6-0 silk; 6-0 chromic gut or plain gut; and 6-0 polypropylene.

The mission of the Level III ophthalmologist is to provide treatments that are as definitive as possible 

within the physical and operational constraints of the care facility. Patients who require more specialized 

surgery, extensive rehabilitation, or are rendered indefinitely combat ineffective will be evacuated to a 

Level IV facility and beyond. Conversely, if a soldier can be treated in-theater and returned to duty within 

Figure 5. Left orbit impaled with large wooden plank. The plank had 

been part of a fence, and the portion embedded in the patient’s face had to 

be broken off in order to facilitate transport from the accident scene.

Figure 6. Removed wooden fragments adjacent to the primarily enucleated 

globe.
Ocular Trauma | 307

a reasonable timeframe, this course of action should be considered. The extent to which host nationals or 

other noncombatants should be treated is determined by the medical commander.

The Level III facility-based ophthalmologist should provide treatments that are as definitive as possible 

within the physical and operational constraints of the facility. For patients requiring evacuation, 

photographic documentation of pertinent clinical findings is helpful to the receiving careproviders.

For patients requiring evacuation out-of-theater, proper medical record keeping is of great importance 

in optimizing follow-up and appropriate treatment by Level IV and V careproviders. Photographic 

documentation of pertinent clinical findings, obtainable through the use of a standard point-and-shoot 

digital camera, can be particularly helpful to careproviders receiving patients evacuated out-of-theater. 

Photographs can be taken externally or through the lens of the operating microscope or slit-lamp 

biomicroscope and electronically transmitted to points of contact at the next level of care.

Levels IV and V 

Definitive and subspecialized ophthalmic care, such as retinal surgery, intraocular foreign body (IOFB) 

removal, or traumatic cataract extraction, is available at Level IV and V facilities located outside the theater 

of operations. Detailed discussion of treatment at this level falls beyond the scope of this chapter. 

Evaluation of the Ocular Trauma Patient 

History

A detailed ocular history aids in the assessment of injury severity and guides subsequent patient 

evaluation. In cases of chemical exposure to the eye, treatment should be initiated immediately while 

history and physical examination are deferred or performed in concert with immediate copious irrigation 

of the eyes. The ophthalmologic history should establish the premorbid visual acuity. It should also 

include the patient’s use of corrective lenses, ophthalmologic medications, tetanus status, and previous 

Figure 7. Ophthalmologic procedure being performed at a Level III 

facility in Balad AFB, Iraq.

Figure 8. Combined ocular and cranial injury caused by gunshot wound. 

Bullet path is demonstrated by cotton-tipped applicators. The patient 

underwent decompressive hemicraniectomy, enucleation of the left eye, and 

left orbital reconstruction.
308 | Ocular Trauma

eye surgery.7,8,9 Patients with a history of prior ocular surgery are at risk for corneal or scleral rupture, even 

with minor trauma.

In cases of chemical exposure to the eye, treatment should be initiated immediately while history and 

physical examination are deferred or performed in concert with immediate copious irrigation of the 

eyes.

In cases of blunt trauma, the mechanism, force, and direction of impact are important in determining 

the extent of injury. A history of ocular exposure to high-speed projectiles should alert the provider to 

the possibility of an IOFB.9

 For penetrating injuries, it is important to determine the composition of the 

potentially retained foreign body. Certain foreign bodies can elicit an intense inflammatory reaction or 

lead to infection within the globe, while others are well tolerated.7

As stated in the introduction to this chapter, combat ocular injuries are often 

found in conjunction with head, face, and neck injuries (Fig. 8). For example, 

during OIF from 2005 to 2006, 33 percent of patients with cranial trauma 

had a concomitant open-globe injury.5

 It is therefore important for CCC 

providers to maintain a high level of suspicion for the presence of ocular injuries 

when trauma to the head, face, or neck is recognized. This is particularly true 

for unconscious patients in whom it is not possible to ascertain the presence of 

ocular pain, decreased vision, or limited motility. 

Visual Acuity

Visual acuity is the vital sign of the eye and its measurement is the first step 

in all ophthalmologic exams. Visual acuity must be measured in all responsive 

patients with ocular trauma, as it is a critical factor in establishing diagnosis, 

guiding treatment, and predicting visual outcome in these patients.10

Visual acuity should be determined independently in each eye using a 

Snellen eye chart at 20 feet or a near card viewed at 14 inches (Fig. 9). The 

best-corrected visual acuity should be obtained using the patient’s spectacle 

correction or a pinhole test. Binocular acuity testing is not useful in the trauma 

setting. Topical anesthetics may facilitate visual acuity testing in patients with 

acute eye pain and blepharospasm. 

Visual acuity is the vital sign of the eye, and its measurement is the first step in all ophthalmologic 

exams.

If an eye chart is unavailable, any form of typed print such as a magazine or packaging from medical 

supplies may be used. If a patient is unable to visualize typed print, visual acuity should be recorded as 

counting fingers at a specified distance, hand motion, light perception, or no light perception.

Figure 9. A Snellen eye chart read 

at 20 feet, or a near card viewed at 

14 inches, should be used to assess 

visual acuity.
Ocular Trauma | 309

Pupil Examination

The pupil should be examined, noting size, shape, 

symmetry, and reaction to light. Pupil size is 

recorded in millimeters (mm). Blunt trauma may 

cause pupillary irregularities or traumatic mydriasis 

(i.e., dilated pupil). A teardrop-shaped pupil is 

suggestive of globe rupture, with the apex of the 

teardrop pointing to the rupture site (Fig. 10). Each 

pupil should be assessed for direct and consensual 

response to light stimulation (i.e., pupillary light 

reflex). Patients should be screened for the presence 

of an afferent pupillary defect (APD), also known 

as the Marcus-Gunn pupil, using the swinging 

flashlight test (Fig. 11). This test is based upon 

the assumption that fellow eyes with normal optic 

nerve function have equal consensual constriction 

to light. When optic nerve function (the afferent visual pathway) is compromised on one side, the pupil 

on the involved side will still constrict when light is shined into the fellow normal eye. However, when the 

light is swung to the abnormal eye, the pupil will be observed to dilate from its once-constricted state, due 

to the decreased input to the Edinger-Westphal nucleus. 

An afferent pupillary defect should alert the examiner to the presence of optic nerve pathology or 

severe retinal injury.

Ocular Motility

The corneal light reflex should be at the same relative position on each cornea and the patient should 

be able to move his or her eyes in all directions of gaze (supraduction, infraduction, adduction, and 

abduction). Limited extraocular motility may indicate orbital fractures, cranial nerve injury, extraocular 

Figure 10. Teardrop-shaped pupil with the apex of the teardrop pointing 

to rupture site. Image courtesy of Swaminatha V. Mahadevan, MD, 

Stanford University.

Figure 11. Afferent pupillary defect. The swinging flashlight test reveals 

an afferent pupillary defect in the left eye.

Right Left

Room Light

Flashlight to Right Eye

Flashlight to Left Eye
310 | Ocular Trauma

muscle injury or entrapment, or restriction of globe motility from intraorbital edema or blood.

It is important to distinguish whether patients complaining of diplopia are experiencing monocular 

versus binocular diplopia. Diplopia that persists when the uninjured eye is covered (i.e., monocular 

diplopia) suggests an abnormality in the ocular media, such as corneal irregularity, lens abnormality, or 

iridodialysis. Diplopia that resolves with occluding either eye (i.e., binocular diplopia) is indicative of a 

defect in coordinated eye movement.

It is important to distinguish whether patients complaining of diplopia are experiencing monocular versus 

binocular diplopia. 

Visual Field Testing

Visual field testing can detect disorders affecting the retina, optic nerve, anterior and posterior visual 

pathways, and visual cortex. Patients with visual complaints irrespective of visual acuity should always 

be screened for visual field defects. Confrontational visual fields are measured one eye at a time and can 

be assessed by comparing the patient’s responses to the examiner’s own field with the opposite eye closed 

(assuming that the examiner has normal visual fields). At a normal conversational distance, any target 

(e.g., fingers or cotton-tipped applicators) can be presented at the periphery of the visual field equidistant 

between the examiner and patient. Care must be taken to ensure that the unexamined eye of the patient is 

completely covered.

Intraocular Pressure Measurement

Intraocular pressure (IOP) may be measured 

using an applanation tonometer, Tono-Pen®, or 

Schiotz tonometer (Fig. 12). However, these devices 

are not usually available at Level I or II facilities. 

Topical anesthesia (e.g., 0.5 percent proparacaine 

or tetracaine) is necessary to enable their use in 

conscious patients. Normal IOP ranges between 

10 and 21 mm Hg. Elevated IOP can result 

from numerous traumatic conditions, including 

hyphema, angle closure, retrobulbar hemorrhage, 

or carotid-cavernous fistula. Decreased IOP can 

result from open-globe injury, uveitis, cyclodialysis 

(separation of the ciliary body from the sclera), or 

retinal detachment.11

If an open-globe injury is suspected, IOP measurements should be deferred to prevent further eye 

injury.

External Ocular Examination

The eyelids and periocular region should be inspected, taking note of asymmetry, edema, ecchymosis, 

lacerations, foreign bodies, or abnormal eyelid position. Ptosis (drooping of the upper eyelid) is common 

Figure 12. The Tono-Pen® is a portable device that can be used by 

ophthalmic and nonophthalmic personnel to accurately measure intraocular 

pressure. 
Ocular Trauma | 311

in trauma settings and is typically the result of edema, but other potential causes include third nerve 

palsy, levator muscle injury, or a traumatic Horner’s syndrome (miosis, ptosis, anhidrosis). Medial eyelid 

lacerations should raise the suspicion of canalicular injury. The presence of fatty tissue within a lid 

laceration indicates violation of the orbital septum, raising the suspicion for orbital injury or foreign body. 

The presence of proptosis (protruding eyeball) should be noted, and may be indicative of a retrobulbar 

hemorrhage or other pathology such as infection, inflammation, or tumor. Looking at the orbits from 

above (bird’s-eye view) or below (worm’s-eye view) can assist in determining the degree of proptosis (Fig. 

13). The orbital rims should be palpated and bony step-offs or tenderness noted. Periorbital subcutaneous 

emphysema is highly suggestive of a fracture involving the orbital floor or medial orbital wall (Figs. 14 

and 15). A detailed discussion of examination for the presence of orbital fractures is presented in the 

Maxillofacial and Neck Trauma chapter. 

Anterior Segment Examination

Gross inspection and slit-lamp examination can detect injuries of the anterior segment including the 

conjunctiva, sclera, cornea, iris, and lens. The conjunctiva and the sclera should be examined for 

injection, bleeding, lacerations, chemosis (i.e., conjunctival edema), exposed tissues (e.g., darkly pigmented 

uveal tissues), and foreign bodies. The presence of hemorrhagic chemosis is suggestive of open-globe injury 

Figure 13. (Above) Frontal view of a patient with right proptosis due 

to a large right orbital tumor. (Top Right) Worm’s-eye view of the same 

patient, showing the degree of proptosis more clearly. (Bottom Right) 

Bird’s-eye view of a different patient demonstrating proptosis of the left 

eye.
312 | Ocular Trauma

(Fig. 16). The cornea should be examined for lack of clarity, surface irregularities, and foreign bodies. 

Fluorescein staining of the cornea may assist with the diagnosis of corneal epithelial defects. Removal of 

contact lenses prior to the application of fluorescein will prevent permanent staining of the contact lens. 

Figure 14. Axial computed tomography image of a patient with 

subcutaneous emphysema in the left upper eyelid resulting from an orbital 

floor fracture.

Figure 16. Presence of hemorrhagic chemosis suggesting open-globe 

injury.

Figure 17. Positive Seidel’s sign identifying aqueous humor leakage. 

Image courtesy of the University of Michigan Kellogg Eye Center.

Figure 15. Coronal computed tomography image of the same patient 

demonstrating the orbital floor fracture.
Ocular Trauma | 313

(Note: in accordance with DA PAM 40-506, chapter 4-13.c, the US Army prohibits the wearing of contact 

lenses in field and combat environments.)

The presence of hemorrhagic chemosis is suggestive of open-globe injury.

In cases of suspected corneal perforation, a Seidel test can identify aqueous humor leakage (Fig. 17). A 

Seidel test is performed by applying a moistened fluorescein strip directly to the area in question, creating 

a puddle of dark orange concentrated fluorescein. Leaking aqueous humor will dilute the fluorescein and 

create a stream that fluoresces bright yellow-green under cobalt blue light. While a positive Seidel test is 

pathognomonic for corneal perforation, a negative test does not necessarily rule it out, as some corneal 

wounds can be self-sealing.

In cases of suspected corneal perforation, a Seidel test can identify aqueous humor leakage. While a 

positive Seidel test is pathognomonic for corneal perforation, a negative test does not necessarily rule 

it out, as some corneal wounds can be self-sealing.

The irides are inspected for color, defects, and irregularities in shape. The crystalline lens is not normally 

visible on gross inspection, and is best examined with a slit-lamp. Traumatic subluxation of the lens often 

manifests as a dark crescent moon in the center of the pupil. Gross examination of the anterior chamber 

may reveal an excessively shallow or deep anterior chamber (in comparison with the opposite eye), 

suggestive of open-globe injury or lens dislocation. Normally, the anterior chamber is optically clear, 

but gross inspection may reveal red blood cells (i.e., hyphema) or purulent exudate (i.e., hypopyon). Cell 

and flare, which are signs of anterior chamber inflammation, can usually only be seen through a slitlamp biomicroscope. The magnified view of the oblique slit beam reveals individual white blood cells or 

proteinaceous debris, which resemble dust particles or smoke within a movie projector beam.8

 

Posterior Segment Examination

The vitreous, retina, and optic disc can be visualized through a careful fundoscopic exam. The fundoscopic 

exam should begin by documenting the status of the red reflex. An abnormal red reflex suggests corneal 

edema, cataract, vitreous hemorrhage, or a large retinal detachment. Any opacity that disturbs the 

transmission of light (e.g., foreign body, corneal laceration, or lens injury) will show up as a dark shadow 

against the red reflex. 

An abnormal red reflex suggests corneal edema, cataract, vitreous hemorrhage, or a large retinal 

detachment.

A complete fundoscopic examination may be facilitated by pharmacologic dilation of the pupils 

with topical mydriatics (e.g., phenylephrine) and cycloplegics (e.g., tropicamide). Prior to inducing 

pharmacologic dilation, patients should have a complete pupillary exam and be screened for 

contraindications to dilation such as significant head trauma or a history of angle-closure glaucoma. All 

patients with possible posterior segment injuries should be referred to an ophthalmologist for a complete 

360-degree retinal examination.
314 | Ocular Trauma

Ocular Imaging Techniques

Plain film radiography, computed tomography (CT), ultrasound, and magnetic resonance imaging (MRI) 

have all been used in the evaluation of ocular trauma. Computed tomography has largely replaced 

conventional plain film radiography for the evaluation of ocular trauma. It is particularly useful in the 

evaluation of orbital fractures, intraocular and orbital foreign bodies, globe rupture, and retrobulbar 

hemorrhage.12,13 However, radiolucent foreign bodies such as glass, plastic, or wood may be difficult to 

detect on CT or plain film.14 Standard CT examination should include both axial and direct coronal 

imaging, although direct coronals are often not obtainable in trauma patients who are unconscious or 

under cervical spine precautions. Contrast administration is not necessary. Thin cuts (e.g., 1 mm) can be 

obtained for specific indications, such as localizing foreign bodies, viewing the optic canal, or for coronal 

reconstruction when direct coronals cannot be obtained (Fig. 18). If CT is unavailable, conventional plain 

films may be used to screen for metallic foreign bodies or evaluate for orbital fractures and sinus injury. 

Within the first 24 to 72 hours following injury, the most valuable imaging modality for the evaluation of 

ocular trauma is CT scanning, which is widely available at Level III facilities.

When ocular examination is obscured by opaque media (e.g., intraocular hemorrhage), B-scan ultrasound 

may provide detailed intraocular anatomic information.15 Ultrasound may detect the presence of an IOFB, 

retinal detachment, choroidal hemorrhage, vitreous hemorrhage, and orbital hemorrhage (Fig. 19).13,16 

Because the transducer applies pressure to the globe, ultrasound testing should be avoided in cases of 

suspected globe violation. 

Within the first 24 to 72 hours following injury, the most valuable imaging modality for the evaluation of 

ocular trauma is CT imaging, which is widely available at Level III facilities. B-scan ultrasound can be useful 

Figure 18. (Left) Axial computed tomography image of a patient with a 

left intraorbital foreign body resulting from an improvised explosive device 

(IED) blast. The metallic foreign body traveled through the right orbit 

and both ethmoid and nasal sinuses before coming to rest in the medial 

left orbit adjacent to the optic nerve. It was successfully removed through a 

transcaruncular medial orbitotomy. 

Figure 19. (Top Right) B-scan ultrasound image showing retinal 

detachment (R). The vitreous cavity is black and the curved surface of 

the posterior sclera (white) is seen on the right side of the image. Image 

courtesy of Mitchell Goff, MD.
Ocular Trauma | 315

in select cases, but its availability at Level III is variable. Magnetic resonance imaging is not particularly 

useful in the setting of acute ocular trauma, and is not generally available prior to Level IV.

Closed Globe Injuries

Corneal Abrasion

In most cases, corneal abrasions (traumatic corneal epithelial defects) can be safely managed by 

nonophthalmic providers. The cause of the abrasion is usually traumatic and the onset of symptoms (pain, 

foreign body sensation, photophobia, and blurred vision) is immediate. The defect can be visualized with 

the aid of fluorescein, which stains exposed epithelial basement membrane and fluoresces bright yellowgreen when viewed under a Wood’s lamp or cobalt blue light (Fig. 20). In most cases, the recommended 

treatment is a prophylactic topical antibiotic (erythromycin, bacitracin ophthalmic ointment, or polymyxin 

B sulfate and trimethoprim [Polytrim®] ophthalmic solution) instilled four times a day. Patching is generally 

discouraged, but sunglasses can provide symptomatic relief. The dispensing of topical anesthetics to any 

patient for any reason is contraindicated, as they can lead to neurotrophic keratopathy and persistent 

epithelial defects.17 Depending on the size of the defect, most corneal abrasions heal spontaneously within 

a few days. Special care must be taken in contact lens wearers or when the presence of an embedded 

corneal foreign body or corneal infection (e.g., corneal ulcer) is suspected. Since slit-lamp biomicroscopy, 

which is not available at Level I or II facilities, is necessary to evaluate and treat these conditions, such cases 

should be referred to an eye care professional (optometrist or ophthalmologist) when operationally feasible.

In most cases, non-ophthalmic providers can safely manage corneal abrasions using a prophylactic topical 

antibiotic. If a superficial foreign body is embedded within or on the surface of the cornea, care must be 

taken to rule out corneal perforation.

Corneal Foreign Bodies

Combat casualties will often present with superficial foreign bodies embedded within or on the surface 

Figure 21. This hyphema demonstrates extensive blood in the anterior 

chamber.

Figure 20. Corneal ulcer. Note the opaque white inflammatory infiltrate 

and overlying epithelial defect. Image courtesy of the University of 

Michigan Kellogg Eye Center.
316 | Ocular Trauma

of the cornea. Without the aid of a slit-lamp, it may be difficult to determine whether the foreign body 

has perforated the cornea, which is only 0.5 to 0.9 mm in thickness.18 In cases where the foreign body is 

thought to be superficial, the first-line treatment should be irrigation of the eye with sterile saline or eye 

wash solution. If irrigation is unsuccessful, instrument removal of the foreign body should be performed 

by an eye care professional. However, if circumstances prevent this from occurring, only experienced 

nonopthalmic personnel should attempt removal of corneal foreign bodies, using slit-lamp or loupe 

magnification, and exercising extreme caution. Seidel testing should be performed following foreign body 

removal and topical antibiotics should be administered until the epitheleal defect has healed. Metallic 

foreign bodies can leave a rust ring in the cornea, which should be removed by an ophthalmologist, ideally 

within several days of the injury.

Hyphema

Hyphema is defined as the presence of blood in the anterior chamber, and is usually caused by blunt 

trauma, unless it is associated with an open-globe injury. The source of bleeding is usually from tears 

in the iris or ciliary body, and irregular mydriasis or iridodialysis (separation of the iris root) is often an 

associated finding. In sufficient quantity, the blood is grossly visible as it layers across the bottom of the 

anterior chamber (Fig. 21). Visual acuity can be affected, depending on the size of the hyphema, and pain 

and photophobia are often present as the result of coexisting injuries, such as traumatic iritis. 

Most hyphemas resolve spontaneously and their treatment is usually nonoperative, consisting of 

observation, eye protection, and bed rest with head elevation. However, complications sometimes arise 

that require medical or surgical intervention. The greatest risk of vision loss from isolated hyphemas 

occurs with rebleeding, which usually occurs two to five days after injury. Permanent vision loss can 

result from hyphema-related complications, which include glaucoma, corneal bloodstaining, and ischemic 

optic neuropathy. Patients with sickle trait or disease are at particular risk for these complications, and all 

hyphema patients of African descent should undergo sickle screening if their status is unknown. 

Most hyphemas resolve spontaneously and their treatment is usually nonoperative, consisting of 

observation, eye protection, and bed rest with head elevation. Small hyphemas (occupying less than 

one-third of the anterior chamber) with normal vision and IOP can potentially be monitored for 

resolution at Level I or II facilities. Patients experiencing vision loss, increased IOP, or larger hyphemas 

(involving one-third or more of the anterior chamber) should be evacuated to a Level III facility for 

ophthalmologic management.

Small hyphemas (occupying less than one-third of the anterior chamber) with normal vision and IOP 

can potentially be monitored for resolution at Level I or II facilities, but eventual evaluation by an 

ophthalmologist is advisable. Patients with vision loss, increased IOP, or larger hyphemas (involving 

one-third or more of the anterior chamber) should be evacuated to a Level III facility for ophthalmologic 

management. Medical treatment includes topical steroids, cycloplegics, and IOP-lowering agents when 

necessary. Aminocaproic acid has been used to prevent rebleeding in select cases, but its marginal 

benefits must be weighed against the potential risks of clotting and stroke. Anterior chamber paracentesis 

with washout is indicated in cases with persistent IOP elevation despite maximal medical therapy, and a 

lower threshold for surgery is maintained for patients with sickle disease.
Ocular Trauma | 317

Traumatic Iritis

Blunt eye trauma can lead to irritation of the iris and ciliary body, inciting an inflammatory reaction 

within the anterior chamber known as traumatic iritis or iridocyclitis. Symptoms include deep eye pain, 

photophobia, and blurred vision. These symptoms may be delayed for 24 to 48 hours following the 

injury. Evaluation of these patients should include a complete slit-lamp exam, fundoscopic exam, and 

documentation of IOP. The key physical exam finding is a mild to severe anterior chamber reaction (cells 

and flare), which, as mentioned previously, can be best appreciated with an oblique slit beam through the 

slit-lamp biomicroscope. Additional findings include perilimbal injection (i.e., ciliary flush), photophobia, 

consensual photophobia (i.e., pain in the affected eye when light is shone in the opposite eye), and 

occasionally decreased vision. Other clues to the diagnosis include pain that does not improve with topical 

anesthetics and pain with accommodation.19,20 Treatment regimens can include cycloplegic drops, topical 

steroids, or topical nonsteroidal antiinflammatory agents (NSAIDs). Isolated traumatic iritis is self-limited 

and carries a good prognosis, and in the absence of findings suggesting coexisting ocular injuries may be 

managed at Level I or II facilities. If symptoms worsen or fail to resolve within one week, ophthalmologic 

evaluation is indicated.

In the absence of findings suggesting coexisting ocular injuries, isolated traumatic iritis is self-limited, 

carries a good prognosis, and may be managed at Level I or II facilities.

Lens Subluxation / Dislocation

Patients with lens subluxation or dislocation can present with a history of ocular trauma, distorted vision, 

monocular diplopia, and pain. Critical findings include a displaced lens on direct ophthalmoscopy, 

phacodonesis (i.e., quivering of the lens), and iridodonesis (i.e., quivering of the iris). Additional findings 

include cataract, acute pupillary block glaucoma, and acquired myopia. Partial disruption of the zonular 

fibers that support the lens will result in subluxation. A subluxed lens can still remain partially visible within 

the pupillary aperture. Complete disruption of the zonular fibers results in lens dislocation, where the lens 

may no longer be visible through the pupillary aperture. 

All patients with lens subluxations or dislocations warrant immediate ophthalmologic consultation. 

A potential vision-threatening complication of lens dislocation is acute pupillary-block glaucoma.21 This 

results from the dislocated lens preventing the aqueous from flowing from the posterior chamber through 

the pupil into the anterior chamber, which pushes the iris forward and closes the anterior chamber angle 

where the aqueous exits the eye. Traumatic cataract, another complication, may follow even the most trivial 

injury to the lens, and can be removed electively at Level IV or V facilities.21 

Vitreous Hemorrhage

Vitreous hemorrhage may occur from a variety of mechanisms including iris injuries, ciliary body trauma, 

vitreous detachment, retinal vessel injury, and choroidal rupture.22 Patients with vitreous hemorrhage can 

present with varying degrees of vision loss, ranging from hazy vision with cobwebs or floaters to bare light 

perception vision.

Visualizing blood within the vitreous cavity with direct or indirect ophthalmoscopy confirms the diagnosis 

of vitreous hemorrhage. It is important to document IOP measurements in these patients, as they are at risk 
318 | Ocular Trauma

for acute glaucoma. The treatment of vitreous hemorrhage involves bed rest (with head of bed elevation), 

a protective eye shield, and analgesics (avoiding aspirin and nonsteroidal antiinflammatory drugs). All 

vitreous hemorrhages, traumatic or otherwise, should be assumed to be secondary to retinal injury and 

referred for immediate ophthalmologic evaluation. 

Retinal / Choroidal Injuries

Ocular trauma may result in a variety of retinal injuries including retinal breaks, retinal detachments, 

choroidal hemorrhage, and choroidal rupture.23 Patients with retinal injuries may present with a recent 

or remote history of ocular trauma. Symptoms include floaters, photopsias (flashes of light), a curtain or 

shadow over the visual field, and varying degrees of vision loss. Peripheral retinal breaks may initially be 

asymptomatic only to later lead to retinal detachment. Detailed dilated fundoscopic examination by an 

ophthalmologist is necessary to diagnose most retinal injuries. 

Commotio retinae (Berlin’s edema) is a retinal injury resulting from a contrecoup mechanism of injury.24

The injury is characterized by a transient whitening of the deep sensory retina following ocular trauma, 

which is visible on direct or indirect ophthalmoscopy. Patients present with variable degrees of vision 

loss, which is more severe with macular involvement. While there is no specific treatment for commotio 

retinae, most cases are self-limited and they rarely result in permanent vision loss.

Patients with retinal injuries may present with a recent or remote history of ocular trauma. Symptoms 

include floaters, photopsias (flashes of light), a curtain or shadow over the visual field, and varying degrees 

of vision loss. Careproviders should be able to identify patients with signs or symptoms consistent with 

retinal injury and refer them for appropriate ophthalmologic consultation.

Combat casualty careproviders must maintain a high suspicion for retinal injuries in all patients with 

significant ocular trauma. The visual morbidity from delayed treatment of these injuries is high. Definitive 

diagnosis of these injuries is well beyond the scope of most physicians. Thus, providers should be able 

to identify patients with signs or symptoms consistent with retinal injury and refer them for appropriate 

ophthalmologic consultation. In some cases, specialized treatment must be performed within 24 to 72 

hours of injury to optimize visual outcomes.25

Open-Globe Injuries

Overview

An open-globe injury is defined as any full-thickness violation of the cornea or sclera. While the 

distinction is largely semantic, a laceration generally implies direct violation by a sharp object, while 

rupture is usually used to describe the forceful splitting of the eye wall induced by blunt trauma. Foreign 

body penetration denotes the entry of an object without exiting the involved structure, while perforation 

indicates the complete through-and-through passage of the object.

Signs and symptoms of open-globe injury include loss of vision, hemorrhagic chemosis, anterior chamber 

asymmetry, intraocular hemorrhage (hyphema or vitreous hemorrhage), uveal prolapse, hypotony (IOP 

less than 5 mm Hg), positive Seidel test, and visible protrusion of a foreign body from the globe (Figs. 
Ocular Trauma | 319

16, 17, and 22). On CT scan, IOFB or air are diagnostic of open-globe injury, and globe deformation, 

intraocular hemorrhage, and lens disruption are highly suggestive (Fig. 23). 

The prognosis for open-globe injury is highly variable and dependent on the severity of the injury. 

According to the Ocular Trauma Score, out of all the prognostic indicators for visual outcome, poor 

initial visual acuity (light perception or worse) is the most important negative predictor.26 This is followed 

by globe rupture, endophthalmitis, perforating injury, retinal detachment, and afferent pupillary defect. 

The prognostic applicability of the Ocular Trauma Score to combat injuries was nicely validated by a study 

from OEF and OIF.27 Corneoscleral laceration length and posterior extension more than five mm past the 

limbus are also negative predictors for globe survival. Barr reported an enucleation rate of 68 percent for 

globes with corneoscleral lacerations over 13 mm in length in contrast to only 4 percent with lacerations 

less than nine mm.28

An open-globe is defined as any full-thickness violation of the cornea or sclera. Signs and symptoms 

of open-globe injury include loss of vision, hemorrhagic chemosis, anterior chamber asymmetry, 

intraocular hemorrhage (hyphema or vitreous hemorrhage), uveal prolapse, hypotony (IOP less than 

five mm Hg), positive Seidel test, and visible protrusion of a foreign body from the globe. Casualties with 

open-globe injuries should undergo eye shielding and be evacuated to a Level III facility.

Initial Management of Open-Globe Injuries

Patients with signs and symptoms consistent with open-globe injury require emergent evacuation to a 

Level III facility for ophthalmologic evaluation. As described above, the eye should be protected with a Fox 

shield and the patient’s tetanus status updated as needed. In anticipation of possible surgery, the patient’s 

last meal should be recorded and they should receive nothing by mouth until they have been evaluated by 

an ophthalmologist. Pain, nausea, and anxiety should be treated if present, as excessive blepharospasm or 

valsalva can increase IOP and exacerbate open-globe injuries.

Figure 22. Signs of open-globe injury: (Left) Uveal prolapse and misshapened globe. (Right) Protruding intraocular foreign body.
320 | Ocular Trauma

Open-Globe Injury Repair

The Level III ophthalmologist is responsible for the definitive treatment of open-globe injuries in the vast 

majority of cases. Even for the most experienced ophthalmologist, the diagnosis of open-globe injury is not 

always clear-cut, and the decision to take the patient to the operating room can be difficult. However, if any 

doubt exists, a low threshold for surgical exploration should be maintained. General anesthesia is required, 

as retrobulbar injection is clearly contraindicated. It has been suggested that the use of depolarizing 

paralytic agents is contraindicated in open-globe injuries due to the risk of increased IOP, but this has never 

been clearly demonstrated to be a problem.29 Intraoperative findings dictate the extent of the exploration, 

but one can never be faulted for performing a 360-degree peritomy in order to directly visualize the 

entire scleral surface. Conjunctival traction sutures (e.g., 4-0 silk) placed at the oblique quadrants can 

improve surgical exposure dramatically (Fig. 24). Scleral lacerations often originate at or extend beneath 

the extraocular muscle insertions, and in these instances it is helpful to detach the muscle at its insertion 

in order to fully visualize and repair the defect. Double-armed 6-0 polyglactin sutures preplaced through 

the tendon can facilitate retraction and exposure of the field, as well as reattachment of the muscle to the 

globe at the end of the case.

The overarching principle in the treatment of open-globe injury is to restore the physical integrity of the 

globe wall. Every attempt should be made to reposit prolapsed intraocular structures prior to wound 

approximation. The exception to this rule is the crystalline lens, which should be removed if it is prolapsed 

into the anterior segment or out of the globe. Viscoelastics are quite useful in preventing incarceration of 

intraocular tissue in the wound during repair. Typically, 10-0 nylon suture is used in the cornea, 9-0 nylon 

at the limbus, and 8-0 nylon in the sclera. If the limbus is involved, it is generally the first structure 

to be sutured, being the most critical and easily recognizable anatomic landmark. Basic wound closure 

principles must be strictly observed, particularly in the cornea. These include: (1) vertical entry and exit 

Figure 23. CT scan findings in open-globe injury: (Left) Intraocular foreign body and air. (Right) Vitreous hemorrhage and lens disruption, right eye. 

Deformed and poorly defined globe, left eye.
Ocular Trauma | 321

of the needle point with respect to the corneal surface; (2) 90 percent-stromal-thickness suture passes; 

(3) exact matching of suture depth and width on each side of the wound; (4) orientation of each suture 

orthogonal to the wound axis; (5) proper and even spacing of interrupted sutures (space between each 

suture slightly less than the suture length); and (6) tying of sutures under proper tension (approximation, 

not strangulation). The use of the adjustable slipknot can greatly aid in achieving the last goal. All corneal 

suture knots should be buried and directed away from the visual axis if possible. 

Occasionally, a watertight closure cannot be achieved with sutures alone, such as in corneal lacerations 

with a stellate pattern or tissue maceration. In these cases, cyanoacrylate glue can be very useful. Prior to 

applying the glue, any residual corneal epithelium should be removed from the surface to which the glue 

will be applied. Nylon 10-0 sutures can then be placed in a criss-crossing or grid pattern to create a scaffold 

across the defect. The glue is drawn up from the ampule in a tuberculin syringe and sparingly applied to 

the defect through a small-gauge needle. A completely dry wound surface is necessary for adherence of 

the glue, but this may be difficult to maintain in the presence of an aqueous leak. Viscoelastic, preferably 

a cohesive type, can be injected directly beneath the laceration to prevent the egress of fluid. A bandage 

contact lens should be placed after the glue is applied, and can subsequently be removed once the plug 

Figure 24. Corneoscleral laceration repair, right eye. The scleral portion of the laceration extends posteriorly beneath the insertion of the medial rectus 

muscle, which has been tagged with a double-armed 6-0 polyglactin suture and detached. Note conjunctival traction sutures.
322 | Ocular Trauma

spontaneously detaches, usually within two to four weeks. Another option for the closure of wounds with 

damaged or missing tissue is the use of allografts or xenografts, such as acellular dermis or processed 

pericardium, which can be cut to the size and shape of the defect and sewn into place as a patch graft 

(Fig. 25). 

The overarching principle in the treatment of open-globe injury is to restore the physical integrity of 

the globe wall. Every attempt should be made to reposit prolapsed intraocular structures prior to wound 

approximation. 

In some cases, intraocular pathology may be addressed during primary globe repair if technically feasible. 

Foreign bodies in the anterior chamber or within easy reach of the anterior segment can often be safely 

removed. Disrupted lens material or prolapsed vitreous may also be removed at the discretion of the 

surgeon. However, as stated above, the primary goal of open-globe repair is to simply close the defect and 

allow the eye an opportunity for further rehabilitation in the future. Procedures that add surgical time or 

increase risk to the globe, such as posterior segment foreign body removal, retinal detachment repair, or 

intraocular lens implantation are not advisable under these circumstances.

Figure 25. Severe corneoscleral rupture with corneal tissue loss repaired with Tutoplast® patch graft.
Ocular Trauma | 323

Intraocular air may be found either clinically or radiographically in some penetrating globe injuries. While 

not a major treatment concern, the presence of air may potentially impact the patient’s ability to safely 

undergo aeromedical evacuation, due to the expansion of gas within the globe at high altitude. However, 

this concern is mitigated by several factors: (1) the rise in IOP at altitude is dependent on the volume of 

air present within the globe, and studies indicate that eyes with less than 10 percent gas fill (0.6 milliliters) 

may safely undergo air travel; (2) the half-life of air in the human eye is only 1.3 days; and (3) most open 

globes, including those that have just undergone repair, are hypotonus and can accommodate moderate 

increases in IOP. 30,31,32 With these considerations in mind, it is advisable for the ophthalmologist to remove 

any air that is easily accessible during the course of open-globe injury repair. However, based upon the 

information provided above, volumes of retained intraocular air less than 0.6 milliliters (approximately 10 

mm in diameter on CT scan) should not prevent aeromedical evacuation of a combat casualty. 

Intraocular air may be found either clinically or radiographically following penetrating globe injuries. 

The presence of air may potentially impact the patient’s ability to safely undergo aeromedical evacuation 

due to the expansion of gas within the globe at high altitude. Volumes of retained intraocular air less than 

0.6 milliliters (approximately 10 mm in diameter on CT scan) should not prevent aeromedical evacuation 

of a combat casualty. 

While definitive evidence proving benefit is lacking, prophylactic administration of systemic antibiotics is 

widely recommended for open-globe injuries.33,34 A variety of single- or multiple-agent regimens have been 

used, including fluoroquinolones, cephalosporins, or beta-lactams. Topical antibiotics are also advisable. 

However, the use of intravitreal antibiotics on a prophylactic basis in this setting is of questionable value.34

A study from OEF and OIF reported no cases of endophthalmitis in 79 eyes with retained IOFBs, despite 

the fact that only three of them received intravitreal antibiotics at the time of primary globe repair.35

Sympathetic Ophthalmia

An uncommon but potentially devastating complication of open-globe injury that can lead to blindness 

in the fellow eye is sympathetic ophthalmia. Defined as a diffuse bilateral granulomatous uveitis following 

penetrating globe injury, sympathetic ophthalmia is believed to represent an autoimmune response to the 

exposure of uveal or retinal antigens previously sequestered within the blood-aqueous or blood-retinal 

barrier. Incidence reports of sympathetic ophthalmia after wartime open-globe injuries vary widely from 

0.02 to 56 percent.36 

It is widely believed that sympathetic ophthalmia can be prevented by enucleating a severely damaged eye 

within two weeks of injury, although this time frame is largely based on anectodal data. Evisceration (i.e., 

removal of the contents of the globe) is generally discouraged in the setting of trauma, due to the potential 

presence of uveal proteins within the emissary canals of the retained scleral shell. The true risk of 

developing sympathetic ophthalmia if enucleation is not performed is unknown. Modern estimates of the 

overall incidence of sympathetic ophthalmia after open-globe injury (including patients who underwent 

enucleation) range from 0.3 to 1.9 percent.36

Globe Repair versus Enucleation

Repair of severe open-globe injuries should be attempted whenever technically feasible, unless proper 

follow-up care is doubtful. Deciding between primary globe repair and primary enucleation can sometimes 
324 | Ocular Trauma

be extremely difficult. In smaller globe lacerations where preoperative vision is at least light perception, 

the decision to repair is clear. On the opposite end of the spectrum, when a globe is so severely 

damaged that repair is not technically possible, enucleation must be performed to prevent sympathetic 

ophthalmia and socket contracture.37,38 In the middle of the spectrum, however, the ophthalmologist will 

encounter cases in which repair is possible, but the ultimate prognosis for vision or globe survival is slim 

to nonexistent. In such cases, it is generally felt that repair should be attempted whenever technically 

feasible. The benefits to the patient are multiple: (1) the patient is assured that a reasonable effort was 

made to try to save the eye; (2) the lack of visual function despite repair is demonstrated to the patient; (3) 

the patient is included in the decision-making process leading to removal of the eye; and (4) the patient 

has time to come to terms with the loss of a major sensory organ before enucleation is performed. This 

guidance is appropriate in cases where the availability of proper follow-up and ophthalmic surgery can be 

reasonably assured, such as is the case for service members being evacuated to higher levels of care (Level 

IV and V facilities). However, if a patient in the same clinical situation may not be able to obtain proper 

follow-up care (e.g., host national in a country with no reliable health care system), primary enucleation 

may be more advisable for the patient’s long-term welfare.

Repair of severe open-globe injuries should be attempted whenever technically feasible, unless proper 

follow-up care is doubtful.

Enucleation

Enucleation, defined as surgical removal of the entire globe, is typically performed under general 

anesthesia, although a retrobulbar block may be utilized if necessary. A 360-degree peritomy is performed, 

sparing as much conjunctiva as possible. Tenon’s capsule is bluntly dissected from the sclera in the oblique 

quadrants with curved blunt scissors. The rectus muscles are isolated with muscle hooks, and double 

armed 5-0 or 6-0 polyglactin sutures can be preplaced before detaching them from the globe at their 

insertions. The oblique muscles are usually cut and not preserved, although some surgeons advocate 

attaching one or both of them to the orbital implant or to the rectus muscles (e.g., the superior oblique 

to the superior rectus and the inferior oblique to the lateral rectus). The globe is then retracted by the 

muscle stumps, with traction sutures (e.g., 4-0 silk 

passed through the limbus), or with an enucleation 

spoon, and the optic nerve is strummed and cut 

with curved scissors (Fig. 26). The length of the 

optic nerve segment is not critical, as long as the 

nerve is severed distal to its entrance into the globe. 

Clamping or cauterizing the optic nerve prior to 

cutting it may assist in hemostasis. Once adequate 

hemostasis is achieved by packing with cold-soaked 

gauze or other hemostatic materials, orbital implant 

sizers can be used to determine the appropriate 

implant size. The implant should provide adequate 

volume replacement while at the same time rest 

easily within Tenon’s capsule without placing 

undue tension on the Tenon’s closure. For ideal 

orbital volume replacement, the optimal implant 

Figure 26. Enucleation of globe. The four rectus muscles are tagged with 

5-0 polyglactin sutures. The globe is retracted with 4-0 silk sutures passed 

through the limbus as the optic nerve is cut.
Ocular Trauma | 325

diameter should be approximately two mm less than the axial length of the globe.39 Given that the average 

axial length of the adult globe is approximately 24 mm, most orbital implants should be between 20 and 22 

mm in diameter, although a smaller size may be used if there is tissue loss or a specific concern for implant 

extrusion. Care should be taken in the presence of large orbital fractures, which may need to be repaired 

in order to prevent implant migration into the maxillary or ethmoid sinus. Much debate remains regarding 

the ideal orbital implant material, and there is insufficient data in the literature to definitively recommend 

one type over another. Once the implant is placed within Tenon’s capsule, the extraocular muscles can 

be attached to the anterior surface of the implant in order to maximize postoperative motility. Tenon’s 

capsule and conjunctiva are then closed over the implant with absorbable sutures. Separate layered closure 

of posterior Tenon’s capsule (with 4-0 polyglactin) and anterior Tenon’s (with 5-0 or 6-0 polyglactin) may 

decrease the risk of postoperative implant extrusion. A conformer is placed into the socket with antibiotic 

ointment, and some surgeons perform a temporary suture tarsorrhaphy, which can be left in place for up to 

three weeks. A pressure patch may also be applied for two to three days to limit postoperative edema. Six 

to eight weeks of postoperative healing should be allowed before ocular prosthesis fitting is attempted.

Intraocular Foreign Body (IOFB)

By definition, IOFBs are open-globe injuries, and the signs and symptoms are the same as those 

described at the beginning of this chapter segment. However, the severity of IOFB injuries varies widely, 

and as one would expect is largely dependent on the size of the offending object. Intraocular foreign bodies 

should be suspected with blast injury mechanisms, sanding, drilling, grinding, or hammering metal-onmetal. High-velocity metal or glass splinters may enter the eye painlessly. The initial ocular examination 

may appear deceptively benign, revealing only slight injection or local discomfort (Fig. 27). Visual acuity 

is typically decreased, but can be normal. Some corneal or scleral perforations can be difficult to detect. 

Additional findings suggestive of an IOFB include conjunctival chemosis, hyphema, localized cataract, iris 

injury, pupillary asymmetry, vitreous hemorrhage, decreased IOP, or an aqueous humor leak (as evidenced 

by a positive Seidel test). CT scanning is helpful in identifying IOFBs in eyes with opaque media. Although 

small pieces of wood, glass, or plastic may not be seen on CT, the majority of IOFBs can be visualized. 

The utility of ultrasonography for detecting IOFBs in the setting of open-globe injury is limited by the need 

to avoid direct pressure to the injured globe.

Figure 27. Penetrating globe injury caused by a rocket-propelled grenade blast fragment. (Left) Anterior segment exam appears relatively benign with 

mild focal corneal edema seen in the inferior cornea. (Right) Posterior segment IOFB is visible on CT scan.
326 | Ocular Trauma

Intraocular foreign bodies are open-globe injuries and should be suspected with blast injury mechanisms, 

sanding, drilling, grinding, or hammering metal-on-metal. Level III facility-based ophthalmologists 

should only remove IOFBs that are easily accessible within the anterior segment. Posterior segment 

foreign bodies should be left for potential future removal by a vitreoretinal specialist at Level IV or V 

facilities.

Management of IOFBs depends on the foreign body size, composition, and location within the eye.40,41 The 

reactivity of IOFBs is highly variable. Wood, vegetable matter, and metals such as iron, copper, and steel 

typically incite an intense inflammatory reaction when left in the eye, and surgical removal is indicated.42

On the other hand, inert foreign bodies such as glass, lead, plaster, rubber, silver, and stone, are often left 

in the eye if they are minimally symptomatic.43 As stated above, Level III facility-based ophthalmologists 

should only remove IOFBs that are easily accessible from the anterior segment. Posterior segment foreign 

bodies should be left for potential future removal by a vitreoretinal specialist at Level IV or V facilities.

Ocular Adnexal Trauma

Eyelid Lacerations

Lacerations of the eyelid and periocular region are common in combat injuries, and can be seen in isolation 

or concomitantly with other ocular injuries (Fig. 28). Proper eyelid function is critical to preserving vision 

and maintaining the health of the ocular surface and cornea. The most important discriminating factor in 

the management of eyelid lacerations is involvement of the lid margin.44 This will be manifested as notching 

or gaping along the lid contour due to violation of the tarsal plate, the dense connective tissue that provides 

structural support to the eyelid. Orbital fat prolapsing thru an eyelid laceration is indicative of violation of 

the orbital septum.

Partial-thickness eyelid lacerations that do not involve the lid margin or violate orbital septum can be 

repaired by careproviders at Level I or II facilities. Absorbable 6-0 or nonabsorbable sutures are generally 

used, and layered closure is recommended for absorbable sutures. Full-thickness lid lacerations should be 

repaired at the earliest opportunity by an ophthalmic surgeon at a Level III facility, preferably within 24 

to 48 hours of injury. If ocular surface exposure is evident prior to evacuation, a lubricating eye ointment 

should be instilled until repair of the laceration can be performed.

The principles of lid laceration repair are simple: (1) reapproximation of vital anatomic landmarks, especially 

the lid margin; (2) preservation of tissues; and (3) avoidance of vertical tension on the lids. While in many 

other body sites, debridement of devitalized or necrotic-appearing tissue is advocated, such is not the case 

with the eyelids. Due to their excellent vascular supply, eyelid tissues that appear to be unsalvageable may 

end up surviving after being anatomically restored. It is also common for lacerated eyelid tissues to roll up 

or retract, giving the false impression of tissue loss. Careful wound exploration often reveals the presence of 

tissue previously thought to be missing, making repair or reconstruction much more achievable (Fig. 29).

Partial-thickness eyelid lacerations that do not involve the lid margin or violate orbital septum can be 

repaired by careproviders at Level I or II facilities. Full-thickness lid lacerations should be repaired by 

an ophthalmologist or facial plastic surgeon. Canalicular involvement must be ruled out in medial eyelid 

lacerations. 
Ocular Trauma | 327

Repair of full-thickness lid lacerations should begin with approximation of the wound at the lid margin. 

This is typically performed at the gray line in a vertical mattress fashion with 5-0 or 6-0 silk or polyglactin 

suture. Additional margin sutures can be placed in similar fashion at the posterior and/or anterior lash 

lines. To avoid contact with the ocular surface, the suture tails can be cut long and tied down with the tails 

of the more anterior sutures. Deep absorbable sutures (e.g., 6-0 polyglactin) should also be used to repair the 

tarsus. The orbicularis and skin can be closed with any of a number of braided or monofilament sutures. 

With lacerations involving the medial eyelid, damage to the lacrimal drainage system should be suspected. 

This can be confirmed by canalicular probing with or without irrigation. Canalicular lacerations should 

be repaired over a silicone stent (e.g., Crawford tubes), which can either be placed through the entire 

nasolacrimal duct system, through the upper and lower canaliculi with a pigtail probe, or through the 

involved canaliculus alone with a monocanalicular stent. The latter option should only be used in proximal 

Figure 28. Stepwise repair of a full-thickness eyelid laceration (demonstrated following a full-thickness wedge resection of the upper lid): (Top Left)

A 6-0 silk suture is passed through the gray line on both sides of the defect, taking healthy bites of the tarsal plate. (Top Right) The same suture is 

passed in a vertical mattress fashion. (Bottom Left) The remainder of the tarsus is repaired with partial thickness passes of 6-0 polyglactin. (Bottom 

Right) The skin is closed with 6-0 fast-absorbing gut sutures. The tails of the margin sutures can be secured with the skin sutures to prevent them from 

contacting the cornea.
328 | Ocular Trauma

canalicular lacerations with a normal punctum. Once the canaliculus is intubated, the pericanalicular tissues 

are approximated with 7-0 or 8-0 polyglactin suture. It should be remembered that damage to the medial 

canthal tendon is often seen with canalicular lacerations. Repair of both the posterior and anterior cruri of 

the medial canthal tendon should be performed as necessary.

Occasionally, lid lacerations will be encountered in association with an open-globe injury or proptotic eye. 

In these cases, it may be advisable to perform a lateral canthotomy and cantholysis to relieve the pressure 

on the globe and decrease the tension on the lid repair. If a significant amount of eyelid tissue is lost, 

reconstruction may be attempted depending on the expertise and comfort level of the ophthalmologist. 

However, it is acceptable to perform a temporary suture tarsorrhaphy and evacuate the patient to Level IV 

or V facility, where ophthalmic plastic and reconstructive surgery services are available.

Conjunctival Lacerations

Patients with conjunctival lacerations following ocular trauma may present with eye pain, foreign body 

sensation, and conjunctival injection or hemorrhage. Physical exam often reveals a conjunctival laceration 

upon white light examination. The damaged conjunctiva typically folds over on itself at the site of the 

laceration providing an unobstructed view of exposed white sclera. The damaged region of conjunctiva 

may fluoresce bright yellow-green following fluorescein staining and cobalt blue light illumination. The 

presence of a conjunctival laceration should raise the suspicion of potential open-globe injury and/or 

IOFB, and merits evaluation by an ophthalmologist.

Patients with small conjunctival defects, less than one centimeter (cm), will typically heal without surgical 

intervention. Patients with conjunctival defects larger than one cm will often need surgical repair, which 

should be performed by an ophthalmologist.45 Aftercare involves topical antibiotic administration for up 

to one week until the affected area has healed.

Figure 29. (Left) Preoperative photograph of a patient who sustained a chainsaw injury to the left globe and orbit. At first glance, a significant amount 

of tissue appears to be missing, but careful wound exploration revealed minimal tissue loss, and primary repair was successfully accomplished. The globe 

was repaired prior to eyelid reconstruction. (Right) Postoperative photograph.
Ocular Trauma | 329

Orbital Trauma

Retrobulbar Hemorrhage

Retrobulbar hemorrhage is typically caused by blunt 

trauma to the orbit, and frequently results in an 

acute orbital compartment syndrome, a true ocular 

emergency.46,47 Another potential cause of orbital 

compartment syndrome in the setting of trauma 

is third-spacing of fluid into the orbit following 

massive fluid resuscitation for burn patients. Signs 

and symptoms of orbital compartment syndrome 

include acute vision loss, eye pain, headache, 

proptosis, resistance to retropulsion, increased IOP 

(typically over 40 mm Hg), afferent pupillary 

defect, ophthalmoplegia (loss of extraocular 

motility), and hemorrhagic chemosis. When orbital 

compartment syndrome is suspected clinically, 

lateral canthotomy and inferior cantholysis should 

be performed immediately. Timing is critical, as 

experimental studies suggest that permanent vision 

loss occurs with orbital ischemia lasting greater than 

100 minutes.48 While imaging studies can help to confirm the presence of retrobulbar hemorrhage, the 

diagnosis of orbital compartment syndrome is clinical, and treatment should not be delayed to obtain a CT 

scan (Fig. 30). 

The goal of lateral canthotomy and inferior cantholysis is to convert the orbit from a closed to an open 

compartment by releasing the attachment of the lower lid to the lateral orbital rim (Fig. 31). Scissors are 

used to make a horizontal cut from the lateral commissure to the orbital rim, effectively separating the lateral 

canthal tendon into its superior and inferior portions (lateral canthotomy). The lower lid is then grasped 

with forceps and pulled away from the rim to place the lateral canthal tendon under tension, and the tendon 

is “strummed” and cut with scissors (inferior cantholysis). The hand grasping the lid during this maneuver 

should feel an immediate release when the tendon is cut. Significant drainage of blood from the orbit is not 

necessary for the procedure to be effective, nor is it expected. However, if the decompressive effect from the 

inferior cantholysis is insufficient, a superior cantholysis can be performed by releasing the upper lid in the 

same manner as the lower. The efficacy of the treatment can be assessed soon after the procedure through 

repeat IOP measurements and visual acuity assessment.

Retrobulbar hemorrhage is typically caused by blunt trauma to the orbit, and frequently results in an 

acute orbital compartment syndrome, a true ocular emergency. When orbital compartment syndrome is 

suspected clinically, lateral canthotomy and inferior cantholysis should be performed immediately. There 

is no other procedure in all of ophthalmology that can more simply, quickly, and dramatically treat and 

prevent such devastating vision loss and so profoundly impact a patient’s final visual outcome.

If orbital ischemia persists despite complete inferior and superior cantholysis, additional maneuvers may be 

attempted. Blunt scissors can be placed through the canthotomy incision and used to spread the orbital fat in 

Figure 30. CT scan appearance of right retrobulbar hemorrhage. Note 

the loculated pattern of blood within the orbital fat, posterior tenting of the 

globe from optic nerve traction, and severe proptosis.
330 | Ocular Trauma

the inferotemporal quadrant, releasing any pockets of loculated blood within the orbit.49 If this maneuver 

fails, the patient may be taken to the operating room for formal orbitotomy and decompression by 

whatever means necessary. Medical therapy with intraocular-pressure-lowering agents such as osmotics 

or aqueous suppressants may also be considered.

The value of canthotomy and cantholysis in the 

setting of orbital compartment syndrome cannot 

be overstated. There is no other procedure in all of 

ophthalmology that can more simply, quickly, and 

dramatically treat and prevent such devastating 

vision loss and so profoundly impact a patient’s 

final visual outcome. Performed promptly enough, 

it can literally make the difference between nolight-perception and 20/20 vision. Given the timecritical nature of this condition, ophthalmologists 

are strongly encouraged to train fellow CCC 

providers on the indications for and use of this 

simple technique.

Orbital Foreign Bodies

Penetrating orbital injury from projectiles or stab 

injuries can result in retained orbital foreign bodies 

(Fig. 32). Patients typically present with varying Figure 32. Orbital foreign body sustained from a blast injury.

Figure 31. Lateral canthotomy and inferior cantholysis. Heavy dotted line represents the orbital rim, lighter dotted lines represent the superior and inferior 

cruri of the lateral canthal tendon. (Left) The lateral canthotomy is created by cutting horizontally from the lateral commissure to the lateral orbital rim. 

(Right) The lower lid is distracted away from the lateral orbital rim and the inferior crus of the lateral canthal tendon is cut, separating the lower lid 

from the lateral orbital rim. Image courtesy of Juan D. Nava, Medical Illustrator, Brooke Army Medical Center.
Ocular Trauma | 331

degrees of periocular edema/ecchymosis, proptosis, impaired ocular motility, decreased vision, and pain. 

Orbital compartment syndrome can also result, and must be managed in the manner described above. As 

is the case with IOFBs, the composition of the object is important in predicting its long-term tolerability 

within the orbit and determining the need for removal. Removal of organic foreign bodies is generally 

recommended, while inorganic foreign bodies can in many cases be observed.50 Complications of orbital 

foreign bodies include vision loss, proptosis, diplopia, cellulitis, or a chronic draining fistula. Foreign 

body removal can be attempted in such cases, although the unique anatomy of the orbit can make this 

procedure technically difficult, and it should only be performed by an experienced orbital surgeon. The 

use of intraoperative fluoroscopy has been described as an adjunct to increase the ease of orbital foreign 

body removal.51

Orbital Fractures

Diagnosis and management of orbital fractures are covered in detail in the Maxillofacial and Neck Trauma 

chapter. 

Miscellaneous Ocular Injuries

Chemical Eye Injuries

Chemical exposure of the eye is a true ophthalmologic emergency and may occur with acid or alkali agents. 

The resulting damage to the eyelids, conjunctiva, cornea, and anterior segment structures may produce 

permanent visual impairment. In general, alkali burns are more severe than acid burns.52 Alkali burns 

cause a liquefactive necrosis, saponifying corneal proteins and initiating corneal collagen destruction. 

Acid burns cause injury through coagulation necrosis and tend to precipitate corneal proteins, which serve 

to limit penetration of the acid. Alkali agents are found in more commercially available products than 

acids, making alkali exposure a relatively more frequent occurrence. Exposure of the eyes to chemical 

warfare agents is also an ocular emergency. Blistering agents such as mustard gas are particularly toxic 

to the ocular surface, and the acute management of exposure to these agents mirrors that for standard 

chemical exposures. 

A patient who presents with chemical exposure should undergo immediate copious irrigation of the 

eye before any time is wasted on additional history and physical examination.53 In terms of efficacy, no 

therapeutic difference exists between normal saline, normal saline with bicarbonate, lactated Ringer’s 

solution, or balanced salt solution.54 Irrigation with a minimum of one liter of irrigating solution is 

recommended. During irrigation, the lids should be retracted and the stream of irrigating fluid should 

be directed onto the globe and conjunctival fornices. The fornices should be carefully swabbed to remove 

any chemical particulate matter. Topical anesthesia will facilitate these maneuvers. Irrigation should 

continue until the pH of the tear film obtained at the inferior conjunctival fornix is neutral, as measured 

with litmus paper or the pH indicator of a urine dipstick.55 Waiting several minutes after completion 

of irrigation will allow for pH equilibration. No attempt should be made to neutralize chemicals with 

either acids or alkalis. The immediate irrigation of metallic sodium, metallic potassium, or yellow or 

white phosphorous has the theoretic potential to initiate further chemical injury. Despite this concern, 

authorities still recommend copious irrigation of eyes exposed to these chemicals.53
332 | Ocular Trauma

Chemical injury to the eye is a true ophthalmologic emergency and may occur with acid or alkali agents. 

A patient who presents following chemical exposure should undergo immediate copious irrigation of the 

eye before any time is wasted on additional history and physical examination. 

The severity of a chemical eye injury is related to the type of chemical, surface area of contact, duration 

of chemical contact, and depth of chemical penetration. If an epithelial defect is highly suspected but 

none is found on initial staining with fluorescein, the procedure should be repeated, as sloughing of the 

corneal basement membrane may result in delayed fluorescein uptake. The ultimate prognosis depends on 

the loss of corneal clarity and degree of limbal ischemia, graded on a scale of I to IV. Patients with mild 

injuries (grade I) may be treated with a cycloplegic (avoiding mydriatics such as phenylephrine due to their 

vasoconstrictor effects), a topical antibiotic (e.g., erythromycin), and oral pain medication. These patients 

should be seen by an ophthalmologist daily until healing is documented, after which they may return to 

duty in the absence of visually significant complications. Patients with moderate to severe injuries (grades II 

to IV) warrant emergent ophthalmologic assessment and evacuation out-of-theater. Subsequent treatment 

will focus on lysis of adhesions, minimizing infection potential, and treatment of iritis and elevated IOP. 

Long-term complications of chemical injuries include corneal scarring and neovascularization, adhesions 

of the lids to the globe (symblepharon), glaucoma, cataracts, and retinal necrosis.

Traumatic Optic Neuropathy

Traumatic optic neuropathy (i.e., injury to the optic nerve) may occur with blunt or penetrating ocular 

trauma. It is often associated with a blow to the eyebrow or forehead, the force of which can be 

transmitted through the orbital roof to the optic canal. Patients with traumatic optic neuropathy typically 

note an immediate and profound loss of vision and present with an afferent papillary defect.56 The optic disc 

usually appears normal upon initial fundoscopic examination, as optic disc pallor can take several weeks to 

develop following the injury. The underlying etiology of nerve injury may be nerve compression, transection, 

or ischemic injury.57 The diagnosis of traumatic optic neuropathy is typically made only after other causes 

of vision loss are excluded by an ophthalmologist. Computed tomography imaging often shows associated 

orbital fractures, but radiographically evident optic canal fractures are much less common.58 Therapeutic 

options for traumatic optic neuropathy include high-dose corticosteroids or surgical decompression of the 

optic nerve if impingement is suspected. However, controversy remains over the efficacy of these treatments. 

The International Optic Nerve Trauma Study, the most extensive prospective study of traumatic optic 

neuropathy to date, showed no definitive benefit from either steroids or surgery, and both of these 

modalities can pose significant potential risks to the multisystem trauma patient.59 The decision to treat 

should be individualized for each patient, taking into account their ocular status, mechanism of injury, 

presence of fracture on CT scan, and comorbid conditions.

Traumatic optic neuropathy may occur following blunt or penetrating ocular trauma. Patients with 

traumatic optic neuropathy typically note an immediate and profound loss of vision and present with 

an afferent papillary defect.
Ocular Trauma | 333

Summary

The basic principles of ocular trauma management in combat do not differ significantly from those followed 

in the civilian sector. Recent developments during OEF and OIF in casualty evacuation and combat trauma 

systems have facilitated the delivery of ocular trauma care which replicates the standards of care maintained 

in civilian trauma system. However, the overall severity and complexity of these injuries are generally much 

greater in combat, calling for the utmost skill and dedication from military ophthalmologists and other 

combat health support personnel. Combat casualty care providers at Level I and II facilities must be 

able to recognize ocular injuries that require further evacuation and take appropriate steps to protect the 

eye during transport. Ophthalmologists at Level III facilities must be prepared to make difficult clinical 

decisions and perform technically challenging surgery within the physical and operational constraints of 

the theater level hospital. Every attempt should be made to repair open-globe injuries, except for severely 

ruptured globes in patients for whom proper access to further ophthalmologic care is doubtful. Given the 

frequent association of ocular injuries with head, face, and neck injuries, ophthalmologists should expect to 

work in close conjunction with surgeons in other specialties, particularly neurosurgery, otolaryngology, 

oral maxillofacial surgery, and facial plastic surgery.

Case Studies

Case 1

A 26-year-old male enlisted soldier arrived intubated at a Level III hospital after sustaining a blast injury 

to his head and face from an IED. Examination of his right eye revealed a large perilimbal scleral 

laceration with uveal prolapse and a large complex laceration to his right upper eyelid and brow (Fig. 

33). His left eye was markedly proptotic and resistant to retropulsion, with marked upper eyelid edema 

and ecchymosis, a mid-dilated non-reactive pupil, and inferior hemorrhagic chemosis (Fig. 34). Based 

Figure 33. Preoperative photograph of a combat casualty following blast 

injury to the head and face from an IED.

Figure 34. Left eye proptosis, lid ecchymosis, hemorrhagic chemosis, 

and mid-dilated pupil indicative of retrobulbar hemorrhage. Lateral 

canthotomy and inferior cantholysis have been performed.
334 | Ocular Trauma

on these clinical findings, a left orbital compartment 

syndrome was suspected and a lateral canthotomy 

and inferior cantholysis were immediately performed 

in the emergency room. Subsequent CT scan revealed 

a misshapened right globe with lens disruption and 

vitreous hemorrhage, fractures of both ethmoid 

sinuses with a metallic foreign body and retrobulbar 

hemorrhage in the left orbit, fractures of both frontal 

sinuses, and a penetrating injury of the right frontal 

lobe (Fig. 35). 

The patient was emergently taken to the operating 

room, where a craniotomy was performed with a 

partial right frontal lobectomy, cranialization of 

the frontal sinuses, and reconstruction of the floor 

of the anterior cranial fossa with titanium mesh, 

fibrin tissue sealant, and a pericranial graft (Fig. 36). Attention was then turned to the right eye, where a 25 

mm scleral laceration was repaired with 8-0 nylon sutures after repositing the prolapsed ciliary body back 

into the globe (Fig. 37). The right upper lid and brow laceration were then addressed (Fig. 38). A lateral 

canthotomy and superior cantholysis were first performed in order to reduce the tension on the eyelid 

reconstruction and prevent undue pressure on the freshly repaired globe. The tarsus was then repaired with 

interrupted 6-0 polyglactin sutures, taking 90 percent-thickness bites of the tarsus and tying the knots on 

the anterior side. The lid margin was approximated at the gray line and lash line with 6-0 silk sutures. The 

remainder of the upper lid and brow laceration was repaired in layers with deep 5-0 polydiaxanone sutures 

Figure 35. Computed tomography image showing: (Left) Severe bilateral frontal sinus fractures and frontal lobe injury. (Right) Deformed right globe 

with intraocular hemorrhage, bilateral ethmoid fractures, and left retrobulbar hemorrhage with intraorbital foreign body. The foreign body has passed 

through the right orbit and both ethmoid sinuses and entered the left orbit.

Figure 36. Intraoperative view of frontal craniotomy showing bilateral 

frontal sinus cranialization and repair of floor of anterior cranial fossa.
Ocular Trauma | 335

Figure 37. Intraoperative photograph of right globe before (Left) and after (Right) scleral laceration repair. Note the prolapsed ciliary body.

Figure 38. Repair of complex right upper lid and brow laceration: (Middle Left) View of defect. (Middle Right) Right lateral canthotomy and 

superior cantholysis. (Bottom Left) Repair of upper tarsus. (Bottom Right) Completed repair of right upper lid and eyebrow.
336 | Ocular Trauma

and interrupted 5-0 Prolene® skin sutures, taking 

care to properly align the brow hairs. Following 

surgery, the patient was promptly evacuated out-oftheater and subsequently received follow-up care at 

a Level V facility. His blind painful right eye was 

enucleated within two weeks of the injury.

This case demonstrates the complexity of the head 

and facial injuries that are often seen concomitantly 

with ocular combat injuries. The vision-threatening 

orbital compartment syndrome of the left eye 

was quickly diagnosed based on clinical findings 

in the absence of radiographic confirmation 

and appropriately treated with canthotomy and 

cantholysis. Surgical intervention proceeded in an 

orderly fashion, dealing with the intracranial injury 

first, followed by the ruptured globe repair, and finally the eyelid and brow laceration repair. Removal of 

the left orbital metallic foreign body was not attempted, as it posed no immediate risk to the globe and very 

little risk of long-term complication.

Case 2

This 24-year-old male enlisted soldier was injured when a rocket-propelled grenade struck the windshield 

of his vehicle. Upon evaluation at the Level III hospital, it was apparent that he had sustained multiple glass 

foreign bodies to his face (Fig. 39). On CT scan, two IOFBs were present in the left eye, along with multiple 

Figure 39. Photograph showing multiple punctate facial lacerations 

caused by glass foreign bodies.

Figure 40. Preoperative CT scan showing glass foreign bodies in the anterior segment (Left) and posterior segment (Right) of the left eye. Note multiple 

additional soft-tissue and subconjunctival foreign bodies.
Ocular Trauma | 337

bilateral subconjunctival foreign bodies (Fig. 40). One of the foreign bodies was located in the anterior 

segment, and the other was in the posterior segment near the posterior pole. The patient was taken to 

the operating room, where the anterior chamber foreign body was easily removed through the corneal 

laceration it had created. The curvilinear inferotemporal laceration was repaired with multiple 10-0 

nylon sutures. The second foreign body had entered the eye through the inferonasal cornea, perforated 

the iris and crystalline lens, and come to rest in the vitreous cavity just over the macula. The resulting 

stellate corneal laceration, although smaller than the first laceration, proved much more difficult to repair. 

A watertight closure could not be achieved with multiple 10-0 nylon sutures placed at all angles across the 

wound. Thus, a plug of cyanoacrylate glue was placed over the suture scaffold, with the aid of viscoelastic 

in the anterior chamber to prevent aqueous leakage (Figs. 41 and 42). Once a watertight seal was obtained, 

a bandage contact lens was placed. No attempt was made to retrieve the posterior segment foreign body. 

Prophylactic topical and intravenous fluoroquinolones were administered. No intravitreal antibiotics were 

used. The patient was evacuated to a Level V hospital, where his traumatic cataract was extracted and the 

retained foreign body was successfully removed by a retina specialist (Fig. 43). Visual acuity at last known 

follow-up was 20/25 with an aphakic rigid gas-permeable contact lens.

This case illustrates the management of corneal lacerations and IOFBs. The size of the corneal laceration 

does not always correlate with the difficulty of wound repair, and cyanoacrylate glue can be a valuable 

tool when sutures alone are inadequate in achieving a watertight closure. Foreign bodies in the anterior 

segment can often be safely removed, but removal of posterior segment foreign bodies should be deferred 

to a vitreoretinal specialist at Level IV or V facilities.

Figure 41. Intraoperative photos before (Left) and after (Right) repair of two separate corneal lacerations, left eye. Note the cyanoacrylate glue plug 

over the inferonasal laceration, which obscures the underlying 10-0 nylon sutures.
338 | Ocular Trauma

Figure 42. (Top Right) Anterior segment and subconjunctival foreign 

bodies after removal.

Figure 43. Intraoperative photographs showing removal of posterior segment foreign body at Level V hospital: (Middle Left) IOFB being grasped 

with basket forceps and (Middle Right) removed through a scleral tunnel incision. (Bottom Left) IOFB after removal. (Bottom Right) Slit-lamp 

photograph at four-month postoperative visit. Images courtesy of Eric D. Weichel, M.D.
Ocular Trauma | 339

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20. Talbot EM. A simple test to diagnose iritis. Br J Med 1987;295(6602):812-813.

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22. Spraul CW, Grossniklaus HE. Vitreous hemorrhage. Surv Ophthalmol 1997;42(1):3-39.

23. Olsen TW, Chang TS, Sternberg P Jr. Retinal detachments associated with blunt trauma. Semin 

Ophthalmol 1995;10(1):17-27.

24. Berlin R. Zur sogenannten commotio retinae. Klin Monatsbl Augenheilkd 1873;11:42-78.

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26. Kuhn F, Maisiak R, Mann L, et al. The Ocular Trauma Score (OTS). Ophthalmol Clin North Am 

2002;15(2):163-165.

27. Weichel ED, Colyer MH, Ludlow SE, et al. Combat ocular trauma visual outcomes during operations 

Iraqi and enduring freedom. Ophthalmology 2008; 115(12):2235-2245.

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285.

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31. Lincoff H, Weinberger D, Stergiu P. Air travel with intraocular gas. II. Clinical considerations. Arch 

Ophthalmol 1989;107(6):907-910.

32. Thompson JT. The absorption of mixtures of air and perfluoropropane after pars plana vitrectomy. 
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Arch Ophthalmol 1992;110(11):1594-1597.

33. Duch-Samper AM, Chaqués-Alepuz V, Menezo JL, et al. Endophthalmitis following open-globe injuries. 

Curr Opin Ophthalmol 1998;9(3):III:59-65.

34. Mittra RA, Mieler WF. Controversies in the management of open-globe injuries involving the posterior 

segment. Surv Ophthalmol 1999;44(3):215-225.

35. Colyer MH, Weber ED, Weichel ED, et al. Delayed intraocular foreign body removal without 

endophthalmitis during Operations Iraqi Freedom and Enduring Freedom. Ophthalmology 2007;114(8):

1439-1447.

36. Albert DM, Diaz-Rohena R. A historical review of sympathetic ophthalmia and its epidemiology. Surv 

Ophthalmol 1989;34(1):1-14.

37. Ward TP. Sympathetic ophthalmia. In Thach AB, ed. Ophthalmic Care of the Combat Casualty. 

Washington, DC: Borden Institute, Walter Reed Army Medical Center; 2003. p. 265-279.

38. DeBacker CM, Holck DEE. Enucleation in orbital trauma. In: Holck DEE, Ng JD, editors. Evaluation 

and treatment of orbital fractures: a multidisciplinary approach. 2nd ed. Philadelphia: Elsevier Saunders; 

2006. p. 365-368.

39. Kaltreider SA, Lucarelli MJ. A simple algorithm for selection of implant size for enucleation and 

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40. Nasr AM, Haik BG, Fleming JC, et al. Penetrating orbital injury with organic foreign bodies. 

Ophthalmology 1999;106(3):523-532.

41. Finklestein M, Legmann A, Rubin PA. Projectile metallic foreign bodies in the orbit: a retrospective 

study of epidemiologic factors, management, and outcomes. Ophthalmology 1997;104(1):96-103.

42. Khani SC, Mukai S. Posterior segment intraocular foreign bodies. Int Ophthalmol Clin 1995;35(1):151-

161.

43. Punnonen E, Laatikainen L. Prognosis of perforating eye injuries with intraocular foreign bodies. Acta 

Ophthalmol (Copenh) 1989;67(5):483-491.

44. Packer AJ. Ocular trauma. Primary Care 1982;9(4):777-792.

45. Cohen EJ, Rapuano CL. Trauma. In: Cullom RD, Chang B, editors. The Wills eye manual: office and 

emergency room diagnosis and treatment of eye disease. 2nd ed. Philadelphia, PA: JB Lippincott; 1994. p. 

27.

46. Fry HJ. Orbital decompression after facial fractures. Med J Aust 1967;1(6):264-266.
342 | Ocular Trauma

47. Hislop WS, Dutton GN, Douglas PS. Treatment of retrobulbar haemorrhage in accident and emergency 

departments. Br J Oral Maxillofac Surg 1996;34(4):289-292.

48. Hayreh SS, Kolder HE, Weingeist TA. Central retinal artery occlusion and retinal tolerance time. 

Ophthalmology 1980;87(1):75-78.

49. Burkat CN, Lemke BN. Retrobulbar hemorrhage: inferolateral anterior orbitotomy for emergent 

management. Arch Ophthalmol 2005;123(9):1260-1262.

50. Ho VH, Wilson MW, Fleming JC, et al. Retained intraorbital foreign bodies. Ophthal Plas Reconstr 

Surg 2004;20(3):232-236.

51. Cho RI, Kahana A, Patel B, et al. Intraoperative fluoroscopy-guided removal of orbital foreign bodies. 

Ophthal Plast Reconstr Surg 2009;25(3):215-218.

52. Pfister RR. Chemical injuries of the eye. Ophthalmology 1983;90(10):1246-1253.

53. Grant WM. Toxicology of the eye. 3rd ed. Springfield, MA: Charles C Thomas; 1986.

54. Herr RO, White GL Jr, Bernhisel K, et al. Clinical comparison of ocular irrigation fluids following 

chemical injury. Am J Emerg Med 1991;9(3):228-231.

55. Wagoner MD. Chemical injuries of the eye: current concepts of pathophysiology and therapy. Survey 

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56. Shoff WH, Sheperd SM. Ocular trauma. In: Ferrera PC, Colucciello SA, Marx JA, et al, editors. 

Trauma management: an emergency medicine approach. 1st ed. St Louis, MO: Mosby; 2001. p. 197-217.

57. Villarreal PM. Traumatic optic neuropathy. A case report. Int J Oral Maxillofac Surg 2000;29(1):29-

31.

58. Wang BH, Robertson BC, Girotto JA, et al. Traumatic optic neuropathy: a review of 61 patients. Plast 

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59. Levin LA, Beck RW, Joseph MP, et al. The treatment of traumatic optic neuropathy: The International 

Optic Nerve Trauma Study. Ophthalmology 1999;106(7):1268-1277.
Chapter 8

TRAUMATIC

BRAIN INJURY

Contributing Authors

Scott A. Marshall, MD

 Randy Bell, MD

 Rocco A. Armonda, MD, LTC, MC, US Army

 Eric Savitsky, MD

 Geoffrey S.F. Ling, MD, PhD, COL, MC, US Army
All figures and tables included in this chapter have been used with permission from Pelagique, LLC, the 

UCLA Center for International Medicine, and/or the authors, unless otherwise noted.

Use of imagery from the Defense Imagery Management Operations Center (DIMOC) does not imply or 

constitute Department of Defense (DOD) endorsement of this company, its products, or services.

Disclaimer

The opinions and views expressed herein belong solely to those of the authors. They are not nor should 

they be implied as being endorsed by the United States Uniformed Services University of the Health 

Sciences, Department of the Army, Department of the Navy, Department of the Air Force, Department of 

Defense, or any other branch of the federal government.
Traumatic Brain Injury | 345

Table of Contents

Introduction........................................................................................................ 347

Pathophysiology of Traumatic Brain Injury ............................................................ 348

Closed Head Injury.............................................................................................. 351

Mild, Moderate, and Severe Brain Injury................................................................ 351

Blast Traumatic Brain Injury ..........................................................................................353

Second Impact Syndrome ................................................................................................354

Focal versus Diffuse TBI...................................................................................................355

Epidural and Subdural Hematomas................................................................................355

Subdural Hematomas........................................................................................................355

Epidural Hematomas.........................................................................................................356

Traumatic Intracerebral Hemorrhage ............................................................................357

Herniation Syndromes .....................................................................................................358

Subfalcine, Central, and Uncal Herniation.......................................................................358

Transcranial and Paradoxical Herniation..........................................................................360

Tonsillar and Upward Herniation .....................................................................................360

Penetrating Traumatic Brain Injury ....................................................................... 361

Infection and Cerebrospinal Fluid Leaks.........................................................................362

Neuroimaging in Penetrating TBI....................................................................................362

Traumatic Brain Injury Management..................................................................... 363

Initial Management (Primary Survey).............................................................................363

Airway and Breathing Management..................................................................................363

Head Position.....................................................................................................................366

Secondary Survey...............................................................................................................366

TBI Management Guidelines and Options ......................................................................367

Airway Management and Ventilation................................................................................367

Role of Hyperventilation ...................................................................................................367

Hemodynamic Management.............................................................................................368

Goals for ICP Management...............................................................................................369

Intracranial Pressure and External Ventricular Drains .....................................................369

Hypertonic Saline and Other Medical ICP Management Options ..................................370

Role of Mannitol............................................................................................................370

Hypertonic Saline (HTS) ................................................................................................372

Other Pharmacologic Agents to Reduce ICP....................................................................373

Induced Hypothermia .......................................................................................................374

Decompressive Craniectomy .............................................................................................374

Current Use of Decompressive Craniectomy with Intractable Intracranial Hypertension ..........375

Anticonvulsant Use in TBI ................................................................................................375

Critical Care and Air Evacuation ......................................................................................376
346 | Traumatic Brain Injury

Other Management Considerations ....................................................................... 377

Summary............................................................................................................ 378

References .......................................................................................................... 379
Traumatic Brain Injury | 347

Introduction

Traumatic brain injury (TBI) occurs whenever a physical force that impacts the head leads to neuropathology. 

This can be as simple as a minor laceration from a small fragment to decapitation. Of all the injuries to the 

head that are concerning, the most worrisome is TBI.

Traumatic brain injury is a leading cause of death and disability from trauma. In the United States (US), 

more than 50,000 patients die from TBI each year, accounting for almost one-third of all civilian traumarelated deaths.1

 Most of these injuries are a direct result of falls, motor vehicle accidents, and assaults. The 

cost for direct TBI medical care is estimated at more than $50 billion per year.2,3 The majority of victims of 

both civilian and military TBI are young male adults.4,5 The societal burden of TBI is staggering. Traumatic 

brain injury accounts for the greatest number of years lived with trauma-related disability.5 Many victims 

of TBI are young and thus require extended rehabilitation and reintegration. Many will likely require 

medical discharge from the armed forces. The young age of many TBI victims is especially unfortunate as 

these patients may no longer be productive members of society at a time in their life when their potential 

contributions are greatest.4

 

Figure 1. A US casualty who sustained explosive blast TBI. 
348 | Traumatic Brain Injury

Traumatic brain injury is a common battle-related injury. In the wars of the 20th century, approximately 

15 to 20 percent of injuries incurred in combat involved the head.6 Evidence suggests that this is also the 

case for casualties sustained in the recent wars, Operation Enduring Freedom (OEF) in Afghanistan and 

Operation Iraqi Freedom (OIF) (Fig. 1).7 Some have speculated that a greater percentage of patients from 

these recent wars have suffered head injury than in prior conflicts.8 This increase in prevalence is thought 

to be a paradoxical consequence of the remarkable improvements in medical care and protective body 

armor.9 These advances have resulted in the lowest killed-to-wounded ratio in modern warfare.10 The 

paradox is that with more wounded warfighters surviving, more are left with severe wounds, especially to 

less protected anatomical regions such as head and extremities. Thus, TBI, traumatic amputations, and 

other such injuries are disproportionally represented. Specifically, TBI resulting from explosive blast has 

become very prominent in the past several years.11,12,13 

Traumatic brain injury is a common battle-related injury. Treatment goals in the first 72 hours of care 

for the injured patient with TBI are to provide clinical stability, arrest any element of ongoing injury, 

preserve neurological function, and prevent medical complications secondary to multisystem trauma.

With advances in battlefield or prehospital clinical management of combat casualties, the outcomes of 

severe conditions such as TBI have improved. Critical elements include improved training and resources 

for far-forward medical providers, a highly efficient modern triage and evacuation system, and dramatically 

shortened length of stay in-theater prior to definitive care in the US.14 There is evidence that the vast 

majority of fatal injuries incurred in combat result from injuries that would be nonsurvivable in any 

setting.15 Thus, those who can be saved are being saved, even under the austere conditions of war. However, 

as long as there are survivors left with chronic disabilities, there is opportunity for improvements in medical 

care.

Treatment goals in the first 72 hours of care for the injured patient with TBI are to provide clinical stability, 

arrest any element of ongoing injury, preserve neurological function, and prevent medical complications 

secondary to severe trauma. Initially, brain injury must be suspected, and this must be followed by 

appropriate field management. Next, TBI patients should be triaged and evacuated to a Level III facility with 

advanced care capability, such as neurosurgery and neurointensive care. Subsequently, as appropriate, TBI 

patients are evacuated from theater to the continental US (CONUS) for advanced definitive treatment. 

The purpose of this review is to outline the intricacies common to both military and civilian TBI, discuss 

different forms of closed and penetrating TBI, and expand upon the distinction between primary and 

secondary brain injuries. A review of the literature outlining various treatment algorithms, both medical 

and surgical, will also be provided.

Pathophysiology of Traumatic Brain Injury

Primary brain injury is tissue destruction that occurs as a direct result of a physiologic trauma. This leads 

to near immediate macroscopic and cellular pathological changes. The severity and location of the primary 

brain injury will dictate the patient’s immediate level of consciousness, mental status, and focal neurologic 

signs. There is no available therapy for primary brain injury at present. The focus of TBI treatment is 

minimizing secondary brain injury. Secondary brain injury refers to the consequences of pathological 
Traumatic Brain Injury | 349

processes that begin immediately after the primary brain injury. Secondary brain injury continues for an 

indefinite period and can cause further dysfunction and death of neurons and glial supporting structures.

The immediate goal of TBI treatment is minimizing secondary brain injury by optimizing cerebral 

blood flow. This involves mitigating elevations in ICP and addressing traumatic intracranial 

hemorrhage, cerebral edema, and metabolic derangements. 

Quantifiably, it is widely held that most of the overall brain injury may be ascribable to secondary injury 

processes. Mechanisms thought to be involved in secondary brain injury include hypoxia, ischemia, free 

radicals, release of neurotransmitters and intracellular elements (e.g., calcium), temperature dysregulation, 

intracranial pressure alterations, gene activation, mitochondrial dysfunction, and inflammation.5,16 Among 

these, hypoperfusion is the main cause of poor outcomes.5,17 This is due to the susceptibility of injured neural 

tissue to ischemia, as it is in a hypermetabolic state following injury. This is exacerbated by dysfunction 

of cerebral vascular autoregulation so that there is insufficient vascular compensation for compromised 

cerebral perfusion. Particularly susceptible areas include the hippocampus and border zone or watershed 

regions such as the high parietal region. It has been hypothesized that delayed neurological dysfunction 

can often be attributed to the effects of delayed ischemia.16,18 To this effect, there is evidence that a single 

episode of hypotension with systolic blood pressures falling below 90 mm Hg is associated with poor 

outcomes in severe TBI.16,18,19 Hypoperfusion itself may result in diffuse microvascular damage and loss 

of blood-brain barrier integrity. This microvascular damage contributes to the prominent pattern of 

vasogenic edema observed after TBI.20 Current guidelines likewise caution of the dangers of hypocapnea 

and hypoxia as markers for poor outcomes following TBI.16,18,19,21

Hypotension (systolic blood pressure less than 90 mm Hg) leading to cerebral hypoperfusion has been 

linked to poor outcomes following severe TBI.

Figure 2. Cerebral blood flow is well-autoregulated when mean arterial pressures are between 50 to 150 mm Hg.

Mean arterial pressure (mm Hg)

Cerebral blood o

w

(mL/100 g/min)

100

50

0

0 50 100 150
350 | Traumatic Brain Injury

Research attempts at developing therapeutic strategies have focused on secondary brain injury processes 

while public health and technological measures have attempted to prevent primary brain injury. 

Currently, clinical management centers on supportive measures to mitigate secondary brain injury 

with particular emphasis on maintaining cerebral perfusion pressure (CPP) and tissue oxygenation, 

minimizing intracranial pressure (ICP) fluctuations, and treatment of cerebral edema. Various alternative 

experimental pharmacological therapies (e.g., free radical scavengers) and neuroprotective strategies have 

been investigated (e.g., therapeutic hypothermia). Unfortunately, none of these experimental therapies or 

strategies has been proven to effectively mitigate secondary brain injury.22

With regard to cerebral autoregulation, cerebral blood flow (normal values 50 to 65 milliliters [ml] per 100 

grams of brain tissue per minute) is well-autoregulated when mean arterial pressures (MAPs) are between 

50 to 150 mm Hg (Fig. 2). Cerebral blood flow (CBF) is a function of cerebral vascular resistance (CVR) and 

cerebral perfusion pressure. Since cerebral vascular resistance is proportional to the fourth power of blood 

vessel radius, even small changes in cerebral vessel caliber translates into significant alterations in CBF. 

Cerebral perfusion pressure is the pressure gradient driving CBF, and is defined as the difference between 

mean arterial pressure and ICP (Equation 1). 

Equation 1: CPP = MAP – ICP 

Equation 2: CBF = CPP/CVR 

Primary brain injuries often lead to alterations in the brain’s ability to autoregulate CBF even within 

the normal autoregulatory range.23 This may further worsen secondary brain injury, in that loss of 

autoregulatory control may lead to increased CBF with changes in blood pressure and resultant increased 

intracranial blood volume and disruption of the blood-brain barrier with vasogenic brain edema formation. 

This may ultimately result in elevated ICP. Alternatively, cerebral ischemia may result if CBF is too low 

(i.e., less than 20 ml per 100 grams of brain tissue per minute), and the neurovasculature is unable to 

compensate by autoregulatory vessel dilation to maintain CBF.

It should be emphasized that hypercapnia is a potent vasodilator of cerebral microvasculature, as is 

hypoxemia. These states may result in cerebral hyperemia and exacerbation of preexisting elevated ICP.24

Hyperventilation with resultant hypocapnia has a profound effect in causing cerebral microvasculature 

vasoconstriction.25 This microvasculature vasoconstrictive response to hypocapnia is often well-preserved, 

even in the setting of devastating brain injury. Hyperventilation leading to hypocapnia will lead to a 

progressive decrease in ICP.25 Loss of ICP responsiveness to hypocapnia is a poor prognostic sign. 

Hypocapnia will also result in decreases in CBF; every one mm Hg decrease in the partial pressure of 

carbon dioxide (PCO2

) will result in a proportionate three percent decrease in CBF.26,27 It is important to 

understand the relationship between hypocapnia and CBF, as well as how hyperventilation and hypocapnia 

relate to ICP.

Hyperventilation leading to hypocapnia will cause a progressive decrease in ICP. Loss of ICP responsiveness 

to hypocapnia is a poor prognostic sign.

Delayed cerebral swelling is the major cause of raised ICP and death. This is often the result of secondary 

brain injury. Persistent bleeding from damaged brain tissue, contusions, impaired autoregulation, and 
Traumatic Brain Injury | 351

breakdown of the blood-brain barrier may all 

contribute to brain swelling (Fig. 3).28 This swelling 

with resultant compression and distortion of brain 

parenchyma further exacerbates the injury cascade. 

The Monroe-Kellie doctrine is a convenient method 

of understanding factors leading to elevated 

intracranial pressures. It postulates that due to 

the fixed size of the intracranial compartment, an 

increase in volume of any of the three intracranial 

constituents (blood, brain, and cerebrospinal fluid) 

must be compensated by a decrease in one or more 

of the other constituents, or ICP will rise.29,30 

Systemic complications directly related to severe 

head injuries are not uncommon. Neurogenic 

pulmonary edema is a well-described phenomenon 

associated with secondary brain injury.31,32 Primary 

myocardial ischemia and dysrhythmias are often 

seen in the setting of secondary brain injury. Although the exact mechanisms are still unclear, it is theorized 

that these processes are the result of greatly elevated circulating catecholamine levels.33 Brain tissue is also rich 

in thromboplastins, and release of these in secondary brain injury patients may result in the development 

of a coagulopathy.34 The syndromes of cerebral salt wasting and the syndrome of inappropriate antidiuretic 

hormone secretion (SIADH) are also seen in the setting of secondary brain injury.35,36

Closed Head Injury

Head injury can be broadly classified into closed versus penetrating head injury (Figs. 4 and 5). With closed 

head injury, the skull and overlying scalp remain intact. In closed head injury, direct impact of brain 

against the skull and shearing force upon neurovascular structures from rotational forces result in cell 

damage at the cell body and axonal level. Among civilians in the US, most closed head injury is due to motor 

vehicle accidents, but other causes include falls, sporting event injuries, and assault.37 In studies analyzing 

US casualties in OIF, some have reported between 5 and 10 percent of all casualties sustained a closed 

head injury.38 Neuronal structures strike the skull in both the direct and opposite planes of motion leading 

to a coup and contrecoup lesion pattern. Contusion or other injury to the brain is seen deep to the site of 

skull impact, as well as 180 degrees opposite the site of impact (Fig. 6). If there is a rotational component, 

structures will torque and twist, and thus shearing can occur. This results in diffuse axonal injury seen 

radiographically as punctuate hemorrhages on computed tomography (CT) or magnetic resonance imaging 

(MRI) at interfaces of grey and white matter. Patients with diffuse axonal injury are often in a coma after 

their trauma without elevations in ICP and often have unsatisfactory clinical outcomes.5

Mild, Moderate, and Severe Brain Injury

The spectrum of TBI is mild, moderate, or severe. Severity is based largely on the presenting Glasgow Coma 

Figure 3. Persistent bleeding from damaged brain tissue, contusions, 

impaired autoregulation, and breakdown of the blood-brain barrier may 

all contribute to brain swelling. Image courtesy of Brian J. Eastridge, 

MD, FACS, COL, US Army
352 | Traumatic Brain Injury

Figure 4. (Top) The distinction between closed head injury and penetrating head injury may be difficult to make based on neurological findings. Here, 

one of the scalp wounds denoted by the arrows, was an entry point for a penetrating fragment that caused brain injury. Image courtesy of the Borden 

Institute, Office of The Surgeon General, Washington, DC.

Figure 5. (Bottom) Axial CT images demonstrate a right frontal extracranial fragment, traumatic subarachnoid hemorrhage, and an intracranial 

fragment. Image courtesy of the Borden Institute, Office of The Surgeon General, Washington, DC.
Traumatic Brain Injury | 353

Scale (GCS) score (Table 1). These classification 

categories have prognostic, monitoring, and 

treatment implications.39 Patients with mild TBI 

have an admission GCS score of greater than 

or equal to 13, with lower scores in this category 

representing more concerning injury. Mild TBI 

may often be referred to as concussion. These 

patients have experienced a brief (less than 30 

min), if any, loss of consciousness or alteration in 

consciousness (less than 24 hrs), and presenting 

complaints include headache, confusion, and 

amnesia.40 The spectrum of presentation and 

sequelae of mild TBI is broad and usually transient. 

When symptoms persist for three months or longer, 

postconcussion syndrome is diagnosed.41 Moderate 

TBI is defined by an admission GCS score of 9 to 

12 and is usually associated with prolonged loss 

of consciousness, abnormal neuroimaging, and 

neurological deficit.42 Injured service members 

with moderate TBI will likely require rapid removal 

from forward areas, subsequent hospitalization, 

and may need neurosurgical intervention. Patients 

with GCS scores of 8 or less have significant neurological injury and are classified as having severe TBI. 

Typically, they have abnormal neuroimaging such as a CT scan demonstrating intracranial hemorrhage, 

often associated with a skull fracture.42 These patients require rapid evacuation to a Level III facility 

and admission to the intensive care unit (ICU) for immediate airway control, breathing support with 

mechanical ventilation, neurosurgical evaluation, and ICP monitoring.

Blast Traumatic Brain Injury 

Explosive blast TBI refers to TBI resulting from explosive blast exposure, and is presently classified as a 

subtype of TBI. The improvised explosive device (IED) is commonly implicated in explosive blast TBI in 

OEF and OIF.5 Blast TBI may occur in isolation or may also be accompanied by closed head injury 

and/or penetrating TBI. The mechanism responsible for causing explosive blast TBI is unclear. The 

Figure 6. Coup and contrecoup patterns of brain injury. An impact to the 

right parietal region has caused a left frontal intraparenchymal contusion.

Table 1. Severity of TBI is based largely on the presenting GCS score. Glasgow Coma Scale scores carry prognostic, monitoring, and treatment 

implications.

Best Eye Opening (E) Best Verbal Response (V) Best Motor Response (M)

Follows commands 6

Oriented, alert 5 Localizes to pain 5

Eyes open spontaneously 4 Confused, appropriate 4 Withdrawal to pain 4

Eyes open to speech 3 Disoriented, inappropriate 3 Flexor posturing 3

Eyes open to pain 2 Incomprehensible speech 2 Extensor posturing 2

No response 1 No response 1 No response 1
354 | Traumatic Brain Injury

overpressure generated by the explosive device is the leading suspect, but other elements of the violent 

explosive event, such as toxins or electromagnetic pulses, might also potentially contribute.43 Once the 

physical force couples to brain, the TBI itself results from a variety of local pathological effects, including 

impaired cerebral vascular homeostasis and formation of reactive oxygen species.44 A recent concern 

is the probable large number of soldiers who have been exposed to blast and suffered a blast TBI but 

did not have their injury recognized or treated. This has resulted in concern over the development of 

psychiatric syndromes that may often be seen with blast TBI, such as post-traumatic stress disorder, anxiety, 

or depression. This is currently under study and the subject of much scientific and political debate.38,45,46,47

Blast TBI is a recently recognized condition for which additional preclinical and clinical research is 

needed.5 

Psychiatric conditions such as post-traumatic stress disorder, anxiety, or depression may be seen following 

blast TBI.

Second Impact Syndrome

An important caveat to the management of TBI is minimizing the risk of second impact syndrome. 

Though relatively uncommon, it can have devastating consequences. Second impact syndrome refers to 

a subsequent head injury during a recovery period from TBI that may result in significant worsening of 

the initial neurotrauma.48 This has been best described among adolescents and younger TBI patients. The 

mechanism underlying second impact syndrome is not fully understood, and the clinical implications of 

second impact syndrome continues to be debated.49,50 It is thought that impaired cerebral autoregulation, 

diffuse cerebral edema, and intracranial hypertension all play a role. The high mortality of second impact 

syndrome, up to 50 percent, is the most concerning aspect.48 The American Academy of Neurology (AAN) 

guidelines for recommended periods of TBI recovery are often used to determine when soldiers with head 

injury may return to duty (Table 2).40 The cited AAN guidelines are currently under review and will be 

updated and published in late 2011.

Symptom Complex First Concussion Second Concussion

Grade I: Transient confusion or 

cognitive impairment lasting less 

than 15 minutes without LOC

Remove from source of injury; 

frequent reevaluation; return to 

duty if normal cognition in 15 

minutes

Return to duty in one week if no 

residual symptoms with physical 

stress or exercise

Grade II: Grade I symptoms but 

lasting greater than 15 minutes 

without LOC

Remove from source of injury; 

frequent reevaluation; no duty 

for one week during which 

medical observation continues

Return to duty in two weeks 

if no residual symptoms with 

physical stress or exercise

Grade III: Any degree of 

cognitive symptoms with LOC

Remove from source of injury; 

trained neurologic evaluation; 

consider imaging; return to duty 

in two weeks if asymptomatic 

with physical stress or exercise

Return to duty in one month 

if no residual symptoms with 

physical stress or exercise

Table 2. Return-to-duty guidelines following concussion. LOC, loss of conciousness. Adapted from the American Academy of Neurology Practice 

Parameter on Management of Concussions.40
Traumatic Brain Injury | 355

Second impact syndrome refers to a subsequent head injury during a recovery period from TBI that 

may result in significant worsening of the initial neurotrauma.

Focal versus Diffuse TBI

Closed TBI may be further classified as focal or diffuse. Focal injuries occur at the site of impact (coup 

injury), with neurological damage localized to those areas. This can occur wherever force is transmitted 

through the skull. The orbitofrontal and anterior temporal lobes are commonly affected in focal contrecoup 

injury. This is due to the tendency for head trauma to occur in an anterior-to-posterior direction causing 

the brain to move along those force vectors. As it moves, the brain traverses over the rough surface of the 

petrous ridge and anterior cranial fossa at the skull base leading to focal injury. 

Diffuse injuries occur without the brain impacting a solid structure. This type of injury is caused by brain 

rotation. Because the brain is tethered by the brainstem, a severe acceleration-deceleration will cause 

it to rotate about this tethered axis. Axons in cerebral white matter will be disrupted, leading to axonal 

swelling and subsequent axonal rupture.51 This condition is known as diffuse axonal injury. It is associated 

with severe neurological deficits and encephalopathy, including coma. The CT appearance of this type of 

injury can be delayed by up to 12 hours following initial trauma.20 Recent evidence also suggests that the 

incidence of diffuse axonal injury may be higher with forces occurring in a lateral orientation, as opposed 

to a frontal or oblique impact common in closed head injury.52

Epidural and Subdural Hematomas

In both focal and diffuse TBI, one must remain vigilant for intracranial hematomas. Such hemorrhages 

occur immediately or can be delayed as long as several days after the inciting trauma.16,18 The highest risk 

of intracranial hematoma is within the first six to nine hours after injury.53

Subdural Hematomas

Subdural hematomas are frequent occurrences in civilian neurosurgical practice (Fig. 7). Subdural 

hematomas account for over 15 percent of combat-related head injuries.11 These lesions often require 

neurosurgical evacuation. The need for surgery is predicated on the clinical status of the patient and 

radiological appearance of the subdural hematoma. Subdural hematomas that require surgery are greater 

than 10 millimeters (mm) or cause more than five mm of midline shift with effacement of the basal 

cisterns. Other indications for surgery are a GCS score of 8 or less with enlarging intracranial lesions 

or deterioration in clinical exam.54 This approach must take into consideration circumstances where 

outcomes are decidedly unfavorable such as advanced age, hematoma volume greater than 90 milliliters, 

presenting GCS score of 3, and time to surgery more than six hours.55,56 There is conflicting evidence 

regarding optimal timing of evacuation, although most favor prompt evacuation once the indication 

exists.56,57,58 Smaller subdural hematomas may be managed conservatively utilizing close neurological 

monitoring and early follow-up neuroimaging.59 If there is concern that a lesion is enlarging, or that 

the patient’s neurologic exam may decline, then immediate transfer to a facility with neurosurgical and 

neurointensivist care is justified. In lieu of the ability to transfer, the placement of burr holes for the 

evacuation of a subdural hematoma by a general surgeon has been described (Fig. 8).60 Treacy et al. 

described a number of neurosurgical procedures (including burr holes) performed on patients in remote 

environments by general surgeons.60 Three hundred and five procedures were performed over a 12-year 
356 | Traumatic Brain Injury

period (including 130 craniotomies, 88 burr holes, 33 extraventricular drains, 25 elevations of fractures, 

four decompressive craniectomies, three posterior fossa craniotomies, and two decompressive frontal 

lobectomies) for an average of over 25 procedures per year.60 Outcomes for patients with epidural and 

chronic subdural hematomas were good, while poor outcomes were noted for patients with acute subdural 

and intracerebral hematomas.60

Operative management of subdural hematomas is indicated for bleeds greater than 10 millimeters, 

those causing more than five millimeters of midline shift with effacement of the basal cisterns, or a 

GCS score of 8 or less in the context of an enlarging intracranial lesion or deteriorating clinical exam.

Epidural Hematomas

Epidural hematomas are especially concerning, even in relatively asymptomatic patients.61 In one case 

series, epidural hematomas occurred in less than 5 percent of combat-related head injury cases.11 Classically, 

an epidural hematoma forms when a skull fracture occurs at the temporoparietal junction causing injury to 

the middle meningeal artery. Epidural hematomas have a distinctive convex lenticular appearance on CT 

imaging (Fig. 9). Epidural hematomas usually require neurosurgical intervention. Definitive indications for 

surgical evacuation include a GCS score less than 8 and a volume greater than 30 milliliters.62 An epidural 

hematoma with less than 30 milliliters of volume, less than 15 mm thick, and with no more than five 

mm of midline shift in a patient who lacks a focal deficit can be managed nonoperatively.62 However, as 

this lesion has a very high potential for progression, such patients must be followed closely with frequent 

neurological examination and serial CT imaging. A study of epidural hematoma patients with GCS score 

greater than or equal to 12 that did not meet criteria for surgery experienced an eventual surgery rate 

Figure 7. Acute subdural hematoma. Figure 8. Cranial landmarks and location for standard burr holes.

Image courtesy of the Borden Institute, Office of The Surgeon General, 

Washington, DC. Illustrator: Bruce Maston.

5–6 cm

1

cm

2 cm 4–5 cm

zygoma
Traumatic Brain Injury | 357

of less than 20 percent with no mortality.63 The presence of a skull fracture, a six-hour delay from injury 

to initial CT scan, or heterogeneous density of epidural hematoma did not influence the likelihood of 

requiring operative management.63

Epidural hematomas have a very high potential for progression. If managed nonoperatively, such patients 

must be followed closely with frequent neurological examination and serial CT imaging.

Traumatic Intracerebral Hemorrhage 

Of the many complications of TBI, the development of traumatic intracerebral hemorrhage is one of 

the most clinically devastating (Fig. 10).53,64 About 40 percent of traumatic intracerebral hemorrhages 

progress in size, and risk factors for enlargement include large initial size, presence of subdural hematoma, 

or associated subarachnoid hemorrhage.53 One must remain aware of the occurrence of delayed traumatic 

intracerebral hemorrhage, which can develop up to several days after the inciting trauma. These delayed 

intracerebral hemorrhages are noted on CT imaging following either focal or diffuse brain injury.16,18

More recent work has identified that CT progression to intracerebral hemorrhage associated with trauma 

is most likely to occur within six to nine hours after head injury.53 Thus, imaging follow-up in conjunction 

with ongoing neurologic evaluation and bedside clinical monitoring is critical.53 Indications for surgical 

evacuation of traumatic intracerebral hemorrhage include the presence of frontal or temporal lobe lesion 

greater than 50 milliliters, a GCS score of 6 to 8 with frontal or temporal lobe lesion greater than 20 

milliliters, effacement of basal cisterns, or midline shift greater than five mm.65 Traumatic intracerebral 

hemorrhage patients not meeting surgical criteria may be treated conservatively. This includes minimizing 

secondary brain injury measures, frequent neurological examinations, and repeated neuroimaging, as 

indicated. Eventual surgical evacuation is more likely for conservatively managed patients with worsening 

GCS scores, hematoma expansion greater than five milliliters or effacement of the basal cisterns.66 

Figure 9. (Above) Acute epidural hematoma.

Figure 10. (Right) Traumatic intracerebral hemorrhage.
358 | Traumatic Brain Injury

Another area of interest is the use of hemostatic agents to arrest ongoing traumatic intracerebral 

hemorrhage. If a traumatic intracerebral hemorrhage patient suffers from thrombocytopenia, platelet 

dysfunction, or coagulopathy, these factors must be corrected rapidly. However, recent trials with the use 

of recombinant factor VIIa (rFVIIa) for traumatic intracerebral hemorrhage have not shown mortality or 

outcome benefit with doses up to 200 micrograms per kilogram.67,68 

Herniation Syndromes

Patients with TBI and intracranial hypertension may progress to a cerebral herniation event. The skull 

is a fixed and rigid container almost completely filled with blood, brain, and cerebrospinal fluid (CSF). 

Any increase in volume from hemorrhage or edema is initially compensated by displacement of blood or 

CSF. When these compensatory mechanisms are exceeded, the brain will herniate out of the cranial vault, 

resulting in a variety of neurologic signs and symptoms (Fig. 11).

Subfalcine, Central, and Uncal Herniation

Subfalcine herniation is a lateral shift of one frontal lobe into the contralateral side and by default occurs 

with any degree of midline shift of the cerebral hemispheres. The most common clinical manifestations 

are increasing lethargy and occasionally neurological deficits related to compromised flow to one or both 

anterior cerebral arteries. Unilateral anterior cerebral artery compromise classically causes weakness of the 

contralateral lower extremity, although involvement of the proximal arm and shoulder is reported.69 

Uncal, or lateral transtentorial herniation, occurs 

when a supratentorial mass pushes the mesial 

temporal lobe and uncus anteriorly and downward 

through the tentorial opening between the ipsilateral 

aspect of the midbrain and the tentorium. This 

can result in the Kernohan’s notch phenomenon, 

with hemiparesis ipsilateral to the side of the 

supratentorial lesion, and is a potentially false 

localizing sign.69 Often, a unilaterally large pupil 

and ensuing third nerve palsy may herald this 

phenomenon. Radiographic findings of uncal 

herniation may be seen with resulting midbrain 

Duret hemorrhages and midbrain ischemia secondary to compromised blood flow to paramedian 

midbrain perforator vessels (Fig. 12).69 Duret 

hemorrhages are small linear hemorrhages along 

the midline of the brainstem and upper pons caused 

by traumatic caudal displacement of the brainstem. 

This is usually an ominous radiographic finding. 

Central herniation is downward movement of the 

brainstem by pressure from the supratentorial brain 

components. Early findings with central herniation 

include cranial nerve (CN) VI palsy manifesting 

Figure 11. Six types of brain herniation: (1) Uncal; (2) Central; 

(3) Subfalcine; (4) Transcranial/extracranial; (5) Upward (upward 

cerebellar or upward transtentorial); (6)Tonsillar (downward cerebellar).

4

2

6

5

1

3
Traumatic Brain Injury | 359

Figure 12. (Top Left) Uncal herniation on initial head CT image. (Top Right) Duret hemorrhages of the midbrain tegmentum on a CT image of 

the same patient days later. (Bottom Left) Duret hemorrhages seen on MRI image. (Bottom Right) Duret hemorrhages and ischemic change seen on 

MRI image of the central midbrain.
360 | Traumatic Brain Injury

as lateral gaze deficits, which can be unilateral or 

bilateral. Like uncal herniation, if this progresses, 

the clinical triad of a CN III palsy (including an 

ipsilateral nonreactive dilated pupil), coma, and 

posturing can occur.70 Occasionally, unilateral or 

bilateral posterior cerebral artery infarctions can 

occur with ongoing central or uncal herniation, due 

to compression of the posterior cerebral artery as it 

passes upwards over the tentorial notch.71 Without 

aggressive management, central herniation is fatal.

Transcranial and Paradoxical Herniation

Transcranial or extracranial herniation occurs when 

the brain breeches through a skull defect. Most 

commonly this occurs after craniectomy, as parts of 

the brain can shift through the surgical site (Fig. 13). 

This can occur in over 20 percent of postsurgical 

TBI patients.72 Essentially, it represents therapeutic 

decompression of intracranial hypertension. 

Untoward complications of extracranial herniation 

do occur, and are related to laceration of cerebral 

cortex and vascular compromise of venous drainage. Making larger rather than smaller craniectomies 

may minimize these complications.72 A less recognized phenomenon is paradoxical herniation, which has 

been reported during lumbar cistern drainage in the setting of a craniectomy. Paradoxical herniation is 

when there is downward movement of brain in the setting of an overall lowered intracranial pressure.73

Only a handful of cases of this type of herniation are reported, although this can also occur in the setting 

of sodium dysregulation and hypernatremia.74 Extracranial herniation may also result from primary 

penetrating injury. 

Tonsillar and Upward Herniation

Tonsillar herniation occurs from downward movement of the cerebellar tonsils into the foramen magnum 

and compression of the lower brainstem. It can result in sudden death from compression of medullary 

respiratory centers and blood pressure instability.69,71 Leading causes of this type of herniation are posterior 

fossa hematomas and obstruction of CSF outflow from the fourth ventricle.71 A posterior fossa hematoma, 

or any significant or increasing fourth ventricular dilation, distortion, or obliteration, requires urgent 

neurosurgical evaluation for possible intervention to include suboccipital craniectomy and placement of an 

extraventricular drain.

Upward herniation is upward movement of the brain through the tentorium into the cranium. It can cause 

brainstem compression and can occur with excessive CSF drainage from an extraventricular drain.75 The 

clinical presentation of upward herniation is not well-described, although as with all herniation syndromes, 

a decrease in mental status progressing to obtundation can be expected.

Figure 13. Extracranial herniation through craniectomy defect.
Traumatic Brain Injury | 361

Penetrating Traumatic Brain Injury

In penetrating TBI, the cranial vault is violated by a foreign body. Foreign bodies affecting soldiers in 

combat include shrapnel fragments and bullets of varying velocities (Fig. 14). Primary brain injury results 

from the projectile passing through the brain, damaging neural, vascular, and support structures along its 

tract. In addition to this damage, high-velocity supersonic projectiles can create a vacuum in their trail, 

giving rise to tissue cavitation. The rapid expansion and retraction of the vacuum cavity compresses and 

stretches neural and support structures, often tearing them. As the cavity may be many times larger than the 

projectile’s tract, injury is much more severe.76 

The majority of military penetrating TBI occurs from penetrating fragment injuries and not from fired 

bullets.77 Historically, penetrating fragment-related TBI had a significantly lower overall mortality than 

military gunshot wound TBI.77 In the past, the clinical management of penetrating TBI involved complete 

neurosurgical removal and debridement of wounds, to include retrieval of any bone and metal fragments 

in the brain.77 This approach was subsequently altered following a detailed analysis of the Israeli-Lebanese 

conflict. This study confirmed that aggressive surgical debridement was unnecessary and may have worsened 

outcomes.78

Figure 14. Common vectors of penetrating TBI. Image courtesy of the Borden Institute, Office of The Surgeon General, Washington, DC. 

Illustrator: Bruce Maston.

Trans-suboccipital

Transtemporal Transfacial/infratemporal

Transorbital

Transfrontal
362 | Traumatic Brain Injury

The majority of military penetrating TBI occurs from penetrating fragment injuries and not from fired 

bullets. Past clinical management of penetrating TBI involved radical wound debridement, surgical 

removal of fragments from the brain, and minimal decompression. Current strategies favor more 

conservative debridement and fragment removal coupled with more aggressive brain decompression.

Today, different management strategies are in effect, especially those based on treatment guidelines for 

penetrating TBI. Evidence suggests that less aggressive neurosurgical management may be warranted.78,79 

Although the level of clinical evidence does not allow for management standards to be issued, current 

guidelines provide clinical management options. Management options include local wound care and 

primary wound closure in penetrating TBI patients who have vitalized scalp without significant intracranial 

pathology, such as midline shift of the falx cerebri, or an intracranial hematoma requiring evacuation. If 

no significant mass effect is evident on CT imaging, debridement along the path of the projectile is not 

recommended.79 If there is tissue devitalization and/or mass effect, then debridement is recommended 

prior to a primary wound closure.79

Infection and Cerebrospinal Fluid Leaks

Infection following penetrating TBI is a concerning complication and can dramatically increase mortality 

and morbidity from head trauma.80 The mechanism by which this occurs involves formation of a dural 

fistula resulting from trauma and subsequent fracture of the skull to which it is adherent. The resulting 

violation of the dura after penetrating TBI predisposes a patient to infection.12,81 If temporary CSF diversion 

(e.g., by lumbar drain) does not lead to spontaneous closure of the CSF leak, surgical correction should be 

considered.82

While the utility of antibiotic prophylaxis following penetrating TBI is unclear, the high likelihood of 

wound contamination has been used to justify the prophylactic use of antibiotics.

The utility of antibiotic prophylaxis following penetrating TBI is unclear. A common practice is the use of 

broad-spectrum antibiotics due to the likely contamination of the wound from foreign bodies, skin, hair, 

and bone fragments.80 In the authors’ opinion, in lieu of standardized guidelines and better evidence-based 

practice on this subject, it may be worthwhile to continue broad-spectrum antibiotic coverage for these 

wounds and subsequently narrow antibiotics based on CSF culture data and the clinical picture of the 

casualty. 

Neuroimaging in Penetrating TBI

Advanced neuroimaging is often necessary in penetrating TBI patients. Acutely, CT generally provides 

sufficient information for appropriate surgical management. Magnetic resonance imaging should not be 

used in the imaging of acute TBI caused by metallic projectiles.83 If a vascular injury is suspected, then 

cerebral angiography is recommended. While conventional angiography is the traditional gold standard 

imaging modality, computed tomography angiography is widely available and typically utilized in-theater 

at Level III facilities for this purpose. The sensitivity to diagnose vascular injury such as traumatic dissection 

of the carotid or vertebral arteries with computed tomography angiography has been reported to be 

similar or even superior to that of magnetic resonance imaging angiography.84,85 In terms of other vascular 

pathology, the incidence of vasospasm in the setting of blast-related penetrating TBI is high, approaching 
Traumatic Brain Injury | 363

50 percent.11 Thus, it is recommended that patients with acute penetrating TBI from explosives undergo 

regular noninvasive vascular assessment via transcranial Doppler, with follow-up invasive digital subtraction 

angiography for definitive diagnosis and endovascular intervention.11 

Patients with acute penetrating TBI from explosives should undergo regular noninvasive vascular 

assessment via transcranial Doppler studies. Digital subtraction angiography is used for definitive diagnosis 

and endovascular intervention.

Traumatic Brain Injury Management

An organized team approach is essential to appropriate TBI management. This begins in the field with 

the medic or corpsman and continues to the CSH and tertiary centers. Proper clinical management in the 

acute period is essential for optimal outcomes. The Guidelines for Field Management of Combat-Related 

Head Trauma (available at www.braintrauma.org) and Advanced Trauma Life Support (ATLS) are both 

useful guides.86 After evaluation and treatment of airway, breathing, and circulatory (ABC) priorities, the 

far-forward careprovider must make a rapid initial neurological evaluation (disability assessment), especially 

determining the patient’s GCS score (Table 1).86 The GCS score is important for triage and is a quantifiable 

measure of impairment, which can help decide early management sequences. This initial exam helps predict 

outcomes of moderate and severe TBI and penetrating TBI.39,87

Initial Management (Primary Survey)

Optimal clinical outcomes depend on proper battlefield care. It is crucial that first responders recognize the 

importance of airway, breathing, and circulatory management in order to optimize cerebral oxygenation 

and perfusion. The brain can tolerate severe hypoxia for a very limited period, and it is well-established 

that the duration and severity of hypoxia and hypotension in this critical early period have dramatic 

consequences on ultimate clinical outcome.21,88 Thus, the goals of early resuscitation are to ensure adequate 

oxygen saturation (greater than 90 percent) and avoid hypotension (systolic blood pressure less than 90 mm 

Hg). Ensuring a secure airway and adequate ventilatory support is critical in the management of moderate 

and severe TBI patients. Circulation management starts with hemorrhage control in concert with damage 

control resuscitation. 

Ensuring a secure airway and adequate ventilatory support is critical to the management of moderate and 

severe TBI patients.

Airway and Breathing Management

The decision to secure a reliable airway in the patient with a severe TBI is most often made by the 

careproviders initially evaluating and treating the patient. Rapid sequence intubation is the method of 

choice. It involves near simultaneous administration of a sedative agent and a neuromuscular blocking 

agent to induce a loss of consciousness and motor paralysis. While the benefit of rapid airway intervention 

in severe TBI patients is without question, the side-effect profiles of the many medications used in rapid 

sequence intubation warrants discussion. The issues of hemodynamic response and intracranial pressure 

response to endotracheal intubation become germane when dealing with severe TBI patients. The 
364 | Traumatic Brain Injury

ideal agent will decrease or stabilize ICP without inducing systemic hypotension during rapid sequence 

intubation efforts. The more commonly used medications will be discussed with a special emphasis on any 

neuroprotective properties they may have. 

Preoxygenation should be performed when possible. Delivering 100 percent oxygen through a nonrebreather 

apparatus will lead to a nitrogen washout from within the lungs. This nitrogen washout may occur over three 

to four minutes and may allow for several minutes of apnea before hypoxemia develops. This will minimize 

the chances of any transient hypoxemia during subsequent attempts at endotracheal intubation. Although 

there are no studies to prove preoxygenation prior to rapid sequence intubation minimizes secondary brain 

injury, the practice intuitively appears beneficial.89

Attempts at endotracheal intubation will elicit gag and cough reflexes, tachycardia, hypertension, and 

increased ICP. The cardiovascular responses are believed to be primarily sympathetic to the mechanical 

stimulation of the larynx and trachea by direct laryngoscopy and intubation. There are a variety of 

premedications touted as being able to blunt these responses. Lidocaine (1.5 milligrams [mg] per kilogram) 

administered intravenously three minutes prior to direct laryngoscopy has been advocated as an agent 

that may blunt reflex cardiovascular and ICP responses.90 The ICP response to endotracheal suctioning 

in intubated TBI patients has been measured at approximately 22 mm Hg.91 Studies that measured 

cardiovascular and ICP responses to endotracheal suctioning or endotracheal intubation using lidocaine 

as pretreatment to blunt these rises revealed mixed results.90,92,93,94,95,96,97 Lidocaine has also been delivered 

topically and in nebulized form, in the hopes of blunting the circulatory response to intubation. The many 

methodologic flaws and conflicting results of these studies preclude drawing any definitive conclusions. 

Lidocaine did not appear to pose any short-term adverse side effects in the setting of severe TBI in any of 

the referenced studies. At best, lidocaine should be regarded as an agent that may have potential benefit in 

blunting ICP rises associated with endotracheal suctioning or intubation. 

Opiates have been advocated as possibly decreasing sympathetic response to endotracheal intubation. 

Fentanyl has specifically been studied in the setting of severe TBI.91,98,99,100 Results of several studies suggest 

it actually causes a paradoxical rise in ICP in this patient subset.101,102 There is not enough evidence to 

advocate the use of fentanyl to attenuate ICP rises associated with endotracheal intubation. Some evidence 

suggests it actually may be harmful. Benzodiazepines are potent sedative hypnotics and have been used 

as adjunctive medications during RSI (rapid sequence intubation). Midazolam, with its rapid onset and 

short duration of action, is a popular choice. There are few studies measuring ICP and CBF responses to 

administration of midazolam in humans. In one of the few studies in the setting of severe TBI, Papazian 

et al. studied the effect of 0.15 mg per kilogram bolus midazolam intravenous infusion on ICP, MAP, and 

CPP. Twelve patients with severe TBI in an ICU received midazolam boluses over one minute.103 In those 

patients, MAP decreased from 89 mm Hg to 75 mm Hg, CPP decreased from 71 mm Hg to 56 mm Hg, 

and no statistically significant change in ICP was noted. The minimum acceptable CPP in the setting of 

severe TBI in many treatment protocols has been set at 70 mm Hg, although current guidelines support 

slightly lower minimum CPP standards.104 This study cautions against the indiscriminate use of midazolam 

in the setting of severe TBI, as it may cause suboptimal CPP in a subset of these patients. At present there is 

insufficient evidence to make any definitive conclusion regarding the neuroprotective benefit of midazolam 

in the setting of RSI of the severe TBI patient.

Etomidate is a short-acting, nonbarbiturate, sedative-hypnotic. A dose of 0.3 mg per kilogram 
Traumatic Brain Injury | 365

administered intravenously over 30 seconds provides rapid sedation with minimal cardiovascular or 

respiratory depression.105,106 It has been shown in some studies to decrease ICP, which makes it an attractive 

option in severe head injury patients.107,108 It has several adverse effects; one being it may produce vomiting if 

not accompanied by a paralytic agent. It has also been reported to temporarily suppress adrenal function with 

as little as one dose.109 There is no evidence to suggest this temporary attenuation of adrenal responsiveness 

is of any clinical significance. There are insufficient studies specifically measuring ICP response in head 

injury patients to the administration of etomidate to make definitive conclusions. However, available evidence 

indicates that 0.3 mg per kilogram etomidate administered intravenously over 30 seconds may be an effective 

adjunct in minimizing secondary brain injury in severe TBI patients.110 Of note, given etomidate’s short 

duration of action, additional sedatives will need to be administered to patients undergoing mechanical 

ventilation. Agents such as propofol and thiopental have been reported to have properties that reduce ICP 

rise associated with endotracheal intubation. Both agents have the propensity to induce systemic hypotension, 

an undesirable side effect for its relationship to CPP in the severe TBI patient. 

Rapid sequence intubation involves the administration of neuromuscular blockade immediately following 

administration of a potent sedating agent and any pretreatment measures for ICP elevation. 

Succinylcholine, a rapid-acting, short duration, depolarizing neuromuscular blocking agent used at a dose 

of 1 to 2 mg per kilogram intravenous bolus, is the traditional first-line agent.111 Administration of this 

drug has been reported to increase ICP directly, although the mechanism remains unclear.112 Estimates of 

the rise in ICP as a direct result of succinylcholine administration in patients with disorders of intracranial 

compliance have been between 4.9 mm Hg to 12.0 mm Hg.113,114 While the exact mechanism is speculative, 

it is suggested that afferent input from muscle spindle receptors to the central nervous system is 

responsible. Administering a defasciculating dose of a nondepolarizing neuromuscular blocking agent 

(pancuronium 0.01 mg per kilogram or vecuronium 0.01 mg per kilogram) intravenously three minutes 

prior to succinylcholine administration has been reported to blunt any subsequent rise in ICP.113,114 An 

alternative to using succinylcholine is the administration of a paralytic dose of vecuronium (0.3 mg 

per kilogram) in an intravenous bolus fashion. This will provide intubating conditions in 100 seconds; 

however, this dose has the potential disadvantage of complete motor paralysis for approximately two 

hours and may complicate further neurologic assessment. Prolonged paralysis is thus discouraged. An 

alternative nondepolarizing paralytic agent with rapid-onset (one to three minutes) and intermediate 

duration of action (30 to 45 minutes) is rocuronium (0.6 mg per kilogram dosing). Rocuronium is not 

contraindicated in the setting of burns, potential hyperkalemia, and myopathies.115,116

Administering a defasciculating dose of a nondepolarizing neuromuscular blocking agent intravenously 

three minutes prior to succinylcholine administration has been reported to blunt any subsequent rise in 

ICP.

Many of the pharmacological agents used to blunt intubation-related elevations in ICP must be 

administered several minutes prior to intubation attempts in order to achieve peak efficacy. Combat 

casualty careproviders must use their judgment in these scenarios. Will several minutes of potential 

hypercarbia or hypoxemia result by waiting for these premedication drugs with theoretical benefit to take 

effect? Would the resultant rise in ICP from increased CBF offset any benefit these medications provide? 

While minimizing transient elevations in ICP with premedication or appropriate muscle blockading agents 

during RSI is theoretically appealing, no definitive proof linking this to improved neurologic outcomes 

exists. 
366 | Traumatic Brain Injury

Head Position

The traditional practice of elevating the head of TBI patients in order to minimize ICP has been 

challenged. Advocates of a supine position argued it would allow for higher cerebral perfusion pressures 

and optimized CBF. Rosner et al. measured the effect of head elevation from zero to 50 degrees on ICP 

and CPP. They concluded that zero degree head elevation maximized CPP.117 Durward et al. studied the 

effect of head elevation at 0, 15, 30, 60 degrees on ICP and CPP. They concluded that 15 to 30 degrees 

of elevation reduced ICP while maintaining CPP. Further elevations of the head to 60 degrees caused an 

increase in ICP and a significant decrease in CPP.118 Feldman et al. measured ICP, CPP, CBF, and mean 

carotid pressures on head injury patients at zero and 30 degrees head elevation. They found mean ICP 

values of 14.1 mm Hg at 30 degrees elevation increased to a mean ICP value of 19.7 mm Hg at zero 

degrees elevation. Mean carotid pressures decreased from 89.5 mm Hg to 84.3 mm Hg when patients 

went from zero degrees to 30 degrees elevation, and no differences in CPP or CBF were noted.119 From 

this data, it appears that elevating the head of severe TBI patients to greater than 30 degrees may be 

detrimental to CBF. Elevation of the head up to 30 degrees may be of some benefit in selected patients 

with TBI with respect to decreasing ICP, although it may be at the expense of diminished CPP and CBF. 

Once ICP monitoring is instituted, a more accurate assessment of the optimal degree of head elevation 

in the patient with severe TBI patient may be made. Of note, any consideration of head position changes 

need to take into account the stability of the cervical spine or potential for injury.

Elevation of the head up to 30 degrees may be of some benefit in selected patients with TBI with 

respect to decreasing ICP, although it may be at the expense of diminished CPP and CBF.

Compromised venous drainage can exacerbate intracranial hypertension. It is prudent to always assume an 

occult cervical spine injury in any TBI patient with altered mental status or blunt injury above the clavicle 

until ruled out by radiographic imaging.86 The cervical spine should be immobilized with a rigid neck collar 

during the initial survey. The neck collar serves a dual purpose. It protects the cervical spine and keeps the 

head midline. Spinal injuries concomitant with TBI are not uncommon, as a recent retrospective review of 

head injury casualties from OEF/OIF included a 16 percent incidence of spinal column trauma of various 

types.12 In a recent retrospective review of the epidemiology of spinal trauma in polytrauma patients, 8 

percent had associated spinal injuries, and the percentages of cervical, thoracic, lumbar, and sacral injuries 

were 35, 19, 37, and 27 percent, respectively.120 It is important to immobilize the spine of a polytrauma 

patient when spinal instability is suspected, and remain vigilant for exam findings, which may be explained 

by occult spinal cord injury.

Assume an occult cervical spine injury is present in any TBI patient with altered mental status or blunt 

injury above the clavicle, until it is ruled out by radiographic imaging and clinical assessment.

Secondary Survey

The secondary survey of a trauma patient follows the primary survey and includes a more detailed yet 

rapid neurologic examination. Examining the patient and detailing the extent of neurologic impairment 

is essential. Ideally, this can be accomplished in advance of sedation and/or paralysis for endotracheal 

intubation and other procedures. The diagnosis of TBI is made on history and physical examination. 

Neuroimaging provides supportive information. It is important to remember that altered mental status or 

obtundation may be due to other causes, including impaired ventilation, oxygenation, perfusion, glycemic 
Traumatic Brain Injury | 367

derangement, or medication/toxin exposure in addition to occult head injury. These conditions must be 

considered during the initial trauma evaluation.86 

TBI Management Guidelines and Options

The overriding concept of management of the moderate and severe TBI patient is the prevention of 

secondary injury. In the initial hours after the inciting trauma, this involves mitigating elevations in ICP, 

traumatic intracranial hemorrhage, cerebral edema, and metabolic derangements. Treatment guidelines 

for the management of severe TBI published by the Brain Trauma Foundation have been instrumental 

in improving care through guiding therapy with evidenced-based recommendations.121 Guidelines for the 

prehospital and field management of brain injury are also published, and all three sets of guidelines can be 

obtained from the Brain Trauma Foundation free of charge (www.braintrauma.org). 

Airway Management and Ventilation

Ensuring adequate oxygenation and appropriate ventilation of the head-injured patient is vital. Oxygenation 

and ventilation goals should be to maintain adequate oxygenation with partial pressure of oxygen in arterial 

blood (PaO2

) greater than 60 mm Hg, and avoid either hypocarbia or hypercarbia by maintaining a PCO2 

in the normal range, except for brief periods of hyperventilation discussed below.21,122 

Oxygenation and ventilation goals should be to maintain adequate oxygenation with PaO2 greater than 

60 mm Hg, and avoid either hypocarbia or hypercarbia by maintaining a PCO2 in the normal range.

In the field, oxygen saturation should be greater than or equal to 90 percent. Hypoxic episodes with 

saturations lower than this are associated with worse outcomes.123,124 Absolute indications for inserting an 

artificial airway are a GCS score of 8 or less or suspicion that the patient’s ability to ventilate or protect 

his or her airway is compromised. Oral endotracheal intubation is preferred in Level III facility settings. 

Nasotracheal intubation is not recommended in the setting of significant head trauma. The possibility 

exists for increasing ICP due to stimulation of the nares as well as displacing occult skull fractures through 

nasopharyngeal manipulation.125,126 Another advantage to intubation is to ensure the maintenance of 

eucapnea (PCO2 of 35 to 40 mm Hg), as hypercapnea will induce increased ICP.127

Role of Hyperventilation

Acute hyperventilation has traditionally been a first-line intervention in rapidly decreasing ICP. As the ability 

to monitor CBF, cerebral metabolism, and cerebral ischemia has improved, new information regarding 

potential pitfalls of hyperventilation has emerged. Recent studies have noted that while hyperventilation 

acutely decreases ICP, it also decreases CBF, and in many cases may induce cerebral ischemia.25,27,128,129

Severe TBI patients have been found to have either increased or reduced CBF during the early phases of 

their injuries. Both states may be associated with elevated ICP. While hyperventilating the TBI patient with 

increased CBF may be desirable, hyperventilation may induce cerebral ischemia in patients with reduced 

CBF. In certain patients with increased CBF, hyperventilation has lead to decreased CBF in uninjured 

areas of the brain, while creating a relative increase in CBF to areas of injured brain. This localized 

increase in CBF to injured areas of brain is thought to occur due to the diminished responsiveness of the 

injured brain’s microvasculature to hypocapnia. 
368 | Traumatic Brain Injury

Optimal titration of hyperventilation therapy requires close monitoring of objective indicators of cerebral 

ischemia.130,131 Objective indicators of cerebral ischemia or CBF include measurement of jugular venous 

saturations, thermal diffusion flowmetry, transcranial Doppler ultrasounds, and xenon-enhanced CT scans. 

These methods of measuring cerebral ischemia or CBF are not widely available to CCC providers. This has 

led to the recommendation that hyperventilation only be used in settings of documented elevated ICP and 

as a temporary and last-line treatment to decrease elevated ICP refractory to other means, such as sedation, 

paralysis, CSF drainage, lowering of brain metabolism, and osmotic therapy. 

Hyperventilation should only be used as a temporary and last-line measure to decrease elevated ICP 

refractory to other means, such as sedation, paralysis, CSF drainage, lowering of brain metabolism, and 

osmotic therapy. Physicians should use a PCO2 level of 30 to 32 mm Hg as their target when they decide 

to institute hyperventilation therapy in the setting of severe head injury.

Prolonged hyperventilation has been clearly associated with exacerbation of cerebral ischemia.132 Very 

brief durations of hyperventilation may be acceptable only as a temporizing measure until other means of 

managing increased ICP are readied. If hyperventilation is continued for longer than 12 hours, metabolic 

compensation negates the ameliorative effects of respiratory alkalosis caused by a hypocapnic state, 

and continued hyperventilation may be harmful.127 The recommended goal for baseline PCO2 levels is 

normocapnia in the 35 to 40 mm Hg range, but during an impending herniation event, hyperventilation 

will acutely lower PCO2 and ICP within seconds. Based on available data, physicians should use a PCO2

level of 30 to 32 mm Hg as their target when they decide to institute hyperventilation therapy in the setting 

of severe head injury. The current recommended PCO2 is to strictly avoid levels below 25 mm Hg.125,127

Hemodynamic Management

The objective of hemodynamic therapy in TBI is to ensure adequate brain perfusion. The specific treatment 

goals are systolic blood pressure greater than or equal to 90 mm Hg, CPP greater than or equal to 60 mm 

Hg, and euvolemia. As discussed above, CPP is MAP minus ICP (Equation 1). Although CPP is neither 

a direct measure of CBF nor regional cerebral flow, it is indicative of the overall adequacy of brain 

perfusion, especially in the context of elevated ICP.

Blood pressure management may be challenging in combat-injured patients. Often, the patient is 

in hemorrhagic shock due to accompanying injuries such as traumatic extremity amputation. As such, 

hypotension is common and independently associated with TBI, poor outcome, and mortality.16,133

Systolic blood pressures less than 90 mm Hg has an especially deleterious effect. When compared to 

hypoxemia, low systolic blood pressure is associated with a worse outcome.17 With head injury, the ability 

of the neurovasculature to autoregulate is impaired, and thus regional cerebral blood flow becomes 

directly dependent on systemic blood pressure.125 Experimental models show that the injured brain is 

highly susceptible to even subtle ischemic states.134 It is therefore imperative to avoid even short episodes 

of hypotension after TBI. Overall fluid balance of head injured patients is also important. Retrospective 

data suggests that TBI patients who were volume depleted by about 600 milliliters developed worse 

outcomes.135

Hypotension is common in combat casualties. Hypotension following severe TBI has been associated with 

poor outcomes and increased mortality.
Traumatic Brain Injury | 369

Hemostasis of the obvious soft-tissue head wound is usually obtained with direct pressure dressing or a 

field dressing such as HemCon® or QuikClot®.Crystalloid fluids are used for fluid resuscitation in the field 

phase of the treatment of the brain-injured patient. Later, blood products may be transfused as needed. 

Analysis of data from OEF and OIF indicates that hemorrhagic shock is best treated with red blood cells 

and plasma using a 1:1 ratio based on volume.15 Colloid and hypotonic fluids are relatively contraindicated 

in TBI. Colloid fluids containing albumin have been shown to increase mortality.136 Hypotonic fluids, such 

as half-normal saline and lactated Ringer’s, have the potential to exacerbate cerebral edema.125 

Colloid and hypotonic fluids are relatively contraindicated in TBI. Colloid fluids containing albumin 

have been shown to increase mortality, while hypotonic fluids, such as half-normal saline and lactated 

Ringer’s, have the potential to exacerbate cerebral edema.

Cerebral perfusion pressure goals are best met with intravenous fluids. If CPP cannot be maintained 

with intravenous fluids alone, vasoactive pharmacologic agents may be considered. Norepinephrine and 

phenylephrine are often used, as they are thought to have minimal effect on cerebral vasomotor tone. If 

vasopressors are used, then continuous hemodynamic monitoring is needed.76 Aggressive use of vasopressor 

agents has been associated with increased incidence of acute respiratory distress syndrome; however, this 

complication potentially could have been the result of exceeding CPP levels of 70 mm Hg.137

Goals for ICP Management

The goal for ICP management in brain-injured patients is to maintain a normal ICP which is generally less 

than 20 cm H2O or 15 mm Hg. Data suggest that elevations over 25 mm Hg are associated with poor outcomes, 

and thus interventions should be aimed at reducing ICP to less than this amount.138 Current guidelines 

recommend instituting measures to control ICP when pressures of 20 mm Hg are reached and aggressive 

means employed to prevent ICP elevations over 25 mm Hg.139 One must keep in mind the achievable 

CPP based on MAP and ICP during therapy, as many interventions to decrease ICP may also have 

systemic effects on peripheral hemodynamics. The maintenance of a CPP of at least 60 mm Hg is strongly 

recommended.104 This is often accomplished with the use of vasopressor agents, although complications, 

including higher incidence of adult respiratory distress syndrome, may result from overshooting the goal 

CPP to greater than 70 mm Hg with vasopressors and intravenous fluids, as previously discussed.137

Intracranial Pressure and External Ventricular Drains

The management of ICP is paramount in neurocritical and neurosurgical care. If ICP progresses 

unchecked, it will culminate in cerebral herniation. Simple therapeutic measures should be instituted in 

every moderate to severe TBI patient so as to minimize increasing ICP. Such simple interventions include 

keeping the head midline, avoiding any circumferential neck dressings for wound hemostasis or securing 

the endotracheal tube, and avoiding placement of internal jugular central venous lines into the dominant 

internal jugular vein. All of these will optimize venous outflow from the head.42 The Trendelenburg position 

should not be used as it will do the opposite.140

All TBI patients with suspected elevated ICP should have an ICP monitor placed. Options include an 

intraventricular catheter, intraparenchymal fiberoptic or solid-state monitor, subdural bolt, and epidural 

fiber optic catheter. The most invasive is the intraventricular catheter. It provides the most accurate 

measurement of ICP as it is placed into the third ventricle that is almost at the center of the cranial 
370 | Traumatic Brain Injury

vault.141 It is also the most consistently reliable as it can be zeroed. The other methods are less invasive 

as they either require only minimal or no penetration of brain parenchyma. As closed systems, they have 

a lower incidence of infection but, unfortunately, also are subject to measurement drift as they cannot 

be zeroed. Another benefit of the intraventricular catheter is that it provides a treatment option for ICP 

management. The intraventricular catheter is also known as an external ventricular drain, as it can be 

used for CSF removal.141 If hydrocephalus is seen on CT, an external ventricular drain is the best option 

(Fig. 15).

There is evidence that with proper training, placement of an external ventricular drain or other ICP 

monitors can be done safely by non-neurosurgeons.

Indications for placing an ICP monitor include a patient with a GCS score less than or equal to 8 (after 

resuscitation) and an acute abnormality on CT, such as traumatic intracerebral hemorrhage, compression 

of the basal cisterns, or evidence of contusion.142 If a patient has two of the following: systolic blood 

pressure less than 90 mm Hg, motor posturing on exam, and/or is greater than or equal to 40 years of 

age, then an ICP monitor should likewise be placed or strongly considered.142 Typically a neurosurgeon 

places these devices. However, there is evidence that with proper training, placement of an external 

intraventricular drain or other ICP monitors can be done safely by neurointensivists and other nonneurosurgeons (Fig. 16).143,144 It should be stated that this is not yet a mainstream position, and that access 

to the cranial vault should ideally only occur with neurosurgical oversight. 

Hypertonic Saline and Other Medical ICP Management Options

Initial medical intervention for elevated ICP includes avoidance of exacerbating factors such as fever, 

seizures, venous outflow obstruction, hyperglycemia, or hypercarbia. The next line of therapy involves 

osmotic therapy. Several agents have been used for this purpose in the past, but currently mannitol and 

hypertonic saline (HTS) are the mainstays of osmotic or hyperosmolar therapy.

Role of Mannitol

Mannitol is an osmotically active agent that has long been used in the management of elevated ICP.145

The mechanism of its action involves multifactorial pathways to lower ICP.146 It has volume expansion and 

rheologic properties making red blood cell mediated oxygen delivery to brain cells more effective. This in 

turn may stimulate reflex cerebral microvasculature vasoconstriction.147,148 Irrespective of the mechanism 

of action of mannitol, its effectiveness in reducing ICP is well documented.147 It will consistently decrease 

ICP by approximately 20 to 35 percent within 10 to 20 minutes of intravenous administration. The 

ICP reduction effect of mannitol typically lasts at least two hours.149,150,151 A common fear of inducing 

acute hypotension in the multiple trauma patient by infusing mannitol precludes its use by many physicians. 

However, in multiple studies, mannitol infusion resulted in acute increases in central venous pressure and mean 

arterial pressures.146,148,150 The osmotic diuresis leading to hypotension was rarely noted. When hypotension 

did occur, it occurred several hours later and was mild and easily treated with volume replacement. Mannitol 

appears to be a safe and effective drug in acutely reducing ICP in severe TBI patients.

Mannitol can decrease ICP by approximately 20 to 35 percent within 10 to 20 minutes of intravenous 

administration, and its effects last for two hours.
Traumatic Brain Injury | 371

Figure 15. Landmarks for placement of intraventricular catheter. Adapted image courtesy of the Borden Institute, Office of The Surgeon General, 

Washington, DC. Illustrator: Bruce Maston.

Midpupillary

line

Aim for nasion or

ipsilateral medial

epicanthus

(coronal plane)

Aim for tragus (sagittal plane)

Tragus line
372 | Traumatic Brain Injury

Mannitol should be given intravenously via a peripheral or central intravenous line at a dose of 0.25 to 

1.0 grams per kilogram. Small doses of mannitol (0.25 grams per kilogram) have been shown to effectively 

reduce ICP in patients with TBI.152 Earlier data shows that mannitol use in TBI correlates with decreased 

ICP and improvements in CBF and CPP.149 Past recommendations for mannitol to be given as bolus 

infusions rather than continuous are no longer supported. Still, in common clinical practice, a single bolus 

dose is most widely used.153 So long as serum osmolality is followed closely, additional doses of mannitol 

can be given. A serum osmolality of 320 milliosmole (mOsm) per liter is generally accepted as a treatment 

endpoint, although some investigators advocate that slightly higher levels can be tolerated with caution.154

Hypertonic Saline (HTS)

Another option for hyperosmolar therapy is HTS. Studies using 7.5% and 23.4% HTS provide evidence 

of clinical benefit.155,156 Recent data support the use of bolus doses of 30 to 60 ml of 23.4% HTS to 

emergently treat a herniation event.156 An additional benefit of using 23.4% HTS is that its ameliorative 

effect on ICP lasts longer than mannitol.157 When used, 23.4% HTS must be administered via a central 

venous line over ten to fifteen minutes to prevent hypotension and phlebitis. A commonly used initial 

treatment goal is to achieve serum sodium levels 145 to 155 milliequivalents (mEq) per liter, which 

is equivalent to a serum osmolality of 300 to 320 mOsm per liter in most patients.140 A continuous 

intravenous infusion of 2% or 3% HTS can be used to maintain high serum osmolality. When doing 

Figure 16. An intraventricular catheter provides the most accurate 

measurement of ICP and is a valuable treatment option for ICP 

management. (Top Left) A hole is drilled through the skull. (Top Right)

The intraventricular catheter is advanced into the third ventricle at the 

center of the cranial vault. (Bottom Right) If needed, CSF can be 

removed if necessary.
Traumatic Brain Injury | 373

so, it is suggested that the fluid be made as a 50%:50% mix of sodium chloride and sodium acetate so 

as to prevent hyperchloremic metabolic acidosis. At 2% concentration, HTS can be given through a 

peripheral intravenous catheter, but at 3% or higher, it must be given via a central line due to its potential 

to cause phlebitis. The infusion rate is set based on a particular patient’s intravascular needs. Typically, 

a maintenance rate of 75 ml per hour is used. However, these solutions can be administered in 250 ml 

boluses to treat episodes of intracranial hypertension or systemic hypotension. 

Studies using 7.5% and 23.4% HTS provide evidence of clinical benefit in reducing ICP in cases of 

refractory intracranial hypertension.

If continuous infusions of hypertonic solutions are used, serum sodium should be monitored frequently, 

at least every six hours. Rapid drops in serum sodium are to be avoided so as not to precipitate cerebral 

edema.140 Dehydration must also be avoided.135 Generally, HTS therapy is maintained for the first four to 

seven days after injury. After the peak edema period elapses, HTS infusion can be switched to normal 

saline or terminated while observing for the slow return to normonatremia.

Other Pharmacologic Agents to Reduce ICP

If ICP remains poorly controlled after the efforts described above, then induced pharmacologic coma 

can be considered. The postulated effect of pharmacologic coma on ICP is through reduction of cerebral 

metabolism with concomitant reductions in CBF and reduced tissue oxygen demand. The most commonly 

used agent for pharmacological coma is pentobarbital. This drug can be administered intravenously at a 

loading dose of 5 mg per kilogram, followed by an infusion of 1 to 3 mg per kilogram per hour. There is 

a high-dose regimen that begins with an intravenous loading dose of 10 mg per kilogram over 30 minutes 

followed by 5 mg per kilogram per hour infusion for three hours, followed by 1 mg per kilogram per hour 

titrated to therapeutic goals, which are either burst suppression on continuous electroencephalography 

(EEG) monitoring or a reduction in ICP.76 If burst suppression is not obtained with this dose, then a 

smaller loading dose and increased rate can be given until a satisfactory EEG tracing is seen or ICP is 

controlled. Other barbiturates may be used including the much shorter acting thiopental, whose half-life 

of five hours is suited for short-term therapy of elevations in ICP.140 Thiopental doses of 200 to 500 mg 

can be given via bolus intravenous push while monitoring for hypotension. 

Another option for pharmacological coma is propofol, which is given at an intravenous loading dose of 2 

mg per kilogram, followed by a titrated infusion of up to 100 micrograms (mcg) per kilogram per minute. 

The use of propofol for this clinical indication is controversial. Long-term and high-dose propofol infusions 

have been associated with the development of hypotension and a newly described metabolic disorder 

termed propofol infusion syndrome.158 This consists of renal failure, rhabdomyolysis, hyperkalemia, 

myocardial failure, metabolic acidosis, lipemia, hepatomegaly, and death. The mechanism for this is not 

fully understood, but significant caution must be used in any infusion over 5 mg per kilogram per hour 

or treatment lasting longer than 48 hours.159 In a study of propofol used for ICP reduction, there was a 

failure to show a six-month outcome benefit.160 If propofol is used for induction of a pharmacological 

coma (and resultant ICP reduction), continuous EEG monitoring will be required to monitor the electrical 

activity of the brain.
374 | Traumatic Brain Injury

Induced Hypothermia 

Induced hypothermia for TBI remains controversial 

but promising. Recent animal data shows 

promise for induced hypothermia with improved 

neurophysiologic metrics in an asphyxial brain 

injury model.161 There is also data in brain trauma 

that induced mild hypothermia (33 to 35 degrees) 

may improve outcomes as far out as two years 

following head injury.162 Current use of prophylactic 

hypothermia for treatment of ICP in severe TBI is a 

second-tier therapy but may be helpful in refractory 

intracranial hypertension. If utilized, modalities 

of induction of hypothermia include skin-applied 

gel cooling systems and intravenous methods, as 

well as traditional air-circulating cooling blankets, 

iced gastric lavage, and surface ice packing.140 The 

goal of maintaining normothermia and avoiding 

hyperthermia in TBI patients, however, remains 

strongly recommended.5 

Decompressive Craniectomy

Decompressive craniectomy is an emerging clinical 

approach to the early intervention and management 

of TBI.163 The reported experience to date is 

conflicting. In a study of 57 young patients (age less 

than 50) with severe TBI, early decompressive craniectomy was associated with a good outcome, defined as 

social rehabilitation, in 58 percent of patients. The authors reported a relatively low mortality of less than 

20 percent.164 A retrospective French study reported a similar outcome in only 25 percent of severe TBI 

patients.165 Older data from the Trauma Coma Data Bank has suggested that even though radiographic 

improvement occurred, there is no significant improvement in patient outcome after craniectomy.166 One 

of the difficulties in interpreting the available data is the lack of agreement as to how the procedure is to 

be performed (e.g., release the dura or not, timing of surgery, cutoff age, and TBI severity on presentation) 

(Fig. 17).167 

The authors’ OEF and OIF neurosurgical experience supports the practice of early decompressive 

hemicraniectomy for treatment of severe blast TBI. From a practical military standpoint, this may 

obviate the need to use more conventional methods to control ICP, such as pharmacologic coma.

Currently, two trials enrolling an estimated combined number of over 800 patients are underway. The 

Randomized Evaluation of Surgery with Craniectomy for Uncontrollable Elevation of Intra-Cranial 

Pressure (RESCUEicp) and the Decompressive Craniectomy (DECRA) trials may better elucidate the role of 

decompressive craniectomy in severe TBI. The RESCUEicp trial is the larger of the two and is a multicenter 

trial in Europe comparing decompressive craniectomy to medical management in TBI.168 The DECRA 

trial has a smaller planned enrollment and is being conducted in Australia, New Zealand, Canada, and 

Figure 17. Early decompressive craniectomy in a patient with blast 

TBI.
Traumatic Brain Injury | 375

Saudi Arabia. The authors’ OEF and OIF neurosurgical experience supports early hemicraniectomy for 

treating severe blast TBI. 

Current Use of Decompressive Craniectomy with Intractable Intracranial Hypertension

From a practical military standpoint, craniectomy provides an additional measure of safety for ICP 

control. Early decompressive craniectomy may obviate the need to use more conventional methods to 

control ICP such as pharmacological coma, which is difficult to execute in a deployed and hostile setting 

due to the limited number of neurological critical care specialists and lack of EEG support in a war 

zone. In a recent paper comparing GCS scores of patients at the time of head trauma and at discharge, 

TBI patients who underwent a craniectomy had lower initial GCS scores than those who underwent 

craniotomy, but at discharge their GCS scores were not significantly different.11 This study implies that 

although these patients were worse initially, they improved after decompressive craniectomy to the point 

where they appeared indistinguishable from those who initially presented with a better neurologic exam. 

In the combat setting, decompressive craniectomy may be a practical, though aggressive, approach to ICP 

management. Future studies on larger cohorts of patients and with more rigorous study design may either 

support or refute this practice (Fig. 18). 

Anticonvulsant Use in TBI

Traumatic brain-injured patients are at risk for both early (less than seven days) and late (more than seven 

days) post-traumatic seizures. This risk is worsened by traumatic intracranial hemorrhage.169 A seizure in 

the acute phase can exacerbate the injury. Phenytoin, a well-established antiepileptic drug, has been shown 

Figure 18. Decompressive craniectomy bone flap and exposed hematoma. Bone may be cut using a power craniotome, or a Hudson brace and Gigli saw. 

Adapted image courtesy of the Borden Institute, Office of The Surgeon General, Washington, DC. Illustrator: Bruce Maston.

Decompressive

craniectomy

skull incision

Dashed lines

(dural incision sites)
376 | Traumatic Brain Injury

to be beneficial in reducing the risk of seizures during the first week after TBI.170 Carbamazepine, 

phenobarbital, and valproate are also effective antiepileptic drugs.171 Unfortunately, no antiepileptic drug 

has been shown to prevent the development of late post-traumatic seizures. Studies have shown that 

when followed for 15 years after significant TBI, approximately 50 percent of patients will develop late 

seizures.172 As 50 percent will not, the recommended approach is to stop antiepileptic drug therapy after 

the first seven days, and only reinstitute treatment should late seizures manifest.173 The potential for 

cognitive side effects of phenytoin make prolonged prophylactic use of this medication less attractive.174

If a patient is unable to take medications orally, alternatives to phenytoin and fosphenytoin are valproate 

and levetiracetam, as all are available in intravenous form. Levetiracetam has not undergone rigorous 

human clinical TBI trials but has been shown to be effective in preclinical TBI models.175

There is little evidence to support or refute the use of antiepileptic drugs for prevention of post-penetrating 

TBI seizures. The risk of seizure following penetrating TBI is much higher than nonpenetrating TBI, 

and thus antiepileptic drugs are prescribed by most providers.176 Management options include the use of 

antiepileptic drugs during the first seven days after penetrating TBI and then to discontinue their use.177

Should the patient suffer a late seizure, the antiepileptic drug therapy can be restarted. Therapeutic options 

are phenytoin, fosphenytoin, carbamazepine, valproate, or phenobarbital.173

The risk of seizures following penetrating TBI is much higher than nonpenetrating TBI. Hence, 

antiepileptic drugs, such as phenytoin, are frequently administered for at least the first seven days 

following injury.

Critical Care and Air Evacuation

After initial emergency care, patients with moderate and severe TBI require close neurological and 

physiological monitoring. This is best done in the ICU of a Level III care facility, where monitors and 

advanced clinical practice nurses are present. Evidence demonstrates improved outcomes when specialized 

neurological intensive care teams, employing evidence-based clinical care, guide management.178 The 

presence of other traumatic injuries may require additional care from trauma, orthopedic, craniofacial 

and other specialists. In this critical injury period, the best measure of efficacy of treatment or worsening 

of condition is the neurologic examination. Thus, regular clinical neurological examination by skilled 

practitioners is needed. In the acute period, it may be as often as every hour and then less frequently if 

the patient remains stable. Intracranial pressure and CPP measurements should be made continuously 

if an ICP monitor is indicated. However, even in the presence of ICP monitoring, the importance of 

the clinical examination and neurological assessment cannot be overstated. The highest risk period for 

deterioration is in the first few days after TBI. The majority of conversion to traumatic intracerebral 

hemorrhage occurs usually within the first nine hours, and generally the peak period of cerebral edema 

is from 48 to 96 hours after TBI.53 Thereafter, these processes wane, and there is clinical improvement 

with better ICP control.76

Evidence demonstrates improved outcomes in patients with moderate and severe TBI when specialized 

neurological intensive care teams apply evidence-based clinical care. This is best done in the ICU of 

Level III care facilities.

Current military policy supports the principle of rapid out-of-theater evacuation to fixed medical 

facilities, although the decision to transfer the severely injured soldier with TBI via air evacuation may still 
Traumatic Brain Injury | 377

be difficult. As discussed above, both the peak period of cerebral edema, as well as the likely conversion 

of TBI to traumatic intracerebral hemorrhage will occur in the hours and days after the initial trauma. 

For this reason, it is wise to have the injured service member out-of-theater and en route to a medical 

center that is part of the casualty evacuation system. Although the risk of transferring a patient who may 

become unstable during air evacuation is disconcerting, a recent review of the Air Force Critical Care Air 

Transport Team’s (CCATT) safety record and census of trauma and nontrauma-related air evacuations 

is reassuring.179 During the period of study, air evacuations via CCATT teams from OIF to Landstuhl, 

Germany, no inflight or 24-hour post-flight fatalities were reported among flights occurring over a oneyear period for the flight time of approximately five hours. In this study, 17 percent of combat casualties 

had neurologic injury, and 9 percent of these patients had an ICP monitor in place with resultant increases 

in ICP during flight occurring in 3 percent of patients. Although the authors of this study credit the intheater medical teams with proper preparation of trauma-related casualties for air evacuation, there is 

data to support the current doctrine of rapid removal of casualties from theater.179 This policy has been 

credited with improved rates of fatalities of soldiers wounded in combat during the conflicts in Iraq and 

Afghanistan.180 

Other Management Considerations

Other important considerations include preventing secondary complications of critical illness including 

venous thromboembolism, gastric stress ulcers, and decubitus ulcers. Injured and immobilized patients 

are at high risk for developing deep venous thrombosis with subsequent venous thromboembolism. The 

optimal approach in severe TBI with intracranial hemorrhage is uncertain. Sequential compression 

devices on the lower extremities are minimally invasive and are not associated with worsening intracranial 

hemorrhage. Thus, they should be placed as soon as possible. The optimal timing of introduction of 

unfractionated or low molecular weight heparin for venous thromboembolism prophylaxis in head 

trauma is less clear. 

However, if there are no contraindications to heparin use (e.g., ongoing coagulopathy, worsening 

thrombocytopenia, or ongoing hemorrhage) then treatment should be started as soon as possible, ideally 

within the first 36 hours of injury.181 A practical guide is to obtain CT imaging of the brain after a period 

of 24 to 36 hours, and if no increase in hemorrhage or new hemorrhage has occurred, then subcutaneous 

heparin can be started. In the setting of any degree of increasing traumatic intracerebral hemorrhage, the 

risks and benefits of heparin must be weighed on an individual basis. The routine placement of inferior 

vena cava filters is controversial, and placement is currently supported only by a low-level recommendation 

in patients with a GCS score of less than 8 and contraindications to anticoagulation.181,182

Gastric stress ulcers may be prevented using either H2-receptor antagonists or proton-pump inhibitors.183

Either one of these medications should be routinely used for gastric stress ulceration prophylaxis in severe 

TBI patients, although the tendency for H2-receptor antagonists to cause thrombocytopenia may limit 

their usefulness.184 Prevention of skin breakdown is a concern in all severely injured trauma patients, and 

care must be taken to reduce the likelihood of decubitus ulcers through frequent repositioning, vigilant 

nursing care, and good skin hygiene practices. 
378 | Traumatic Brain Injury

Summary

Medical management of the combat TBI patient is challenging. The field and hospital care of TBI is 

largely confined to supportive efforts to minimize secondary brain injury for optimal neurologic recovery. 

This is accomplished through maintaining cerebral perfusion, controlling ICP, and preventing morbidity 

associated with critical illness. Routine or prolonged hyperventilation, as discussed previously, is harmful 

and should be avoided.27 As new pharmacologic and medical approaches are introduced, there will be 

increasing opportunity to better manage these patients and enhance their long-term neurologic outcomes. 
Traumatic Brain Injury | 379

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Trauma 2002;53(1):142-164.

182. Marion DW. Head and spinal cord injury. Neurol Clin 1998;16(2):485-502.

183. Daley RJ, Rebuck JA, Welage LS, et al. Prevention of stress ulceration: current trends in critical care. 

Crit Care Med 2004;32(10):2008-2013.

184. Ropper AH, Gress DR, Diringer MN, et al. Head injury. In: Ropper AH, Gress DR, Diringer MN, 

et al., editors. Neurological and neurosurgical intensive care. 4th ed. Philadelphia, PA: Lippincott Williams 

& Wilkins; 2004. p. 189-207.
392 | Traumatic Brain Injury
Chapter 9

EXTREMITY INJURY

Contributing Authors

John F. Kragh, Jr., MD, COL, MC, US Army

 Jess M. Kirby, MD, MAJ, MC, US Army

James R. Ficke, MD, COL, MC, US Army
All figures and tables included in this chapter have been used with permission from Pelagique, LLC, the 

UCLA Center for International Medicine, and/or the authors, unless otherwise noted.

Use of imagery from the Defense Imagery Management Operations Center (DIMOC) does not imply or 

constitute Department of Defense (DOD) endorsement of this company, its products, or services.

Disclaimer

The opinions and views expressed herein belong solely to those of the authors. They are not nor should 

they be implied as being endorsed by the United States Uniformed Services University of the Health 

Sciences, Department of the Army, Department of the Navy, Department of the Air Force, Department of 

Defense, or any other branch of the federal government.
Extremity Injury | 395

Table of Contents

Introduction........................................................................................................ 397

Burden of Extremity Injury................................................................................... 398

Extremity Injury-Associated Mortality ................................................................... 400

Emergency Tourniquet Application........................................................................ 403

Limb Compartment Syndrome.............................................................................. 405

Introduction......................................................................................................................406

Definition, Mechanisms, and Risk...................................................................................406

Clinical Findings...............................................................................................................407

Diagnosis...........................................................................................................................408

Treatment .........................................................................................................................409

Fasciotomy Techniques ......................................................................................................412

Lower Leg Fasciotomy.....................................................................................................412

Thigh Fasciotomy ...........................................................................................................413

Upper Arm Fasciotomy....................................................................................................413

Forearm Fasciotomy ........................................................................................................413

Hand Compartment Fasciotomy........................................................................................413

Conclusions.......................................................................................................................413

Traumatic Limb Amputations .............................................................................. 415

Introduction......................................................................................................................415

Initial Assessment ............................................................................................................415

Initial Resuscitation .........................................................................................................417

Primary (Completion) Amputation....................................................................................417

Wound Debridement .........................................................................................................417

Fasciotomy .........................................................................................................................419

Surgical Amputation and Wound Care ............................................................................420

Delayed Amputation .........................................................................................................420

Rehabilitation ...................................................................................................................422

Combat Casualty Wound Care............................................................................... 422

Introduction......................................................................................................................423

Extremity Resuscitation and Wound Management ........................................................423

Special Wounds.................................................................................................................424

Vascular Injury...................................................................................................................424

Muscle, Tendon, and Ligament ........................................................................................424

Open Joint Injury...............................................................................................................425

Nerve Repair......................................................................................................................426

War Wound Closure.............................................................................................. 426

Introduction......................................................................................................................427
396 | Extremity Injury

Timing of Wound Closure ................................................................................................427

Wound Closure Techniques..............................................................................................427

Wound Coverage................................................................................................................430

Preventing War Wound Infections .......................................................................... 431

Wound Debridement and Irrigation ................................................................................431

Introduction .......................................................................................................................431

Wound Flora ......................................................................................................................431

Wound Irrigation ...............................................................................................................432

Timing of Irrigation .......................................................................................................432

Volume of Irrigation........................................................................................................432

Irrigants and Additives ....................................................................................................432

Irrigation Devices............................................................................................................432

Wet-to-Dry Dressing Debridement....................................................................................433

Surgical Wound Debridement ...........................................................................................434

Assessing Muscle Viability...............................................................................................437

Massive Wounds (Upper Thigh and Buttock)....................................................................437

Negative-Pressure Wound Dressings .............................................................................438

Antibiotic Impregnated Pellets and Cement Bead Therapy............................................439

Antibiotics and Tetanus Immunization...........................................................................439

Prophylaxis.........................................................................................................................440

Fracture Management ......................................................................................... 441

Introduction......................................................................................................................441

Initial Fracture Wound Management ..............................................................................443

Initial Fracture Stabilization............................................................................................443

Open Fracture Management ............................................................................................444

External Fixation of Extremity Fractures........................................................................445

Upper Extremity Fracture Fixation ...................................................................................447

Lower Extremity Fracture Fixation....................................................................................448

Femur Fracture Fixation ....................................................................................................449

Pelvic Fracture Fixation......................................................................................................450

Open Pelvic Trauma........................................................................................................452

Associated Injuries .............................................................................................................453

Genitourinary Complications ............................................................................................453

Hip Dislocations.............................................................................................................453

Acetabular Fractures........................................................................................................454

Summary............................................................................................................ 455

References .......................................................................................................... 456

Appendices ......................................................................................................... 469
Extremity Injury | 397

Introduction

Combat casualty care (CCC) poses unique challenges. “Special experience is required to handle war 

injuries” and a good trauma surgeon is not necessarily a good war surgeon.1 The goal of this chapter is to 

translate lessons learned during Operation Enduring Freedom (OEF) and Operation Iraqi Freedom (OIF) 

into a useful guide for managing combat casualties with extremity injuries. 

• A majority (54 percent to 82 percent) of casualties at far-forward hospitals have extremity injuries.2,3

• The severity of limb injury encountered during CCC is far greater than that encountered in civilian 

care (Fig. 1).

• General surgeons often need to perform orthopaedic procedures such as complex wound debridement, 

external fixation of fractures, and fasciotomy for compartment syndrome. 

• Extremity injury care underscores one of the most obvious differences between military and civilian 

scope of practice for nonorthopaedic CCC providers.

 

Figure 1. The severity of limb injury encountered during CCC is far greater than that encountered in civilian care. Image courtesy of Harold Bohman, 

MD, CAPT, MC, US Navy.
398 | Extremity Injury

Burden of Extremity Injury

Extremity injuries in battle casualties are common, 

disabling, and costly.2,4,5 Much of war surgery is 

orthopaedic related. Extremity injuries were noted 

in 54 percent of casualties from OEF and OIF.2

Furthermore, the casualties with extremity injuries 

consume the most care at the first hospital as 

evidenced by operating room time used, proportion 

of surgeries performed, and number of occupied 

beds.3 Data collected from 2003 to 2006 in OIF 

indicate that extremity injuries have increased 

in severity (Fig. 2).6 Despite the increase in injury 

severity, more casualties with more severe limb 

injuries are surviving and undergoing rehabilitation 

in large part due to improved CCC. 

Extremity injuries were noted in 54 percent of casualties from OEF and OIF.

Extremities are particularly vulnerable to combat-specific injury mechanisms like parachuting and fastroping injuries, which are similar to falls from height.7,8,9,10 The proportion of casualties with major limb 

trauma has doubled during the course of the OIF (from 21 percent to 44 percent).11 In OEF and OIF, 

battlefield casualties with limb injuries consume about 65 percent of inpatient care, cause the greatest 

number of disabled soldiers, and result in the greatest projected disability costs.5

Extremity injury is of great importance as casualties can be saved with proper care and, conversely, 

endangered with inappropriate care (Fig. 3). The scope of practice for most careproviders expands when 

one goes to war. In the words of Sir Robert Jones who was knighted for his CCC in World War I, “the War 

has taught the orthopaedic surgeon that he has to be more of a general surgeon; it has taught the general 

surgeon that he should be more of an orthopaedist.”12

Extremity injury care is a prime example of this 

expanded scope of practice, as nonorthopaedists 

are often responsible for providing limb-saving 

interventions and care. Orthopaedic workload at 

times necessitates nonorthopaedic trained surgeons 

to perform extremity procedures such as: (1) 

complex wound debridement; (2) external fixation 

of fractures; and (3) fasciotomy for compartment 

syndrome (Fig. 4). These procedures are technically 

challenging, and if performed late or not at all, 

they are associated with increased mortality and 

morbidity rates.13,14 Other critical interventions 

include applying extremity tourniquets and 

managing traumatic amputations. 

Figure 2. Annual proportion of US casualties with severe limb injuries 

during OEF and OIF. 

Figure 3. Nonorthopaedists are often responsible for providing limbsaving interventions and care.

0%

10%

50%

2003

20%

30%

40%

2004 2005 2006

21%

27%

35%

44%

Proportion

Year
Extremity Injury | 399

General surgeons often need to perform orthopaedic procedures such as complex wound debridement, 

external fixation of fractures, and fasciotomy for compartment syndrome.

Combat casualties with multiple injuries can 

rapidly overwhelm orthopaedic service capacity 

(Fig. 5). Orthopaedists should anticipate this 

challenge and be prepared to help manage trauma 

system resources according to a preexisting

 protocol. Delegating cases, training colleagues, 

extending care through ancillary careproviders, 

and delegating nonorthopaedic tasks (e.g., casualty 

triage) to others will maximize available orthopaedic 

resources. In the setting of multiple casualties, 

the scope of practice for orthopaedists widens 

to include burn care, escharotomies, assisting in 

damage control surgery and resuscitation, and 

soft-tissue repairs, flaps, and reconstructions.

Figure 4. General surgeons often need to perform orthopaedic procedures 

such as: (Top Right) complex wound debridement, (Bottom Left)

external fixation of fractures, and (Bottom Right) fasciotomy for 

compartment syndrome. Fasciotomy image courtesy of Defense Imagery 

Management Operations Center (DIMOC).

Figure 5. White board demonstrating numerous combat casualties with 

multiple injuries. Image courtesy of the Borden Institute, Office of The 

Surgeon General, Washington, DC.
400 | Extremity Injury

Extremity Injury-Associated Mortality

A common preventable cause of battlefield death is limb hemorrhage.

• Casualty fatality rates have remained at an all-time low, while injury severity has increased because of 

lifesaving care such as emergency tourniquet use and improved patient resuscitation.

• A persistent, difficult to manage cause of death is limb hemorrhage too proximal for tourniquet or direct 

pressure control.

• United States (US) military hospital casualty death rates (casualties who died of wounds received in 

action, after arrival at a hospital) are 5 percent despite high injury severity. 

• The orthopaedist is considered the subject matter expert on musculoskeletal injures, tourniquet use, and 

proximal limb hemorrhage. 

Battlefield survival is at an all-time high for US casualties during OEF and OIF. Casualty fatality rates 

have remained at an all-time low while the injury severity has increased because of lifesaving care such as 

improved body armor, emergency tourniquet use, and improved patient resuscitation.15,16,17,18 Orthopaedic 

trauma was the main cause of death in about 7 percent of casualties who were killed in action before 

arrival at a hospital in recent wars (e.g., Somalia, Vietnam), and the most common mechanism of death 

in this cohort was exsanguination.19,20,21,22 Those casualties who died of wounds received in action after 

arrival at a hospital died of a myriad of traumatic sequelae. These included exsanguination, shock, and 

sepsis.20 The rate of those who died of wounds, usually above 10 percent prior to 1900, has decreased 

with treatment advancements. As of 2009, the rate of those who died of wounds is about 5 percent (Fig. 

6).23,24,25,26

Varying definitions of combat casualties who died of wounds make historical comparisons between 

individual wars difficult. Casualty statistics come predominantly from the war victors of modern nations, 

so there is a reporting bias. Although died of wounds is a phrase with a commonly accepted innate 

Figure 6. Rates over time of casualties who died of wounds.

0%

4%

1850

8%

12%

16%

1910 1930 2010

Died of Wounds Rate

Year

1870 1890 1950 1970 1990
Extremity Injury | 401

meaning, its operational definition is very specific 

and less appreciated. Died of wounds received 

in hostile action is a specific casualty category; it 

excludes victims of a terrorist activity and includes 

those who die of wounds or other injuries received 

in action after having reached a medical treatment 

facility. The died of wounds rate generally goes up 

when prehospital care is optimized, as the casualties 

arriving alive at the first hospital generally are 

more severely injured than if prehospital care is 

suboptimal. If prehospital care is suboptimal, the 

killed in action rate generally goes up, and the died 

of wounds rate goes down.27

Battlefield tourniquet use has been shown to be 

a lifesaving intervention when tourniquets are 

applied for limb exsanguination (Fig. 7).15,28 The 

proportion of casualties dying from isolated limb 

exsanguination has dropped from 7 percent to 2 

percent during the course of OEF and OIF. This decrease in mortality is likely due to improved resuscitation, 

better battlefield bandages, and more frequent use of tourniquets in the prehospital setting.6,15,17

The incidence of combat casualties suffering extremity wounds that arrive alive at CCC facilities has 

not changed much over time. Improved survival to hospital discharge is likely the result of resuscitation 

improvements, more rapid evacuation, body armor, and early forward surgery.29,30 The proportion of 

survivors with extremity wounds increases when body armor is used compared to when it is not used. 

The greater lethality of head and torso war wounds results in casualties killed in action, disproportionate 

to casualties with isolated limb injury. The proportion of casualties arriving alive at the hospital with 

extremity injuries is 54 percent in OEF and OIF.2 This is similar to the average projected body surface 

area for the extremities (61 percent) vulnerable to penetrating trauma in adult males proposed by Burns 

and Zuckerman.4,30 Prolonged evacuation times due to tactical situations or other reasons generally 

increase the rates of those killed in action and generally decrease the rates of those who died of wounds 

in a delayed fashion. Shorter evacuation times usually reverse the aforementioned trends.25,29 Recent 

medical advancements and body armor may have saved preferentially more torso-wounded casualties.29 

The proportion of casualties dying from isolated limb exsanguination has dropped from 7 percent to 2 

percent during the course of OEF and OIF. This decrease in mortality is likely due to improved resuscitation, 

better battlefield bandages, and more frequent use of tourniquets in the prehospital setting.

Case fatality rates for limb trauma patients admitted to hospitals have changed dramatically in the last 

century.31 For example, case fatality rates for femur fractures have dropped from 80 percent in early World 

War I to less than 1 percent recently because of such advancements as the use of the Thomas splint before 

arrival at a hospital, intramedullary nailing, and early mobilization rather than bed rest and traction.25,32

Gas gangrene, tetanus infections, and wound sepsis, common in World War I, are uncommon in OEF and 

OIF because of improved surgical debridement, wound irrigation, tetanus immunization, and antibiotic 

advancements.6,25

Figure 7. Battlefield tourniquets applied for limb hemorrhage control 

are a lifesaving intervention. If one tourniquet is ineffective, side-byside (in sequence longitudinally) dual tourniquet use may be effective. 

Image courtesy of the Borden Institute, Office of The Surgeon General, 

Washington, DC.
402 | Extremity Injury

Combat casualty mortality is predominantly related to vascular trauma and hemorrhage for those killed in 

action and those who died of wounds.6,25 Observational data indicate that the type of tissue injured (e.g., 

artery, vein, or muscle), location (proximal versus distal) of the wound, and the mass of tissue wounded are 

associated with trauma outcomes such as death and survival.25,33 For example, pelvic vessel disruption has 

had intermediate lethality between femoral and thoracoabdominal vessel disruption.25 Proximal traumatic 

amputations are more lethal than distal amputations, and traumatic amputations of the lower limbs are 

more lethal than those of the upper limbs.25 Multiple traumatic amputations are more lethal than single 

amputations.20 These findings all converge on the idea that for combat casualties, the larger vessels bleed 

more, and greater tissue loss is associated with greater blood loss and higher mortality (Fig. 8). 

Observational data indicate that the type of tissue injured (e.g., artery, vein, or muscle), location of the 

wound (proximal versus distal), and the mass of tissue wounded are associated with trauma outcomes 

such as death and survival.

Hemorrhage control (in general) and tourniquet use (in particular) have been associated with improved 

combat casualty survival.15,34,35 Emboli and intravascular clots, including deep venous thrombosis, 

Figure 8. Combat casualty mortality is predominantly related to vascular trauma and hemorrhage. Note pressure being applied to bilateral transected 

femoral arteries in this casualty. Image courtesy of the Borden Institute, Office of The Surgeon General, Washington, DC.
Extremity Injury | 403

pulmonary embolism, air embolus, and missile emboli, are uncommon but potentially preventable causes 

of extremity injury-associated death.20 Multiple organ failure and sepsis are additional causes of death that 

are potentially preventable.6,20,25

Since the majority of the combat casualties suffer extremity trauma, orthopaedists are a cornerstone of 

CCC. Orthopaedists should prepare to train, educate, and extend the scope of practice of other CCC 

providers and ancillary staff regarding orthopaedic trauma. The orthopaedist is considered the subject 

matter expert on musculoskeletal injures, tourniquet use, and proximal limb hemorrhage control. 

Emergency Tourniquet Application

Tourniquet use is probably the single most obvious difference in practice between combat and civilian 

casualty care.35

• The objective of emergency tourniquet use is to extinguish the distal pulse, thereby controlling 

bleeding distal to the site of tourniquet application. 

• Tourniquets provide maximal benefit the earlier they are applied following difficult to control extremity 

hemorrhage.

• Improvised (windlass) tourniquets should be applied only when scientifically designed tourniquets are 

absent. A windlass is a lever that can be wound to tighten a tourniquet.

• Tourniquets work better when applied distally (forearms and calves) than when applied more 

proximally (upper arms or thighs).

• Remove clothing and other underlying materials prior to tourniquet application (when possible) to 

ensure a tight and secure tourniquet fit. 

• Remove the clothing surrounding a tourniquet to enable identification of all surrounding wounds and 

injuries.

• Do not apply tourniquets directly over joints as compression of vascular structures and bleeding 

control is limited by overlying bone.

• If one tourniquet is ineffective, side-by-side (in sequence longitudinally) dual tourniquet use may be 

effective.

The current indication for emergency tourniquet use in combat is any compressible limb wound that the 

first responder assesses as possibly lethal.36 Tourniquet use for this indication has demonstrated favorable 

results following optimization of tourniquet design, training, doctrine, casualty evacuation, and tourniquet 

research.15,28 The goals of emergency tourniquet use are to control bleeding and to extinguish the distal 

pulse. Timing and speed of application are vital because tourniquet placement before shock onset saves 

about 20-fold more casualties than placement after shock onset (96 percent survival with use before onset 

of shock versus 4 percent survival after onset of shock). Early prehospital tourniquet application saves 

about 11 percent more lives than delayed in-hospital use.15 Tourniquet use in combat is recommended 

before casualty extraction or transport.36

Tourniquets provide maximal benefit the earlier they are applied for difficult to control extremity 

hemorrhage. Tourniquet placement before the onset of shock is associated with 96 percent survival 

versus 4 percent survival after the onset of shock.
404 | Extremity Injury

How tourniquets are applied has direct patient survival implications. Loose, misplaced, unattended, and 

broken devices have been associated with loss of hemorrhage control and death.15,35 Materials under a 

tourniquet should be removed at the first opportunity to ensure optimal tourniquet constriction.36 Periodic 

reassessment of tourniquets and casualties is vital. For example, a thigh tourniquet can loosen during 

patient transport or manipulation and thus permit rebleeding, especially when there is clothing or gear 

between the tourniquet and the skin.36 A previously tight thigh tourniquet can loosen after exsanguination 

from non-extremity bleeding (e.g., chest, abdomen, or pelvis injuries). A significant loss of total body 

blood volume (e.g., 3.75 liters) will diminish the thigh circumference (volume) under and proximal to 

the tourniquet and will cause tourniquet loosening. Hence serial evaluations and tourniquet retightening 

are vital, when indicated.36 However, reassessment should not include loosening and reapplication until 

surgeons are prepared to directly address the source of hemorrhage.

The objective of emergency tourniquet use is to extinguish the distal pulse, thereby controlling 

bleeding, distal to the site of tourniquet application.

Clothing about a tourniquet should be removed at the first opportunity (when the tactical situation 

permits) to allow detection of all wounds. Undetected wounds are associated with uncontrolled hemorrhage 

and death.36 Surveys are cursory when the applier and the casualty are under gunfire. Hastily performed 

casualty examinations often miss injuries; hence, casualties should be routinely reexamined at each level 

of care. Scientifically designed, laboratory tested, and clinically validated tourniquets should be used 

whenever possible.36,37 The Combat Application Tourniquet (C-A-T®) is the most effective prehospital 

tourniquet (of tourniquets that have undergone clinical trials), and the Emergency & Military Tourniquet 

(EMT) is the most effective emergency department tourniquet.36 Tourniquet effectiveness was defined by 

stopping visible bleeding and elimination of a palpable pulse (Fig. 9). Improvised windlass tourniquets 

should only be used when well-designed and clinically validated tourniquets are unavailable. A windlass is 

a lever that can be wound to tighten a tourniquet.

Figure 9. The indication for emergency tourniquet use in combat is any compressible limb wound that the first responder assesses as potentially lethal.

(Left) The Combat Application Tourniquet® is effective in a prehospital setting. (Right) The Emergency & Military Tourniquet is effective in an 

emergency department setting. Images courtesy of North American Rescue, LLC and Delfi Medical Innovations, Inc.
Extremity Injury | 405

Improvised (windlass) tourniquets should be applied only when scientifically designed tourniquets are 

unavailable.

Tourniquet use over the distal segment of Hunter’s canal near the knee should be avoided because 

prominent bones and tendons risk ineffectiveness. Tourniquets work well, provided they are applied 

proximal to wounds. They work better on the forearm or calf area and need not be reserved for the 

thigh or upper arm as is sometimes recommended for control of distal limb hemorrhage.36 A common 

misconception is that a tourniquet has a lower effectiveness on two-boned segments (forearm and lower 

leg) than on one-boned segments (upper arm and thigh). A tourniquet actually has higher, rather than 

lower, effectiveness on two-boned limb segments.36 The main determinant of effectiveness in well-designed 

tourniquets is the ratio of device width-to-limb circumference.36,38 If one tourniquet is ineffective, then 

side-by-side (in sequence longitudinally) use can extinguish the distal pulse and stop bleeding, as such use 

widens the compressed area. 

If one tourniquet is ineffective, side-by-side (in sequence longitudinally) dual tourniquet use may be 

effective.

Misconceptions regarding tourniquets are rampant and take time and effort to correct.36,38,39,40 Tourniquet 

education, training, and doctrine are vital and should be refined based on clinical evidence. Orthopaedists 

are looked to for tourniquet advice because they commonly use tourniquets during their day-to-day surgical 

practice. Orthopaedists are often asked to educate CCC providers on how and when tourniquets should be 

applied and how to detect and manage tourniquet-related problems. Orthopaedists may even be asked to 

build and steward tourniquet programs (i.e., find, order, store, test, clean, and fix devices, educate users, and 

document adverse events).15,36 

Combat Application Tourniquet (C-A-T®): Application Steps (see Appendix 1)

(1) Route band around injured limb

(2) Pass band through the outside slit

(3) Pull band tight

(4) Twist windlass rod until bleeding has stopped and distal pulse is extinguished

(5) Lock the rod with the clip

(6) Secure the rod with the strap

(7) Record time tourniquet was applied

Limb Compartment Syndrome

• Compartment syndrome continues to cause significant morbidity in OEF and OIF.

• Over-resuscitation with crystalloids can cause compartment syndrome.

• Compartment syndrome is a clinical diagnosis.

• Pressure manometry-based diagnosis of compartment syndrome in combat settings is unreliable.

• Lethal mistakes include delayed or limited fasciotomy skin incisions.

• Fasciotomy is not indicated in patients with prolonged compartment syndromes (warm ischemia 

duration exceeding 12 hours).
406 | Extremity Injury

Introduction

Compartment syndrome is a significant cause of combat-related morbidity in OEF and OIF and is highly 

varied in its presentation.11 For US military casualties with limb injury in OEF and OIF, the incidence 

of compartment syndromes at or before arrival at Landstuhl Regional Medical Center, Germany, is 

15 percent (Kragh, in press).11 Combat casualty careproviders must often manage multiple cases of 

compartment syndrome prior to mastering the subtleties of diagnosis, treatment, and developing the 

ability to identify injured limbs at risk for developing the condition.13

Compartment syndrome continues to cause significant morbidity in OEF and OIF, with an incidence of 

15 percent at or before arrival at Landstuhl Regional Medical Center, Germany.

Definition, Mechanisms, and Risk

Compartment syndrome is defined as an increased interstitial pressure within an enclosed osteofascial 

space (compartment) that reduces capillary blood perfusion below a level necessary for tissue viability.41

As with all ischemia-reperfusion syndromes, duration of ischemia affects severity. Two basic mechanisms 

that cause compartment syndrome are an increase in the volume of tissue within an enclosed space and a 

decrease in the size of the enclosed space. 

The compartment syndrome is common with injuries such as fractures that have severe swelling or 

bleeding.41 Interestingly, open fractures have a higher rate of compartment syndrome than closed fractures 

despite the fascial rents seen with open fractures (Fig. 10). This is likely due to the higher injury force 

seen with open fractures resulting in greater tissue trauma, swelling, and bleeding.41 The occurrence of 

compartment syndrome in a fractured limb has recently been associated with slower subsequent fracture 

healing rates.42 The interstitial pressure of limbs also plays an important role in the mobilization of 

interstitial fluids into the intravascular space in response to distant hemorrhage and the tamponade of 

local intracompartmental hemorrhage. 

The list of causes or risk factors for compartment 

syndrome is long and diverse (Appendix 2).41 In 

combat casualties, more than one contributing 

factor is often present. Current data indicate 

that the most obvious determinant of fasciotomy 

frequency in OEF and OIF is the injury severity of 

the limb wound, based on the Abbreviated Injury 

Scale (AIS) of the most severe extremity wound.11

Limb interstitial tissue pressures increase with 

resuscitation.41 Hence, care must be taken to avoid 

excessive administration of crystalloid fluids that can 

worsen compartment syndrome. The overall injury 

severity score (ISS), frequency of tourniquet use, 

shock, and hypoperfusion also confer compartment 

syndrome risk.11

Over-resuscitation with crystalloids can cause compartment syndrome.

Figure 10. Open fractures have a higher rate of compartment syndrome 

than closed fractures despite the fascial rents seen with open fractures.
Extremity Injury | 407

Clinical Findings

The classic findings seen with acute limb ischemia (i.e., pain, pallor, paresthesias, pulselessness, and 

poikilothermia) are not clinically reliable for the diagnosis of compartment syndrome and often manifest 

only in the late stages of compartment syndrome.41 The finding of distal limb pulselessness is due to 

compression of arteries within the compartment. Civilian literature reports that pulselessness is a late 

clinical finding in compartment syndrome.41 The authors’ experiences in OIF revealed similar findings. 

Pulselessness is rarely seen, and it is usually a late finding when it is documented. In an alert and cooperative 

patient, compartment syndrome is manifest by pain out of proportion to the physical injury observed. The 

pain is typically worse with passive stretch of the muscles within the ischemic compartment. This pain on 

passive stretch is a sensitive indicator of compartment syndrome as it occurs early in its course; however, 

it is not specific.43,44 While a palpably tense compartment is a specific clinical finding, it is not highly 

sensitive.45 Sensory symptoms such as paresthesias are often an early indicator of nerve ischemia.46 

Compartment syndrome is a clinical diagnosis. Clinicians must weigh the mechanism of injury and 

suggestive clinical findings, including pain with passive stretch, palpable tenseness of the affected 

compartment, and neurovascular examination to arrive at the diagnosis.

The time of onset of compartment syndrome is often hours following injury, but it can occasionally 

present within minutes of injury.47 The authors have seen florid compartment syndrome cases in OIF 

that presented within 15 to 45 minutes of injury with pulselessness that was rapidly reversed following 

fasciotomy.47 Clinical findings in casualties with compartment syndromes can be classified as early and 

late. Early findings such as a palpably tense compartment, pain out of proportion to the injury, and pain 

with passive stretch of involved muscles are due to the elevated hydrostatic pressure within the fascial 

compartment.41 Late findings of paresthesias and paralysis are due to the duration of tissue ischemia, 

particularly of nerves and muscle, respectively. Permanent nerve palsy is uncommon with compartment 

syndrome. The etiology of extremity weakness may be difficult to differentiate clinically from myopathy 

of ischemia-reperfusion, which is common and associated with the duration of ischemia.41 The pressure 

gradient applied to the nerve (such as with a tourniquet) deforms the nerve at the point of maximal 

gradient (e.g., at the tourniquet edge) and is the cause of the nerve palsy. Nerve palsy clinically resolves 

slower than nerve ischemia but usually completely resolves.36 Nerve ischemia is zonal, not focal, and is 

rarely severe in the emergency setting. It is associated with prolonged ischemia time.36 Muscle is the tissue 

most sensitive to the duration of ischemia, the nerve is less so. 

The rate of limb swelling is greatest early after injury, as tissue compartments are more pliable. Limbs 

typically reach maximum swelling 36 to 48 hours following injury.48 Resolution of limb swelling occurs 

over a similar duration.49 Comorbidities such as hemorrhagic shock and treatments (e.g., tourniquets and 

resuscitation) may alter swelling timelines, such that maximal swelling occurs up to five days following 

injury. This can result in discordant total body fluid intake and output measurements.49 This means that 

compartment syndrome can be absent early at a forward treatment facility, yet occur from one to four 

days later during evacuation to rearward hospitals.13 Furthermore, even if a fasciotomy is performed at 

a forward hospital, continued swelling can cause recurrent compartment syndrome if the release was 

not complete. This occurrence is associated with increased amputation and mortality rates.13 The degree 

of swelling is also associated with the degree of injury and the degree of over-resuscitation, particularly 

with fluids more dilute than plasma.13,49
408 | Extremity Injury

Recurrent compartment syndrome can be seen with incomplete release of compartments and is 

associated with increased amputation and mortality rates.

Prevention and identification of compartment syndrome are difficult. Historically, under-resuscitation 

was associated with acute renal failure. Subsequently, over-resuscitation with excessive fluids was linked to 

excessive limb edema and compartment syndromes, even in uninjured limbs.50,51 Over-resuscitation leading 

to limb compartment syndrome is analogous to over-resuscitation leading to abdominal compartment 

syndrome.50,52 Modern resuscitation has evolved towards physiologically-based targets (e.g., controlled 

hypotension with adequate perfusion), rather than simply replacing the estimated volume of blood loss with 

crystalloid fluids. Over-resuscitation has become less common recently.16,53

Diagnosis

The diagnosis of compartment syndrome in war is based on clinical findings. Clinicians must weigh 

the mechanism of injury (e.g., blast) and suggestive clinical findings, including pain with passive stretch, 

palpable tenseness of the affected compartment, and neurovascular examination to arrive at the diagnosis. 

Common laboratory tests suggestive (but not diagnostic) of late or missed compartment syndrome, 

include elevated serum levels of creatinine kinase and urine myoglobinuria.41 Due to limited sensitivity 

and specificity of clinical and laboratory findings, the diagnosis of compartment syndrome in the civilian 

sector is highly dependent on measuring tissue compartment pressures.54 It is common civilian practice 

to measure compartment pressure before and after fasciotomy to confirm both the diagnosis and the 

efficacy of fascial release.54 The accuracy of manometric-based diagnosis of compartment syndrome is 

unreliable in combat settings, and its use is not recommended.47 Limb tissues such as muscle compartments 

are not incompressible matter (such as water) and do not transmit pressures fully or immediately like 

incompressible fluids. Time and distance attenuate high pressures within limb tissues. Failure to measure 

tissue pressure in proximity (e.g., within five centimeters) to the zone of peak pressure may result in a 

serious underestimation of the maximum compartment pressure.55

Manometric-based diagnosis of compartment syndrome in combat settings is unreliable and not 

recommended.

Even the methods and pressure threshold used for 

diagnosis are controversial. Pressures are indirect 

indicators of ischemia, and the amplitude of 

the pressure does not account for the ischemic 

duration, individual tolerance of ischemia, 

variations of anatomic compartments, and location 

of measurement versus pathology, such as fracture 

site.54 No consensus exists on whether the pressure 

threshold within the compartment should be 

30 or 45 mm Hg (4 to 6 kilopascals) or whether 

the difference between the intracompartmental 

pressure from the blood pressure such as the 

diastolic blood pressure (delta pressure) should be 

30 or 40 mm Hg (4 to 5.33 kilopascals).54 There is Figure 11. Manometric-based diagnosis of compartment syndrome in 

combat settings is unreliable.
Extremity Injury | 409

even a lack of consensus regarding the type of catheters (slit, wick, and ultrafiltration) that should be used 

to measure compartmental pressures (Fig. 11).43 

Observation and serial clinical examination of patients with limb trauma and equivocal compartment 

syndrome clinical findings are common in civilian settings. In such cases, recent interventions (e.g., 

aggressive fluid resuscitation) combined with mechanism of injury and evolving physical findings, such 

as a palpably tense compartment, can facilitate early diagnosis. In the mentally impaired (e.g., sedated, 

intubated, or unconscious) casualty, diagnosis of compartment syndrome is difficult because the clinical 

examination is less sensitive. Similarly, in combat settings, serial examinations may be impossible or 

unreliable because patients are often evacuated long distances under austere conditions. In such scenarios, 

prophylactic fasciotomies are recommended prior to transport based on clinical findings, extent of softtissue injury, anticipated resuscitation, and potential ischemia time.56 Circular casts, which are common 

in civilian settings, are usually avoided in war, since evacuation over distances and time without close 

monitoring permit the onset of compartment syndrome without detection or treatment.13,57

Delayed attempts at therapeutic fasciotomies are suboptimal and are associated with increased morbidity 

and mortality. Certain clinical findings – wounds with extensive soft-tissue injury, anticipated lengthy 

resuscitation, and potential extended ischemia time – should prompt prophylactic fasciotomies prior to 

evacuation of patients. 

Failure to detect compartment syndrome early risks rhabdomyolysis, renal failure, Volkmann’s ischemic 

contracture (ischemic muscle necrosis), and permanent limb dysfunction.41 Delayed attempts at therapeutic 

fasciotomies are suboptimal and are associated with increased morbidity and mortality.13

Treatment

The definitive treatment for acute compartment syndrome is therapeutic fasciotomy. When compartment 

syndrome is risked or is impending during the lag time from injury to syndrome onset, the fasciotomy is 

termed prophylactic.47

Evidence indicates a delayed fasciotomy is not indicated for casualties with a prolonged compartment 

syndrome (i.e., warm ischemia duration greater than 12 hours).14,58 Fasciotomy in this subset of patients 

will increase infection rates and will decrease survival.47 An algorithm for clinical decision making on 

compartment syndrome management in a combat setting is provided in Figure 1 within Appendix 2.

Fasciotomy is not indicated for casualties with a prolonged compartment syndrome (i.e., warm ischemia 

duration greater than 12 hours).

Temporizing measures such as removing circumferential dressings or casts, removing sutures from tightly 

bound closures, and placing the affected limb at the level of the heart to balance inflow and venous return 

do no harm but are inadequate to treat an established compartment syndrome. In a casualty, marked 

elevation or dependence of the injured limb relative to the heart can increase risk of compartment 

syndrome, especially if the casualty is at risk for or is in hemorrhagic shock.41 Extremity elevation is 

contraindicated because it decreases arterial blood flow and the arteriovenous pressure gradient and thus 

worsens the ischemia.

59
410 | Extremity Injury

Marked elevation or depression of the injured limb relative to the heart can increase the risk of 

compartment syndrome.

The sequelae of neglected or delayed treatment of compartment syndrome are ischemic contractures, 

nerve injury (due to nerve ischemia), potential amputation, systemic effects of myonecrosis, and death.13,54 

The morbidity risk and sequelae of compartment syndrome and fasciotomy are outlined in detail in 

Table 1.

Figure 12. The fasciotomy skin incision should be long, approximating 

the proximal to distal length of the compartment to be released. Image 

courtesy of the Borden Institute, Office of The Surgeon General, 

Washington, DC.

Figure 13. Limited fasciotomy skin incisions, as seen above, should be 

avoided.

Morbidity Risk and Sequelae of Compartment Syndrome and Fasciotomy

Potential Morbidity:

Compartment Syndrome 

and Early Fasciotomy

Skin scar, scaly skin, ulceration, tethered tendons

Postoperative arterial or graft thrombosis, thromboembolic disease wound 

infection, nonhealing fasciotomy wounds

Limb swelling or chronic edema, shape change of limb, muscle hernia

Pain, paresis or paralysis, paresthesia

Coverage challenge: primary closure, delayed primary closure, skin graft, flap

Possible repair of arterial injury worsening ischemia-reperfusion injury

Potential Sequelae List: 

Compartment Syndrome 

with Late or Incomplete 

Fasciotomy

Mortality, sepsis, multiple organ failure, acute kidney failure

Myonecrosis, myoglobinemia, myoglobinuria, or rhabdomyolysis

Paresis or paralysis

Stiffness or contracture

Limb amputation, tissue loss (e.g., muscle debridement)

Table 1. Morbidity risk and sequelae of compartment syndrome and fasciotomy.
Extremity Injury | 411

Fasciotomy Surgical Steps (Leg as an Example)

1. Initiate surgical positioning (supine); palpate bony landmarks and septum between anterior and 

lateral compartments.

2. Plan and mark incisions for dermotomies; do not use one-incision technique; use two-incision 

technique.

3. Make a medial skin incision: longitudinal posterior to tibia margin; avoid saphenous vein and nerve; 

from proximal tibia near the pes anserinus to the proximal ankle flexor retinaculum; do not use 

short skin incisions.

4. Make a lateral skin incision: near the septum between the anterior and the lateral compartments; 

avoid the superficial peroneal nerve from the proximal tibia margin near iliotibial band insertion on 

Gerdy’s tubercle to the proximal ankle extensor retinaculum; do not use short skin incisions.

5. Expose the lateral leg fascia for a visual and palpable check of bony landmarks and septum between 

the anterior and the lateral compartments.

6. Divide the lateral fascia transversely at the septum to confirm entry into both the anterior and the 

lateral compartments. Extend this fasciotomy anterior and posterior enough for confirmation; use 

instrument or finger to confirm entry into both compartments.

7. Divide the lateral leg fascia longitudinally from the transverse fasciotomy; do this both proximally 

and distally for both the anterior and the lateral compartments.

8. Anterior compartment fasciotomy goes from the proximal tibia margin near the iliotibial band 

insertion on Gerdy’s tubercle to the proximal ankle extensor retinaculum. Partially release onequarter inch of the retinaculum; do not use short fascia incisions.

9. Superficial medial fasciotomy releases the posterior superficial compartment and goes from the 

proximal tibia margin near the pes to the proximal ankle flexor retinaculum. Partially release onequarter inch of the retinaculum; do not use short fascia incisions.

10. Deep medial fasciotomy releases the deep posterior compartment and goes along the posterior 

medial tibia margin. Release the medial soleus margin from the tibia; check especially deep and 

proximal.

11. Check muscle bulge after fasciotomy; palpably confirm the adequacy of all releases.

Table 2. Fasciotomy surgical steps using the leg as an example.
412 | Extremity Injury

Fasciotomy Techniques

Extremity fasciotomy can be performed as an emergent bedside procedure but is preferably undertaken in 

the operative suite where anesthesia, sterile conditions, adequate lighting, and appropriate equipment are 

readily available (Table 2). Skin incisions (dermotomies) provide nearly no compartment release in and of 

themselves. The fasciotomy skin incision should be long because fasciotomy will need to span the length of 

the compartment itself.54 The skin incision approximates the proximal to distal length of the compartment to 

be released (Figs. 12 and 13). Long skin incisions permit proper palpation and inspection of the compartment 

pressure and fascial release. Fasciotomies in civilian settings are often shorter because injury severities and 

compartment syndromes are less severe than in military settings and because reassessments are easier. 

A detailed outline of compartment names and corresponding main muscle groups and diagnostic and 

procedural codes used for CCC documentation are provided in Table 4 within Appendix 2. An operative 

note template for dictation, surgical planning, and data collection is provided in Table 5 within Appendix 2.

Limited fasciotomy skin incisions should be avoided. Skin incisions should be long, as a fasciotomy will 

need to span the length of the compartment itself.

Lower Leg Fasciotomy

For the lower extremities, the common compartments that need release are in the lower leg (calf) and 

thigh. The four compartments of the lower leg consist of the anterior, lateral, superficial posterior, and 

deep posterior compartments. These compartments are typically released with longitudinal medial and 

lateral incisions (two skin incisions) (Fig. 14). One skin incision versus two skin incisions risks incomplete 

Figure 14. The four compartments of the lower leg are typically released 

with longitudinal lateral and medial skin incisions as demonstrated in the 

adjacent images. Images courtesy of the Borden Institute, Office of The 

Surgeon General, Washington, DC.
Extremity Injury | 413

fascial release since it is associated with both an inadequate inspection and inadequate palpation of 

muscles and fascia; this includes an inadequate check of the completeness of the release. The lower leg 

compartments are the ones most commonly released late, and should be released earlier in such cases 

prior to swelling reaching its maximum at the index surgery.13 The anterior leg compartment fasciotomy in 

war can include a partial (five millimeter) release of the proximal portion of extensor tendon retinaculum 

near the ankle. This should ensure that the distal extent of the fasciotomy is sufficiently complete.

A double-skin incision technique should be used to release the four compartments of the lower leg in 

combat casualties.

Thigh Fasciotomy

The thigh has three large compartments (anterior, posterior, and adductor), which are released with 

longitudinal medial and lateral incisions. The lateral thigh incision, used to access both the anterior and 

the posterior thigh compartments, can be extended to release the hip abductor muscles, tensor fascia lata, 

and gluteal muscles (Fig. 15).41

Upper Arm Fasciotomy

The upper arm contains three compartments: one anterior, one posterior, and one for the deltoid muscle. 

These compartments are typically approached with medial and lateral skin incisions, and the lateral incision 

may also be extended to include release of the deltoid compartment.41

Forearm Fasciotomy

In the forearm, the three compartments are dorsal, volar, and mobile wad muscles. The forearm fascial 

release is typically through one volar skin incision and one dorsal skin incision. The volar skin incision 

provides access to the mobile wad, superficial, and deep volar musculature and may be extended distally 

for the carpal tunnel release. The dorsal skin incision is used to release the contents of the dorsal forearm 

compartment. Individual forearm muscle epimysium, the layer of connective tissue that ensheaths an 

entire muscle, may be as robust as the superficial fascia of the forearm resulting in elevated pressures 

within individual muscle belly sheaths. Thus, each muscle belly, especially volar, should be inspected for 

possible release (epimysiotomy) in addition to release of the forearm fascia (Fig. 16).41

Hand Compartment Fasciotomy

Hand compartments can be released through five skin incisions: two dorsally-based incisions over the 

index and ring finger metacarpals; one radial incision over the thenar muscles; one ulnar incision over 

the hypothenar muscles; and the final skin incision for the carpal tunnel release (Fig. 17).41 Carpal tunnel 

release is commonly performed too late. The carpal tunnel should be released at the index surgery before 

swelling has reached its maximum.13

Conclusions

Short skin incisions and incomplete fasciotomies risk mortality and morbidity.13 Long skin incisions should 

be made to ensure adequate exposure of the deepest portion of the wound.60 A single skin incision of the 

lower leg for a four-compartment fasciotomy may work well in civilian care, but it has not worked well in 

war. A double-skin incision technique should be used in combat casualties. Orthopaedists serve patients 

well if they make themselves widely available for consultation regarding combat casualties at risk for 

compartment syndrome.
414 | Extremity Injury

Figure 15. The lateral thigh incision can be used to access the anterior 

and posterior thigh compartments and can be extended to release the hip 

abductor muscles, tensor fascia lata, and gluteal muscles. Image courtesy of 

Defense Imagery Management Operations Center (DIMOC).

Figure 16. Volar forearm debridement and fasciotomy. Each muscle 

belly should be inspected for possible release (epimysiotomy) in addition to 

release of the forearm fascia. Image courtesy of the Borden Institute, Office 

of The Surgeon General, Washington, DC.

Figure 17. (Middle Left) Hand compartment syndrome. (Middle Right) Dorsal skin incisions. (Bottom Left) Carpal tunnel release. (Bottom 

Right) Skin closure at 96 hours. Images courtesy of Rady Rahban, MD.
Extremity Injury | 415

Traumatic Limb Amputations 

• Blast injury is a common cause of traumatic limb amputation.

• Traumatic limb amputations may be multiple and can result in lethal hemorrhage.

• Careproviders should provide immediate lifesaving interventions and avoid becoming distracted by 

visually disturbing limb amputations. 

• The distal segments of amputated limbs should be checked for viable autologous vein graft sources 

before disposal. 

• Traumatic fasciotomies are not a substitute for the purposeful and complete surgical release of 

compartment fascia.

• The preservation of vital tissues achieved through atypical delayed surgical amputations may result in 

better functional outcomes than limb shortening in order to get a conventional wound closure.

Introduction

The term amputation can refer to an injury, an emergent procedure, a delayed procedure in planned 

staged care, a delayed procedure for treatment or prevention of a complication, an elective procedure 

perhaps for limb dysfunction, or an outcome. Thus, the context of usage for the term amputation should 

be made explicitly clear in medical communications and records by the provider and coder (Appendix 3). 

Care notes are often written with indelible markers on adhesive tape applied to the casualty in order to get 

important information to rearward hospitals when records are otherwise at risk of being lost (Fig. 18). 

Historically, most major limb amputations in combat settings were injuries as the result of extensive 

limb trauma, a surgery for consequence of severe infection, or a surgery for irreparable major arterial 

injury.61,62,63 The percentage of limbs lost because of major vascular trauma and severe infection had 

decreased in modern warfare. However, the greater use of explosive weapons in OEF and OIF has resulted 

in a steady number of limbs lost because of massive blast injuries.64 Traumatic limb amputation accounts 

for 7.4 percent of major limb injuries in OEF and OIF; it was 8.3 percent in the Vietnam War.61,64

Blast injury is a common cause of traumatic limb amputation; traumatic limb amputation accounts for 

7.4 percent of major limb injuries in OEF and OIF.

Limb salvage can occur when war surgeons use damage control vascular surgery principles and a team 

approach to injury triage and patient resuscitation.65,66,67 It is important to note that surgical amputation 

(when indicated) should not be considered a failure of care, but rather, a key step of maximizing limb 

function. After debridement of all nonviable tissues, a reconstructive mindset and approach by careproviders 

are critical. A second operation to check the wound for possible debridement should be routinely planned 

24 to 48 hours after the initial debridement, depending on the amount of initial tissue destruction and 

wound contamination. A fracture proximal to a traumatic amputation should be stabilized and is not an 

indication for more proximal amputation since successful fixation can help retain a longer and possibly 

more functional residual limb. The principle is to retain the maximum number of options for definitive 

care.63

Initial Assessment

The closer the limb is to the explosion, the higher the likelihood of amputation. Casualties closer to 
416 | Extremity Injury

explosions may have multiple amputations. The amputation site generally correlates with lesion severity as 

in the Abbreviated Injury Scale (AIS); more proximal lesions are more severe and lethal. Traumatic limb 

amputations are visually very disturbing, even to seasoned careproviders and can distract CCC providers 

from delivering optimal patient care (Fig. 19). Traumatic limb amputations are devastating injuries; 

however, if appropriately managed, patient morbidity and mortality can be minimized.15,63 

The initial therapeutic approach to the patient with a traumatic amputation should follow the same protocol 

as with all combat casualties. The emphasis should be placed on identifying and treating immediately lifethreatening conditions first. Once immediate life-threats are mitigated, further evaluation of a traumatic 

limb amputation is warranted. The zone of injury may be wide and not limited to the direct penetrating 

portion of the explosion, as the blunt effects may be proximal to the open wound. The degree of wound 

contamination can be severe. 

Traumatic limb amputations may be multiple and can result in lethal hemorrhage. Careproviders should 

provide immediate lifesaving interventions and avoid becoming distracted by visually disturbing limb 

amputations.

Severe limb injuries, like subtotal traumatic amputations and mangled limbs, have been evaluated using 

a scale and assigned a score in order to help assess treatment options, such as the likelihood of successful 

limb salvage. Such efforts have been limited in their ability to predict outcomes or dictate care.68 Similarly, 

the prognostic value of the insensate foot in association with limb salvage or surgical amputation has been 

evaluated. Researchers concluded that the insensate foot at presentation is neither prognostic of long-term 

plantar sensory status nor functional outcome, and should not be a component of a limb-salvage decision 

algorithm.69 Two small case series have described how the technique of shortening and angulation of 

extremities with significant soft-tissue and bone loss can facilitate soft-tissue coverage.70,71 Delayed gradual 

distraction of the shortened extremities is performed with a hinged circular external fixator. Further studies 

of this promising technique are required. 

Figure 18. Improvised patient information communication strategy. 

Patient information is written directly onto the dressing of a patient 

emerging from surgery. Image courtesy of Harold Bohman, MD, CAPT, 

MC, US Navy.

Figure 19. Although traumatic limb amputations are devastating injuries, 

patient morbidity and mortality can be minimized with appropriate 

management. Image courtesy of the Borden Institute, Office of The 

Surgeon General, Washington, DC.
Extremity Injury | 417

Initial Resuscitation

Massive extremity hemorrhage is often an immediate life-threat in patients with traumatic proximal 

limb amputations.36 An appropriately applied tourniquet on the residual proximal limb can be a firstline lifesaving intervention in such patients.15 Proximal surgical control of the vascular structures can 

control distal sources of hemorrhage. Following the control of active limb hemorrhage, the patient can be 

evaluated for other life-threatening conditions followed by resuscitation of the casualty and the residual 

limb. Tactical situations such as extraction of casualties entrapped within vehicles (under enemy fire) 

may present unusual circumstances for prehospital surgical amputation. The amputated limb should 

accompany the casualty and should be assessed as a possible source of autologous vein graft harvesting.66

Ideally, only the treating surgeon should discard the distal limb in order to ensure its therapeutic value to 

patient care has been fully assessed.

An amputated limb should be assessed as a possible source of autologous vein graft harvesting and 

discarded only after its therapeutic value to patient care has been fully considered.

Primary (Completion) Amputation

In traumatic limb amputations, the nonviable distal 

portion is often attached to the proximal portion by 

a small skin bridge or a few intact tendons that span 

a segment of lost tissue. Transecting such bridging 

tissue is called a primary or completion amputation 

(Fig. 20). Primary amputation is indicated if the 

limb cannot be reconstructed or salvaged. This 

procedure is occasionally done in the emergency 

department, but it is typically performed during the 

first visit to the operating room. Other indications 

for primary (completion) amputation include: (1) 

ischemic limbs with irreparable vascular injury; (2) 

hemorrhage control refractory to other means; 

and (3) enabling lifesaving resuscitation in a patient 

whose injury physiologic burden (e.g., ongoing 

shock, hypothermia, acidosis, coagulopathy, or 

infection) will not permit limb salvage.63 The latter 

exemplifies when limb-salvage techniques are 

beyond the physiologic capacity of the patient.65

Primary amputation is indicated if a limb cannot be reconstructed or salvaged. Primary amputation 

indications include ischemic limbs with irreparable vascular injury, hemorrhage control refractory to 

other means, or when limb salvage is beyond the physiologic capacity of the patient.

Wound Debridement

Successful debridement depends on the surgeon’s capacity to assess tissue for viability and the ability of the 

surgeon to remove contaminants.72 Wounds associated with traumatic limb amputation are often grossly 

Figure 20. Primary amputation is indicated if a limb cannot be 

reconstructed or salvaged. Image courtesy of the Borden Institute, Office of 

The Surgeon General, Washington, DC.
418 | Extremity Injury

contaminated and contain nonviable tissue in need of surgical debridement and copious irrigation (Fig. 21). 

During surgical debridement, all viable and uncontaminated tissues, however random in nature, should 

be retained with the hope of preserving maximal limb length and function.73 Retention of maximum 

nerve length, especially in the upper extremity, has value since targeted reinnervation is possible later.74

Therefore, in the initial surgery, resection of nerves should not be routinely performed. 

During surgical debridement for completion amputation, all viable and uncontaminated tissues should 

be retained with the hope of preserving maximal limb length and function.

Certain types of wound contaminants may require special care. Oil-laden wounds may require soap 

or an additive that may safely aid in the removal of what is not water-soluble. Unfortunately, there is 

little data to determine best practices. White phosphorus is a chemical that is in some munitions used 

for illumination. White phosphorus is actually a yellow, waxy chemical that ignites spontaneously when 

exposed to air.75 It is used as a filling for various projectiles, as a smoke-producing agent, and has an 

incendiary effect. White phosphorous smoking wounds can be covered in saline, but this only temporarily 

staves off recombustion. There is a thermal component to the injury when there is combustion as it is an 

exothermic process. Most of the cutaneous injury resulting from white phosphorus burns is due to the 

Figure 21. (Left) Wounds associated with traumatic limb amputation are 

often grossly contaminated and contain nonviable tissue in need of surgical 

debridement and copious irrigation. (Above) During surgical debridement, 

all viable tissues should be retained with the hope of preserving maximal 

limb length and function. Images courtesy of Glenn J. Kerr, MD, MAJ, 

MC, US Army.
Extremity Injury | 419

ignition of clothing and is treated as a conventional 

burn. Copper sulfate was once recommended 

for aid in locating the white phosphorus during 

debridement, but this is no longer recommended 

as copper sulfate use is associated with fatal 

hemolysis.75 If copper sulfate solutions are used, 

they should be washed away immediately and not 

used as a wet dressing. White phosphorus-injured 

patients should be dressed with saline-soaked 

dressings to prevent reignition of the phosphorus 

by contact with the air.76 Members of the US 

Army Burn Center have patented a gel for use in 

treatment of white phosphorus wounds, but there 

is little data regarding its use in a combat setting. 

Fasciotomy

Fasciotomy is often necessary in limbs with 

traumatic amputations. It would be a mistake to 

think that surgical fasciotomies are not necessary 

following traumatic amputations. While traumatic 

limb amputations create fascial disruptions, 

these traumatic fasciotomies (disruptions) do not 

adequately reduce intracompartmental pressures 

and do not equate to a surgical fasciotomy. 

Traumatic fasciotomies are not a substitute for 

the purposeful and complete surgical release of 

compartment pressures.41 The injury proximal to 

Figure 22. Surgical limb preparation should be quite proximal because 

the zone of injury or planes of traumatic dissection may be more proximal 

than suspected on physical examination.

Figure 23. Combat extremity wounds should not be closed primarily. 

This residual proximal limb wound was dressed with bulky dry dressings. 

Image courtesy of Glenn J. Kerr, MD, MAJ, MC, US Army

Figure 24. Skin traction remains an option to preserve limb length if there 

is a planned four (or more) day interval between surgeries. Image courtesy 

of the Borden Institute, Office of The Surgeon General, Washington, DC. 

Illustrator: Jessica Shull.
420 | Extremity Injury

the amputation may also warrant fascial release. The fascial compartments of the residual proximal limb 

should be examined and fasciotomies performed if necessary for treatment or prevention of compartment 

syndrome.

Traumatic fasciotomies are not a substitute for the purposeful and complete surgical release of 

compartments.

Surgical Amputation and Wound Care 

Surgical limb preparation should be very proximal (sometimes more proximal than the groin or axilla) 

because the zone of injury or planes of traumatic dissection are more proximal than suspected on 

physical examination (Fig. 22). Proximal control of arteries may require access to the pelvis, abdomen, 

or chest. Use of a tourniquet during the surgery is common to help with hemorrhage control. Ligation 

of distal major artery and vein injuries is indicated to avoid rebleeding after resuscitation, transport, 

limb mobilization, or dressing changes. Traumatic nerve stumps have gentle traction applied and are 

sharply transected proximal to the zone of injury and proximal enough so that the nerve retracts under 

soft-tissue. Large nerves, such as the sciatic nerve, may require ligation if the vessels within them bleed. 

Failure to ligate such nerves may risk rebleeding. 

Combat extremity wounds are not closed primarily. The skin can often be loosely approximated with 

a few sutures to keep some skin tension and coverage while allowing drainage from the open wounds 

during transport (Fig. 23). Skin traction remains an option to preserve limb length if there is a planned 

four or more day interval between surgeries. Skin traction technique and postoperative management 

are described well in the Emergency War Surgery Manual (Figs. 24 and 25).63 The residual proximal 

limb should be dressed with bulky dry dressings. While data are limited to anecdotal reports by war 

surgeons, negative-pressure wound therapy appears best avoided at the initial surgery for wounds at risk 

for rebleeding. Negative-pressure wound dressings can be considered after the casualty and wounds are 

stable without bleeding for 48 hours (following initial resuscitation) (Fig. 26). 

Delayed Amputation 

Indications for delayed limb amputation may include complications like refractory wound sepsis, failed 

Figure 25. A bivalved transportation cast (prior to patient transport) 

allows for continuous traction. Image courtesy of the Borden Institute, 

Office of The Surgeon General, Washington, DC. Illustrator: Jessica 

Shull.

Figure 26. Negative-pressure wound dressings can be considered after the 

casualty is stable and wounds are without bleeding for 48 hours following 

initial resuscitation.
Extremity Injury | 421

flap coverage or limb salvage (due to vascular or musculoskeletal causes), and selective amputation to 

optimize limb function (e.g., relieve pain or prosthetic fitting).77 Selective amputation is performed when 

the distal salvaged limb function is less than that with a prosthetic. This decision is typically deferred 

to the definitive treatment facility after discussion with the casualty. Standard, conventional amputation 

levels were developed mostly from patients with diabetic vasculopathies. These standard civilian-based 

practices do not apply to most combat casualties. Positive outcomes have been documented for amputees 

undergoing delayed surgical amputations of atypical configurations (level and flaps).77 Atypical surgical 

amputations do not employ standard or traditional levels of bony cuts, standard (textbook) skin incisions, 

or typical musculofascial flaps to cover the cut bone and conform to conventional prosthetic fittings.77

Initial efforts to maximally salvage viable tissue following atypical limb amputations enable broader 

future treatment options for the distal limb. Thus, preservation of viable tissues appears to result in better 

outcomes than limb shortening in order to get a typical wound closure.77 Open guillotine amputations have 

fallen out of favor and are only performed based on the specific margins of tissue loss or necrosis.77 The 

US Army recommends performing atypical amputations so that rearward care can optimize outcomes.78

Tissue viability is used to determine the extent of debridement. The initial surgery is performed without 

regard for the likely subsequent amputation level. 

The preservation of vital tissues achieved through atypical delayed surgical amputations may result 

in better functional outcomes than limb shortening performed in order to get a conventional wound 

closure.

Atypical stump flaps (sometimes called flaps of opportunity) can be used in later surgeries to close the 

wound when it is ready for closure (Fig. 27). Such flaps are not fashioned during the initial surgery. For 

example, short (as little as one- to two-centimeter stumps) and even incomplete transtibial stumps can 

help avoid problems with through-the-knee amputations like the retraction of tendons or skin that may 

force more proximal amputation later for definitive wound closure. 

Figure 27. Atypical stump flaps (sometimes called flaps of opportunity) can be used in later surgeries to close the wound when it is ready for closure. 

Images courtesy of Robert R. Granville, MD, COL, MC, US Army.
422 | Extremity Injury

Rehabilitation

Rehabilitation services at specialized amputee centers have been documented to result in improved 

outcomes.79 Besides the surgical reconstruction of residual limbs (flaps, bone grafting, amputation revision), 

casualties undergo a comprehensive evaluation and treatment plan for a broad spectrum of issues like 

traumatic brain injury, tympanic membrane rupture, and psychological and social screening. Currently 

in the US military, a physiatrist is often the leader of the rehabilitation team. Each casualty is routinely 

assigned a case manager for coordination of the myriad of medical and administrative issues they will face. 

Casualties are sent to the most appropriate facility based on injury severity. Rehabilitative care may be 

provided at a small base and hospital (simple injuries) or may occur at a tertiary medical center (complex 

injuries). One tertiary care center is San Antonio Military Medical Center (formerly Brooke Army Medical 

Center), which is a Level I trauma center with a burn center and a rehabilitative and amputee center called 

the Center for the Intrepid.80,81,82 In summary, refinements in traumatic amputation care, amputation 

surgery, and aftercare have led to improved patient outcomes.83,84

Combat Casualty Wound Care

• The management of combat wounds differs from civilian wound care. 

• Combat wounds differ in degree and number from wounds occurring in the civilian sector.

• Combat wounds evolve more rapidly than civilian wounds and require more frequent reevaluation 

following injury.

• Initial postoperative dressings on blast injuries should routinely be dry, bulky dressings.

Figure 28. Combat wounds evolve more rapidly than civilian wounds and require more frequent reevaluation following injury. Over time, bleeding and 

swelling ensue and resolve, while tissues can become devitalized and revitalized. This sequence of images shows the initial wound on day one (Top Left) 

and evolution (Left to Right) of the wound in response to multiple debridements over a two-week timeframe (Bottom Right).
Extremity Injury | 423

Introduction

War wounds are often the result of higher-energy mechanisms than those in civilian sector. As such, 

combat wound size, severity, and lethality are often greater.56 Combat-associated wounds evolve in the 

hours to days following the initial injury. What one careprovider sees at the point-of-injury often differs 

substantially from what is seen at the forward hospital (hours later) and then the rearward hospitals (days 

later) (Fig. 28). Over time, bleeding and swelling ensue and resolve while tissues can become devitalized 

and revitalized. Wound edema typically peaks at one to two days following the initial injury.48,56 However, 

the consequences of initial treatments (e.g., tourniquet ischemia reperfusion and resuscitation fluid edema) 

may delay the timing of maximal edema to five days.56 Both the magnitude of tissue edema and the 

variability of the time lag from initial injury to maximal edema can be startling to careproviders who have 

minimal CCC experience.13

Combat wounds evolve more rapidly than civilian wounds and require more frequent reevaluation 

following injury.

Extremity Resuscitation and Wound Management

Following injury (battle conditions permitting), initial wound treatment involves covering of wounds with 

sterile dry dressing bandages and splinting of bony injuries to prevent further injury.85 Combat casualty 

care providers should address obvious life-threatening priorities first. The life-over-limb principle always 

applies. Uncontrolled limb wound hemorrhage is often identified as an immediate priority. Hemorrhage 

control options include: (1) manual direct pressure over the wound or proximal pressure points; (2) limb 

elevation; (3) hemostatic dressings; and (4) extremity tourniquet application. Tourniquets, a hemorrhage 

control adjunct to damage control resuscitation, provide maximal benefit the earlier they are applied 

following difficult to control extremity wound hemorrhage.15 

Once the patient has been evacuated from the point-of-injury to the next echelon of care, the combat 

casualty should be reassessed. Immediate life-threats need to be addressed, including the control of any 

persisting wound hemorrhage. Subsequent to addressing immediate life-threats, limb wound management 

should consist of neurovascular examination of the limb, wound inspection, and wound irrigation with the 

goal of removing gross contamination.85 If limb salvage is an option, limb perfusion must be optimized 

Care of A Combat Limb Wound

• Control hemorrhage; tourniquets are temporary adjuncts

• Prevent or treat shock, hypothermia, and coagulopathy

• Immobilize limb fractures and joint dislocations to minimize further injury

• Limit wound contamination to reduce infection risk

• Debride wounds by removing devitalized tissue, while maximally retaining viable tissue

• Keep wounds clean by repeated irrigation and debridement

• Cover wounds to reduce infection risk

• Prevent deep venous thrombosis and emboli

• Provide reconstructive care to maximize casualty and limb function

• Provide limb care within comprehensive rehabilitation

Table 3. Key steps in the care of a combat limb wound.
424 | Extremity Injury

and further injury must be prevented. Immediate priorities include: (1) diagnosis and treatment of vascular 

injury and compartment syndrome; (2) shunting, vein grafting, or primary repair of arterial injuries; (3) 

immobilization of unstable bony injuries; and (4) prevention of wound infection. A summary of key steps 

in the care of combat limb wounds is provided in Table 3.

Special Wounds

Vascular Injury

The optimal management of extremity vascular injuries sustained in war requires collaboration between 

orthopaedists, general surgeons, and vascular surgeons. The process may involve temporizing vascular 

shunts, definitive repairs, or vascular reconstructions (Fig. 29).86 The challenge of emergently addressing 

extremity vascular injury repair can tax a trauma system’s personnel, supplies, and operative resources.87

Ideally the regional trauma system serves to direct available resources towards providing optimal care. 

Optimal management of these complex injuries requires up-front planning, coordination of care, and 

frequent process improvements. 

Vascular injuries may be treated with temporizing vascular shunts or limited vascular procedures at 

Level II facilities, whereas definitive repairs or vascular reconstructions can be provided at Level III 

facilities. 

Currently in the US military, Forward Surgical 

Teams can perfuse limbs with shunts or perform 

limited vascular procedures. Most Combat Support 

Hospitals (Level III facilities) provide extensive limb 

revascularization capacity. The scope of practice 

for orthopaedic surgeons and general surgeons in 

war broadens and demands that they perform more 

vascular procedures than they would otherwise 

perform in more controlled environments. Damage 

control principles should be applied to the care of 

acute wartime vascular injuries with emphasis on 

the effective correction of physiologic shock.65,66 To 

this end, surgical time must be limited to essential 

resuscitative procedures, with the goal of returning 

to the operating room after physiologic parameters 

are restored and stabilized. A detailed discussion 

of vascular injury repair is provided in the Damage 

Control Surgery chapter.

Muscle, Tendon, and Ligament 

Skeletal muscle repair is an uncommon surgical task in early CCC, but it is sometimes needed after the 

first debridement and surgery. Complete disruption or transection of a muscle belly or tendon can lead 

to morbidity without surgical repair. Hence, if no agonist muscle exists (or is too small), surgical repair 

may be indicated for improved future muscle strength, patient satisfaction, or cosmetic results.88 Also, 

Figure 29. Temporizing vascular shunt placed in the brachial artery at 

a Level II facility. Image courtesy of the Borden Institute, Office of The 

Surgeon General, Washington, DC. 
Extremity Injury | 425

the need to cover underlying tissues such as nerve, tendon, or bone may also prompt surgical repair of 

muscle transections. Recent advancements in skeletal muscle repair have emphasized epimysium-based 

suturing.89,90,91,92,93 Crushed limbs or those entrapped and ischemic for prolonged times pose management 

difficulties. A delayed fasciotomy (greater than 12 hours following injury) may increase sepsis and mortality 

rates compared to conservative care.14

Ligament repair can be done early, but not necessarily at the first surgery, for complete disruption of 

major ligaments leading to joint instability. Large ligaments with joint instability may be repaired end-toend, oversewn, reinforced, or reinserted anatomically into their bony origins with nonabsorbable suture 

when the wound is clean. In the setting of gross wound contamination, a knee-bridging external fixator 

and serial surgical debridements prior to primary ligament repair or reconstruction are indicated. Serial 

assessment of joint stability and stiffness over time can help guide follow-on care. 

Blood vessels, tendons, nerves, bone, and open joint spaces should be covered throughout care, at least 

temporarily by loose apposition of the surrounding tissue or skin so that the delicate tissues do not dry 

out. This drying (with resultant stiffness) risk is greatest in exposed segments of immobilized open joints.94

However, good results with motion of open joints can be attained if the joint is mechanically stable.94 All 

other soft-tissue wounds should be left open so that drainage may occur.

Blood vessels, tendons, nerves, bone, and open joint spaces should be covered by loose apposition of 

the surrounding tissue or skin, so that the delicate tissues do not desiccate. All other soft-tissue wounds 

should be left open so that drainage may occur.

Open Joint Injury

A penetrating wound near a joint such as the knee may cause a traumatic arthrotomy, a communication 

between the wound and joint space where foreign matter or bacterial contamination may remain in the 

joint and lead to septic arthritis (Fig. 30). Retained foreign matter or contamination in diarthrodial (freely 

moveable) joints is an indication for early surgical debridement and irrigation of the joint space and 

wound. 

If a traumatic arthrotomy is suspected, a saline 

load test can be performed to help ascertain if 

the wound communicates with the joint space. 

A saline load test is the needle administration of 

sterile normal saline into the joint space through 

an uncontaminated route through the skin and softtissues. Enough saline is injected into the joint space 

to cause visible leakage if traumatic arthrotomy is 

present. The leakage may be seen in the wound if 

there is enough saline and limited blood and other 

obscurants. The saline load test is positive if the 

leakage is detected and negative if not detected. 

The saline load test has limitations in clinical 

practice. In a study, false positive clinical results 

occurred in 39 percent and false negative results in 

Figure 30. Traumatic arthrotomy with extensive soft-tissue and bone 

injuries of the elbow due to a gunshot wound. Image courtesy of the 

Borden Institute, Office of The Surgeon General, Washington, DC. 
426 | Extremity Injury

43 percent of casualties; there were no complications from the use of the test.95 In several studies using 

the saline load test to evaluate small lacerations around the knee, saline loads of less than 145 to 194 

milliliters were of questionable sensitivity. The authors concluded small volume saline load tests should 

not be used to rule out open knee injuries.96,97 The injection of methylene blue has traditionally been used 

as an alternative agent for detecting open joint injuries. The performance characteristics of intraarticular 

injection of methylene blue for detecting open joint injuries remain poorly defined. Of note, the use of 

high-dose intravenous methylene blue as a diagnostic agent (for alternative procedures) has been linked to 

a variety of neuropsychiatric adverse side effects.98,99,100,101 These rare cases were possibly associated with 

concomitant patient use of medications affecting serotonin metabolism.

If doubt exists as to whether a wound communicates with a major joint space, the principle of 

exploration of the traumatic wound, followed by debridement and irrigation, should be practiced.

Nerve Repair

Penetrating war trauma with associated peripheral nerve injury is uncommon.4 When such injuries occur, 

they can be severe, require complicated care, and result in persistent disability.102,103 Historically, advances in 

nerve repair, grafting, tendon transfers, and rehabilitation have been developed in part through CCC.103 

The 1988 edition of the Emergency War Surgery Manual provides a detailed discussion of the management 

of peripheral nerve injury.104 It details arteriovenous fistulas, clots and contusions, missile fragments, and 

causalgia associated with nerve injury. The 2004 edition of the Emergency War Surgery Manual discourages 

primary repair of peripheral nerve injuries in war wounds and advocates for prevention of desiccation by 

soft-tissue coverage of the nerve.105 Specifically, debridement of nerve is not indicated except for grossly 

destroyed areas of the nerve and trimming frayed edges.105 Recent advancements in the field of targeted 

reinnervation in the setting of upper extremity amputations have led to the goal of limiting initial nerve 

debridement to just the nonviable portions and preserving nerve length so that reinnervation, if chosen, 

is assisted with longer nerve stumps.

74 Surgeon experience is needed for the surgical repair of peripheral 

nerves. Loupe magnification is recommended for surgeons, and fascicular and epineurial repair appears 

prudent in most simple cases. The tagging of nerve with a fine, monofilament, nonabsorbable suture (e.g., 

6-0 nylon) is not mandatory but can assist in identifying nerves during later surgeries. 

Primary repair of nerve injuries should not be performed in combat settings. Initial objectives 

include judicious debriding of nonviable neural tissue and avoiding desiccation by ensuring adequate 

soft-tissue coverage of wounds. Definitive nerve repair can be accomplished at rearward facilities 

following patient evacuation.

War Wound Closure

• Extremity combat wounds should not be closed primarily.

• Cover bone, tendons, nerves, vessels, or joints with loosely apposed skin to prevent desiccation of 

underlying tissue and minimize risk of wound contamination. 

• Wound closure decreases nosocomial infections, but closure too early risks wound infections associated 

with devitalized tissue. 

• Zig-zag use of suture or vessel loops can provide wide wounds with some tension in order to aid in 

closure.
Extremity Injury | 427

Introduction

No extremity wound sustained during combat should be closed primarily at the first debridement because 

the risk of infection from residual contamination is very high.105 The one exception is closing soft-tissues 

over open joint injuries following thorough joint washout and wound debridement in an operating room. 

Definitive closure of combat wounds can be done in several ways: (1) delayed primary closure; (2) negativepressure wound dressings; (3) skin grafting; (4) local or free tissue transfer; and (5) healing by secondary 

intention. One or a combination of the above methods may be selected based on the nature and location 

of the wound, material available, and skill of the careprovider and treating facility resources.106 From 

non-US casualties treated in a Combat Support Hosptial in Iraq, gram-negative bacteria were the most 

commonly isolated pathogens.107 Cultures of respiratory fluid yielded positive results earlier than cultures 

of wound or blood samples and potentially serve as an earlier marker of future infections. Continued 

aggressive infection control for all casualties is needed.107

With the exception of open joint injuries, no extremity wound sustained during combat should be closed 

primarily.

Timing of Wound Closure

While primary closure of wounds within the strict controls of mature civilian trauma centers has shown good 

results, primary closure of war wounds is deemed inappropriate by experts in CCC.108,109,110 Preparation 

of a wound for closure requires clinical judgment and is based upon: (1) the appearance of the tissue 

(i.e., clean, granulating, healthy tissue versus foul smelling and purulent tissue); (2) the absence of active 

infection; and (3) the ability to achieve a tension-free closure. 

Classically, war wounds are not closed primarily since the wounds are often severe and contaminated. 

Occasionally the US Army has had to mandate delayed closure guidelines, such as in World War II.111

Part of the problem is that the surgeon cannot see all types of contamination such as bacteria or fine 

particulate matter.72 Another problem is that the wound core may include obviously nonviable tissue 

but there is a surrounding zone of tissue that may be devitalized but not dead, such that there is limited 

perfusion, a so-called zone of stasis that may evolve and swell over time.72 The surrounding zone of stasis 

may be susceptible to over-resuscitation or may be responsive to negative-pressure therapies that may 

reduce swelling locally.72

Timing of wound closure is dependent upon the appearance of the tissue, absence of infection, and 

ability to achieve a tension-free closure. 

Wound Closure Techniques

Delayed primary closure of war wounds can be effectively performed after planned, staged wound 

debridements.56 The stapling of a zig-zag pattern of suture or vessel loops across wide wounds with some 

tension can aid in closure by keeping the skin from passively retracting further (Fig. 31). Mild drainage 

and granulation can occur before closure. Such suture patterns can be periodically retightened by pulling 

on the suture and adding a staple in incremental closure, perhaps avoiding an operative visit.

Early in OEF and OIF, CCC providers became familiar with negative-pressure wound dressing devices, 
428 | Extremity Injury

as did civilian careproviders in the US. As familiarity and positive clinical outcomes became common, 

more frequent use ensued for a wider spectrum of wounds.56 In areas of skin loss with adequate muscle 

or granulation tissue coverage, a skin graft may be the treatment selected to cover the wound. Most 

commonly, a meshed split-thickness (0.015 inch) graft is used over the exposed soft-tissues.56 Meshing the 

graft allows for more area coverage per donor site harvested, but more highly meshed grafts will contract 

more as they heal and are less cosmetically acceptable (Fig. 32).56 Full-thickness skin grafting is considered 

for areas such as the palms of the hand where contracture of the graft is undesirable (Fig. 33). The skin 

graft may also be used in combination with delayed primary closure of a wound to first make the area 

needing a skin graft smaller. After serial debridements, the wound edges are approximated primarily, and 

then a skin graft is used to cover areas that cannot be closed because of tissue loss. 

Local rotational tissue transfer (local flaps) can be a reliable way to achieve wound closure in areas 

lacking muscle or granulation tissue coverage (Fig. 34).56 Common reliable rotational flaps in the lower 

extremity include the medial and lateral gastrocnemius flaps, soleus flap, and the reverse sural artery 

flap (Fig. 35).56 In the upper extremity, the radial forearm flap is reliable.56 Free tissue transfer or flaps are 

options as well, but it must be remembered that the zone of injury in war wounds is often larger than the 

open wound itself.56 This makes flap anastomosis within the zone of injury complicated.106,110,112 

Figure 31. (Top Left) The stapling of a zig-zag pattern of suture or 

vessel loops across wide wounds can aid in closure by keeping the skin from 

passively retracting further. Such patterns may be periodically retightened 

through increased tension.

Figure 32. (Top Right) In areas of skin loss with adequate muscle or 

granulation tissue coverage, a skin graft may be the treatment selected to 

cover the wound.

Figure 33. (Bottom Right) Meshing of the skin allows for greater graft 

coverage, improved conformity of the graft, and drainage of serous fluid.
Extremity Injury | 429

Figure 34. Gastrocnemius muscle flap: (Top) A large anterior leg wound with exposed tibia due to fragmentation injury. (Bottom) The gastrocnemius 

was exposed, divided, and passed through a subcutaneous tunnel to cover the defect. Images courtesy of the Borden Institute, Office of The Surgeon 

General, Washington, DC, and Michael Shaun Machen, MD, COL, MC, US Army.
430 | Extremity Injury

Definitive closure of combat wounds can be achieved through delayed primary closure, negativepressure wound dressings, skin grafting, local or free tissue transfer, or healing by secondary intention.

Wound Coverage

The timing of wound coverage is complex. As previously noted, war wounds and their management 

differ significantly from wounds seen in the civilian sector. Early coverage of war wounds is often 

associated with inadequate wound debridement and increased infection rates, while delayed coverage 

is also associated with increased nosocomial infection rates.110 More studies need to be done to define 

optimal wound coverage practices and minimize complications such as nonunion, flap failure, and 

infection.110 

Early coverage of war wounds is often associated with inadequate wound debridement and increased 

infection rates, while delayed coverage is associated with increased nosocomial infection rates.

Figure 35. Sural nerve flap: (Right) Fragmentation injury to the heel of 

the foot with exposed bone. (Bottom Left) A segment of skin, subcutaneous 

fat, and fascia are fashioned at the midcalf. (Bottom Right) A flap is 

rotated and sutured into place. Images coaaurtesy of the Borden Institute, 

Office of The Surgeon General, Washington, DC, and Michael Shaun 

Machen, MD, COL, MC, US Army.
Extremity Injury | 431

Preventing War Wound Infections

 

Wound Debridement and Irrigation

• All war wounds should be considered dirty and contaminated.

• Thorough wound debridement and irrigation are the main defenses against combat wound infection.

• Recent evidence shows that high-pressure pulsatile lavage traumatizes wounds and complicates 

healing.

• Copious low-pressure irrigation balances the need for contaminant removal with maintaining 

structural integrity of viable tissues.

Introduction

Although the sepsis rate in trauma is roughly 0.75 percent, the mortality of such cases is about 4 

percent.113 As such, the prevention of infection is an important imperative in trauma systems.85 After 

casualty evacuation from the point-of-injury to a safe area, the CCC provider can evaluate the wound and 

manually remove or irrigate away gross contamination. Initial wound irrigation is sometimes performed 

in the prehospital setting before reapplication of a wound dressing.114 The nonoperative debridement 

and irrigation of wounds as a bedside procedure can be done in the emergency department. The process 

typically consists of superficial wound inspection with lavage or irrigation of blood, debris, and loose bone 

fragments. Irrigation is often done at the first inspection of the wound to limit emergency department 

dressing changes. The promptness of the initial wound irrigation may have a slight effect on decreasing 

infection risk, but studies supporting this conclusion are limited.115 All but the smallest and most superficial 

of war wounds should undergo such irrigation. Wound infections tend to increase hospital length of stay, 

cost of care, and complication rates.107,113,114

Wound Flora

The bacteria within a war wound are often thought to contaminate the wound at the time of injury or 

soon thereafter.113,114 The natural history of such wound flora is not clearly known, but there are seasonal 

and geographic variations.113,114 The flora change over time and this likely occurs as a result of host, injury, 

treatment, and yet undefined reasons.113,114 Early wound flora is a mix of gram-positive and gram-negative 

bacteria including anaerobes.116 By day five, Pseudomonas aeruginosa is commonly noted.116 Later-stage flora 

includes gram-negative bacteria such as Pseudomonas aeruginosa, Klebsiella pneumonia, and Proteus spp.116 

Early in OEF, the extremity infection rate was reported as 3.8 percent (two of 52 casualties) but another 

report noted 77 percent (27 of 35) of deep cultures of tibia fractures were positive, and five went on 

to amputation with four associated with ongoing infections.116,117,118 According to a review by Yun (from 

2003 and 2006) there were 2,854 OEF or OIF admissions to Brooke Army Medical Center; 664 (23 

percent) patients were admitted to the orthopaedic service with approximately 13 percent developing 

osteomyelitis. A total of 25 percent of these patients developed recurrent osteomyelitis.116,119 Gramnegative bacterial pathogens were primarily responsible for the initial infections. Of those who had 

subsequent recurrent infections, initial gram-negative pathogens were typically eradicated and the 

subsequent infections were the result of gram-positive infections, primarily staphylococcus species. 

Murray et al. pointed out that the latter-stage infections were the result of nosocomial infections and 

were not present at the time of initial injury.116
432 | Extremity Injury

Wound Irrigation

Wound irrigation and debridement are the most common of all surgical procedures in war hospitals, 

particularly for limb wounds. The sheer number of these cases taxes the system, surgeons, and 

perioperative services.3 The volume of such cases leads to familiarity but also breeds complacency. The 

skill, diligence, and experience needed to do these procedures optimally are paramount to reducing 

infections. 

Timing of Irrigation

Early irrigation in contaminated wound model experiments has resulted in superior bacterial removal 

than when delayed irrigation is used.115 Clinical evidence supports early irrigation within six to eight 

hours of injury.116 The optimal time to repeat irrigation is unclear. Given that bacteria counts rebound 

in wound models within 48 hours, performing serial wound irrigation every two days is a reasonable 

choice.113,114,115,116,120,121

Clinical evidence supports early irrigation of wounds within eight hours of injury.

Volume of Irrigation

Copious initial wound irrigation should be performed to minimize bacterial contamination, which will 

decrease subsequent wound infection rates.77 The actual amount of fluid required is debatable, but ideally 

enough is used so that any gross material is removed and the wound grossly appears clean.85 Current 

US military (Joint Trauma Theater System) wound irrigation guidelines recommend nine liters or more 

of sterile saline be used for large traumatic wounds, six liters or more for moderate-size wounds, and 

three liters as a minimum for small traumatic wounds.77,122 These are ideal amounts, and the amount and 

type of irrigant may be constrained by actual supplies and resources. Recent evidence indicates that the 

irrigant volume decreases bacterial load in an approximation of a natural logarithmic decay. A point of 

diminishing returns occurs near nine liters for average-size wounds.77,121

Irrigants and Additives

Traditionally, the preferred wound irrigant has been sterile saline or sterile water.77 Recent studies have 

demonstrated that potable (drinking) water may also be used.85,123 Appendix 4 provides the Joint Trauma 

Theater System (JTTS) Clinical Practice Guidelines (CPG) for Irrigation in War Wounds recommended 

by the United States Army Central Command. Additives (e.g., antibiotics, surfactants, soaps, or antiseptics) 

to irrigants have been used with the intent of decreasing local bacterial contamination.122 Many of these 

additives are potentially cytotoxic to the cells of the wound.109 There is no evidence to suggest additives 

to standard wound irrigants are more beneficial than irrigants without additives. Wound irrigant additive 

use for war wounds is not recommended.77,121,122 The optimal irrigant temperature is unclear, but casualty 

hypothermia should be avoided, so warm irrigants should be chosen as indicated.

There is no evidence to suggest additional benefit to supplementing standard wound irrigation 

solutions with chemical additives.

Irrigation Devices

High-pressure lavage devices should be avoided because they can cause further tissue injury and push 

contamination deeper between tissue planes.77,122 Copious low-pressure irrigation balances the need for 

contaminant removal while protecting wounded tissues (Appendix 4).115,120,122,123 Low-pressure pulsatile 
Extremity Injury | 433

lavage, gravity-fed irrigation, and manual bulb-syringe irrigation are currently all techniques successfully

used in CCC (Fig. 36).77,12,

High-pressure lavage devices should be avoided because they can further tissue injury and drive 

contaminants deeper between tissue planes.

Wet-to-Dry Dressing Debridement

Initial postoperative dressings on blast injuries should be dry, bulky dressings, which will be able to absorb 

the copious amounts of wound drainage seen early in this injury pattern (Fig. 37).56,77 As the wound 

begins to drain less, a wet-to-dry debridement dressing change schedule can be started, if superficial 

debridement is desired. The use of wet-to-dry dressings is a debridement technique in which dry dressings 

are removed two or three times daily and replaced with damp, sterile ones. As the damp dressing dries, 

local tissue adheres. When this dressing is removed, it also removes the superficial wound serous drainage 

and provides a small amount of superficial debridement.56,77

Initial postoperative dressings on blast injuries should be bulky dry dressings.

Figure 36. (Top Left) Copious low-pressure wound irrigation should 

be performed to minimize bacterial contamination. High-pressure lavage 

should be avoided. 

Figure 37. (Top Right) Initial postoperative dressings of blast injuries 

should be bulky dry dressings, which will allow absorption of the copious 

amounts of wound drainage.

Figure 38. (Bottom Right) Plaster casts must be bivalved and the cast 

padding cut down to the skin to prevent excessive pressure on the enclosed 

limb. Image courtesy of Defense Imagery Management Operations Center 

(DIMOC).
434 | Extremity Injury

Reevaluation of wounds should occur frequently since wounds evolve with time. Dressing wounds tightly 

with gauze may prohibit drainage and risk infection.60 Initial postoperative limb dressings should be made 

with the injury severity in mind. Severe injuries can swell so much that dry, bulky dressings are needed to 

permit swelling while absorbing copious serous wound drainage. 

When plaster casts are applied for the immobilization of fractures, two lateral longitudinal half-inch 

segments should be removed from the cast’s entire length (bivalving) and the circular dressings cut down 

to the skin (Fig. 38). This procedure prevents undue pressure on the enclosed limb when swelling occurs.41

The military air evacuation system in OEF and OIF prohibits casts that are not split (bivalved) in this 

manner because of the risk of limb swelling during aeromedical transport.57

Circumferential plaster casts should be bivalved to prevent excessive pressure on the enclosed limb.

Surgical Wound Debridement

Following evacuation of the casualty to a facility with surgical capability, early and assertive surgical 

debridement of grossly contaminated and nonviable tissues is the first step in infection control.113,114,116

Inadequate wound debridement has been cited as the most common cause of war wound infection.116

War wound surgery involves careful exploration of all wounds (i.e., closed wounds, entry and exit 

wounds, missile tracks between entry and exit, and secondary missile tracks caused by fragmentation of 

the munitions after entering the body).60

Inadequate wound debridement has been cited as the most common cause of war wound infection. 

Fasciotomy is often integral to debridement.

A systematic approach to wound evaluation will help the surgeon avoid missing areas of a large 

wound. This involves: (1) starting by exploring the most superficial wound first; (2) debriding the skin 

and subcutaneous tissue; (3) then debriding muscle and fascia; (4) fasciotomy and hematoma removal; 

and (5) finishing deep wound debridement of periosteum and bone. Fasciotomy is often integral to 

debridement. Debridement’s core meaning includes unbridling the wound, which includes removal of 

expanding hematomas and relieving compartment pressure. Diligent wound exploration is required to 

avoid iatrogenic injury to the traversing vessels and nerves within the wound. In the authors’ experience 

a geographic approach to wound evaluation, dividing it into quadrants and addressing all pathology in 

each quadrant before moving to the next one, has been successful. 

The broad spectrum of foreign matter found within war wounds is remarkable. Over time, CCC 

providers will document everything from blast injury victim bone fragments to palm dates and even 

insects within war wounds (Table 4). Of note, the anatomic location of a foreign body does not indicate 

what path it took to get there. For example, a casualty in OIF with a traumatic amputation above the left 

knee was found to have a large foreign body in his right chest on radiography (Fig. 39). The foreign body 

was initially thought to be something on the cassette he was lying upon, until a repeat chest radiograph 

reconfirmed its presence. An 18 x 2 x 1⁄4 inch explosion-related fragment had entered his right lung 

via his abdomen from his knee wound. The missile track was confirmed surgically. It traversed the 

bladder, rectum, kidney, intestines, liver, diaphragm, and lung. Missile tracks following blast injuries are 

notoriously difficult to precisely and reliably identify.
Extremity Injury | 435

Foreign Matter Identified During Debridement

• Dirt, soil, mud, sand, rocks, road debris, dust, and compost

• Bullets, shrapnel, ordnance fragments, uniform bits, clothing, and 

equipment

• Other casualty items blasted into the wound, bones, clothing, boots, kit, 

and gear

• Animal matter such as insects, worms, carcass fragments, excrement, and 

leather

• Plant matter such as wood, grass, leaves, roots, and nuts

• Manmade items: glass, car or building parts, concrete, pipes, nails, 

batteries, nuts, bolts, screws, and metal can parts

• Water, sewage, water plants, and frog fragments

• Chemical matter, phosphorous, acids, liquids, and smoked or charred 

items

Table 4. Foreign matter identified in explosion-related wounds.

Figure 39. Missile tracks following blast injuries are difficult to identify: 

(Top Left) Combat casualty with a traumatic amputation above the left 

knee. (Top Right) Foreign body noted on chest radiograph. (Bottom 

Left) Explosion-related fragment that had entered the chest cavity via the 

casualty’s abdomen from the knee wound. Images courtesy of John B. 

Holcomb, MD, COL(Ret.), MC, US Army. 
436 | Extremity Injury

Missile tracks following blast injuries are difficult to reliably identify. Large missile fragments in soft-tissue 

wounds are often removed, whereas small fragments are only removed if they are readily accessible.

Sharp surgical debridement of devitalized and grossly contaminated tissues is the primary surgical means 

of infection prevention.114,124 However, the innate meaning of devitalized (that which is less than fully vital) 

is operationally problematic, as devitalized tissues range from bruised or edematous to blackened eschar. 

Muscle rigor, a feature of rigor mortis, is rarely seen in the living casualty. 36,125 Analyzing how effectively 

surgeons classify viable versus nonviable tissue during debridement efforts is rarely researched. Ensuring 

CCC providers new to war are adequately trained in this process is critical.60,126

Generous surgical extension of the wound in order to see the damaged tissues adequately (around the 

wound recesses) is important. This process enables complete inspection and removal of devitalized 

tissues and foreign material that may have traveled along or through fascial planes.60 Such extension 

of traumatic wounds often includes longitudinal skin incisions and compartmental fasciotomy. Fascia 

is generously released.54 Judicious excision of skin margins, often just a millimeter or two, will remove 

devitalized or grossly contaminated edges while maintaining as much cover as practical (Fig. 40). Grossly 

contaminated skin edges are often identified following irrigation and removal of dried blood. The skin 

edges’ white fibrous strands are often covered with dark particulate debris such as sand. Contaminants 

tightly adhere to these fibers, which can be a millimeter or longer. These contaminated and difficult to 

clean fibrous strands are useless and risk infection. 

There is little beyond expert opinion on which to base tissue fragment management recommendations.127

Large missile fragments (shrapnel) in soft-tissue wounds are typically removed, whereas small fragments 

are removed only if they are easily accessible.60 If iatrogenic trauma would result from the removal 

of smaller fragments, they are allowed to remain in place.60 Shrapnel is a term used classically for 

fragments from preformed antipersonnel munitions, but is now commonly used by lay people to indicate 

metal fragments from explosive shells. 

When wound tracks from entry-to-exit are long relative to their width, debris such as bone fragments 

and blood clots can be debrided without fully opening the wound. This can be accomplished by passing 

Figure 40. Early and assertive surgical debridement of nonviable tissue is a critical step in infection control.
Extremity Injury | 437

a small but long surgical sponge across the track, often by a clamp, such that the wound floss can help 

pull the debris out the dependent opening. Similarly, the dependent opening can be used for drainage, 

and if the opening is not large enough for adequate drainage, then it can be enlarged. If the track is 

blind in that it has no exit, and the entry is not dependent, then a counterincision can be made in a 

dependent area. The dependent drainage by gravity is usually for the casualty in the supine position, 

and can simplify care while decreasing complications. 

Wound drains are routinely placed by surgeons in war wounds with the intent of decreasing infection 

rates. While data are limited, existing studies suggest that open surgical drains are associated with more 

complications (e.g., infections) as compared to no drains or closed drains.128 A Cochrane review of closed 

drains following orthopaedic surgery in a civilian patient population concluded there is insufficient 

evidence to support the routine use of closed suction drainage following orthopaedic surgery.129 Further 

studies are required to better define the role of surgical drains for war wounds.

Assessing Muscle Viability

The most challenging and problematic tissue to debride in wounded limbs is skeletal muscle. Muscle, 

in particular, can be judged as living or dead roughly based on the four C’s of muscle viability. These 

include (1) color (red versus pale or brown); (2) consistency (not waxy or stewed); (3) contractility (on 

being pinched with the tips of a forceps); and (4) capacity to bleed (capillary bleeding when cut).126 Tissue 

discoloration or staining from surface hemorrhage on wound surfaces or small hemorrhages within 

tissue such as skeletal muscle should be differentiated from large hematomas, contamination, and tissue 

ischemia. Color is not as reliable as the other C’s. Dead muscles can bleed from larger blood vessels 

within the skeletal muscle itself, so this capacity to bleed should be differentiated from the capacity to 

bleed from capillaries.14 The former is a false positive indicator of viable tissue, while the latter is a true 

indicator of tissue viability. Muscle injury, particularly when large and associated with ischemia, can be 

associated with coagulopathy. Hence, careproviders must be aware that slow, venous oozing from cut 

muscle may also be a false positive indicator of tissue viability. Medications such as aspirin, nonsteroidal 

antiinflammatory drugs, and anticoagulants may accentuate such bleeding in casualties.130

Muscle viability can be assessed based on the four C’s: color, consistency, contractility, and capacity to 

bleed.

Massive Wounds (Upper Thigh and Buttock)

Massive wounds of the upper thigh and buttock are problematic in two aspects; control of hemorrhage 

and determination of the amount of muscle to be excised (Fig. 41).36 The wound may be too 

proximal for a tourniquet. Oozing may persist and may be associated with coagulopathy in need of 

correction.35,131 Placement of an emergency tourniquet as proximal as possible, while still partially 

covering the wound, can be temporarily effective in hemorrhage control. However, this approach risks 

failing to extinguish the arterial pulse and may lead to complications (e.g., expanding hematomas and 

compartment syndrome).36 Surgical preparation with the tourniquets in place, within the operative 

field, can maintain hemorrhage control and allow more time for surgical team preparation.15,36,65,66,67

In large wounds of the buttock and upper thigh, repeat wound inspection on the second or third 

postoperative day are indicated. These repeat inspections during staged debridements and irrigations 

can ensure any remaining devitalized tissue is recognized sooner for further debridement.56
438 | Extremity Injury

In large, complex wounds it is difficult to 

determine the amount of muscle to excise. 

Residual devitalized tissue in wounds risk 

infection. With high-energy mechanisms, damage 

along fascial planes and between muscle bundles 

occurs, which may further devitalize deep muscle 

as some muscle perfusion comes from adjacent 

planes. Surgeons digitally probing for debris or 

hematomas should be aware that the technique 

of using their fingers to circumferentially dissect 

around small muscles can damage vasculature 

structures. Muscles like the sartorius in the 

thigh can be inadvertently stripped of their 

segmental blood supply through circumferential 

digital dissection, resulting in muscle necrosis 

and infection. The intramuscular vascular 

patterns of muscles are poorly known.132 After 

sharp debridement, copious low-pressure wound 

irrigation can be used to remove loose debris, missile fragments, and decrease wound surface bacterial 

contamination (Appendix 4).115,121,122,123

Negative-Pressure Wound Dressings 

• Negative-pressure wound dressings are commonly used in OEF and OIF.

• Appropriately applied and managed negative-pressure wound dressings result in improved wound 

healing rates.

• Placement of a negative-pressure dressing should occur only after thorough debridement of devitalized 

and contaminated tissues. 

• A wound vacuum device is available and approved for aeromedical transport use in OEF and OIF.

Negative-pressure wound dressings have been used successfully in the treatment of war injuries.133,134 The 

negative-pressure dressing provides a closed environment for the wound and resorbs the large amounts of 

serous fluids that drain from blast injuries.135 This closed system may reduce hospital-acquired infections 

because these wounds are less prone to repeated inspection and manipulation. 

Negative-pressure wound dressings are commonly used in OEF and OIF.

Inappropriate use of negative-pressure wound dressings has been associated with infectious complications. 

Placement of a negative-pressure dressing should occur only after thorough debridement of devitalized 

and contaminated tissues.56,133 Use of the negative-pressure dressing overlying dead tissues can create a 

closed space. This closed space creates an ideal environment for abscess formation, which would lead to 

local and potential systemic infectious complications.56 This closed wound environment provides the ideal 

media for bacterial growth if the vacuum device fails, or is left in place too long between debridements.136

Loss of vacuum suction or tube blockage can have similar outcomes as device failure.134 If suction is lost, 

the tube or dressing can be cut to allow drainage or the negative-pressure dressing can be replaced by dry 

Figure 41. Hemorrhage from massive wounds of the upper thigh and 

buttock may be difficult to control, and determining the amount of muscle 

to debride is often difficult. Images courtesy of John B. Holcomb, MD, 

COL (Ret.), MC, US Army.
Extremity Injury | 439

bulky dressings. As previously mentioned, based on anecdotal reports by war surgeons, negative-pressure 

wound therapy appears best avoided at the initial surgery for wounds at risk for rebleeding. Negativepressure wound dressings can be considered after the casualty and wounds are stable without bleeding for 

48 hours (following initial resuscitation).

Placement of a negative-pressure dressing should occur only after thorough debridement of devitalized 

and contaminated tissues. Negative-pressure dressings should be avoided in wounds at risk for 

rebleeding.

Negative-pressure wound therapy can facilitate the delayed closure of large traumatic wounds. It does so 

by decreasing the size of the wound over time. The device applies tension to the skin and removes thirdspace fluids. The device can be an adjunct in split-thickness skin grafting. During OEF and OIF, a wound 

vacuum device (The V.A.C. Freedom® Therapy System, Kinetic Concepts, Inc. or KCI, San Antonio, TX) 

was approved for aeromedical transport in OEF and OIF. The wound vacuum assisted closure or V.A.C., 

is a proprietary label for KCI’s negative-pressure wound therapy system, a common one used currently in 

the US military. Devices have to be approved by the military for safe aircraft use prior to implementation 

during aeromedical transportation in casualty care. 

Antibiotic Impregnated Pellets and Cement Bead Therapy

An adjunctive measure that can be used with 

or without the negative-pressure dressings is 

antibiotic-impregnated beads (Fig. 42). Such beads 

are usually made of polymethylmethacrylate, a 

type of bone cement, with a heat stable antibiotic 

additive such as tobramycin. The polymerization of 

the polymethylmethacrylate powder with the liquid 

catalyst is exothermic in forming the cement, so the 

antibiotic powder needs to be heat stabile, or it will 

be inactivated in bead formation. Antibiotic bead 

pouch use reduces bacterial growth in an anaerobic 

environment.116 Antibiotic beads may offer some 

benefit in the prevention of infection at the local 

site, but no data exists on their efficacy in war 

wounds or long-term effect on wound infection.116

Preparation of antibiotic bead pouches consumes valuable time and operative resources; ideally these 

should be prepared ahead of time.116 Effective local antibiotic delivery can be obtained with both 

commercially available calcium sulfate pellets and with handmade polymethylmethacrylate beads.137

Tobramycin-impregnated calcium sulfate pellets have been shown to effectively prevent infection in a 

contaminated wound model.138

Antibiotics and Tetanus Immunization

• Systemic antibiotic administration should occur within three hours of sustaining combat wounds.

• Antibiotic guidelines for routine combat wounds should be followed.

Figure 42. Antibiotic beads may offer some benefit in the prevention 

of local infection, but definitive data are lacking on their efficacy in war 

wounds.
440 | Extremity Injury

• Ensuring up-to-date tetanus immunization status following combat wounds is important to eliminating 

tetanus infections.

• The main risk for developing wound infection in casualties is the severity of the injury.

Prophylaxis

Prevention of infection in war wounds is an important goal.139 Injury severity and wound management 

practices are important determinants of subsequent infection.128 The benefits and risks of current antibiotic 

wound prophylaxis practices to prevent infections in combat casualties have yet to be fully defined.85,140

Early wound cleansing and surgical debridement, antibiotics, bony stabilization, and maintenance of 

infection control measures are essential to diminish or prevent infections.85 Antibiotic prophylaxis or 

therapy is an adjunct to adequate surgical debridement of war wounds.116 Prophylactic antibiotics have 

been associated with high rates of drug-resistant organisms.116

Initial care of combat wounds occurs at the point-of-injury, where a sterile bandage may be applied and 

oral antibiotic administered as prophylaxis.139 Prophylactic antibiotics in tactical CCC settings have been 

recommended for all open wounds. If the evacuation time of the casualty is expected to be more than 

three hours, the use of oral antibiotics is recommended within three hours of injury.85 Recommendations 

for initial antibiotic prophylaxis in OEF and OIF for open extremity wounds with oral antibiotics are 

moxifloxacin (400 milligrams orally, one single dose in the field) or as an alternative levofloxacin (500 

milligrams orally, one single dose in the field), but empiric evidence is scant regarding effectiveness or 

outcomes.85

Prophylactic antibiotics in tactical CCC settings have been recommended for all open wounds and should 

be administered within three hours of sustaining combat wounds.

Antibiotic recommendations for OEF and OIF casualties with open fractures arriving at a treatment 

facility that possesses intravenous antibiotic supplies are one gram of cefazolin (also known as cephazolin) 

intravenously every eight hours for 72 hours. An alternative to cefazolin is clindamycin (900 milligrams 

intravenously every eight hours for 72 hours). The clindamycin dosing used in war wounds differs 

from 450 milligrams every six hours civilian sector dosing. Clinical evidence supporting this practice is 

limited. Subsequent use of antibiotics (beyond 72 hours) should be reserved for treatment of documented 

infections, as opposed to prophylaxis, in order to limit the selection of multidrug-resistant organisms. 

In patients who present more than 72 hours after injury, or are injured with antipersonnel land mines 

(implying soil contamination), metronidazole should be added as well to the treatment for 48 hours 

intravenously and then orally until delayed primary wound closure is complete.85 Evidence is scant 

regarding effectiveness or outcomes of aforementioned recommendations. 

Wounds should only be cultured routinely when an infection is suspected. Antibiotic selection is ideally 

based on results of wound cultures and bacterial antibiotic sensitivities. Recent hospital and regional 

bacterial flora should influence antibiotic selection. Temporal and geographic variations occur with the 

organisms isolated from combat wounds.113,114 Longstanding systematic tetanus immunization programs 

for US military personnel have largely prevented tetanus infections.113 New cases of tetanus in military 

personnel are rarely seen today.113,114 If a combat casualty (e.g., host national) has not received a primary 

immunization series against tetanus infection, primary tetanus immunization and passive prophylaxis 

(tetanus immune globulin) should be administered.85 
Extremity Injury | 441

All penetrating combat wounds should be considered tetanus-prone, and patients should be provided a 

tetanus toxoid booster immunization if more than five years have passed since their most recent tetanus 

immunization.

Fracture Management 

• Fractures stabilization decreases pain, eases wound care, and improves soft-tissue and vascular repair 

outcomes.

• Initial fracture stabilization is performed in a damage control manner in war and is not definitive. 

• Most hand and foot fractures can be adequately stabilized for transport with simple splints applied 

over dressings.

• External fixators can loosen with patient transport; so the clamps should be periodically retightened 

(e.g., 24 to 48 hours) after application.

Introduction

Extremity trauma with bony fractures is a common war injury.60 About 26 percent of casualties with 

Figure 43. Radiographic evaluation of the traumatized limb should (at a minimum) include biplanar radiographs to fully delineate the bony injury. 

Here, (Left) PA and (Right) lateral radiographs demonstrate a midfemoral fracture and the metallic fragment that caused the injury. Images courtesy of 

the Borden Institute, Office of The Surgeon General, Washington, DC. 
442 | Extremity Injury

extremity wounds in OIF have a fracture. The majority of these injuries (82 percent) are open fractures 

where the soft-tissue envelope around the fracture has been physically disrupted, and the bone has been 

exposed to the external environment.2,4 Inexperienced providers can underestimate wounds by thinking 

that a skin wound does not communicate with a nearby fracture when it actually does, so a high index of 

suspicion should persist pending orthopaedic evaluation. 

Eighty-two percent of extremity fractures in OIF are open fractures.

Radiographic evaluation of the traumatized limb should (at a minimum) include biplanar radiographs 

to fully delineate the bony injury (Fig. 43). Stabilization of these fractures has several benefits, including 

patient comfort, protection of the surrounding soft-tissues, protection of vascular repairs, and improved 

wound care.116 The goals of fracture management in the combat setting are to prevent infection, preserve 

options for limb reconstruction or limb salvage, and prevent further tissue injury and hemorrhage 

during patient treatment and transport.57 Simple, early management of fractures can avoid long-term 

complications such as osteomyelitis and nonunion. 

Goals of fracture management in the combat setting are to prevent infection, preserve options for 

limb reconstruction or limb salvage, and prevent further tissue injury and hemorrhage during patient 

treatment and transport.

Figure 44. (Left) Limb deformity due to displaced fractures can 

compromise the vascular supply to the distal limb. If compromised 

perfusion is detected, immediate longitudinal traction should be applied.

Figure 45. (Above) When possible, fixation devices should be placed in 

a location that avoids traversing the traumatic wound or hematoma itself.
Extremity Injury | 443

Initial Fracture Wound Management

Initial limb deformity due to displaced fractures can compromise the vascular supply to the distal limb 

(Fig. 44). The CCC provider should respond to the limb with compromised perfusion and displaced 

fracture with longitudinal limb traction, which will grossly realign the limb at its proper length, thereby 

reducing the fracture shortening and typically improving distal perfusion. The fracture reduction can be 

maintained with manual traction if necessary; or if supplies and time allow, temporary plaster splints can 

be applied to hold the limb out-to-length. 

In this type of unstable skeletal injury, the distal pulses should be checked frequently and more definitive 

fracture fixation should be sought. If fracture reduction is successfully performed and the vascular supply 

to the distal extremity remains compromised, an arterial injury should be assumed until proven otherwise. 

Careproviders are advised to immediately transfer such cases to an echelon of care capable of providing 

vascular repair (typically a Level III facility). Periarticular fracture reduction is also important for limb 

perfusion, length, soft-tissue balance, joint surface reduction, and follow-on care.

If vascular supply distal to a skeletal injury remains compromised following successful fracture 

reduction, arterial injury should be assumed present and the casualty transferred to a Level III facility 

for further evaluation.

Initial Fracture Stabilization

Initial fracture stabilization should be viewed as part of limb resuscitation and not definitive fixation.141

Care should be taken to first do no further harm by ensuring the placement of fixation devices is away 

from nerves and vessels. When possible, to minimize risk of infection, fixation devices should be placed 

in a location that avoids traversing the traumatic wound or hematoma itself (Fig. 45). Half-pin frame 

external fixators, K-wires (Kirschner wires), splints, and skeletal traction can all be used for fracture 

stabilization.142 Skeletal traction is fast but limited to patients not needing further evacuation because 

traction must be removed for transport. External splints allow for noninvasive fracture stabilization 

and provide a cradle for the injured soft-tissue envelope (Fig. 46). The disadvantage of splinting is the 

potential for loss of fracture reduction with motion in the splint and the inability to easily inspect the 

wounds underlying the splint unless it is removed. 

Initial fracture stabilization should be viewed as part of damage control limb resuscitation and not as 

definitive fixation.

External fixators and K-wires provide skeletal fixation and are indicated for long-bone and periarticular 

fractures in which stability cannot be achieved by splinting.77 Commonly, the fixator will be applied 

concurrently with a vascular procedure to provide a stable limb and protect the site of vascular repair 

or shunting (Fig. 47). Segmental metacarpal and metatarsal fractures with bony loss can be spanned 

longitudinally with K-wires to reduce soft-tissue contractures during transport. Such wires can be 

straight or have 90-degree bends to block the fractures’ ends out at their reduced positions for optimal 

soft-tissue lengths (Fig. 48). There is no single, ideal form of resuscitation fixation, but the options used 

should first do no further harm and, second, provide a stable extremity for transport out of the theater 

of operations.77
444 | Extremity Injury

External fixators and K-wires provide skeletal fixation. They are indicated for long-bone and periarticular 

fractures in which stability cannot be achieved by splinting.

Open Fracture Management

The approach to an open fracture should proceed with similar tenets as for other contaminated wounds. 

Initial open fracture wound irrigation can be performed as part of the wound inspection in the emergency 

department. This initial inspection and irrigation should not be considered definitive treatment. Copious 

Figure 46. (Right) External splints allow for noninvasive fracture 

stabilization. In this combat casualty, additional surgery was deferred 

until the patient was stable. Image courtesy of the Borden Institute, Office 

of The Surgeon General, Washington, DC. 

Figure 47. (Bottom Left) This open femur fracture was rapidly 

stabilized with external fixation while a shunt of the superficial femoral 

artery was placed. The external fixator provided added protection to the 

site of vascular shunting.

Figure 48. (Bottom Right) Segmental metacarpal and metatarsal 

fractures with bony loss can be spanned longitudinally with K-wires to 

reduce soft-tissue contractures. The K-wire is bent four times (90-degree 

corners) so when the ends are inserted in the bone marrow, the corners 

hold the soft-tissues out the length of the bone depth.
Extremity Injury | 445

intraoperative wound irrigation and sharp surgical 

debridement are indicated with adjunctive, broadspectrum, intravenous antibiotic prophylaxis 

(Fig. 49).77,116 Nonviable tissues, including bone 

fragments stripped of their soft-tissues, should be 

removed (Fig. 50). An exception to this removal 

may include retention of large articular bony 

fragments regardless of soft-tissue attachments 

as long as they are not grossly contaminated and 

appear suitable for articular reconstruction.77

Internal fixation of fractures should be delayed 

until the patient has been resuscitated and the 

soft-tissue injury has been treated.77 With rapid 

aeromedical evacuation of combat casualties to 

Level IV and V facilities, there are no compelling 

indications for internal fracture fixation of US 

and coalition forces in-theater during OEF and 

OIF. Internal fixation of host nation patients after 

a clean wound bed has been obtained has been 

performed in OEF and OIF.77 Certain fracture 

types (e.g., displaced femoral neck and talus 

fractures) have, in the past, been considered a 

dilemma for CCC providers, as delay in fracture 

reduction was believed to increase risk of avascular 

necrosis. Recent studies have shown no difference 

in results, and therefore the increased risk, and 

often increased reduction difficulty, favor early 

evacuation and fixation out-of-theater.

With rapid aeromedical evacuation of combat casualties to Level IV and V facilities, there are no compelling 

indications for internal fracture fixation of US and coalition forces in-theater during OEF and OIF. 

Most of the initially placed frames will eventually be removed or modified to allow for definitive fracture 

fixation.143,144 Bony stabilization of the extremities is indicated to hold alignment of the long bones to 

prevent laceration of soft-tissue structures by the fracture surfaces, prevent injury to vascular shunts or 

grafts, and provide comfort to patients during transport. External splinting may be appropriate for more 

distal fractures. Such fractures are closed, low-energy, and stable fractures. External splinting can also 

serve as an adjunct to external fixation (e.g., a posterior leg splint to keep the foot out of equinus with 

a half-pin frame on a tibia fracture). If a circumferential cast is used, it and the cast padding must be 

bivalved prior to aeromedical evacuation. 

External Fixation of Extremity Fractures

External fixation is invasive and is generally reserved for long-bone and periarticular fractures not 

amenable to splinting. External fixation preserves access to the wound and soft-tissues for serial evaluation 

Figure 49. The approach to an open fracture should proceed with similar 

tenets as for other contaminated wounds. Copious intraoperative wound 

irrigation and sharp surgical debridement are indicated with adjunctive 

broad-spectrum intravenous antibiotic prophylaxis. Image courtesy of 

the Borden Institute, Office of The Surgeon General, Washington, DC. 

Illustrator: Jessica Shull.
446 | Extremity Injury

Figure 50. Open fracture management: (Top Left) Casualty with open 

tibial and fibular fractures at presentation. (Top Right) Appearance 

of wound following irrigation, sharp surgical debridement, removal of 

nonviable tissue, and external fixation. (Bottom Left) Bone fragments 

stripped of their soft-tissues. (Bottom Right) Radiographic appearance 

of the injured limb following external fixation.
Extremity Injury | 447

and debridement while providing rigid skeletal fixation, and it may save time during damage control 

interventions.109 Disadvantages of external fixation are the potential for iatrogenic vessel or nerve injury, 

pin site infections, lack of soft-tissue support, and possibly fewer surgical options if pin complications 

occur.77,145 General surgeons should be familiar with the standard constructs of external fixation for use 

in initial care of battle casualties and have a thorough understanding of limb anatomy to ensure safe pin 

placement.57 External fixation constructs may be applied without fluoroscopy and without the need for 

power tools.

General surgeons should be familiar with the standard constructs of external fixation for use in initial care 

of battle casualties and have a thorough understanding of limb anatomy to ensure safe pin placement.

For effective external fixation, a minimal number 

of pins should be used to provide skeletal stability 

during resuscitation. This stabilization is commonly 

performed with two half-pins on both proximal 

and distal sides of the fracture (Fig. 51). Other 

factors that can make the external fixator frames 

more rigid are bony cortical contact of the reduced 

fracture edges, larger diameter half-pins, pin pairs 

spread farther apart (each pair on either side of the 

fracture), number of bars used in the frame, use of 

bars in multiple planes in the frame, and lessening 

the distance from the bone to the closest bar.142

Basic principles of external fixation dictate that the 

half-pins used should be bicortical (as opposed to 

unicortical) with avoidance of all neurovascular 

structures, joints, open wounds, fractures, and 

fracture hematoma.142,145 As with any fracture work, care must be paid to the surrounding neurovascular 

structures before, during, and after provisional fracture reduction. 

Principles of external fixation dictate that half-pins should be bicortical (as opposed to unicortical) and 

should avoid all neurovascular structures, joints, open wounds, fractures, and fracture hematomas.

External fixation of a distal femur fragment at distal Hunter’s canal involves placing the half-pin tip in 

close proximity to neurovascular structures. Care must be exercised to avoid inadvertent injury to the 

superficial femoral artery as it courses through Hunter’s canal.145 Distal pulses should be reevaluated 

if limb manipulation is performed and after external fixation pins are placed. Clinical examination of 

peripheral nerves is important because external fixation pins can injure nerves.145 An excellent atlas for 

review of safe tissue intervals for placement of external fixation half-pins is the Atlas for the Insertion of 

Transosseous Wires and Half-Pins: Ilizarov Method.142

Upper Extremity Fracture Fixation

Upper extremity fractures are typically stabilized with splints or external fixators. Most fractures of the 

hand and upper extremity can be managed with external splints applied to the injured limbs (Fig. 52). 

Figure 51. Stabilization with external fixation is commonly performed 

with two half-pins on both proximal and distal sides of the fracture. 

Image courtesy of the Borden Institute, Office of The Surgeon General, 

Washington, DC. Illustrator: Bruce Maston.
448 | Extremity Injury

These splints should be well-padded. If the splints span across the wrist, they should place the wrist and 

hand in the neutral or safe position (wrist is placed in 20 degrees of extension, metacarpophalangeal 

joints are positioned at 70 degrees of flexion, and interphalangeal joints are straight), whenever possible. 

External fixation of upper extremity fractures can be of value in cases with marked soft-tissue injury, 

vascular shunt or repair, and segmental bone loss. Additionally, metacarpal fractures with bony loss may 

benefit from internal K-wire fixation to maintain bony length and prevent soft-tissue contracture during 

evacuation out of theater and initial limb resuscitation and wound debridements.77 With external fixation 

of smaller diameter bones, the inserted pin diameter size should be kept to less than one-third of the 

diameter of the bone to limit the risk of fracture upon half-pin removal. When severe bony loss shortens 

the injured limb (e.g., segmental loss of multiple metacarpal shafts), K-wires (0.065 inch) can be placed in 

the proximal and distal bone fragments after four 90-degree bends are made at the desired bone length 

in order to keep limb length ideal during planned staged care (Fig. 53). If the hand maintains its good 

perfusion, it can be relatively resistant but not immune to infections and infected hardware. Fixation of 

hand fractures is often delayed until the wounds are clean and otherwise generally follows most civilian 

care principles. The priority in hand injuries in war are restoring perfusion and providing soft-tissue care 

followed by fracture care. 

External fixation of humerus fractures should be reserved for those fractures with risk of vascular or 

neurologic injury due to fracture displacement. Often a coaptation splint or cuff and collar sling can 

suffice in simple fracture patterns, but if vascular structures have been shunted or repaired, more rigid 

skeletal fixation is indicated. Bony loss around the elbow joint may also be an indication for spanning 

external fixation, as this injury treated with a splint may displace and put traversing arteries and nerves at 

risk. Forearm fractures can also be managed with splinting or external fixation depending on the degree 

of soft-tissue injury, vascular status, and risk of displacement in a splint. 

Lower Extremity Fracture Fixation

Similar to the upper extremity injuries, lower extremity fractures are amenable to splinting or external 

fixation depending on the soft-tissue injury, risk of fracture displacement, and risk to vascular structures 

or repairs if the fractures displace. Foot injuries can be treated in a similar fashion as hand fractures; 

Figure 53. In this pediatric hand injury with segmental loss of multiple 

metacarpal shafts, K-wires were used to preserve bony length.

Figure 52. Most fractures of the hand and upper extremity can be 

managed with external splints applied to the injured limbs. Image courtesy 

of Defense Imagery Management Operations Center (DIMOC).
Extremity Injury | 449

K-wires can be fashioned to maintain metatarsal length if segmental loss is present. A plantar or posterior 

splint can be used for simple fracture patterns of the ankle and feet. If a splint is used across the ankle 

joint, the ankle should be placed in neutral dorsiflexion. Tibia fractures should be closely evaluated for 

presence of or potential to develop compartment syndromes. Simple closed fractures can be treated in 

a splint but may need additional time in-theater to allow for serial compartment checks during the first 

24 to 48 hours of fracture swelling. Commonly, open tibia fractures are initially treated with external 

fixation. This allows for wound care, protection of neurovascular structures, and patient comfort during 

evacuation. Injuries of the proximal tibia and distal femur may warrant a knee-spanning external fixation 

to prevent knee dislocation or fracture displacement. 

Femur Fracture Fixation

Femur fractures can present with a markedly shortened, floppy limb with severe hemorrhage (both 

internal and external to the limb).146 Restoration of the bony length reduces pain, blood loss, and risk 

of neurovascular injury from the sharp bony fracture surfaces.146 Initially external traction splints can 

achieve some stability and bony alignment for safe patient transport (Fig. 54). For example, a Thomas 

splint, which is similar to the modern Hare traction splint, is the only other first-aid device besides the 

tourniquet evidenced to save lives of the limb injured (Fig. 55).146 However, these traction splints rely on 

pressure on the ischial tuberosity proximally for their mechanical effect to hold the limb out to length. If 

such splints are misused or unattended, risk of sciatic nerve compression and possible risk of tourniquetlike effect by tight straps can occur. Such problems underscore the importance of periodic reassessment 

and adjustment of splints. 

Figure 54. (Left) An external traction splint can help stabilize and 

align displaced femur fractures. Image courtesy of Defense Imagery 

Management Operations Center (DIMOC).

Figure 55. (Above) Restoration of the bone length reduces pain, blood 

loss, and risk of neurovascular injury from sharp fracture fragments.
450 | Extremity Injury

Proximal tibial or distal femoral traction pins 

can be used to bring the femoral fracture out to 

length as well, but they cannot be used routinely 

during interhospital patient transport (Fig. 56). Hip 

spica casting of femur fractures should be avoided 

because wound access and visibility are poor, and 

the heavy logistical burden outweighs the benefit 

of the cast.147 A common form of femoral fracture 

immobilization is half-pin external fixation in a 

unilateral frame configuration (Fig. 57). Safe areas 

for half-pin placements are from anterior in the 

thigh to lateral in the thigh (i.e., half-pin placement 

across the anterolateral quadrant is safe).142,148 Care must be taken to avoid placing pins into the knee joint, 

as this risks septic arthritis and iatrogenic cartilage injury. Care in not overdrilling the pins through the 

far cortices and into the distal Hunter’s canal is needed to avoid arterial injury.145 Hip or knee-spanning 

frames may be used as well for very proximal and distal fractures, respectively. 

Pelvic Fracture Fixation

The evaluation of patients sustaining pelvic trauma is a critical component of trauma care. Severe pelvic 

injuries result from high-energy trauma and are associated with a variety of injuries. A multidisciplinary 

Figure 57. For femoral fracture immobilization, half-pins may be safely placed across the anterolateral quadrant of the thigh. Images courtesy of 

David Carmack, MD, and Michael Shaun Machen, MD, COL, MC, US Army.

Figure 56. Proximal tibial or distal femoral traction pins can be used 

to bring a femoral fracture out to length. Image courtesy of the Borden 

Institute, Office of The Surgeon General, Washington, DC. 
Extremity Injury | 451

approach to the early care of the casualty with pelvic trauma is important. Further discussion of acute 

surgical issues associated with pelvic trauma is provided in the Damage Control Surgery chapter. 

Early pelvic stabilization can control hemorrhage and reduce mortality.

Pelvic fractures in combat settings can present with severe and difficult to control hemorrhage.149 The goals 

of resuscitation are to first stop the bleeding in the pelvis and then identify all open wounds. A patient 

with a pelvic fracture needs a thorough external and internal physical examination (including rectum and 

vagina) to identify any open fractures. The sources of bleeding from a pelvic fracture are venous, arterial, 

and bony fracture surfaces themselves. Errors in early assessment or management can increase mortality.150

Fecal contamination and associated injuries can complicate care.

Patients with a pelvic fracture need a thorough external and internal physical examination (including 

rectum and vagina) to identify open pelvic fractures.

If the pelvic fracture pattern is unstable, initial stability may be improved with a pelvic binder or 

sheet around the patient’s hips (greater trochanters) to reduce motion in an unstable pelvis (Fig. 58).77

Pelvic binders should be avoided in lateral compression fractures because they add to the compression 

laterally by their pressure on the greater trochanters; in this way, pelvic binders can worsen fracture 

displacement.151

Eastridge et al. noted the importance of pelvic fracture pattern in guiding management in a civilian patient 

population suffering from pelvic ring disruption and hemorrhagic shock.149 These authors noted that 

Figure 58. (Left) Pelvic stability may be improved with application of 

a pelvic binder or bed sheet around the patient’s hips. Image courtesy of 

Pelvic Binder, Inc.

Figure 59. (Below) Selective use of external fixation of the pelvis should 

be considered in patients with mechanical pelvic instability and persistent 

hemorrhage. Image courtesy of Trauma.org.
452 | Extremity Injury

casualties with signs of ongoing shock with stable 

pelvic fracture patterns and hemoperitoneum 

require celiotomy as the initial intervention, as 

the site of major hemorrhage is predominantly 

intraperitoneal. In patients with unstable fracture 

patterns, even in the presence of hemoperitoneum, 

consideration should be given to angiography before 

celiotomy.149 Extraperitoneal pelvic packing has 

been used as an adjunctive measure to angiographic 

embolization to achieve direct hemostasis and 

control venous bleeding following massive 

traumatic pelvic hemorrhage.151,152 Further studies 

are required to define the utility of this approach. 

Interventional radiology capacity (therapeutic 

angiography) is limited in OEF and OIF, thus 

making pelvic packing a primary consideration in 

patients with massive pelvic hemorrhage. 

If pelvic mechanical instability and hemodynamic 

instability persist, selective use of external fixation 

of the pelvis should be considered.151 Rigid bony 

stability may allow for hemostasis, as the hematoma and vessels may be protected from further injury 

during initial management.151 Of note, external fixators can displace pelvic fractures with posterior 

element (sacroiliac joint) instability and result in anterior pelvic compression and posterior pelvic element 

distraction, which can exacerbate pelvic hemorrhage (Fig. 59).151 This phenomenon is possible with 

overcompression of the anterior ring resulting in diastasis of the posterior injury.

An anterior pelvic fixator can be placed without power tools and without fluoroscopic assistance. The 

half-pins can be tightened into a T-handled chuck for bony insertion as the half-pin’s threads can cut into 

bone. The half-pins that are specifically designed with blunt tips for pelvic bone insertion in the Stryker’s 

Hoffman® II External Fixation System are commonly used in the US military. The blunt tipped half-pins 

tend to stay within the bone between the two tables of the pelvic bone instead of sharply cutting through 

the inner or outer tables, and thereby with more bony purchase have better skeletal fixation. Through a skin 

incision and finger dissection yielding direct digital palpation of the inner and outer cortices of the pelvis 

with the surgeon’s thumb and forefinger, half-pins are typically inserted through the bone cortex two to four 

centimeters posterior to the anterior superior iliac spines aligned with and between the inner and outer 

tables of the pelvis. This distance posterior to the anterior superior iliac spine has the greatest amount of 

bone available for optimal pin placement and will avoid the lateral femoral cutaneous nerve (Fig. 60).

Open Pelvic Trauma

Open pelvic fractures are uncommon in war.153 When they do occur, they can present with severe 

hemorrhage that is difficult to control. Open pelvic fractures often result from penetrating trauma that 

causes less skeletal instability but higher rates of arterial hemorrhage relative to closed pelvic fractures 

(Figs. 61 and 62). Damage control surgery such as emergent laparotomy, proximal control of vessels, and 

pelvic packing may be indicated, although there is little evidence to guide management. The resuscitation 

Figure 60. External fixator placement in the iliac crests allows for the 

most direct control of the pelvis. Image courtesy of the Borden Institute, 

Office of The Surgeon General, Washington, DC.
Extremity Injury | 453

requirements in such cases can be extreme and mortality rates high.153 If the open fracture has 

radiographic findings suggestive of pelvic fracture instability commonly associated with blunt trauma, 

then the principles of care from blunt pelvic trauma still probably apply as discussed previously.149 

However, additional principles of open pelvic trauma may also apply and include consideration for 

massive transfusion and pelvic packing.152,154 

Open pelvic fractures are uncommon in war. When present, they require immediate hemorrhage 

control, aggressive and thorough debridement, pelvic stabilization, and a diverting colostomy in the 

presence of wounds at risk for fecal soilage.

Associated Injuries

Genitourinary Complications

The genitourinary injuries found in association with pelvic injuries are discussed in the Damage Control 

Surgery chapter.

Hip Dislocations

Hip dislocations are often associated with pelvic (e.g., acetabular fractures) trauma.155 Hip dislocations 

are classified as posterior (80 to 90 percent), anterior (10 to 15 percent) and central (2 to 4 percent). All 

hip dislocations must be regarded as true orthopaedic emergencies (Fig. 63). Following a hip dislocation, 

traction on the blood vessels supplying the femoral head can result in ischemia. Prompt reduction of 

hip dislocations is necessary to minimize the incidence of avascular necrosis of the femoral head.156

Figure 61. (Left) Open pelvic fractures can present with severe 

hemorrhage that is difficult to control. This casualty required 200 units 

of blood in 24 hours. Image courtesy of Leopoldo C. Cancio, MD, 

FACS, COL, MC, US Army. 

Figure 62. (Below) Open pelvic fractures require immediate hemorrhage 

control, aggressive and thorough debridement, pelvic stabilization, and a 

diverting colostomy in the presence of wounds at risk for fecal soliage. 

Image courtesy of Raymond F. Topp, MD, LTC, MC, US Army.
454 | Extremity Injury

Classic teaching is that all hip dislocations should be reduced within six hours.157,158 The sooner the hip is 

reduced the better. The longer a hip is dislocated, the greater the risk of avascular necrosis. The timing 

and method of reduction depend on the patient’s condition, the type of dislocation, and associated 

fractures. Adequate relaxation ensures the greatest chance for success. Patients will need to undergo deep 

sedation. 

All hip dislocations must be regarded as true orthopaedic emergencies. Prompt reduction of hip dislocations 

is necessary to minimize the incidence of avascular necrosis of the femoral head.

Most anterior hip dislocations reduce easily with 

traction in line with the deformity. Posterior hip 

dislocations may be reduced by the Allis or Stimson 

maneuvers. In the Allis maneuver, an assistant 

stabilizes the anterior superior iliac spines while 

the patient is supine. First the knee is flexed, then 

the hip is flexed, and traction is applied below the 

knee pulling it upward. The leg is internally and 

externally rotated until reduction is achieved. The 

Stimson maneuver requires the patient to lie prone 

with the affected extremity completely off the 

table or stretched. The hip and knee are flexed to 

90 degrees, and downward pressure is placed on 

the flexed knee. The leg is gently externally and 

internally rotated until reduction is accomplished.

Following hip reduction, an abduction pillow is placed between the patient’s thighs and holds them widely 

apart to maintain the reduction. A post-reduction hip radiograph should be obtained to confirm adequate 

reduction and document any fracture fragments. Occasionally, a hip dislocation may be irreducible due to 

the incarceration of a tendon, joint capsule, or fracture fragment. These cases will need closed reduction 

under general anesthesia or open (i.e., operative) reduction.

Acetabular Fractures

Fractures of the acetabulum represent 20 percent of all pelvic fractures.159 There are four types of 

acetabular fractures: posterior rim, transverse, iliopubic (i.e., anterior column) and ilioischial (i.e., posterior 

column). Posterior rim fractures represent the most common form of acetabular fracture. They are almost 

always associated with posterior hip dislocations. Transverse acetabular fractures may be associated with 

central hip dislocations. Iliopubic column acetabular fractures may be associated with central or anterior 

hip dislocations. Ilioischial column fractures have an associated sciatic nerve injury in 25 to 30 percent of 

cases.160 The general treatment of acetabular fractures includes analgesia, CT imaging with thin sections 

to further characterize the injury, hospitalization, and orthopaedic consultation. The goal of treating 

acetabular fractures is to reestablish the normal femoral head and acetabular relationship. Associated hip 

dislocations require prompt reduction to avoid long-term complications.

Figure 63. Example of a left hip dislocation. All hip dislocations should 

be treated as true orthopaedic emergencies and reduced as soon as possible.
Extremity Injury | 455

Summary

The frequency and severity of extremity injuries in OEF and OIF are substantial. Extremity injury 

care underscores one of the most obvious differences between military and civilian scope of practice 

for nonorthopaedic CCC providers. Combat casualty careproviders need to have a solid understanding 

of the general principles of combat extremity wound and injury management. General surgeons will 

often need to perform orthopaedic procedures such as complex wound debridement, external fixation 

of fractures, and fasciotomy for compartment syndrome. For experienced orthopaedists, the means and 

goals of CCC differ slightly in context. For example, host nation casualty management is aimed more 

towards providing definitive care, to the extent local logistical constraints allow. Definitive care of US 

military casualties is typically deferred to Level V facilities. Balancing ideal versus practical casualty care 

in a combat theatre will challenge even the most seasoned careprovider.
456 | Extremity Injury

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464 | Extremity Injury

116. Murray CK, Hsu JR, Solomkin JS, et al. Prevention and management of infections associated with 

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118. Johnson EN, Burns TC, Hayda RA, et al. Infectious complications of open type III tibial fractures 

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Afghanistan. J Trauma 2008;64(2 Suppl):S163-168; discussion S168.

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131. Nelson DE. Coagulation problems associated with multiple transfusions secondary to soft-tissue 

injury. USARV Medical Bulletin 1968;3(5):40-49. 

132. Bowden RE, Gutmann E. The fate of voluntary muscle after vascular injury in man. J Bone Joint 

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133. Leininger BE, Rasmussen TE, Smith DL, et al. Experience with wound VAC and delayed primary 

closure of contaminated soft tissue injuries in Iraq. J Trauma 2006;61(5):1207-1211.

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466 | Extremity Injury

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2003;73(6):453-459.

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157. Rodríguez-Merchán EC. Osteonecrosis of the femoral head after traumatic hip dislocation in the 

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Extremity Injury | 467

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468 | Extremity Injury

Appendices

1. Combat Application Tourniquet (C-A-T®) Application Steps

2. Joint Theater Trauma System Clinical Practice Guideline — Compartment Syndrome (CS) and the 

Role of Fasciotomy in Extremity War Wounds

3. Glossary and Classification of Amputations

4. Joint Theater Trauma System Clinical Practice Guideline — Irrigation of War Wounds
Extremity Injury | 469

Appendix 1
470 | Extremity Injury
Extremity Injury | 471

Appendix 2
472 | Extremity Injury
Extremity Injury | 473
474 | Extremity Injury
Extremity Injury | 475
476 | Extremity Injury
Extremity Injury | 477
478 | Extremity Injury
Extremity Injury | 479
480 | Extremity Injury
Extremity Injury | 481

Appendix 3

Glossary and Classification of Amputations

Mechanism

•	 Traumatic amputations are injuries, not procedures.

Timing of amputation procedure

•	 Originally, the use of primary, secondary, and intermediate amputation dealt with the timing of suppuration, but recently the usage of primary has generally meant early and secondary meant late. 

•	 Primary amputation is a procedure done at the first surgery; it means the same as a debridement

amputation or completion amputation (terms which are less specific). Synchronous amputations:

multiple amputations when occurring simulataneously as when two or more operative teams work 

together on different limbs.

Degree of amputation (limb transection)

•	 Partial (or subtotal) traumatic amputation is preferable to near complete amputation since complete

traumatic amputation is confusable with completion amputation which is a procedure. Total traumatic amputation is preferable to complete traumatic amputation. 

•	 Open traumatic amputation is the norm, but closed traumatic amputations occur rarely while involving disruption of most of the limb yet have intact skin.

•	 Site of major amputation

•	 On physical examination before the results of the radiographs are available, providers can simply 

use the word ‘about’ (as in ‘amputation about the knee’) instead of speculating what exactly the

amputation site may be. 

•	 Trans-pelvic

•	 Through the hip

•	 Transfemoral is preferable to above knee which is less specific

•	 Through the knee

•	 Transtibial is preferable to below knee which is less specific.

•	 Through the ankle 

•	 Fore quarter (interscapulothoracic)

•	 Hind quarter (interilioabdominal or internnominoabdominal)

•	 Major amputation: amputation of upper extremity proximal to the wrist and lower extremity proximal to the ankle (‘proximal’ is more precise than ‘above’).

•	 Minor amputation: amputation of the smaller parts such as fingers, toes, hands or feet.

Number of limbs

•	 Single amputation: amputation of one limb only

•	 Double amputation: amputation of two limbs

•	 Triple amputation: amputation of three limbs

•	 Quadruple amputation: amputation of four limbs

Surgical Technique

•	 The ‘guillotine amputation’ technique was a rapid procedure that was done with a circular sweep 

of the knife and cut of the saw through bone transverse to the long axis of the limb with the crosssection being left open when the primary closure was not indicated. The guillotine amputation label 
482 | Extremity Injury

was later superseded by the open circular amputation which actually permitted the different tissue 

cuts to be at different levels. The current preferred term is open, length-preserving amputation in 

order to emphasize the principle of preserving the maximum distal tissue as practical instead of following an arbitrary or transverse direction that wastes normal tissue. 
Extremity Injury | 483

Appendix 4
484 | Extremity Injury
SPINAL TRAUMA

Contributing Authors

Raymond F. Topp, MD, LTC, MC, US Army

 Eric Savitsky, MD

 William P. Cranston, PA, CPT, SP, US Army

Chapter 10
All figures and tables included in this chapter have been used with permission from Pelagique, LLC, the 

UCLA Center for International Medicine, and/or the authors, unless otherwise noted.

Use of imagery from the Defense Imagery Management Operations Center (DIMOC) does not imply or 

constitute Department of Defense (DOD) endorsement of this company, its products, or services.

Disclaimer

The opinions and views expressed herein belong solely to those of the authors. They are not nor should 

they be implied as being endorsed by the United States Uniformed Services University of the Health 

Sciences, Department of the Army, Department of the Navy, Department of the Air Force, Department of 

Defense, or any other branch of the federal government.
Spinal Trauma | 487

Table of Contents

Introduction........................................................................................................ 489

Epidemiology...................................................................................................... 490

Levels of Combat Casualty Care............................................................................ 490

Level I................................................................................................................................491

Level II ..............................................................................................................................491

Level III.............................................................................................................................492

Level IV .............................................................................................................................492

Level V...............................................................................................................................492

Emergency Management ...................................................................................... 493

Spinal Shock .....................................................................................................................496

Spinal Immobilization .....................................................................................................496

Tactical Combat Casualty Care ............................................................................. 497

Spinal Resuscitation............................................................................................. 498

Neurogenic Shock .............................................................................................................499

Restoring Spinal Alignment .............................................................................................499

Role of Glucocorticosteroids ............................................................................................499

Detailed Assessment of Spinal Injury..................................................................... 500

Spinal Anatomy ................................................................................................................500

Radiographic Considerations...........................................................................................501

Determining Spinal Stability............................................................................................503

Spinal Cord Injury Patterns.............................................................................................503

Complete Cord Syndrome.................................................................................................503

Incomplete Cord Syndromes.............................................................................................504

Anterior Cord Syndrome...................................................................................................504

Central Cord Syndrome....................................................................................................504

Brown-Séquard Syndrome................................................................................................506

Cauda Equina Syndrome...................................................................................................506

Spinal Nerve Root Syndromes...........................................................................................506

Spinal Cord Injury Without Radiographic Abnormality ..................................................506

Spinal Injury Management Considerations ............................................................. 507

Spinal Immobilization and Transport Considerations ..................................................507

Timing of Surgical Interventions .....................................................................................507

Spinal Reduction Interventions .......................................................................................508

Axial Traction ....................................................................................................................508

Penetrating Injury to the Spine ........................................................................................510

Management......................................................................................................................510

Mechanical Stability .......................................................................................................510
488 | Spinal Trauma

Infection Control .............................................................................................................511

Complications: Penetrating Spine Trauma........................................................................512

Cerebrospinal Fluid Fistulae.............................................................................................512

Spinal Infections .............................................................................................................513

Vascular Injuries.............................................................................................................514

Projectile in the Disc Space ..............................................................................................514

Projectile in the Spinal Canal...........................................................................................515

Summary............................................................................................................ 516

References .......................................................................................................... 517
Spinal Trauma | 489

Introduction

Combat casualty care (CCC) providers play a vital role in the diagnosis and initial management of acute 

spinal injury patients. Combat casualty care frequently presents patient care challenges that are beyond 

the scope of Advanced Trauma Life Support (ATLS) training.1 Failure to recognize and appropriately 

manage unstable spinal injuries may result in the development or the progression of neurologic injury.2 The 

optimal management of spinal injuries is dictated by a CCC provider’s skill set, support staff, and access to 

equipment necessary to achieve desired outcomes.

Two broad categories of spinal trauma on the battlefield are penetrating and blunt injuries. Penetrating 

spinal injuries in combat are most often the result of gunshot wounds or fragmentation injuries from blast 

mechanisms.3,4,5 Blunt trauma can result from falls, tertiary injury from blasts, combat vehicle collisions, and 

numerous other mechanisms. The early identification and management of open spinal injuries are critical. 

A direct path from the skin through the dura defines an open spinal injury. All spinal injuries associated with 

penetrating trauma should be deemed open spinal injuries, until proven otherwise (Fig. 1). Conversely, blunt 

Figure 1. Pediatric host nation patient with penetrating trauma to his back. Here, exposed spinal cord with cerebrospinal fluid leak is noted at 

the lumbar (L3) level. The spine was stable with only posterior spinal column involvement. Image courtesy of the Borden Institute, Office of The 

Surgeon General, Washington, DC.
490 | Spinal Trauma

trauma leading to spinal injury, needs to be classified on a case-by-case basis based on physical findings (e.g., 

open wound in proximity to spinal injury). Regardless of the etiology, spinal trauma represents a critical 

wounding pattern that increases the morbidity and mortality of soldiers injured on the battlefield.6

All soldiers injured on the battlefield, including soldiers with spinal cord injuries, are treated within the 

Health Service Support (HSS) system. This system comprises established levels of CCC. Each level of care, 

starting at the point of injury to medical centers within the continental United States (CONUS), varies 

in respective capacity to manage spinal trauma. Each level of care (Level I thru Level V) is designed to 

deliver a progressively greater degree of care and resources. Careproviders working in Level I thru Level III 

facilities will face the challenge of providing initial care for a significant number of penetrating spinal trauma 

casualties. This will be a markedly different experience for CCC providers trained in civilian centers, where 

blunt trauma mechanisms of spinal injury predominate.7,8,9 This chapter will discuss the varying levels of 

CCC, relevant anatomical considerations and spinal cord injury patterns, and the optimal management of 

the spinal injury patient within a CCC environment.

Epidemiology

As of June 2010, 37,669 combatants were listed as wounded in action from Operation Enduring Freedom 

(OEF) and Operation Iraqi Freedom (OIF). Total soldier deaths from these two conflicts over the same time 

period was 5,425. In an attempt to report and study the injuries from this conflict, Holcomb et al. have 

created the Joint Theater Trauma Registry (JTTR) database. From this database, the rate of spine injury 

from OEF and OIF is 1.4 percent.10 Therefore, CCC providers will need to be proficient in the management 

of combatants with spine injuries.

Levels of Combat Casualty Care

Civilian medical care for spinal injuries relies on the ability of emergency medical services (EMS) personnel 

to stabilize spinal injuries and directly transport the patient, using spinal immobilization, to a trauma 

center for definitive care. Typically, the civilian transport process takes less than an hour. In extenuating 

circumstances, if the patient is located in a remote location at the time of injury, transport time may be 

extended to several hours. In contrast, CCC provided from the point of injury to CONUS medical centers 

proceeds through varying stages of care. Typically, it takes 72 to 96 hours for a combat casualty to reach a 

Level V facility (Fig. 2).11,12,13 Combat casualty care is not only complicated by long distance air evacuation 

(AIREVAC) through multiple facilities and careproviders, but also by unpredictable weather conditions and 

the inherent hostility of the battlefield.

Figure 2. Evacuation chain for combat casualties.

Echelon I Echelon II Echelon III Echelon IV Echelon V

Self-aid, 

buddy-aid, 

medic,

Battalion Aid 

Station

Forward 

Surgical Team

Combat

Support 

Hospital

Landstuhl,

Germany

CONUS

Facility
Spinal Trauma | 491

Level I 

Level I CCC refers to the initial care an injured soldier receives in the battlefield. This level of care is often 

provided by a combat medic trained at an emergency medical technician–basic (EMT-B) level. There are 

times when a careprovider with a higher level of training (e.g., special forces medic, physician assistant, or 

physician) is present at the point of injury. However, CCC providers at this level are limited by available 

resources and their environment. Level I care is often provided while the initial conflict or battle is in 

progress (Fig. 3). Casualty evacuation (CASEVAC) times may be delayed because of the ensuing battle or 

the hostility of the terrain. 

Because of the possibility of exposing themselves to hostile fire, CCC providers may not be able to safely 

provide proper spinal immobilization for those injured on the battlefield (e.g., care-under-fire scenario). It 

is recommended that spinal immobilization be performed once the injured soldier has been moved to a 

safer location, such as a casualty collection point.

Although battlefield heroics often prevail, 

careproviders risk injury or death by exposing 

themselves to direct fire from the enemy in order 

to provide CCC. Current ATLS guidelines 

recommend all patients with an injury above 

the clavicle or a head injury resulting in a loss 

of consciousness be immobilized in a semi-rigid 

cervical collar and a backboard.1

 This is not 

always appropriate on the battlefield because 

proper placement of a cervical collar and spinal 

immobilization could involve multiple personnel 

exposing themselves to hostile fire, thereby 

increasing the likelihood of more injured soldiers. 

In a retrospective study of penetrating trauma to the 

neck in the Vietnam War, Arishita et al. discovered 

that roughly 1.4 percent of the casualties treated 

with cervical spine precautions actually had a spinal 

injury that would have benefited from cervical spine 

immobilization.14 The authors concluded that mandatory cervical spine immobilization of all penetrating 

neck trauma sustained in an environment hostile to careproviders had an unfavorable risk-to-benefit ratio. 

For this reason, it is recommended that spinal immobilization be performed once the injured soldier has 

been moved to a safer location, such as a casualty collection point. 

Studies performed in civilian and combat settings suggest that most patients with normal neurological exams 

following penetrating trauma to the neck will not have a mechanically destabilized spinal column.15,16 

Level II

Level II care expands upon Level I care by providing a designated CCC facility that is more removed 

from direct conflict. This facility is staffed with greater numbers of careproviders with access to laboratory 

and medical imaging technology. Radiographic studies are usually limited to plain radiography and handFigure 3. On the battlefield (e.g., care-under-fire scenario), preservation 

of the lives of the casualty and medic is of paramount importance. Spinal 

immobilization of the injured soldier is performed once they have been 

moved to a safer location. Image courtesy of the Borden Institute, Office of 

The Surgeon General, Washington, DC.
492 | Spinal Trauma

carried ultrasonography. Computed tomography (CT) and magnetic resonance imaging (MRI) are typically 

not available at these facilities. The main mission of Level II facilities is to recognize and treat injuries that 

compromise a casualty’s airway, breathing, and the circulatory system. Treatment initiated at this level 

typically follows the established protocols found in ATLS.1 Combat casualties with suspected unstable spinal 

injuries undergo spinal immobilization at Level II facilities. Spinal injury patients who are experiencing 

neurogenic shock are treated with supportive care. Operative interventions aimed at stabilizing spinal 

injuries are not typically performed at these facilities. 

Level III

Level III care facilities are represented by a field hospital environment such as a Combat Support Hospital 

(CSH), described as a Mobile Army Surgical Hospital (MASH) in previous conflicts. Level III facilities 

provide highly trained and specialized careproviders, extensive medical imaging capacity (e.g., CT scans), 

laboratory support, and blood bank services. In addition, they provide dedicated operating rooms with 

specialized surgical capabilities, and it is not uncommon to have vascular surgeons, neurosurgeons, 

orthopaedic surgeons, and trauma surgeons available.

This is the first CCC environment where more definitive stabilization of life-threatening injuries can be 

achieved. With regard to spinal injury, this level of care allows for better delineation of spinal column injury 

via CT imaging. Computed tomography has the ability to detect even the most subtle bone pathology. 

In addition, as the patient is further evaluated, tertiary examination of the casualty often confirms or 

refutes the presence of spinal injury. Once a spine injury is recognized, a Level III CSH provides the 

human and logistical resources needed to maintain strict spinal immobilization and ensure optimal patient 

transportation. If the patient cannot be treated definitively at this level with subsequent return-to-duty, the 

primary mission of the CSH is to stabilize all injuries such that the casualty can tolerate intertheater air 

evacuation to a higher level of care.

Level IV

Level IV facilities (e.g., Landstuhl Medical Center in Germany) are major medical centers that have 

the capacity to diagnose and treat complex injuries. They are often located out-of-theater and provide 

maintenance of stabilization and ongoing resuscitation. These treatment facilities provide a broad spectrum 

of specialty and subspecialty medical care, advanced diagnostic capability (e.g., MRI, angiography suites, 

nuclear medicine), surgical interventions, and stabilization prior to the patient reaching Level V care. 

Level V

Level V facilities (e.g., Brooke Army Medical Center-BAMC) provide stabilization, definitive care, and 

reconstructive surgical capabilities. Level V is the highest level of medical treatment available to combat 

casualties. Definitive surgical repair and reconstruction of all injuries is provided at this level of care. With 

regard to spine injuries, definitive stabilization optimally occurs at Level V, unless it is medically necessary 

to perform at preceding levels of care (e.g., a case of progressive neurologic deterioration with documented 

cord compression). 
Spinal Trauma | 493

Unless it is medically necessary to perform an operation at preceding levels of care (e.g., progressive 

neurologic deterioration with documented cord compression), a definitive stabilization procedure 

optimally occurs at Level V facilities.

Battlefield spinal injuries will challenge CCC providers. Given the limited capabilities to recognize and 

definitively treat spinal trauma in Level I and II settings, the main goal of management is to maintain spinal 

immobilization and initiate spinal cord resuscitation pending better delineation of spinal injury. Level III 

facilities will enable optimal radiographic imaging of spinal injuries, while definitive surgical stabilization 

typically occurs at Level IV and V facilities. 

Emergency Management

Forty-seven percent of patients with spinal trauma 

and 64 percent of patients with spinal cord injuries 

have concomitant injuries in civilian studies.17,18

Head, chest, and long-bone injuries are the most 

frequently associated injuries. Similarly, a majority 

of spinal injuries sustained in combat environments 

will be associated with concurrent injuries.3,4,5,6

In the setting of multiple trauma, in which most 

spinal injuries occur, assessment and management 

of airway, breathing, and circulatory system 

compromise take priority. The assessment and 

management of airway, breathing, and circulation 

issues and the simultaneous identification of 

neurologic disability with exposure of the casualty 

constitute the primary survey. Immediately 

following initial stabilization, a careful neurologic examination is warranted. Spinal cord injuries have 

important physiologic consequences. A cervical or high thoracic spinal cord injury often results in a loss 

of phrenic and/or intercostal nerve function with resultant compromise of diaphragmatic and chest 

wall excursion. This is of special concern in patients with concurrent head, chest wall, or lung injury. 

All patients with high-level spinal cord injuries require close observation to ensure that ventilation and 

oxygenation remain adequate. 

All patients with high-level spinal cord injuries require close observation to ensure that ventilation and 

oxygenation remain adequate. 

Once primary survey issues are addressed, a secondary survey is performed. The secondary survey consists 

of performing a focused physical examination. Palpation of the entire spinal column and a more detailed 

neurological exam are performed during the secondary survey. Spinal injuries are typically documented 

during this phase of casualty management. Special attention must be paid to identifying physical findings 

suggestive of open spinal injuries (e.g., open wound in proximity to spinal injury) and detecting neurologic 

deficits suggestive of spinal injury (Fig. 4). The neurologic exam does not have to be extensive but should 

document the basic sensory and motor function of the combat casualty. 

Figure 4. Open spinal injury. Image courtesy of Joint Combat Trauma 

Management Course, 2007.
494 | Spinal Trauma

A direct path from the skin through the dura defines an open spinal injury. All spinal injuries associated 

with penetrating trauma should be deemed open injuries, until proven otherwise.

In a responsive patient, light touch examination attempts to localize the lowest dermatome with normal 

sensation equilaterally. The sensation of pain may be of limited utility, as most casualties will have been 

made more comfortable with the use of narcotics or may have altered mental status due to concurrent 

injuries. However, motor function can be readily assessed in a cooperative patient. An intact motor level is 

recorded as that level that maintained enough muscular function to resist gravity (3 out of 5 motor strength) 

(Table 1).19 Special attention must be paid to documenting rectal tone, sacral sensation, and bowel and 

bladder function to avoid missing injuries to the terminal spinal cord (conus medullaris) and cauda equina. 

Neurologic assessment in unresponsive patients is 

much more limited. The exam consists of observing 

spontaneous movements, the patient’s motor 

responses to painful stimuli, the presence or absence 

of deep tendon reflexes, and rectal sphincter tone.

A complete secondary survey includes careful 

examination of the entire length of the patient’s 

spine. This is performed by gently logrolling the 

patient to his or her side while supporting the 

patient’s spine with a cervical collar and in-line 

immobilization (Fig. 5). The patient’s back should 

be inspected for open wounds, deformity, and 

ecchymosis. The spine should be palpated for a 

step-off or interspinous widening. The locations 

of lacerations and abrasions on the skull may help 

determine the mechanism of cervical injuries. 

Occipital lacerations suggest flexion injuries, 

0 Total paralysis

1 Palpable or visible contraction

2 Active movement, full range of motion, gravity eliminated

3 Active movement, full range of motion, against gravity

4 Active movement, full range of motion, against gravity and provides some resistance

5 Active movement, full range of motion, against gravity and provides normal resistance

5* Muscle able to exert, in examiner’s judgment, sufficient resistance to be considered normal 

if identifiable factors were not present

NT Not testable. Patient unable to reliably exert effort or muscle unavailable for testing due to 

factors such as immobilization, pain on effort, or contracture

Table 1. American Spinal Injury Association Muscle Grading Score.

Figure 5. During the secondary survey, patients should be logrolled, and 

the entire length of their backs should be inspected for tenderness, open 

wounds, deformities, or ecchymoses. Image courtesy of Defense Imagery 

Management Operations Center (DIMOC).
Spinal Trauma | 495

whereas frontal or superior injuries suggest extension or axial compression, respectively. The presence of 

a single spinal injury does not preclude careful evaluation of the rest of the spine. Eight to 28 percent of 

patients with a spinal column injury have additional noncontiguous spinal injuries, and it has been noted 

that up to 30 percent of these injuries are not initially recognized.20,21,22,23,24 The upper and lower extremities 

are examined for motor function by nerve root level. Tables 2 and 3 outline how upper and lower extremity 

spinal nerve roots relate to muscle function, sensation, and reflex activity. The motor examination also 

includes a digital rectal examination for voluntary or reflex bulbocavernosus anal sphincter contraction.

Eight to 28 percent of patients with a spinal column injury have additional noncontiguous spinal injuries, 

and up to 30 percent of these injuries are not initially recognized.

Areas of sensory deficit should be accurately recorded, dated, and timed on the medical record progress 

note or spinal injury flow sheet and demarcated with ink at the affected level on the patient’s skin.

The sensory examination includes testing of dermatomal pattern skin sensation. The light touch sensation 

Root Reflex Muscles Sensation

C5 Biceps Deltoid, biceps Lateral arm

C6 Brachioradialis Wrist extension, 

biceps

Lateral forearm, 

thumb, index finger

C7 Triceps Wrist flexion, finger 

extension, triceps

Middle finger

C8 Finger flexion Medial forearm

T1 Finger abduction Medial arm

Table 2. Upper extremity spinal nerve roots with respective muscle function, sensation, and reflex activity.

Root Reflex Muscles Sensation

L1, L2 Hip flexion Inguinal crease (L1), 

anterior thigh (L2)

L2, L3 Knee extension Anterior thigh (L2), 

anterior thigh just 

above knee (L3)

L4 Patellar tendon Ankle dorsiflexion Medial leg, medial 

foot

L5 None Extensor hallucis 

longus extension

Lateral leg, foot 

dorsum 

S1 Achilles tendon Ankle flexion Lateral foot, sole

Table 3. Lower extremity spinal nerve roots with respective muscle function, sensation, and reflex activity.
496 | Spinal Trauma

of a cotton-tipped applicator (Q-tip®) rubbed lightly over the skin is a quick and reliable examination 

maneuver. Sensation should also be tested in the perianal region. The areas of sensory deficit should be 

accurately recorded, dated, and timed on the medical record progress note or a spinal injury flow sheet. It 

is also recommended that the sensory level be marked, dated, and timed in ink on the patient’s skin at the 

affected level. The practice of marking the sensory level on the skin can avoid much uncertainty when a 

number of examiners are involved. A known challenge of CCC is adequate hand-off or transfer of notes 

between the levels of care. When available, permanent markers can be used on the injured soldier’s skin to 

aid the documentation process. 

Spinal Shock

Spinal shock is defined as the loss of spinal reflexes after injury to the spinal cord, which affects the muscles 

innervated by the cord segments situated below the site of the lesion.25 The loss of reflex function is most 

severe closest to the site of spinal cord injury. Patients with high-level cervical cord injuries may retain some 

distal sacral reflex function (bulbocavernosus reflex and anal wink) despite loss of more proximal reflex 

function.26,27 The documentation of the bulbocavernosus reflex is a key early determinant of whether spinal 

shock has resolved in patients that had initially lost distal sacral reflex function. Return of spinal reflex function 

occurs in a caudal to rostral direction. The return of the bulbocavernosus reflex marking the end of spinal 

shock is variable but often occurs within 24 hours of cord injury.26,27,28,29,30 The bulbocavernosus reflex is 

elicited by simultaneous digital rectal exam and lightly squeezing the glans penis (males) or by gently tugging 

on a placed Foley catheter in female or male patients. An involuntary increase in tone around the examiner’s 

digit with these maneuvers indicates the presence of an intact bulbocavernosus reflex (normal). The absence 

of a bulbocavernosus reflex implies the patient is still in spinal shock. When the bulbocavernosus reflex is 

absent, the prognostic value of the motor exam following a spinal injury is inconclusive. The prognosis of 

a spinal injury patient with a complete cord syndrome, following the return of the bulbocavernosus reflex, 

is poor. Complete cord syndrome patients have a less than 5 percent chance of functional recovery if no 

motor function improvement is documented at 24 hours following return of the bulbocavernosus reflex.29,31

Spinal shock following spine trauma should be differentiated from neurogenic shock, an injury syndrome 

characterized by flaccid paralysis, moderate hypotension, and varying degrees of bradycardia.32

The absence of a bulbocavernosus reflex implies the patient is still in spinal shock, and the prognostic 

value of the motor exam following a spinal injury is inconclusive. The return of the bulbocavernosus 

reflex marking the end of spinal shock is variable but often occurs within 24 hours of cord injury.

Spinal Immobilization

If following the initial patient evaluation suspicion exists for a spinal cord injury, strict spinal cord injury 

precautions must be observed until spinal injury has been ruled out (provided battlefield conditions 

allow). Civilian studies have suggested that neurologic deficits progress as a result of inadequate spinal 

immobilization in up to 5 percent of hospitalized patients during their initial stay.2,33 Keeping the combat 

casualty immobilized on a full-length backboard during the initial resuscitation often facilitates patient care. 

This method of stabilization facilitates patient transportation and allows for rapid logrolling of the patient 

to prevent aspiration in case of vomiting. 

Upon identifying a potentially unstable spinal injury on standard radiography, CT imaging is often the next 
Spinal Trauma | 497

step in defining the injury. The most conservative management style is to maintain spinal immobilization 

until a CT scan is performed to better delineate the mechanical stability of the injured spine. Aggressive 

pain management will often be necessary to alleviate the discomfort resulting from immobilization on a 

hard backboard. Special care (e.g., padding hard surfaces) will need to be taken to avoid pressure necrosis 

of the skin and underlying tissue that can develop within hours of immobilization on a hard surface.34,35

Pressure necrosis of the skin and underlying tissue can develop within hours of immobilization on a hard 

surface.

The most effective method of initial cervical immobilization is the use of bilateral neck supports (e.g., 

sandbags or rolled towels) and taping of the patient across the forehead to a spine board, along with the 

use of a rigid cervical collar (which serves to limit extension) (Fig. 6).36,37 In unstable cervical spine injuries, 

a soft collar, extrication collar, hard collar, or Philadelphia collar alone is not sufficient for immobilization.36

A poster brace (e.g., four-poster brace) or sternal occipital mandibular immobilizer (SOMI brace) is not 

utilized on the battlefield. Securing a patient 

to a standard long spine board is also standard 

practice for immobilization of the thoracolumbar 

spine. This enables rotating of the patient (e.g., if 

they need to clear their airway and vomit) while 

providing maximal support to the thoracolumbar 

spine.36 Cadaveric studies of recreated unstable 

spinal injuries suggest that significant translational 

and rotational spinal movement still occurs, despite 

in-line traction and backboard immobilization 

during logrolling maneuvers.38,39,40 Hence, rotational 

movement of suspected spinal injury patients should 

be minimized. Spinal immobilization is discontinued 

only after radiographic and clinical evaluation have 

excluded unstable spinal injury. This usually occurs 

at the CSH where trauma surgeons and radiologists 

are available to interpret radiographic imaging and 

further assess patients.

The most effective method of initial cervical immobilization is the use of bilateral neck supports (e.g., 

sandbags) and taping of the patient across the forehead to a spine board (stretcher or litter), along with 

the use of a rigid cervical collar.

Tactical Combat Casualty Care

Care-under-fire or at the point of injury is dictated by the tactical situation. The combat casualty may 

have to be moved to a safer location before an assessment can be accomplished. In battlefield conditions, 

rapid casualty evacuation is often a life-threatening process. When only one person is available to assist the 

combat casualty, the casualty is carried or often dragged to a safer location. Patients with suspected spine 

Figure 6. Image demonstrating appropriate initial cervical immobilization 

with the use of bilateral neck supports, taping of the patient’s forehead to 

a spine board, and use of a rigid cervical collar.
498 | Spinal Trauma

injuries should undergo spinal immobilization as soon as it is feasible. Strict spinal cord injury precautions 

are ideally observed until spinal injury has been ruled out.

In care-under-fire tactical situations without 

direct confirmation of spinal injury, the presence 

or absence of associated risk factors should be 

identified. Associated risk factors for spinal injuries 

include bullet, fragmentation, and stab wounds, and 

direct trauma to the face, neck, head, or back. One 

may also include extreme twisting of the trunk and 

major blows to the head or chest that may occur 

from large blast injuries or body impact from landing 

following the blast wave (tertiary blast injury). Along 

with documented neurologic deficits, a Glasgow 

Coma Scale (GCS) score of 8 or below is associated 

with a higher risk (odds ratio = 2.77) of cervical 

spine injuries when associated with traumatic brain 

injuries.41

The standard battlefield cervical collar is the Vertebrace® Extrication Collar (VEC) (Fig. 7). Many Level I 

careproviders not only carry the VEC, but also have access to long spineboards that can be attached to the 

military litter prior to transport. Medical and rescue personnel should make every attempt to control the 

spine during initial extrication and evacuation until proper cervical and thoracolumbar spine precautions can 

be provided. Documentation of known injuries and neurological deficits must occur during the stabilization 

and resuscitative phases of treatment, often taking place prior to the injured combatant reaching a Level 

III care facility. 

Spinal Resuscitation

Once spinal injury is recognized, it is important to begin resuscitative efforts as soon as possible. The ATLS 

guidelines have been designed to ensure full body resuscitation of the traumatized patient.1 It is important 

to note that the injured spinal cord itself needs to be carefully resuscitated. In general terms, resuscitation 

of the spinal cord implies that perfusion with oxygenated blood to the injured area is restored to begin the 

process of healing and prevent further injury.42,43

Resuscitation of the spinal cord involves minimizing secondary injury due to hypoxemia, hypoperfusion, 

and mass effect.

Definitive evidence of discrete hemodynamic resuscitation parameters leading to improved clinical 

outcomes following spinal injury does not exist. A series of animal and human studies do support the 

concept of optimizing spinal cord perfusion following spinal cord injury.44,45 Suggested treatment options 

include ensuring hemodynamic stability and maintaining mean arterial pressures greater than or equal to 

80 mm Hg to optimize spinal cord perfusion.30,42,43,46,47,48,49,50,51 Similarly, ensuring adequate oxygen delivery 

Figure 7. Example of a rigid cervical collar applied to a combat casualty 

with head trauma.
Spinal Trauma | 499

to the spinal cord is important. This often requires supplemental oxygenation via breathing apparatus and 

the application of pulse oximetry. Likewise, airway, breathing, and circulatory compromises need to be 

corrected to ensure optimal resuscitation of the injured spine. Maintaining a minimum hemoglobin value 

of 7 grams per deciliter in trauma patients is recommended, and the timing of blood transfusion (triggers) 

should be based on bedside clinical findings rather than absolute hemoglobin values.52

Neurogenic Shock

Spine trauma may result in neurogenic shock, a syndrome characterized by flaccid paralysis, moderate 

hypotension, and varying degrees of bradycardia.32,53 The typical neurogenic shock patient will have 

suffered a traumatic spinal cord injury, resulting in disruption of T1 to L2 sympathetic outflow.54 Vagal tone 

is unopposed, and moderate hypotension and bradycardia ensue. Bradycardia is a distinguishing sign in 

neurogenic shock as opposed to other shock states where tachycardia is often observed. 

Neurogenic shock is a diagnosis of exclusion and should be made only after life-threatening hemorrhage 

has been excluded, as hypovolemic shock is the most common shock state observed after battlefield trauma. 

Recognition of neurogenic shock will minimize excessive use of crystalloid fluids and resultant dilutional 

coagulopathy and pulmonary edema. Vasopressors may be used following the restoration of intravascular 

volume to maintain normal blood pressures and minimize excessive fluid administration.55

Neurogenic shock, a syndrome characterized by flaccid paralysis, moderate hypotension, and varying 

degrees of bradycardia, is a diagnosis of exclusion and should be made only after life-threatening 

hemorrhage has been excluded.

Restoring Spinal Alignment

An immediate initial treatment priority is to realign the spine. Subluxed or dislocated spinal segments often 

result in additional mechanical stress and ischemic injury to the spinal cord. Alignment of the spine is 

accomplished through a variety of interventions ranging from traction devices to operative interventions. 

Spinal realignment requires specialized equipment, spine surgeons, and support staff. Hence, attempts at 

spinal realignment must typically await transfer of the spinal injury patient to Level III or higher facilities.

Role of Glucocorticosteroids

The use of steroids in the battlefield for treatment of spinal injury is not recommended.56,57,58,59 The role 

of glucocorticosteroids in the treatment of the acute spinal cord injury has long been controversial. The 

purported mechanisms through which steroids exert their effects following spinal cord injury are unclear. 

There is no evidence to suggest administration of glucocorticosteroids results in neurologic improvement 

following penetrating spinal trauma, and some studies suggest increased harm.58,60,61,62 Inconsistency in 

study methodology and reporting has largely discredited any pre-existing civilian data, such as the National 

Acute Spinal Cord Injury Studies (NASCIS), suggesting benefit to the administration of glucocorticosteroids 

following blunt spinal trauma.56,57,58,62,63,64,65,66,67,68

The use of steroids following penetrating spinal injury is not recommended as there is no evidence to 

suggest improved neurologic outcomes, and some studies suggest increased harm.
500 | Spinal Trauma

Detailed Assessment of Spinal Injury

A complete and thorough understanding of spinal anatomy and spinal cord function is integral to the 

appropriate recognition and subsequent management of spinal injuries. In-depth assessments of spinal 

injuries are performed after patients are removed from immediate danger, immobilized, hemodynamically 

stabilized, and transferred to appropriate levels of care. This level of assessment and evaluation is typically 

performed in Level III and higher facilities. Computed tomography evaluation and serial neurological 

evaluations constitute the critical elements that help careproviders further assess and subsequently manage 

spinal injuries.

Spinal Anatomy

Due in large part to its flexibility and exposure, the cervical segment is the most commonly injured part of 

the spinal cord.69 In contrast, the thoracic spine (T1 to T10 vertebral bodies) is a rigid and fixed structure. 

This results from ribs attaching to their respective transverse processes and forming articulations anteriorly 

with the sternum. Cervical nerve roots exit the spinal canal above their respective vertebral bodies. 

Thoracolumbar nerve roots exit the spinal canal below their respective vertebral bodies. The neural canal 

is narrower in the thoracic spine than in the cervical or lumbar spine. These anatomic characteristics and 

the fact that great force is required to damage the thoracic spine probably account for the high incidence of 

significant neurologic injuries following fractures of the thoracic spine.69,70 Because of its unique anatomy, 

the thoracolumbar junction is the second most injured area of the spine.69,70 Unlike the other ribs, the 

11th and 12th ribs do not articulate with the sternum, nor do they attach to their respective transverse 

processes. 

Due in large part to its flexibility and exposure, the cervical segment is the most commonly injured part 

of the spinal cord, while the thoracolumbar junction is the second most injured area.

The orientation of lumbar vertebral body articulating facets and thicker lumbar intervertebral discs allow 

for more flexion, extension, and lateral bending of the lumbar spine. Thus, the rigidly fixed thoracic 

spine abruptly transitions to a less rigidly supported lumbar spine. This abrupt transition likely explains 

the susceptibility of the thoracolumbar junction (T11 to L2 vertebral bodies) spinal segment to injury.69

The spinal canal is relatively wide at this region. Hence, thoracolumbar junction injuries often result in 

incomplete cord lesions. The spinal cord’s terminal segment is called the conus medullaris. It terminates 

at the first lumbar (L1 vertebral body) level in adults and at the L2 or L3 vertebral body level in pediatric 

patients. Individual nerve roots extending distal to this segment constitute the cauda equina. The lower 

lumbar and sacral segments are less prone to spinal cord injury, and the neurologic sequelae are usually less 

severe.69,71

The blood supply to the spinal cord consists of the anterior and posterior spinal arteries and radicular arteries 

(Fig. 8). The anterior spinal artery perfuses the anterior and central cord, and the posterior spinal artery 

supplies the posterior one-third of the spinal cord. The anterior and posterior spinal arteries ascend from 

the vertebral arteries and travel downward along the anterior and posterior aspects of the spinal cord. With 

the exception of the cervical region, these small arteries inadequately maintain the viability of the spinal 

cord. Radicular arteries serve to augment the blood supply to the spinal cord in areas where the anterior 
Spinal Trauma | 501

and posterior arteries alone are insufficient. The radicular arteries arise from the thoracoabdominal aorta, 

among other sources. They form anastomotic tracts with the spinal arteries. The midthoracic region of 

the spinal cord is described as a watershed area. This region has limited blood flow and is located between 

the well-perfused superior and inferior segments of the spinal cord. One of the larger radicular arteries 

is the great radicular artery of Adamkiewicz. It enters the spinal canal between the T10 and L2 vertebral 

bodies. Injury to this artery explains how neurologic deficits resulting from spinal cord ischemia may extend 

cephalad from a more caudal vertebral body fracture or dislocation.29,72

Radiographic Considerations

Plain radiography, CT imaging, and MRI are 

used in the evaluation of spinal injuries. In civilian 

studies, up to 5 percent of trauma patients who 

are unable to give a reliable history or have a 

painful distracting injury have a spinal injury.73,74,75

Conversely, the patient who has neither spinal pain 

or midline tenderness on palpation nor neurologic 

signs or symptoms and is awake, alert, and without 

major distracting injuries does not require routine 

spinal radiographs.76 While indications for plain 

radiography of the thoracolumbar spine have not 

been clearly defined, the application of criteria 

developed for cervical spine radiography appears 

reasonable.77,78

A standard trauma spinal series should include a 

cross-table lateral and an anterior-posterior (AP) 

view radiograph. An open-mouth odontoid view 

is needed for cervical spine evaluation. While the 

Figure 8. Cross-section illustration of spinal cord anatomy demonstrating its vascular supply.

Figure 9. Axial CT image demonstrating C3 vertebral body fracture.

Posterior Spinal Artery

Radicular Trunk

Aortic Spinal Ramus

Anterior Spinal Artery
502 | Spinal Trauma

sensitivity and specificity of these views are controversial, a normal and technically optimal study is widely 

considered adequate to exclude major fractures and dislocations. The primary exceptions include patients 

with unexplained neurologic deficits or underlying musculoskeletal conditions (e.g., severe spondylosis). 

Patients with unexplained neurologic deficits or a major fracture or dislocation identified on plain 

radiographs should undergo CT scan to further define the extent of injury. Patients with inadequate plain 

films or areas of suspicion on plain radiographs typically undergo CT scanning.76,79

Patients with inadequate plain films, unexplained neurologic deficits or a major fracture or dislocation 

identified on plain radiographs should undergo CT imaging to further define the extent of injury.

Computed tomography imaging is more accurate than plain radiography in delineating the extent of 

fractures and bone fragment displacement.76,79,80 A CT scan is also useful in identifying minor fractures, 

many of which are missed on plain radiography. Standard axial CT images are adequate to delineate 

most injuries (Fig. 9). Chance fractures and odontoid fractures are exceptions.18,81,82,83,84 Their detection 

often requires sagittal reconstruction of CT or MRI images and concurrent plain radiographs (Fig. 10).83,84

Computed tomography imaging fails to adequately visualize the spinal cord, hence it cannot give direct 

evidence of spinal cord injury. The excellent bone visualization, wide accessibility, and speed of CT imaging 

make it the primary supplementary method of imaging the spine.

Figure 10. Sagittal reconstruction of CT images demonstrating a Chance 

fracture. Adapted image courtesy of LearningRadiology.com.

Figure 11. MRI, available at Level IV or V facilities, allows precise 

visualization of the spinal cord. MRI imaging is more sensitive than CT 

imaging for ligamentous and soft-tissue injury.
Spinal Trauma | 503

Magnetic resonance imaging plays a vital role in spinal cord injury evaluation (Fig. 11). More sensitive 

than CT scan for ligamentous and soft-tissue injury, MRI also allows precise visualization of the spinal 

cord.85,86 Logistical difficulties, including limited accessibility, limited ability to monitor the patient while in 

the scanner, and prolonged imaging time, currently prevent routine use of MRI in the evaluation of acute 

spinal injury patients. MRI is not available until Level IV or V care for combat casualties.

Determining Spinal Stability

Determining the stability of the spinal column is an important initial step in the evaluation of spinal injuries. 

White and Panjabi provided a widely accepted definition of spinal stability.87,88 They defined spinal stability 

as the ability of the spine, under physiologic loads, to limit patterns of displacement, to preclude damage 

and irritation to the neural elements, and to prevent incapacitating deformity or pain due to structural 

changes. 

While White and Panjabi’s definition lends itself to the subjectivity of the examiner, the use of CT allows 

for a much more objective approach to determining mechanical stability. The advent of CT led to an 

evolution of theory regarding the determinants of spinal column stability. In 1983, Denis devised an 

anatomic three-column theory of stability based on a retrospective review of 412 spinal injuries and their 

CT features (Fig. 12).89 Denis divided the spinal column into anterior, middle, and posterior columns. The 

anterior column consists of the anterior longitudinal 

ligament, anterior half of the vertebral body, and 

the annulus fibrosus. The middle column consists of 

the posterior half of the vertebral body, posterior 

longitudinal ligament, and posterior part of the 

annulus fibrosus. The posterior column consists 

of the neural arch, ligamentum flavum, facet joint 

capsules, and the supraspinous and interspinous 

ligaments. Denis concluded that the integrity of the 

middle column determines the stability of the spine. 

Experience over subsequent years has generally 

supported this concept. Therefore, a definitive 

assessment of the integrity of the middle column is 

made at a facility where CT imaging is available, 

typically at a Level III CSH. 

Spinal stability is defined as the ability of the spine, under physiologic loads, to limit patterns of 

displacement, preclude damage and irritation to neural elements, and prevent incapacitating deformity 

or pain due to structural changes. 

Spinal Cord Injury Patterns

Complete Cord Syndrome

A complete spinal cord syndrome is characterized by flaccid paralysis and loss of sensation below the 

level of spinal cord injury.78 Deep tendon reflexes and the bulbocavernosus reflex are absent in the acute 

Figure 12. Three-column Denis classification of the spine. The posterior 

column consists of the posterior ligamentous complex. The middle column 

includes the posterior longitudinal ligament, posterior annulus fibrosus, and 

posterior wall of the vertebral body. The anterior column consists of the 

anterior vertebral body, anterior annulus fibrosus, and anterior longitudinal 

ligament.
504 | Spinal Trauma

phase. This reflex is useful in assessing the integrity of the lower sacral cord segments. The return of the 

bulbocavernosus reflex marking the end of spinal shock is variable but often occurs within 24 hours of cord 

injury.26,27,30,90 The development of spasticity, clonus, hyperreflexia, and Babinski reflexes is more variable. 

These findings develop days to months after injury. Functional motor recovery following a complete cord 

syndrome injury is extremely poor. Complete injuries have a less than 5 percent chance of functional motor 

recovery if no improvement occurs within 24 hours of injury, and virtually no chance of recovery after 48 

hours.29,31,90 Therefore, intervening surgically on a complete injury typically is futile if the goal is neurologic 

recovery. The restoration of mechanical stability following a complete cord syndrome injury can be delayed 

until the combat casualty reaches Level IV and V facilities. 

Restoration of mechanical stability following a complete cord syndrome injury can be delayed until 

the combat casualty reaches Level IV or V facilities. With incomplete cord syndromes, a delay in 

decompression and stabilization is tolerated until the evacuee arrives at Level IV or V facilities, unless the 

combatant’s neurologic condition is deteriorating.

Incomplete Cord Syndromes

A spinal cord injury is termed incomplete if there is some sparing of motor or sensory function below 

the level of injury. Incomplete spinal cord syndrome patients usually improve from their presenting 

condition, with some patients regaining the ability to ambulate.28,78,91,92,93,94 The decision of where and 

when to surgically intervene remains a challenge for battlefield surgeons. Unless the combatant’s neurologic 

condition is deteriorating, a delay in decompression and stabilization is tolerated until the evacuee arrives 

at Level IV and V facilities. In an unpublished analysis of combat-related spine injuries, zero of 52 patients 

evacuated from OEF/OIF had deterioration in neurologic status (Bellabarba, personal communication, 

2009). Therefore, it stands to reason that if a combat casualty has tolerated evacuation from the point of 

injury to a Level III facility without neurologic deterioration, decompression with or without spinal fusion 

can often be delayed until evacuation to Level IV and V centers. In the presence of neurologic deterioration, 

the judgment of whether to proceed with surgery in-theater rests with the careprovider at that given level.

Anterior Cord Syndrome 

The anterior cord syndrome is the result of an injury to the anterior two-thirds of the spinal cord (Fig. 13). 

The syndrome typically results from anterior spinal cord compression by adjacent bone or disc fragments 

following a hyperflexion injury.93 Hyperextension is a less common mechanism of injury. Anterior cord 

syndrome is characterized by immediate, complete paralysis with hypesthesia to the level of the lesion, 

with preservation of light touch, motion, position, and part of vibration sense. This syndrome has a 

better prognosis for recovery than a complete spinal cord syndrome.92,93 In one of the earliest descriptions 

of anterior cord syndrome, Schneider reported that five of 11 patients in his case series regained the 

ability to ambulate.92 This potential for recovery underscores the importance of a careful neurologic 

examination aimed at detecting any residual neurologic function in spinal cord injury patients.95 

Central Cord Syndrome

The central cord syndrome commonly occurs in the cervical region and typically occurs in the setting of 

preexisting degenerative spine disease. The spinal cord is thought to be compressed between the ligamentum 

flavum posteriorly and osteophytes anteriorly during hyperextension. As a result, centrally located spinal 

tract fibers are injured. Weakness is greater distally than proximally and worse in the upper extremities than 
Spinal Trauma | 505

Figure 13. The anterior cord syndrome is typically the result of anterior spinal cord compression following a hyperflexion injury. It is characterized by 

immediate, complete paralysis with hypesthesia to the level of the lesion, with preservation of light touch, motion, position, and part of vibration sense.

Figure 14. The central cord syndrome is typically seen following a hyperextension injury. Weakness is greater distally than proximally and worse in the 

upper extremities than in the lower extremities. Sensory loss is variable.

Figure 15. The Brown-Séquard syndrome is characterized by ipsilateral proprioceptive and motor loss and contralateral loss of pain and temperature 

sensation.

Anterior Cord Syndrome

 Central Cord Syndrome

Brown Séquard-Syndrome
506 | Spinal Trauma

in the lower extremities. Sensory loss is variable. In severe cases, upper extremity paralysis, loss of sensation, 

and urinary retention may occur.96 The lower extremities are relatively spared. The recovery potential with 

this syndrome is favorable.70 Previous studies of central cord syndrome patients have revealed that more 

than 50 percent become ambulatory and regain functional use of their hands (Fig. 14).94,97,98

Brown-Séquard Syndrome

The Brown-Séquard syndrome is characterized by ipsilateral proprioceptive and motor loss and contralateral 

loss of pain and temperature sensation (Fig. 15).99 Anatomically, only one-half of the spinal cord is damaged. 

This results in spinothalamic tract, corticospinal tract, and dorsal column injury. This syndrome, which was 

previously thought to occur only in penetrating trauma, is increasingly described following blunt trauma. 

The prognosis for recovery in this syndrome is good. Several case series have documented functional 

recovery in up to 75 percent of patients with Brown-Séquard syndrome.91,94,98

Cauda Equina Syndrome

The cauda equina syndrome results from injury to the lumbosacral nerve roots within the neural canal. The 

clinical manifestations vary and include sensorimotor deficits of the lower limbs and bowel and bladder 

areflexia. The prognosis for recovery is similar to peripheral nerve injuries and is significantly better than 

that for spinal cord injuries.

Spinal Nerve Root Syndromes

Nerve root syndromes deserve special mention because they often occur in the setting of spinal fractures 

and facet dislocations. The spinal nerve root can be injured along with the spinal cord, or an isolated nerve 

root injury can occur. Motor and sometimes sensory deficits will be found in the distribution of one or 

several contiguous nerve roots. The prognosis for recovery from these lesions is good, provided adequate 

reduction and anatomic restoration of the vertebral column occurs.100,101,102 Given that nerve root injuries 

have a good prognosis for recovery, nerve root decompression may be delayed until patients reach Level IV 

and V facilities, unless a progressive loss of neurologic function occurs.

Nerve root decompression may be delayed until patients reach Level IV or V facilities unless a progressive 

loss of neurologic function occurs.

Spinal Cord Injury Without Radiographic Abnormality

Spinal cord injury without radiographic abnormality (SCIWORA) is a post-traumatic myelopathy with no 

radiographic evidence of fracture or dislocation on plain radiography and CT scan evaluation.86,103,104,105 

Although the syndrome was initially described in children, it can occur in the adult population as well.106

Anatomic differences of the pediatric spine allow for significant intersegmental movement without 

bony column disruption. The spinal cord does not share the same degree of elasticity, thus contusions, 

transections, infarctions, and stretch injuries result. While the exact mechanism for SCIWORA in adults 

is varied, patients with underlying stenosis, either congenitally or degeneratively, are at considerably much 

higher risk.106
Spinal Trauma | 507

Spinal Injury Management Considerations

Spinal Immobilization and Transport Considerations

Once an unstable spinal injury is identified at a Level III facility, full spinal immobilization pending definitive 

stabilization is indicated. The medical evacuation network in the theater of operation has greatly reduced 

the evacuation and transport time for injured combatants. If a prolonged delay in definitive care exists, 

moving the patient to a bed using strict spinal cord injury precautions is often attempted. The risk of 

worsening the patient’s neurologic status must be weighed against the risk of pressure necrosis of the skin 

and degree of patient discomfort resulting from the backboard.34,35,107 Level I care is often limited to hard 

cervical collars, Kendrick Extrication Device (K.E.D.®) short boards, and long spineboards placed on a 

military stretcher. Due to the space limitations inherent in casualty evacuation (ground ambulance and 

helicopter), the equipment used on the battlefield for spine immobilization is limited. 

When a prolonged delay in definitive care of unstable spinal injuries exists, the risk of worsening the 

patient’s neurologic status during transfer to a bed must be weighed against the risk of pressure necrosis 

of the skin, and degree of patient discomfort, resulting from full spinal immobilization on a backboard.

Patients at greatest risk for pressure sores are those who remain on the spine board for more than two hours 

without being repositioned.34,35 Careproviders must use their discretion. If enough manpower is not present 

to move the patient safely, or there is any doubt about the patient’s ability to cooperate with spinal injury 

precautions, the patient should be kept immobilized on the backboard. The patient should be moved as little 

as possible as even minimal movement may worsen the neurologic deficit in an unstable spinal injury. If a 

spine injury is excluded or deemed to be a stable injury, prompt removal of the patient from the backboard 

to a more comfortable setting is indicated.

Timing of Surgical Interventions

The role and timing of operative intervention in patients with acute spinal cord injury are 

controversial.108,109,110,111,112 The paucity of prospective randomized trials defining operative indications for 

acute spinal injury results in a disparate approach to these injuries among spine specialists. Issues germane 

to CCC providers may be addressed by using three clinical categories: (1) patients with complete spinal 

cord syndromes; (2) patients with incomplete but progressive spinal cord syndromes; and (3) patients with 

incomplete but nonprogressive spinal cord syndromes.

Emergency spine surgery for penetrating or closed injuries of the spinal cord is indicated only in the 

presence of neurologic deterioration.

If a spinal cord neurologic injury can be determined to be a complete injury (i.e., the bulbocavernosus 

reflex is intact and complete loss of sensorimotor function, including proprioception exists), spinal segment 

realignment may proceed at a less urgent pace. There does not seem to be any evidence to indicate that 

early surgical treatment can alter the prognosis of patients who present with complete cord syndromes.113

Although this subset of patients may need subsequent stabilization of the spine, they do not require 

emergency surgery. An exception may be in the cervical spine, where urgent reduction may improve the 

rate of “root-sparing” recovery.114,115
508 | Spinal Trauma

There is broad support for emergency surgery for patients with incomplete but progressive spinal cord 

syndromes. This syndrome is rare, but may result from progressive spinal cord injury via fracture 

displacement, bone fragment compression, expanding hematoma, spinal cord edema, or infarction.116

Animal studies have indicated that immediate decompression of neural elements is associated with reduction 

of permanent neurologic sequelae.117,118 In combat environments, transport times and access to Level III, 

IV, and V care must be weighed by CCC providers when considering the timing of surgical interventions.

While there does not seem to be any evidence to indicate that early surgical treatment can alter the 

prognosis of patients who present with complete cord syndromes, there is broad support for emergency 

surgery for patients with incomplete but progressive spinal cord syndromes.

Management of incomplete and nonprogressive spinal cord syndromes involves rapid spinal segment 

reduction and stabilization to minimize neurologic injury. In the cervical spine, such management 

frequently involves the application of skull traction devices at Level III or higher facilities. In the 

thoracolumbar spine, traction is less successful, so if neutral supine body positioning does not restore 

anatomic alignment, definitive correction of the malalignment will typically be performed at the time of 

stabilization surgery (typically at Levels IV and V).

Spinal Reduction Interventions

Axial Traction

Prior to any attempt at reduction of a malaligned 

cervical spine, the entity of atlanto-occipital 

disassociation must be excluded (Fig. 16). When 

severe hyperflexion or hyperextension combined 

with distraction occurs in the upper cervical spine, 

atlanto-occipital disassociation may occur. Atlantooccipital disassociation (dislocation) is characterized 

by complete disruption of ligamentous attachments 

between the occiput and the atlas.119,120 Death 

commonly occurs due to concurrent injury to the 

brainstem.119,121,122 Radiographically, pathologic 

separation between the base of the occiput and 

the arch of atlas is noted.120 Cervical traction is 

absolutely contraindicated with atlanto-occipital 

disassociation since further stretching of the 

brainstem can occur. Atlanto-occipital disassociation 

may initially be evaluated with lateral plain 

radiographs, but it is most reliably detected with CT 

imaging. 

An unstable or malaligned cervical spine requires 

either more stable immobilization or axial traction 

to achieve reduction.123,124,125 Two types of axial Figure 16. Atlanto-occipital disassociation.
Spinal Trauma | 509

traction devices are available: Gardner-Wells tongs and the halo ring apparatus (Tables 4 and 5).126,127,128

Gardner-Wells tongs are a simple, effective means of applying axial traction for reduction, but they do not 

significantly limit voluntary rotation, flexion, or extension in an uncooperative patient (Figs. 17 and 18). 

Gardner-Wells tongs can be applied with minimal skin preparation and without assistance. In contrast, the 

halo ring allows axial traction for reduction and provides rather stable immobilization with the application 

of a vest but its application requires an assistant, and it takes longer to apply than Gardner-Wells tongs. 

Traction devices are typically utilized at the Level III CSH where appropriate radiographic support and a 

more secure setting are found.

Halo Ring Application

• The correct ring size is selected according to head circumference 

• The ring is placed around the head, at a level one centimeter above the eyebrows and is held 

temporarily with plastic pod attachments

• After the patient’s eyelids are closed, the skin is prepared, and local anesthetic is infiltrated through 

the ring holes

• Pins are then placed through the ring holes and are torqued down in an opposing fashion to 8 inchpounds in adults and 4 inch-pounds in pediatric patients 8 years or younger 

• After 24 hours, these pins will require reevaluation of proper torque as they often loosen early on

Table 5. Halo Ring application.

Gardner-Wells Tong Application

• After the patient is placed in a supine position, the provider identifies the external auditory meatus, 

bilaterally 

• A position on the skin is marked one centimeter (cm) superior and one cm anterior to the external 

auditory meatus 

• The skin is infiltrated with lidocaine with epinephrine to assist with pain control and bleeding from 

the scalp 

• The tongs are placed over the crown of the head with the pins positioned on the skin prepared area

• The pins are inserted into the skull by symmetrically tightening the knobs 

• Weights are then applied to the tongs such that the traction vector is directed superiorly 

• Traction should be initiated at 10 pounds (lbs) and increased by five- to 10-lb increments (5 lb 

weight added for each spinal level)

• Reduction should be performed in awake patients with administration of intravenous sedation and 

analgesia, as necessary 

• Fluoroscopy or serial radiographs and serial neurologic examinations should be performed to detect 

excessive distraction of spinal segments

• In patients with neurologic symptoms or signs or one centimeter distraction of a disk space, closed 

reduction should be stopped and further images taken

Table 4. Gardner-Wells Tong application.
510 | Spinal Trauma

If traction is applied, radiographs must be obtained to ascertain that no undiagnosed ligamentous injury 

has been exacerbated by the added weight. 

A halo ring can be applied when definitive treatment is anticipated to be in a halo or in cases in which 

distraction cannot be achieved with Gardner-Wells tongs. Placing a halo vest underneath the patient, prior 

to or during transfer to the bed, can help attach the ring to the vest while the patient is in traction after 

reduction. Open halo rings offer the advantage over previous whole rings in their ability to be placed 

without putting the patient’s head on a head holder off the stretcher. 

Penetrating Injury to the Spine

Management

Mechanical Stability

The majority of gunshot wounds to the spine in patients with normal neurological exams are mechanically 

stable.14,15,16 In assessing the stability of the cervical spine, it has been noted that 36 percent of the weight of 

the head is carried by the anterior vertebral bodies and disks and 32 percent by each of the two posterolateral 

columns, which are composed of facet joints and lateral masses.

129 In the vast majority of cases, the projectile 

does not destabilize the spine, and collars or any other type of bracing are not necessary. However, the 

cervical collar does have the benefit of maintaining a neutral neck position that may be important in the 

setting of head injuries.

The majority of gunshot wounds to the spine are mechanically stable in patients with normal neurological 

exams. Unlike closed spinal cord injuries, it is rarely necessary to operate on gunshot wounds to the spine 

for purposes of establishing mechanical spinal stability.

In the thoracic and lumbar spine, the three-column concept of Denis can be applied, but the careprovider 

Figure 17. Gardner-Wells tongs are applied when cervical spine traction 

is desired. Image courtesy of the Borden Institute, Office of The Surgeon 

General, Washington, DC.

Figure 18. Atlanto-occiptal disassociation must be ruled out prior to 

application of cervical traction with Gardner-Wells tongs. Image courtesy 

of Jonathan Martin, MD, Connecticut Children’s Medical Center.
Spinal Trauma | 511

should understand that the mechanism of destruction is considerably different from that in the closed 

injuries for which this classification was designed.129 When destruction is limited to one of the three 

columns, then no particular immobilization is needed (Fig. 19). If two or three columns are compromised 

by the gunshot wound, then use of spine precautions and immobilization are recommended until definitive 

management occurs at Level IV and V facilities.

Unlike closed spinal cord injuries, it is rarely necessary to operate on gunshot wounds of the spine for 

purposes of establishing stability. The length of immobilization for mechanically unstable injuries of the 

cervical, thoracic, or lumbar spine is normally six to eight weeks. At that time, further radiographic imaging 

of the affected region is performed to establish whether the spine has adequately healed and is stable.

Infection Control

Disruption of the dura (e.g., open spinal injury) is associated with a significant risk of central nervous 

system infection.130 Reports from combat settings (i.e., Iran-Iraq, Vietnam, and Lebanese conflicts) have 

documented infection rates of 4 to 11 percent following penetrating brain injuries.131,132,133 The benefits of 

administering prophylactic antibiotics prior to elective neurosurgical procedures have been used to justify 

the administration of prophylactic antibiotics following penetrating injuries to the spine.134

Prophylactic antibiotics may be of benefit following open spinal injury given the significant risk of central 

nervous system infection. 

If a hollow viscus is not violated with penetrating spine injuries, the administration of three to five days 

of prophylactic parenteral antibiotics has been recommended.135 Cefazolin, one gram intravenously every 

8 hours, is often given in these situations.136 If a concern for meningitis exists, as in the case of persistent 

Figure 19. The majority of gunshot wounds to the spine are mechanically stable in patients with normal neurologic exams: (Left) This patient sustained 

a transthoracic gunshot wound. Right-sided hemothorax is noted and the missile is resting in the subcutaneous space of the posterior thorax.(Right)

Mechanical stability was determined when CT images demonstrated isolated injury to the posterior column.
512 | Spinal Trauma

cerebrospinal fluid (CSF) leakage after dural violation by a projectile, ceftriaxone (one gram intravenously 

every 12 hours) is often prescribed.137 Better defining the role (e.g., optimal duration of therapy, choice of 

antibiotic) of these treatment regimens requires future study. 

It is also important to consider associated hollow viscus injuries in patients with penetrating projectile 

injury to the spine. If the projectile has potentially penetrated the pharynx, esophagus, or colon, then extra 

precautions should be taken to prevent spine infection.129 This is essential only when the bullet has first 

penetrated the viscus and then penetrated the spine, and it does not seem to be clinically important if the 

bullet first traversed the spine before perforating the viscus. In contrast to prior recommendations, which 

promoted radical spine debridement, the best results have been reported by Roffi and coworkers, who 

recommended minimal spine debridement and one to two weeks of prophylactic parenteral antibiotics.138

The parenteral antibiotics should be broad-spectrum agents directed at the particular bacteria normally 

associated with hollow viscus injury.139

In contrast to prior recommendations that advocated radical spine debridement for cases of penetrating 

spinal injury with associated hollow viscus violation, current evidence supports minimal spinal debridement 

in conjunction with parenteral antibiotics.

Complications: Penetrating Spine Trauma

Complications from penetrating injuries to the spine are a concern for CCC providers. Even in the face 

of proper initial triage and management, these complications may present either early in the treatment 

course or up to several weeks later. It is absolutely critical that CCC providers promptly recognize and treat 

these complications as they can have devastating effects on patients. Cerebrospinal fluid fistulae, infection, 

and vascular injuries are some of the more common situations that may be faced by the battlefield medical 

team.3,4,5,131,132,133

Cerebrospinal Fluid Fistulae

Cerebrospinal fluid fistulae have been recognized after penetrating injuries, and they are defined as an 

abnormal CSF conduit within either the skin or body cavities.4,31 Stauffer et al. studied bullet removal 

following penetrating spinal injury and found that CSF fistulae commonly occurred after surgical treatment 

with laminectomy.140 The incidence of CSF fistulae was 6 percent in patients treated with laminectomy, 

debridement, irrigation and bullet removal.140 As previously stated, routine surgical intervention following 

spine injuries with stable neurological exams does not change neurologic outcomes.141 The fact that most CSF 

fistulae occur following surgical interventions is yet another reason to reserve surgical intervention for later 

in the treatment course, unless emergent decompression due to neurological deterioration is indicated. 

If emergency spinal surgery is performed (e.g., due to neurologic deterioration), it is imperative that 

meticulous dural repair occurs. Augmentation of dural repair with tight closure of the paraspinal muscles, 

fascia, and skin will minimize the occurrence of postoperative CSF fistulae.

Meningitis is a devastating complication of persistent CSF leakage and it is imperative to avoid 

this dreaded complication.4,142 When spinal surgery is performed, meticulous dural repair is essential. 

Augmentation of dural repair with tight closure of the paraspinal muscles, fascia, and skin will minimize 

the occurrence of postoperative CSF fistulae (Fig. 20). Likewise, it is advised that an intraoperative valsalva 
Spinal Trauma | 513

maneuver should be performed after the dural leak is repaired to ensure the seal is watertight, and if 

persistence of the leakage occurs, a lumbar drain should be placed. Most Level II and III facilities will 

not have subarachnoid (lumbar) drains on-hand, thus providing another reason to delay elective surgical 

interventions. 

CSF fistulae can either track cutaneously (externally) or into other body cavities (internally). The cutaneous 

variety typically are easily identifiable. However, fistulae emptying into a deep body cavity can be 

overlooked. When a penetrating spinal injury patient has persistent postural headaches, the existence of 

a CSF fistulae with a course that tracks to an internal cavity should be suspected. Radionucleotide studies 

can be effective in confirming the diagnosis and localizing the tract.143 However, these studies require 

introduction of the radionucleotide into the subarachnoid space and are not available to Level II and 

III CCC providers. When a CSF fistula is suspected, the placement of a lumbar (subarachnoid) drain is 

recommended followed by supine patient body positioning pending resolution of the leak.

Spinal Infections

Spinal infections following penetrating spinal injury are often accompanied by perforation of a hollow 

Figure 20. Pediatric host nation patient with penetrating spinal injury (patient’s lumbar region). After wound debridement, a gluteal flap was created and 

rotated over the spinal canal to prevent CSF leakage and infection. Image courtesy of the Borden Institute, Office of The Surgeon General, Washington, 

DC.
514 | Spinal Trauma

viscus.138 Postoperative spine infections can be another common scenario in association with penetrating 

spinal injury. Stauffer found the rate to be 4 percent after decompressive laminectomy with projectile 

removal.140 For these reasons, perioperative antibiotic prophylaxis and the administration of antibiotics 

for up to 14 days post-injury have been recommended when a dural tear is in communication with a 

hollow viscus injury.144 In such patients, an internal fistula may also be present in association with the spine 

infection. It is virtually impossible to resolve a spine infection unless the fistula is corrected. General surgery 

techniques such as diversion of the drainage with nutritional hyperalimentation may be necessary when a 

deep space CSF fistula is present. 

Local surgical exploration, debridement, or diversion may be required in cases of penetrating spinal 

injury associated with hollow viscus involvement, given the risk of infection.

In the face of progressive paralysis or deformity in association with spine infection, the necessity to identify 

an organism, problematic foreign body, or failure of nonoperative management are all indications to 

proceed with exploratory surgery. In most cases, spine infections may not be readily apparent until later in 

the evacuation of the battlefield trauma patient, and CT-guided biopsy with abscess drainage along with 

parenteral antibiotic administration is the typical management strategy. Routinely, the Level V facility has 

this capability.

 

Vascular Injuries

Vascular injury must be considered in all patients with penetrating injury to the spine. The vertebral arteries 

within the transverse foramina of the cervical spine, the thoracic aorta associated with the thoracic spine, 

and the iliac vessels anterior to the lumbar spine are vulnerable to injury following penetrating spine trauma. 

Suspicion for vascular injury should be further heightened in the face of progressive anemia or persistent 

hypotension in the spine trauma patient. Current recommendations advise that wounds should be explored 

when significant warning signs for vascular injury are present.145,146 Hard signs such as pulsatile bleeding, 

neurovascular compromise, an expanding hematoma, and a palpable thrill are obvious warning signs for 

vascular injury. 

Projectile in the Disc Space

Several factors have traditionally been considered in deciding whether surgery is indicated when projectiles 

are located in the disk space. The first consideration is whether lead poisoning (plumbism) or other 

projectile-associated toxicity will develop. Reports in the literature suggest that the lead is leached out 

of a bullet that is bathed in synovial fluid, and lead poisoning can subsequently occur.129 Plumbism is a 

late complication and is typically not an immediate concern for CCC providers. Second, the careprovider 

should determine whether mechanical disruption of physiologic spinal segment movement has resulted 

from the presence of a projectile within the disk. Mechanical stability is an issue when the patient is placed 

upright and typically can be dealt with at higher levels of care outside of the battlefield. Lastly, it must be 

determined whether disk extrusion has resulted from a penetration of the disk space by the projectile. If 

disk extrusion leading to symptomatic neural compression occurs, neural decompression and removal of 

the disk fragments are indicated. This occurrence is extremely uncommon, but it has been reported in the 

literature.129 
Spinal Trauma | 515

The need to remove a projectile resting in the disk space is rare. If this operative intervention is required, 

it should be performed at Level IV or V facilities, unless progressive neurologic deterioration is noted at a 

Level III facility and skilled spine surgeons are available to operatively intervene.

Projectile in the Spinal Canal 

Many anecdotal articles have been written concerning removal of bullets (projectiles) from the spinal 

canal.97,140,147,148,149,150 Prior to the 1990’s, this topic had not been studied in a methodologically rigorous 

manner. For study conclusions to be robust, the two study groups must have equivalent pathology, with one 

group having bullets removed and the other group having bullets left in place. It is also important that this 

study be done on a prospective basis, recording adequate neurologic information as well as quantitative 

assessment of clinical variables (e.g., pain). A well-designed study of the removal of bullets from within 

the spinal canal was performed by Waters et al.31 The study reviewed 90 cases of patients with bullets 

lodged within their spinal canals, of whom 32 had bullets removed and 58 had bullets left in place. They 

concluded that between the T12 (thoracic) to L5 (lumbar) spinal levels statistically significant neurologic 

motor improvement occurred with removal of the bullet from the spinal canal. There was no difference, 

however, in sensation or in pain experienced by the patients. In thoracic spine injuries, from T1 to T11, 

no statistical difference was seen for either complete or incomplete injuries, whether or not the bullet was 

removed. Similarly, no difference was seen with bullet removal in the cervical spine; however, the authors 

suggest that the patient numbers were too small to be able to draw statistical conclusions about the cervical 

spine. 

The medical literature does not support the routine removal of projectiles resting in the spinal canal when 

located between T1 to T12 vertebral bodies. For projectiles in the canal inferior to T12 vertebral body, 

removal of the projectile in-theater should only be attempted if the neurological exam is deteriorating. If 

the exam remains unchanged or improves, then removal may occur at Level IV or V facilities. There is 

insufficient data to provide more definitive recommendations regarding cervical spinal canal bullet fragment 

removal.

Elective removal of projectiles from within the spinal canal should ideally be performed seven to 10 days 

following the injury. This time lag will minimize many cases of CSF leakage and considerably simplify 

dural tear management.

Once the decision has been made to surgically remove the projectile from the spinal canal, it is essential that 

a scout radiograph be taken in the operating room before the incision is made. The reason for this is that 

the projectile can occasionally migrate within the spinal canal, depending on the position of the patient.129

This is especially true for patients with large spinal canals and relatively small embedded projectiles. Elective 

removal of projectiles from within the spinal canal should ideally be performed seven to 10 days following 

the injury. This time lag will minimize many cases of CSF leakage and considerably simplify dural tear 

management.129
516 | Spinal Trauma

Summary

Spinal injuries cause significant morbidity. Spinal injury patients often have multiple coexisting, lifethreatening injuries. Knowledge of spinal anatomy is necessary to accurately evaluate and manage spinal 

injury patients. Combat casualty care providers must have an accurate understanding of the emergency 

management, diagnostic evaluation (e.g., radiological studies), transport considerations, and therapeutic 

management of spinal injury patients. 
Spinal Trauma | 517

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528 | Spinal Trauma
Chapter 11

PEDIATRIC TRAUMA

Contributing Authors

Philip C. Spinella, MD

 Jonathan Martin, MD

Kenneth S. Azarow, MD, FACS, FAAP, COL (Ret), MC, US Army
All figures and tables included in this chapter have been used with permission from Pelagique, LLC, the 

UCLA Center for International Medicine, and/or the authors, unless otherwise noted.

Disclaimer

The opinions and views expressed herein belong solely to those of the authors. They are not nor should 

they be implied as being endorsed by the United States Uniformed Services University of the Health 

Sciences, Department of the Army, Department of the Navy, Department of the Air Force, Department of 

Defense, or any other branch of the federal government.
Pediatric Trauma | 531

Table of Contents

Introduction........................................................................................................ 533

Epidemiology...................................................................................................... 533

Anatomic Considerations ..................................................................................... 534

Airway...............................................................................................................................534

Head and Spinal Cord ......................................................................................................537

Skeletal and Body Surface Area........................................................................................540

Physiology.........................................................................................................................541

Vital Signs and Other Physiologic Parameters ..................................................................541

Fluids, Electrolytes, Nutrition, and Glucose Metabolism ..................................................542

Respiratory System ............................................................................................................544

Pharmacology ....................................................................................................................545

Patient Monitoring Considerations....................................................................................546

Resuscitation ...................................................................................................... 548

General Considerations....................................................................................................548

Airway and Breathing.......................................................................................................548

Rapid Sequence Intubation ...............................................................................................549

Vascular Access.................................................................................................................550

Circulation ........................................................................................................................551

Blood Product Transfusion ................................................................................................553

Specific Medical Condition Management................................................................ 553

Acute Respiratory Distress Syndrome (ARDS) ................................................................553

Severe Sepsis and Septic Shock........................................................................................553

Cerebral Herniation Syndromes......................................................................................556

Seizure Management........................................................................................................556

Pediatric Advanced Life Support (PALS) ..........................................................................558

Cardiac Rhythm Disturbances.........................................................................................558

Asystole and Pulseless Electrical Activity ...........................................................................558

Pulseless Ventricular Tachycardia and Ventricular Fibrillation .........................................559

Bradycardia with Poor Perfusion........................................................................................559

Narrow Complex (Supraventricular) Tachycardia.............................................................560

Wide Complex (Ventricular) Tachycardia..........................................................................560

Surgical Considerations ...................................................................................................560

Thoracic Interventions.......................................................................................................560

Abdominal Interventions ...................................................................................................561

Burn Care..........................................................................................................................564

Neurosurgical Interventions ............................................................................................565

Forward Neurosurgical Care by Non-Neurosurgical Careproviders .................................565

Surgical Management of Head Injuries.............................................................................566

Triage and Initial Assessment...........................................................................................566
532 | Pediatric Trauma

Repair of Scalp Injuries ..................................................................................................568

Intracranial Pressure Monitoring.......................................................................................572

Management of Skull Fractures........................................................................................573

Management of Intradural and Extradural Hemorrhage .....................................................576

Spinal Injuries ..................................................................................................................576

Closed Injuries ...................................................................................................................576

Penetrating (Open) Injuries................................................................................................580

End-of-Life Care................................................................................................................580

References .......................................................................................................... 581
Pediatric Trauma | 533

Introduction 

The care of injured children from combat-related injuries is an unfortunate but consistent consequence 

of all conflicts. The ability to provide care to injured children is complicated by unfamiliarity with treating 

severely injured children by most deployed United States (US) combat casualty care (CCC) providers. In 

addition, lack of pediatric-sized equipment and medications to care for severely injured children increases 

the difficulty in caring for these patients. The anxiety and emotion that are invoked by an injured child further 

complicates their management. United States military doctrine clearly states that during combat operations 

health careproviders are to resuscitate all patients with injuries that threaten life, limb, or eyesight. The 

care of children injured during combat is an opportunity for military personnel to show compassion and 

to strengthen relationships with the civilian population. Appropriate care and attention towards wounded 

children are critical and provide opportunities to strengthen mutual respect and understanding. 

Epidemiology 

Multiple publications have described the epidemiology of injuries suffered by children (patients less than 

18 years of age) treated at US military medical facilities in both Iraq and Afghanistan.1,2,3,4,5 These reports 

indicate that CCC providers will frequently treat children. These children often sustain severe injuries that 

are associated with increased mortality compared to adults. 

The relative distribution of pediatric admissions to Level III care facilities between Operation Enduring 

Freedom (OEF) in Afghanistan (53 percent) and Operation Iraqi Freedom (OIF) in Iraq (47 percent) is 

similar, as is the mean age of pediatric patients (10 years, ± 5) in both locations.6 Children account for 4 to 

7 percent of all admissions to US military hospitals in OEF and OIF, and they account for 10 to 12 percent 

of all hospital bed days.1,5 In Afghanistan, these proportions are increased with children comprising 15 

percent of all admissions and 25 percent of all hospital bed days. The mean hospital length of stay, 7 days, 

is similar in both locations.6 In both Iraq and Afghanistan, penetrating trauma accounts for approximately 

75 percent of pediatric traumatic injuries. In Iraq, gunshot wounds are the mechanism of injury for 57 

percent of pediatric admissions compared to 21 percent in Afghanistan. In Afghanistan, burn and landmine 

explosive injuries account for 15 percent of admissions each, while in Iraq they are the mechanism of injury 

for 6 percent and 1 percent of pediatric admissions, respectively.6 

Combat casualty careproviders will frequently treat children who often sustain severe injuries that are 

associated with increased mortality compared to adults. Children account for 4 to 7 percent of all 

admissions to US military hospitals in OEF and OIF, and 10 to 12 percent of all hospital bed days.

When data from Iraq and Afghanistan are combined, the overall primary causes of death are traumatic 

brain injury (29 percent) and burns (27 percent) (Fig. 1).6

 Death as a result of infection was more common 

in Afghanistan (12 percent) than Iraq (2 percent), whereas death from penetrating abdominal and thoracic 

injuries was more common in Iraq (13 percent) than Afghanistan (5 percent).6

 In a review of children 

treated at a Combat Support Hospital (CSH) in Iraq, children less than eight years of age, as compared 

to older children and adults, had an increased severity of injury according to the Injury Severity Score 

(ISS) and an increased incidence of death after adjusting for increased severity of injury.7 
534 | Pediatric Trauma

Anatomic Considerations

Airway

The pediatric airway is significantly different than an adult airway. In addition to the obvious size differences 

in airway anatomy, the infant and young child’s (less than eight years of age) oropharyngeal cavity is 

relatively smaller due to a larger tongue-to-cavity ratio in the child. The larger head in relation to body 

size also makes visualization of the larynx with laryngoscopy more difficult and often requires elevating 

the shoulders and upper thorax to allow for a more direct line of site of the larynx. The epiglottis in a child 

is typically omega-shaped (long and narrow) and attached at the vocal cords at an acute angle. The vocal 

cords are more cephalad and anterior compared to those in an adult. The subglottic area is narrower and 

cone-shaped, rather than more cylindrical in shape. An endotracheal tube (ETT) that passes easily through 

the vocal cords may encounter resistance in the subglottic area. Furthermore, children less than 12 years of 

age have a small, pliable, mobile larynx and cricoid cartilage making a surgical cricothyrotomy difficult to 

perform.8

Figure 1. Resuscitative efforts in progress at a CSH. This host nation toddler was injured in a civilian motor vehicle accident and sustained 30% TBSA 

second- and third-degree burn wounds and severe inhalation injury.
Pediatric Trauma | 535

The pediatric airway differs significantly compared to an adult airway. The larynx is more difficult to 

visualize during laryngoscopy, and the subglottic area is narrow and cone-shaped. An ETT that readily 

passes through the vocal cords may still encounter resistance in the subglottic area. Furthermore, children 

less than 12 years of age have a small, pliable, mobile larynx and cricoid cartilage making a surgical 

cricothyrotomy difficult to perform.

Selecting an appropriately sized ETT is a crucial first step when preparing to intubate a pediatric trauma 

victim. A number of methods intended to assist physicians with selecting the optimal ETT have been 

published. Using the internal diameter of the 

external nasal nares or nailbeds of the fifth 

digits of the child has been reported to facilitate 

the selection of an appropriately sized ETT.9

While these approaches may provide reasonable 

approximations of ETT sizing, they require the 

physical presence of the patient. This precludes 

the ability of careproviders to have this equipment 

prepared prior to patient arrival. Using the age (in 

years) added to 16 divided by 4 to represent the 

internal tube diameter in millimeters has also been 

recommended.9

 Irrespective of the initially selected 

tube size, the physician should always be prepared 

to use either smaller or larger diameter tubes if the 

patient’s airway dictates it (Table 1). The Broselow® 

tape is a commonly used and helpful method to 

standardize the approach to the resuscitation of 

children.10 It provides a valuable reference source for 

the appropriate sizing of pediatric airway equipment 

and dosing of medications. 

Age Preterm Newborn Infant 1 Yr 3 Yrs 6 Yrs 10 Yrs 14 Yrs

Laryngoscope 

Blade Size 0 1 1 1 to 2 2 2 2 to 3 3

ETT Size 2.5 to 3.0 3.0 to 3.5 3.5 to 4.0 4.0 to 4.5 4.5 to 5.0 5.0 to 5.5 6.0 to 6.5 6.5 to 7.0

Suction 

Catheter (Fr)

5 6 8 8 8 to 10 10 10 10 to 14

Chest Tube 8 to 10 10 to 12 10 to 12 16 to 20 16 to 20 20 to 28 28 to 32 32 to 40

NG Tube 

or Foley 

Catheter (Fr)

5 5 to 8 5 to 8 8 8 to 10 10 to 12 12 to 14 14 to 18

Table 1. Equipment size according to the age of the patient.

Figure 2. Cuffed versus uncuffed endotracheal tubes. With an uncuffed 

ETT, the narrowed subglottic space should provide an adequate seal 

around an appropriately selected ETT. Cuffed tubes are likely just as safe 

as uncuffed tubes, and may protect against tube dislodgment and gastric 

content aspiration by creating tighter seals.
536 | Pediatric Trauma

The issue of whether or not to use cuffed or uncuffed ETT in younger children often arises (Fig. 2). 

Advocates for using uncuffed tubes contend there is no need for a cuffed tube in children less than eight 

years of age.11,12 Their rationale is that the narrowest part of a young child’s airway is subglottic in location. 

The narrowed subglottic space should provide an adequate seal around an appropriately selected ETT. 

Cuffed tube critics also believe these tubes decrease tracheal mucosal blood flow and increase the incidence 

of post-extubation laryngeal edema and tracheal stenosis.13 Proponents of using cuffed tubes believe that 

modern day low pressure (less than 25 cm H2O), high-volume ETT cuffs are safer than the older models. 

They claim appropriately used, cuffed endotracheal tubes are just as safe as uncuffed endotracheal tubes.14

They believe cuffed tubes provide added protection against tube dislodgment and gastric content aspiration 

by creating tighter seals. Special caution must be exercised to avoid overinflating ETT cuffs. Monitors are 

now available that will measure cuff pressures and should be used to maintain cuff pressures less than or 

equal to 25 cm H2

O to minimize the incidence of cuff-related tracheal injury.14

Selecting an appropriately sized ETT is crucial; (age + 16)/4 may help in selecting ETT diameter. 

Current pediatric standards taught in the Pediatric Advanced Life Support (PALS) course recommend the 

use of cuffed endotracheal tubes to optimize oxygenation and ventilation in all children. 

One method of providing an immediate surgical 

airway for a child less than 12 years of age is to 

perform a needle cricothyrotomy and initiate 

percutaneous transtracheal ventilation (PTTV)

(Fig. 3).15,16 Percutaneous transtracheal ventilation 

is performed by having a 14- or 16-gauge 

angiocatheter inserted through the cricothyroid 

membrane, positioned intratracheally, and attached 

to a high-flow oxygen source.17 Regular oxygen 

tubing may be attached to a three-way stopcock, 

which is attached to the angiocatheter. Alternatively, 

a 14- or 16-gauge angiocatheter may be attached to 

one prong of a dual-pronged nasal cannulae, while 

the other end of the nasal cannulae is attached to a 

high-flow oxygen source. A one-second inspiratory 

and three-second expiratory cycle will allow time for 

adequate oxygenation and ventilation. The oxygen 

source should provide at least 50 pounds per square 

inch of air pressure (i.e., deliver flow rates of 15 

liters per minute). Unfortunately, PTTV will not protect the airway from aspiration of gastric contents. 

In addition, this technique may eventually fail to provide adequate ventilation. Over time, progressive 

hypercarbia and acidemia may ensue. Percutaneous transtracheal ventilation technique should be viewed as 

a temporizing measure until a definitive airway in the form of a tracheostomy is established. If high-oxygen 

flow (jet) ventilation is not possible, an adapter from a 2.5 millimeter or 3.0 millimeter-sized ETT can be 

used to attach the angiocatheter to bag-valve-mask, thus enabling manual ventilation. 

Figure 3. Percutaneous transtracheal ventilation (PTTV). Illustrator: 

Chris Gralapp.
Pediatric Trauma | 537

One method of providing an immediate surgical airway for a child less than 12 years of age is to perform 

a needle cricothyrotomy and initiate PTTV. Percutaneous transtracheal ventilation should be viewed as a 

temporizing measure until a definitive airway in the form of a tracheostomy is established. Percutaneous 

transtracheal ventilation will not protect the airway from aspiration of gastric contents, and the technique 

may eventually fail to provide adequate ventilation.

It is the opinion of the authors and many experienced pediatric surgery and otolaryngology specialists that 

when a surgical airway is emergently needed in a child less than six years of age, a tracheotomy should be 

performed. At this age, cricoid cartilage versus tracheal anatomy is difficult to discern. Extra care needs 

to be exercised to stay well below the cricoid cartilage in order to avoid subglottic stenosis during the 

healing phase after the surgical airway. In younger children (e.g., less than three years of age), the concern 

with performing a needle cricothyrotomy is that it will be very difficult to place the needle in the airway. 

This is due to the laxity of the airway, and since the diameter of the airway is so small the risk of going 

through its posterior wall is high. The neck anatomy is better defined in older children (i.e., over six years 

of age), and it is easier to perform a needle cricothyrotomy. The choice of performing a surgical airway 

versus needle cricothyrotomy in children of all ages is dependent upon the comfort and experience of 

the provider in performing these procedures. If tracheostomy is attempted, the use of a cuffed ETT will 

be required. Accessing the correctly sized tracheostomy tube (lengthwise) will be nearly impossible in a 

combat environment where supplies are limited. Cuffed ETT of all sizes are not always available. As a 

result, advanced planning will be required regardless of the type of airway intervention. 

Head and Spinal Cord 

The risk of head injury is higher in children compared to adults, while the risk of spinal cord injury is 

lower.18,19,20 This is a result of the relative increase in head-to-body size and more flexible cervical ligaments 

of children compared to adults. There is also less subarachnoid space and fluid in children compared to 

adults. The anatomy of an infant’s head with an open fontanelle and mobile cranial sutures allows for 

significant isolated intracranial bleeding. In addition, extracranial bleeding such as caput succedaneum, 

cephalohematoma, or subgaleal hematoma can cause severe anemia and hyperkalemia secondary to 

bleeding and eventual thrombolysis.19,20,21,22,23 The incidence of spinal cord injury in children is low and is 

likely related to flexible vertebral interspinous ligaments and anteriorly wedged vertebrae. As a result, with 

flexion injuries vertebral bodies slide forward minimizing the risk of spinal cord injury. However, spinal 

cord injury without radiographic abnormality (SCIWORA) does exist, and children injured by way of blast 

mechanisms are at risk. Diagnosis is difficult. Attention needs to be given to the presence of pain, tenderness 

on palpation of the spine, and the neurologic examination. 

The risk of head injury is higher in children compared to adults. The anatomy of an infant’s head 

with an open fontanelle and mobile cranial sutures allows for significant isolated intracranial bleeding. 

Extracranial bleeding such as caput succedaneum, cephalohematoma, or subgaleal hematoma can cause 

severe anemia and hyperkalemia secondary to bleeding and eventual thrombolysis.

There are several important radiographic variations in the pediatric cervical spine that warrant mentioning. 

Being aware of these variations is necessary in order to avoid misinterpreting these normal findings as 

injured spinal segments. The prevertebral soft-tissue of the pediatric cervical spine is prone to great 

variation. Emergency radiologic evaluation of the pediatric cervical spine can be challenging because of 
538 | Pediatric Trauma

the confusing appearance of synchondroses, normal 

anatomic variants, and injuries that are unique to 

children.24 Cervical spine injuries in children are 

usually seen in the upper cervical region owing 

to the unique biomechanics and anatomy of the 

pediatric cervical spine. Knowledge of the normal 

embryologic development and anatomy of the 

cervical spine is important to avoid mistaking 

synchondroses for fractures in the trauma setting. 

Familiarity with anatomic variants is also important 

for correct image interpretation.24 These variants 

include pseudosubluxation, absence of cervical 

lordosis, wedging of the cervical vertebra, widening 

of the predental space, prevertebral soft-tissue 

widening, intervertebral widening, and “pseudo 

Jefferson fracture” (normal C1 vertebra variant 

in young children).24 In addition, familiarity with 

mechanisms of injury and appropriate imaging 

modalities will aid in the correct interpretation of 

radiologic images of the pediatric cervical spine.24

Using prevertebral soft-tissue swelling to detect 

injury is neither a sensitive nor specific indicator 

of acute injury in pediatric patients. In adults, a 

predental space of greater than three millimeters is 

regarded as abnormal. Children have more laxity 

of their spinal segments, and a predental space of up to five millimeters in children age 13 or younger is 

deemed within normal limits.25

The most prominent abnormality in pediatric cervical spine films is the physiologic pseudosubluxation of 

the C2 on C3 vertebral body (Fig. 4).25 Physiologic pseudosubluxation may occur at several levels between 

C2 to C5. There may be up to four millimeters of subluxation at the C2 to C3 junction as part of normal 

variation in children up to the age of 16 years.25 This pseudosubluxation pattern is unusual beyond the 

age of 16. Use of the spinolaminar line (also known as the posterior cervical line) as a reference may be 

helpful in differentiating acute injuries from normal anatomical variants. The spinolaminar line junction 

of the C2 vertebral segment should be within two millimeters of a line drawn between the C1 and C3 

spinolaminar line junction.26 If the C2 spinolaminar line junction is offset by two or more millimeters, 

the radiograph should be interpreted as abnormal and suspicious for an injury.26,27 The spinolaminar line 

should only be applied in cases where anterior displacement of the C2 on C3 vertebral body exists. When 

the C2 and C3 vertebral bodies are in a neutral or extended position, an offset of two millimeters or more 

of the C2 spinolaminar line may be a normal finding.

Figure 4. Physiological pseudosubluxation on pediatric cervical spine 

radiograph. Normal displacement of C2 on C3 may be so pronounced as 

to be mistaken for a pathologic condition. Image courtesy of Swaminatha 

V. Mahadevan, MD, Stanford University..
Pediatric Trauma | 539

Emergency radiologic evaluation of the pediatric cervical spine can be challenging because of the confusing 

appearance of synchondroses, normal anatomic variants, and injuries that are unique to children. Due 

to unique pediatric anatomy, cervical spine injuries are usually seen in the upper cervical spine. The 

synchondrosis at the junction of the dens and body of C2 is often the site of injury. The most prominent 

abnormality in pediatric cervical spine films is the physiologic pseudosubluxation of the C2 on C3 

vertebral body, which may be mistaken for pathologic motion.

The synchondrosis at the junction of the dens and 

body of C2 is often the site of injury.28,29 The dens 

and body of the axis synchondrosis may remain 

unfused up to the age of seven, mimicking a dens 

fracture. Any anterior angulation of the dens should 

be viewed as suspicious for injury.27 The anterior 

vertebral bodies of C3, C4, and C5 will often have a 

wedged appearance mimicking wedge compression 

fractures (Fig. 5). As their ossification sites fully 

calcify, they will take on the appearance of adult 

vertebral bodies. Small calcifications may sometimes 

be seen inferior to the cervical vertebral bodies. 

These represent normal ring epiphyses. Looking 

for any subluxation, soft-tissue swelling, or any 

clinical evidence of injury at those levels is helpful 

in deciding whether any radiographic abnormalities 

in those regions represent acute injuries. Children 

suffer a disproportionate number of high cervical 

spine injuries.18 Children are also still vulnerable to 

lower cervical spine injuries, although injury in this 

location is not as common.18

Spinal cord injury without radiographic abnormality (SCIWORA) is a post-traumatic myelopathy 

that results from acute spinal cord or nerve root 

injury and results in some combination of sensory 

and motor deficit.30 Spinal cord injury without radiographic abnormality is defined as a post-traumatic 

myelopathy that occurs without radiographic evidence of fracture or dislocation on plain radiography 

and computed tomography (CT) scan evaluation. Anatomic differences of the pediatric spine allow for 

significant intersegmental spinal movement without bony column disruption. The spinal cord does not 

share the same degree of elasticity as the spinal column. This explains why, despite the lack of radiographic 

evidence of spinal column disruption, spinal cord injury may still occur. In a recent meta-analysis of 

pediatric studies describing SCIWORA syndrome, 27 percent of patients (24/88) experienced delayed 

onset of symptoms.30 Paralysis developed hours to days after patients’ initial injuries. The prognosis of 

patients with SCIWORA syndrome is better than patients with similar neurologic deficits who exhibit 

radiographic evidence of bony column disruption. Nevertheless, patients with complete cord syndromes 

or severe deficits on initial examination generally do not recover.31 In more recent studies, SCIWORA 

syndrome has been documented in adult patients as well.30

Figure 5. Wedge-shaped appearance of vertebral bodies, most prominent 

at C3, should not be confused with compression fractures. The vertebrae 

take on a more rectangular appearance with age. Image courtesy of 

Swaminatha V. Mahadevan, MD, Stanford University.
540 | Pediatric Trauma

Spinal cord injury without radiographic abnormality is defined as a post-traumatic myelopathy that occurs 

without radiographic evidence of fracture or dislocation on plain radiography and CT scan evaluation.

Trauma victims who complain of either transient or persistent symptoms potentially attributable 

to a spinal cord injury should be assumed to have an unstable spinal column until proven otherwise. 

Radiographic evaluation often involves plain radiography and CT. High-dose glucocorticosteroid 

(i.e., methylprednisolone) therapy was the standard of care in adult patients with blunt trauma and 

clinical evidence of spinal cord injury. That was largely based on the results of the National Acute 

Spinal Cord Injury Study (NASCIS) II trial, which have since been called into question.32 This trial 

did not include any patient age 12 or younger. There are no published trials that support administering 

high-dose methylprednisolone in children age 12 and younger with spinal cord injuries. The benefits of 

administering high-dose glucocorticosteroids following blunt spinal cord injury has been refuted by many 

experts who feel the practice is of no value and possibly harmful.33

There are no published trials that support administration of high-dose methylprednisolone in children 

age 12 and younger with spinal cord injuries.

Skeletal and Body Surface Area 

Due to incomplete calcification and multiple unfused growth plates, the skeleton of a child is more pliable 

than an adult skeleton. As a result, significant internal organ injury can occur in children without notable 

overlying skeletal findings.34,35 For example, pulmonary contusions commonly occur in children, without 

associated rib fractures. Conversely, rib fractures denote significant trauma and are commonly associated 

with underlying injuries.34,35 Thus, when a rib or central bony structure is fractured, a diligent search for 

underlying internal organ injuries should follow, irrespective of how hemodynamically stable the child 

initially appears. The head is another area where a skull fracture may not occur, but there can be 

significant underlying cerebral pathology.36 Skin surface-area-to-body-volume ratio is highest at birth and 

decreases with age.37 As a result, heat transfer occurs much more rapidly in smaller children. Therefore, 

injured children are prone to hypothermia and must be evaluated and monitored vigilantly.

The skeleton of a child is more pliable than an adult skeleton. As a result, significant internal organ injury 

can occur without notable overlying skeletal injuries.

Age (years) Weight (kg) Respiratory Rate Pulse

Less than 1 3 40 to 60 130 to 150

1 to 5 10 to 20 20 to 40 110 to 130

6 to 10 20 to 35 12 to 20 75 to 100

11 to 18 35 to 70 12 to 20 70

Table 2. Physiologic parameters for respiratory rate and pulse rates in children.
Pediatric Trauma | 541

Physiology 

Vital Signs and Other Physiologic Parameters 

Normal respiratory and pulse rates vary with age as is described in Table 2. The definition of hypotension 

(less than fifth percentile) according to systolic blood pressure is less than 70 mm Hg for infants, less than 

70 mm Hg + 2 x (age in years) for children one to 10 years of age, and for children older than 10 years of 

age, it is less than 90 mm Hg.38 Children also have a smaller circulating blood volume than adults. Using 80 

milliliters of blood volume per kilogram of body weight will allow for an accurate estimation of a child’s 

intravascular blood volume. For example, the calculated intravascular blood volume for a five-kilogram 

infant would be 400 milliliters.

The definition of hypotension according to systolic blood pressure for infants is less than 70 mm Hg, for 

children one to 10 years of age is less than 70 mm Hg + 2 x (age in years), and for children older than 10 

years of age is less than 90 mm Hg. 

Normal intracranial pressure (ICP) in a child is similar to an adult and ranges between five to 15 mm Hg in 

the supine position with the exception of infants with an open fontanel where the ICP will be slightly lower. 

Similar to adults, the standard goal is to maintain ICP less than 20 mm Hg.39 The threshold to treat low 

cerebral perfusion pressure (CPP), defined by mean arterial pressure minus ICP, in children is dependent 

upon their age. In general, CPP should be maintained greater than 40 mm Hg for children under two years 

of age, greater than 50 mm Hg for those two to six years of age, greater than 60 mm Hg for those six to 12, 

and greater than 70 mm Hg for patients older than 13 years of age.39

Normal central venous pressures in children range between three to five mm Hg. Since children rarely 

have diastolic dysfunction, the central venous pressure is a relatively accurate measure of intravascular 

volume. For patients requiring positive-pressure mechanical ventilation, the intrapulmonary pressure that 

is transmitted to the intrapleural space will elevate the measured central venous pressure.40 The amount 

of central venous pressure elevation will be dependent upon the degree of compliance of the lungs, with 

increased lung compliance causing less transmission of pressure and therefore less effect on the measured 

central venous pressure.41 Intraabdominal pressure in children can be approximated with any device that 

measures urinary bladder pressure or intragastric pressure as is done in adults. Normal intraabdominal 

pressure in children is less than 10 mm Hg and typically three to five mm Hg, which is similar to adults, 

and in critically ill children requiring mechanical ventilation without signs of abdominal compartment 

syndrome, normal intraabdominal pressures were reported to be seven ± three mm Hg.42 

Abdominal compartment syndrome has been loosely defined in children, as in adults, by an intraabdominal 

pressure greater than 20 mm Hg.43 Children may develop abdominal compartment syndrome at lower 

pressures compared to adults.43 Splanchnic perfusion pressure, defined as mean arterial pressure minus 

intraabdominal pressure, may also be calculated. Splanchnic perfusion pressure is as a more accurate 

marker of splanchnic blood flow, and a decrease in splanchnic perfusion pressure may be the most sensitive 

early finding of abdominal compartment syndrome.44 Aggressive volume resuscitation in combination 

with inflammatory processes that promote capillary leak syndrome increases the risk of abdominal 

compartment syndrome, which can manifest as renal failure, decreased pulmonary compliance, and 

multiorgan failure.43
542 | Pediatric Trauma

Aggressive volume resuscitation in combination with inflammatory processes that promote capillary leak 

syndrome increases the risk of abdominal compartment syndrome, which can manifest as renal failure, 

decreased pulmonary compliance, and multiple organ system failure.

Due to higher metabolic rates, oxygen consumption is increased in infants and younger children compared 

to adolescents and adults.45 A significant related consequence is that younger children will become 

hypoxemic more rapidly during rapid sequence intubation. Methods to monitor the relationship between 

oxygen delivery and consumption in children are similar to what is practiced in adults. Blood gas analysis of 

arterial partial pressure of oxygen, base deficit or lactate concentrations, central venous oxygen saturations, 

and systemic arterial and cerebral tissue oxygen saturation monitoring are all used to directly or indirectly 

measure oxygen delivery, consumption, and cardiac output. 

Higher oxygen consumption in infants and young children combined with decreased functional 

residual capacity compared to adults causes children to become hypoxemic more rapidly during rapid 

sequence intubation.

Fluids, Electrolytes, Nutrition, and Glucose Metabolism 

Daily fluid requirements in children are dependent upon their weight (Table 3).46 For children who 

present with intravascular volume depletion due to fluid losses, these deficits should be replaced with 

non-dextrose containing isotonic saline rapidly if the child is hemodynamically compromised and more 

gradually (e.g., over 24 hours) if the losses have been subacute and the child is hemodynamically stable. 

Determining intravascular volume in pediatric patients is difficult since there is no direct method to 

measure it. Patient vital signs, physical exam findings, urine output, hemodynamic parameters, and 

laboratory values must be collectively evaluated to estimate the patient’s intravascular volume status. 

When intravenous fluids are used, close attention needs to be paid to the child’s electrolyte status. Critical 

illness in children increases antidiuretic hormone production, which increases free water retention. The 

risk of hyponatremic seizures increases with the use of hypotonic saline such as one-quarter normal saline 

(0.22 percent NaCl).47 Therefore, one-half normal saline (0.45 percent NaCl) to isotonic fluids such as 

Weight (kg) Hourly Rate of Fluids

3 to 10 4 milliliters (ml) per kilogram per hour

11 to 20 40 ml per hour + 2 ml per kilogram per hour

20 to 70 60 ml per hour + 1 ml per kilogram per hour

e.g., for weight of 13 kg, maintenance fluid requirement is 40 ml/hr + 2(3) ml/hr = 46 ml/hr

e.g., for weight of 37 kg, maintenance fluid requirement is 60 ml/hr + 1(17) ml/hr = 77 ml/hr

The exception is day 1 to day 2 of life in full-term neonates. Day 1 use = 60 to 80 ml per 

kilogram per day. Day 2 use = 80 to 100 ml per kilogram per day.

Table 3. Daily maintenance fluid requirement for pediatric patients, based on weight.
Pediatric Trauma | 543

normal saline (0.9 percent NaCl) or lactated Ringer’s solution should be used to provide maintenance 

fluids in critically ill children. This is a change from classical teaching that stressed the use of hypotonic 

fluids. Recent literature shows that the use of hypotonic fluids provides too much free water and should be 

abandoned.47 

Intravascular volume depletion should be rapidly reversed with non-dextrose containing isotonic saline if 

the child is hemodynamically unstable, and more gradually reversed if the fluid deficit is subacute and 

the child is hemodynamically stable.

Potassium daily requirements are 1 to 2 milliequivalents (mEq) per kilogram per day.48 In children less 

than one month of age this can be achieved with the addition of 10 mEq per liter of potassium chloride 

and in children greater than three months of age by adding 20 mEq per liter of potassium chloride to 

their intravenous fluid solution. The standard maximum potassium chloride concentrations suggested 

for peripheral intravenous (IV) solution is 80 mEq per liter and is 200 mEq per liter for central line 

administration.48 In non-immediately life-threatening scenarios, the maximum IV rate of potassiumcontaining solutions is 0.5 mEq per kilogram per hour with a maximum of 40 mEq per hour for children 

weighing greater than 40 kilograms.49 To minimize the risk of significant electrolyte disturbances, serum 

electrolytes should be monitored at least daily in all children requiring intravascular fluids. 

Children in areas of combat operations are 

often malnourished. Consequently, nutritional 

deficiencies are common, which increases the risk of 

many nutritional comorbid disorders such as sepsis 

and poor wound healing.50,51 A major difference 

between children and adults is caloric requirements. 

Daily caloric resting energy requirements decrease 

with age (Table 4). The standard caloric requirement 

or resting energy expenditure for an infant is 90 

to 120 kilocalories (kcal) per kilogram per day 

compared to 25 to 30 kcal per kilogram per day in 

adults.46 There is no one simple formula that can 

be used to calculate critically ill patients’ total caloric requirements. This requires direct calorimetry, which 

will not typically be available at Combat Support Hospitals. Alterations in energy expenditure as a result of 

critical illness in children cannot be estimated accurately, therefore nutritional support should be provided 

according to measurement of resting energy expenditure to avoid the consequences of overfeeding or 

malnutrition.52 

Enteral feeding compared to parenteral is preferred since it preserves gastrointestinal function and has been 

associated with decreased infections and length of hospital stay in critically ill children.53 Enteral feeds are 

indicated early in the course of critical illness as soon as enteric peristalsis is established, unless there is a 

medical or surgical contraindication. Post-pyloric feeds are advantageous due to less gastric distention and 

decreased risk of gastroesophageal reflux compared to gastric feeding.53 Nasoduodenal tubes can often be 

placed blindly 30 minutes after the administration of a prokinetic agent with the child in the right lateral 

decubitus position. Promotility agents can be used to improve gastric motility, and non-narcotic agents can 

be used for sedation to decrease the risk of ileus.54

Age (Years) Kcal/kg

0 to 1 90 to 120

1 to 7 75 to 90

7 to 12 60 to 75

12 to18 30 to 60

Greater than 18 25 to 30

Table 4. Daily maintenance caloric requirements in children. Note the 

decrease of caloric requirements associated with age.
544 | Pediatric Trauma

Children in areas of combat operations are often malnourished, which increases the risk of many 

comorbid disorders such as sepsis and poor wound healing. Enteral feeding is preferred to parenteral 

feeding since it preserves gastrointestinal function and has been associated with decreased infections and 

length of hospital stay in critically ill children.

Hypoglycemia is a significant risk in young children if glucose is not provided (in some form) early after 

initial resuscitation. This is due to decreased hepatic stores of glycogen and increased metabolism in 

children.55 For neonates it is standard to provide 10 percent dextrose (D10) when parenteral fluids are 

required and 5 percent dextrose (D5) for all other ages until adolescence.48 Clinical signs and symptoms 

of hypoglycemia may not be easily recognized in sedated and mechanically ventilated children. The risk 

of hypoglycemia makes it necessary to evaluate serum glucose values at least once a day if not more 

frequently in these critically ill children. Adolescent age children have larger glucose stores and are able 

to temporarily tolerate maintenance fluids without dextrose, similar to adults. Table 5 summarizes the 

range of acceptable choices of solutions, with dextrose concentrations and additives. For the treatment 

of symptomatic hypoglycemia in neonates and infants, it is preferred to give 4 ml per kilogram of D10 

solution by intravenous bolus infusion and to check the glucose concentration within 15 to 30 minutes. 

The use of D25 and D50 solutions should be avoided in neonates and infants due to the theoretical risk of 

intraventricular hemorrhage following the rapid infusion of a hyperosmotic agent and the risk of infiltration 

and tissue injury when administered into a peripheral vein.48

Hypoglycemia is a significant risk in young children if glucose is not provided in some form early after 

initial resuscitation. The use of D25 and D50 solutions should be avoided in neonates and infants due to 

the theoretical risk of intraventricular hemorrhage with the rapid use of a hyperosmotic agent and the 

risk of infiltration and tissue injury when used within a peripheral vein.

Respiratory System 

While there are age-dependent changes in pulmonary compliance and resistance and chest wall compliance, 

in children as compared to adults, these differences have minimal effect on the treatment of respiratory 

failure once it has occurred in children.56 Increased resistance due to smaller airways and increased 

metabolic rates and lower functional residual capacities may increase the risk of respiratory failure in 

Age Dextrose 

(Percent)

Solution Potassium 

Chloride (KCl)

0 to 2 Days 10 Water + 2 mEq/kg NaCl + 1 mEq/kg KCl

3 Days to 1 Month 5 or 10 0.45 Normal Saline 10 mEq per liter

1 Month to 1 Year 5 0.45 to 0.9 Normal Saline or LR 20 mEq per liter*

1 to 8 Years 5 0.45 to 0.9 Normal Saline or LR 20 mEq per liter*

8 to 18 Years 0 or 5 0.45 to 0.9 Normal Saline or LR 20 mEq per liter*

*Potassium chloride should not empirically be added to lactated Ringer’s (LR) solution if not required.

Table 5. Appropriate range of fluid solutions and additives in children.
Pediatric Trauma | 545

young children. Once a child is intubated, the same open-lung or low-lung tidal volume strategies that 

are applied in adults should also be applied in children (e.g., 5 ml per kilogram as an initial tidal volume). 

Principles of permissive hypercapnia and permissive hypoxemia to prevent ventilator-associated lung injury 

are also practiced in children.57 Complications of hypercapnia are minimal as long as the pH of the blood 

is medically controlled at a pH of 7.1 or above. 

Once a child is intubated, the same open-lung or low-lung tidal volume strategies that are applied 

in adults should also be applied. Principles of permissive hypercapnia and permissive hypoxemia to 

prevent ventilator-associated lung injury are also applied to children.

Pharmacology 

The dosing of most, if not all, medications for children is weight-based. Multiple references for 

appropriate dosing and how to adjust for renal and hepatic impairment in addition to contraindications 

and adverse reactions are available and must be used for the safe and appropriate use of medications in 

children. The Harriet Lane Handbook is a small soft-cover book that is an invaluable resource for pediatric 

medication dosing and adjustment.58 All Combat Support Hospitals should have this reference available.

The Harriet Lane Handbook is a small soft-cover book that is an invaluable resource for pediatric 

medication dosing and adjustment.58 Level III care facilities should have this reference available.

Succinylcholine and propofol are two pharmaceutical agents that are commonly used for patients with 

traumatic injuries that have added risks or considerations in children compared to adults.59 Succinylcholine 

has historically been the paralytic of choice for true rapid sequence induction due to its rapid onset of action 

(30 seconds) and brief duration of action (five to six minutes).8 This was undoubtedly true, especially 

when there were no other similar profile agents. The increased risks associated with succinylcholine in 

children must be recognized and alternative choices should at least be considered. The major risk associated 

with its use is life-threatening hyperkalemia, which is increased when used in children with undiagnosed 

neuromuscular disorders, massive multiorgan trauma, widespread intestinal ischemia, and subacute burn 

injuries.59 In addition, risks associated with succinylcholine use include malignant hyperthermia, masseter 

spasm, increased intracranial, intraocular, and gastric pressure, sinus bradycardia with hypotension, 

and pulmonary edema.59 Several methods of blunting the transient rise of ICP directly resulting from 

succinylcholine administrations have been studied. The use of lidocaine (1 to 1.5 milligrams [mg] per 

kilogram) IV has shown mixed results in the literature; the studies demonstrating benefit required a 

minimum of three minutes of time to pass prior to administering succinylcholine.60 The administration of a 

defasciculating dose (0.01 mg per kilogram) of a nondepolarizing paralytic agent such as pancuronium has 

been shown to decrease succinylcholine-associated rises in ICP.59 Administration of atropine will eliminate 

the risk of bradycardia with laryngoscopy.59 The use of these premedication agents often negates the rapid 

onset of action of succinylcholine since it takes time for these agents to be administered and take effect. If 

succinylcholine is used in pediatric patients, infants may require 2 to 3 mg per kilogram and children 1 to 2 

mg per kilogram of succinylcholine compared to the adult intravenous dose of 1 to 1.5 mg per kilogram.59

An alternative agent that has near similar onset of action that should be considered in children is rocuronium. 

Rocuronium at a dose of 0.6 mg per kilogram typically produces paralysis at 50 to 80 seconds, and using an 

increased dose of 0.8 mg per kilogram will decrease the average time to 30 seconds.59 The duration of action 
546 | Pediatric Trauma

in children is typically 30 to 40 minutes, which is much longer than succinylcholine since it is an intermediateacting nondepolarizing paralytic.59 Hence, careproviders will need to provide airway and breathing support 

for this extended period of time if endotracheal intubation is unsuccessful. Hemodynamic effects include 

mild increase in heart rate. It is metabolized primarily by the liver and excreted by the kidneys. Since there 

are now suitable alternatives to succinylcholine, many in the pediatric emergency medicine and critical care 

communities discourage its use and support the alternative use of agents such as rocuronium.59

Succinylcholine has historically been the paralytic of choice for true rapid sequence induction due to 

its rapid onset of action and brief duration of action. An alternative agent that has near similar onset 

of action that should be considered in children is rocuronium. 

Propofol is an intravenous anesthetic agent that gained wide acceptance for long-term sedation in adult 

intensive care units as a result of its potent anesthetic properties, fast-onset, and short duration of action. 

Propofol’s attractive rapid-onset and rapid-offset pharmacologic profile has resulted in extending its use to 

critically ill pediatric patients (e.g., enabling near-term neurologic exams in patients with head injuries). Shortterm use of propofol for procedural sedation and operative cases has not been shown to be a problem, but 

the use of propofol for prolonged sedation in the critical care setting has raised concerns. A fatal metabolic 

acidosis syndrome associated with prolonged use of propofol has been described. The mechanism is 

unclear, but duration of therapy and higher doses are the most commonly cited factors associated with 

the syndrome. Notably, children have been reported to develop a rapidly fatal metabolic acidosis syndrome 

when higher doses of propofol have been used for sedation for more than two to three days.61,62,63,64 While 

this has also been reported in adults, it has been more commonly associated with pediatric use (specifically 

in brain injury and burn patients), hence the black box warning for long-term use in children.65

Propofol has an attractive rapid-onset and rapid-offset pharmacologic profile, which has resulted in 

extending its use to critically ill pediatric patients. The use of propofol for prolonged sedation in the 

critical care setting has raised concerns. With prolonged sedation of more than two to three days, a fatal 

metabolic acidosis syndrome, also known as propofol infusion syndrome, can occur.

Fatal metabolic acidosis, also known as propofol infusion syndrome, can present with the following 

signs and symptoms: lactic acidosis, rhabdomyolysis, elevated hepatic enzymes, and fatal dysrhythmias. 

Discontinuation of propofol and supportive care is the only treatment.61,62,63,64 Since there are alternative 

agents that can produce adequate deep sedation such as fentanyl, remifentanil, midazolam, ketamine, 

barbiturates, and dexmedetomidine, the use of propofol for greater than 24 hours must be carefully 

considered. If propofol is used for long-term sedation, patients should be carefully monitored for the 

development of propofol infusion syndrome.

Patient Monitoring Considerations 

Standard monitoring of vital signs in children includes continuous end-tidal carbon dioxide monitoring 

for children who are intubated.66 A main benefit of continuous end-tidal carbon dioxide monitoring is the 

rapid recognition that the ETT has been displaced out of the airway. Children, due to their shorter tracheas 

and difficulty in maintaining adequate sedation, are at increased risk of accidental extubations (Fig. 6). 

Immediate recognition of ETT displacement before the child becomes hypoxemic will minimize adverse 

outcomes. Continuous end-tidal carbon dioxide waveform analysis monitoring improves the recognition 
Pediatric Trauma | 547

of obstructive airway disease, whether it is from reactive airways or mucus plugging.66 It is also beneficial 

for the child with severe traumatic brain injury where the goal is to keep the arterial partial pressure of 

carbon dioxide (PCO2) within a certain range and can also be used to estimate pulmonary dead space.66

Once correlated with the arterial PCO2, the end-tidal carbon dioxide can be used to titrate ventilation and 

has the potential to minimize phlebotomy. 

Because children are at increased risk of accidental extubations, standard monitoring should include 

continuous end-tidal carbon dioxide monitoring, which may aid in rapid recognition of a displaced 

ETT.

The use of intracranial ventriculostomy catheters for patients with severe traumatic brain injury is 

standard practice in children.39 Diagnostic benefits include the monitoring of ICP, while therapeutic 

benefits include the ability to drain cerebrospinal fluid (CSF) via the catheters when intracranial pressures 

become elevated. Compared to intraparenchymal pressure monitoring devices, there is an increased 

infection risk with the use of ventriculostomy catheters, but this risk is still very low and the therapeutic 

benefits outweigh the risks.39

Figure 6. A pediatric victim of an IED blast undergoing mechanical ventilation with cardiac and respiratory monitoring in place. 
548 | Pediatric Trauma

Resuscitation 

General Considerations 

Advanced Trauma Life Support (ATLS) course 

principles all apply for children. The Broselow® 

tape is a commonly used and helpful method to 

standardize the approach to the resuscitation of 

children (Fig. 7).10 It provides a valuable reference 

source for the appropriate sizing of pediatric 

resuscitation equipment and dosing of medications. 

Airway and Breathing

For the conscious child with an obstructed airway, 

back blows or the Heimlich maneuver should be 

performed to dislodge any foreign body.38 Attempts 

Figure 7. Pediatric resuscitation of a host nation casualty cared for at a 

Level III facility. By measuring the patient’s body length, the Broselow® 

tape allows careproviders to rapidly determine appropriate resuscitation 

equipment and medication dosing.

Figure 8. A pediatric patient who sustained multiple traumatic injuries. A right mainstem intubation is noted, with hyperinflation of the right lung.
Pediatric Trauma | 549

to manually remove the obstruction should only occur if a foreign body is visible.38 In cases where positivepressure ventilation is indicated, the use of an oral airway will greatly improve the ability to bag-valvemask ventilate a young child since the tongue often obstructs a child’s airway. The use of a Miller blade 

and the Sellick maneuver will often improve your ability to visualize the larynx in a young child. 

Always consider ETT misplacement (e.g., right mainstem bronchus intubation) if it is difficult to increase 

a child’s arterial oxygen saturations or if the peak inspiratory pressures are higher than expected. The 

trachea of a child is much shorter than it is in an adult and it is easy to mistakenly advance the ETT into 

the right mainstem bronchus (Fig. 8). The proximal airways in an intubated child obstruct very easily due 

to their small size. Nebulized hypertonic saline, respiratory vibratory and percussive therapy, and the use 

of mucolytics (nebulized or instilled) can be considered and have been used with mixed results to minimize 

airway obstruction in a variety of conditions.67,68,69 

The trachea of a child is much shorter than it is in an adult, and it is easy to mistakenly advance the 

ETT into the right mainstem bronchus. Always consider ETT misplacement (e.g., right mainstem 

bronchus intubation) if it is difficult to increase a child’s arterial oxygen saturations or if the peak 

inspiratory pressures are higher than expected.

Current pediatric standards taught in the Pediatric Advanced Life Support (PALS) course advise the use 

of cuffed endotracheal tubes to optimize oxygenation and ventilation in all children. The primary benefit 

is to secure the tube and prevent significant air leaks around the ETT. With the use of cuffed ETT tubes 

comes the responsibility of maintaining the appropriate ETT cuff pressure (less than 25 cm H2

O). This 

will minimize the risk of subglottic stenosis that may occur from ischemic injury to this area from over 

inflated endotracheal cuffs.70 The short length of the trachea especially in infants can make it very difficult 

to keep the ETT in proper midtracheal position. To minimize the risk of accidental extubations it is wise 

to: (1) keep the infant and young child well-sedated; (2) ensure the ETT is securely taped; (3) immediately 

change the tape if it loosens (e.g., due to oropharyngeal secretions); (4) obtain daily chest radiographs to 

determine the position of the ETT; and (5) always use continuous end-tidal carbon dioxide monitoring 

to enable immediate recognition of ETT dislodgment. In circumstances where it is difficult to maintain 

an orally-placed ETT in proper position, considerations should be given to performing nasotracheal 

intubation.

Rapid Sequence Intubation 

Careproviders need to consider multiple important factors when performing rapid sequence intubation in 

young children. Atropine should be strongly considered as a premedication prior to intubation in infants 

and young children. Infants have a strong vagal response to laryngoscopy and can develop significant 

bradycardia as a result.70 Oropharyngeal secretions in young children can make airway visualization 

difficult during laryngoscopy. This is especially true with the use of ketamine, which is a potent sialogogue. 

Atropine has been shown to decrease oral secretions and may also reduce the risk of vomiting during 

recovery from ketamine use.71 Interestingly, while glycopyrrolate and atropine have been traditionally used 

to minimize secretions, recent studies have found that neither drug has been shown to decrease serious 

adverse respiratory events associated with ketamine use.72,73 
550 | Pediatric Trauma

Infants and young children have a strong vagal response to laryngoscopy and can develop significant 

bradycardia as a result. Atropine should be strongly considered as a premedication prior to intubation of 

infants and young children.

Due to increased metabolic rates and decreased 

functional residual capacity compared to adults, 

children will undergo arterial oxygen desaturation 

more quickly with rapid sequence intubation.74

This is especially true for children with nutritional 

deficiencies and decreased muscular strength 

and those with distended abdomens either 

from malnutrition or hepatic enlargement. For 

children who require bag-valve-mask ventilation 

prior to intubation, intragastric air can increase 

intraabdominal pressure significantly enough 

to decrease pulmonary compliance and make it 

more difficult to maintain adequate oxygenation 

(Fig. 9). To minimize increased intragastric air 

accumulation, the Sellick maneuver should be used 

during bag-valve-mask ventilation once the child 

is sedated. If gastric distension still occurs, the 

placement of a nasogastric tube to decompress the 

stomach should also be considered. 

Vascular Access 

Rapid resuscitation of a child is best accomplished through the largest peripheral intravascular access 

that can be obtained. If a child is in need of immediate intravascular access and standard peripheral 

or central intravenous access cannot be rapidly established, an intraosseous (IO) needle should be 

inserted.70 

Intraosseous needles can be inserted by hand or with the use of a tool such as the EZ-IO® (Fig. 10).75

The preferred landmark for IO line placement is two centimeters inferior to the tibial tuberosity and 

perpendicular to the medial flat surface of the tibia. Local anesthetic (e.g., lidocaine) injected at the 

site of needle insertion several minutes prior to needle insertion will minimize procedural discomfort. 

Alternative sites include the distal tibia, distal femur, and proximal humerus (Fig. 11). All resuscitative 

medications and blood products that can be given intravenously can be administered via an IO needle.70

Marrow sinusoids drain into venous channels, which lead into nutrient and emissary veins, which in turn, 

drain into the systemic venous system. Medications infused via intraosseous lines can reach the central 

circulation rapidly and in a similar timeframe compared to peripheral injections, even in hypoperfused 

states. Pressure bags or manual syringe infusion are the recommended methods for attaining adequate 

infusion rates. Passive flow rates (i.e., gravity infusion of hanging saline bags) are suboptimal. Blood can 

also be sampled from an IO needle for laboratory analysis.76

Figure 9. For children who require bag-valve-mask ventilation prior 

to intubation, intragastric air can increase intraabdominal pressure 

significantly enough to decrease pulmonary compliance and make it 

more difficult to maintain adequate oxygenation. In such cases, prompt 

nasogastric tube decompression is warranted.
Pediatric Trauma | 551

If a child is in need of immediate intravascular access and standard peripheral or central intravenous 

access cannot be rapidly established, an IO needle should be inserted. All resuscitative medications and 

blood products that can be given intravenously can be administered via an IO needle. Pressure bags 

or manual syringe infusion are the recommended methods for attaining adequate flow rates, as passive 

flow rates are suboptimal. 

Complications of IO lines include subcutaneous extravasation of infusate, extremity compartment 

syndrome, tibial fracture, and osteomyelitis.75 Intraosseus line utilization should be regarded as temporary 

vascular access and should be replaced with traditional IV access within 24 hours. This is due to the 

concern that there is an increased risk of osteomyelitis with prolonged IO access.77 Close monitoring for 

extravasation of fluid is crucial. Early recognition of a malfunctioning IO line will minimize the risk of 

compartment syndromes at IO infusion sites.

Circulation

Damage control or hemostatic resuscitation principles can be applied to children in hemorrhagic shock.78

There is no contraindication to the use of appropriately cross-matched whole blood for children who 

Figure 10. Vascular access in this patient includes bilateral proximal tibia IO lines. All resuscitative medications and blood products that can be given 

intravenously can be administered via an IO needle.
552 | Pediatric Trauma

present in hemorrhagic shock. In fact, the only randomized controlled trial of whole blood was performed 

in children after cardiac surgery.79 In this study, whole blood was transfused in both the operating room 

and intensive care unit, and outcomes were statistically adjusted. The results indicated that whole blood 

transfusion compared to blood product components decreased postoperative blood loss.79 This study is 

often compared to another that reported increased length of stay with the use of whole blood compared 

to components.80 It is important to realize that in this study by Mou et al., whole blood was only transfused 

in the operating room, and the analysis did not adjust for other factors associated with length of stay.80

The use of type O whole blood should only be considered when there is no other alternative, and the 

child is in immediate risk of death. Every effort should be made to use type-specific whole blood when it is 

indicated. All vasoactive agents used in adults to increase cardiac output can be used in children, including 

vasopressin.81,82 Relative adrenal insufficiency is common in critically ill children.83 Hydrocortisone is used 

for its treatment with reported dosing that varies from 2 mg per kilogram IV every 4 hours to a 50 mg per 

day continuous infusion.84 Of note, the benefit of low-dose hydrocortisone in critically ill children in septic 

shock remains poorly defined. The recognition of low ionized calcium concentrations and its treatment 

in hypotensive children is important since correction improves myocardial contractility and vasomotor 

tone.81

Damage control or hemostatic resuscitation principles can be applied to children in hemorrhagic shock, 

as in adults. Standard volumes for red blood cell, fresh frozen plasma, and platelet transfusions range 

from 10 to 15 ml per kilogram. For children requiring massive transfusion, which is typically defined as 

more than one blood volume (70 to 80 ml per kilogram) in 24 hours, hypothermia, hyperkalemia, and 

hypocalcemia are all risks.

Figure 11. Sites for IO line placement. The preferred landmark for IO line placement is two centimeters inferior to the tibial tuberosity and perpendicular 

to the medial flat surface of the tibia. Alternative sites include the distal tibia, distal femur, and proximal humerus. Image courtesy of Elsevier. In: Roberts 

JR and Hedges JR. Clinical Procedures in Emergency Medicine. 4th ed. Philadelphia (PA): WB Saunders; 1998.
Pediatric Trauma | 553

Blood Product Transfusion 

Standard volumes for red blood cell, fresh frozen plasma (FFP), and platelet transfusions range from 10 

to 15 ml per kilogram. Cryoprecipitate dose is 1 to 2 units per 10 kilograms bodyweight.85 For children 

requiring massive transfusion, which is typically defined as more than one blood volume (70 to 80 ml 

per kilogram) in 24 hours, hypothermia, hyperkalemia, and hypocalcemia are all risks.86 As a result, the 

use of a blood warmer should be strongly considered, and frequent electrolyte monitoring is required. 

The treatment of hypocalcemia is important for patients with coagulopathy since calcium is required for 

optimal coagulation factor function.86 This is critical in the patient requiring massive transfusion. The 

large citrate load in packed red blood cells binds calcium, increasing the risk of hypocalcemia.86 If left 

uncorrected, this will lead to decreased cardiac function.87 In addition, for children requiring massive 

transfusion, the treatment of acidosis with alkaline solutions with either sodium bicarbonate or THAM 

(tromethamine) can be considered.86 Adjunctive pro-hemostatic agents such as recombinant factor 

VIIa (rFVIIa) and antifibrinolytics can also be considered.78,86 If rFVIIa is given, anecdotal experience 

and preliminary data indicate that it works best when used in conjunction with cryoprecipitate.88 If 

thromboelastography is available, it can be used to direct hemostatic resuscitation and specifically 

determine if rFVIIa or antifibrinolytics are indicated.78 For children who are hemodynamically stable 

without active bleeding, a hemoglobin concentration below 7 grams per deciliter is an appropriate red 

blood cell transfusion trigger.89

Specific Medical Condition Management

Acute Respiratory Distress Syndrome (ARDS) 

Acute respiratory distress syndrome (ARDS) in children is defined as it is in adults: (1) Partial pressure 

of oxygen in arterial blood (PaO2)/fraction of inspired oxygen (FiO2) ratio less than 200 mm Hg; (2) 

presence of bilateral lung infiltrates on the chest radiograph; (3) no clinical evidence of heart failure; 

and (4) absence of COPD or other chronic pulmonary disorders. Principles practiced in adults regarding 

ventilator (e.g., permissive hypercapnia) and fluid management are also used for children.57 Goals include 

keeping peak inspiratory pressures less than 30 cm H2O with the use of tidal volumes between 4 to 6 

ml per kilogram bodyweight.57 In addition, judicious fluid administration is recommended to prevent an 

excessive fluid balance since it has been associated with worse outcomes in adults with ARDS.90 There is 

no limit to the amount of positive end-expiratory pressure that can be used to support oxygenation, and 

the prone position is also commonly used to attempt to improve oxygenation indices.57 Nonconventional 

modes of ventilation, such as alternating pressure release ventilation (APRV) and high-frequency 

oscillation ventilation (HFOV), and alternative therapies, such as nitric oxide and surfactant therapy, are 

not currently available at Combat Support Hospitals.

Acute respiratory distress syndrome in children is defined as it is in adults. Principles practiced in adults 

regarding ventilator (e.g., permissive hypercapnia) and fluid management are also used for children. 

Nonconventional modes of ventilation are not currently available at Combat Support Hospitals.

Severe Sepsis and Septic Shock

Children respond differently hemodynamically to sepsis than adults.81 Children typically have decreased 
554 | Pediatric Trauma

Figure 12. Protocol for early goal-directed therapy.91 CVP denotes central venous pressure, MAP mean arterial pressure, and ScvO2 central venous oxygen 

saturation. Image courtesy of Massachusetts Medical Society.

<8 mm Hg

Supplemental oxygen ±

endotracheal intubation and

mechanical ventilation

Central venous and

arterial catheterization

Sedation, paralysis

(if intubated),

or both

CVP

MAP

ScvO2

Goals

achieved

Hospital admission

Crystalloid

Colloid

Vasoactive agents

Transfusion of red cells

 until hematocrit ≥ 30%

Inotropic agents

<65 mm Hg

>90 mm Hg

8–12 mm Hg

≥65 and ≤90 mm Hg

No

Yes

<70%

<70%

 ≥70%

≥70%
Pediatric Trauma | 555

myocardial function and compensate with increased systemic vascular resistance commonly referred to 

as “cold shock.” This is in contrast to adults who conversely first develop loss of vasomotor tone and 

compensate with increased cardiac function or what has been termed “warm shock.”81 

Adhering to principles of goal-directed therapy for treatment of patients with severe sepsis and septic 

shock is warranted (Fig. 12).91,92 Therefore, the standard approach to septic shock in children is early 

administration of antibiotics and volume resuscitation, while correcting hypoglycemia and low ionized 

calcium concentrations. Correcting hypocalcemia is important since cardiac contractility is dependent 

upon normal serum ionized calcium concentrations. These interventions are coupled with infection source 

control (e.g., debridement of infected tissue). Either dopamine or epinephrine is appropriate as the initial 

inotrope.82 If cold shock persists and intravascular volume is adequate (determined primarily by a central 

venous pressure of greater than 8 mm Hg), the use of an afterload reducing agent, either dobutamine 

or milrinone, is appropriate. If warm shock develops, norepinephrine, phenylephrine, or vasopressin is 

appropriate. Hydrocortisone should be used for patients with catecholamine-resistant shock.82 Pulmonary 

artery catheters and other methods of determining cardiac output are not usually available at Combat 

Support Hospitals. 

Figure 13. Careproviders reviewing a CT scan of the brain demonstrating an epidural hematoma.
556 | Pediatric Trauma

Adhering to principles of goal-directed therapy for treatment of patients with severe sepsis and septic 

shock is warranted. The standard approach to septic shock in children is early administration of antibiotics 

and volume resuscitation while correcting hypoglycemia and low ionized calcium concentrations.

Cerebral Herniation Syndromes 

Several immediate interventions are indicated when a child has signs and symptoms of impending 

cerebral herniation (hypertension, bradycardia, abnormal breathing pattern, and posturing). These 

include hyperventilation by manual bag-valve-mask as a temporizing measure while initiating additional 

interventions. Additional measures include elevation of the head of the bed to approximately 30 degrees, 

and the rapid administration of an osmotic agent. Mannitol or hypertonic saline can be used as osmotic 

agents.39 If the patient is hypovolemic and volume resuscitation is problematic, mannitol should not be 

used since it will often have a diuretic effect several hours after infusion. The decrease in mean arterial 

pressure from diuresis will translate into decreased cerebral perfusion pressure.93 Hypertonic saline may be 

a better choice in hypovolemic pediatric patients. The dose of 3% hypertonic saline is 10 ml per kilogram 

IV (maximum dose 250 ml per bolus) and should be given as a fast intravenous push for impending 

herniation. Pediatric dosage handbooks mention it is preferable to use a central line with hypertonic saline 

since there is a risk of thrombophlebitis when used peripherally.49 This risk has also been noted with 

mannitol.94 Therefore, the safest approach may be to use either agent with a central line. 

If a child displays evidence of impending cerebral herniation, hyperventilation, elevation of the head 

of the bed, and infusion of mannitol or hypertonic saline are indicated.

Concurrent efforts (cranial computed tomography scanning) should be made to determine whether a 

neurosurgically treatable intracranial lesion exists (e.g., epidural hematoma) (Fig. 13). Prompt neurosurgical 

consultation will also enable placement of intracranial ventriculostomy tubes, which can real-time monitor 

intracranial pressures and provide a method to decrease intracranial pressure through the removal of 

CSF.39

Seizure Management 

The etiology of seizures in children that are evacuated to a Combat Support Hospital after an acute injury 

is likely to be related to traumatic brain injury or a consequence of hypoxic ischemic injury (Fig. 14). 

Hypoglycemia, hyponatremia, and other electrolyte disturbances should always be immediately ruled out 

as the cause of seizure. The differential diagnosis should also include meningitis, epilepsy, hypertension, 

and drug ingestion. 

After determining that the patient’s airway is patent and breathing and circulation are adequate, oxygen 

should be applied and vascular access obtained. A rapid-acting benzodiazepine such as lorazepam (0.1 

mg per kilogram) or diazepam (0.2 mg per kilogram) should be administered intravenously as a first-line 

therapeutic agent if continued tonic-clonic seizure activity persists beyond one minute. If the seizure persists 

beyond several minutes, repeat dosing of rapid-onset benzodiazepines is indicated. Alternative routes of 

benzodiazepine administration include intraosseous, intranasal, buccal, and rectal administrations. If 

seizures recur or persist in the minutes that follow infusion of first-line agents (benzodiazepines), secondline therapy is indicated. Second-line agents include intravenous administration of phenytoin (18 to 20 
Pediatric Trauma | 557

mg per kilogram) or fosphenytoin (15 to 20 mg phenytoin equivalents per kilogram).95 If phenytoin is 

administered, the rate should not exceed 1 mg per kilogram per minute (maximum infusion rate 50 mg per 

minute) due to the risk of fatal dysrhythmias.95 Fosphenytoin has become the preferred second-line agent 

for the acute management of seizures in children for several reasons. While fosphenytoin will not work any 

faster than phenytoin and is more expensive, it does not have the serious risk of tissue necrosis that phenytoin 

possesses upon extravasation into soft tissues and can be administered intramuscularly or intravenously.96

Phenobarbital (15 to 20 mg per kilogram) can be used in children instead of phenytoin or fosphenytoin 

as a second-line antiepileptic agent. Phenobarbital carries a profound respiratory depressant effect and 

can also cause hypotension upon intravenous administration.95 Careproviders must be prepared to treat 

hypotension and/or apnea subsequent to infusion of barbiturates or multiple doses of benzodiazepines to 

control seizure activity. 

The etiology of seizures in children that are evacuated to a Combat Support Hospital after an acute 

injury is likely to be related to traumatic brain injury or hypoxic ischemic injury. A rapid-acting 

benzodiazepine such as lorazepam (0.1 mg per kilogram) or diazepam (0.2 mg per kilogram) should 

be administered intravenously as a first-line therapeutic agent if continued tonic-clonic seizure activity 

persists beyond one minute.

Figure 14. A critically ill head-injured child at high risk for seizure activity.
558 | Pediatric Trauma

Pediatric Advanced Life Support (PALS) 

The Pediatric Advanced Life Support (PALS) course concepts have been developed to improve the 

recognition and treatment of cardiopulmonary failure in children. Early recognition of respiratory or 

cardiac failure and its reversal is obviously optimal. However, if a child arrests and cardiopulmonary 

resuscitation (CPR) is initiated, the following principles should be applied: the rate of cardiac compression 

should be 100 per minute, and full elastic recoil should occur with compressions to improve venous return 

into the thoracic cavity. Efficacy of CPR can be most effectively assessed by evaluating the diastolic 

pressure on the invasive arterial blood pressure monitor. The respiratory rate should not exceed 12 

breaths per minute as hyperventilation will decrease venous return.70 The differential diagnosis for all 

nonperfusing, bradycardic, and tachycardic rhythms include: hypoxemia, hypovolemia, hypothermia, 

hyper/hypokalemia, acidosis, tamponade physiology, tension pneumothorax, drug overdose, trauma, and 

thromboembolism.

For a pediatric cardiac arrest, the cardiac compression rate should be 100 compressions per minute. Full 

elastic recoil of the chest should occur between compressions to improve venous return to the thoracic 

cavity. The respiratory rate should not exceed 12 breaths per minute as hyperventilation will decrease 

venous return.

Cardiac Rhythm Disturbances

Treatment of cardiac rhythm disturbances must 

occur with the clinical context of the patient in 

mind. The treatment of pulseless electrical activity 

in the setting of hypovolemic shock due to traumatic 

hemorrhage will be futile unless concurrent efforts to 

restore blood volume and stop ongoing hemorrhage 

are undertaken. However, CCC providers should 

be familiar with standard therapies for the 

more commonly encountered cardiac rhythm 

disturbances encountered in critically ill children. In reality, many cases will involve immediately initiating 

cardiac rhythm disturbance treatments while identifying and treating concurrent contributory medical 

conditions. It is important to note that the QRS complex is age-dependent. A wide QRS complex is 

defined as greater than or equal to 80 milliseconds in infants and young children up to age three years; 

greater than 80 milliseconds in children ages four to nine years; greater than 90 millseconds between ages 

nine and 11 years; and greater than 100 milliseconds in children age 12 and above (Table 6).97,98

Combat casualty careproviders should be familiar with standard therapies for the more commonly 

encountered cardiac rhythm disturbances encountered in critically ill children.

Asystole and Pulseless Electrical Activity 

Rapid initiation of CPR should occur followed by 0.1 ml per kilogram of epinephrine (1:10,000) or 0.01 mg 

per kilogram of epinephrine IV injection every three to five minutes while attempting to reverse the cause 

of the arrest.70

Age (Years) Time

Infants to 3 ≥ 80 milliseconds

4 to 9 > 80 milliseconds

9 to 11 > 90 milliseconds

12 and above > 100 milliseconds

Table 6. Definition of wide QRS complex based on patient’s age.
Pediatric Trauma | 559

Pulseless Ventricular Tachycardia and Ventricular Fibrillation 

Standard treatment includes the rapid initiation of CPR, then defibrillation at 2 joules per kilogram, 

another five cycles of CPR, defibrillation at 4 joules per kilogram, then epinephrine (1:10,000) 0.1 ml per 

kilogram IV, five cycles of CPR, defibrillate at 4 joules per kilogram, then amiodarone (5 mg per kilogram) 

IV, while attempting to identify and reverse the cause of the arrest.70

Bradycardia with Poor Perfusion

Cardiopulmonary resuscitation should be initiated for a pulse rate less than 60 with poor perfusion, then 

epinephrine, atropine, and cardiac pacing should be considered while attempting to identify and reverse 

the cause of the arrest. Keep in mind that bradycardia is a very common manifestation of hypoxemia 

in children.70 Conversely, bradycardia with good perfusion occurs with severe traumatic brain injury and 

herniation syndrome. 

Bradycardia is a very common manifestation of hypoxemia in children.

Figure 15. The left anterior fifth intercostal space is used as the standard approach for resuscitative thoracotomies in pediatric patients, as in adults. 

Image courtesy of J. Christian Fox, MD, University of California, Irvine.
560 | Pediatric Trauma

Narrow Complex (Supraventricular) Tachycardia 

If good perfusion is noted, administer adenosine 0.1 mg per kilogram IV as a fast-push infusion. Since the 

half-life of adenosine is five seconds, the use of a three-way stopcock with another syringe in-line for a flush 

allows for rapid bolus administration. A repeat dose of adenosine at 0.2 mg per kilogram IV can be given 

if needed.70 Amiodarone 5 mg per kilogram over 20 to 60 minutes can be used as a second-line agent in 

refractory cases. If poor perfusion is noted, synchronized cardioversion with 0.5 to 1 joules per kilogram is 

indicated followed by adenosine and amiodarone administration as indicated.70

Wide Complex (Ventricular) Tachycardia 

If good perfusion is noted, amiodarone, 5 mg per kilogram IV over 20 minutes should be administered. 

Administration of adenosine, 0.1 mg per kilogram IV fast-push can be considered in patients with 

adequate perfusion who are suspected of having supraventricular dysrhythmias with associated 

bundle branch block(s) resulting in wide complex QRS rhythms. If poor perfusion is noted, synchronized 

cardioversion of the patient with 0.5 to 1 joules per kilogram is indicated. This is followed by administration 

of amiodarone, and then adenosine as indicated.70

Surgical Considerations

Thoracic Interventions

Resuscitative thoracotomies are best done for 

penetrating trauma when vital signs have been 

present within minutes of patient arrival to the 

trauma suite (Fig. 15).99 Resuscitative thoracotomies 

for blunt trauma are almost uniformly unsuccessful 

when vital signs have been lost prior to arrival in the 

trauma suite.100 A left anterior fifth intercostal space 

is the approach most commonly employed during 

emergency resuscitative thoracotomy. Advantages 

of this approach include ease of access to the heart 

and great vessels. The disadvantage is that access to 

the lower lobes of the lung becomes more difficult. 

Regardless of the approach, Rummel tourniquets 

should be available on all resuscitative thoracotomy 

trays for children and infants (Fig. 16). This obviates 

the concern about the appropriate-sized vascular 

clamp. The other point unique to children is that 

pneumonectomies in the very young will lead to 

scoliosis and lack of chest wall development on that 

side (post-pneumonectomy syndrome).101 Thus, 

trauma pneumonectomy should be considered 

only as a last resort. As in adults, the vast majority 

of chest trauma can be managed with either 

observation or tube thoracostomy alone.102

Figure 16. Appropriately-sized vascular clamps are not always available 

in combat settings. As an alternative, Rummel tourniquets may be used 

for vascular control. A tourniquet is fashioned by passing umbilical tape 

around a vessel, threading both ends through a short rubber catheter, and 

securing with a perpendicularly placed hemostat.

tape

rubber 

tube

artery
Pediatric Trauma | 561

Resuscitative thoracotomies for penetrating trauma are most successful when vital signs have been present 

within minutes of patient arrival to the trauma suite. Resuscitative thoracotomies for blunt trauma are 

almost uniformly unsuccessful in patients arriving without signs of life.

Abdominal Interventions

For children less than two years of age, a transverse laparotomy is thought to provide adequate exposure 

to the entire abdomen, has a lower dehiscence rate, and is generally the accepted approach for elective 

operations.103 While this is true for elective operative cases, many surgeons would argue for an alternative 

incisional approach in the case of traumatic injury.104 A midline laparotomy allows for supraceliac aortic 

control as well as iliac control with minimal changes in retraction (Fig. 17).104 The approach should be 

dependent upon the mechanism and severity of the injury, as well as the hemodynamic instability of the 

patient. 

Pediatric surgeons favor splenic salvage whenever possible. An important point in splenic preservation is 

complete mobilization of the spleen prior to addressing the hilum. The goal is to spare at least 30 percent 

of the spleen for immunologic function, as less than that will not yield a benefit.105 Also, it is important to 

Figure 17. Laparotomy in a 5-year-old male performed through a midline incision. A midline laparotomy allows for supraceliac aortic control as well 

as iliac control with minimal changes in retraction. Image courtesy of the Borden Institute, Office of The Surgeon General, Washington, DC.
562 | Pediatric Trauma

remember that associated injuries (especially head) 

represent relative contraindications to attempting 

nonoperative splenic preservation.

When dealing with a liver injury, the decision 

whether to pack or repair the injury is critical. 

Some advocate that this decision should be delayed 

until the liver has been fully mobilized. This 

requires division of both triangular ligaments as 

well as the falciform ligament from their respective 

diaphragmatic attachments. Only then can adequate 

compression be applied and the decision to pack 

versus repair be made. However, others are in favor 

of preserving ligamentous attachments to achieve 

more effective packing. If repair is attempted, 

blood flow to the liver needs to be temporarily 

controlled in order to prevent overwhelming blood 

loss.106 The correct size of vascular clamps is not 

always available in the pediatric-aged population, 

thus Rummel tourniquets are extremely helpful to 

control the portal hilum as well as the hepatic veins, 

retrohepatic cava, and inferior vena cava in order to 

achieve complete vascular isolation of the liver. 

While the surgical approach to retroperitoneal injuries (pancreas, duodenum, aorta) represents a chapter 

in and of itself, the following principles hold true. Prior to entering a zone I (central) retroperitoneal 

hematoma, vascular control of the aorta and vena cava, respectively, needs to be achieved (Fig. 18). For 

any central hematoma involving the duodenum or pancreas, a full Kocher maneuver to elevate the head 

of the pancreas and to inspect the posterior duodenum needs to be performed. This will assist in vascular 

control and allow for complete inspection of the head of the pancreas and duodenum. Finally, for all 

injuries requiring surgery for the pancreas and/or duodenum, wide drainage should be employed before 

closing the abdomen.

For traumatic injuries of the pancreas involving ductal disruption, there has been support for a nonoperative 

approach.107 Operative intervention will necessitate full hospital and ancillary support (e.g., parenteral 

nutrition), prolonged hospitalization, and interventional radiology support to address complications.108 If 

resources are at a premium, major pancreatic ductal disruptions need to be surgically corrected either with 

distal pancreatectomy or a Whipple procedure depending upon injury location. There has been a recent 

case report of a minimally invasive splenic preserving approach to pancreatic injury.109 It is the authors’ 

opinion that splenic preservation and a minimally invasive approach are not part of the algorithm for the 

operative management of severe pancreatic traumatic disruptions in a combat environment. The limited 

resources in most CCC environments make nonoperative management of such injuries difficult.

In the case of major penetrating duodenal injury, there is paucity in the literature of long-term outcomes or 

even large series in children. It is generally accepted that children tolerate primary duodenal repair better 

Figure 18. Zones of the retroperitoneum. Image courtesy of the Borden 

Institute, Office of The Surgeon General, Washington, DC.

Zone I

Zone II Zone II

Zone III
Pediatric Trauma | 563

than their adult counterparts, and this needs to be considered if the head of the pancreas is spared in 

the face of a duodenal injury. This approach will decrease the operative time and eliminate the need for 

future intervention. However in the authors’ opinion, when in a combat theater where total parenteral 

nutrition, intensive unit care, blood products, and preoperative factors such as the nutritional status and 

immunologic status of the patients are questionable, primary repair should either be avoided or performed 

in carefully selected patients. In the event of significant additional injuries (e.g., burns) that may affect 

healing, primary repair may give way to a more complex approach that involves isolation, exclusion, and 

drainage maneuvers that are well developed in adults.110 These include pyloric exclusion proximal to a 

duodenal repair and gastrojejunostomy or tube externalization of the duodenum, t-tube decompression 

of the biliary system, gastrostomy, and jejunostomy with or without antrectomy and establishment of 

gastrointestinal continuity.111

When encountering intestinal perforations, the decision to exteriorize the injury or primarily repair it has 

its evidence-based background embedded in military history. Once again, there is a lack of evidencebased literature in children, so our practice relies on the adult experience. The state of the art has gone 

from initial primary repair, to exteriorization of all colon injuries, to a physiologic basis for our operative 

decisions.112 The decision to perform colostomies or small intestinal stomas should be based upon the 

degree of hemodynamic instability, shock, and the presence of other injuries, rather than the degree of 

destruction of the colon or small intestine.113

Finally, the single most important decision when performing a trauma laparotomy is when and how to close. 

Deciding that any procedure is only for “damage control” is best done within the first 20 minutes of the 

procedure.114,115 Children, like adults, do not tolerate abdominal compartment syndrome. Unlike adults, 

the physiologic response in children is not one of gradual and progressive hemodynamic compromise 

(i.e., decreased urine output, development of hypotension, response to volume and pressors, and then 

continued deterioration). Children often develop increased intraabdominal pressure with less overt signs 

and symptoms and then unexpectedly suffer a major cardiorespiratory event.116 This may be due to the 

fact that abdominal compartment syndrome is underrecognized in children.

Monitoring of intraabdominal pressure and 

following a calculated splanchnic perfusion pressure 

has been useful in managing other models of 

abdominal compartment syndrome, specifically 

gastroschisis.44 The placement of silon sheeting 

has been the traditional approach to this problem 

in congenital anomalies.117 This is suboptimal in a 

traumatic situation where drainage and monitoring 

of the intraabdominal fluid has both diagnostic and 

therapeutic value. The development and use of the 

wound vacuum-assisted closure (V.A.C.®) devices 

or “trauma vac” have become a useful adjunct to 

control fascial contraction, allow for abdominal wall 

expansion, monitor for bleeding, manage fluids, 

and allow instant access for reoperation (Fig. 19).118

In addition, the concern of increased morbidity 

Figure 19. Pediatric damage control laparotomy following fragmentation 

injuries from an IED blast. Given the susceptibility of children to 

abdominal compartment syndrome, the abdominal wall was left open and 

covered with a wound V.A.C.®
564 | Pediatric Trauma

from bowel fistulization has not been born out in the recent literature.119 In the authors’ opinion, use of 

this system alleviates the need for constant intraabdominal pressure monitoring and should be employed 

liberally as part of the damage control procedure in children. In addition, one can achieve a V.A.C.®-

like closure with any sterile adhesive plastic drape, sponges, sterile plastic sheets, and a suction apparatus. 

These materials are typically available in a Combat Support Hospital.

The single most important decision when performing a trauma laparotomy is when and how to close 

the abdomen. Deciding that any procedure is only for damage control is best done within the first 20 

minutes of the procedure. 

Burn Care 

Differences in burn care for children versus adults 

are minimal and predominantly involve fluid and 

nutritional management (Fig. 20). For children 

less than 30 kg, glucose should be added to the 

intravenous maintenance fluids that are in addition 

to the amount of fluid replacement calculated 

based upon the Parkland or any other formula that 

is used.120 The body surface area burned is based 

upon second- and third-degree burns and can be 

estimated according to age-based charts.120 In 

general, the size of the child’s palm is equal to one 

percent of body surface area. 121

Both hyper- and hypoglycemia should be avoided. 

There is always a risk of over-resuscitating a patient 

with burn injuries when algorithmic fluid infusion 

and urine output alone are used to guide fluid replacement. Vital signs and hemodynamic parameters 

should also be utilized to determine the patient’s intravascular volume status. The development of 

conditions associated with over-resuscitation such as acute respiratory distress syndrome or abdominal 

compartment syndrome should be closely monitored. It is critical to avoid over-resuscitation in a combat 

environment while remembering that most burns encountered in a combat environment are almost 

always associated with blast injuries. Thus underlying muscle damage causing myolysis and eventual renal 

failure are accentuated with low urine output states. Early excision and grafting for all nonviable skin are 

recommended. When dealing with large volume surface area burns, care must be taken to preserve all 

viable skin surface. The availability of artificial skin barriers and temporary skin coverage may be limited 

and the only viable grafting material may be the patient’s surviving skin. Finally, transfer to a burn unit, 

while always the first option, may not be possible or available; thus, a clean environment needs to be 

established for the acute and chronic care of these patients. 

Differences in burn care for children versus adults are minimal and predominantly involve fluid and 

nutritional management. There is always a risk of over-resuscitating a patient with burn injuries when 

algorithmic fluid infusion and urine output alone are used to guide fluid replacement. Vital signs and 

hemodynamic parameters should also be utilized to determine the patient’s intravascular volume status.

Figure 20. Pediatric burn patient with injuries sustained from a civilian 

motor vehicle accident. The patient developed capillary leak syndrome, 

acute respiratory distress syndrome, and abdominal compartment syndrome.
Pediatric Trauma | 565

Neurosurgical Interventions

Forward Neurosurgical Care by Non-Neurosurgical Careproviders

Non-neurosurgical providers are increasingly tasked with the care of neurotrauma patients in a CCC 

environment. Unconventional warfare places children in harm’s way, where the combination of their 

natural curiosity, disproportionate head size, and lack of protective equipment can lead to tragic results. 

Local geography, weather, tactical considerations, medical rules of engagement, and limited subspecialty 

availability often conspire to bring these casualties to the door of facilities staffed with non-neurosurgical 

careproviders. Caring for these patients is resource intensive and emotionally taxing for all members of the 

health care team. It requires both a clear understanding of coalition and host nation medical capabilities 

and advanced preparation on the part of providers and facilities. 

While a complete review of forward neurosurgical care is beyond the scope of this chapter, careproviders 

should acquire technical and decision-making skills in neurotrauma prior to deployment. The training of 

non-neurosurgical personnel for this task is not a new concept, but surprisingly little progress has been 

made in this area since World War I.122 However, past successes in civilian settings both in the United 

States and elsewhere speak to the potential of this approach.123,124 Resources include formal courses,

informal courses by local neurosurgical providers, and self-education through literature review.125,126

While deployment may require a careprovider to reach into the periphery of clinical comfort zones, some 

lines are better not crossed. Each careprovider should carefully assess his or her ability to perform select 

critical neurosurgical interventions in a forward environment. Critical interventions include: (1) scalp 

closure; (2) ICP monitoring; and (3) limited craniectomy for extradural hemorrhage. Individual nonneurosurgical careproviders will need to decide whether they are competent to perform such procedures 

when clinically indicated in a forward environment. Palliative care remains a viable option for patients 

with devastating neurological injuries and is often the prudent course of action in a CCC environment 

with limited resources.

Non-neurosurgical providers are increasingly tasked with the care of neurotrauma patients in a CCC 

environment. Careproviders should acquire technical and decision-making skills in neurotrauma prior 

to deployment. Critical interventions include: (1) scalp closure; (2) ICP monitoring; and (3) limited 

craniectomy for extradural hemorrhage.

Additional Instruments Suggested Disposables

• Raney clip applier

• Hudson brace

• Disposable perforator bit (Codman®)

• Penfield dissectors #1, #4

• Leksell rongeur, large

• Kerrison rongeur, 3 mm or greater

• Adson cerebellar retractor

• Bipolar cautery unit (if available)

• Raney clips

• Gelfoam®

• ThrombinTM

• Surgicel®

• Bone wax

• 35 cm-ventricular catheter with trochar

• Lumbar drain catheter

• ICP monitor system

Table 7. Instruments typically available for neurosurgical interventions at a Level III facility.
566 | Pediatric Trauma

Local facility considerations are of paramount importance (Table 7). Medical rules of engagement, 

equipment availability, careprovider skill sets, imaging capabilities, and coalition and host nation 

medical assets all influence medical decision making in a deployed environment. Pediatric neurotrauma 

patients are particularly problematic from a disposition standpoint, as many resource-constrained 

nations are not equipped to provide supportive care for patients whose needs exceed the limited holding 

capabilities of deployed medical facilities. It is the responsibility of facility leadership to address these 

issues, prospectively if possible, and to ensure that care delivery does not place unsustainable burdens 

on host nation medical facilities. This may involve difficult ethical decisions that are among the most 

challenging aspects of deployment medical care.

Surgical Management of Head Injuries

The principles of caring for adult and pediatric neurotrauma patients are more similar than different. 

However, the assessment and management of pediatric neurotrauma patients do provide unique 

challenges in the delivery of care.

Triage and Initial Assessment

Good triage requires the timely consideration of pertinent clinical information about multiple casualties 

within the framework of resources available. In a deployed environment, this may result in decisions to 

delay or even withhold treatment that would be readily offered in a civilian environment. As host nation 

citizens, pediatric casualties must be treated with the intention to return them to host nation medical 

facilities within a timeframe that is compatible with the treating facility’s holding capacity and mission. 

Presenting neurologic status is consistently cited as a valuable tool in predicting outcome from both closed 

and penetrating head injuries.127,128 A complete, concise neurologic assessment is therefore invaluable to 

the triage officer in evaluating salvageability of casualties in a deployed environment. In the authors’ 

opinion, the presenting exam is the most valuable information available for determining prognosis of 

a casualty. For the exam to be valid, it must be obtained following appropriate resuscitation and in the 

absence of confounding medications including sedatives, hypnotics, analgesics, and muscle relaxants. 

This requires resuscitation to normotension, normothermia, and restoration of physiologic arterial 

oxygen and carbon dioxide pressures. 

Presenting neurologic status is consistently cited as a valuable tool in predicting outcomes following 

head injuries. For the exam to be valid, it must be obtained following appropriate resuscitation and 

in the absence of confounding medications including sedatives, hypnotics, analgesics, and muscle 

relaxants. 

On occasion, some patients may require administration of appropriate weight-based medication reversal 

agents and twitch-monitor assessment to ensure pre-facility medications do not interfere with a baseline 

exam (Table 8). Reversal of medications with antiepileptic properties (e.g., benzodiazepines) in the setting 

of head injury may precipitate seizure activity, which would further secondary brain injury. Alternative 

approaches include providing supportive care pending metabolism and elimination of confounding 

medications.

Pupillary exam is an important indicator of outcome in civilian closed and penetrating head injuries. In 

the setting of epidural hematoma, latency to treatment exceeding 90 minutes after the development of 
Pediatric Trauma | 567

anisocoria has been shown to correlate with dramatic increase in mortality.129 In penetrating injury, 

bilaterally fixed and dilated pupils have been shown to be highly predictive of mortality.130 Pupil 

responsiveness is an objective finding that is easily assessed regardless of patient age. A common 

misconception by careproviders is that muscle relaxants and paralytic medications (e.g., pancuronium) 

impair pupil responsiveness. They do not. Among medications frequently used during resuscitation in 

children, atropine and epinephrine are likely to impair pupillary responsiveness, with effects varying 

from minutes to several hours.131

GCS Pediatric GCS Infant FACE Scale

Eyes

1 No opening No opening No opening

2 Open to pain Open to pain Open to pain

3 Open to voice Open to voice Open to voice

4 Spontaneous Spontaneous Spontaneous

Verbal

1 No response No response No facial expression to pain

2 Incomplete sounds Inconsolable, agitated Grimaces to pain

3 Inappropriate words Inconsistently 

inconsolable

Cries to deep pain only

4 Confused Cries, consolable Cries to minor pain, alternating with sleep

5 Oriented Smiles, tracks 

appropriately

Cries to minor pain, alternating with wakefulness

Motor

1 No response No response Flaccid

2 Decerebrate Decerebrate Decerebrate

3 Decorticate Decorticate Abnormal rhythmic movements (seizure-like)

4 Flexion withdrawal Withdraws to pain Nonspecific movements to deep pain

5 Localization Withdraws to touch Hypoactive spontaneous movements

6 Follows commands Purposeful Normal spontaneous movements

Table 9. Modified scales of neurologic assessment in pediatric patients.

Weight-Based Dosing of Reversal Agents

• Neostigmine (50 micrograms [mcg] per kilogram)

• Glycopyrrolate (10 mcg per kilogram)

• Naloxone (0.1 mg per kilogram)

• Flumazenil (10 mcg per kilogram)

Table 8. Weight-based dosing of agents to assist with pharmacologic reversal of 

sedation/paralysis.
568 | Pediatric Trauma

Pupillary responsiveness is an objective finding that is easily assessed regardless of patient age and is an 

important indicator of outcome. Muscle relaxants and paralytic medications (e.g., pancuronium) do not 

impair pupillary responsiveness.

The Glasgow Coma Scale (GCS) is a highly effective tool in the assessment of neurotrauma patients. 

Developed to improve communication about the neurologic state of comatose patients, the GCS is an 

excellent predictor of neurologic outcome in head-injured patients.132,133 Glasgow Coma Scale scores in 

preverbal children are more problematic due to immature motor pathways and limited or absent verbal 

skills on an age-related continuum. Alternative grading scales such as the pediatric GCS or Infant FACE 

Scale should be utilized in these patients (Table 9).134

Glasgow Coma Scale scores in pre-verbal children are problematic due to immature motor pathways 

and limited verbal skills. Alternative grading scales include the pediatric GCS or Infant FACE scales.

Neuroimaging, when available, is another valuable 

tool for patient triage. Computed tomography 

(CT) scanners are currently available at Level III 

facilities in both Afghanistan and Iraq (Fig. 21). 

Reliable forward imaging technology has been a 

major advance of the past decade. The Traumatic 

Data Coma Bank Classification Scale identified 

two findings that were consistently predictive of 

worsened neurologic outcome: compression or 

absence of patent basal cisterns and degree of 

midline shift (Fig. 22).135 Additional anatomic 

information regarding relative distribution 

(lateralized versus diffuse pathology), location 

(intradural versus extradural and frontal/

temporal/parietal), and reversibility of injuries 

can also be determined for both adult and 

pediatric patients by cranial CT. In the clinically unstable patient, ICP monitoring can also be used as 

a triage tool. Uncontrolled intracranial hypertension has been associated with a high rate of mortality 

and poor neurologic outcome.136 Unstable patients undergoing emergent laparotomy/thoracotomy with 

suspected severe head injuries can undergo simultaneous ICP monitor placement, facilitating decisions 

on cessation of clinical efforts for overwhelming injuries. The authors employed the following algorithm 

in the management of pediatric head trauma patients in 2007 at a Level III facility with neurosurgical 

support and a two-week patient holding capacity (Table 10).

Repair of Scalp Injuries

Early and aggressive treatment of scalp injuries is perhaps the most important technical skill for 

careproviders to acquire in the management of the forward head-injured patient (Fig. 23). Adequate 

exposure of injuries is essential, and aggressive shaving of the scalp is often required to fully identify what 

are frequently multiple injuries (Fig. 24). The value of routine practice of shaving scalp wounds has been 

questioned, and civilian studies have linked routine preoperative skin shaving with increased infection 

Figure 21. CT scanners are currently available at Level III facilities in 

both Afghanistan and Iraq.
Pediatric Trauma | 569

Figure 22. (Top Left) Axial image demonstrating the pentagon-shaped suprasellar cistern. (Top Right) Axial image demonstrating the ‘smile’-shaped 

quadrageminal plate cistern. Normal head CT demonstrating patency of basal cisterns in the setting of normal ICP. These small-volume spinal fluid 

spaces are excellent indirect markers of ICP. (Bottom Left) Despite trajectory of fragment across the midline and ventricular system, no midline shift 

is present and the basal cisterns remain patent. The patient required limited debridement only and was discharged from the hospital on post-injury day 

four. (Bottom Right) In this patient who suffered a blast-related injury, marked midline shift is present with effaced basal cisterns. Palliative care was 

elected, and the patient expired. 
570 | Pediatric Trauma

Figure 23. Local advancement flaps to address scalp defect: (Left) One-year-old female with midfrontal penetrating fragment head injury. (Right)

Opposing advancement flap closure of scalp defect performed after wide local shaving, exposure, and management of intracranial injury.

1. Assess Pupils

• Palliative care if bilateral fixed and dilated pupils or unilateral fixed and dilated pupils documented for 

greater than 90 minutes without signs of direct trauma to the globe

2. Perform GCS Score or Age-Equivalent Assessment

• GCS scores 9 to15 mandate aggressive intervention

• GCS scores 6 to 8 consider intervention based on available resources. Imaging helpful in 

identifying favorable prognosis

• GCS scores 3 to 5 indicate palliative care

3. Review imaging if available

• Favorable prognosis: Basal cisterns patent, less than 1 centimeter midline shift, focal extraaxial 

mass lesion

• Unfavorable prognosis: Basal cisterns effaced, greater than 1 centimeter midline shift, intraaxial 

hemorrhage, diffuse injury pattern

Table 10. Suggested algorithm for neurosurgical triage at Level III facilities.
Pediatric Trauma | 571

rates.137,138,139,140,141 In civilian practice, routine scalp shaving has given way to clipping, cutting hair with 

scissors, or using lubricant gel to congeal and move hair away from wound margins. The complex wound 

patterns seen in combat and difficulty identifying multiple scalp injuries are cited as reasons for shaving 

of the scalp to enable better wound bed visualization. 

Early and aggressive treatment of scalp injuries is perhaps the most important technical skill for 

careproviders to acquire in the management of the forward head-injured patient. 

Judicious debridement techniques, identifying 

vascular pedicles, simple rotational and 

advancement flap techniques, and two-layer 

closure techniques (galea and skin) can be rapidly 

learned by all clinicians with even limited surgical 

skill. Excellent reviews of these techniques are 

readily available in the literature.142 Scalp closure 

alone, as opposed to more extensive cranial 

operative intervention, is often the primary surgical 

intervention required to manage patients with lowvelocity, fragmentary (e.g., shrapnel) penetrating 

head injuries.143 For example, Taha et al. found 

that 32 such patients with a GCS score of 10 or 

higher, entry wounds less than two centimeters in 

size, and treated within six hours of injury who had 

negative CT scans for intracranial bleeding, did well 

with scalp wound closure alone in the emergency 

department.143

Pediatric patients with limited circulating blood 

volume are highly susceptible to hypovolemic 

shock from scalp injuries. Beyond common-sense 

measures such as the application of pressure, 

management of scalp lacerations associated with 

closed head injuries can be facilitated by the use of 

local vasoconstricting agents such as Xylocaine® 

(0.5% lidocaine with epinephrine 1:100,000), with 

weight-based lidocaine with epinephrine dosing not to exceed 7.5 mg per kilogram. Use of lidocaine in 

penetrating head injuries should be tempered by the potential for subarachnoid infusion with seizure 

induction. Simple hemostatic devices can also be utilized. Raney clips are widely available within surgical 

sets at Level III facilities (Fig. 25). They are of lower utility in infants and toddlers due to limited scalp 

thickness in these patients. Another technique is the application of Dandy clamps (hemostats) along the 

galea with the application of upward traction or reflection of the clamps outward. 

With smaller circulating blood volumes, pediatric patients are highly susceptible to hypovolemic shock 

from scalp injuries.

Figure 24. Aggressive shaving of the scalp allows for identification and 

exposure of all injuries and is essential in the management of wartime 

penetrating head injuries.
572 | Pediatric Trauma

Intracranial Pressure Monitoring 

Intracranial pressure monitors and intraventricular drainage catheters are powerful tools that provide 

valuable diagnostic information and therapeutic benefits for head-injured patients. Both parenchymal 

and fluid-coupled systems are currently available in the US military medical supply system (Fig. 26). 

The Codman® ICP EXPRESS (Codman, USA) is the standard intraparenchymal monitoring system 

utilized, while several vendors have 35-centimeter ventricular catheters with trochars available. Insertion 

techniques for these systems are easily taught to careproviders with basic surgical skills, and relative 

complication rates for insertion are low.144 In the authors’ experience, infection rates for intraventricular 

catheters placed in a field environment are high, and the choice for insertion of these catheters over 

parenchymal monitors should be weighed carefully. Appropriate indications for intraventricular catheter 

placement include management of refractory intracranial hypertension and spinal fluid leak.39

Intracranial pressure monitors and intraventricular drainage catheters are powerful tools that provide 

valuable diagnostic information and therapeutic benefits for head-injured patients. Insertion techniques 

for these systems are easily taught to careproviders with basic surgical skills, and relative complication 

rates for insertion are low.

While anatomic landmarks for insertion are identical to those used for adult patients, differences in scale 

between the two populations can lead to errors in the choice of insertion site resulting in preventable 

complications. The coronal suture is readily palpable in infants and toddlers. It is essential that the 

monitor or catheter be placed at or in front of this landmark and a minimum of two centimeters off of 

the midline to avoid the motor cortex and superior sagittal sinus, respectively (Fig. 27). The lateral edge 

of the anterior fontanelle is an acceptable point of entry in very young children. Regardless of patient 

age, parenchymal monitors should be placed to a depth of one to two centimeters. Ventricular catheters 

are inserted to depths along an age-based continuum: three to four centimeters in infants, four to five 

centimeters in toddlers, and five to six centimeters in older children and adults. When used for CSF 

drainage, replacing the volume removed (5 to 10 ml per hour on average) with 0.9% NaCl + 20 mEq KCl 

per liter to avoid hyponatremia and hypokalemia from solute loss in CSF has been recommended.145 

Figure 25. Application of Raney clips to the scalp and galea is a valuable 

technique for hemostasis in the surgical management of head injuries.

Figure 26. Intracranial pressure monitoring systems can readily be inserted 

in an austere environment to assist with the diagnosis and management of 

the head-injured patient.
Pediatric Trauma | 573

Management of Skull Fractures

Treatment of fractures along the skull convexity in a forward environment is limited to the care of 

associated injuries. Closed skull fractures without significant neurologic impairment such as so called 

ping-pong fractures in infants or minimally depressed fractures do not require specific treatment in a CCC 

environment (Fig. 28). Closed fractures are often encountered in combination with underlying intradural 

and extradural hemorrhage. Under those circumstances, surgical management may be appropriate as 

discussed later (see Management of Intradural and Extradural Hemorrhage).

Open skull fractures require irrigation and judicious debridement to remove devitalized tissue and reduce 

risks of infection. In the current environment of counterinsurgency warfare (OEF and OIF), most of 

these injuries are the result of low-velocity projectiles. Aggressive debridement and watertight dural 

closure were advocated in the past.146 This form of management is unnecessary for most low-velocity 

projectile injuries encountered in OEF and OIF. Long-term follow-up of patients who underwent wide 

margin, aggressive debridement of embedded bone fragments has not been demonstrated to reduce 

infection and is technically more challenging for non-neurosurgical providers.147 Attempts at watertight 

Figure 27. Landmarks for insertion of intracranial monitoring systems. The drill hole should be placed two centimeters off of midline, just anterior to 

the coronal suture, to avoid the superior sagittal sinus and motor strip. In children over the age of five, the average distance posterior to the nasion is nine 

centimeters.

Age-based depth

Three to six centimeters

Landmarks for ICP monitor placement

Superior sagittal sinus

Coronal suture

Motor strip

2

cm.

X

9 cm.
574 | Pediatric Trauma

dural closure can add significant time to the surgical intervention, and in the authors’ opinion, is not 

required for supratentorial injuries. Onlay dural substitutes (DuraGen® Dural Graft Matrix, Integra 

Neurosciences) are widely available for the coverage of these injuries. Complete coverage of any dural 

defect with this material followed by meticulous scalp closure is acceptable in such patients. 

Open skull fractures require irrigation and judicious debridement to remove devitalized tissue and 

reduce infection risk. Antibiotic administration following open fractures with embedded fragments 

is controversial, and no standard guidelines regarding either choice or duration of antibiotic therapy 

exist.

Antibiotic coverage for open fractures with embedded fragments is controversial. No standard guidelines 

regarding either choice or duration of antibiotic therapy exist.130 The presence of both gram-positive and 

gram-negative organisms in abscesses resulting from penetrating head injuries has resulted in widespread 

use of broad-spectrum coverage for three days to two weeks by some practitioners.148 Single agent grampositive antibiotic therapy has been shown to be effective in reducing wound infection rates following open 

skull fractures.143 In the authors’ experience, patients receiving prompt care with debridement and layered 

closure without subsequent CSF leakage did well with a single dose of an appropriately selected antibiotic 

(based on local resistance patterns) against skin flora. 

Fractures or penetration of the anterior or lateral skull base carry additional risks of spinal fluid leakage 

and subsequent infection (Fig. 29).149 Pediatric patients harbor a lower risk of spinal fluid leakage from 

Figure 28. (Left) Linear skull fracture. (Right) Ping-pong fracture.
Pediatric Trauma | 575

injuries to the anterior cranial fossa due to age-related pneumatization of the paranasal sinuses, which

is complete by the mid-teens.150 When CSF leaks do occur, conservative management through head 

elevation is advocated. Inflammation following the initial injury may result in closure of a persistent CSF 

fistula; therefore, time may be all that is needed in this circumstance. In the authors’ opinion, prophylactic 

antibiotics for spinal leaks should be avoided, since it may increase the risk of selecting out resistant 

organisms without any known benefit. Refractory spinal fluid leaks in pediatric patients are not acute 

medical issues and require subspecialty consultation for management with a trial of lumbar drainage or 

surgical management by craniotomy and/or sinus exenteration. While leptomeningeal cysts or growing 

Figure 29. Penetrating injuries involving the anterior skull base: (Top 

Left) Vertex view of the scalp in a child impaled with rebar rod. Note 

the site of penetration and mild proptosis of the right eye. (Top Right)

Coronal CT reconstruction demonstrating penetrating injury extending 

through the right frontal bone, orbital roof, and maxilla. (Bottom Right)

Intraoperative photograph following right frontal craniotomy demonstrating 

penetration of the floor of the anterior cranial fossa.
576 | Pediatric Trauma

skull fractures can result from open fractures with dural disruption in infants and toddlers, they are a more 

chronic concern that is beyond the scope of deployed medical elements.151

Fracture or penetration of the anterior or lateral skull base carries an additional risk of CSF leakage 

and subsequent infection. Cerebrospinal fluid leaks are conservatively managed. Refractory CSF leaks 

in pediatric patients are not acute medical issues and require subspecialty consultation for management 

with a trial of lumbar drainage or surgical management by craniotomy and/or sinus exenteration.

Management of Intradural and Extradural Hemorrhage

Indications for performance of a limited craniotomy 

or craniectomy by a non-neurosurgical provider 

on a pediatric patient in a deployed environment 

are limited. The treatment of intradural injuries 

(e.g., subdural hematoma and intraparenchymal 

hemorrhage) requires advanced surgical training 

and clinical experience (Fig. 30). The surgical 

management of such injuries is beyond the scope 

of practice of forward non-neurosurgical CCC 

providers. On occasion, events may conspire to 

place a well-prepared careprovider in the presence 

of an acutely deteriorating patient with clinical or 

radiologic findings supportive of an underlying 

epidural hematoma (Fig. 31). A clinically significant 

extradural hemorrhage is one form of injury 

likely to benefit from surgical intervention by 

non-neurosurgical careproviders under these 

circumstances.152

Techniques for expedient craniotomy/craniectomy are similar between pediatric and adult patients. 

Patients are positioned supine with a bolster under the ipsilateral shoulder and hip with the head in a gel 

roll or equivalent. Generous hair removal assists with visualization of landmarks. Scalp opening should be 

well controlled and minimized to reduce blood loss. In the case of image confirmed epidural hemorrhage, 

placement of a burr hole over the site of injury followed by enlargement with rongeurs is both technically 

easier to accomplish and more expedient than turning a bone flap (Fig. 32). Exploratory burr holes can 

be performed with enlargement if a bloodclot is identified at the operative site. Complete removal of 

the hemorrhage is not essential; decompression of the hemorrhage is usually sufficient to resolve acute 

neurologic changes. Use of a Hemovac® or Jackson-Pratt® drain under the scalp is useful to prevent 

blood reaccumulation.

Spinal Injuries

Closed Injuries

Management of closed pediatric spinal injuries in a deployed environment is primarily nonoperative. 

While spinal instrumentation and intraoperative fluoroscopy are available at select deployed facilities, 

Figure 30. Intradural neurotrauma surgery poses significant operative 

challenges to the inexperienced careprovider.
Pediatric Trauma | 577

most injuries can be managed locally with more modest resources. The majority of closed spinal column

injuries are biomechanically stable. In a neurologically intact patient, upright and weight-bearing films 

can establish the stable nature of these injuries. For the patient with neurologic impairment or unstable 

fracture, forward facilities are poorly equipped to deal with short- or long-term issues faced by these 

patients. Realistic goals include restoration of anatomic alignment and immobilization. 

Management of closed pediatric spinal injuries in a deployed environment is primarily nonoperative. 

Forward facilities are poorly equipped to deal with short- or long-term issues faced by patients with 

neurologic impairment or unstable fractures. Realistic goals include restoration of anatomic alignment 

and immobilization. 

Gardner-Wells tongs are available in surgical sets for Level III facilities; they are a low-cost means of 

obtaining or maintaining alignment in the cervical spine (Fig. 33). In children older than two years of 

age, application is identical to adult patients. When utilized appropriately, torque application should not 

result in penetration of the skull in these patients.153 In the authors’ experience, less weight is generally 

required to achieve reduction: two pounds (lbs) per level compared to five to 10 lbs in adult patients. 

Immobilization can be achieved with bedrest for thoracolumbar fractures, or with appropriately-sized 

commercial collars for cervical spine fractures. In the absence of appropriate collar sizes, field-expedient 

Figure 31. Epidural hematoma: (Top Left) In the patient harboring an 

epidural hematoma, impaired neurologic examination including pupillary 

asymmetry and GCS of 9 or less are independent predictors of poor 

outcomes. (Top Right) CT scan demonstrating a large right parietal 

epidural hematoma in a toddler. Note the mixed density of the collection 

indicative of active hemorrhage and marked midline shift. (Bottom Left) 

Intraoperative image demonstrating a large epidural hematoma following 

removal of the overlying calvarial bone.
578 | Pediatric Trauma

Figure 32. Damage control craniectomy. Extradural hemorrhage localized or extending into the middle cranial fossa is an ideal indication for this 

procedure. (Top Left) The scalp incision extends from the root of the zygoma toward the frontal hairline. The incision extends through the underlying 

temporalis fascia to expose the lateral surface of the middle cranial fossa. (Top Right) Schematic of burr hole sites for middle fossa craniectomy. Note 

location of posterior-inferior burr hole immediately above the zygomatic root. Craniectomy proceeds between burr holes and extends anteriorly along the 

greater wing of the sphenoid as indicated. (Bottom Left) Burr hole placed by a non-neurosurgical provider. Note fracture line that resulted in underlying 

intracranial injury. (Bottom Right) Image following completion of craniectomy and evacuation of local epidural hemorrhage. This craniectomy is 

ideally located low in the middle cranial fossa resulting in relief of brainstem compression along the medial aspect of the affected temporal lobe.
Pediatric Trauma | 579

Figure 33. (Left) Gardner-Wells tongs are a simple device capable of 

assisting with the stabilization and reduction of cervical spinal column 

injuries.

Figure 34. (Below) Thecal sac ligation following penetrating injuries to 

the spine. Blast injuries can result in massive tissue loss with devastating 

injuries to the spinal axis and thecal sac. In this case, an IED blast 

caused extensive destruction of the dorsal elements of the lumbar spine and 

dura. The ventral surface of the dura is indicated by the arrow. A staged, 

collaborative surgical approach allowed for ligation of the thecal sac to 

prevent spinal fluid leak, staged debridement, and spinal stabilization and 

flap-assisted wound closure.
580 | Pediatric Trauma

collars can be custom contoured with SAM® SPLINTS or other materials. Pediatric-sized halo vests 

are rarely available in a deployed environment. In the exceptional case that an appropriately-sized vest 

is available, application differs from adult patients in the number of pins used and torque applied.154 Six 

to eight pins with an applied torque of four inch-pounds (in-lbs) are sufficient to secure the halo ring in 

children aged two through eight years of age. Adult application guidelines can be used in children age nine 

and above. 

Penetrating (Open) Injuries

The acute management of penetrating injuries of the spine mirrors that of adult patients with these 

injuries. Depending on the trajectory of the projectile, abdominal and thoracic injuries are addressed 

first. Antibiotic therapy is tailored to the individual needs of injuries in these adjacent compartments. 

Penetrating injuries rarely produce acute spinal instability; however, children with neurologic impairment 

are at high risk for developing late spinal deformity.155,156 Such concerns are beyond the capabilities of 

forward CCC providers. 

The acute management of penetrating injuries of the spine mirrors that of adult patients with similar 

injuries. Depending on the trajectory of the projectile, abdominal and thoracic injuries are addressed 

first. Penetrating injuries rarely produce acute spinal instability. Local debridement and wound closure are 

appropriate at the time of presentation. Massive injuries with extensive tissue loss and spinal cord avulsion 

are best managed through ligation of the thecal sac.

Local debridement and wound closure are appropriate at the time of presentation. Cerebrospinal fluid 

fistulae, either externally or into adjacent cavities such as the thorax, are infrequent but challenging 

problems. Massive injuries with extensive tissue loss and spinal cord avulsion are best managed through 

ligation of the thecal sac (Fig. 34). In injuries with less tissue destruction, visualization of the leak is more 

limited. It is the authors’ opinion and experience that local tissue patch with external spinal fluid diversion 

is a rapid and technically less demanding option for these patients. Lumbar drainage systems are available 

through the military supply system and are an invaluable adjunct for such patients. Catheters can be placed 

at the time of exploration, or percutaneously by anesthesia providers at the L4 to L5 interspace when the 

fistula is recognized in patients as young as two years of age. It is the authors’ opinion and experience that 

height-controlled drainage of 10 to 15 ml per hour is usually sufficient to stop the flow of spinal fluid with 

closure of the fistula within 72 hours in most cases.

End-of-Life Care 

While children are very resilient, there are times when enough is enough and it is more appropriate to halt 

the resuscitation or to recognize that certain wounds are not treatable and further care is futile. In these 

circumstances, treatment should be focused on providing the appropriate level of pain relief and comfort. 

It is often very hard for practitioners to recognize when care is futile in children since the death of a child 

is a very emotional event. The medical team needs to remain objective and truly balance the benefits 

and risks of treating certain injuries with providing comfort care if the wounds are lethal or severely 

neurologically debilitating. Balancing what you can do for a child with what can be handled medically in 

the host nation is a very difficult task, but this dichotomy must be recognized. 
Pediatric Trauma | 581

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147. Amirjamshidi A, Abbassioun K, Rahmat H. Minimal debridement of simple wound closure as 

the only surgical treatment in war victims with low-velocity penetrating head injuries: indications and 

management protocol based upon more than 8 years follow-up of 99 cases from Iran-Iraq conflict. Surg 
Pediatric Trauma | 591

Neurol 2003;60(2):105-111.

148. Carey ME, Young H, Mathis JL, et al. A bacteriological study of craniocerebral missile wounds from 

Vietnam. J Neurosurg 1971;34(2 pt 1):145-154.

149. Arendall RE, Meirowsky AM. Air sinus wounds: an analysis of 163 consecutive cases incurred in the 

Korean War, 1950-1952. Neurosurgery 1983;13(4):377-380.

150. Fatu C, Puisoru M, Rotaru M, et al. Morphometric evaluation of the frontal sinus in relation to age. 

Ann Anat 2006;188(3):275-280.

151. Singhal A, Steinbok P. Operative management of growing skull fractures: a technical note. Childs 

Nerv Syst 2008;24(5):605-607.

152. Rosenfeld JV. Damage control neurosurgery. Injury 2004;35(7):655-660.

153. Lerman JA, Dickman CA, Haynes RJ. Penetration of cranial inner table with Gardner-Wells tongs. J 

Spinal Disord 2001;14(3):211-213.

154. Arkader A, Hosalkar HS, Drummond DS, et al. Analysis of halo-orthoses application in children

less than three years old. J Child Orthop 2007;1(6):337-344.

155. Waters RL, Sie IH. Spinal cord injuries from gunshot wounds to the spine. Clin Orthop Relat Res 

2003;408:120-125.

156. Lancourt JE, Dickson JH, Carter RE. Paralytic spinal deformity following traumatic spinal-cord 

injury in children and adolescents. J Bone Joint Surg Am 1981;63(1):47-53.
592 | Pediatric Trauma
Chapter 12

ACUTE BURN CARE

Contributing Authors

Evan M. Renz, MD, FACS, LTC(P), MC, US Army

Leopoldo C. Cancio, MD, FACS, COL, MC, US Army
All figures and tables included in this chapter have been used with permission from Pelagique, LLC, the 

UCLA Center for International Medicine, and/or the authors, unless otherwise noted.

Use of imagery from the Defense Imagery Management Operations Center (DIMOC) does not imply or 

constitute Department of Defense (DOD) endorsement of this company, its products, or services.

Disclaimer

The opinions and views expressed herein belong solely to those of the authors. They are not nor should 

they be implied as being endorsed by the United States Uniformed Services University of the Health 

Sciences, Department of the Army, Department of the Navy, Department of the Air Force, Department of 

Defense, or any other branch of the federal government.
Acute Burn Care | 595

Table of Contents

Introduction........................................................................................................ 596

Combat versus Civilian Burns ............................................................................... 597

Initial Evaluation and Management ....................................................................... 598

Primary and Secondary Survey.......................................................................................599

Patient Inspection and Decontamination........................................................................600

Airway and Breathing Interventions................................................................................601

Comorbid Life-Threatening Injury Care..........................................................................603

Burn Wound Evaluation and Patient Resuscitation................................................... 603

Estimating Depth of Burns...............................................................................................604

Estimation of Burn Severity ..............................................................................................606

Burn Location....................................................................................................................606

Initial Fluid Resuscitation................................................................................................607

Modified Brooke Formula..................................................................................................609

Complications of Burn Injury ..........................................................................................611

Abdominal Compartment Syndrome ................................................................................611

Traumatic Rhabdomyolysis ...............................................................................................612

Electrolyte Disturbances ....................................................................................................612

Escharotomy and Fasciotomy ............................................................................................613

Initial Wound Care ...........................................................................................................615

Patient Exposure and Hypothermia ..................................................................................616

Pain Control.......................................................................................................................617

Advanced Burn Wound Care ............................................................................................617

Wound Excision .................................................................................................................617

Tangential Excision.........................................................................................................619

Fascial Excision..............................................................................................................619

Skin Grafting......................................................................................................................621

Harvesting of Skin..........................................................................................................622

Meshed Skin Grafts.........................................................................................................623

Full-Thickness Skin Grafts..............................................................................................625

Engraftment ...................................................................................................................625

Infection Control...............................................................................................................626

Metabolic and Nutritional Considerations......................................................................627

Aeromedical Transport and Definitive Care ...................................................................628

Summary ..........................................................................................................................629

References .......................................................................................................... 631
596 | Acute Burn Care

Introduction

The harsh cruelty of war, as witnessed by those 

who treat the wounded, would be intolerable if it 

were not for the belief that the art of medicine is 

advanced with each lesson learned. In order to pay 

proper respect to those who have suffered from their 

wounds, physicians must be dedicated to advancing 

and applying these lessons of combat casualty care 

(CCC) (Fig. 1).

Many of the lessons learned from Operation 

Enduring Freedom (OEF) in Afghanistan and 

Operation Iraqi Freedom (OIF) relate to problems 

that have existed as long as wars have been waged. 

Problems include: the remote and often austere 

environment in which the battle occurs; the presence, 

experience, and capability of CCC providers at 

each level of care; access to necessary supplies and 

equipment to implement care; the need to transport casualties expeditiously across dangerous terrain to a 

safe environment for further recovery; and the inevitability that innocents, too often children, will present 

among the wounded and require care.1

Children with severe burns are part of the reality of war, and their arrival at field hospitals should come 

as no surprise to anyone, least of all the surgeon. Care of pediatric burn patients should be anticipated.

The ultimate hope of all those associated with 

providing burn care is that prevention and safety 

programs will mitigate, if not minimize, thermal 

injury as a cause of mortality and morbidity. 

Unfortunately, military operations are often 

accompanied by sophisticated means of destroying 

the enemy, and explosives are often part of this 

equation. Despite methods of protection nearly as 

advanced as the weaponry, combatants on both 

sides are subject to the thermal effects of the tools 

of war. Such has been true for many decades, and 

recent events in Iraq and Afghanistan have proved 

to be no exception (Fig. 2).

Figure 1. Burn patients are frequently encountered in combat. This 

photograph demonstrates Iraqi burn patients on board the USNS Comfort 

hospital ship in 2003 in the Persian Gulf.

Figure 2. A host nation burn victim undergoing wound care at Balad 

AB, Iraq.
Acute Burn Care | 597

Combat versus Civilian Burns

Analysis of burn injuries sustained in the civilian United States (US) population compared to those observed 

in combat zones reveals both similarities and differences. Severe burn injury occurs in approximately 5 to 

10 percent of combat casualties.2 Casualties may sustain thermal injuries from a variety of mechanisms, 

including the explosion of incendiary devices, as well as the secondary fires that occur as nearby combustible 

materials ignite. However, in the austere environment of the overseas military post, the hazards associated 

with everyday life, such as burning refuse or refueling operations, also contribute to injury.3

Whether the injury occurs in a combat or civilian environment, the severity of burn is generally determined 

by the intensity of the thermal energy to which the patient is exposed, the duration of exposure, and the 

total body surface area (TBSA) burned. The pattern of injury for military casualties is also related to the 

protective equipment worn at the time of burn. Unless specifically working in an environment associated 

with high-risk thermal or chemical exposure, such as firefighting, most civilians are wearing everyday 

clothing at the time of burn. By contrast, military personnel routinely wear durable uniforms; body armor 

provides additional protection to the torso. Despite efforts to improve protection against burn injury for 

combatants, the face and hands continue to be the least protected, resulting in significant numbers of burns 

to these areas (Fig. 3).4

 

Burns involving the hands are common on the battlefield and are associated with devastating disability, 

making fire-resistant gloves essential gear for at-risk military personnel.

The civilian burn patient is generally assessed and treated near the place of injury by emergency medical 

services personnel. The patient is rapidly transferred by ground or air ambulance to the closest available 

medical facility, which may then transfer the patient to a regional burn center. The civilian patient is 

typically admitted to no more than two medical facilities during his or her hospital course. Although 

transport distances may be considerable for persons living in remote regions within the US, most civilian 

Figure 3. US soldier injured by a vehicle-borne improvised explosive device (IED) with fragmentation and burn injury to the face, torso, and extremities 

(following escharotomies). Note the escharotomy incision along the ulnar aspect of the hand has extended slightly deeper than intended through the fascia 

with protrusion of muscle.
598 | Acute Burn Care

burn patients can be transported from the site of 

injury to a definitive care facility within a few 

hours. In contrast, US military casualties are often 

transported to one or more intermediary facilities 

prior to final air evacuation over thousands of miles 

back to the US for definitive care.5,6 

Triage is an important consideration in military 

burn care. North American Treaty Organization 

(NATO) triage criteria define the expectant category 

as including patients in whom there are signs of 

impending death, or in whom there are injuries 

requiring an expenditure of resources exceeding 

those available.7

 The latter subset of expectant 

category triaged patients may include patients with 

burns of greater than 85% TBSA.8

 Sound clinical 

judgment is required to appropriately allocate 

resources during times of excessive patient influx.

Of note, young casualties with severe burns, even those with greater than 90% TBSA involvement may 

now survive to leave the hospital, provided rapid resuscitation and evacuation are available.9 Even the 

most severely burned combat casualty will likely tolerate evacuation back to the US to receive care, with 

the support of family and friends at his or her bedside (Fig. 4). Providers are encouraged to contact US 

Army Institute of Surgical Research (USAISR) Burn Center staff at Brooke Army Medical Center for 

advice and assistance should survivability become a factor in decisions concerning continuation of care or 

evacuation. Providers are encouraged to call (210) 916-2876 or DSN (312) 429-2876 to contact the burn 

center attending surgeon. Consultation may also be initiated by sending an email message (burntrauma.

consult@us.army.mil) to US Army Medical Department (AMEDD) burn consultants.

Young casualties with severe burns, even those with greater than 90% TBSA involvement, will usually 

tolerate long-range evacuation provided adequate resuscitative support is available, making expectant 

status rare for US casualties.

The process of caring for burn patients in a combat zone can also be complicated by the presence of 

multiple open wounds sustained in a dirty environment, combined with hemorrhage related to the injury. 

Operative intervention for lifesaving treatment or stabilization of concurrent injuries is not uncommon 

before the combat casualty is evacuated out of the theater of operations. Associated nonthermal trauma is 

more common in combat than in non-combat burn injury patients.6

 

Initial Evaluation and Management 

Perhaps the single most important lesson to learn when providing acute care for the burn casualty is to 

remember that burn patients are trauma patients. The visible nature of burn injury should not distract CCC 

Figure 4. US Army Burn Flight Team assists in rapid evacuation of 

severely burned combat casualties back to the US.
Acute Burn Care | 599

providers from the fact that the patient may have several other life-threatening injuries. This is particularly 

true when managing blast injury casualties (Fig. 5).6,10,11

Burn casualties are trauma patients, and as such deserve a complete evaluation for associated injuries 

beyond burn. Treat the patient, not the burn.

Primary and Secondary Survey

Successful treatment of burn patients starts with a thorough primary and secondary survey of the patient. 

In a combat zone this often requires a combined strategy of airway and breathing evaluation and protection 

and hemorrhage control. It is very easy for the careprovider unaccustomed to severe burns to become 

fixated on the horrendous tissue damage, particularly that involving the face (Fig. 6). Combat casualty 

care providers must resist becoming distracted by burn injuries and identify and manage immediately lifethreatening injuries, which are often less visually graphic in nature (e.g., airway edema and obstruction or 

internal hemorrhage from concurrent solid organ injury). 

The initial management of the combat burn casualty proceeds in a stepwise process as outlined by the 

Advanced Trauma Life Support (ATLS) guidelines of the American College of Surgeons Committee on 

Trauma, modified for the special needs of the burn patient. The principles described in the Advanced 

Figure 5. Combat casualty care providers must resist becoming distracted by burn injuries and identify and manage immediately life-threatening injuries, 

which are often less visually graphic in nature (e.g., airway edema and obstruction).
600 | Acute Burn Care

Burn Life Support (ABLS) curriculum sponsored by the American Burn Association (ABA) reflect these 

modifications.12 As an important example, the two-liter bolus of lactated Ringer’s solution described in 

ATLS is contraindicated in the hemodynamically stable burn patient, as this likely contributes to edema 

formation with no lasting benefit. 

Patient Inspection and Decontamination

Despite many improvements in military clothing and equipment, including fire-resistant uniforms, military 

burn casualties need to be disrobed just like any other trauma patient in order to fully examine them and 

ensure that thermal or chemical tissue injury is stopped. Chemical burn injury can occur when a patient 

comes in contact with an acid, base, or toxic organic compound. The incidence of chemical burn injury in 

OEF and OIF has been very low.11 Petroleum-based products are best removed with soap and water. Brush 

off any debris on a patient prior to irrigation. 

White phosphorous is an incendiary munition that is also found in civilian products such as fertilizers, 

fireworks, and pesticides. While rarely encountered in OEF and OIF, white phosphorous exposure can 

result in severe, combined thermal and chemical injuries. White phosphorous is extremely volatile and can 

ignite spontaneously upon exposure to air. In addition, phosphoric acids form during combustion and cause 

further tissue injury.13,14,15

Figure 6. This visually distracting and severe burn to a casualty’s head and neck region poses a significant immediate risk to the airway.
Acute Burn Care | 601

A Woods lamp can be used to identify embedded white phosphorous particles, which fluoresce under 

ultraviolet light. Treatment of patients with these embedded particles involves: (1) immediate debridement 

of visible debris; (2) copious irrigation; (3) coverage of exposed areas with saline or liquid-soaked gauze pads 

that must be kept wet; and (4) cardiac monitoring and serial measurement of serum electrolytes and calcium 

correction.13,14 Profound hypocalcemia, hyperphosphatemia, and sudden death have been associated with 

white phosphorous chemical injury.15

Careproviders must take precautions to ensure that they do not sustain injuries in their attempt to clean and 

treat the casualty. Standard universal precautions (i.e., face mask, gloves, and gown protection) should be 

routinely practiced. The location in which patient decontamination is performed needs to be individualized 

based on the nature of the chemical exposure and characteristics of the care facility. Providers need to 

minimize secondary contamination of patient care areas. In the authors’ experience, the combined thermal 

and chemical burn injuries most commonly encountered in OEF and OIF have not (thus far) routinely 

necessitated a separate area for patient decontamination.

Identify the cause of the burn and ensure that the thermal or chemical tissue injury process is stopped. 

Careproviders should use standard universal precautions when caring for patients with possible chemical 

agent injury, and prevent secondary contamination of patient care areas.

Electrical injuries deserve special mention as 

they typically cause a disproportionate degree of 

underlying deep tissue injury relative to visible burn 

injury to the skin.16,17 Electrical burns are most 

severe at the source of electrical contact (e.g., hands) 

and ground contact points (e.g., feet).18 As such, 

careproviders should carefully evaluate electrical 

burn patients for systemic complications and 

specifically for rhabdomyolysis and compartment 

syndromes.18

Airway and Breathing Interventions

Patients with facial burns or large surface area 

burns who receive a large volume of resuscitation 

often develop progressive upper airway edema 

in the first 48 hours following injury. This makes 

delayed intubation difficult, if not impossible. 

This distortion of upper airway anatomy is a 

consequence of massive anasarca and occurs 

even in the absence of inhalation injury.19 Early 

prophylactic intubation of patients with greater 

than 40% TBSA involvement or deep facial burns 

is recommended. Burn casualties, at risk for upper 

airway edema, who require long-range transport 

should have a definitive airway established prior to Figure 7. Fiberoptic laryngoscopy can be used to assess the upper airway 

for evidence of burn injury or edema.
602 | Acute Burn Care

movement between medical treatment facilities.20

Inhalation injury is relatively uncommon, being 

diagnosed in approximately 10 percent of burn 

injuries.21 Casualties with facial burns, large TBSA 

burn size, and those who are trapped within a 

burning vehicle or structure are those most at risk 

for inhalation injury.21 Clinical findings such as 

stridor or production of carbonaceous sputum 

should increase suspicion of inhalation injury, but 

are by no means definitively diagnostic.22 Fiberoptic 

laryngoscopy (if available) can be used to assess the 

upper airway for evidence of burn injury or edema 

in equivocal cases (Fig. 7). Patients suspected of 

suffering significant inhalation injury benefit from 

early airway protection by endotracheal intubation 

and subsequent support with mechanical ventilation. 

Figure 8. (Above) Circumferential burns to the chest may impair effective 

ventilation and should be treated with thoracic escharotomy.

Figure 9. (Right) Effective chest excursion was achieved after thoracic 

escharotomy in this pediatric burn patient.
Acute Burn Care | 603

As in the case of large burn size, the authors’ experience is that it is better to err on the side of earlier rather 

than later intubation of patients with inhalation injury.23

Treatment of life-threatening airway or breathing compromise and bleeding wounds takes priority over 

initial burn wound care. Prophylactic intubation of the patient with extensive burns or inhalation injury 

is advisable, especially if ongoing resuscitation is required. Protect the burn patient’s airway and establish 

effective ventilation in preparation for aeromedical evacuation.

Patients with inhalation injury should be intubated with the largest size endotracheal tube possible. 

Sloughing of tissue from the friable airway following inhalation injury, coupled with blood and secretions, 

may quickly occlude an endotracheal or tracheostomy tube. Larger-sized endotracheal tubes will mitigate 

this process and facilitate subsequent interventions (e.g., bronchoscopy). Interval suctioning of the airway 

is important. The use of aerosolized heparin alternating with aerosolized N-acetylcysteine in burn 

patients with inhalational injury requiring ventilatory support has been shown to decrease the incidence 

of reintubation for progressive respiratory failure, decrease atelectasis, and reduce mortality in adults and 

children with massive burn and inhalation injury.24,25 Fiberoptic bronchoscopy is also recommended to 

document extent of injury, as well as to remove large plugs under direct visualization.20

Patients who sustain circumferential burns of the chest, especially full-thickness burns resulting in a tight 

eschar, are at risk of respiratory impairment (Fig. 8). Effective chest excursion can be markedly impeded by 

thoracic eschar, resulting in hypercapnia, hypoxia, and respiratory arrest.26 Such patients require thoracic 

escharotomy (Fig. 9).

Circumferential burns involving the chest can impair ventilation and/or oxygenation due to reduced 

thoracic excursion. Thoracic escharotomy, performed at the bedside, can be a lifesaving intervention. 

Comorbid Life-Threatening Injury Care

The purpose of the primary and secondary trauma survey is to rapidly assess a combat casualty and identify 

and mitigate imminent threats to life. Combat casualties, including those with burns, are most likely to die 

within the first 24 hours from exsanguination related to a penetrating wound.27 Airway, breathing, and 

hemorrhage control must be addressed immediately in all casualties. Treatment of life-threatening airway 

or breathing compromise and bleeding wounds takes priority over initial burn wound care.

In addition to burn wounds, primary and secondary surveys of the casualty may reveal intraabdominal 

injuries as well as significant soft-tissue wounds and long-bone fractures, an observation noted among a large 

percentage of military burn casualties injured from explosions.28 Military personnel may also sustain burn 

injuries while traveling in moving vehicles attacked with improvised explosive devices (IEDs), mandating 

evaluation for blunt trauma, as well as for penetrating injuries. 

Burn Wound Evaluation and Patient Resuscitation

In a deployed environment, burn patients are routinely transported to the operating room not only for 

treatment of associated injuries, but also for debridement and dressing of all wounds. The operating room 
604 | Acute Burn Care

provides the most sterile environment available 

for such interventions (Fig. 10). The presence of 

anesthesia staff to provide pain control and sedation 

during debridement and dressing changes makes 

the operating room an optimal location for these 

procedures.10 

Estimating Depth of Burns

Burns are classically described as first-degree, 

second-degree (partial-thickness), or third-degree 

(full-thickness) in depth. First-degree burns affect a 

variable portion of the epidermis, feature erythema 

without extensive blistering, and heal within a few 

days. An example is a mild sunburn. For purposes 

of CCC (to include calculation of total burn size 

and fluid resuscitation needs), first-degree burns are 

of no consequence. Second-degree (partial-thickness) burns affect the entire thickness of the epidermis and 

a variable portion of the dermis. An example is a blistered scald burn. Because these burns spare the hair 

follicles and other epidermal analogs, they are capable of spontaneous healing. However, the healing time is 

highly variable. For this reason, second-degree burns are further subdivided into superficial second-degree 

burns (those that will heal with rapid reepithelialization and minimal scarring within 14 days) and deep 

second-degree burns (those that will heal after 14 days or more). Finally, third-degree (full-thickness) burns 

destroy the entire depth of the epidermis, dermis, and epidermal analogs. An example is a flame burn from 

gasoline, a house fire, or an IED. The burned skin may appear leathery, pale, or charred. These wounds are 

incapable of healing spontaneously, except by wound contraction, and almost always merit excision and 

Figure 10. The operating room provides the most sterile environment for 

debridement and dressing of burn wounds.

Degree of Burn Depth of Wound Wound Description

First Epidermis Pink or red, without blister formation; 

capillary refill and sensation intact

Second (partial-thickness)

 • Superficial partial-thickness Epidermis, papillary 

layer of dermis

Blistering of skin, exposed dermis is red 

and moist; capillary refill and sensation 

intact, painful

 • Deep partial-thickness Epidermis, papillary and 

reticular layers of dermis

Blistering of skin, exposed dermis is pale, 

white to yellow; capillary refill is absent, 

pain sensation is diminished

Third (full-thickness) All epidermal and 

dermal structures are 

destroyed

Charred, pearly white, or leathery 

appearance; capillary refill absent, 

insensate

Fourth Epidermis, dermis, fat/

muscle/bone

Variable appearance; thrombosed blood 

vessels, insensate

Table 1. Classification of burn depth.
Acute Burn Care | 605

grafting. The term fourth-degree burns is sometimes used to describe burns that affect even deeper layers, 

such as fat, muscle, and/or bone (Table 1 and Fig. 11). 

Accurate burn classification is needed to identify which burns require skin grafting to accelerate healing, 

improve cosmetic results, and prevent contractures. Time to healing and scar development is retrospectively 

used to grade burns that were not initially excised and grafted. Partial-thickness burns that heal prior to 

14 days are unlikely to scar, while those that take over 21 days to heal will likely scar and/or result in 

contractures (Fig. 12).

Accurate estimation of a patient’s burn size, expressed as the percentage of the TBSA burned, is the most 

important component in determining the severity of burn injury, and should be done in collaboration 

with consulting burn surgeons.

Clinical assessment of burn depth is fairly accurate for distinguishing first- and third-degree burns. 

Unfortunately, it is less accurate for determining which second-degree burns would benefit from immediate 

excision and grafting, and which will heal spontaneously within 14 days.29,30 Expert burn surgeons are 

only 60 to 75 percent accurate in correctly classifying partial-thickness burn depth and recovery potential 

at time of initial injury.30 To address this problem, a variety of standard (e.g., biopsy and histology) and 

advanced technologies (e.g., thermography, dye studies, laser Doppler imaging, noncontact high-frequency 

ultrasonography) have been used to assess tissue characteristics and/or perfusion as methods for 

determining burn depth. 

Figure 11. (Left) Schematic cross section of skin anatomy demonstrating 

layers involved with differing burn depths.

Figure 12. (Below) A severe hand burn, now with scarring and 

contractures. Early excision and grafting, followed by timely splinting and 

rehabilitation, are essential to prevent outcomes like this in the treatment of 

burns of the hands and across major joints.

epidermis

dermis

subcutaneous

tissue

muscle/bone

1st-degree

2nd-degree

3rd-degree

4th-degree
606 | Acute Burn Care

Combat casualty careproviders in OEF and OIF will need to make clinical assessments of burn depth in

collaboration with consulting burn surgeons. Burns that do not heal within 14 days following injury are 

likely to benefit from excision and grafting, as well as from advanced rehabilitation, to ensure optimal 

cosmetic and functional outcomes.

Estimation of Burn Severity

Accurate estimation of a patient’s burn size, expressed as the percentage of the TBSA burned, is the most 

important component in determining the severity of burn injury. Total body surface area burned is an 

important predictor of mortality (along with other factors including age, inhalation injury, and concurrent 

injuries). Total body surface area burned is the most important factor to consider when initiating burn 

resuscitation. The “Rule of Nines” is a commonly used, but relatively inaccurate, tool for estimating TBSA 

(Fig. 13).31 The Lund-Browder chart is a more accurate (but more time-consuming) tool for assessing and 

documenting the extent of burn injury that takes into account differences in patient age (Fig. 14).31

Burn Location

As previously noted, circumferential burns (e.g., thorax and extremities) are at high risk for compromising 

tissue perfusion. Full-thickness and partial-thickness burns to critical areas such as the face, ears, hands, 

feet, perineum, and genitalia are also considered high-risk injuries and require burn specialist consultation. 

In addition, full-thickness or partial-thickness burns over joint areas need careful follow-up evaluation and 

management to prevent contractures.

Figure 13. (Above) Estimation of body surface area using the Rule 

of Nines is relatively inaccurate. Image courtesy of the Borden Institute, 

Office of The Surgeon General, Washington, DC.

Figure 14. (Right) Estimation of body surface area using a LundBrowder chart is an accurate tool for assessing extent of burn injury.

9%

9%

18% 18%

9%

1%

18%

18%
Acute Burn Care | 607

Initial Fluid Resuscitation

Intravenous (IV) fluid resuscitation is typically required for all burn patients with greater than 20% TBSA 

involvement, and for some with greater than 10% TBSA involvement. Before any resuscitative fluids can 

be administered, IV access is required. Thermal burns often increase the difficulty of establishing and 

maintaining IV access. Problems include loss of normal landmarks, loss of skin pliability, and difficulty in 

penetrating the eschar with the catheter. Although it is preferable to establish IV access through unburned 

skin, access through burned skin is acceptable. When a peripheral IV catheter cannot be placed, central 

venous or intraosseous access should be obtained without delay.32

It is acceptable to establish IV access through burned skin, if necessary. When a peripheral IV catheter 

cannot be placed, central venous or intraosseous access should be obtained without delay.

Once adequate IV access is established, the catheter 

must be secured. The routine use of adhesive tape 

or transparent dressings does not work over burned 

skin. Securing the IV catheter to skin (or eschar) 

with sutures or surgical staples is a very effective 

method (Fig. 15). Redundant access (i.e., at least two 

IV catheters) is essential prior to transporting the 

patient, especially during the critical phase of burn 

resuscitation. 

Placement of a urinary catheter should be performed 

early during patient resuscitation, as urine output 

is an important indicator of the adequacy of 

resuscitative efforts. Burns to the genitalia and/

or the perineal region are not contraindications 

to Foley catheter placement. The CCC provider 

may need to remove eschar on the glans penis to 

visualize the urethral meatus to enable placing the 

catheter. This simple intervention is far superior 

to placement of a suprapubic catheter and the 

complications associated with inadvertent violation 

of the peritoneal cavity. 

One of the most challenging and controversial aspects of burn care continues to be providing optimal 

resuscitation during the initial 24 to 48 hours following injury.33 Severe burns lead to massive fluid shifts 

from the intravascular space to the interstitium in both burned and nonburned tissues. The hypovolemia 

caused by this shift and an increase in systemic vascular resistance leads to a reduction in cardiac output and 

decreased end-organ perfusion. Early volume replacement with crystalloid solutions to maintain adequate 

perfusion of vital organs reverses burn shock and can be lifesaving. Excessive fluid resuscitation, beyond the 

minimum required to maintain end-organ perfusion, exacerbates tissue edema, contributes to devastating 

complications such as abdominal compartment syndrome, and leads to increased mortality.34

Figure 15. An IV catheter is secured to the skin using sutures.
608 | Acute Burn Care

Figure 16. The standardized Burn Flow Sheet has improved documentation, communication, and outcomes following battlefield burn 

resuscitation. Image courtesy of the Borden Institute, Office of The Surgeon General, Washington, DC.

Pre-burn Est.

Wt (kg) %TBSA 1st 8 hrs 2nd 16th hrs 24 hr Total

Fluid Volume ACTUALLY received

Page 2 (24-48 hrs) Page 3 (48-72 hrs)

Pre-burn Est.

Wt (kg) %TBSA 1st 24 hrs 2nd 24 hrs 48 hr Total

Fluid Volume ACTUALLY received

[11] [13] [15] [16] [17] [18] [19] [20]

[14a]

[12]

[1] Date: Today's date

[2] Initial Treatment Facility: Where this form is initiated

[3] Name: Patient’s name

[4] SSN: Patient’s social security number

[5] Weight (Kg): Estimated weight PRE-BURN “dry weight”

[6] % TBSA: Total body surface area burned

[7] 1st 8 Hrs: 1⁄2 total calculated fluids per burn resuscitation

formula (ABLS), given over 1st 8 hrs post-burn

[8] 2nd 16 Hrs: Remaining 1⁄2 of the calculated fluids over the 

next 16 hrs

[9] Estimated Total Fluids: Total fluids calculated for the first 

24 hrs post-burn injury

[10] Time of Injury: Time the patient burned, NOT the time

patient arrived at the facility

[11] Treatment (Tx) Site/Team: Facility, CCATT or care team

providing care at specified hour

[12] Hour From Burn: “1st” hour is the first hour post burn. For 

example: pt arrives @ facility 3 hrs post-burn. Clinicians will

start their charting for the “4th” hour. Enter IVF & UOP totals

from level I & II care, prior to arrival at the current facility, in

the “3rd” hour row.

[13] Local Time: Current time being used by recorder

[14a] Crystalloid (mL): Total crystalloid volume given over last

hour (LR, NS, etc.)

[14b] Colloid (mL): Total colloid volume given over the last

hour (Albumin 5%-25%, blood products, Hespan, etc.) Note 

when using Albumin: With large resuscitations, start 5%

Albumin at the 12 hour mark; with normal resuscitations, start at 

the 24 hour mark.

[15] Total: Total volume (crystalloid + colloid) for the hour

[16] UOP: Urine output for last hour

[17] Base Deficit: enter lab value, if avail. (indicates acidemia) 

[18] BP: Systolic BP / Diastolic BP

[19] MAP/CVP: MAP and/or CVP if available.

[20] Pressors: Vasopressin, Levophed, etc., and rate/dose

[21] 12-hr Total: Total IVF & UOP for 1st 12 hours post-burn

[22] 24-hr Total: Total IVF & UOP for 1st 24 hours post-burn

[14b]

Burn Flow Sheet Documentation

The guidelines for page 2 remain the same as for page 1, with

the exception of the calculation table. On page 2, the values in

[a] and [c] are the actual volumes delivered and recorded from 

page 1, blocks 21 & 22. [b] is the actual volume delivered 

from the 9th hour through the 24th hour. These values allow 

caregivers to re-calculate the mL/kg/% TBSA, and evaluate for 

over-resuscitation

[a] [b] [c] [d] [e] [f]

The guidelines for page 3 remain the same as for pages 1 & 2, 

with the exception of the calculation table. On page 3, the values

in [d] and [e] are the actual 24 hour fluid totals recorded from

pages 1 & 2. [f] is the total volume delivered over the first 48

hrs ([d] + [e]). Once again, these values allow caregivers to recalculate the mL/kg/% TBSA, and evaluate for over-resuscitation

JTTS Burn Resuscitation Flow Sheet Page 1

Date: Initial Treatment Facility:

Name SSN

Pre-burn est.

wt (kg) % TBSA 1st 8 hrs 2nd 16th hrs Est. Total 24 hrs

[5] [6] [7] [8] [9]

[2]

[3] [4]

[1]

Date & Time of Injury [10] BAMC/ISR Burn Team DSN 312-429-2876

Estimated fluid vol. pt should receive

Tx Site/ 

Team

HR from

burn

Local 

Time

UOP Base

Deficit

BP Pressors

(Vasopressin 0.02-0.04 

1st u/min)

2nd

3rd

4th

5th

6th

7th

8th

9th

10th

11th

12th

13th

14th

15th

16th

17th

18th

19th

20th

21st

22nd

23rd

24th

Total Fluids:

Total Fluids 1st 12 hrs:

Crystalloid

Colloid TOTAL MAP 

(>55) (ml) CVP

[21]

[22]
Acute Burn Care | 609

Excessive fluid administration (over-resuscitation), beyond the minimum required to maintain end-organ 

perfusion, produces its own constellation of complications termed resuscitation morbidity. Resuscitation 

morbidity includes upper airway obstruction, pulmonary or cerebral edema, and compartment 

syndromes affecting the extremities and abdomen.

Patients presenting with concurrent injuries, which require fluid administration unrelated to burn 

treatment, complicate resuscitation of military burn casualties. Resuscitation is also made complex by 

virtue of multiple careproviders with varying backgrounds providing burn care during the patient’s initial 

management and subsequent aeromedical evacuation and care. The implementation of a standardized 

Burn Resuscitation Flowsheet and Burn Resuscitation Guidelines (Fig. 16), by improving documentation 

and inter-echelon communication, has improved outcomes following battlefield burn resuscitation.35,36 

Modified Brooke Formula 

The current clinical practice guideline for resuscitation of the military burn casualty recommends initiating 

fluid resuscitation utilizing the modified Brooke Formula: lactated Ringer’s solution totaling (2 ml x %TBSA 

burned x kilogram weight) divided over 24 hours, with half of the total amount administered during the 

first 8 hours following injury.37 An abbreviated method of calculating the initial fluid resuscitation rate (only 

applicable to adults weighing over 40 kilograms) is to multiply the estimated %TBSA burned x 10. Coined 

the “Rule of Ten” at the USAISR (Chung KC, unpublished data 2009), this simple equation provides the 

initial hourly infusion rate for lactated Ringer’s solution (Fig. 17). 

Figure 17. (Above) Ongoing resuscitation of a burn victim with 

lactated Ringer’s infusion during critical care transport.

Figure 18. (Right) Patient monitoring during air evacuation.
610 | Acute Burn Care

USAISR Rule of Ten for Burn Resuscitation of Adults: 

%TBSA burned x 10 = Initial Hourly IV Fluid Infusion Rate

For children, body weight remains a critical consideration, and the modified Brooke Formula for children 

is used: (3 ml x %TBSA burned x kilogram weight) divided over 24 hours, with half of the total amount 

programmed for administration during the first eight hours following injury.38 In addition, children require 

a maintenance fluid, which is not adjusted during resuscitation.

Modified Brooke Formula:

Lactated Ringer’s total (2 ml x %TBSA burned x kilogram weight); first half infused in first eight hours

Modified Brooke Formula for Children:

Lactated Ringer’s total (3 ml x %TBSA burned x kilogram weight); first half infused in first eight hours

These estimates, or any other burn resuscitation formulas, simply provide a point at which to start the 

resuscitation. Burn resuscitation must be closely monitored and adjusted based on clinical response and 

endpoints. Administer no more fluid than is necessary for end-organ perfusion as observed by adequate 

urine output, generally accepted as 30 to 50 ml per hour in adults, and 1 to 2 ml per kilogram per hour 

in children.39 Intravenous fluid rates should be adjusted hourly, avoiding boluses of fluid and making 

incremental adjustments by 20 to 25 percent up or down, based on urine output. Current research and 

development efforts are underway to improve this process though the development of decision-assist 

software.40

Optimal Burn Resuscitation: 

 Estimate  Initiate  Monitor  Adjust  Document 

Repeat monitoring and adjustment process at hourly intervals to optimize resuscitation

Inadequate resuscitation can lead to ischemia of renal and mesenteric vascular beds and can worsen 

end-organ injury.41,42 Excessive fluid administration (over-resuscitation) produces its own constellation of 

complications termed resuscitation morbidity. Resuscitation morbidity includes upper airway obstruction, 

pulmonary or cerebral edema, and compartment syndromes affecting the extremities and abdomen.43

Patient monitoring becomes more advanced as the patient is transported to better-resourced facilities 

(Fig. 18). Vital sign monitoring (assessment of pulses and manual measurement of blood pressure) rapidly 

advances as the patient is evacuated to higher levels of care, to include continuous electrocardiographic 

monitoring, pulse oximetry, and interval automated blood pressure measurements. Placement of arterial 

and central venous catheters provides continuous measurements of arterial and central venous pressures. 

An improving base deficit has also been identified as a helpful indicator of resuscitation efficacy.44

While central venous pressure, central venous saturation, and arterial base deficit are often followed during 

resuscitation, there are no accepted guidelines with respect to use of these variables as endpoints.45 Adequate 

end-organ perfusion, manifested by a urine output of 30 to 50 ml per hour in adults (1 ml per kilogram 

per hour in children less than 30 kilograms), is the primary index of resuscitation adequacy used in burn 

patients. 
Acute Burn Care | 611

While hemodynamic variables (e.g., hypotension) are helpful in identifying uncompensated shock, they 

inadequately detect hypoperfusion in compensated shock states. Patients with compensated shock may 

appear normotensive, yet still suffer from regional hypoperfusion, as evidenced by progressive metabolic 

acidosis. Current methods for assessing the adequacy of fluid resuscitation in critically ill patients are 

suboptimal. While much emphasis has been placed on defining markers of global perfusion adequacy (e.g., 

base deficits), future efforts will likely involve better defining markers of regional perfusion adequacy (e.g., 

gastric intramucosal pH monitoring) and endpoints for resuscitation. 

Adequate end-organ perfusion, manifested by a urine output of 30 to 50 ml per hour in adults (1 ml per 

kilogram per hour in children less than 30 kilograms), is the primary index of resuscitation adequacy used 

in burn patients. 

Complications of Burn Injury

Abdominal Compartment Syndrome

Patients with significant burns are at risk for 

developing abdominal compartment syndrome. 

This risk increases with the volume of fluid infused 

over the first 24 hours following burn injury. 

Infusion of fluid volumes exceeding 250 ml per 

kilogram within the first 24 hours following injury 

is particularly hazardous.46 Thus, initiation of serial 

measurements of the bladder pressure may be 

prudent as soon as a patient, during the first 24 hours 

post-burn, receives greater than 200 ml per kilogram 

of fluid infusion. Other risk factors for abdominal 

compartment syndrome include extensive TBSA 

involvement and full-thickness burn size, aggressive 

fluid resuscitation in the early resuscitative period, 

and deep or circumferential burns to the abdomen 

and thorax.47

If abdominal compartment syndrome develops, a decompressive laparotomy will likely be required.

If intraabdominal hypertension occurs (i.e., bladder pressure greater than 25 mm Hg): (1) escharotomies of 

any eschar involving the abdominal wall are warranted; (2) every effort should be made to reduce the fluid 

infusion rate; and (3) bedside placement of a peritoneal drain should be considered to remove ascites.46,48,49

If these methods fail to reduce bladder pressure and if the patient develops abdominal compartment 

syndrome (e.g., intraabdominal hypertension with rising airway pressures, cardiovascular collapse, and/or 

oliguria despite adequate preload), a decompressive laparotomy will likely be required (Fig. 19).50 Because the 

open abdomen becomes heavily contaminated and may be impossible to close, decompressive laparotomy 

is a high-risk procedure in burn patients.46,49,50 In the authors’ experience, such an intervention is associated 

with a mortality exceeding 80 percent. Techniques proposed to reduce the fluid infusion rate in patients with 

intraabdominal hypertension include early use of colloid and use of hypertonic crystalloid solutions.51,52,53

Figure 19. This image illustrates an open abdomen following 

decompressive laparotomy for abdominal compartment syndrome.
612 | Acute Burn Care

Both over-resuscitation and under-resuscitation of burn patients must be avoided; each invokes unique 

morbidity.

Traumatic Rhabdomyolysis

Patients with traumatic rhabdomyolysis are at risk of acute kidney injury and acute tubular necrosis.54 

These patients present with gross myoglobinuria, which can be distinguished from hematuria by a urinalysis 

that is dipstick positive for blood but microscopically negative for red blood cells. The diagnosis is further 

supported by documenting elevated levels of serum creatine phosphokinase (CPK). Once diagnosed, 

rhabdomyolysis is treated with an increase in the intravenous fluid rate in order to achieve a target urine 

output of 1 ml per kilogram per hour (i.e., commonly 75 to 100 ml per hour in adults), to clear the tubules 

of myoglobin. In addition, urgent fasciotomy and/or debridement of necrotic muscles may be required 

to eliminate sources of ongoing pigment release (tissue injury). If these measures fail to produce a gradual 

clearing of pigment from the urine (as determined by visual inspection over several hours) or a decline in the 

serum CPK level, then infusion of mannitol and/or administration of bicarbonate to alkalinize the urine 

should be considered.18,54,55 The efficacy of mannitol and bicarbonate therapy for rhabdomyolysis remains 

controversial.56,57,58,59

Electrolyte Disturbances

Burn patients may present with a variety of electrolyte disturbances. Patients with massive tissue destruction, 

such as those with traumatic rhabdomyolysis, are at risk for hyperkalemia. Loss of the evaporative barrier to 

water loss leads to very large insensible water losses and thus to hypernatremia. This mandates intravascular 

volume replacement with hypotonic intravenous (such as D5W) and/or oral solutions, beginning about 

48 hours post-burn.60 The amount of these losses can be roughly estimated by the formula, daily water 

requirement = (1 ml x TBSA burned x weight in kilograms). However, patients are also at risk of 

hyponatremia because of abnormalities in the thirst mechanism and in some cases the syndrome of 

inappropriate secretion of antidiuretic hormone (SIADH).61 

The rate of serum sodium correction depends on the severity of symptoms and rate at which the 

derangement developed (acute versus chronic).62 The treatment of acute (less than 48 hours duration) 

hyper- and hyponatremia associated with burn injury involves correcting intravascular volume deficits and 

correcting hyper- or hypotonicity. The serum sodium should be corrected at an initial rate of 1 mEq per liter 

per hour. Serial serum electrolyte measurements should be performed every one to two hours during initial 

treatment phases. The correction of chronic sodium disturbances (greater than 48 hours duration) should 

be at a rate not to exceed 0.5 mEq per liter per hour.63 Serum sodium correction is performed more rapidly 

if a neurological complication, such as ongoing seizure activity, is attributed to sodium derangement.

The predictive accuracy of formulas for serum sodium and intravascular volume repletion is limited.64

Lindner et al. studied the predictive accuracy of formulaic approaches to serum sodium correction and 

found that individual patient variability of response to treatment dictates such formulas should only be 

used as a guide. Serial measurements of serum sodium are recommended to ensure appropriate treatment.

Finally, burn patients may develop severe hypophosphatemia during the first three to five days post-burn, 

most likely reflecting the tremendous increase in metabolic demand that occurs during this period.65 Thus, 

serum electrolytes must be monitored frequently (minimum of twice daily) in patients with major burns. 
Acute Burn Care | 613

Escharotomy and Fasciotomy

Circumferential burns of the extremities and torso are prone to the compressive effect of eschar. Fluid 

resuscitation can rapidly exacerbate such compression through increased tissue edema, with resultant 

vascular obstruction, ischemia, and limb loss.26 This most commonly occurs in the setting of circumferential 

full-thickness burns, but does on occasion occur with deep partial-thickness burns, or noncircumferential 

burns. Elevation of burned extremities well above the level of the heart is a simple but critically important 

intervention that will minimize tissue edema in the initial 48 hours following burn injury. Elevate burned 

limbs and evaluate them hourly during patient resuscitation (Fig. 20). This can be done with pillows and 

blankets, or better yet, with slings constructed of surgical netting hung from IV poles. When this fails 

to maintain adequate distal blood flow, escharotomy (a longitudinal incision through the burned skin) is 

required (Fig. 21).

Elevation of burned extremities well above the level of the heart is a simple but critically important 

intervention that will minimize tissue edema in the initial 48 hours following burn injury.

Progressive diminution of pulsatile arterial flow by Doppler flowmetry is the primary indication for 

escharotomy. Other indications include cyanosis of distal unburned skin, impaired capillary refill, or 

progressive neurological deficits.66 Such neurologic deficits include paresthesias progressing to hypesthesia 

or loss of motor function. In addition, early escharotomy should be considered for any patient with deep, 

Figure 20. (Left) With circumferential burns, elevation of the burned 

extremity and frequent evaluation are extremely important.

Figure 21. (Bottom Left and Bottom Right) Extremity 

escharotomies following circumferential burns.
614 | Acute Burn Care

circumferential extremity burns who is being evacuated between military medical treatment facilities on the 

battlefield.

Escharotomy is considered to be a relatively urgent procedure and can be performed at the bedside, using 

sharp incision with a knife or electrocautery device. Regardless of the technique used, escharotomies should 

be performed in the most sterile environment possible. The burned skin is incised down to the subcutaneous 

level, providing decompression through the incision sites.26 Escharotomies are generally performed on the 

lateral and medial aspects of the limbs, avoiding any underlying neurovascular structures, and without 

entering the deep (investing) fascia (Fig. 22). Pain control during this procedure should be managed 

with titrated doses of intravenous narcotics or ketamine. Once the escharotomy has been completed, 

neurovascular examination is serially repeated to verify effectiveness. 

Early escharotomy should be considered for patients with circumferential, deep burns involving the 

extremities, especially in anticipation of long-range aeromedical transport.

Except in cases involving high-voltage electrical injury, fractures deep to the burn, or vascular injury to the 

limb, fasciotomies of burned extremities are rarely required.2,67 If compartment syndrome is suspected in a 

circumferentially burned limb, escharotomies should be performed, and the patient reevaluated (to include 

neurovascular exam and measurement of intracompartmental pressures). 

Figure 22. (Left) Hand escharotomies. Burned skin is incised to the 

subcutaneous level, providing decompression while avoiding deeper 

structures.

Figure 23. (Below) Compartment syndrome is unusual following thermal 

injury. Unlike circumferential eschar, which is treated with escharotomy, a 

true compartment syndrome requires fasciotomy as demonstrated here.
Acute Burn Care | 615

Fasciotomies are performed only when clinical findings indicate intracompartmental hypertension 

(compartment syndrome). They should not be performed prophylactically, solely on the basis of 

circumferential burns.

A delay in performing a clinically indicated escharotomy, or an inadequately performed escharotomy, 

may lead to a true compartment syndrome mandating fasciotomy (Fig. 23).67 In addition, massive fluid 

resuscitation can result in a compartment syndrome in a normal (unburned) limb.68 In the authors’ 

experience, the regions most sensitive to post-burn compartment syndrome are the anterior lower leg 

and the forearm. Fasciotomies of the thigh and upper arm as part of post-burn management are rarely 

indicated. Post-burn compartment syndromes of the hand do occur, and are best managed by a surgeon 

with appropriate expertise (e.g., hand plastic surgeon).69,70 

External fixation is generally the preferred treatment option for combat casualties with major burns and 

underlying extremity fractures, as these wounds are assumed to be contaminated.71 Although the presence 

of nonviable tissue at the pin sites is far from ideal, alternative treatment options are even less attractive. 

The use of external fixation does not contribute to an increase in compartment pressures and it allows 

for ease of monitoring of tissue edema and viability during burn resuscitation.72 Internal fixation may be 

considered in selected cases, provided there are clear advantages over external fixation and the operation 

can be performed before the wound becomes heavily colonized (i.e., within the first one to two days postburn).72

External fixation is generally the preferred treatment option for combat casualties with major burns and 

underlying extremity fractures, as these wounds are assumed to be contaminated.

Initial Wound Care

When considering the acute management of the burn wound, it is crucial to remember that the skin is 

intimately linked at a physiologic level to the function of every other organ system. Generally speaking, the 

larger the burn wound, the greater the adverse effect on each of those systems. The sooner the burn wound 

is addressed, the sooner the patient can commence recovery. A thorough and continuous assessment of the 

burn and its healing status are paramount.

The term ‘wound care’ includes multiple activities often performed in a progressive manner from point of 

injury through initial hospital resuscitation, wound management, and rehabilitation. From the perspective 

of the first responder, the primary activities related to wound care involve halting the burning process and 

protecting the skin from further injury. In some cases, this may mean quite literally extinguishing the fire, 

or more often, simply removing any residual clothing or equipment that may be retaining heat, thereby 

furthering the insult to the tissue. 

Cleansing and debridement of the burned skin follow as the next logical step in care of the burn wound. 

This action may include cleaning of the patient’s skin with a disinfectant soap and warm water. For patients 

with burns related to possible chemical exposure, irrigating the skin with copious amounts of water is crucial. 

Brush off debris before irrigation as the damaging effects of certain chemical agents can be compounded 

with irrigation.
616 | Acute Burn Care

Initial debridement of patients with large 

surface area burns is best performed in a clean, 

warm operating room with anesthesia support, 

resuscitation capability, adequate lighting, and 

appropriate dressing materials. In the combat 

environment, this means formal debridement may 

have to be delayed until the patient is evacuated 

to a Level III Combat Support Hospital (CSH). 

Casualties with partial-thickness burns often 

demonstrate blisters as the epidermis separates 

from the dermis and fluid (similar in composition 

to plasma) fills the void (Fig. 24). In the field, it is 

recommended that blisters be left intact until such 

time as formal wound care, in a clean environment, 

can be performed.73 A clean, dry bed sheet will 

usually provide adequate protection of the blistered 

skin. 

The choice of topical burn dressings and when to apply them is based on several factors: materials on-hand, 

provider preference, adjacent wounds, and the anticipated time and distance between successive medical 

facilities. Providers in the field should simply cover burns with a clean, dry dressing and avoid applying 

any topical ointments, including burn creams, to the wounds.73 This approach eliminates the need for 

careproviders to later have to remove creams when patients present at the next facility in the evacuation 

chain. The use of a silver-impregnated dressing such as Silverlon®, Acticoat®, or SilverSeal® as the initial 

dressing is a reasonable alternative, since these materials are relatively easy to apply, provide a topical 

antimicrobial effect, and do not impede the subsequent examination and debridement process.74

Providers in the field should simply cover burns with a clean, dry dressing and avoid applying any topical 

ointments, including burn creams, to the wounds.

Once the burns have been formally cleansed and debrided, dressing the wound in a silver-impregnated 

dressing covered by layer of gauze provides a clean, protective milieu that utilizes the silver ion as the 

antimicrobial agent.74 This dressing is effective for many hours to several days. This eliminates the need for 

twice daily reapplication of topical creams such as Silvadene® or Sulfamylon®.75,76 However, we caution 

that silver dressings do not take the place of meticulous care when wounds are contaminated or infected. 

Thus, burn patients with such wounds will continue to require once or twice daily dressing changes, 

cleansing with chlorhexidene gluconate, and reapplication of topical antimicrobial creams. 

Burns sustained in combat often involve adjacent areas of open soft-tissue wounds that result from direct 

tissue loss, degloving injuries, or surgical debridement. Wounds of this nature are left open for serial 

debridement and until definitive coverage or closure can be performed. 

Patient Exposure and Hypothermia

Just as it is very important to completely expose the burn patient during the initial assessment, it is also 

crucial to remember that burn casualties are predisposed to hypothermia. Burn patients with large surface 

Figure 24. Partial-thickness burns demonstrate fluid-filled blisters that 

should be left intact until formal wound care is performed. Image courtesy 

of Robert H. Demling, MD, Harvard Medical School.
Acute Burn Care | 617

area burns can quickly become hypothermic due to loss of normal skin thermoregulatory function.77

Hypothermia is even more likely in the burn patient who also has severe trauma and blood loss. Burn patients 

are prone to hypothermia during multiple phases of care, including operating room wound debridement, 

routine dressing changes, and transport. 

Burn patients with large surface area burns, especially those with traumatic injuries resulting in blood 

loss, can quickly become hypothermic due to loss of normal skin thermoregulatory function.

Because of this high risk of hypothermia, the burn casualty in the prehospital setting should be kept 

warm and dry (e.g., covered with a clean sheet and a warm blanket). Use of hypothermia prevention 

kits is recommended during all phases of transport. Do not wet the patient and do not apply wet sheets. 

The operating room should be kept as warm as possible for the casualty. Warmed intravenous fluids 

should be used during the resuscitation process. Research is ongoing to further evaluate the feasibility of 

internal warming using specialized venous catheters during the early phases of resuscitation of the military 

casualty.

Pain Control

The severity of pain reported by burn casualties varies greatly. This variability is due, in part, to the extent 

that pain receptors are affected, the presence of concurrent injuries, and subjective components related to 

pain. 

The judicious administration of intravenous narcotics is generally effective in controlling pain for the 

burn patient. Indiscriminate dosing of narcotics may cause adverse consequences such as hypotension 

and respiratory depression.

Intermittent dosing of intravenous morphine or fentanyl is effective for controlling background burn 

injury pain. The addition of IV ketamine (0.25 to 1.0 mg per kilogram) provides very effective analgesia 

(disassociative sedation at higher doses) during dressing changes and other painful procedures.78 More 

recently, the use of oral transmucosal fentanyl citrate (Actiq®, Cephalon Inc., Fraser, PA) has been used 

for acute pain management in combat.79 Sedation using a benzodiazepine in small doses decreases anxiety 

and is an important adjunct to pain control. The routine use of continuous infusions of these drugs in 

CCC settings is discouraged unless the patient can be closely monitored to ensure optimal pain control, 

sedation, and immediate detection of adverse effects (e.g., respiratory depression and hypotension).

Advanced Burn Wound Care

Wound Excision 

The surgical process of sharply excising burned skin (excision) and replacing it with autologous skin 

(grafting) is based on sound principles of general surgical wound management. Expediting this process 

has been shown to decrease mortality and morbidity in US burn centers.80,81 The process of excision and 

grafting requires a substantial commitment of resources (personnel, supplies, and hospital support services). 

Excision and grafting are ideally postponed until the casualty arrives at a Level V care facility such as a burn 

center that is fully staffed and equipped to complete all phases of care, including rehabilitation.
618 | Acute Burn Care

Early (in-theater) excision and grafting are not recommended for any patient who can be evacuated to a 

designated burn center within one to two weeks of burn injury. To intentionally excise the burned skin, 

without a means of covering the exposed tissue bed, invites unnecessary contamination and may ultimately 

impede definitive wound closure. Similarly, to proceed with skin grafting prior to arrival at the burn center 

would place the fresh grafts at undue risk for shear force injury and loss during the transport process. 

On the other hand, experiences in the current conflicts in Afghanistan and Iraq have provided numerous 

examples of the need for forward-deployed surgeons to perform excision and grafting of burn patients 

who cannot be evacuated.1 This primarily involves host nation patients whose only hope of recovery often 

rests with the facility at which they initially present (Fig. 25). As a consequence, staff at deployed military 

hospitals should be prepared to provide definitive burn care. 

Early (in-theater) excision and grafting are not recommended for any patient who can be evacuated to 

a designated burn center within one to two weeks of burn injury. However, forward-deployed surgeons 

should be familiar with this procedure for treatment of those who cannot be evacuated or host nationals.

Unlike US military casualties who are usually evacuated to medical treatment facilities within hours of 

injury, host nation casualties often present several days to weeks after injury. The surgeon must assess such 

patients with respect to wound contamination, determine whether an infection is present, and decide 

whether autografting would be prudent. Host nation patients presenting in a delayed fashion with invasive 

burn wound infections pose special management challenges (see Infection Control). A viable option 

for treatment of dirty or contaminated burns is to excise the wound to healthy-appearing tissue and to 

perform scheduled dressing changes using negative-pressure wound therapy (NPWT) until the bed appears 

optimal for grafting (Fig. 26).82 Placement of allograft (cadaver skin, with or without NPWT) as a temporary 

Figure 25. (Left) Treatment of host nation patients may require surgeons 

to provide definitive burn care with excision and grafting.

Figure 26. (Below) Placement of a negative-pressure wound dressing on 

the lower extremities following excision and grafting is one way to achieve 

postoperative splinting of freshly grafted wounds.
Acute Burn Care | 619

measure to prime the wound bed is an option, if available.83 Gammagraft® (Promethean LifeSciences, 

Inc., Pittsburgh, PA), an irradiated allograft product with a long shelf-life, may be considered when no 

other source of allograft exists.1

Tangential Excision

Dermal burns are excised with multiple tangential passes of a manual dermatome (such as a Blair, Humby, 

Brown, Braithewaite, Watson, or Goulian-Weck instrument) until viable tissue is reached (Fig. 27). This 

method of tangential excision allows maximum preservation of viable dermis and subcutaneous fat. This 

leads to better long-term results in the quality of the healed grafts and improved mobility and range of 

motion for the patient. Regardless of the instrument used, the key is to remove only that which is deemed 

nonviable and to preserve that which may heal. Areas requiring intricate or delicate work, such as the 

hand and fingers, are best approached using small instruments like the Goulian dermatome, with shallow 

penetration and multiple passes.84 

Fascial Excision

Subdermal burns extending well into the subcutaneous tissue, and those that are heavily colonized or 

Figure 27. The technique of tangential excision can be rapidly accomplished with a large hand dermatome. Note the potential for massive blood loss 

associated with this operation.
620 | Acute Burn Care

infected, are often best excised primarily to the level of the investing fascia (Fig. 28). Excision to this level 

can proceed rapidly using a knife, scissors, or electrocautery device. Fascial excision often results in less 

overall blood loss compared to tangential excision, as excision proceeds in a rapid manner along the fascial 

planes, removing all eschar with the underlying subcutaneous tissue. This process can result in the removal 

of a significant amount of tissue, especially in obese patients, with marked step-offs and associated softtissue defects.85

Engraftment of autograft onto fascia is often better than when grafting onto subcutaneous tissue, thereby 

speeding wound closure. The undesirable aspects of fascial excision and grafting include: (1) inferior 

cosmetic appearance, (2) increased edema in distal extremities due to the loss of venous and lymph vessels, 

and (3) decreased sensation and inferior functional results.86 Each of these factors must be considered when 

deciding which technique to use when removing burned tissue.

Areas that have been adequately debrided show brisk punctate bleeding in healthy-appearing dermis. 

Poor bleeding in grayish-colored dermis indicates inadequate debridement, requiring deeper excision. As 

Figure 28. Excision to fascia of deep burns of the lower extremity at a Level III facility. Excision to fascia is indicated for deep third-degree burns and 

infected burns. A marked step-off will be created by this soft-tissue defect.
Acute Burn Care | 621

debridement progresses deeper into and through the dermis, more fat appears and capillary bleeding gives 

way to flow from larger arterioles and veins. The total amount of blood loss from extensive excision may be 

massive, and the surgical team must endeavor to monitor the wound bed for excessive bleeding and temper 

the pace of excision to address hemostasis.85

Effective excision of burned skin uncovers the underlying vascular bed. The surgeon must monitor the 

pace and extent of surgical excision to ensure hemostasis is achieved.

Hemostasis in the debrided wound bed is routinely 

obtained using pinpoint electrocautery. Repetitive 

dabbing of the excised wound bed with a dry 

gauze sponge is an effort in futility. Instead, a bulb 

syringe can be used to irrigate blood off of the 

field during electrocautery. Compressive dressings 

soaked in dilute (1:100,000 or 0.01 mg per milliliter) 

epinephrine placed on the exposed capillary bed 

are effective adjunctive methods of achieving 

hemostasis (Fig. 29).85 A nonadherent, perforated, 

polyester-film material such as TELFATM (Kendall 

Brands, Covidien Inc., Mansfield, MA) can be used 

with the epinephrine-soaked gauze to help prevent 

clot dislodgment from the wound surface when the 

gauze is removed. Local pressure and the use of 

temporary elastic bandages can improve hemostasis. 

Recombinant human thrombin or fibrin sealants 

can also be used.87,88 

Whether utilizing tangential or fascial techniques to excise burned skin, blood loss can be significantly 

reduced with the use of pneumatic tourniquets in conjunction with temporary exanguination of the 

extremity. Since bleeding from the wound bed cannot be utilized as an indicator of tissue viability when 

using tourniquets, the operating surgeon must possess experiential knowledge of the desired appearance 

of the wound bed to avoid unnecessary or inadequate depth of excision. Regardless of which debridement 

option the surgeon chooses, he or she must be prepared for the blood loss associated with excision of burns. 

Two to six units of packed red blood cells should be typed and crossed for the patient in anticipation of 

excisions involving greater than 10% TBSA. Estimation of blood loss is difficult even for experienced burn 

care teams. It is recommended that less experienced teams limit their excisions to less than 10% TBSA at a 

time, or two hours in duration.

Two to six units of packed red blood cells should be typed and crossed for the patient in anticipation of 

excisions involving greater than 10% TBSA.

Skin Grafting

Coverage of open wounds, following either excision of burns or debridement of injured soft-tissue, can be 

accomplished using autograft, allograft, or biosynthetic products. Ultimate wound closure involves use of 

Figure 29. Compressive dressings soaked in dilute epinephrine placed on 

the exposed capillary bed are effective hemostatic adjuncts.
622 | Acute Burn Care

autologous tissue, either in the form of split- or fullthickness grafts or flaps.

Harvesting of Skin 

An autograft in the form of a split-thickness skin graft 

(STSG) is routinely harvested at a depth of between 

0.006 to 0.012 inches using either a manual, or more 

commonly, a powered dermatome. The advantages 

of using powered dermatomes are uniformity 

and speed in the harvesting process. Use of dilute 

(1:1,000,000) epinephrine in lactated Ringer’s 

solution injected by clysis into the subcutaneous 

space aids in hemostasis and assists in “leveling” of 

the operative field prior to harvesting (Fig. 30).89 The 

use of a 60-ml syringe coupled to a 18- to 16-gauge 

needle works satisfactorily for the clysis procedure, 

and can be performed fairly rapidly even for a large 

surface area.

The selection of donor site dressing is largely a matter of operator preference.85 Xeroform® gauze is 

commonly available, even in the deployed military environment, and has proven to be effective. Donor sites 

generally heal in about 10 to 14 days and may be reharvested multiple times once healed.

Survival of the combat burn casualty is linked to wound closure, and the surgeon must exploit all possible 

donor sites to facilitate coverage. The scalp is an excellent donor site and should not be overlooked.

A STSG may be placed on the wound bed as either a sheet graft or meshed graft (Figs. 31 and 32). 

Typically, a properly placed STSG is adherent to the wound bed in three to five days and is durable 

enough for fairly aggressive cleansing after about seven days. Cleansing of the healing graft is important, 

especially when debris fills the interstices, impeding wound closure.

Excellent functional outcomes with STSG coverage can be achieved with early and progressive rehabilitation 

and through close communication between the surgeon, wound care team, and rehabilitation team to 

determine a safe and effective rehabilitation plan. Rehabilitation efforts involving grafted areas should be 

minimized during the first three days following graft placement. Mobilization activities such as transfers 

can be performed during this time if the area of grafting can be safely protected from shear forces. As 

the STSG matures, rehabilitation activities may be advanced, but every consideration must be given to 

protection of the healing graft until durable adherence is confirmed, usually around postoperative day 

seven. 

Areas of burn graft in which an optimal functional or cosmetic result is desirable should be covered with 

thick unmeshed STSGs (Fig. 33).90 Examples of areas best served by sheet grafting versus meshed skin 

grafting include the face, neck, and dorsum of the hand. Availability of adequate donor sites affects how 

much grafting can be accomplished using sheet grafts.91

Figure 30. Subdermal clysis aids in hemostasis and “leveling” of the 

operative field prior to skin harvesting.
Acute Burn Care | 623

Meshed Skin Grafts

Meshing of skin allows for greater graft coverage from available donor sites, improves conformity of 

the graft, and provides a route of escape for serous fluid beneath the graft. Instrumentation used to 

reproducibly mesh skin comprises a mechanical device that allows the surgeon to expand the skin in ratios 

between 1:1 and 6:1. As the expansion ratio increases, the cosmetic quality of the skin decreases, and the 

healing time increases. A meshing ratio of 3:1 or less is employed for most circumstances due to the friability 

and prolonged healing associated with wider expansion.91 There are times, however, when donor sites are 

so limited as to demand that ratios of 4:1 or higher are used. Using a “sandwich” technique in which 

widely meshed autograft is covered with sheet allograft serves to protect the underlying tissue bed during 

prolonged healing.91

There are several different types of meshing devices available to the surgeon (Fig. 34). Some devices utilize a 

flat carrier upon which the skin is placed prior to being passed through the cutting blades. Another version 

of this device utilizes carriers with fine ridges, which work with the mesher blades to create the desired 

Figure 31. Harvesting of a split-thickness skin graft at a depth of 10/1,000 inch is facilitated by subdermal clysis with a solution of epinephrine 

(concentration 1:1,000,000) in lactated Ringer’s, injected using a 60-milliliter syringe and an 18-gauge needle. Harvesting is performed by use of an 

air or electric-powered dermatome. Xeroform gauze is stapled into place, followed by a dry gauze dressing and a compressive wrap such as an Ace® 

bandage or surgical netting (depending on location).
624 | Acute Burn Care

Figure 32. Placement of meshed split-thickness skin graft on the lower extremity following excision to fascia, performed at a Level III facility. Excision 

and grafting at hospitals in the combat zone are generally not performed, except in cases of host national casualties who do not have other treatment 

options.

Figure 34. Meshing of the skin allows for greater graft coverage, 

improved conformity of the graft, and drainage of serous fluid.

Figure 33. Unmeshed split-thickness skin grafts should be used in areas 

where optimal function or cosmetic result is desirable.
Acute Burn Care | 625

pattern. A third type uses no carrier, requiring only that the skin be fed through the cutting rollers in a 

uniform manner.

Regardless of the type of mesher utilized, it is imperative that both the surgeon and the operating room 

technician know how to use the meshing device prior to starting the case to avoid wasting any valuable 

donor autograft.

Full-Thickness Skin Grafts

The most common alternative to the STSG is a full-thickness skin graft (FTSG). The main advantages of using 

the FTSG are durability of the healed wound, minimal contracture, and cosmesis.90 The disadvantages 

of using a FTSG include loss of valuable donor site and necessity for excellent vascularization for graft 

survival. The technique of harvesting a FTSG involves sharply incising the skin into the subcutaneous layer, 

then preparing the FTSG by removing as much of the subcutaneous tissue as possible from the dermis. 

Donor sites for a FTSG may be closed primarily or covered with a STSG. Most FTSGs heal in 10 to 14 

days.91

Regardless of the type of graft used, protection of the graft with proper limb splinting and positioning is 

essential.85 Mobilization activities such as transfers and ambulation can be performed within the first few days 

after grafting, provided that the graft site can be safely protected. Excellent functional outcomes with FTSG 

coverage can be achieved with early and progressive rehabilitation and through close communication 

between the surgeon, wound care team, and rehabilitation therapists.

Engraftment

Meticulous wound management during the immediate postoperative period is vital to graft viability and 

patient survival due to the importance of burn wound closure. Movement of the graft or shear is the 

principal cause of graft failure; infection is the second.92,93 Securing the graft to the wound bed is important 

because unintended motion disrupts neovascularization, leading to death of the graft.

Movement of the graft or shear is the principal cause of graft failure; infection is the second.

To minimize the possibility of movement, grafts are typically secured with staples or sutures. Surgical 

staples are quickly applied and relatively easy to remove. Advantages of sewing the grafts in place include 

more precise placement and the ability to use absorbable suture, eliminating the need for later removal. 

Suturing generally takes considerably longer than stapling. Adhesives such as fibrin glue may be used 

to supplement adherence, especially in areas with irregular contours.87 When using biological glue, it is 

important to ensure that any dressing applied over the graft does not adhere to wound. 

Splints incorporated into the final dressing help maintain the desired limb position and help prevent graft 

loss due to shear, especially over joints. The use of negative-pressure wound dressings has increased in 

popularity due to their effectiveness in promoting engraftment and protection against shear, provided that 

negative pressure is maintained. At the first dressing change, the nonadherent dressing can be left in place, 

provided there are no signs of infection. This layer is removed over the course of the next two to three days 

as the graft interstices close. Removal of the dressing in contact with the graft is facilitated by soaking the 

dressing with 5% solution of Sulfamyalon® or saline prior to removal.
626 | Acute Burn Care

Infection Control

Despite many advances in burn care, local infection related to unhealed burn wounds can lead to systemic 

illness and death.94 Measures to prevent burn wound infection include meticulous wound care. This includes 

effective topical antimicrobial therapy, removing all nonviable tissue (tissue debridement), and timely 

excision and grafting when indicated. Contact precautions, including isolation in private rooms, should 

be liberally employed in the treatment of burn patients. The use of gloves and gowns when in contact 

with the burn patient assists in minimizing nosocomial spread of infection. Meticulous and regular use of 

antimicrobial hand cleanser should be the rule for all providers caring for burn patients.95

Measures to prevent burn wound infection include topical antimicrobial therapy, tissue debridement, 

and timely excision and grafting when indicated. The use of prophylactic antibiotics in burn patients is 

not recommended except perioperatively.

Burns should be considered contaminated wounds, and casualties should have their tetanus immunization 

status updated accordingly. The use of prophylactic antibiotics in burn patients is not recommended except 

perioperatively (in association with excision and grafting procedures).96 A rim of mildly erythematous tissue 

often surrounds healing burns, but extension of the erythema more than two centimeters past the wound 

margin implies cellulitis, which should be treated with antibiotics aimed at beta-hemolytic streptococcal 

and staphylococcal infections (Fig. 35).97 Such gram-positive infections are highly responsive to therapy.95

Figure 35. Streptococcal cellulitis in a burn patient.
Acute Burn Care | 627

By contrast, when burn patients demonstrate systemic evidence of sepsis, particularly when coupled with 

color changes in the wound, an invasive gram-negative burn wound infection should be suspected and treated 

aggressively (Fig. 36). In the absence of effective topical antimicrobial therapy, the risk of gram-negative 

wound infection is a function of burn size (i.e., patients with larger burns are more likely to present with and 

die from such infections).98 These patients require: (1) aggressive resuscitation (early goal-directed therapy 

treatment for sepsis); (2) topical therapy with mafenide acetate cream (Sulfamylon®); (3) treatment with 

antibiotics effective against gram-negative organisms (the authors currently use imipenem-cilastatin, and 

amikacin, to cover multiple-drug-resistant Pseudomonas spp. and Klebsiella pneumoniae); (4) prompt infection 

source control by excision to fascia; (5) a scheduled second-look operation; and (6) subsequent grafting.95

In addition, post-excision topical use of 5% Sulfamylon® solution, or of dilute Dakin’s solution (0.025% 

sodium hypochlorite), may be used to combat gram-negative colonization.99 

Metabolic and Nutritional Considerations 

Burn patients demonstrate extraordinary increases in metabolic rate, as a function of burn size.100,101 There 

are several important consequences of this. Patients demonstrate a persistent tachycardia that makes heart 

Figure 36. Host nationals may present with sepsis due to infected burn wounds several days after injury. In this photograph, subeschar bacterial 

proliferation and suppuration have occurred. After resuscitation, this patient’s burns were excised primarily to fascia.
628 | Acute Burn Care

rate a poor indicator of both effective resuscitation and suspected sepsis. Elevated core temperature is also 

common. Therefore, the usual definitions of fever need to be adjusted upwards, accepting core temperature 

values of up to 38.5°C before antipyretics are given.102,103 The massive caloric requirements engendered 

by this hypermetabolic state cannot be met by oral alimentation alone. Therefore, patients with burns 

totaling greater than 30% TBSA require Dobhoff or nasogastric tube feeding. Early enteral nutrition is 

encouraged, provided the patient is not hemodynamically unstable or requiring pharmacological support 

with vasopressor agents.104 Immediate post-burn administration of acid-suppressive medications (protonpump inhibitors, H2

-blockers, or antacids) is critical for preventing gastroduodenal ulceration (Curling’s 

ulcer).105,106,107,108 

Aeromedical Transport and Definitive Care

All military burn casualties who require the level of care offered by a burn center are transferred to the 

USAISR Burn Center at Brooke Army Medical Center in San Antonio, Texas (Fig. 37). The ability to 

safely transport burn casualties across long distances, while continuing resuscitation, allows rapid transfer 

of patients to facilities capable of providing definitive care. This capability facilitates the overall process of 

burn care for combat casualties as it enables early excision and grafting and early rehabilitation therapy. 

Evacuation policies regarding burn casualties are similar to guidelines published by the American Burn 

Association (ABA) for burn center admission criteria. Both are based on the severity of burn injury, the 

presence of inhalation injury, and other associated 

injuries (Table 2).109

Critically injured burn casualties, typically those 

with large surface area burns and/or inhalation 

injury, are transported to the burn center by one 

of the US Army’s Burn Flight Teams. Each team 

consists of a general surgeon, a registered nurse, a 

licensed vocational nurse, a respiratory therapist, 

and an operations officer, each of whom work daily 

in the intensive care units of the burn center.110 Burn 

casualties not requiring Burn Flight Team support, 

but with one or more other critical problems of 

lesser severity, are transported by a US Air Force 

Critical Care Air Transport Team (CCATT). The 

CCATT crews consist of a physician, registered 

nurse, and respiratory technician, each trained in the 

management of critically ill patients in flight.111,112,113

For patients requiring mechanical ventilation 

during flight, the choice of ventilator and ventilator 

mode during transport is based on the patient’s 

severity of injury, pulmonary status, and response 

to ventilatory support. Patients with inhalation 

injury may require significant ventilatory support 

beyond the capabilities of conventional ventilators 

Figure 37. Staff at the USAISR Burn Center take a call from a referring 

hospital. Early and frequent communication between the referring medical 

treatment facility and the burn center are absolutely essential to successful 

transfer of a patient with severe thermal injury.
Acute Burn Care | 629

used for evacuation. Extensive use of the Volumetric Diffusive Respiration ventilator (VDR-4®) by the 

USAISR Burn Center to treat patients with inhalation injury and other severe pulmonary problems led 

to extensive use of the VDR-4® in patient transport.20 The TXP® pressure-controlled ventilator is also 

used in the evacuation of patients because of its simplicity, compact size, and effectiveness in this patient 

population.114 Both the VDR® and TXP® are powered by compressed air or oxygen, have no electrical 

requirements, and are approved for use on all military aircraft.

As with the interfacility transfer of any critically ill or injured patient, communication between the 

sending and accepting physician is essential for optimal continuity of care. Staff at the USAISR Burn 

Center is available 24 hours per day, seven days per week, to respond to questions and to facilitate evacuation 

of seriously injured burn casualties. 

Providers are encouraged to call (210) 916-2876 to contact the burn center attending surgeon, or DSN 

(312) 429-2876 if commercial access is not available. Consultation may also be initiated by sending an 

email message to US Army Medical Department burn consultants (burntrauma.consult@us.army.mil).

Summary 

Critical elements of caring for burn patients in a combat environment are: (1) careful titration of fluid 

resuscitation (neither too much, nor too little) during a burn shock period that lasts at least 48 hours; (2) 

awareness of the risks of over-resuscitation and prompt recognition and management of such complications 

(e.g., abdominal and extremity compartment syndromes); (3) strategically-timed aeromedical evacuation, 

Burn Center Referral Criteria

A burn center may treat adults, children, or both.

Burn injuries that should be referred to a burn center include the following:

1. Partial-thickness burns of greater than 10% of the total body surface area

2. Burns that involve the face, hands, feet, genitalia, perineum, or major joints

3. Third-degree 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 complex cases, if the trauma poses the greater immediate 

risk, the patient’s condition may be stabilized initially in a trauma center before transfer to a burn 

center. Physician judgment will be necessary in such situations and should be in concert with the 

regional medical control plan and triage protocols.

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

Table 2. Evacuation policies surrounding burn casualties mirror ABA burn center admission criteria.109
630 | Acute Burn Care

which balances the need for close monitoring and hemodynamic stability during the burn shock period 

against the need for early excision of large burns in a dedicated burn center; and (4) recognition of the 

scope and burden of civilian burn care during combat (e.g., definitive surgical care that includes excision 

and grafting of burned children and adults). 
Acute Burn Care | 631

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the efficacy and safety of Acticoat silver-coated dressing for the treatment of burn wounds. J Burn Care 

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77. Gore DC, Beaston J. Infusion of hot crystalloid during operative burn wound debridement. J Trauma 

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78. Owens VF, Palmieri TL, Comroe CM, et al. Ketamine: a safe and effective agent for painful procedures 

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80. Wolfe RA, Roi LD, Flora JD, et al. Mortality differences and speed of wound closure among specialized 

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87. Foster K, Greenhalgh D, Gamelli RL, et al. Efficacy and safety of a fibrin sealant for adherence of 

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88. Greenhalgh DG, Gamelli RL, Collins J, et al. Recombinant thrombin: safety and immunogenicity in 

burn wound excision and grafting. J Burn Care Res 2009;30(3):371-379.

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291-324.

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Chapter 13

CRITICAL CARE

Contributing Authors

David Norton, MD, LTC, MC, US Air Force

 Phillip Mason, MD, MAJ, US Air Force

Jay Johannigman, MD, COL, US Air Force Reserves
All figures and tables included in this chapter have been used with permission from Pelagique, LLC, the 

UCLA Center for International Medicine, and/or the authors, unless otherwise noted.

Disclaimer

The opinions and views expressed herein belong solely to those of the authors. They are not nor should 

they be implied as being endorsed by the United States Uniformed Services University of the Health 

Sciences, Department of the Army, Department of the Navy, Department of the Air Force, Department of 

Defense, or any other branch of the federal government.
Critical Care | 641

Table of Contents

Introduction........................................................................................................ 643

Mechanical Ventilation......................................................................................... 643

Key Concepts ....................................................................................................................643

Ventilator-Induced Lung Injury .......................................................................................646

Barotrauma ........................................................................................................................646

Volutrauma ........................................................................................................................646

Atelectotrauma...................................................................................................................646

Biotrauma ..........................................................................................................................647

Basic Modes of Positive-Pressure Ventilation .................................................................648

Overview............................................................................................................................648

Assist-Control (A/C) ..........................................................................................................649

Synchronized Intermittent Mandatory Ventilation (SIMV) ..............................................649

Pressure-Control Ventilation (PCV)...................................................................................650

Pressure-Support Ventilation (PSV) ...................................................................................651

Advanced Modes of Positive-Pressure Ventilation..........................................................652

Airway Pressure Release Ventilation (APRV).....................................................................652

Pressure-Regulated Volume Control (PRVC).....................................................................652

High-Frequency Ventilation (HFV)....................................................................................653

Basic Ventilator Settings When Lungs Are Normal .........................................................653

Pulmonary Contusion .......................................................................................... 655

Basic Concepts ..................................................................................................................655

Management.....................................................................................................................657

Airway Protection and Pulmonary Toilet ..........................................................................657

Positive-Pressure Ventilation ..............................................................................................659

Adjunctive Strategies..........................................................................................................659

Acute Respiratory Distress Syndrome (ARDS) ......................................................... 661

Basic Concepts ..................................................................................................................661

Mechanical Ventilation.....................................................................................................663

Tidal Volume .....................................................................................................................663

Positive End-Expiratory Pressure (PEEP) ..........................................................................665

Airway Pressure Release Ventilation (APRV).....................................................................667

Adjunctive Strategies..........................................................................................................668

Fluid Management............................................................................................................669

Role of Corticosteroid Therapy........................................................................................669

Role of Prone Positioning.................................................................................................670

Nutritional Goals..............................................................................................................671

Summary ..........................................................................................................................671

Endpoints of Resuscitation ................................................................................... 672

Basic Concepts ..................................................................................................................672

Lactate...............................................................................................................................673
642 | Critical Care

Base Deficit .......................................................................................................................674

Supraphysiologic Oxygen Delivery Attainment ..............................................................675

Mixed Venous Oxygen Saturation / Central Venous Oxygen Saturation .......................676

Gastric Intramucosal pH (pHi) ........................................................................................677

Sublingual PCO2

 (PslCO2 ) ................................................................................................677

Tissue Carbon Dioxide and Oxygen Assessment............................................................678

Summary ..........................................................................................................................678

Sepsis................................................................................................................. 679

Definition of Sepsis ...........................................................................................................679

Pathophysiology ...............................................................................................................680

Prognosis ..........................................................................................................................680

Management.....................................................................................................................680

Infection Source Control....................................................................................................682

Resuscitation Goals............................................................................................................682

Intravascular Volume .........................................................................................................683

Role of Vasopressors..........................................................................................................684

Role of Corticosteroids......................................................................................................685

Assessing Adequacy of Oxygen Delivery...........................................................................686

Blood Product Transfusion ................................................................................................687

Role of Inotropic Therapy.................................................................................................688

Role of Recombinant Human Activated Protein C (rhAPC) ............................................689

Management of Hyperglycemia........................................................................................689

Role of Bicarbonate Therapy ............................................................................................690

Nutritional Goals ...............................................................................................................690

Summary............................................................................................................................690

Basic Care Considerations in the Combat Casualty Care ICU ................................... 692

Combat-Associated Pneumonia Prevention....................................................................692

Deep Venous Thrombosis Prophylaxis............................................................................694

Gastrointestinal Bleeding Prophylaxis............................................................................695

Preventive Care and Infection Control ............................................................................695

Structure of the Combat Casualty Care ICU....................................................................696

Critical Care Air Transport Team (CCATT)............................................................. 697

Historical Background and System Basics......................................................................697

Challenges Associated with Critical Care in the Air........................................................699

Summary............................................................................................................ 700

References .......................................................................................................... 701

Appendix ............................................................................................................ 719
Critical Care | 643

Introduction

The provision of critical care in the combat environment is never a passive process. There is always 

an opportunity to affect great change that can alter the course of a patient’s recovery. A command of 

several core concepts is vital for those who practice in the combat intensive care unit (ICU). This chapter 

will review basic mechanical ventilation, pulmonary contusion management, acute respiratory distress 

syndrome management, endpoints of resuscitation, sepsis, several basic ICU care considerations for the 

combat casualty care (CCC) patient, and the critical care air transportation system. In a given day at 

a wartime trauma resuscitation hospital, a clinician will encounter every one of these issues. They are 

fundamental, common, and important to master.

Mechanical Ventilation

The birth of the intensive care unit can be traced back to the application of invasive positive-pressure 

mechanical ventilation during the polio epidemic of 1952 in Denmark.1

 Prior to that time, positivepressure ventilation (PPV) had been used only sparingly for a few decades by anesthesiologists in the 

operating room. Most of the mechanical ventilation provided to patients with neurologic disorders or 

respiratory failure prior to 1952 was done with negative-pressure ventilation (NPV) devices such as the 

cuirass respirator or the iron lung (tank respirator). While negative-pressure ventilation more accurately 

simulates normal physiologic breathing, positive-pressure ventilation is used almost exclusively in modern 

critical care, mainly due to improved access to the patient. 

Mechanical ventilation has evolved as a discipline quite rapidly over the last few decades, and lessons 

learned are now paying substantial dividends with respect to morbidity and mortality. This section will 

focus primarily on the use of invasive mechanical ventilation to support the trauma patient encountered 

in the combat critical care setting. The use of noninvasive mechanical ventilation will be discussed in 

certain settings below where it may have a role, such as mild pulmonary contusion. The most important 

aspect of mechanical ventilation is defining the goals associated with its use in a given setting. A clear 

understanding of the clinical endpoint for this therapy will allow earlier liberation and improved 

outcomes. 

Key Concepts

Many trauma patients are placed on invasive mechanical ventilation primarily for airway protection 

early in a resuscitation or during perioperative periods. The method used to secure an airway depends 

upon the nature of the injury and the expected clinical course. Options include endotracheal intubation, 

nasotracheal intubation, cricothyroidotomy, and formal operative tracheotomy. Ensuring a stable, secure 

airway is always the first priority of any resuscitation. As vital as this step is, it is only the beginning. 

Mechanical ventilation is primarily a supportive therapy that buys time for an injury to heal, but it also 

has the ability to cause great harm if not used appropriately. A basic understanding of pulmonary system 

compliance, gas exchange, and ventilator-induced lung injury (VILI) is vital for its rational use.

A clear understanding of the goals and clinical endpoint of mechanical ventilation will allow for earlier 

weaning and improved outcomes.
644 | Critical Care

Compliance is defined as a change in volume divided by a change in pressure. In a given system, it may 

describe the change in volume expected if a given pressure is applied or vice versa. A system is said to be 

highly compliant when a large change in volume is associated with a small change in pressure. 

With respect to invasive mechanical ventilation, pulmonary system compliance is assessed by the machine 

at bedside. This measurement is made at some distance from the patient, and its significance depends 

upon the clinical setting. Pulmonary system compliance is a combination of the pulmonary compliance 

and that of the chest wall. The lungs have a tendency to pull the chest wall centrally while the chest 

wall is inclined to pull the lungs outward. The balance of these two forces defines the pulmonary system 

compliance in a given patient. A lung that is stiff due to pulmonary edema surrounded by a normal chest 

wall may generate a similarly decreased pulmonary system compliance as a normal lung enclosed within 

a chest whose motion is restricted by a circumferential burn eschar. While esophageal manometry can be 

used to distinguish chest wall versus pulmonary contributions to the overall system compliance, bedside 

clinical assessment will need to be relied upon during CCC.

When a compliance abnormality is identified, it is helpful to classify it as a static or dynamic defect. If 

using a conventional volume-control mode, as described later in this chapter, a compliance defect will 

result in an elevated peak pressure. The peak pressure is the highest pressure generated as the machine 

pushes a given volume of gas into a patient’s lungs. Once the initial portion of the breath is introduced, 

a more stable plateau pressure is reached until the end of inhalation. 

A static compliance abnormality is one in which there is an elevated peak pressure as well as a similarly 

elevated plateau pressure. No matter how long the inspiration period lasts, an elevated pressure 

will continue to be noted that is similar to the peak pressure. Conditions causing stiff lungs such 

as pulmonary edema or a stiff chest wall will result in a static compliance abnormality. A dynamic 

compliance abnormality is characterized by an elevated peak pressure that is significantly higher than 

the plateau pressure, the breath has difficulty getting into the lungs initially, but then is able to overcome 

the obstruction. A common example of this is mucus or other secretions in the airways that is significant 

enough to hamper, but does not completely obstruct airflow. 

Gas exchange in the lungs is accomplished at the level of the alveolar capillary interface. Ideally, flow of 

air into an alveolus and flow of blood into a surrounding capillary vessel bed should be matched. Areas 

of ventilation (V) should generally correspond to areas of perfusion (Q); V/Q = 1. When ventilation 

is present in the absence of blood flow (V/Q = infinity), this is known as dead-space ventilation.2

 The 

dead-space fraction is the ratio of dead-space (Vd) to tidal volume (Vt). The dead-space fraction is the 

portion of each breath that is unavailable for gas exchange. A normal person has a dead-space fraction of 

approximately 30 percent at rest that decreases to 18 percent at maximal exercise.3 A higher dead-space 

fraction results in difficulty eliminating carbon dioxide. 

Perfusion in the absence of ventilation makes it impossible for oxygen to diffuse from the airways into the 

blood and bind hemoglobin. Areas with preserved blood flow but an absence of ventilation (V/Q = 0) 

cause a right-to-left shunt.2

 The proportion of blood that passes from the right side of the heart to the left 

without being exposed to adequately ventilated alveoli is called the shunt fraction. 

In the normal lung, there are three physiologically distinct zones with respect to gas exchange as described 
Critical Care | 645

by West.4 From the top to the bottom of the lungs, there is an increase in alveolar ventilation as well as 

an even greater relative increase in blood flow. The uppermost portions of the lung are characterized by 

West Zone 1 physiology and are defined by an alveolar pressure (Palv) that is greater than the pulmonary 

artery systolic (PAs) and pulmonary artery diastolic (PAd) pressures. In West Zone 1 conditions, deadspace ventilation always exists since V/Q is by definition infinite. In West Zone 2 sections, PAs pressure 

is greater than Palv, which is greater than PAd pressure. Finally, in West Zone 3 sections, PAs pressure 

is greater than PAd pressure, which is greater than Palv. The majority of gas exchange happens in West 

Zone 3 conditions in the spontaneously breathing adult in the mid and basilar portions of the lungs.4

Positive-pressure invasive mechanical ventilation is often used to support patients who have inadequate 

oxygenation (respiration). Options available to improve respiration include increasing the fraction of 

inspired oxygen (FiO2

) or increasing the mean airway pressure. There are several ways to increase 

the mean airway pressure including inverse ratio ventilation, application of positive end-expiratory 

pressure (PEEP), and purposefully allowing the development of intrinsic PEEP. Treatment of hypoxemic 

respiratory failure will be covered in more detail later in this chapter when pulmonary contusion and 

acute respiratory distress syndrome are addressed.

Augmentation of oxygenation and elimination of carbon dioxide may be achieved though invasive 

mechanical ventilation.

Augmentation of carbon dioxide elimination (ventilation) is often facilitated with invasive mechanical 

ventilation. Each breath that is provided for the patient (Vt) can be thought of as a combination of a 

portion used for gas exchange (effective alveolar ventilation [Va]) and that lost to dead-space ventilation 

(Vd). Thus, Vt = Va + Vd. If one considers these components over the course of a minute (by multiplying 

each by the respiratory rate per minute), minute ventilation (Ve) = Va + Vd. Rearranging the equation 

for effective alveolar ventilation (Va) yields: Va = Ve – Vd = Ve (1 – Vd/Vt). 

The actual partial pressure of carbon dioxide in arterial blood (PaCO2

) is a function of how much CO2

is generated by the body (VCO2) and how much is eliminated (largely dependent upon Va): 

PaCO2 = k(VCO2)/Va = k(VCO2)/Ve(1 – Vd/Vt).

The CO2 production is generally proportional to the basal metabolic rate, and increases in times of 

physiologic stress and with temperature elevation. The respiratory quotient (RQ = VCO2/VO2) of 

enteral and parenteral feeds may also impact CO2 production in some critical care patients. Other than 

manipulating the RQ of feeds or controlling temperature, effective control of the PaCO2 is largely a 

function of mechanical ventilation and the ability to control the minute ventilation (Ve), which is equal to 

the respiratory rate ( f ) multiplied times tidal volume (Ve = f x Vt). It should be noted that overdistension 

of alveoli with excessive ventilator pressures or intravascular volume depletion can both lead to an increase 

in West Zone 1 conditions by increasing the dead-space fraction. This can happen in an unpredictable 

manner at times, but should be considered when carbon dioxide elimination is proving difficult with 

positive-pressure ventilation.
646 | Critical Care

Ventilator-Induced Lung Injury

One of the unfortunate lessons of critical care has been the realization that positive-pressure mechanical 

ventilation has the capacity to cause significant harm. Injury caused to the lung as a direct result of the use 

of a ventilator is called ventilator-induced lung injury (VILI). The pathophysiology of VILI is complex, 

but includes the effects of extrapulmonic air trapping (see barotrauma below) as well as the development 

of diffuse alveolar damage that is indistinguishable from that seen in acute respiratory distress syndrome 

(ARDS). As our understanding of VILI increases, so does the nosology to classify it. At present, it is 

helpful to think of four distinct subsets: barotrauma, volutrauma, atelectotrauma, and biotrauma.

Morbidity associated with positive-pressure mechanical ventilation is termed ventilator-induced 

lung injury (VILI). It may be broadly classified into barotrauma, volutrauma, atelectotrauma, and 

biotrauma.

Barotrauma

Barotrauma describes the most commonly appreciated adverse effects, such as the development of air 

collections outside of the lung, due to the use of inappropriately high pressure levels for a given clinical 

condition. While it is possible for a pneumothorax to develop directly at the periphery of the lung as a 

direct result of pressure changes, it is more frequently observed that air ruptures into the bronchovascular 

bundles first and dissects proximally resulting in a pneumomediastinum. Since the pleural space and the 

mediastinal space are separated by a pleural reflection on each side, a pneumothorax may or may not 

develop. Any subsequent pneumothorax will not necessarily form on the side of the initial airway defect. 

Finally, air may dissect in a cephalad or caudal direction, resulting in palpable air collections in the skin of 

the face, neck and chest, or intestinal wall (pneumatosis intestinalis) (Fig. 1).

Volutrauma

Volutrauma describes a physical overdistension of alveolar lung units that leads to pulmonary inflammation 

and can trigger the development of diffuse alveolar damage. It may occur in association with barotrauma, 

especially when excessive ventilatory pressures are used. Volutrauma is most likely to be a problem in 

conditions characterized by uneven ventilation such as pulmonary contusion or ARDS. Air becomes 

preferentially diverted to alveolar units with preserved compliance, leading to their overdistention. Animal 

models demonstrate that alveolar overdistention is likely a larger contributor to the development of VILI 

than elevated intraalveolar pressures.5

 From a pressure standpoint, it is the transalveolar pressure that is 

most dangerous, rather than the absolute pressure applied by the ventilator. The transalveolar pressure 

is directly correlated with the subsequent volume of expansion and therefore the potential development 

of volutrauma. 

Atelectotrauma

Atelectotrauma refers to the repetitive opening and closing of alveolar lung units, which can lead to the 

development of local inflammation and diffuse alveolar damage. This occurs because opening and closing 

of alveoli that are adjacent to alveoli that are incapable of opening contribute to a shearing stress at their 

interface. Cytokines are released that perpetuate the local inflammatory response and may serve as a 

catalyst for injury in other parts of the body. This is one hypothesized mechanism for the development 

of multiple organ dysfunction syndrome and is more likely to be a major player in VILI associated with 

asymmetric lung injury.5
Critical Care | 647

Biotrauma

An emerging concept that links the three aforementioned mechanisms of VILI is that of biotrauma. 

Biotrauma describes the impact on the lungs and body of biologically active molecules such as 

inflammatory mediators that are released as a direct result of positive-pressure ventilation. Alveolar 

volume, pressure, and cyclical opening have all been associated with the development of biotrauma.6,7 It 

is likely that biotrauma is a final common pathway resulting in lung injury for many otherwise seemingly 

disparate mechanisms. Use of antiinflammatory agents to prevent or mitigate the impact of VILI has 

thus far been unsuccessful, further underlining the importance of prevention.8

Oxygen toxicity primarily leads to the development of pulmonary fibrosis. Efforts to limit the FiO2

should be made whenever possible (FiO2 less than 50 percent) to minimize this complication.

Oxygen toxicity should also be considered a local form of biotrauma. There is no “safe” level of 

oxygen supplementation since its presence in any concentration will be associated with some degree 

of oxidation and damage to tissues. Animal models have convincingly demonstrated that higher levels 

Figure 1. Four-year-old child with severe ARDS at a Level III facility. Very high mean airway pressure requirements to maintain minimal oxygenation 

resulted in severe barotrauma.
648 | Critical Care

of oxygen supplementation lead to the development of a form of VILI that is independent of the 

effects of pressure, volume, and cyclical changes.9 Oxygen toxicity leads primarily to the development of 

pulmonary fibrosis and efforts to limit the FiO2 should be made whenever possible. While no completely 

safe threshold has been demonstrated convincingly in clinical trials, most advocate decreasing the FiO2

to less than 50 percent as soon as possible.10

Basic Modes of Positive-Pressure Ventilation

Overview

The provision of positive-pressure ventilation can be accomplished in an ever-increasing variety of 

ways. The increasing complexity of computer-driven algorithms can be confusing, but focusing on the 

fundamentals can help the clinician choose an appropriate mode for a given clinical situation. This 

section reviews some basic concepts applicable to all methods of providing positive-pressure ventilation 

and how they apply to more common modes of ventilation in clinical use. At the heart of understanding 

the different modes of ventilation is appreciating the impact of compliance and how the ventilator and 

patient communicate with each other. As discussed previously, compliance is the change in volume over 

the change in pressure. At any given point in time, the pulmonary system has a given overall compliance 

that will dictate the pressure change expected if a volume is provided by the ventilator. Conversely, if 

a pressure is provided by the ventilator, the compliance will determine the volume that is generated. 

Generally, a positive-pressure breath provides a volume or a pressure as an independent variable to the 

patient, and the compliance of the pulmonary system determines the value of the dependent variable. 

Communication between the ventilator and the patient is what defines the actual mode of ventilation. 

When a given mode of ventilation is chosen, a set of rules for communication between the patient and 

ventilator is established. At a basic level, the defining questions are as follows: (1) how does the machine 

know when to start a breath?; (2) how does the machine provide the breath?; and (3) how does the 

machine know when to stop giving the breath? The combination of answers to these three questions 

defines the basic rules of communication and, therefore, the ventilator mode.

The trigger is the signal to the ventilator that it is time to provide a positive-pressure breath. For the 

common modes of ventilation, the trigger for a given breath is time (a breath is delivered at a set rate 

regardless of patient effort) or patient-driven. A patient-triggered breath is provided when the patient 

initiates a predetermined negative inspiratory pressure or a change in flow in the ventilator circuitry. 

This is interpreted by the machine as a desire on behalf of the patient to receive a breath. Some modes 

have both time and patient triggers (assist-control), as will be discussed later.

Provision of a breath to the patient depends on whether the machine or the patient initiated the breath. 

When the breath is given to the patient in accordance with a predetermined rate, it is said to be a control 

breath. A breath that is given by the machine in response to initiation by the patient is said to be an 

assist breath. Occasionally, the patient may initiate a breath that is in close proximity to when a control 

breath was going to be given by the machine. Most current ventilators recognize this and provide the 

planned control breath rather than an assist one in order to maintain minimum minute ventilation and 

avoid patient-ventilator synchrony problems.
Critical Care | 649

Modes of ventilation are generally referred to as volume-control or pressure-control modes. Volume control 

is unfortunately a misnomer. A volume-control breath delivers a set volume to the patient; however, flow 

is actually the controlled variable. A specific flow is given by the machine until a predetermined volume 

is achieved. It is more accurate to think of volume control as volume set and flow control. A pressurecontrol mode of ventilation does deliver a set pressure using a pressure control and is therefore an accurate 

description. The cycle defines how the machine knows to stop giving a breath to the patient and allow 

exhalation to begin. Available cycle mechanisms commonly used include time, volume, pressure, and 

flow. Time cycles are often used in both pressure- and volume-control modes where a set inspiratory to 

expiratory (I:E) ratio is important to maintain. Flow cycles are frequently applied to pressure-supported 

assist breaths in modes such as pressure-support ventilation, as will be described below. 

With this brief background, it is now time to consider how trigger, control, and assist breath delivery and 

cycle define the modes that are commonly used for positive-pressure ventilation. A few less conventional 

modes will also be described that may be of use in the combat casualty critical care setting today or in 

the near future. 

Assist-Control (A/C)

Trigger: Time (controlled breaths), Patient (assisted breaths)

Breath Delivery: Control (volume set and flow controlled) 

 Assist (volume set and flow controlled)

Cycle: Time or Volume

In A/C mode, a respiratory rate, tidal volume, and inspiratory flow rate are set by the operator. The 

combination of these three variables will define the I:E ratio. The patient can trigger an assist breath 

that is recognized by the machine as either a negative pressure or change in flow in a closed circuit. The 

assist breath given has an identical tidal volume to the control breaths. Cycling depends on the ventilator 

manufacturer. In the past, a volume cycle was used for both the controlled and assisted breaths, and an 

operator set flow rate would determine the I:E ratio. Most current ventilators provide a mechanism for 

setting an I:E ratio, and the machine will automatically determine a time cycle based on the average 

number of total breaths the patient is breathing per minute. To achieve the desired I:E ratio, the machine 

may vary the flow and/or have a built-in inspiratory hold after the set volume is applied in order to 

achieve the desired I:E ratio. 

Synchronized Intermittent Mandatory Ventilation (SIMV)

Trigger: Time (controlled breaths), Patient (assisted breaths)

Breath Delivery: Control (volume set and flow controlled)

 Assist – none (SIMV) versus pressure-support (SIMV/PSV)

Cycle: Time or Volume (controlled breaths), Flow (assisted breaths)

With SIMV mode ventilation, the operator determines a set respiratory rate and tidal volume, and cycling 

of controlled breaths is identical to that described in the A/C section. In fact, in a patient who takes no 

spontaneous breaths, SIMV mode is identical to A/C mode. Assisted breaths that are initiated by the 

patient have a trigger that can be either a change in flow or the generation of a predefined negative 
650 | Critical Care

inspiratory pressure. When SIMV is used alone, there is no support given by the ventilator during an assist 

breath. The machine recognizes that a spontaneous breath has been initiated and responds by opening a 

valve that allows the patient to take as deep a breath without support as the patient can. Frequently, SIMV 

is combined with pressure-support ventilation (PSV). The combined SIMV/PSV mode allows an operator 

determined pressure-support to be applied by the ventilator through the inspiratory phase of an assist 

breath. The resulting tidal volume will be determined by the pulmonary system compliance at the time the 

breath is delivered and may or may not be similar to the set tidal volume delivered on controlled breaths. A 

flow cycle is used to terminate assist breaths in both SIMV and SIMV/PSV. The machine determines the 

maximal inspiratory flow at breath initiation and cycles the breath off when the inspiratory flow generated 

by the patient declines to a predetermined point, such as 20 to 25 percent of the maximal value. 

Although SIMV is frequently used in critical care units today, it cannot be recommended as a weaning 

mode of ventilation. The rationale for its use as a maintenance mode of ventilation, above other 

modes, has little support in the literature.

Synchronized intermittent mandatory ventilation was initially designed as a weaning mode where an 

operator could transition a patient to a completely spontaneous mode of ventilation from a completely 

controlled mode simply by decreasing respiratory rate over time. Unfortunately, SIMV performed 

inferiorly to PSV and T-piece trials in two major prospective, randomized weaning studies and delayed 

overall extubation time.11,12 Several hypotheses have been proposed to explain these findings, many 

relating to the way in which SIMV was applied. Of note, research indicates that as the set respiratory 

rate declines as a percentage of the overall respiratory rate, the work of breathing goes up substantially.13

Assisted breaths in the SIMV mode can be quite variable and may not be adequate. Proponents of 

SIMV argue that combining SIMV with PSV allows assist breaths that have less variability relative to the 

control breaths and therefore decreased work of breathing. Others argue that titrating PSV to achieve 

assist breaths that are similar to control breaths in SIMV/PSV is no different from what can more easily 

be accomplished with A/C. Although SIMV is frequently used in critical care units today, it cannot be 

recommended as a weaning mode, and the rationale for its use as a maintenance mode of ventilation 

above other modes has little support in the literature.11,12,14 

Pressure-Control Ventilation (PCV)

Trigger: Time (controlled breaths), Patient (assisted breaths)

Breath Delivery: Control (pressure controlled)

 Assist (pressure controlled)

Cycle: Time or Pressure

Pressure-control-ventilation mode is identical to A/C mode with the exception that the breath delivered 

in the control or assist setting is a pressure breath set by the operator. This mode is frequently utilized 

in disease states where pulmonary system compliance is limited, and it is perceived by the clinician that 

using a predefined pressure control will decrease the likelihood of barotrauma. It is also used in situations 

where manipulation of the I:E ratio to greater than or equal to 1:1 (inverse ratio ventilation) is felt to be 

advantageous. When volume control A/C is set appropriately, there is little advantage to the use of PCV 

even in disease states where both such concerns manifest, such as ARDS. Pressure-control ventilation and 

volume-control A/C are in actuality very similar modes of ventilation, and either can be used in most 

cases, the choice being largely related to operator comfort.
Critical Care | 651

Pressure-control ventilation mode is frequently utilized in disease states where pulmonary system 

compliance is limited and where pressure control will decrease the likelihood of barotrauma.

Understanding the concept of compliance is key. A given volume can be given that will generate a certain 

pressure. Conversely, a pressure can be given that will generate a certain volume. The relationship between 

the volume and pressure is defined by the system compliance, and whether the breath is given as a volume 

or a pressure is largely irrelevant in most circumstances. When pressure-controlled breaths are used in 

conditions characterized by reduced pulmonary system compliance, inadequate tidal volumes are possible 

and should be watched for closely. Occult air trapping with significant intrinsic PEEP that is unrecognized 

will also result in a lower than expected tidal volume when using pressure-controlled breath delivery.

Pressure-Support Ventilation (PSV)

Trigger: Patient

Breath Delivery: Pressure support

Cycle: Flow

Pressure-support ventilation is a mode of ventilation that is strictly an assist mode. The patient triggers 

the ventilator by generating a change in flow or a negative inspiratory pressure that is recognized by the 

ventilator. The machine then provides an operator defined pressure support throughout the inhalation 

portion of the breath until a flow cycle is reached. The breath cycles off typically when inspiratory flow 

drops below 20 to 25 percent of the maximal inspiratory flow. One concern related to PSV is the potential 

for its application in patients who have an inadequate respiratory drive or respiratory muscle strength. 

In either case, an inadequate minute ventilation may result. Most modern ventilators that have PSV as 

an option also allow a predefined backup control mode such as A/C that is automatically initiated when 

the minute ventilation is below a certain threshold. Some proprietary programs will only augment the 

number of breaths needed at a given time to achieve the minimum minute ventilation and will continue to 

allow the patient to otherwise remain in PSV. Pressure-support ventilation is commonly used as a weaning 

mode in the ICU, although with enough pressure support this mode can also be used quite effectively as 

a fully supportive mode, as long as the patient is able to generate an adequate respiratory effort. 

Pressure-support ventilation is an assist mode commonly used to wean patients in the ICU.

Patients with significant air trapping may become dysynchronous with PSV. Prolonged exhalation times due 

to increased airway resistance (inflammation, secretions, etc.,) or increased compliance (emphysema) may 

result in incomplete alveolar emptying and the development of air trapping. Patients who have significant 

air trapping will be noted at end-exhalation to have a pressure within the lungs that is above atmospheric 

pressure (Patm). This is referred to as intrinsic positive-end expiratory pressure (iPEEP) or autoPEEP. 

The pressure difference between the intrinsic PEEP and atmospheric pressure can establish a significant 

expiratory flow between the gas exchanging units and the mouth, even when the patient considers the 

breath complete. This flow can be recognized by the ventilator and complicate the ability of the machine 

to accurately determine the proper time to end the inhalation portion of a breath that is flow cycled as in 

PSV. The machine may terminate the breath at a different time than the patient would prefer, creating the 

potential for significant dysynchrony. While use of PSV in patients with the potential for air trapping is not 

absolutely contraindicated, close attention should be paid to patient ventilator interaction.
652 | Critical Care

The basic modes of ventilation, as presented here, represent the most commonly utilized methods of 

delivering positive-pressure breaths today. They are, however, very rudimentary modes with respect to 

their ability to accommodate the underlying neuromuscular processes involved in producing a patient 

breath. Several newer modes of ventilation are currently being evaluated and can be expected to be seen 

shortly in modern critical care units. Three of these modes are discussed below as they are used from time 

to time in the current combat casualty critical care environment.

Advanced Modes of Positive-Pressure Ventilation

Airway Pressure Release Ventilation (APRV)

Airway pressure release ventilation (APRV) is a time-triggered, pressure-controlled, time-cycled mode 

used in conditions where limiting airway pressure and manipulating the I:E ratio are both desirable, 

such as ARDS. High PEEP (PEEPh) and low PEEP (PEEPl) levels are set, as are the amount of time to 

be spent at the high PEEP level (Th) and the time to be spent at the low PEEP level (Tl). The patient 

spends at least 60 percent of the respiratory cycle at PEEPh, typically closer to 80 to 90 percent. If the 

patient attempts to take a spontaneous breath, the trigger can be either flow or a negative inspiratory 

pressure. Generally, spontaneous breaths in APRV are unassisted when taken while at PEEPh. They may 

be assisted by preset pressure support when taken during PEEPl; however, often they are not when the Tl 

is of a very short duration. When pressure support is used to assist a spontaneous breath taken at PEEPl, 

it is often set to be equal to the difference between PEEPh and PEEPl. 

Airway pressure release ventilation (APRV) is a time-triggered, pressure-controlled, and time-cycled 

mode used in conditions where limiting airway pressure and manipulating the I:E ratio are both 

desirable (e.g., ARDS).

The advantage of APRV is the ability to control mean airway pressure by varying the I:E ratio without 

having to force the patient to complete an entire respiratory cycle with each spontaneous breath. For 

instance, if a patient were undergoing inverse ratio ventilation using either A/C or PCV, each spontaneous 

breath would force an entire iteration of the breathing cycle. This can be extremely uncomfortable to 

a patient and frequently mandates very high levels of sedation or even chemical paralysis. With APRV, 

a spontaneous breath does not change where the patient is in the time-triggered, pressure-controlled, 

time-cycled breath. If a breath is taken, the patient takes what he can and returns immediately to the 

PEEPh or PEEPl plateau that he was previously on. This is more comfortable for the patient, in spite of 

the maintenance of a significantly inversed I:E ratio. As the lung injury improves, the Th and Tl can be 

manipulated to a more normal I:E ratio over time, allowing an easy transition to more traditional modes 

of ventilation, particularly PSV. 

Pressure-Regulated Volume Control (PRVC)

Pressure-regulated volume control (PRVC) is a time- and patient-triggered, volume set/pressuresupported, time-cycled (set inspiratory time, Ti) mode of ventilation that adjusts the pressure support over 

the course of several breaths to achieve a preset tidal volume. This ensures adequate minute ventilation 

while augmenting patient efforts to the minimal extent necessary. PRVC use can be difficult in patients 

with significant variability in spontaneous respiratory breath generation. The ventilator looks at the 
Critical Care | 653

tidal volume achieved with a given pressure support during the set inspiratory time over the last several 

breaths and compares the average tidal volume achieved to the desired tidal volume. By calculating a 

compliance using the average tidal volume and the difference between the pressure support and the 

PEEP, the ventilator determines what increase in pressure support is necessary to achieve a target tidal 

volume. Unfortunately, variable pressure swings on a breath to breath basis can cause the ventilator to 

over or underestimate the optimal pressure support. Cough, significant patient movement, or tachypnea 

may all render PRVC a difficult mode to use and result in extreme patient work of breathing variability.

High-Frequency Ventilation (HFV)

High-frequency ventilation (HFV) has several variants that are all based on the idea of providing very low 

tidal volumes at very high respiratory rates. The most commonly studied of the HFV modes are highfrequency jet ventilation (HFJV) and high-frequency oscillatory ventilation (HFOV). High-frequency jet 

ventilation uses pulses of gas to generate very small tidal volumes at frequencies of one to 10 hertz (Hz). 

The mode was used initially for thoracic surgery involving the major airways, but today is generally 

limited to the pediatric critical care population. High-frequency oscillatory ventilation uses even higher 

frequencies of five to 50 Hz along with exceptionally small tidal volumes to maintain a predefined mean 

airway pressure in lung conditions with extremely limited pulmonary system compliance such as ARDS. 

Because of the extremely small tidal volumes being used, the method of gas exchange is fundamentally 

different when HFV is used relative to more conventional modes of ventilation. Chan et al. provided an 

excellent review of HFOV in the treatment of ARDS.15 The use of HFOV in ARDS will be discussed in 

further detail below.

Basic Ventilator Settings When Lungs Are Normal

When mechanical ventilation is used for patients with normal lungs, it is being done for airway protection 

during the initial resuscitative period (Fig. 2). When employing mechanical ventilation, careproviders must 

avoid VILI. Finally, some lung conditions not appreciated initially may evolve or develop over time, such 

as pulmonary contusions, tracheal injury, or acute lung injury. The initial ventilator settings considered 

here assume normal pulmonary system compliance and an absence of identifiable lung injury.16,17,18

It is recommended that most be placed on traditional A/C ventilation as follows: FiO2 = 100 percent, f = 

16 to 20, Vt = 5 to 8 milliliters (ml) per kilogram (predicted body weight), PEEP = 5 centimeters (cm) 

H2O and flow = 60 liters per minute.19

The FiO2 can be turned down quickly after intubation to the lowest amount necessary to keep pulse 

oximeter oxygen saturation (SpO2) greater than 92 to 94 percent (a higher SpO2 may be desired when 

shock states are present). In cases of hypoperfusion where the SpO2 cannot be measured accurately, serial 

arterial blood gas assessments may need to be obtained to appropriately titrate the FiO2. 

The FiO2 should be titrated downward after intubation to the lowest amount necessary to keep SpO2

greater than 92 to 94 percent.

The minute ventilation (Ve = f x Vt) adequacy is determined primarily by the pH. Whatever minute 

ventilation is necessary to achieve an adequate pH is the goal of mechanical ventilation. Efforts to achieve a 

normal partial pressure of carbon dioxide in arterial blood (PaCO2

) are not generally productive. Partial 
654 | Critical Care

pressure of carbon dioxide in arterial blood manipulation should be more appropriately considered as 

a way of achieving a desired pH. In most patients, a pH above 7.25 is adequate, although 7.35 to 7.40 

is ideal in most settings. In some conditions, such as those associated with significant cerebral edema, 

low pH should be rigorously avoided.20,21 The tidal volume described here of 5 to 8 ml per kilogram is 

lower than the 8 to 12 ml per kilogram classically described for initial settings in a patient with normal 

lungs and more closely resembles recommendations for ventilation of ARDS patients. This is because a 

significant body of data is beginning to emerge that VILI also develops in normal lungs at volumes that 

were previously considered safe.22,23 It is important to note that the weight used in these formulas is the 

predicted (ideal) body weight (PBW) as used in the ARDSnet trials (see section on ARDS):

PBW in kilograms (male) = 50 + 2.3 x (height in inches – 60)

PBW in kilograms (female) = 45.5 + 2.3 x (height in inches – 60)

To compensate for the lower tidal volume recommended here, a higher respiratory rate will also be 

necessary. Adjustments in the respiratory rate should be made as necessary to achieve the pH goals outlined 

previously, as long as the patient’s spontaneous rate does not already exceed the machine set rate. If the 

Figure 2. Intubation of a patient with blast injury to the head and neck is performed during primary trauma survey to protect his airway.
Critical Care | 655

spontaneous rate does already exceed the set rate, the set rate should be established as approximately 80 

percent of the total rate, and further changes in the pH can be achieved with tidal volume manipulation. 

As the patient rate decreases, a decrease can be made in the set rate while attempting to keep the ratio 

of machine breaths to total breaths constant at about 80 percent. If the total rate does not exceed the set 

rate, then the set rate can be manipulated as necessary to achieve the pH goals described.

In the absence of any lung injury, PEEP greater than 5 cm H2O is generally not initially necessary. As 

the amount of time spent on the ventilator increases, dependent atelectasis frequently develops and can 

create a very significant shunt leading to hypoxemia. Increased levels of PEEP may need to be applied 

in order to combat the development of atelectasis or to counteract the effects of lung injury in evolution. 

The manipulation of PEEP will be discussed in more detail below as it pertains to pulmonary contusion 

and ARDS. 

In the absence of lung injury, PEEP greater than 5 cm H2O is generally not initially necessary. Increased 

levels of PEEP may be needed in order to prevent the development of atelectasis or to counteract the 

effects of lung injury in evolution.

There is rarely a significant benefit to the manipulation of flow. In patients with prolonged exhalation 

times, such as asthma and chronic obstructive pulmonary disease (COPD), flow is frequently increased in 

an attempt to decrease the I:E ratio and allow more time for exhalation. However, at a standard flow of 

60 liters per minute, a tidal volume of 500 ml is supplied in 0.5 seconds (60 liters per minute = 1000 ml 

per second). Therefore, doubling the flow rate to 120 liters per minute will decrease the inspiratory time 

to 0.25 seconds, extending the exhalation time by only 0.25 seconds. Simply decreasing the respiratory 

rate from 20 to 12 will increase the expiratory time by two seconds without having to manipulate the flow 

at all. 

Pulmonary Contusion

Basic Concepts

Pulmonary contusion represents a heterogeneous, generally asymmetric, lung injury that is associated 

with blunt trauma or blast injury (Fig. 3).24,25 It frequently evolves over hours to days and can result in 

significant right-to-left shunt as well as impaired ventilation. Associated injuries may include injury to 

the pulmonary vasculature and the airways. If a major airway injury occurs in association with blunt 

trauma, it frequently will appear within 2.5 cm of the carina and may not be appreciated during the 

initial resuscitation.26 Blast injury to the lungs can result from primary blast effects, penetrating trauma 

(projectiles), or blunt trauma that results in pulmonary contusion. The blunt trauma that is applied to the 

chest in the case of blast injury may be either from physical contact (being thrown against an object) or 

from air pressure waves. The development of pulmonary contusion in the setting of blast injury was said 

to be unlikely in the absence of tympanic membrane perforation.27 Recent reports dispute the reliability 

of tympanic membrane rupture as a sensitive screening tool for primary blast injury detection.28,29
656 | Critical Care

Blast injury to the lungs can result from primary blast effects, penetrating trauma (projectiles), or 

blunt trauma that results in pulmonary contusion. The blunt trauma that is applied to the chest in the 

case of blast injury may be either from physical contact (being thrown against an object) or from air 

pressure waves.

Contusion in the pulmonary parenchyma is 

characterized by collections of blood and exudative 

fluid in alveoli in response to destruction of the 

alveolar capillary interface by transmitted pressure. 

As the pressure waves propagate through the lung 

tissue, they transmit less energy per unit of lung 

tissue so the destruction is greatest closer to the 

point of impact. This is the primary reason for the 

asymmetric nature of the injury. Lobar collapse 

and focal atelectasis may also occur due to the 

collection of blood, blood clots, reactive airway 

secretions, mucus plugging, and occasionally 

aspirated secretions or foreign bodies such as teeth or 

food particles. All of these factors create significant 

regions of lung that have minimal ventilation but 

relatively preserved blood flow, resulting in right-toleft shunt development. The resulting hypoxemia 

may present fairly abruptly many hours after the initial injury.

Pulmonary system compliance decreases significantly with blunt trauma that is substantial enough to 

result in pulmonary contusion. Fractured ribs may limit the efficiency of rib cage movement, as may 

resultant pain. The particular condition of flail chest is characterized by the presence of two or more 

adjacent ribs that each have at least two sites of fracture (Fig. 4). Inspiration in the spontaneously breathing 

patient normally results from chest wall expansion and diaphragm contraction that generates a negative 

intrathoracic pressure relative to atmospheric pressure. This serves to draw the flail segment inward 

during inspiration and contributes to respiratory compromise. It also may not be recognized when a 

person is on positive-pressure mechanical ventilation because there is no mechanism for the flail chest to 

develop. The presence of significant chest wall injury of any kind can be expected to decrease the chest 

wall compliance.

The alveolar injury pattern described previously creates a decrease in lung compliance. The compliance 

is further decreased by any postobstructive atelectasis associated with airway occlusion by blood or other 

secretions. Inability to take deep breaths due to pain will contribute to the development of dependent 

atelectasis as well as make postobstructive atelectasis more likely. Decreased chest wall compliance 

and lung compliance both contribute to a limited total pulmonary system compliance. The limited 

compliance decreases the tidal volume that a patient is able to generate. In addition, given that a normal 

pair of lungs has a given amount of dead-space, a decreased tidal volume by necessity implies a greater 

dead-space fraction. A larger dead-space fraction means that there will be increased difficulty getting rid 

of carbon dioxide, so the body must compensate by increasing the minute ventilation (Ve = f x Vt). Since 

tidal volume is limited, patients with significant pulmonary contusions are often noted to breath shallowly 

Figure 3. Pulmonary contusion represents a heterogeneous, generally 

asymmetric, lung injury that is associated with blunt trauma or blast 

injury. 
Critical Care | 657

and rapidly as they try to increase respiratory rate. However, once tidal volume becomes sufficiently 

shallow and dead-space fraction significantly large, the patient is at great risk for the development of 

hypercarbic respiratory failure.

Management 

Airway Protection and Pulmonary Toilet

Airway protection and ventilator support are extremely important facets of pulmonary contusion 

management. Upper airway control with endotracheal intubation or tracheostomy is generally 

accomplished early in the resuscitation of severely injured patients. Due to the progressive nature of 

pulmonary contusion symptomatology, careproviders should obtain early airway control and provide 

ventilator support for all moderate to severely symptomatic pulmonary contusion patients. Mildly 

symptomatic cases may be managed with supplemental oxygen, serial observation, and pulse oximetry.30

Occasionally, patients may benefit from the use of noninvasive positive-pressure ventilation (NIPPV) if 

they are alert.31

Figure 4. Flail chest is described as the paradoxical movement of a segment of chest wall due to fractures of two or more ribs in at least two different 

sites. Here, multiple left-sided posterior rib fractures are noted.
658 | Critical Care

Due to the progressive nature of pulmonary contusion symptomatology, early airway control and 

ventilator support should be provided to all moderate to severely symptomatic patients. Mildly 

symptomatic cases may be managed with supplemental oxygen, serial observation, and pulse 

oximetry.

The concept of airway protection in the case of pulmonary contusion also extends to airways that can be 

reached by flexible fiberoptic bronchoscopy easily, such as those serving the major pulmonary segments 

(Fig. 5). Bronchoscopy allows removal of clots and secretions, thereby decreasing the percentage of 

lung that may have been prone to postobstructive atelectasis.32 A survey can be performed with flexible 

fiberoptic bronchoscopy to rule out any evidence of major airway injury and localize any major bleeding 

that may be present from vessel injury. Serial flexible fiberoptic bronchoscopy as the contusion progresses 

may be necessary to maintain adequate pulmonary toilet by clearing mucus plugging or inspissated 

secretions that may contribute to the late development of atelectasis. It should be noted that flexible 

fiberoptic bronchoscopy does not have the ability to clear blood or exudative secretions at the level of the 

alveoli.

Figure 5. Flexible fiberoptic bronchoscopy allows removal of blood clots and secretions, thereby decreasing the likelihood of postobstructive atelectasis.
Critical Care | 659

Positive-Pressure Ventilation

Positive-pressure ventilation has a key role in the care of pulmonary contusions by supporting adequate gas 

exchange.24 The application of a positive-pressure breath can augment the tidal volume enough to allow 

an adequate minute ventilation. The minute ventilation necessary may also be decreased by the use of 

positive-pressure ventilation since a more effective tidal volume will lead to a decreased dead-space fraction. 

Remembering that the PaCO2 is inversely related to Ve (1–Vd/Vt), it is easy to see that an augmented tidal 

volume will significantly improve ventilation in the setting of pulmonary compliance limitations.

As discussed earlier, positive-pressure ventilation can augment respiration (oxygenation) in two ways: 

increasing the FiO2 and increasing the mean airway pressure. Increasing the mean airway pressure can 

be accomplished in several ways, but is easiest to do in the setting of pulmonary contusion by increasing 

the PEEP. Positive end-expiratory pressure results in an increased functional residual capacity (FRC), 

which is the volume of the lung at end-tidal exhalation. The increased functional residual capacity 

helps to maintain the patency of alveoli and counteract the tendency towards atelectasis and shunt 

development. The application of PEEP may also open some previously closed alveoli, further improving 

the shunt fraction.

Positive-pressure ventilation is instrumental in the care of pulmonary contusions by supporting adequate 

gas exchange. 

One potential complication of excessive PEEP application results from the asymmetric nature of the 

lung injury.24 Any pressure applied by the ventilator will preferentially go first to portions of the lung 

with relatively normal compliance such as those that are not affected by the contusion. Serial increases 

in PEEP may paradoxically result in decreasing oxygenation if overdistension of normal lung becomes 

severe enough to decrease blood flow by the creation of West Zone 1 conditions. West Zone 1 conditions 

comprise alveolar pressures greater than pulmonary artery systolic pressures greater than pulmonary artery 

diastolic pressures. Blood will then preferentially flow to the contused lung units where ventilation is poor, 

increasing the shunt fraction and worsening hypoxemia. Increasing areas of West Zone 1 conditions by 

definition imply larger areas of dead-space ventilation, and the dead-space fraction is therefore increased 

leading to less effective ventilation. It is difficult to know in a given patient what level of PEEP may prove 

to be too much, but progressively worsening hypoxemia and hypercapnea in the setting of increasing 

levels of PEEP may imply that the level of PEEP being applied is excessive. 

It is important to remember that positive pressure can be applied noninvasively (NIPPV). This is an excellent 

option for patients with mild pulmonary contusions, who otherwise are not in need of invasive mechanical 

ventilatory support. The appropriate use of NIPPV can be expected to result in decreased ventilatorassociated pneumonia.31 However, as contusions may heal slowly and may progress over several days, the 

decision to use NIPPV should be accompanied by aggressive serial clinical evaluations. Use of NIPPV also 

makes the use of flexible fiberoptic bronchoscopy for airway survey and serial pulmonary toilet difficult.

Adjunctive Strategies

For patients with isolated pulmonary contusion, intravascular volume should be minimized to that 

necessary to ensure adequate systemic perfusion.31 This will minimize the adverse effects on pulmonary 

physiology. When pulmonary contusion is encountered in the multisystem trauma patient, it may not be 

the dominant or most life-threatening injury. In such cases, intravascular volume should be maintained as 
660 | Critical Care

dictated by the overall injury pattern, but fluid minimization should be accomplished when possible. Even 

in the setting of isolated pulmonary contusion, forced diuresis does not have a role except in patients who 

are otherwise intravascularly volume overloaded, as in the case of a congestive heart failure patient who 

may have sustained blunt thoracic trauma.31

In patients with isolated pulmonary contusion, intravascular volume administration should be kept to 

the minimum amount necessary to maintain adequate systemic perfusion.

Pain control is vital, as is stabilization of the chest wall. In the case of rib fractures, the application of 

positive-pressure ventilation may be all that is necessary for chest wall stabilization.33 Direct fixation of 

rib fractures may be necessary in some cases, particularly when large areas of flail chest are involved.33

Adequate pain control may be aided greatly by the use of epidural anesthesia and paravertebral blocks.34

Such techniques may be especially effective in the marginal, unintubated patient. Most deployed medical 

facilities that have anesthesia support should be facile in these methods of achieving pain control.

Figure 6. Patient with severe ARDS following trauma. ARDS is a clinical syndrome characterized by noncardiogenic pulmonary edema in response to 

lung injury.
Critical Care | 661

Control of cough is debatable, and it is difficult to offer guidance that applies to all cases.35 Cough is 

beneficial in that it may allow improved pulmonary toilet by dislodging clot and secretions in the airway, 

thereby decreasing postobstructive atelectasis. On the other hand, cough that is associated with significant 

chest wall pain may prolong the period where patients feel incapable of taking adequate deep breaths. 

This may contribute to hypercarbic respiratory failure as well as the development of more atelectasis. 

Cough in general should probably be encouraged, but any associated pain should be treated aggressively. 

Cough should only be suppressed when the pulmonary contusion is accompanied by active, uncontrolled 

pulmonary hemorrhage and intractable pain. 

Cough should only be suppressed when a pulmonary contusion is accompanied by active, uncontrolled 

pulmonary hemorrhage, or intractable pain. Otherwise, coughing should probably be encouraged, and 

any associated pain should be treated aggressively. 

Chest physical therapy is often prescribed for patients in the ICU, but there is almost no literature supporting 

its use in any setting outside of that associated with bronchiectasis.36,37 Some describe benefits in cases 

where postobstructive focal atelectasis is present, such as that associated with a maturing pulmonary 

contusion. If chest physical therapy is used for a pulmonary contusion patient, pain control is vital for the 

same reasons as outlined above with respect to cough. 

The significant shunt associated with pulmonary contusion is due to a heterogenous, largely asymmetric 

process.24,31 The injury process and resultant shunting associated with acute lung injury and the acute 

respiratory distress syndrome are also heterogenous but more likely to be symmetric (Fig. 6). There are 

significant differences in the management of these conditions as will be outlined in the next section.

Acute Respiratory Distress Syndrome (ARDS)

Basic Concepts

Acute lung injury (ALI) and ARDS both describe a common clinical syndrome characterized by the 

development of noncardiogenic pulmonary edema in response to a direct or indirect lung injury.38

Both processes have an identical pathophysiologic origin and management is the same.39 The difference 

between ALI and ARDS is one of severity with respect to the partial pressure of oxygen in arterial blood 

(PaO2

)/FiO2 ratio and is therefore somewhat arbitrary. For this reason, ARDS will be used exclusively in 

this review to describe any patient with a clinical syndrome compatible with either ALI or ARDS. The 

American-European Consensus Criteria for ALI and ARDS both include the following characteristics: 

acute onset (less than seven days), diffuse bilateral patchy infiltrates seen on standard chest radiography, 

and an absence of left atrial hypertension clinically (or with a pulmonary capillary wedge pressure 

[PCWP] less than 18 mm Hg if a pulmonary artery catheter is already in place). As noted previously, ALI 

and ARDS differ only in the PaO2/FiO2 used for their definition. Acute respiratory distress syndrome is 

notable for a PaO2/FiO2 less than 200, while that of ALI is between 200 and 300.39

Acute respiratory distress syndrome can be caused by both direct and indirect injuries.40 Direct causes 

include aspiration, pneumonia, blunt trauma to the chest, and other pulmonary processes that may 

trigger a significant inflammatory response. Indirect injury may cause ARDS by triggering systemic 

inflammation through the release of cytokines. Examples of indirect injury relevant to the critical care 
662 | Critical Care

ICU environment include multisystem trauma, shock, blood product transfusion, and sepsis. The common 

pathway for both direct and indirect causes is inflammation. When ARDS presents clinically, it usually 

develops several hours to days after the initial precipitating injury.40,41

Acute lung injury and ARDS both describe a common clinical syndrome characterized by the 

development of noncardiogenic pulmonary edema in response to a direct or indirect lung injury.

The likelihood of ARDS development secondary to an underlying insult rises with the age of the patient. 

The mortality attributable to ARDS is approximately 40 percent but increases with the number of 

concomitant organ system failures.40 The development of renal failure in the setting of ARDS denotes 

a particularly poor prognosis. A recent study demonstrated that the likelihood of eventual death due to 

ARDS is related to dead-space fraction on presentation.42 Those with a higher dead-space fraction had 

a higher mortality. The mortality due to ARDS is improving with aggressive supportive therapy and 

an increasing appreciation of the role that mechanical ventilation can play in both recovery and injury 

propagation.10

The pathology associated with ARDS is that of diffuse alveolar damage, regardless of the inciting injury, 

which may represent a stereotypic lung injury and healing response.40 There are two distinct clinical phases 

in the evolution of the lung injury: an exudative phase that predominates in the first five to seven days, 

followed by a proliferative phase after this point.40 Cytokines and other inflammatory mediators initiate 

changes that lead to disruption of the normal alveolar-capillary interface and the introduction of exudative 

fluid into the alveolus. This causes two major changes: the first is inactivation of surfactant, and the second 

is sloughing of the alveolar and bronchial epithelial cells. Loss of surfactant function makes alveolar collapse 

more likely, and the loss of epithelial cells leads to hyaline membrane formation on the denuded basement 

membrane. The injury leads to attraction of neutrophils as well as stimulation of alveolar macrophages. 

These cells release several cytokines, proinflammatory agents as well as some antiinflammatory mediators. 

On balance, there is a net effect to perpetuate the inflammatory process and to recruit other neutrophils. 

It is not clear to what extent local release of these agents impacts other organ systems.

The late phase of ARDS evolution, the proliferative phase, is notable for the development of fibrotic 

changes in the interstitium and alveolar spaces.40 There may be significant architectural distortion, and it is 

common to see an increase in dead-space fraction that may manifest as an increased PaCO2 or a suddenly 

increased spontaneous minute ventilation. While it is convenient to think of ARDS pathophysiology as 

having two distinct phases, there is evidence of abnormal fibroproliferation early in the syndrome, and 

fibroblast mitogenic activity on bronchoalveolar lavage specimens has been correlated with mortality.43

Most patients who die as a direct result of ARDS will do so during the exudative phase of the syndrome, 

but there is still a significant mortality risk for those in the fibroproliferative stage who require prolonged 

ventilation.40 Their mortality is increasingly likely to be related to nosocomial complications as well as 

failure of other organ systems.

In a clinical sense, there are three distinct lung zones created in patients with ARDS. There are significant 

portions of the lung that are dominated by shunt physiology secondary to alveolar filling and atelectasis, 

associated both with the loss of surfactant and dependent collapse. Most of these areas will either heal 

or they will not irrespective of interventions. Vigorous efforts to open involved alveoli are unlikely to be 

of benefit and may be harmful to more compliant areas of the lungs. A second important lung zone is 
Critical Care | 663

characterized by significant atelectasis or alveolar-capillary barrier damage that may be reversible. Some 

areas in this region may even open with the introduction of a positive-pressure breath but close as the breath 

is allowed to exit the lung. The cycle then repeats with each subsequent breath. This area is the battleground 

for ARDS supportive management. The goal is to utilize this region for gas exchange as much as possible 

while simultaneously protecting it from further injury evolution. The third lung zone is a relatively normal 

one. It is likely that there are significant inflammatory changes taking place in these regions as well, but 

from a gross macroscopic standpoint, this zone appears to behave in a normal physiologic manner. As 

described for the second region, one of the fundamental goals of ARDS care is to protect this normal 

lung zone from injury. Gattinoni et al. have used the term “baby lungs” when thinking about mechanical 

ventilation of ARDS patients, since a smaller than normal lung volume is actually available to perform the 

necessary physiologic function normally accomplished by the uninjured pulmonary system.44

The edema and atelectasis create a significant amount of physiologic right-to-left shunt that generally leads 

to progressive, severe hypoxemia. These changes also cause a significant reduction in lung compliance. 

Efforts to provide “normal” tidal volume breaths using a traditional volume-control mode will result 

in the development of very high peak and plateau pressures.40,45 Use of a pressure-control mode with 

the intent of limiting these high pressures will often lead to very low tidal volumes.46,47 Strategies for 

addressing both the shunt and compliance abnormalities will be discussed in further detail below.

Ventilator-induced lung injury is one of the significant dangers associated with the care of the ARDS 

patient.7 Volutrauma in ARDS has been noted with excessive tidal volumes in both retrospective and 

prospective human trials and demonstrated convincingly in animal studies.10 Volutrauma is felt to be one 

of the primary mediators of VILI in ARDS patients and has been the impetus for the low-tidal-volume 

strategies described below. Barotrauma was seen frequently in the past when overaggressive positivepressure ventilation was applied to ARDS patients with severely limited lung compliance, resulting in very 

high transalveolar pressures. Atelectotrauma due to cyclic opening and closing of alveoli is of greatest 

concern at the edges of portions of the lung that are densely consolidated. Alveoli that open and close 

adjacent to those that are incapable of opening create a shearing force with each cycle. This shearing 

force may disrupt the alveolar-capillary interface and perpetuate the lung injury. Finally, biotrauma 

associated with mechanical ventilation use will exacerbate the underlying inflammatory milieu already 

present in the ARDS patient and may serve to encourage further lung injury. With this as a background, 

attention now turns to the complex task of ARDS management. Goals for management of ARDS include: 

(1) eliminate the source of the ARDS; (2) provide aggressive supportive care to allow time for healing to 

take place; and (3) do not cause further harm with iatrogenic interventions. 

Goals for management of ARDS include: (1) eliminate the source of the ARDS; (2) provide aggressive 

supportive care to allow time for healing to take place; and (3) do not cause further harm with iatrogenic 

interventions. 

Mechanical Ventilation 

Tidal Volume

Volutrauma has long been noted in animal models to both perpetuate existing ARDS and to cause a lung 

injury de novo with pathology consistent with diffuse alveolar damage. It was therefore hypothesized 
664 | Critical Care

that using a lower tidal volume with mechanical ventilation may result in improved outcomes. Four 

randomized controlled trials conducted using so-called lung protective strategies were published in the 

late 1990’s.48,49,50,51 Only one of the four was able to demonstrate a statistically significant improvement 

in mortality.48 A consortium of institutions known as the Acute Respiratory Distress Syndrome Clinical 

Trials Network (ARDSnet) led by the National Heart Lung and Blood Institute was formed in the mid 

1990’s to coordinate ARDS research efforts. They conducted a large phase III randomized controlled 

trial comparing a low tidal volume (4 to 6 ml per kilogram) versus high (conventional) tidal volume (12 

ml per kilogram) that was published in 2000.52 The low-tidal-volume intervention resulted in statistically 

significant improvements in mortality, ventilator-free days and organ-failure-free days. It should be noted 

that the weight used for the tidal volume calculation is the predicted body weight. This same low-tidalvolume strategy was used in subsequent ARDSnet studies described later that addressed issues such as 

optimal PEEP settings, fluid strategy and corticosteroid use in ARDS. A reproduction of the ARDSnet 

low-tidal-volume strategy is included in the Appendix.

An early criticism of the low-tidal-volume ARDSnet trial was that it is unclear from the design of the study 

that a low tidal volume of 4 to 6 ml per kilogram is optimal. Another explanation of the study findings 

perhaps is that a tidal volume of 12 ml per kilogram may be excessive and did not represent the common 

standard of care at the time the study was done.53 The criticism has been countered by survey data from 

the mid 1990s demonstrating that average tidal volumes in use at the time of the study design were in fact 

similar to those produced in the ARDSnet study control group. At this point in time, the ARDSnet lowtidal-volume strategy is considered the standard of care for initial ventilator management of ARDS, and 

deviations from this basic protocol should only be made when it has failed in a given clinical setting. 

Low-tidal-volume strategy is considered the standard of care for initial ventilator management of 

ARDS.

Based on the ARDSnet study findings, initial ventilator settings for a patient with ARDS are illustrated 

below.52 For patients who were previously receiving invasive mechanical ventilation prior to the diagnosis 

of ARDS, adjust the FiO2 and PEEP as indicated in the Appendix. For patients who were intubated at 

the same time that the initial diagnosis of ARDS was made, begin with an FiO2 of 100 percent, a PEEP 

of 10 cm H2O and titrate both according to the Appendix. 

1. Assist-Control (A/C) Mode (volume set/flow controlled for assist and control breaths)

2. Initial Vt = 8 ml per kilogram (PBW)

PBW in kg (male) = 50 + 2.3 x (height in inches – 60)

PBW in kg (female) = 45.5 + 2.3 x (height in inches – 60)

3. Reduce Vt by 1 ml per kilogram until Vt = 6 ml per kilogram

4. Adjust f (up to 35) and Vt (4 to 6 ml per kilogram) to achieve peak plateau pressure (Pplat) less than

30 cm H2O and pH 7.3 to 7.45

5. Bicarbonate can be added if pH is less than 7.3 and if f is maximal at 35.

6. Initial FiO2 and PEEP levels were not predefined in the ARDSnet low-tidal-volume study. 

An important concern related to the use of low tidal volumes to limit plateau pressures in ARDS patients 

is the development of clinically significant respiratory acidosis. Previous research has demonstrated that 
Critical Care | 665

moderate degrees of respiratory acidosis are well tolerated in most instances and therefore represent a 

small price to pay relative to the benefits of decreasing volutrauma and barotrauma.54 This trade-off 

of ventilation for lung function preservation became known as permissive hypercapnia. The ARDSnet 

protocol allowed for the use of bicarbonate to help counteract the effects of hypercapnia and normalize 

the pH.52 There was little difference in pH between intervention and control groups after the initial 72 

hours. Other options in clinical practice include the use of proton scavengers such as tromethamine and 

less commonly limiting CO2 production by manipulating the respiratory quotient of feeds, decreasing 

body temperature, or minimizing metabolic rate through deep sedation or paralysis. The use of 

permissive hypercapnia in the setting of a severe elevation in intracranial pressure should be avoided 

due to associated worsening elevations in intracranial pressure.20,21,55,56

The use of low tidal volumes to limit plateau pressures in ARDS patients can lead to clinically significant 

respiratory acidosis. When permissive hypercapnia is practiced, the resultant acidemia can be mitigated 

by use of bicarbonate or other interventions.

Positive End-Expiratory Pressure (PEEP)

The optimal PEEP to be used for mechanical ventilation of the ARDS patient is an area of great interest 

and few definite answers.57 The maintenance of pressure in the airways at end-exhalation should help to 

prevent collapse of alveoli and preserve the current functional residual capacity, which is the volume in 

the lungs at the end of tidal exhalation. In ARDS, progressive atelectasis is a problem due to progression 

of the injury itself, as well as the effects of compression by a heavy, edematous lung on more dependent 

portions. The use of PEEP can counteract this trend. 

An intuitive approach to the application of PEEP would involve the examination of a static pressurevolume curve as represented in Figure 7. Pressure is applied initially to the lung in an effort to cause 

inflation. The initial portion of the curve is characterized by little change in volume in spite of pressure 

application, which represents alveoli that are closed and will not open without a significant amount of 

energy. Once a critical opening pressure is reached, the compliance of the system improves markedly, 

and the lung opens quickly with relatively little subsequent pressure application. This critical opening 

pressure is referred to as the lower inflection point. At some point, the lung cannot expand further 

and compliance again drops drastically yielding no significant gain in volume regardless of the further 

application of pressure. This point of sudden decrease in compliance is called the upper inflection 

point. 

Many experts have argued that the optimal PEEP should be one that is just above the lower inflection 

point, since the fundamental goal of PEEP is to prevent collapse of alveoli and loss of functional residual 

capacity. Others argue that it is more effective to use a higher level of PEEP just below the upper inflection 

point in order to maximize the ability to keep the lungs open. A third opinion relates to the fact that a 

static pressure-volume curve in ARDS often demonstrates a degree of hysteresis. The sigmoidal shape 

curve seen as air is pushed into the lungs is not identical to that seen when air is allowed to passively 

leave on exhalation. The exhalation curve is typically shifted slightly to the left, implying a higher lung 

volume at any given transpulmonary pressure relative to that seen on inhalation. Some advocate using 

the exhalation curve to determine the optimal PEEP rather than any point on the inhalation curve, since 

the goal is to help alveoli remain open as air leaves the lungs.
666 | Critical Care

Several ventilator packages have sophisticated software algorithms available that can project a pressurevolume curve. However, measurement of a true static pressure-volume curve involves paralyzing the 

patient and serially measuring pressures after different volumes are introduced into the patient. In the 

day-to-day clinical management of an ARDS patient, this process is time consuming, risky for the patient, 

and not practical to consider several times a day when compliance may be expected to change rapidly. 

Attempts to define the optimal use of PEEP have resulted in the evolution of two schools of thought, 

one advocating more moderate levels of PEEP and one favoring a high level of PEEP.58,59

Potential problems may be envisioned with both approaches. If a low-PEEP strategy is used, it may not 

be adequate enough to maximally prevent alveolar collapse. Additionally, worsening compliance due to 

evolution of the lung injury may lead to the emergence of an inadequate level of PEEP within hours or 

days that may have been adequate at the time it was set. If a low-PEEP strategy is used, close attention 

must be paid to the development of worsening compliance and shunt. The use of very high levels of PEEP 

may result in overdistension of relatively normal lung tissue. Excessive alveolar distending pressures may 

cause diversion of blood to less ventilated sections of the lung. This creates increased dead-space in the 

more compliant areas of lung and increased shunt in the more consolidated areas. Other complications 

to consider in the scenario would be atelectotrauma exacerbation at the interfaces between more and 

less compliant areas of lung, as well as volutrauma and possibly barotrauma in the overdistended lung 

regions. All of these effects would perpetuate biotrauma and add the effects of VILI to those already 

ongoing due to the ARDS.

Figure 7. An ARDS static compliance curve. Once a critical opening pressure is reached (B), the compliance of the system improves markedly and the 

lung opens quickly with relatively little subsequent pressure application.

A

B

C

D

500

250

0 15 30

Pressure (cm H2O)

Volume (ml) Alveoli

Lower inflection point

Upper deflection 

point
Critical Care | 667

In 2004, the ARDSnet published the results of a multicenter randomized controlled trial comparing 

a low-PEEP/high FiO2 strategy to a high-PEEP/low FiO2 strategy known as the Assessment of Low 

Tidal Volume and Elevated End-Expiratory Lung Volume to Obviate Lung Injury (ALVEOLI) trial.59

The study enrolled 549 patients to completion and did not show a significant difference in terms of 

hospital mortality or ventilator-free days. The average PEEP in the low-PEEP group was 8.3 cm H2O 

compared to 13.2 cm H2O in the high-PEEP group. A subgroup analysis of the ALVEOLI trial compared 

the effects of recruitment maneuvers in ARDS patients who were ventilated in the high-PEEP group. 

Recruitment maneuvers were performed by transitioning the patient from A/C to continuous positive 

airway pressure (CPAP) with a pressure of 35 cm H2O and maintaining this pressure for 30 seconds 

before transitioning back to A/C. There were some transient improvements in SpO2 in some patients, 

but no sustained improvements after an hour were noted. Some patients experienced desaturation and 

hypotension as complications. A recent study compared the use of a moderate level of PEEP (5 to 9 cm 

H2O; the minimal distension group) to an increased recruitment approach (increasing the PEEP to reach 

a plateau pressure of 28 to 30 cm H2O).60 All patients received a low-tidal-volume (6 ml per kilogram) 

strategy with volume set/flow controlled, A/C as the mode of mechanical ventilation. There was no 

significant difference in mortality, but the increased recruitment strategy led to a statistically significant 

improvement in the number of ventilator-free days and organ failure-free days. It should also be noted 

that adjunctive therapies such as prone positioning and inhaled nitric oxide were used more frequently 

in the minimal distension group. Meade et al. compared an “open-lung” strategy of ventilation versus 

the now standard ARDSnet low-tidal-volume algorithm in a multicenter randomized controlled trial 

published in 2008 involving 983 patients with ARDS.61 The intervention group received a plateau pressure 

limit of 40 cm H2O, pressure-control ventilation, and a significantly higher PEEP than that seen in the 

2000 ARDSnet low-tidal-volume trial. There was no difference in mortality, but there was a statistically 

significant decrease in refractory hypoxemia and the use of rescue therapy (inhaled nitric oxide, prone 

positioning, high frequency oscillatory ventilation and extracorporeal membrane oxygenation) in the 

intervention group. 

In most cases of ARDS, the optimal PEEP is likely at least 10 to 12 cm H2O. Higher levels should 

be attempted in patients with more severe ARDS manifestations, while close attention is paid to the 

development of iatrogenic complications.

Conclusions regarding PEEP remain a source of great debate. The data appears to favor a higher PEEP 

with respect to oxygenation, but there does not appear to be a mortality benefit to this approach.59,61

Concern exists that excessively high levels of PEEP may perpetuate VILI, exacerbate hypoxemia and 

hypercapnia, and may cause hypotension.62 The optimal PEEP is likely at least 10 to 12 cm H2O in most 

cases, and higher levels should probably be attempted in patients with more severe ARDS manifestations 

while close attention is paid to the development of iatrogenic complications.59,61

Airway Pressure Release Ventilation (APRV)

Airway pressure release ventilation (APRV) has been used as an alternative mode of mechanical 

ventilation in the ARDS patient.63,64 As discussed earlier, it involves controlling the mean airway pressure 

by cycling between two different levels of PEEP. The ability to generate a high mean airway pressure 

augments oxygenation, while the upper PEEP level serves to limit the plateau pressure generated by 

driving air into a noncompliant lung. The ability to limit the plateau pressure is an attractive feature of 

this mode of ventilation in ARDS, as is such a precise ability to control the mean airway pressure. The 
668 | Critical Care

fact that the ventilator does not have to change its controlled pressure release cycle based upon patient 

effort is also very helpful and allows the use of very aggressive inverse ratio ventilation with less patient 

discomfort.63 This allows a decreased requirement for sedation and chemical paralysis.65

One drawback of APRV mode is that the tidal volume generated by the controlled breaths is determined 

by the difference between the high PEEP and low PEEP levels. Most who use APRV tend to use relatively 

aggressive PEEPh levels but PEEPl levels of 0 to 5 cm H2O. This large difference creates the potential for 

excessive tidal volume generation greater than 6 ml per kilogram and therefore may perpetuate VILI. The 

development of intrinsic PEEP may mitigate this concern somewhat since the time spent at the PEEPl 

is frequently very short. The time at the PEEPl is often set so that the expiratory flow versus time curve 

is only 80 to 90 percent of the way back to a baseline of zero flow when the machine cycles back to the 

PEEPh level. Significant intrinsic PEEP will cause the tidal volume to be proportional to the difference 

between the PEEPh and intrinsic PEEP rather than the larger difference between PEEPh and PEEPl. 

There is no data to support the use of APRV over other modes of ventilation in the setting of ARDS. It 

should be thought of as a potentially useful salvage therapy in the critical care setting for patients who 

have failed a traditional ARDSnet low-tidal-volume strategy.

At this time, there are no data to support a benefit of this mode of ventilation versus any other mode in the 

setting of ARDS. There are studies that describe the successful application of APRV for ARDS patients, 

and some major medical centers have a great deal of experience with the mode.66 A randomized, open 

labeled, parallel assignment study comparing APRV to the ARDSnet low-tidal-volume standard of care 

for ALI/ARDS is currently enrolling patients.67 At this time, APRV should be thought of as a potentially 

useful salvage therapy in the CCC setting for patients who have failed the traditional ARDSnet low-tidalvolume strategy.

Adjunctive Strategies

Inhaled nitric oxide (iNO) has been used to cause selective pulmonary artery vasodilation in several 

conditions, including primary pulmonary hypertension, pulmonary reperfusion lung injury after 

pulmonary thromboendarterectomy, and ARDS in both adults in infants.68,69,70 Inhaled nitric oxide is 

very short-acting and does not enter the systemic circulation to an appreciable extent. Its effects are 

therefore locally confined to well-ventilated alveoli, serving to improve ventilation-perfusion matching. 

Importantly, perfusion is diverted away from poorly ventilated regions, which has the effect of decreasing 

the shunt fraction and therefore improving hypoxemia. Several clinical trials have evaluated the use of 

iNO in ARDS with variable designs and outcomes. A recent meta-analysis concluded that there is a small 

but significant improvement in PaO2

/FiO2 at 24 hours but no improvement in mortality and potential 

harm (renal dysfunction). Thus it cannot routinely recommended at this time.69

Although there is a small but significant improvement in PaO2/FiO2 at 24 hours, inhaled nitric oxide 

fails to improve mortality, and cannot be routinely recommended for treatment of ARDS.

High-frequency oscillatory ventilation is the intellectually extreme manifestation of the low-tidal-volume 

approach. The majority of clinical experience with this mode of ventilation and its application in ARDS 

is confined to a few major academic medical centers. A study published by Derdak et al. in 2002 compared 
Critical Care | 669

the use of HFOV versus a more conventional mode of ventilation.71 There was no mortality benefit 

noted in that study, although there was a trend towards improved survival noted as many as 90 days after 

randomization (p = 0.1, 148 patients enrolled in the study). The average tidal volume in the conventional 

ventilation group was 10 ml per kilogram. There has not been a prospective randomized controlled 

trial comparing HFOV to the ARDSnet low-tidal-volume strategy. High-frequency oscillatory ventilation 

should be thought of as a rescue therapy only in centers with significant experience in its use. It may find 

wider application in the future as further prospective studies are conducted.

Extracorporeal membrane oxygenation (ECMO) has been used in neonatal intensive care for ARDS for 

several decades with success.72 The therapy involves diverting blood through a filter outside of the body 

to allow gas exchange and then reintroducing the treated blood into the vasculature. A large prospective 

study evaluating the use of ECMO in adults with severe acute respiratory failure during the 1970’s failed 

to show a significant benefit to the therapy.73 Extracorporeal membrane oxygenation is used as therapy for 

ARDS in a few large medical centers today with relatively stringent criteria used for selection of patients 

believed to derive benefit. A portable extracorporeal carbon dioxide removal (ECCO2R) device called 

the NovaLung® has been used in the ICU as rescue therapy for United States (US) service members 

wounded in Iraq with severe ARDS and for their critical care air transport out-of-theater. Rationale 

for this approach stems from allowing the use of very low minute ventilation in an effort to minimize 

ventilator induced lung injury.74 Experience is limited, but anecdotal success has been encouraging.75

Randomized controlled trials further evaluating ECMO and ECCO2R technology relative to ARDSnet 

low-tidal-volume standards are needed.

Fluid Management 

A recent study compared a conservative versus liberal fluid management strategy in ARDS.76 The study 

also compared the use of a central venous catheter in the internal jugular or subclavian position versus 

a pulmonary artery catheter to guide assessment of intravascular volume status. The conservative fluid 

strategy limited fluid infusion and encouraged early diuresis. There was a profound difference in cumulative 

fluid balance between the liberal and conservative fluid groups by day seven after randomization. Of note, 

the cumulative fluid balance curves for the initial ARDSnet low-tidal-volume and ALVEOLI studies were 

almost identical to the liberal fluid curve in the Wiedeman et al. study.52,59,76 With respect to fluid balance 

approaches, there was no significant difference in mortality; however, an improvement was noted in both 

ventilator-free days and ICU-free days in the conservative fluid group. There was no difference in any 

major outcome when comparing the use of a standard central venous catheter versus a pulmonary artery 

catheter. It is recommended that outside of the initial resuscitation for hypovolemic shock, intravascular 

volume be minimized to the extent possible. There does not appear to be a significant role for the routine 

use of a pulmonary artery catheter for the management of ARDS.

Apart from the initial resuscitation for hypovolemic shock, intravascular fluid administration should be 

minimized during management of ARDS.

Role of Corticosteroid Therapy

Corticosteroids have been evaluated in both the early and late phases of ARDS in several well-designed 

randomized controlled trials over the last fifteen years. An ARDSnet trial published in 2006 evaluating 

the efficacy and safety of corticosteroid use for persistent ARDS did not demonstrate a mortality benefit 
670 | Critical Care

to their use.77 In fact, corticosteroids started more that two weeks after onset of ARDS were associated 

with an increased mortality. There was a statistically significant improvement in ventilator-free days in 

the treatment group through 28 days after randomization. Two meta-analyses published recently arrived 

at conflicting conclusions.78,79 Agarwal et al. were unable to find any benefit in mortality with the use of 

corticosteroids for ARDS in either the early or late phase.78 Meduri et al. found a statistically significant 

improvement with the use of corticosteroids with respect to ventilator-free days as well as mortality.79

The routine use of corticosteroids in either the early or late phase of ARDS is not recommended at this 

time. 

Currently evidence suggests there may be some physiologic improvement with the use of corticosteroids 

for ARDS, particularly when started before the development of a significant amount of fibrosis.80 There 

does not appear to be a consensus that mortality is improved with the therapy, and the potential for 

complications directly related to the therapy is significant. The routine use of corticosteroids in either the 

early or late phase of ARDS is not recommended at this time. 

Role of Prone Positioning

Prone positioning has been advocated as an 

adjunctive therapy for ARDS to improve 

oxygenation and has been studied prospectively 

in several trials.81,82,83,84,85,86 The physiologic basis 

for improvements in oxygenation is not entirely 

clear, but is hypothesized to involve improved 

ventilation perfusion matching, regional changes 

in ventilation, and decreased compression of 

the dependent portions of the left lower lobe 

by the heart. Proning a patient with ARDS can 

be a difficult undertaking and requires a special 

bed that can assist in the position change and 

several personnel. In the CCC environment, a 

frame made by the Stryker company is available 

that can be used in the ICU and during critical 

care air transportation (Fig. 8). The potential for 

dislodgement of endotracheal tubes and lines is 

significant and may be life threatening for a patient 

with marginal oxygenation at baseline. 

Gattinoni et al. were unable to demonstrate a mortality benefit to prone positioning for 304 ARDS patients 

enrolled in a randomized controlled trial, but a significant improvement in PaO2

 was noted in 70 percent 

of patients in the experimental group.83 A post-hoc analysis was able to demonstrate an improvement in 

mortality in the quartile of patients with the lowest PaO2

/FiO2 on enrollment as well as in the quartile 

of patients with the highest simplified acute physiology score (SAPS) II at enrollment. One criticism of 

the study was the relatively short duration of prone positioning. Of note, there was no difference in the 

number of endotracheal tubes that were dislodged between the experimental and control groups.

Figure 8. A Stryker frame allows a patient to be turned to the prone 

position as a single unit without individually moving parts of the body.
Critical Care | 671

A 2002 review of the literature for the use of prone positioning with ARDS concluded that 

improvement in oxygenation can be expected in 70 to 80 percent of early ARDS patients undergoing 

prone positioning, but the effects of this improvement are not seen after seven days.82 There does not 

appear to be a substantial mortality benefit and significant care must be taken during patient position 

changes. Finally, the incidence of pressure sores was increased in patients who were proned and related 

directly to the duration of time in the prone position. A recent prospective randomized trial evaluated 

the use of prone positioning for periods of at least 20 hours at a time for the treatment of moderate 

and severe ARDS.86 The primary endpoint of all-cause mortality at 28 days was equivalent for both the 

supine and prone patient groups, as was a secondary endpoint of mortality at six months. In the severe 

ARDS patient group, there was a slight trend towards benefit with respect to mortality at both time 

points, but the difference did not reach statistical significance.86

Prone positioning is not recommended for routine therapy of ARDS patients at this time.

Prone positioning is not recommended for routine therapy of ARDS patients at this time. It is recommended 

as an adjunctive therapy in patients with severe hypoxemia. Care should be taken to closely coordinate 

the efforts of those involved in proning the patient, and dislodgement of the endotracheal tube should be 

prevented at all costs. 

Nutritional Goals 

Nutrition in the ICU is increasingly being appreciated as an active therapy with the potential for a 

significant impact on patient outcomes.87 The patient with ARDS has an injury that is driven to a great 

extent by inflammatory mediators. Using any therapy, including nutrition, to help modulate the pathologic 

response is desirable. Several small studies suggest a possible benefit to the use of omega-3 fatty acids in 

ARDS as a mechanism for reducing inflammation.88,89,90 The balance of fat versus carbohydrate in enteral 

feeds also significantly impacts the respiratory quotient and therefore the carbon dioxide production. An 

increased CO2 production may complicate efforts to use permissive hypercapnia as a strategy in the 

management of ARDS.

A recent study evaluated the effect of a specific enteral feed on patients with sepsis and respiratory 

failure.90 The experimental group was given a feed with significant amounts of omega-3 fatty acids 

(replacing omega-6 fatty acids which are metabolized to inflammatory mediators) as well as borage oil. 

They noted a statistically significant improvement in mortality and PaO2

/FiO2 (at days four and seven) as 

well as an increase in ICU-free days and ventilator-free days. A major prospective randomized controlled 

trial that will address nutrition specifically in ARDS patients is currently underway in the ARDSnet 

consortium of research centers. 

While definitive data supporting the use of specific enteral feeds in ARDS are still lacking, the 

preponderance of available data at this time supports the use of feeds high in omega-3 fatty acids. 

Summary

Acute respiratory distress syndrome (ARDS) is a diffuse, heterogenous disorder resulting in significant 

shunt physiology and pulmonary compliance limitations that are seen commonly in the CCC ICU. The 
672 | Critical Care

use of a low-tidal-volume, open-lung strategy can improve mortality by limiting the propagation of the 

lung injury and possibly decreasing the incidence of multisystem organ failure.

Endpoints of Resuscitation

Basic Concepts

At the most basic level, shock is defined as a state where there is inadequate oxygen available relative to 

the metabolic needs of the intracellular processes.91 This may be a result of decreased oxygen delivery, 

increased oxygen requirement in the setting of fixed delivery, or an inability to utilize oxygen at the 

cellular level. It is important for the clinician to have a solid appreciation of oxygen delivery (DO2), aerobic 

metabolic demand, oxygen uptake (VO2), the oxygen extraction ratio (ER), and their interrelationships. 

In the normal healthy state, the oxygen uptake correlates directly with aerobic metabolic demand. As 

will be discussed shortly, conditions that affect the mitochondrial electron transport chain will influence 

the relationship between aerobic metabolic demand and oxygen uptake. Failure of appropriate aerobic 

metabolism defines the presence of shock, and resultant adverse outcomes are related both to the severity 

of the failure as well as its duration.92

Ensuring adequate resuscitation and early recognition of hypoperfusion is critical in the treatment of 

shock. 

Oxygen delivery is directly proportional to the oxygen content of the blood as well as the volume of blood 

transmitted to the body per-unit-time. The most important components of oxygen delivery are therefore 

hemoglobin (Hgb), oxygen saturation of hemoglobin (SaO2

), and the cardiac output (Q). The amount 

of oxygen dissolved in the blood is very small relative to that bound to hemoglobin. While the PaO2 is 

included in the definition of oxygen delivery, it is physiologically of little importance. 

Q = Stroke Volume x Heart Rate

DO2 = Q x [1.39 x Hgb x SaO2 + 0.0031 x PaO2]

The interrelationship of oxygen uptake and oxygen delivery in the normal state is affected greatly by 

the integrity of the mitochondrial electron transport chain. Generally, there is an abundance of oxygen 

delivery relative to oxygen uptake. Efforts to increase oxygen delivery will not result in increased oxygen 

uptake. Below a critical oxygen delivery, the oxygen uptake is said to be supply dependent as the 

reduction-oxidation (redox) state of the mitochondrial electron transport chain changes towards a more 

reduced state in response to the oxygen delivery. The amount of oxygen utilized will mirror that which 

is provided, and the relationship is defined by the oxygen extraction ratio (ER = VO2

/DO2). In a nonsupply-dependent state where there is an abundance of oxygen delivery relative to oxygen uptake, the 

redox state of the electron transport chain adjusts towards increased oxidation to yield a progressively 

lower oxygen extraction ratio as oxygen delivery increases. A normal oxygen extraction ratio in this 

setting is approximately 15 to 30 percent. When oxygen delivery is limited enough to become supply 

dependent, a maximum oxygen extraction ratio is established by a maximally reduced electron transport 

chain. A normal global oxygen extraction ratio in the supply dependent setting is in the range of 60 to 

70 percent; however, it should be recognized that each tissue has its own oxygen extraction ratio that may 

play a large role in determining its risk of injury in a given low oxygen supply state. 
Critical Care | 673

In patients who have sustained prolonged or severe decreases in oxygen delivery, expected redox changes 

may fail, leading to inefficient activity of the electron transport chain. The result is a lower than expected 

oxygen extraction ratio and the development of an oxygen uptake that becomes supply dependent across 

all levels of oxygen delivery. The inability to move away from supply dependence, even with supranormal 

oxygen delivery, signifies a failure of the expected change towards oxidation of the electron transport 

chain. Decoupling of the electron transport chain redox state from the oxygen delivery can result in the 

production of free radical mediated damage as well as the generation of reactive oxygen species. This 

decoupling is a commonly described phenomenon in patients who eventually develop progressive organ 

dysfunction as the trauma resuscitation evolves. Inefficient oxygen utilization can be difficult to detect at 

bedside, but inadequate oxygen availability at the cellular level will lead to increased rates of anaerobic 

metabolism that can be detected in a variety of different ways. Most methods investigated to detect 

the presence of anaerobic metabolism rely on secondary acid-base physiology changes reflecting the 

increased production of lactate and the increased consumption of bicarbonate. 

In the CCC setting, hypovolemic shock is seen most frequently initially, and many patients may go on to 

develop distributive shock secondary to the systemic inflammatory response syndrome. Rapid resolution 

of the etiology is the most critical aspect of the management of either, but aggressive supportive care 

directed at normalization of oxygen delivery is vital. 

Hypovolemic shock is seen in the immediate phase of resuscitation, but distributive shock may follow, 

secondary to the systemic inflammatory response syndrome.

Markers of global perfusion adequacy do not necessarily mean that regional perfusion is intact. 

Inadequate regional perfusion that is clinically unrecognized is common and may be seen in as many 

as 85 percent of patients with normal bedside hemodynamics early in a major trauma resuscitation.93,94

Uncompensated shock is generally easy to diagnose at bedside, as it is heralded by decreased urine output, 

tachycardia, and hypotension. Compensated shock is a condition characterized by normal bedside markers 

of resuscitation with underlying evidence of regional oxygen delivery inadequacy such as a progressive 

metabolic acidosis. It is clear that traditional bedside parameters available to the clinician are inadequate 

to establish an effective resuscitation endpoint. Available options for defining such an endpoint follow.

Clinical markers such as decreased urine output, tachycardia, and hypotension may herald 

uncompensated shock. Conversely, clinical markers may be normal in compensated shock, and 

additional biochemical markers may be necessary to establish an effective resuscitation endpoint. 

Lactate 

The use of lactate to assess resuscitation adequacy follows logically from the recognition that anaerobic 

metabolism leads to increased production. Understanding its strengths and weaknesses in this regard 

follow from an appreciation of how it is formed and subsequently cleared. Glycolysis, whether anaerobic 

in the cytoplasm or aerobic in the mitochondria, results in the production of a small amount of adenosine 

triphosphate (ATP) and pyruvate. Any stress state will increase the rate of glycolysis and result in increased 

pyruvate production. In an anaerobic environment, pyruvate is converted almost exclusively to lactate. 

In an aerobic environment, the majority of pyruvate is consumed by the tricarboxylic acid (TCA) cycle 

resulting in efficient production of ATP. However, even in an aerobic environment, there is a fixed ratio 
674 | Critical Care

of lactate to pyruvate (a normal lactate to pyruvate ratio [L:P] is 10:1). Any increase in pyruvate production 

will also result in increased lactate production regardless of the availability of oxygen, but the percentage 

of pyruvate used to create lactate increases in the anaerobic environment (L:P greater than 30:1). Lactate 

is cleared from the body by actions of the liver (60 percent), kidney (30 percent), and muscle (10 percent).

Lactate should not be used as a sole marker for adequacy of resuscitation in the CCC environment. 

Lactate is increased in trauma resuscitation patients who are nonsurvivors relative to those who survive.95

Time to resolution of lactic acidosis appears to be predictive of survival in the setting of trauma 

resuscitation as well as postoperative surgical patients being cared for in the ICU.96,97 Use of lactate as 

an endpoint for resuscitation is appealing given its ease of measurement. However, its use is complicated 

by the fact that its generation is not completely related to the presence of anaerobic conditions, and its 

clearance may be delayed when liver or kidney damage is present. As a real-time marker of perfusion, 

both of these are important considerations. An elevated lactate level can serve as a useful prognostic 

marker. 

In summary, an elevated lactate level has prognostic value, but a normal level is not helpful. Lactate 

should not be used as a sole marker for adequacy of resuscitation in the CCC environment. 

Base Deficit

The base deficit is a theoretical construct designed to simplify acid-base interpretation and has no true 

physiologic basis. It is the amount of bicarbonate in millimoles (mmol) per liter required to titrate one 

liter of whole blood to achieve a pH of 7.4, assuming the PaCO2 of the patient is 40 mm Hg. The base 

deficit does not have any relationship to the cause of the acidemia, and the amount of base predicted 

assumes a stable acid-base system at the time of measurement. 

One of the few areas in the critical care literature where base deficits have been shown to be of clinical 

benefit is in the setting of early trauma resuscitation.98,99,100 This is a reflection of the fact that most cases 

of acidemia seen in this setting result from hypovolemic shock leading to inadequate oxygen delivery 

and the subsequent development of lactic acidosis. A progressively worsening base deficit argues that 

the resuscitative efforts are not adequate and should prompt the clinician to ensure adequate hemostasis, 

intravascular volume repletion, and replacement of hemoglobin. 

Base deficit has been shown to be of clinical benefit in guiding the management of hypovolemic 

patients during early trauma resuscitation. The base deficit should not be used to guide therapy after 

the initial resuscitative period, as too many variables affecting acid-base physiology are likely to exist.

Scenarios that will complicate the use of base deficit as an endpoint of resuscitation include any condition 

that impacts the acid-base status other than lactic acidosis.95,101 A non-anion gap metabolic acidosis is 

frequently seen after aggressive crystalloid resuscitation, particularly if saline is used. This will worsen 

the base deficit and may not reflect inadequate resuscitation at all. Respiratory acidosis will worsen 

a base deficit, and a respiratory alkalosis will improve it. Exogenous bicarbonate therapy or buffers 

used in total parenteral nutrition (TPN) may also complicate the use of the base deficit as a marker of 

resuscitation adequacy. A final problem with the base deficit is that it is a more appropriate marker of 

global resuscitation than regional resuscitation.
Critical Care | 675

An increased base deficit in the trauma resuscitation period has been correlated with increased resuscitation 

requirements in terms of fluid and blood as well as increased mortality.99,102,103 The progression of the 

base deficit during resuscitation has also been correlated with worsened outcomes.104 Serum bicarbonate 

levels correlate well with base deficit in trauma patients, but the serum lactate level is not well-predicted 

by the base deficit.95,105

Base deficit has value in predicting prognosis and guiding resuscitation in the hypovolemic patient. It is easy 

to measure at the bedside in austere environments and can be calculated with reasonable accuracy during 

critical care air transport using portable handheld arterial blood gas analyzers based upon measured pH 

and PaCO2 values. It is not recommended for use as a resuscitation endpoint in patients who have other 

sources of acid-base physiology derangement, such as those who have received a significant amount of 

crystalloid fluid therapy. The base deficit should not be used to guide therapy after the initial resuscitative 

period, as too many variables affecting acid-base physiology are likely to exist other than lactic acidosis 

related to inadequate intravascular volume. Finally, the base deficit may be insensitive to the existence of 

regional hypoperfusion, and a normal base deficit should be therefore greeted with guarded optimism.

Supraphysiologic Oxygen Delivery Attainment

The development of supply dependence of oxygen uptake on oxygen delivery has long been recognized 

in shock resuscitation as a marker of suboptimal oxygen utilization at the cellular level. Patients 

demonstrating decoupling of the electron transport chain demonstrate supply dependence across all 

levels of oxygen delivery and a lower maximal oxygen extraction ratio. It has been hypothesized that: (1) 

patients who are unable to generate an adequate oxygen delivery to meet the basic oxygen uptake needs 

of the body will do poorly; (2) increased aerobic metabolic needs in a time of stress will necessitate the 

generation of a higher than normal oxygen delivery, particularly when supply dependent physiology is 

present; and (3) the presence of a lower than normal maximal oxygen extraction ratio will also necessitate 

the generation of a supraphysiologic oxygen delivery.

Groundbreaking work by Shoemaker and colleagues found that high-risk surgical patients who survived 

were able to generate significantly higher cardiac indices and oxygen delivery values than nonsurvivors.106,107

Early efforts to incorporate supraphysiologic oxygen delivery as a goal of resuscitation resulted in 

improved outcomes.108,109 Subsequent studies using cardiac index and oxygen delivery goals defined by 

the experience of Shoemaker et al. were not successful in improving outcomes.110,111 A study comparing 

clinical resuscitation using an oxygen delivery goal of 500 ml/min/m2

 versus the value of 600 ml/min/

m2 found no significant difference in outcomes.112 There is difficulty in interpreting these studies because 

of significant variations in study design and patient population. A recent meta-analysis failed to show an 

overall benefit to the use of supraphysiologic oxygen delivery in surgical patient resuscitation.113 However, 

a subset analysis of patients who had the intervention initiated before the onset of organ dysfunction did 

show a significant benefit. 

Supraphysiologic oxygen delivery achievement is not recommended as a resuscitation endpoint for 

trauma patients encountered in the combat environment. Measurement is difficult to perform, and the 

data does not support a specific oxygen delivery goal that is absolutely better than any other in all patient 

populations. While it is true that severely ill patients are more likely to need a supraphysiologic oxygen 

delivery to meet oxygen uptake goals, the necessary oxygen delivery should be determined by targeting 

other endpoints of resuscitation. 
676 | Critical Care

Mixed Venous Oxygen Saturation / Central Venous Oxygen Saturation

In a stressed patient with an intact ability to appropriately adjust the redox state of the mitochondrial 

electron transport chain toward reduction, supply dependence will develop below a critical oxygen 

delivery, and a maximal global oxygen extraction ratio of 65 to 70 percent can be expected. Measurement 

of the mixed venous oxygen saturation (SvO2) in this case will yield a value of 30 to 35 percent, if one 

assumes that the SaO2 is 100 percent. In the nonstressed state, the redox state of the electron transport 

chain favors oxidation, and the global oxygen extraction ratio is much lower than in the stressed state 

(typically less than 30 percent). Measurement of the mixed venous oxygen saturation in this setting, again 

assuming a SaO2 of 100 percent, will be greater than 70 percent.

Measurement of mixed venous oxygen saturation has been hypothesized to be a useful endpoint of 

resuscitation because changes in its value theoretically reflect the balance between oxygen utilization and 

oxygen demand. A lower value, particularly less than 60 to 70 percent, indicates a relative inadequacy of 

oxygen delivery and a trend towards increased electron transport chain reduction in order to maintain 

adequate oxygen uptake relative to intracellular oxygen demand. A problem with this concept is 

commonly seen in the resuscitation of septic patients where decoupling is commonly seen, and oxygen 

uptake demonstrates supply dependence across a very broad range of oxygen delivery values, and a lower 

maximal oxygen extraction ratio is also seen. This reflects a significant inefficiency in oxygen utilization at 

the cellular level; however, the lower than expected oxygen extraction ratio may mask the inefficiency. A 

very low oxygen extraction ratio will result in a normalization of the mixed venous oxygen saturation that 

does not draw attention to the dysfunctional oxygen utilization at the cellular level. This scenario may 

also be observed in severely injured trauma patients who develop the systemic inflammatory response 

syndrome.

The measurement of mixed venous oxygen saturation is made using blood drawn from the distal tip 

of a pulmonary artery catheter. Efforts have been made to correlate the value of mixed venous oxygen 

saturation and the central venous oxygen saturation (ScvO2

) obtained from the distal tip of a central 

venous catheter positioned in the superior vena cava. It is normally expected that the two values will be 

slightly different owing to the contribution of blood from the coronary sinus as well as variable extraction 

of blood returning to the heart from the inferior vena cava relative to the superior vena cava. Several 

studies have noted a tight correlation between mixed venous oxygen saturation and central venous oxygen 

saturation, even if the actual values varied by a few percentage points.114,115,116 

The mixed venous oxygen saturation was used as one of three goals for resuscitation in a prospective 

study of critically ill patients.117 Patients were either resuscitated to a normal cardiac index, a supranormal 

cardiac index, or a mixed venous oxygen saturation of 70 percent. There were no differences in mortality 

or the development of multiple organ dysfunction syndrome.117 Rivers et al. used a central venous oxygen 

saturation of 70 percent as one endpoint in their groundbreaking study of early goal-directed therapy in 

the treatment of severe sepsis and septic shock and demonstrated improved mortality.118

Central venous oxygen saturation is recommended as one easily measured endpoint for resuscitation 

in the combat care environment. Central venous oxygen saturation less than 60 to 65 percent signifies 

inadequate resuscitation.

Central venous oxygen saturation is recommended as one easily measured endpoint for resuscitation in the 
Critical Care | 677

combat care environment. A frankly low central venous oxygen saturation that is less than 60 to 65 percent 

should be taken as a marker of inadequate resuscitation.119 Efforts should be made to ensure hemostasis, 

adequate intravascular volume, optimization of hemoglobin concentration, and oxygen saturation. 

Inotropic therapy can be considered if these parameters are all adequate but the central venous oxygen 

saturation remains low. There is no benefit to be gained from the placement of a pulmonary artery 

catheter specifically to measure the mixed venous oxygen saturation.

A normal central venous oxygen saturation should not be interpreted as confirming adequate resuscitation. 

Poor oxygen utilization at the cellular level may lead to a normalized central venous oxygen saturation 

while significant intracellular hypoxia continues. Efforts to confirm adequacy of regional oxygenation 

should continue if the central venous oxygen saturation is normal.

Gastric Intramucosal pH (pHi)

Blood flow is not uniform across the tissues of the body, and decreased systemic perfusion pressures cause 

redistribution away from tissues that are not immediately necessary for survival. In hypovolemic shock, 

blood flow redistributes away from the gut mucosa early on and does not return until relatively late in the 

recovery process. Gut mucosa is one of the regions that is most sensitive to decreased perfusion pressure 

and therefore represents an excellent location to assess the adequacy of regional oxygen delivery.

Anaerobic metabolism in the gut mucosa leads to the increased production of tissue pressure of carbon 

dioxide (PCO2

), which rapidly equilibrates with the gastric secretions and lowers the gastric intramucosal 

pH (pHi). The gastric intramucosal pH can be measured using a gastric tonometry balloon or a 

continuous monitoring CO2 electrode. A normal gastric intramucosal pH suggests adequate regional 

oxygen delivery, while an abnormally low gastric intramucosal pH suggests inadequate resuscitation in 

spite of possibly normal vital signs or markers of global oxygenation.

If available, gastric intramucosal pH is recommended for the assessment of the adequacy of regional 

oxygen delivery in trauma patients in the combat care environment.

Several studies have noted a statistically significant correlation between a low gastric intramucosal pH 

and mortality.120,121,122,123 When used as a prospective endpoint for a protocol driven resuscitation, a 

delay in achieving the gastric intramucosal pH goal was associated with increased mortality and the 

development of organ system failure.124,125 

Gastric intramucosal pH is recommended for the assessment of the adequacy of regional oxygen delivery 

in trauma patients in the combat care environment if available. Gastric tonometry performed using saline 

filled probes with semipermeable membranes is unlikely to be widely used in most wartime critical care 

units, but continuous gastric CO2 monitoring capability may be available in the near future as validation 

of increasingly portable technology continues. Such a capability would also be extremely useful in the 

critical care air transport setting.

Sublingual PCO2 (PslCO2 ) 

The measurement of sublingual PCO2 (PslCO2) concentrations is easy to do at the bedside and correlates 

well with gastric intramucosal pH.126,127 A handheld monitor is used in much the same way as an oral 
678 | Critical Care

temperature probe. The implications of an elevated sublingual PCO2 are identical to those of a low 

gastric intramucosal pH, and a normal value is felt to represent normal regional oxygen delivery.

The measurement of sublingual PCO2 concentrations may be useful in assessing adequacy of resuscitation 

of trauma patients.

The use of sublingual PCO2

 as a noninvasive surrogate marker of gut mucosa perfusion has been 

described in two studies.129,128 The sublingual PCO2 has also been used in a prospective fashion to identify 

hemorrhage in penetrating trauma patients.129 The degree of sublingual PCO2 elevation correlated with 

the volume of blood loss.

The technology surrounding sublingual PCO2 may be a very useful adjunct to the care of the combat 

trauma patient and represents a cheap, easily transportable method of assessing adequacy of resuscitation 

in austere environments. It is likely to offer the same benefits as gastric intramucosal pH assessment but 

will be much easier to perform. 

Tissue Carbon Dioxide and Oxygen Assessment

Transcutaneous oxygen content (PO2) is expected to decrease when oxygen delivery is inadequate to meet 

demand. The development of anaerobic metabolism leads to the elevation of tissue PCO2 in a fashion 

that is analogous to that described in the gut mucosa. Electrodes have been used to assess transcutaneous 

PO2 and PCO2 in critically ill trauma patients. Lower PO2 values and higher PCO2 values were associated 

with increased mortality.130 One problem with older methods of assessing transcutaneous PO2 and 

PCO2 is that they were invasive. Near infrared spectroscopy (NIRS) offers a noninvasive method of 

assessing skeletal muscle oxyhemoglobin levels, which have been hypothesized to correlate with adequate 

regional oxygenation. Oxygen saturation of hemoglobin in tissue (StO2) is the percentage of oxygenated 

hemoglobin relative to total hemoglobin. The oxygen saturation of hemoglobin in tissue was studied 

during the resuscitation of trauma patients and found to correlate well with oxygen delivery, lactate, and 

base deficit and less so with gastric intramucosal pH.131 A prospective randomized observational study 

found that oxygen saturation of hemoglobin in tissue using NIRS technology was able to reliably identify 

severe shock but may not be able to reliably identify mild shock states.132

Tissue assessment of oxygenation may be useful as a resuscitation endpoint for trauma patients in the 

future, and NIRS technology may ensure ease of its application in the combat setting. At this time, it 

cannot be recommended as an endpoint of resuscitation due to its lack of demonstrated ability to identify 

early shock. 

Summary

Several of the commonly used endpoints of resuscitation such as mixed venous oxygen saturation, lactate 

concentration, and base deficit are useful in identifying global deficiencies in oxygen delivery. Increased 

sensitivity is required to identify patients with regional oxygen delivery abnormalities, and this capability 

is becoming available in the form of gastric intramucosal pH monitoring, sublingual PCO2

 assessment, 

and oxygen saturation of hemoglobin in tissue analysis. Markers of regional perfusion adequacy will 

likely largely replace global perfusion assessment in the future. Technological advancements will allow 

these more sensitive endpoints to be assessed in austere combat environments and during critical care air 
Critical Care | 679

transport. A future frontier will involve the sensitive detection of oxygen utilization abnormalities at the 

cellular level. However, this capability will only be useful if therapies can be developed in the future that 

can act upon the information in a beneficial manner. 

Sepsis

Definition of Sepsis 

Sepsis is a clinical syndrome that is extremely common in the multisystem trauma patient and associated 

with great morbidity, mortality, and cost of care.133,134 The presence of sepsis can be a challenge to 

identify in the combat casualty population since there are frequently numerous reasons for the presence 

of a systemic inflammatory state. However, early recognition and aggressive management of sepsis are 

necessary to maximize the chance of patient survival. Severe organ dysfunction associated with untreated 

infection has been recognized for over a millennium. Attempts to define the syndrome of sepsis did not 

become formalized in a largely agreed upon manner until 1991.135 This consensus definition described 

the systemic inflammatory response syndrome (SIRS) as a condition that may result from either an 

infectious or noninfectious etiology. Sepsis was defined as the presence of SIRS most likely due to 

infection. 

The traditional SIRS criteria are as follows:

• Temperature greater than 38oC or less than 36oC

• Heart rate greater than 90 beats per minute

• Respiratory rate greater than 20 breaths per minute or PaCO2

 less than 32 mm Hg

• White blood cells (WBCs) greater than 12,000 cells per cubic millimeter; less than 4,000 cells per 

cubic millimeter; or with greater than 10 percent band forms

SIRS and Sepsis Definition

SIRS

(Systemic Inflammatory 

Response Syndrome)

Two or more of the following criteria:

• Temperature > 38oC or <36oC 

• Heart rate > 90 beats per minute

• Respiratory rate > 20 breaths per minute or PaCO2 < 32 mm Hg

• WBCs > 12,000 cells per cubic millimeter or < 4,000 cells per cubic 

millimeter or > 10 percent immature (band) forms

Sepsis Documented infection together with two or more SIRS criteria

Severe Sepsis Sepsis associated with organ dysfunction, including, but not limited to, lactic 

acidosis, oliguria, hypoxemia, coagulation disorders, or an acute alteration in 

mental status

Septic Shock Sepsis with hypotension, despite adequate fluid resuscitation, along with 

the presense of perfusion abnormalities. Patients who are on inotropic 

or vasopressor agents may not be hypotensive at the time when perfusion 

abnormalities are detected.

Table 1. Definition of SIRS and sepsis syndromes.
680 | Critical Care

Severe sepsis was defined as sepsis associated with evidence of organ dysfunction, hypoperfusion, 

or hypotension. Septic shock was defined as the persistence of organ dysfunction, hypoperfusion, or 

hypotension in spite of adequate fluid resuscitation. The diagnostic criteria for sepsis were revised in 2001 

in an effort to incorporate new biomarkers of inflammation and offer an improved system for staging 

sepsis.136 The PIRO staging system takes into account predisposition toward sepsis, the infectious insult 

likely to have caused the condition, the response of the body (SIRS), and evidence of organ dysfunction 

(Table 1). From a clinical standpoint, the initial consensus definitions offered in 1991 are most useful and 

worth committing to memory for every physician in the combat environment. The revised guidelines 

from 2001 are most useful for research protocol development, but the definitions of organ dysfunction 

can serve to remind the trauma critical care clinician of relevant physiologic variables to trend.

Pathophysiology

Sepsis is characterized by four basic clinical defects: vasodilation, leaky endothelial membranes, 

disseminated intravascular coagulation, and cellular oxygen utilization inefficiency.137 In a given patient, 

some of these defects may be more relevant than others. A distributive shock pattern with relative 

intravascular volume depletion is frequently seen, leading to organ hypoperfusion. Disseminated 

intravascular coagulation contributes significantly to ineffective end-organ oxygen delivery and can 

induce a systemic hypocoagulable state. The inefficient utilization of oxygen at the cellular level is a 

result of decoupling at the level of the mitochondrial electron transport chain as described in the previous 

section on endpoints of resuscitation. Mitigating the adverse impact of each of the aforementioned 

defects defines the goals of sepsis management.

Prognosis 

Severe sepsis and septic shock are associated with mortality rates of 30 to 60 percent.133,134,138,139 In spite of 

improvements in critical care and the development of several broad-spectrum, highly active antibiotics, 

the mortality associated with sepsis has not improved greatly in the last several decades.133,134 This is 

likely due to several factors, among them being a larger number of immunosuppressed patients, a higher 

proportion of elderly patients, and the emergence of several virulent pathogens with challenging patterns 

of antimicrobial drug resistance.

The expected mortality associated with infection is directly related to the development of severe sepsis 

or septic shock.140 Multiple organ dysfunction syndrome as a result of inadequate oxygen delivery and 

ineffective oxygen utilization at the cellular level is a poor prognostic marker, and the mortality is related 

to the number of organ system failures present.141 In the setting of sepsis some specific organ system 

dysfunctions are associated with higher odds of subsequent death, with hematologic and neurologic 

failure both being particularly concerning.142

Management 

Critical care is a process rather than the definition of a form of medicine that happens only in an ICU. 

Over the last two decades, the importance of an institutional approach to several complex care issues has 

been demonstrated. The management of sepsis involves the coordinated efforts of numerous healthcare 

providers and the synthesis of a large body of clinical data. It is vital that each institution adopt an 

aggressive, protocolized approach to the resuscitation of the septic patient. 
Critical Care | 681

Figure 9. Early goal-directed therapy protocol used by Rivers et al. in the management of severe sepsis. Image courtesy of Massachusetts Medical 

Society.118

<8 mm Hg

Supplemental oxygen ±

endotracheal intubation and

mechanical ventilation

Central venous and

arterial catheterization

Sedation, paralysis

(if intubated),

or both

CVP

MAP

ScvO2

Goals

achieved

Hospital admission

Crystalloid

Colloid

Vasoactive agents

Transfusion of red cells

 until hematocrit ≥ 30%

Inotropic agents

<65 mm Hg

>90 mm Hg

8–12 mm Hg

≥65 and ≤90 mm Hg

No

Yes

<70%

<70%

 ≥70%

≥70%
682 | Critical Care

The use of an early goal-directed therapy protocol for the management of severe sepsis has been 

shown to significantly improve mortality.

The use of an early goal-directed therapy protocol for the management of severe sepsis has been shown 

to significantly improve mortality (Fig. 9).118 One of the most important aspects of this study was that 

resuscitations were initiated early in the emergency room setting and continued in the ICU.118 Waiting for 

transfer to the ICU to begin aggressive resuscitation should never be considered an appropriate strategy. 

Several subsequent studies have described morbidity, mortality, and economic benefits associated with a 

protocolized, institutional approach to sepsis resuscitation.143,144,145,146 Rivers et al. published an excellent 

review of one approach to implementation of an institutional commitment to sepsis resuscitation.147

Infection Source Control

Perhaps the most important aspect of the management of the septic patient involves identification of 

the etiology of infection and ensuring adequate infection source control. While this seems intuitive, it 

is often forgotten as a fundamental priority during the initial activity surrounding other aspects of the 

resuscitation. Source identification and efforts to control the infection should be considered part of the 

initial resuscitation.147,148,149 Timing of transport for radiologic studies or operative intervention will need 

to be individualized based on patient stability.

The most important aspect of the management of the septic patient involves identification of the source 

of infection and achieving infection source control.

When drawing blood cultures, two or more cultures should be obtained.150,151,152 Patients with indwelling 

catheters that have been in place for greater than 48 hours should have blood drawn through each 

lumen of each catheter.148 The vascular device is more likely to be the source of the infection if cultures 

drawn through the line become positive more than two hours prior to cultures simultaneously drawn 

peripherally.153,154 In the CCC setting, the use of empiric antibiotics is necessary while attempting to 

achieve successful source control. This involves the early identification of the etiology of infection as 

well as an understanding of the most likely associated microorganisms and any common antimicrobial 

resistance patterns. A recent series of articles regarding combat related infections and the experience in 

Operation Enduring Freedom (OEF) and Operation Iraqi Freedom (OIF) is helpful for physicians taking 

care of patients in these settings.155,156 

Resuscitation Goals 

The Surviving Sepsis Campaign 2008 guidelines recommend the following initial resuscitation goals:148

1. Central venous pressure (CVP) 8 to 12 mm Hg 

 8 mm Hg for unintubated patients

 12 mm Hg for intubated patients 

2. Mean arterial pressure (MAP) greater than or equal to 65 mm Hg

3. Urine output greater than 0.5 ml per kilogram per hour

4. Central venous oxygen saturation (ScvO2

) greater than or equal to 70 percent or mixed venous oxygen 

saturation (SvO2

) greater than or equal to 65 percent.
Critical Care | 683

The resuscitation goals offered here are similar to those used in the early goal-directed therapy study 

by Rivers et al.118 They do not offer a mechanism for evaluating regional oxygen delivery adequacy and 

should be supplemented at a given institution with intramucosal gastric pH, sublingual PCO2, or oxygen 

saturation of hemoglobin in tissue assessment if available. In the typical CCC scenario, however, the 

resuscitation goals above are likely to be the best available.

Intravascular Volume

Relative intravascular volume depletion is seen in sepsis as a result of vasodilation and endothelial 

leak. Hemorrhage in the trauma patient may also be a complicating factor. Maintaining an adequate 

intravascular volume is necessary to ensure adequate cardiac preload and therefore cardiac output. 

Decreased cardiac output will, by necessity, lead to a decrease in oxygen delivery which can be particularly 

important in sepsis where oxygen consumption may be supply-dependent. 

Static measures are most often used in the ICU setting to estimate intravascular volume. The CVP is 

most often used at the bedside due to its ease of measurement, and there is no advantage to obtaining a 

pulmonary capillary wedge pressure over the CVP. Unfortunately, CVP is a very poor predictor of the 

intravascular volume status in the septic patient.157 As an example, a CVP less than 5 mm Hg in sepsis has 

only a 47 percent positive predictive value for the presence of intravascular volume depletion.158 Changes in 

intrathoracic pressure due to any cause may cause CVP to be an inaccurate representation of intravascular 

volume status. In the trauma ICU, mechanical 

ventilation and abdominal compartment syndrome 

are common complicating factors.159,160

Dynamic measures such as pulse pressure variation 

are better predictors of intravascular volume 

status in sepsis than CVP.161,162 As technology 

evolves, it is likely pulse pressure variation 

measurement capability will be available in the 

CCC setting. Transthoracic and transesophageal 

echocardiography have both been shown to be 

excellent markers of intravascular volume status 

as well.163 Small portable ultrasound machines are 

commonly available at Level III facilities and may 

be useful when CVP and the clinical exam do not 

correlate (Fig. 10).

Bedside ultrasonography available in Level III facilities has been shown to be an excellent marker of 

intravascular volume status.

The type of fluid used for resuscitation may depend on associated injuries, such as traumatic brain 

injury accompanied by intracranial pressure elevation, where hypertonic saline may be a preferred 

resuscitation fluid.164,165 A recent large trial failed to show a benefit to the use of albumin or normal 

saline during the resuscitation of patients in the ICU.166 However, the same outcomes were obtained 

using smaller resuscitation volumes in the colloid group. Two reviews of the topic also failed to show a 

significant outcome benefit using one or the other approach.167

Figure 10. Portable ultrasound machines, available at Level III facilities, 

may be used for hemodynamic assessment.
684 | Critical Care

Fluid should be given in an aggressive manner early in sepsis resuscitation using boluses of greater than 

1,000 ml crystalloid or greater than 300 to 500 ml colloid at a time until adequate cardiac filling pressures 

are obtained (Fig. 11).148 After this point, intravascular volume supplementation should be eliminated until 

evidence of intravascular hypovolemia is once again demonstrated. Fluid balance is directly proportional 

to mortality. To some extent, this may reflect the severity of the underlying disease, but even when this 

is controlled for, there appears to be a benefit to minimizing intravascular volume overload after the 

initial resuscitation period.168

Role of Vasopressors

The use of a vasopressor may be beneficial in the management of sepsis and should be thought of as a 

temporizing measure that is only used as long and as much as necessary.148,169 A mean arterial pressure 

goal of 65 mm Hg is sufficient for most, but higher goals may be necessary as a way of preserving cerebral 

perfusion pressure in those with an elevated intracranial pressure. The human body tightly autoregulates 

blood flow to a given organ or tissue. This means that over a large range of blood pressure variation, 

the actual blood flow is controlled fairly precisely. In very low-pressure states, the blood pressure may 

fall below the pressure necessary for autoregulation, and the blood flow becomes linearly related to the 

pressure. In this setting, immediate improvement of the blood pressure will improve blood flow and 

oxygen delivery.170,171 Patients with a history of essential hypertension may benefit from a higher mean 

arterial pressure due to a rightward shift in their normal autoregulatory range. Myocardial perfusion is a 

function of the difference between the diastolic blood pressure and the ventricular end-diastolic pressure. 

While the end-diastolic pressure is typically low early in the resuscitation of severe sepsis, it will normalize 

with resuscitation. Ensuring an adequate diastolic blood pressure can prevent myocardial ischemia or 

infarction.

Figure 11. Intravenous fluid administration should be performed aggressively during sepsis resuscitation.
Critical Care | 685

The optimal vasopressor in sepsis depends upon the individual patient scenario.169 The Surviving Sepsis 

Campaign 2008 guidelines suggest that either norepinephrine or dopamine be used as a first-line agent.148

Patients who fail to respond should have epinephrine added to the vasopressor regimen. Vasopressin or 

phenylephrine can be considered for patients who are still hypotensive in spite of the above measures 

and who have been adequately volume resuscitated. Some studies have suggested that norepinephrine 

is a better first line choice of vasopressor in severe sepsis than dopamine. These studies evaluated the 

hemodynamic effects of norepinephrine versus dopamine in septic patients and demonstrated improved 

clinical outcomes and improved splanchnic circulation in patients treated with norepinephrine.172,173,174

Recent studies analyzing the use of norepinephrine in septic shock have come to opposite conclusions, 

linking the use of norepinephrine to worse or equivalent outcomes relative to alternative vasoactive 

agents.175 Epinephrine is an alternative vasopressor. It has been associated with elevation of lactic acid 

levels in the serum independent of oxygenation or blood flow. This is likely secondary to increased 

glycolysis and production of higher amounts of pyruvate with a normal L:P ratio of 10:1.176

Vasopressin levels are decreased in patients with severe sepsis and those who die from sepsis, when 

compared to those with mild sepsis and those who survive.177 Two clinical studies have demonstrated 

a hemodynamic and vasopressor sparing benefit to the addition of a low-dose vasopressin infusion in 

patients with septic shock.178,179 No mortality benefit was identified in either study. The recently completed 

Vasopressin and Septic Shock Trial (VASST) trial did not demonstrate a mortality benefit by adding 

vasopressin to a patient already being managed with norepinephrine.180

Dopamine is not recommended specifically for the prevention or management of acute renal failure 

in the septic patient. Several trials have failed to demonstrate benefit, while noting a decrease in 

splanchnic perfusion, associated with the use of dopamine (versus norepinephrine) in patients with severe 

sepsis.181,182,183,184 Consensus opinion currently is that there is potential harm that may be expected when 

low-dose dopamine is used for renal failure prevention or management in the critically ill patient.148,185

Vasopressors may be of benefit in the management of sepsis, but they should be viewed as a temporizing 

measure.

Role of Corticosteroids

Corticosteroids should be added in total daily dose equivalents of hydrocortisone less than or equal 

to 300 milligrams (mg) intravenously daily in patients with hypotension associated with septic shock 

that is unresponsive to vasopressors or is of prolonged duration.148,186 If a steroid is used with less 

mineralocorticoid activity than hydrocortisone, fludrocortisone can be added in a dose of 50 mcg per 

day. Three randomized controlled studies have shown clinical benefit to the use of corticosteroids in 

the setting of septic shock.187,188,189 The first of these three studies was able to demonstrate a mortality 

reduction for patients who failed to increase their cortisol level more than 9 mcg per deciliter after 

an adrenocorticotropic hormone (ACTH) stimulation test.187 The recently completed Corticosteroid 

Therapy of Septic Shock (CORTICUS) trial failed to show a mortality benefit to the use of corticosteroids 

in the setting of septic shock but did demonstrate faster resolution of shock in patients who were given 

steroids.190 The response to an ACTH stimulation test did not predict those who responded to steroid 

therapy and those who did not. It is not clear from the study why improved resolution of the shock state 

with corticosteroids did not translate into a meaningful outcome advantage. 
686 | Critical Care

The use of steroids in the management of refractory septic shock should be limited to patients who have 

failed at least two vasopressor agents.

The shock state associated with sepsis is frequently complicated by absolute or relative adrenal 

insufficiency. Unfortunately, the data supporting a benefit to the use of corticosteroids is minimal. 

Corticosteroids should be used in those with a previous condition requiring replacement and should be 

considered early in those who are likely to have secondary adrenal insufficiency due to chronic steroid 

therapy prior to the sepsis interval. The use of steroids strictly for the management of refractory septic 

shock should be limited to patients who have failed vasopressor therapy with at least two agents. 

Assessing Adequacy of Oxygen Delivery

An assessment of the adequacy of oxygen delivery with central venous oxygen saturation was part of the 

Rivers et al. early-goal directed therapy strategy for severe sepsis management and is recommended by 

the most recent Surviving Sepsis Campaign 2008 guidelines.118,148 The goals are a central venous oxygen 

saturation greater than or equal to 70 percent or a mixed venous oxygen saturation greater than or equal 

to 65 percent depending on which is being followed in a given patient. 

The topic of assessing adequacy of resuscitation was discussed in more detail previously, but a few 

concepts should be emphasized for the patient with severe sepsis. First, both central venous oxygen 

saturation and mixed venous oxygen saturation are markers of global oxygen delivery and may not be 

sensitive to regional inadequacy.191 Where possible, technology to assess regional perfusion should be 

employed to supplement the data gained from the central venous oxygen saturation or mixed venous 

oxygen saturation. Just as a normal blood pressure does not mean that a patient is necessarily adequately 

resuscitated, neither does a normal central venous oxygen saturation.

A second important point regarding mixed venous oxygen saturation assessment is that a high value 

is commonly seen in very advanced septic shock. Because patients with septic shock frequently have 

decoupling of the mitochondrial electron transport chain, their oxygen consumption is supply dependent 

across most values of oxygen delivery, and the maximal oxygen extraction ratio may be profoundly 

decreased. A normal mixed venous oxygen value may be measured in spite of significant intracellular 

hypoxemia.191 This perpetuates a shock state that may lead to death through the development of 

progressive multiple organ dysfunction.

The central venous oxygen saturation or mixed venous oxygen saturation is useful in identifying those 

with a need for further resuscitation when the values are low, but they are of little use when normal.191

When low, the defective component of oxygen delivery must be identified, remembering that oxygen 

delivery is a function of cardiac output and oxygen content of the blood. If the central venous oxygen 

saturation or mixed venous oxygen saturation is low, efforts to ensure adequate hemoglobin oxygen 

saturation should be made first. Second, transfusion to a hemoglobin value of at least 10 g per deciliter 

should be considered.148 Finally, if the mixed venous saturation remains low, an inotrope can be added 

with the intent of increasing cardiac output. The necessity of maintaining adequate intravascular volume 

during this process should be emphasized since an inadequate cardiac output can result from inadequate 

preload, direct myocardial suppression by cytokines in sepsis, or from myocardial infarction. 
Critical Care | 687

Central venous oxygen saturation or mixed venous oxygen saturation is useful in identifying patients 

needing further resuscitation when the values are low, but are of little use when normal.

Blood Product Transfusion

The transfusion of blood products carries the 

potential for great benefit but also great harm to 

the patient and cost to society. In the CCC setting, 

it may be a very limited resource that must be used 

judiciously. Massive transfusion during a trauma 

resuscitation or transfusion goals associated with 

inadequately controlled hemorrhage are separate 

topics than the use of blood products strictly 

for the management of sepsis. Sepsis frequently 

develops during the course of care of the trauma 

patient rather than being present during the 

initial patient resuscitation. For the management 

of sepsis, component therapy is recommended 

rather than the use of whole blood.148 Component 

therapy allows correction of identifiable defects 

(Fig. 12). Specific goals for the transfusion should 

be defined and effects of the therapy subsequently 

assessed.192

The most likely component to be considered 

for transfusion is packed red blood cells. The 

Transfusion Requirements in Critical Care 

(TRICC) trial demonstrated the adequacy of 

a conservative transfusion strategy in critically 

ill patients.193 In spite of the linear relationship 

between oxygen uptake and oxygen delivery over a 

broad range of oxygen delivery, ineffective oxygen utilization precludes a significant oxygen uptake benefit 

from very aggressive red blood cell (RBC) transfusion in the setting of severe sepsis.194 It is recommended 

that packed red blood cell therapy only be used when hemoglobin concentrations are less than 7 g 

per deciliter unless evidence of ongoing oxygen delivery inadequacy (e.g., low central venous oxygen 

saturation, myocardial ischemia, cerebral hypoperfusion) exists or active hemorrhage is present.148 In that 

case, a hemoglobin goal of at least 10 g per deciliter is prudent, although overaggressive transfusion may 

be potentially harmful in the multisystem trauma patient, and these competing goals must be balanced 

carefully.195 Once adequate oxygen delivery is felt to be present based upon available assessment tools, 

efforts to minimize red blood cell transfusion should be made.

It is recommended that packed red blood cell therapy only be used when the hemoglobin value is less than 

7 g per deciliter, unless evidence of ongoing oxygen delivery inadequacy exists, or active hemorrhage is 

present.

Figure 12. Selective blood component therapy is recommended in the 

setting of sepsis complicated by coagulopathic bleeding.
688 | Critical Care

Erythropoietin should not be used to improve hemoglobin or prevent future potential blood transfusions 

in the setting of sepsis. Two prospective clinical trials failed to demonstrate a significant benefit to the use 

of erythropoietin supplementation in critically ill patients.196,197 Both of these studies show erythropoietin 

results in increased hemoglobin concentrations and decreased need for blood transfusion, but there is no 

data showing improved survival or clinical outcomes. Thus, it is not recommended in surviving sepsis 

guidelines.148

Correction of coagulopathy due to factor depletion or thrombocytopenia is not recommended strictly 

for the management of sepsis.148,198 There may be settings where correction is desirable, as in the case 

of early trauma resuscitation, uncontrolled intracranial hemorrhage, or spinal surgery. Strict goals for 

resuscitation that are well-validated remain elusive and largely a matter of opinion. In the setting of 

sepsis, a platelet count of less than 5,000 per cubic millimeter should prompt transfusion, as should 

values of 5,000 per cubic millimeter to 30,000 per cubic millimeter when active bleeding is present.148

Some procedures may require higher transfusion goals. There is no absolute international normalized 

ratio (INR) that should prompt transfusion of fresh frozen plasma in the absence of active bleeding or 

an anticipated procedure, but the risk of spontaneous intracranial hemorrhage correlates directly with 

anticoagulation intensity.199,200

Disseminated intravascular coagulation (DIC) results from an abnormal balance of procoagulant and 

anticoagulant factors in the blood that ultimately results in excessive accumulation of fibrin in the 

microvasculature. This contributes to organ dysfunction and may eventually lead to a generalized inability 

to form clot due to excessive consumption of coagulation factors. In the setting of active bleeding due to 

DIC, fresh frozen plasma may be considered in an attempt to improve the overall coagulopathy, platelet 

transfusion may be of benefit, and cryoprecipitate can be used to correct the fibrinogen deficiency. It is 

important to emphasize that all of these therapies are likely to be ineffective unless the source of the DIC 

is corrected. Specific goals for the supportive management of DIC will depend upon a bedside clinical 

assessment of any resulting hemorrhage.

Role of Inotropic Therapy

The necessity of inotropic therapy may be suggested by the presence of a decreased central venous oxygen 

saturation in the setting of adequate intravascular volume repletion, hemoglobin oxygen saturation, and 

hemoglobin content.170 If a pulmonary artery catheter is in place, a decreased cardiac output in the 

setting of normal or high cardiac filling pressures suggests a role for inotropic therapy. A pulmonary 

artery catheter is not necessary for the identification of the need for inotropic therapy or the utilization 

of an inotrope but may allow more accurate dose titration.

Dobutamine is the inotrope of choice in septic patients.148,170,201 Dobutamine increases oxygen utilization, 

and care must therefore be exercised in states where cardiac oxygen delivery is marginal. When started, it 

is started at 5 micrograms (mcg) per kilogram per minute and titrated to a maximum dose of 20 mcg per 

kilogram per minute. If using a central venous catheter with the tip in the superior vena cava, the central 

venous oxygen saturation can be used to guide therapy. The dose is increased until the central venous 

oxygen saturation normalizes or the maximum dose is reached. Arrhythmias may complicate the ability 

to titrate dobutamine. If a pulmonary artery catheter is in place, the cardiac index can be trended, as can 

the mixed venous oxygen saturation. 
Critical Care | 689

A large part of the blood pressure improvement seen when dopamine is used as a vasopressor at moderate 

doses may be due to increased stroke volume; therefore, it can be considered an inotrope as well.169

Norepinephrine has some inotropic properties, but its major mode of improving blood pressure is through 

peripheral vasoconstriction.169

Role of Recombinant Human Activated Protein C (rhAPC)

The Recombinant Human Activated Protein C Worldwide Evaluation in Severe Sepsis (PROWESS) 

trial was the first to demonstrate a mortality benefit with the use of an agent (recombinant human 

activated protein C [rhAPC]) designed to prevent abnormal clotting in severe sepsis.202 Subset analysis 

of the PROWESS trial found the greatest benefit in patients with more severe manifestations of sepsis. 

The process by which the PROWESS study was conducted and its conclusions (i.e., based on subgroup 

analysis) have generated controversy.203 The limitations of rhAPC were delineated by the Administration 

of Drotrecogin Alfa (activated) in Early Stage Severe Sepsis (ADDRESS) trial, which was designed to 

evaluate the use of rhAPC in patients with severe sepsis but a low risk of death.204 It was stopped early 

due to futility, and a subset analysis of patients with recent surgery and only a single-organ dysfunction 

had a significantly higher 28-day mortality if they received rhAPC. The study concluded that rhAPC 

(drotrecogin alfa or Xigris®) “should not be used in patients with severe sepsis who are at low risk for 

death, such as those with single-organ failure or an APACHE II score less than 25.”

Recombinant human activated protein C has been recommended by some for patients with severe sepsis 

and either multiple organ failures or an APACHE II score greater than 25.148 Use of rhAPC, specifically in 

the combat trauma population, needs to be tempered by a higher risk of bleeding noted in national surveys 

relative to that reported in the initial PROWESS trial.205,206 Risks and benefits must be carefully assessed, 

and adequate hemostasis must be ensured. When used, it is best to initiate therapy with rhAPC as soon as 

the need is identified, since outcomes appear to be best when the therapy is introduced early.207,208,209 The 

cost-effectiveness of administering rhAPC in all severe sepsis patients has been questioned, and calls for 

more selective use in this subset of high-risk patients have been made.203

Management of Hyperglycemia

The publication in 2001 of a significant mortality benefit in critical care patients treated with an intensive 

insulin therapy protocol with resultant glucose values of 80 to 120 mg per deciliter was met with great 

enthusiasm.210 Because this initial experience was primarily with surgical ICU patients, a subsequent 

study by the same author was conducted in the medical ICU population.211 The medical ICU study was 

able to demonstrate a mortality benefit only in those patients with a length of stay greater than three days, 

which cannot be predicted when patients are admitted. It is important to note as well that the rate of 

significant hypoglycemia was 18 percent, relative to the 6.2 percent seen in the 2001 surgical ICU study. 

Both of these studies were performed at a single institution. While tight glucose control was adopted 

quickly by several major clinical organizations, the results of other studies have failed to demonstrate 

similar outcomes, and in fact, not only show no benefit, but provide evidence of harm.212,213 

The recently completed Normoglycemia in Intensive Care Evaluation – Survival Using Glucose Algorithm 

Regulation (NICE-SUGAR) study randomized 6,104 critical care patients into intensive glucose control 

(81 to 108 mg per deciliter) versus conventional glucose control (180 mg per deciliter or less) groups 

and followed a number of variables over 90 days from enrollment.214 The results are striking in their 

demonstration of a 2.6 percent mortality increase at 90 days in those treated with an intensive approach, 
690 | Critical Care

although there was no significant difference in mortality at 28 days. Subgroup analysis in the NICESUGAR study noted a trend toward improved outcomes with conventional control in patients with severe 

sepsis, as well as those with an APACHE II score greater than 25 on admission. 

Moderate glucose control (less than 150 mg per deciliter) should be achieved using insulin infusion 

protocols in patients with sepsis.

Of particular relevance to the trauma critical care population was a trend toward improved outcomes 

in trauma patients with intensive insulin control. Excitement over this result should be tempered by the 

wide confidence intervals (0.50 to 1.18) and the fact that there was a statistically significant improvement 

in operative admission patients who were treated with conventional control. Hyperglycemia has been 

associated with worsened outcomes following traumatic brain injury and sepsis. At this time, it is 

recommended that moderate glucose control (less than 150 mg per deciliter) be achieved using insulin 

infusion protocols in patients with sepsis.148 Future studies are needed to help clarify what degree of 

glucose control is most beneficial for the critically ill patient. 

Role of Bicarbonate Therapy

Bicarbonate therapy has been used in clinical practice for years in an attempt to mitigate the effects of 

acidemia caused by numerous metabolic and respiratory challenges. In the setting of sepsis-induced 

lactic acidosis, there does not appear to be any benefit to the routine use of bicarbonate therapy.215,216

It is hypothesized that conformational changes at the level of the sympathetic receptor occur at very 

low pH values that may lead to unresponsiveness to vasopressor therapy. There is no firm clinical data 

supporting an absolute pH where such an effect may occur. In the aforementioned studies, the number of 

patients enrolled with pH less than 7.15 was small.215,216 The use of bicarbonate is associated with volume 

overload that may complicate other goals of sepsis therapy, particularly after the initial resuscitation 

phase. It is recommended in the Surviving Sepsis Campaign 2008 guidelines that bicarbonate not be used 

for the sole purpose of raising pH greater than 7.15 in an effort to improve hemodynamics.148

In the setting of sepsis-induced lactic acidosis, there does not appear to be any benefit to the routine use 

of bicarbonate therapy.

For patients with profound acidemia, raising the pH may be an immediate lifesaving maneuver.217

Manipulation of mechanical ventilation may allow a sufficient respiratory alkalosis to improve the overall 

pH adequately, or bicarbonate therapy may be utilized. In a theoretical sense, bicarbonate combines with 

hydrogen ions and eventually creates water and carbon dioxide via the action of carbonic anhydrase. 

Carbon dioxide readily crosses cell membranes and may therefore contribute to intracellular pH reduction 

in spite of improved pH in the blood. This might be more significant when sepsis is associated with 

ARDS or other conditions where ventilation is limited and carbon dioxide elimination is suboptimal. 

The potential for poor outcomes due to intracellular pH decrease associated with bicarbonate therapy 

has not been demonstrated conclusively in a prospective clinical fashion.

Other options for raising the pH include the use of tromethamine, which is a proton scavenger that is 

eliminated renally.218 The tromethamine solution is hypertonic and has a pH of 8.6. The hypertonic nature 
Critical Care | 691

of the solution can induce a mild osmotic diuresis and will result in improved urine output, but it should 

not be used as an agent to prevent or treat acute renal failure. For those with established renal failure, 

tromethamine is not appropriate given the necessity of renal clearance. Bicarbonate therapy is associated 

with a significant sodium load and increased generation of carbon dioxide; therefore, tromethamine may 

be preferred in patients with hypernatremia or a limited minute ventilation.218 There is no evidence that 

outcomes are better with tromethamine versus bicarbonate therapy versus no therapy at all in the setting 

of lactic acidosis associated with severe sepsis. 

Unfortunately, there is no clear guidance than can be offered for pH values less than 7.15. Until better 

data emerges, the decision to correct the pH and the best way to accomplish this goal are both up to the 

bedside clinician.

Nutritional Goals 

The literature regarding optimal nutrition for the septic patient continues to evolve, but few firm 

recommendations can be made at this time. It appears that septic patients have a higher basal energy 

expenditure than nonstressed patients.219,220 Glutamine and arginine supplementation may be of 

benefit.221,222 The method by which critical care patients are fed has generally received as much attention 

as what is fed (Fig. 13). Enteral nutrition is preferred over total parenteral nutrition when possible.223,224

Enteral feeding is cheaper, preserves the integrity of the gut mucosa (possibly decreasing the incidence 

of multiple organ dysfunction syndrome), and has a lower rate of secondary infection. The exact timing 

of feed initiation is unclear. It seems intuitive that earlier achievement of adequate caloric intake would be 

beneficial. This has been demonstrated in the hypercatabolic adult burn patient population.225 However, 

in the sepsis population undergoing initial resuscitation, it is unclear whether the body is able to use the 

nutrients provided to it. Decreased gut perfusion may also make the use of enteral nutrition risky, and 

total parenteral nutrition may be favored earlier if feeds are started during the periresusciation period. 

It is probably best to achieve adequate caloric intake as early as possible after the initial resuscitation 

period with enteral nutrition being favored over total parenteral nutrition unless there are significant 

contraindications (severe ileus, recent gastrointestinal surgery, etc.). The choice of feeds remains an 

unsettled matter with many favoring antioxidant formulas, although there is little outcome data at this 

point to argue for or against such recommendations. 

Enteral nutrition is preferred over total parenteral nutrition when possible and should be started as early 

as possible after the initial resuscitation period.

Summary

The sepsis syndrome is characterized by vasodilation, leaky endothelial membranes, DIC, and ineffective 

oxygen utilization at the cellular level. It is associated with a high mortality. Early syndrome recognition, 

infection source control, and a protocolized approach to resuscitation are key factors for ensuring patient 

survival. Components of supportive therapy include maintenance of adequate intravascular volume, 

vasopressor support, inotropic support, moderate glucose control, rhAPC in select patients with severe 

sepsis, and the rational use of blood products. There may be a role for the use of corticosteroids in some 

patients, and the optimal nutrition strategy continues to emerge.
692 | Critical Care

Basic Care Considerations in the Combat Casualty Care ICU

Combat-Associated Pneumonia Prevention

Ventilator-associated pneumonia (VAP) is a frequent complication of prolonged mechanical ventilation that 

leads to increased duration of mechanical ventilation, prolongation of ICU care, and, most importantly, 

an increase in mortality.226 Ventilator-associated pneumonia is defined as a pneumonia that arises after 

48 to 72 hours of endotracheal intubation (Fig. 14).227 Multidrug-resistant bacteria of nosocomial origin 

are more likely to be associated with ventilator-associated pneumonia after the first four to five days of 

hospitalization as the patient becomes colonized with organisms that live in an environment characterized 

by extraordinary antibiotic selection pressure. Organisms such as methicillin-resistant Staphylococcus aureus

(MRSA) and multidrug-resistant gram-negative organisms such as Pseudomonas aeruginosa and Acinetobacter 

baumanii are commonly encountered.227

Ventilator-associated pneumonia is a frequent complication of prolonged mechanical ventilation 

that leads to increased duration of mechanical ventilation, prolongation of ICU care, and increased 

mortality.

The flow of combat casualties out-of-theater in OEF and OIF for the vast majority of critically ill patients 

involves a handful of medical centers (Fig. 15). This is done to consolidate medical resources in a few 

locations and because patient flow via the air evacuation system uses aircraft of opportunity that are 

flying regularly established mission routes. Multidrug-resistant organisms are extremely common in these 

node locations, and patients who become colonized tend to carry such organisms to each successive 

node.228 Of particular concern has been the emergence of extremely virulent multidrug-resistant 

acinetobacter and pseudomonas strains that have been associated with ventilator-associated pneumonia. 

The concept of “combat-associated pneumonia” as a variant of ventilator-associated pneumonia has 

emerged to accentuate the importance of these extremely difficult to treat, multidrug-resistant organisms 

as a cause of nosocomial pneumonia.229 Combat-associated pneumonia also highlights the role that the 

nodal structure of patient flow plays in the emergence of multidrug-resistant organisms at each successive 

military treatment facility.228

Figure 13. Enteral nutrition is preferred over total parenteral nutrition. Figure 14. Ventilator-associated pneumonia is defined as a pneumonia 

that arises after 48 to 72 hours of endotracheal intubation.
Critical Care | 693

Prevention of combat-associated pneumonia in ventilated patients is vital since treatment is extremely 

difficult. The development of ventilator-associated pneumonia prevention bundles is now common 

practice in critical care units. A suggested combat-associated pneumonia bundle is depicted in Table 

2. Posting these recommendations at bedside can serve as a helpful reminder for clinicians, nurses, and 

respiratory therapists. Such recommendations should also be included in standard ICU admission order 

Figure 15. Multidrug-resistant organisms are common in the evacuation chain, and patients who become colonized tend to carry such organisms to each 

successive facility.

Combat-Associated Pneumonia Prevention Bundle

1. Keep head of bed elevated greater than 30 to 45 degrees at all times, unless contraindicated

2. Daily sedation interruption

3. Gastrointestinal bleeding prophylaxis

4. Deep venous thrombosis (DVT) prophylaxis

5. Heat and moisture exchanger (HME) use unless otherwise specified; no daily changes of HMEs

6. Oral care every two hours, with chlorhexidine every 12 hours

7. Consider vaccination with pneumovax® and influenza vaccine 

8. Continuous subglottic suctioning endotracheal tube if duration of intubation expected to be 

greater than or equal to four days

9. No routine ventilator circuit changes

Table 2. Combat-associated pneumonia prevention interventions.
694 | Critical Care

sets. Critical care air transport teams can continue all of these recommendations during flight and should 

be encouraged to do so prior to each movement of an intubated patient.

In combat critical care units, consideration should be given to relatively liberal use of an invasive 

diagnostic strategy to confirm suspected cases of combat-associated pneumonia. Options include flexible 

fiberoptic bronchoscopy (with or without protected specimen brush) and blind bronchoalveolar lavage 

(BAL) using specially designed catheters. This will decrease the use of broad-spectrum antibiotics and 

hopefully decrease some of the selection pressure that exists in downrange ICUs.

Deep Venous Thrombosis Prophylaxis

Multisystem trauma patients have numerous risk factors for the development of venous thromboembolic 

disease. In the combat environment, there is a higher likelihood of intravascular dehydration prior 

to injury that may contribute to an increased risk over that seen in the civilian trauma population 

in the US.230 A more important distinction between the two populations is the periods of prolonged 

immobilization that will necessarily accompany air evacuation out of the combat theater.

Representatives from the American College of Chest Physicians recently reviewed the literature 

regarding a number of common patient populations encountered in the combat environment such as 

those with head and spine injuries, orthopedic injuries, and multisystem trauma.231 Several insightful 

recommendations for each population are made and levels of evidence are reviewed. 

When possible, trauma patients should receive either graded compression stockings or intermittent 

pneumatic compression devices, given the higher than normal risk for venous thromboembolism in the 

combat environment.

Given the higher than normal risk for venous 

thromboembolism in the combat environment, it 

is recommended that each patient receive either 

graded compression stockings or intermittent 

pneumatic compression devices unless injury 

severity does not allow the placement of such 

devices on any extremity (Fig. 16). In addition, lowmolecular-weight heparin dosed as 30 mg injected 

subcutaneously twice daily should be used unless 

contraindicated by active uncontrolled hemorrhage 

or recent intracranial bleeding.231,232 An aggressive 

approach to venous thromboembolism prophylaxis 

in the combat trauma environment is wise since 

treatment with full-dose anticoagulation for DVT 

or pulmonary embolism (PE) may be problematic 

in patients with ongoing hemostasis inadequacy 

or who may need repeated trips to the operating 

room. 

Figure 16. Intermittent pneumatic compression devices are used for venous 

thromboembolism prophylaxis. Image courtesy of DJO, LLC.
Critical Care | 695

Gastrointestinal Bleeding Prophylaxis

Stress gastritis is a common complication in critical care patients.233 Significant risk factors for gastrointestinal 

bleeding due to stress gastritis include mechanical ventilation greater than 48 hours, coagulopathies, 

shock, sepsis, hepatic failure, renal failure, multiple trauma, greater than 35 percent total body surface 

area burn, head/spinal cord trauma, and a prior history of upper gastrointestinal hemorrhage.234

All patients admitted to a combat ICU should be treated with an intravenous proton-pump inhibitor or 

H2-receptor antagonist due to risk of stress gastritis.

All patients admitted to a combat ICU should be treated with an intravenous proton-pump inhibitor 

or H2

-receptor antagonist. This is generally continued even when the patient is tolerating enteral feeds, 

although some experts would consider discontinuation of prophylaxis at that point.233

Preventive Care and Infection Control

Exposure keratopathy is common in the critical care setting when the eye is left exposed to dry air in 

patients who are not capable of spontaneously blinking (e.g., chemical sedation or central nervous system 

injury).235 Efforts to protect the eyes with the regular application of lubrication is a basic necessity of care 

that can be overlooked during combat critical care with devastating consequences. Exposure keratopathy 

may lead to the development of infections that are extremely difficult to eradicate and frequently result 

in permanent loss of vision.235

Aggressive skin care is extremely important in the multisystem trauma patient due to the prolonged 

periods of immobility that often accompany convalescence.236 Decubitus ulcers can develop quickly in 

dependent regions where weight is focused on a single point and allowed to compress the soft-tissue 

underneath. Common ulcer locations include the sacral region, heels, and portions of the body that 

are left pressed up against solid objects such as a bedrail. What appear at first to be small areas of 

redness can evolve over hours to days into large, poorly healing regions of necrotic soft-tissue that may 

require extensive debridement and occasional skin grafting.237 There is also a risk for the development of 

osteomyelitis in exposed bone. Prevention involves frequent turning in an effort to continually redistribute 

pressure points as well as the use of foam blocks under the feet and legs.

Aggressive skin care is extremely important in the multisystem trauma patient in order to prevent 

decubitus ulcers. Efforts to protect the eyes with regular application of lubrication are necessary to 

prevent exposure keratopathy.

Intensive care unit infection control measures are extremely important in the current mature theaters of 

combat in Afghanistan and Iraq. The spread of multidrug-resistant pathogens needs to be limited as much 

as possible in an effort to improve outcomes. The epidemiology, history, prevention, and treatment of 

combat-related infections were outlined in a recent series of articles.155,228,238,239,240 Basic recommendations 

for preventing the spread of nosocomial multidrug-resistant pathogens include universal standard 

precautions, contact precautions with all direct patient care, consideration of cohorting patients who are 

likely to be in the ICU less than 72 hours, and antibiotic control. Antibiotic control recommendations 

include avoiding unnecessary use of broad-spectrum empiric antibiotics, establishment of a local 

antibiogram that can be used to guide initial therapy, and limiting antibiotic therapy duration as much 

as possible.156
696 | Critical Care

Structure of the Combat Casualty Care ICU 

Critical care is a process that begins at the point of injury and continues until resolution of 

the physiologic insult. Care that is provided in the ICU is one piece of a larger systemic effort to 

provide care. The ICU is a complicated environment charged with the coordination of the efforts 

of many as a wealth of data is prioritized and 

acted upon. Traditionally, physicians have 

practiced in a relatively independent manner, and 

several different approaches to a given disease 

process may be expected at a given institution. 

Numerous studies in the last two decades have 

demonstrated that protocolized approaches to 

complex disease processes can result in better 

patient outcomes.120,241,242,243 In many instances, 

the improved outcomes are as likely to be due to 

the development of an institutional approach to a 

given problem rather than the intervention per se. 

An institutional approach allows multiple services 

to prepare for involvement in a predictable fashion 

and improve efficiency. Additionally, a protocol 

allows more frequent adjustment of therapies 

in response to real-time data collection than is 

possible when decisions are deferred to once or 

twice daily physician rounds. 

The importance of multidisciplinary rounds cannot be overemphasized. While it has been demonstrated 

during the current OEF and OIF conflicts that an intensivist-directed ICU team improves outcomes in 

the combat theater, every member of the critical care team has a role to play and an expertise to bring 

to the bedside.244 Simply adding a clinical pharmacist to daily rounds in the ICU improves mortality.245

Multidisciplinary rounds offer both a chance to share ideas and impressions about a patient’s care as well 

as a method of communicating a plan simultaneously to all of the care team members.

Telemedicine is in its infancy as a specialty but will be seen with increasing frequency in the combat 

environment in the next decade. The technology behind telemedicine is evolving rapidly and allows a 

limited resource to be in many places at once. It is a medicine force-multiplier that has the potential to 

help minimize the forward-positioned medical logistical footprint. 

A final key concept regarding the structure of the combat casualty care ICU is the need for flexibility. The 

combat care environment is fluid and frequently unpredictable. Large numbers of patients may appear 

suddenly at anytime (Fig. 17). The ability to adapt the available, sometimes limited, resources to the needs 

of many will in large part dictate the success or failure of a combat ICU.246 Deviations from optimum 

care are to be expected, but a firm understanding of the relevant medical concepts will help prioritize 

efforts and maximize the chances for a successful patient outcome.

Figure 17. The ability to adapt available resources to the needs of many 

will dictate the success or failure of a combat ICU. Image courtesy of 

Harold Bohman, MD, CAPT, MC, US Navy.
Critical Care | 697

Critical Care Air Transport Team (CCATT)

Historical Background and System Basics

All coalition patients with critical care requirements in the current conflicts in Afghanistan (OEF) and 

Iraq (OIF) are flown out-of-theater to Germany with the assistance of a Critical Care Air Transport Team 

(CCATT) (Fig. 18). A CCATT is composed of a physician with some critical care training, a critical care 

nurse, and a respiratory therapist. They are prepositioned in the area of operation to facilitate transport 

to Landstuhl Regional Medical Center (LRMC) in Germany, and more teams are prepositioned in 

Germany for transport back to the continental US.247,248 Each team has a specified equipment allowance 

standard that is designed to support between three and six patients, with the number on a given mission 

being determined in part by the severity of illness. A CCATT represents an additional critical care 

capability that augments the capabilities of an air evacuation team. Air evacuation teams are composed 

of two to three nurses and four to seven technicians that provide care to non-critically injured patients 

and act as the liason between the CCATT and the aircraft crew members.248,249

All coalition patients with critical care requirements in the current conflicts in Afghanistan (OEF) and 

Iraq (OIF) are flown out-of-theater to Germany with the assistance of a CCATT. Critical Care Air 

Transport Teams facilitate the rapid evacuation of severely ill patients, which translates both into better 

patient care as well as a significantly decreased forward medical footprint.

The birth of the CCATT asset can be traced back 

to 1988, when the program was first proposed by 

then Col PK Carlton, USAF, MC. Subsequent 

experiences in the Gulf War and Somalia 

highlighted a need for a coordinated approach to 

augmenting the in-flight critical care capability of 

standard air evacuation teams. A pilot program 

was formed in 1994 and the program was later 

formally adopted in 1996. The role of CCATT 

in patient movement has matured in the OEF 

and OIF areas of operation since 2001 and 2003, 

respectively.250 Critical Care Air Transport Teams 

facilitate the rapid evacuation of severely ill 

patients, which translates both into better patient 

care as well as a significantly decreased forward 

medical footprint. The evolution of this unique 

capability has been one of the great success stories of military medicine during the current conflicts.

The overall approach to care of the severely injured trauma patient has evolved in parallel with the 

CCATT system. The concept of damage control resuscitation emphasizes a first surgery to control 

immediately life-threatening hemorrhage while delaying more definitive surgical therapy until after a 

period of resuscitation that may take several hours to days.251 In practice in OEF and OIF, patients will 

often have a first damage control surgery at a forward surgical location and are transported to a larger 

military trauma center in-theater by helicopter that is colocated with a CCATT. A second washout surgery 

Figure 18. A CCATT transports critically injured soldiers out-of-theater.
698 | Critical Care

may be performed at the trauma center and then the patient is flown with a CCATT to Germany.252

During the five to nine hours in the air, the CCATT is able to continue an aggressive resuscitation and 

deliver a patient to Landstuhl that is better prepared for more definitive surgical therapy. The success of 

damage control resuscitation in civilian trauma settings and in other military conflicts has lent itself well 

to the CCATT concept, and the presence of this new capability allows damage control to be pursued 

without delaying patient transport.

The US Air Force used to have a fleet of dedicated air evacuation aircraft, the majority of which were 

C-9 aircraft based on the DC-9 airliner airframe (Fig. 19). A set fleet of aircraft was found to be expensive 

and inflexible since all of the aircraft had identical capabilities in terms of range and logistics footprint 

and were located in only a few locations worldwide. Today, the air evacuation system uses “aircraft of 

opportunity.” Air evacuation and CCATT teams are designed to be modular and have been trained 

to use the unique capabilities of numerous aircraft to allow patient transport. Today, the majority of 

CCATT missions are flown on C-17 and C-130 aircraft. Refueling aircraft such as the KC-135 and KC10 have been used, as has the largest aircraft in the US inventory, the C-5. CCATT missions in-theater 

are occasionally flown on HH-60 Black Hawk helicopters, and some missions in the continental US and 

Europe are conducted with the C-21, which is the military version of a standard Learjet. 

When the critical care team downrange identifies the need for CCATT transport, an air evacuation liason 

officer is contacted. The air evacuation liaison officer notifies a local flight surgeon who can evaluate the 

patient and identify any special needs the patient may have in flight. The request is then forwarded to a 

Joint Patient Movement Requirement Center (JPMRC) in-theater. The request is cleared, and an effort is 

coordinated with the Tanker Airlift Control Center (TACC) to find an aircraft in the theater that can be 

made available for patient movement. The patient, an air evacuation team, and a CCATT are then assigned 

Figure 19. C-17 aircraft is commonly used for CCATT missions.
Critical Care | 699

to that aircraft and preparations are made in the critical care unit for flight. While the system seems at 

first glance to be complex, it has become relatively efficient and results in much faster patient evacuation 

than in any prior conflict as well as a significantly decreased need for forward medical resources.253

Challenges Associated with Critical Care in the Air

Critical care in the back of an aircraft can be challenging and represents a significant physiologic stressor 

for the patient. Older aircraft may have poor temperature control and are typically very cold in flight. 

While flying in-theater below a certain threshold altitude, aircraft are kept dark inside to minimize the 

chances of being shot down. Vibration and noise are common factors that make patient monitoring 

more difficult than on the ground. Aircraft cabins are typically pressurized to 6,000 to 8,000 feet leading 

to lower oxygen content in the air as well as a tendency for any gas contained within an enclosed space 

to expand. This can complicate the care of patients with closed eye injuries associated with air pockets 

in the vitreous or patients with unrecognized pneumothoraces. Finally, acceleration changes associated 

with steep combat takeoffs and landings may contribute to the development of increased intracranial 

pressures in patients with traumatic brain injury.254,255

Physiologic stressors associated with cabin temperature, vibration and noise, air pressure, and steep 

combat takeoffs and landings may compound patient morbidity.

Perhaps the biggest challenge facing the CCATT when caring for a patient is the reality that there are 

limited options for assistance. The medical equipment that accompanies a CCATT is designed to support 

numerous interventions such as endotracheal intubation, central venous catheter insertion, arterial line 

placement, emergent tracheostomy, and chest tube thoracostomy. However, there are occasions when it 

is necessary to divert an aircraft to allow urgent transport of a patient to a ground based medical facility. 

Luckily, this has been a rare occurrence. A specialized Acute Lung Rescue Team (ALRT) is positioned 

at Landstuhl Regional Medical Center to assist in the evacuation of OEF/OIF patients with profound 

respiratory failure that may exceed basic CCATT capabilities.76

The relatively austere, resource-limited environment that a CCATT practices within demands that every 

effort be made prior to the flight to anticipate complications that may arise. With experience during a 

deployed rotation, the sending ICU teams and CCATTs become very adept at anticipating the needs 

of a patient. Those with marginal oxygenation on the ground should be intubated prior to flight.256

Developing extremity compartment syndromes should be addressed with fasciotomies, and abdominal 

compartment syndromes should lead to laparotomy and the placement of an adjustable temporary 

abdominal closure.250,257 Patients with suspected intracranial pressure elevations should be considered 

for early placement of intracranial pressure monitoring capability.255 Blood products that may be needed 

for resuscitation and medications such as antibiotics and vasopressors should be identified prior to the 

mission.

The biggest challenge facing the CCATT when caring for a patient is that there are limited options for 

assistance, and every effort must be made prior to the flight to anticipate complications that may arise.

The use of the air evacuation system with CCATT augmentation has resulted in excellent patient 

outcomes, increased speed of evacuation, and a decreased downrange medical footprint. Even in its 
700 | Critical Care

relative infancy, the CCATT capability is demonstrating a new way to allocate medical resources in the 

combat care environment. The successful evolution of the system has created a new paradigm for how 

major industrialized countries involved in protracted wartime operations will address the care of their 

wounded warriors.

Summary

Aggressive, attentive, evidence-based critical care is a key component of recovery for the multisystem 

trauma patient. The ability to adapt the lessons of the medical literature to the challenges of the combat 

environment often determines the difference between a successful or poor patient outcome. Those who 

have the privilege of caring for our nation’s heroes will always look back on the experience as one of the 

defining moments of their lives. Even in the most austere settings, there is no limit to the good that can 

be done.
Critical Care | 701

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Appendix

NIH ARDS 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;342:1301-1308. Copyright © 2000 Massachusetts Medical Society. All rights reserved.
720 | Critical Care
Abbreviations and Acronyms

A

AAN: American Academy of Neurology

ABA: American Burn Association

ABC: airway, breathing, and circulation

ABLS: Advanced Burn Life Support

A/C: assist-control 

ACTH: adrenocorticotropic hormone

ADDRESS: Administration of Drotrecogin Alfa (activated) in Early Stage Severe Sepsis (trial)

AFSOC: Air Force Special Operations Command

AFTH: Air Force Theater Hospital

AIREVAC: air evacuation

AIS: Abbreviated Injury Scale

ALI: acute lung injury

ALRT: Acute Lung Rescue Team

ALVEOLI: Assessment of Low Tidal Volume and Elevated End-Expiratory Lung Volume to Obviate Lung Injury (trial)

AMEDD: US Army Medical Department

ANFO: ammonium nitrate/fuel oil

AOR: area of responsibility

AP: anteroposterior

APD: afferent papillary defect

aPLT: apheresis platelet

APRV: alternating pressure release ventilation

aPTT: activated partial thromboplastin time

ARDS: acute respiratory distress syndrome

ARDSnet: Acute Respiratory Distress Syndrome Clinical Trials Network

ATLS: Advanced Trauma and Life Support

ATP: adenosine triphosphate

B

BAL: bronchoalveolar lavage

BAMC: Brooke Army Medical Center

BP: blood pressure

BSMC: Brigade Support Medical Company

BSS: balanced salt solution

BTBIS: Brief TBI Screen

BUMED: Bureau of Medicine and Surgery

C

CASEVAC: casualty evacuation

CBF: cerebral blood flow

CCATT: Critical Care Air Transport Team/Critical Care Aeromedical Transport Team

CCC: combat casualty care

CDC: Centers for Disease Control and Prevention

CENTCOM: US Central Command

CHS: combat health support

cm: centimeter

CN: cranial nerve

COG: Clinical Operating Guidelines

CONUS: continental United States

COPD: chronic obstructive pulmonary disease

CORTICUS: Corticosteroid Therapy of Septic Shock (trial)

CPAP: continuous positive airway pressure

CPG: Clinical Practice Guidelines

CPK: creatinine phosphokinase

Abbreviations and Acronyms | xv
xvi | Combat Casualty Care

CPP: cerebral perfusion pressure

CPR: cardiopulmonary resuscitation

CRTS: Casualty Receiving and Treatment Ship

CS: compartment syndrome

CSH: Combat Support Hospital

CT: computed tomography

CTA: computed tomographic angiography

CVP: central venous pressure

CVR: cerebral vascular resistance

D

D10: 10% dextrose

D25: 25% dextrose

D5: 5% dextrose

D50: 50% dextrose

DCR: damage control resuscitation

DCS: damage control surgery

DECRA: Decompressive Craniectomy (trial)

DIC: disseminated intravascular coagulation

DIMOC: Defense Imagery Management Operations Center

DO2: oxygen delivery

DOD: Department of Defense

DVT: deep venous thrombosis

E

ECCO2R: extracorporeal carbon dioxide removal

ECMO: extracorporeal membrane oxygenation

ED: emergency department

EFP: explosively formed projectile

EMEDS: Expeditionary Medical Support

EMF: Expeditionary Medical Facility

EMS: emergency medical services

EMT: emergency medical technician; also Emergency & Military Tourniquet

EMT-B: emergency medical technician–basic

ENT: ear-nose-throat

EOD: explosive ordnance disposal

ER: oxygen extraction ratio

EtCO2/ETCO2: end-tidal carbon dioxide

ETT: endotracheal tube

exam: examination

F

FAST: Focused Assessment with Sonography for Trauma

FDA: Food and Drug Administration

FFP: fresh frozen plasma

FiO2: fraction of inspired oxygen

Fr: French (gauge system used to measure catheter size)

FRC: functional residual capacity

FRSS: Forward Resuscitative Surgical System

FST: Forward Surgical Team

FTSG: full-thickness skin graft

FWB: fresh whole blood

G

g: gram

GCS: Glasgow Coma Scale

GSW: gunshot wound
Index | xvii

H

HEAT: high-explosive antitank

HFJV: high-frequency jet ventilation

HFOV: high-frequency oscillation ventilation

HFV: high-frequency ventilation

Hgb: hemoglobin

HIV: human immunodeficiency virus

HME: heat and moisture exchanger

HMMWV: High-Mobility Multipurpose Wheeled Vehicle (“Humvee”)

HMX: cyclotetramethylene tetranitramine

HPMK: Hypothermia Prevention and Management Kit

HPPL: high-pressure pulsatile lavage

HR: heart rate

HSS: Health Services Support

HTS: hypertonic saline

I

I:E: inspiratory to expiratory ratio

ICP: intracranial pressure

ICRC: International Committee for the Red Cross

ICU: intensive care unit

IED: improvised explosive device

I MEF: First Marine Expeditionary Force

in-lbs: inch-pounds

iNO: inhaled nitric oxide

INR: international normalized ratio

IO: intraosseous

IOFB: intraocular foreign body

IOP: intraocular pressure

IPEEP: intrinsic positive end-expiratory pressure

ISS: Injury Severity Score

IV: intravenous

IVC: inferior vena cava

J

JP: Jackson Pratt

JPTA: Joint Patient Tracking Application

JTTR: Joint Theater Trauma Registry

JTTS: Joint Theater Trauma System

K

KCl: potassium chloride

K.E.D.: Kendrick® Extrication Device

KIA: killed in action

K-wires: Kirschner wires

L

labs: laboratory tests

LMA: laryngeal-mask airway

LOC: loss of consciousness

LOS: length of hospital stay

L:P: lactate to pyruvate ratio

LR: lactated Ringer’s 

LRMC: Landstuhl Regional Medical Center

LZ: landing zone

Abbreviations and Acronyms | xvii
xviii | Combat Casualty Care

M

MACE: Military Acute Concussion Evaluation

MAP: mean arterial pressure

MASH: Mobile Army Surgical Hospital

mcg: microgram

MEDEVAC: medical evacuation

mEq: milliequivalent

METTAG: Medical Emergency Triage Tag

METT-TC: mission, equipment, terrain and weather, time, troops, and civilians

MFST: Mobile Field Surgical Team

mg: milligram

ml: milliliter

mm: millimeter

MODS: multiple organ dysfunction syndrome

mOsm: milliosmole

MRAP: mine-resistant ambush-protected (vehicles)

MRI: magnetic resonance imaging

MRSA: methicillin-resistant Staphylococcus aureus

m/sec: meters per second

MTF: Medical Treatment Facility

N

NASCIS: National Acute Spinal Cord Injury Study

NATO: North Atlantic Treaty Organization

NG: nasogastric

NICE-SUGAR: Normoglycemia in Intensive Care Evaluation-Survival Using Glucose Algorithm Regulation (study)

NIPPV: noninvasive positive-pressure ventilation

NIRS: near infrared spectroscopy

NOE: naso-orbito-ethmoid

NPO: nil per os (nothing by mouth)

NPV: negative-pressure ventilation

NS: normal saline

NSAID: nonsteroidal anti-inflammatory drug

O

OEF: Operation Enduring Freedom

OIF: Operation Iraqi Freedom

OR: operating room

OTFC: oral transmucosal fentanyl citrate

P

PA: posterior-anterior

PAd: pulmonary artery diastolic

PAI-1: plasminogen-activator inhibitor type 1

PALS: Pediatric Advanced Life Support

Palv: alveolar pressure

2-PAM: pralidoxime chloride

PaO2: partial pressure of oxygen in arterial blood/arterial blood gas

PAs: pulmonary artery systolic

Patm: pressure above atmospheric pressure

PBW: predicted (ideal) body weight

PCO2: partial pressure of carbon dioxide

PCR: patient care report

PCV: pressure-control ventilation

PCWP: pulmonary capillary wedge pressure

PE: pulmonary embolism

PEEP: positive end-expiratory pressure
Index | xix

PEEPh: high positive end-expiratory pressure

PEEPl: low positive end-expiratory pressure

PETN: pentaerythritol tetranitrate

pHi: gastric mucosal pH

PPE: personal protective equipment

Pplat: peak plateau pressure

PPV: positive-pressure ventilation

PRBCs: packed red blood cells

PROWESS: Recominant Human Activated Protein C Worldwide Evaluation in Severe Sepsis (trial)

PRVC: pressure-regulated volume control

PslCO2: sublingual PCO2

PSV: pressure-support ventilation

PT: prothrombin time

PTSD: posttraumatic stress disorder

PTTV: percutaneous transtracheal ventilation

Q

Q: cardiac output; also areas of perfusion

R

RBC: red blood cell

RDX: cyclotrimethylene trinitramine

REACH: Registry of Emergency Airways at Combat Hospital

RESCUEip: Randomized Evaluation of Surgery with Craniectomy for Uncontrollable Elevation of Intra-Cranial Pressure (trial)

RFVIIa: recombinant factor VIIa

RhAPC: recombinant human activated protein

RPG: rocket-propelled grenade

RR: respiratory rate

RSI: rapid sequence intubation

RTS: Revised Trauma Score

S

SALT: Sort, Assess, Life-Saving, Triage/Treat/Transport

SaO2: oxygen saturation of hemoglobin

SAPS: simplified acute physiology score

SBIR: Small Business Innovation Research

SBP: systolic blood pressure

SCIWORA: spinal cord injury without radiographic abnormality

ScvO2: central venous oxygen saturation

SEAL: Sea-Air-Land (US Navy)

SIADH: syndrome of inappropriate antidiuretic hormone 

SIMV: synchronized intermittent mandatory ventilation

SIRS: systemic inflammatory response syndrome

SOF: Special Operations Forces

SOMI: sternal occipital mandibular immobilizer

SPO2: pulse oximeter oxygen saturation

SSTP: Surgical Shock Trauma Platoon

START®: Simple Triage And Rapid Treatment

StO2: oxygen saturation of hemoglobin in tissue

STP: Shock Trauma Platoon

STSG: split-thickness skin graft

SvO2: mixed venous oxygen saturation

T

TACC: Tanker Airlift Control Center

TACEVAC: tactical evacuation

TATRC: Telemedicine and Advanced Technology and Research Center

Abbreviations and Acronyms | xix
xx | Combat Casualty Care

TBI: traumatic brain injury

TBSA: total body surface area

TCA: tricarboxylic acid

TCCC: Tactical Combat Casualty Care

Th: high PEEP level

THAM: tromethamine

TIC: Troops in Contact

Tl: low PEEP level

TNT: 2,4,6-trinitrotoluene

TOC: Tactical Operations Center

TPN: total parenteral nutrition

TRICC: Tranfusion Requirements in Critical Care

U

US: United States

USAF: United States Air Force

USAISR: United States Army Institute of Surgical Research

USMC: United States Marine Corps

USN: United States Navy

USSOCOM: US Special Operations Command

UXO: unexploded ordnance

V

V: areas of ventilation

Va: alveolar ventilation

V.A.C.®: vacuum-assisted closure

VAP: ventilated-associated pneumonia

VASST: Vassopressin and Septic Shock Trial

VBIED: vehicle-borne improvised explosive device

VCO2: carbon dioxide generated by the body

Vd: dead-space ventilation

VDR-4®: Volumetric Diffusive Respiration (ventilator)

Ve: minute ventilation

VEC: Vertebrace® Extrication Collar

VILI: ventilator-induced lung injury

VO2: oxygen uptake

VS: vital signs; also Valsella Meccanotechnica SpA (producer of the VS-16 Italian antitank blast mine)

Vt: tidal volume

VTOL: Vertical Take-Off and Landing

W

WBB: walking blood bank

WBC: white blood cell

WDMET: Wound Data and Munitions Effectiveness Team

WRAMC: Walter Reed Army Medical Center

WWI: World War I

WWII: World War II
Index | xxi

Index

A 

A/C. See Assist-control

AAN. See American Academy of Neurology

ABA. See American Burn Association

Abbe-Estlander flaps, 266

Abbreviations and acronyms, xv–xx

Abdominal compartment syndrome

burn care, 611–612

effects of, 194–195

pediatric, 541–542

prevention of, 27

Abdominal injuries

abdominal wall closure, 194–195

damage control laparotomy, 184–192

duodenal injury, 187–188

hepatic parenchymal injury, 186–187

intestinal injuries, 192–193

large soft-tissue wounds, 192

pancreatic injury, 187–188

pediatric, 561–564

perihepatic vascular injury, 186

rectal injury, 193

renal injury, 188–190

retrohepatic hematoma, 186

retroperitoneal wounds, 192

splenic injury, 190–192

ureteral injury, 190–191

Abdominal packing, 27–28

ABLS. See Advanced Burn Life Support

Acceleration-deceleration injuries, 58

Acetabular fractures, 454

Acid burns. See also Chemical burn injuries

eye injuries, 331–332

Acidemia, 23, 139

Acidosis

damage control resuscitation, 22–23, 124–125

damage control surgery and, 170

ACTH. See Adrenocorticotropic hormone

Acute airway obstruction, 97–98

Acute burn care

abdominal compartment syndrome, 611–612

aeromedical transport, 628–629

airway and breathing interventions, 601–603

burn center referral criteria, 629

Burn Flow Sheet documentation, 608

burn severity estimation, 606

combat compared to civilian burns, 597–598

comorbid life-threatening injury care, 603

complications, 611–615

decontamination, 600–601

degree of burn, 604–605

depth of burn estimation, 604–606

electrolyte disturbances, 612–613

engraftment, 625

escharotomy, 613–615
xxii | Combat Casualty Care

fascial excision, 619–621

fasciotomy, 613–615

fluid resuscitation, 607–611

full-thickness skin grafts, 625

hypothermia, 616–617

infection control, 626–627

initial evaluation and management, 598–603

location of burn, 606

meshed skin grafts, 623–625

metabolic considerations, 627–628

modified Brooke Formula, 609–611

nutritional considerations, 627–628

overview, 596

pain control, 617

patient exposure, 616–617

patient inspection, 600–601

patient resuscitation, 603–630

primary survey, 599–600

Rule of Nines, 606

Rule of Ten, 609–610

secondary survey, 599–600

skin grafting, 621–625

skin harvesting, 622

tangential excision, 619

total body surface area, 597–598, 606, 610

traumatic rhabdomyolysis, 612

triage criteria, 598

wound care, 615–627

wound evaluation, 603–630

wound excision, 617–621

Acute lung injury, 661

Acute respiratory distress syndrome

adjunctive strategies, 668–669

airway pressure release ventilation, 667–668

basic concepts, 661–663

corticosteroid therapy, 669–670

fluid management, 669

mechanical ventilation, 663–669

nutritional goals, 671

pediatric, 553

positive end-expiratory pressure, 665–667

prone positioning, 670–671

tidal volume, 663–665

Acute Respiratory Distress Syndrome Clinical Trials Network, 664

ADDRESS trial. See Administration of Drotrecogin Alfa (activated) in Early Stage Severe Sepsis

Adenosine, 560

Administration of Drotrecogin Alfa (activated) in Early Stage Severe Sepsis, 689

Adrenocorticotropic hormone, 685

Advanced Burn Life Support, 599–600

Advanced Trauma Life Support, 22, 599–600

Aeromedical evacuation system, 21. See also MEDEVAC

Afferent pupillary defect, 309

Afghanistan. See also Operation Enduring Freedom

Combat Support Hospitals, 19

landmine prevalence, 47

AFTH. See Air Force Theater Hospitals

Air Ambulances. See MEDEVAC units

Air evacuation. See Patient evacuation
Index | xxiii

Air Force

combat health support, 109

Expeditionary Medical Support, 7, 108

Mobile Field Surgical Teams, 7, 108

Air Force Theater Hospitals, 19, 108

Air medical evacuation. See MEDEVAC

Airway compromise

acute airway obstruction, 97–98

awake endotracheal intubation, 245–246

burn care, 601–603

confirmation of endotracheal tube placement, 246–247

crash endotracheal intubation, 246

cricothyroidotomy, 97, 247–250

difficult airways, 250–251

endotracheal intubation preparation, 243–244

endotracheal intubation technique, 244–247

initial management, 251–256

maxillofacial injuries, 237–242

neck injuries, 281

pediatric, 534–537, 548–550

preventable death from, 88–89

pulmonary contusion, 657–658

rapid sequence intubation, 245

surgical airway management, 247–250

traumatic brain injuries, 363–365, 367

Airway pressure release ventilation, 652, 667–668

ALI. See Acute lung injury

Alkali burns. See also Chemical burn injuries

eye injuries, 331–332

Allograft, 618–619

Alternating pressure release ventilation, 553

Alveolar pressure, 645

ALVEOLI trial. See Assessment of Low Tidal Volume and Elevated End-Expiratory Lung Volume to Obviate Lung Injury

American Academy of Neurology, 354

American Burn Association, 600, 628

Aminocaproic acid, 144

Amiodarone, 560

Ammonium nitrate/fuel oil, 45

Amputations

degree of, 481

delayed amputation, 420–421

fasciotomy, 419–420

initial assessment, 415–416

initial resuscitation, 417–421

mechanism of, 481

number of limbs, 481

primary amputation, 417

rehabilitation, 422

surgical amputation, 420–421

surgical technique, 481–482

timing of, 481

wound care, 420–421

wound debridement, 417–419

Anaerobic metabolism, 23

Analgesics, 102

ANFO. See Ammonium nitrate/fuel oil

Angiography. See also Computed tomographic angiography

pelvic injuries, 205
xxiv | Combat Casualty Care

Anterior cord syndrome, 504–505

Antibiotics

antibiotic impregnated pellets, 439

extremity injuries, 439–441

maxillofacial wound infection management, 261

prophylactic use, 102, 259, 362, 440

Anticonvulsants, 375–377

Antiepileptic drugs, 376

Antifibrinolytics, 144

Antipersonnel landmines, 46–47

Antitank landmines, 54

Antitank munitions, 52–54

Anxiety disorders, 354

Aprotinin, 144

APRV. See Airway pressure release ventilation; Alternating pressure release ventilation

ARDS. See Acute respiratory distress syndrome

ARDSnet. See Acute Respiratory Distress Syndrome Clinical Trials Network

Army

combat health support, 109

Forward Surgical Teams, 5, 7–8, 17–19

Medical Treatment Facilities, 7

Arterial injuries, 195–200

Assessment of Low Tidal Volume and Elevated End-Expiratory Lung Volume to Obviate Lung Injury, 667

Assist-control positive-pressure ventilation, 649

Asystole, pediatric, 558

Atelectotrauma, 646

Atlanto-occipital disassociation, 508

ATLS. See Advanced Trauma Life Support

Atypical stump flaps, 421

Audiology, 60

Awake endotracheal intubation, 245–246

Axial traction, 508–510

B

Bacteria. See Wound flora

Bag-valve-mask ventilatory support, 97

Ballistic injuries, 54

Barotrauma, 646

Base deficit, 674–675

Battalion Aid Stations, 103

Bedside clinical findings, 133–134

Benzodiazepines, 364, 556, 617

Berlin’s edema, 318

Bicarbonate therapy, 690–691

Biotrauma, 647–648

Bladder injuries, 208–210

Blast landmines, 47–48

Blast traumatic brain injuries, 353–354

Bleeding. See Hemorrhage

Blood pH, 23

Blood transfusions. See Transfusions

Body armor, 15

Bone fractures. See Fractures

Bone grafting

mandibular reconstruction, 276

“Bouncing Betty,” 49

Bounding fragmentation landmines, 48–49

Bowstring test, 270
Index | xxv

Bradycardia, pediatric, 559

Brain injuries, traumatic. See Traumatic brain injuries

Brain Trauma Foundation, 367

Breathing support

acute airway obstruction, 97–98

awake endotracheal intubation, 245–246

burn care, 601–603

confirmation of endotracheal tube placement, 246–247

crash endotracheal intubation, 246

cricothyroidotomy, 97, 247–250

difficult airways, 250–251

endotracheal intubation preparation, 243–244

endotracheal intubation technique, 244–247

initial management, 251–256

maxillofacial injuries, 237–242

neck injuries, 281

pediatric, 534–537, 548–550

preventable death from airway compromise, 88–89

pulmonary contusion, 657–658

rapid sequence intubation, 245

surgical airway management, 247–250

traumatic brain injuries, 363–365, 367

Brief TBI Screen, 64

Brigade Support Medical Company, 103, 107–108

Bronchopleural fistulas, 62

Bronchoscopy, fiberoptic, 658

Brooke Army Medical Center, 19

Brooke Formula, modified, 609–611

Brown-Séquard syndrome, 505–506

BSMC. See Brigade Support Medical Company

BTBIS. See Brief TBI Screen

Bureau of Medicine and Surgery, 93

Burn care

abdominal compartment syndrome, 611–612

aeromedical transport, 628–629

airway and breathing interventions, 601–603

burn center referral criteria, 629

Burn Flow Sheet documentation, 608

burn severity estimation, 606

combat compared to civilian burns, 597–598

comorbid life-threatening injury care, 603

complications, 611–615

decontamination, 600–601

degree of burn, 604–605

depth of burn estimation, 604–606

electrolyte disturbances, 612–613

engraftment, 625

escharotomy, 613–615

facial, 267–268

fascial excision, 619–621

fasciotomy, 613–615

fluid resuscitation, 607–611

full-thickness skin grafts, 625

hypothermia, 616–617

infection control, 626–627

initial evaluation and management, 598–603

location of burn, 606

meshed skin grafts, 623–625
xxvi | Combat Casualty Care

metabolic considerations, 627–628

modified Brooke Formula, 609–611

nutritional considerations, 627–628

overview, 596

pain control, 617

patient exposure, 616–617

patient inspection, 600–601

patient resuscitation, 603–630

pediatric, 564

primary survey, 599–600

Rule of Nines, 606

Rule of Ten, 609–610

secondary survey, 599–600

skin grafting, 621–625

skin harvesting, 622

tangential excision, 619

total body surface area, 597–598, 606, 610

traumatic rhabdomyolysis, 612

triage criteria, 598

wound care, 615–627

wound evaluation, 603–630

wound excision, 617–21

Burn Flight Team, 628

Buttock wounds, 437–438

C

Cantholysis, inferior, 329–330

Canthotomy, lateral, 329–330

Carbamazepine, 376

Cardiac rhythm disturbances

pediatric, 558–560

Cardiopulmonary resuscitation, 14, 558–559

Care-under-fire, 93–94

Case studies

damage control resuscitation, 29–31

damage control surgery, 29–31

eye injuries, 333–338

out-of-hospital care, 89–91, 111–112

CASEVAC. See Casualty evacuation

Casualty evacuation. See also Patient evacuation

considerations, 18, 20

Tactical Combat Casualty Care, 104

Casualty Receiving and Treatment Ships, 7

Catecholamine-resistant shock, 555

Catecholamines, 143

Cauda equina syndrome, 506

CBF. See Cerebral blood flow

CCATT. See Critical Care Air Transport Teams

CCC. See Combat casualty care

CeloxTM powder, 17

Cement bead therapy, 439

Centers for Disease Control and Prevention, 111

Central brain herniation, 358–360

Central cord syndrome, 504–506

Central venous oxygen saturation, 676–677, 686–687

Central venous pressure, 682–683

Cerebral blood flow, 350, 367–368

Cerebral edema, 349
Index | xxvii

Cerebral herniation, 358–360, 556

Cerebral hypoperfusion, 100, 349

Cerebral perfusion pressure, 350, 364–366, 368–369, 541

Cerebral vascular resistance, 350

Cerebrospinal fluid fistulae, 512–513

Cerebrospinal fluid leaks, 362

Cervical spine injuries, 242–243

Chemical burn injuries, 419, 600–601

Chemical eye injuries, 331–332

Children. See Pediatric trauma

Chitosan dressings, 129

Choroidal injuries, 318

Civilian casualties

explosive-related injuries, 55–56

Claymore mine, 49–50

Clinical Practice Guidelines, 64, 471–480, 483–484

Closed wounds

globe injuries, 315–318

head injuries, 351

spinal injuries, 576–580

Clot-promoting agents, 17

Coagulopathy

damage control resuscitation, 22–23, 124–125

damage control surgery and, 170

massive transfusion-associated, 138–140

Codman

® ICP EXPRESS, 572

Cold shock, 555

Colloid solutions, 142, 369

Colostomy, 193

Combat Application Tourniquets, 128, 404–405, 469–470

Combat-associated pneumonia prevention, 692–694

Combat casualty care

adjusting to the environment, 5–8

causes of preventable death, 11–13, 88–89

challenges, 4

damage control strategies, 22–29

damage control surgery, 170–172

echelons of care, 17–20

equipment advancements, 15–17

extremity injuries, 422–426

ICU structure, 696

levels of ophthalmic care, 304–307

organizational innovations, 17–22

out-of-hospital care, 89–92, 111–112

spinal injuries, 490–493

tactical care, 92–107

training advancements, 13–14

Combat Gauze

TM, 17, 95, 130

Combat health support, 109

Combat injury patterns, 11

Combat Support Hospitals

evacuation times, 5–6

function of, 19

Commotio retinae, 318

Compartment syndrome, abdominal. See Abdominal compartment syndrome

Compartment syndrome, limb. See Limb compartment syndrome

Complete cord syndrome, 503–504

Completion amputation, 417
xxviii | Combat Casualty Care

Composition C4, 45

Compressible hemorrhage

pressure points, 17, 126–127

preventable death from, 88–89

Computed tomographic angiography

neck injuries assessment, 283, 285

traumatic brain injuries, 362

Computed tomography imaging

facial injuries, 262

maxillofacial wound infection diagnosis, 260–261

ocular injuries, 314–315

pediatric injuries, 568–570

pelvic injuries, 204–205

spinal injuries, 501–503

traumatic brain injuries, 351–352, 357, 359, 362–363

Conflagration, 45

Conjunctival lacerations, 328

Continuous positive airway pressure, 667

Copper sulfate, 419

Corneal abrasion, 315

Corneal foreign bodies, 315–316

Corneal perforation, 313

Corneoscleral laceration, 321–322

Corticosteroid Therapy of Septic Shock trial, 685

Corticosteroids, 669–670, 685–686

CORTICUS. See Corticosteroid Therapy of Septic Shock trial

Cough control, 661

Coup injuries, 355

CPAP. See Continuous positive airway pressure

CPGs. See Clinical Practice Guidelines

CPP. See Cerebral perfusion pressure

CPR. See Cardiopulmonary resuscitation

Cranialization, 270

Craniectomy, decompressive, 374–377

Cricothyroidotomy, 97, 247–250

Critical care

acute respiratory distress syndrome, 661–672

airway pressure release ventilation, 667–668

assist-control positive-pressure ventilation, 659

atelectotrauma, 646

barotrauma, 646

biotrauma, 647–648

central venous oxygen saturation, 676–677

combat-associated pneumonia prevention, 692–694

combat casualty care ICU structure, 696

Critical Care Air Transport team, 697–700

deep venous thrombosis prophylaxis, 694

gastric intramucosal pH, 677

gastrointestinal bleeding prophylaxis, 695

high-frequency ventilation, 653

infection control, 695

lactate, 673–674

mechanical ventilation, 643–655, 663–669

mixed venous oxygen saturation, 676–677

positive end-expiratory pressure, 665–667

positive-pressure ventilation, 648–653

pressure-control ventilation, 650–651

pressure-regulated volume control, 652–653
Index | xxix

pressure-support ventilation, 651–652

preventive care, 695

pulmonary contusion, 655–661

resuscitation endpoints, 672–679

sepsis, 679–691

sublingual PCO

2

, 677–678

supraphysiologic oxygen delivery attainment, 675

synchronized intermittent mandatory ventilation, 649–650

tissue carbon dioxide and oxygen assessment, 678

traumatic brain injuries, 376–377

ventilator-induced lung injury, 646–648

ventilator settings for normal lungs, 653–655

volutrauma, 646

Critical Care Air Transport Teams, 20–21, 172, 377, 697–700

CRTS. See Casualty Receiving and Treatment Ships

Crush syndrome, 68

Crystalloid solutions, 22–23, 142, 369

CSH. See Combat Support Hospitals

CT. See Computed tomography imaging

CTA. See Computed tomographic angiography

CVP. See Central venous pressure

CVR. See Cerebral vascular resistance

Cyclotetramethylene tetranitramine, 45

Cyclotrimethylene trinitramine, 45 D

Damage control resuscitation

adjunctive measures, 140–144

Advanced Trauma and Life Support, 22

antifibrinolytics, 144

bedside clinical findings, 133–134

blood product transfusion ratios, 24–26

blood products transfusion, 135–138

case study, 29–31

coagulopathy, 138–140

colloid solutions, 142

crystalloid solutions, 142

electrolyte disorders, 138

fibrinogen, 137

fresh frozen plasma transfusion, 136–137

fresh whole blood transfusion, 137–138

goal of, 23

hemorrhage control techniques, 126–127

hemostatic dressings, 127–130

hypotensive resuscitation, 140–142

hypothermia prevention, 130–131

key components of, 125–126, 171

laboratory testing, 134

lethal triad, 22–23, 124–125

massive transfusion-associated complications, 138–140

massive transfusion need prediction, 132–135

massive transfusion prevention, 126–131

mechanism of injury, 132–133

new technologies, 134–135

nonsurgical hemostatic agents, 143–144

pediatric, 551–552

permissive hypotension, 24

platelets transfusion, 137
xxx | Combat Casualty Care

recombinant factor VIIa, 143–144

red blood cells transfusion, 135

role of fresh whole blood, 26–27

role of recombinant factor VIIa, 27

topical sealants, 143

tourniquets, 127–130

vasoactive agents, 143

Damage control surgery

abdominal injuries, 184–195

neck injuries, 181–183

pelvic injuries, 202–211

peripheral vascular injuries, 195–201

principles of, 27–31, 169–172

thoracic injuries, 173–181

Dandy clamps, 571

DCR. See Damage control resuscitation

DCS. See Damage control surgery

Dead-space ventilation, 644

Debridement, 259, 261, 417–419, 433–438

Decompressive craniectomy, 374–377

Decompressive Craniectomy trial, 374–375

Decontamination plans, 72

DECRA, 374–375

Decubitus ulcers, 377

Deep venous thrombosis prophylaxis, 694

Defense and Veterans Brain Injury Center, 64

Dental injuries, 253–254

Depression, 354

Dermatomes, 619

Destot’s sign, 203

Dextrose, 544

Diazepam, 556

DIC. See Disseminated intravascular coagulation

Diffuse traumatic brain injuries, 355

Digital subtraction angiography, 362

Dilutional coagulopathy, 140

Diplopia, 310

Direct pressure, 17

Directional fragmentation landmines, 49–50

Disseminated intravascular coagulation, 140, 688

Distal pancreatectomy, 187

Dobutamine, 555, 688–689

Dopamine, 555, 685

Doppler ultrasonography, 363

Drotrecogin alfa (activated), 689

Duodenal injuries, 187–188, 562–563

Duodenojejeunostomy, 187

Dural substitutes, 574

DVBIC. See Defense and Veterans Brain Injury Center

Dynamite, 45

E

Ear injuries, 58–60

Echelons of care, 17–20, 104

ECMO. See Extracorporeal membrane oxygenation

EEG. See Electroencephalography

EFP. See Explosively formed projectile

Electrical injuries, 601
Index | xxxi

Electrocautery, 621

Electroencephalography, 373

Electrolyte disorders, 138, 612–613

Embedded unexploded ordnances, 72–73

EMEDS. See Expeditionary Medical Support

Emergency and Military Tourniquets, 404

Emergency medical services, 91–92

Emergency medical technicians, 91

Emergency thoracotomy, 173–175

EMF. See Expeditionary Medical Facilities

EMS. See Emergency medical services

EMTs. See Emergency medical technicians

En-route nursing care, 21

End-of-life care, pediatric, 580

End-tidal carbon dioxide detection, 246–247, 546–547

Endotracheal intubation

awake endotracheal intubation, 245–246

combat casualty care, 97

confirmation of tube placement, 246–247

crash intubation, 246

displacement, 546–547

pediatric, 535–537, 549

preparation, 243–244

rapid sequence intubation, 245

technique, 244–247

Engraftment, 625

Enteral feeding

pediatric, 543, 544

sepsis, 691

Enteric injuries, 192–193

Enucleation, 323–325

EOD. See Explosive ordnance disposal

Epidural hematomas, 355–357

Epinephrine, 555

Epsilon aminocaproic acid, 144

Equipment advancements, 15–17

Erythropoietin, 688

Escharotomy, 613–615

Esophageal gastric tube airways, 97

Esophageal injuries, 180–181, 286–287

Etomidate, 364–365

ETT. See Endotracheal intubation

Evacuation. See Patient evacuation

Expeditionary Medical Facilities, 108

Expeditionary Medical Support

function of, 108

transporting casualties, 7

Explosive ordnance disposal, 73

Explosive-related injuries

categories, 58–73

civilian casualties, 55–56

embedded unexploded ordnances, 72–73

management considerations, 72

military casualties, 54–55

patterns, 54–56

potentiators, 56–57

primary blast injuries, 58–65

quaternary blast injuries, 69–70
xxxii | Combat Casualty Care

quinary blast injuries, 70–72

secondary blast injuries, 65–68

tertiary blast injuries, 68–69

Explosively formed projectile, 52–54

Explosives

antipersonnel landmines, 46–47

antitank munitions, 52–54

blast landmines, 47–48

devices, 46–54

directional fragmentation landmines, 49–50

fragmentation landmines, 48–49

high-order, 45–46

improvised explosive devices, 50–52

low-order, 45

physics of, 44–45

rocket-propelled grenades, 50

unexploded ordnances, 46–47

Exsanguinating oropharyngeal hemorrhage, 283

External fixation

initial fracture stabilization, 443–444

pelvic injuries, 206

External ventricular drains, 369–370

Extracorporeal membrane oxygenation, 669

Extradural hemorrhages, 576

Extremity injuries

acetabular fractures, 454

amputation, 415–422, 481–482

antibiotic impregnated pellets, 439

antibiotics, 439–441

assessing muscle viability, 437

burden of, 398–399

cement bead therapy, 439

combat casualty wound care, 422–426

debridement, 431, 433–438

emergency tourniquet application, 403–405

external fixation of fractures, 445–454

extremity resuscitation, 423–424

fasciotomy surgical steps, 411

fasciotomy techniques, 412–414

femur fracture fixation, 449–450

forearm fasciotomy, 413

fracture management, 441–454

genitourinary complications, 453

hand compartment fasciotomy, 413

hip dislocations, 453–454

infection prevention, 431–441

irrigation, 432–433, 483–484

Joint Theater Trauma System guidelines, 471–480

ligament injury, 424–425

limb compartment syndrome, 405–414

lower extremity fracture fixation, 448–449

lower leg fasciotomy, 412–413

massive wounds, 437–438

morbidity risk, 410

mortality, 400–403

muscle injury, 424–425

negative-pressure wound dressings, 438–439

nerve repair, 426
Index | xxxiii

open fractures, 444–445

open joint injury, 425–426

open pelvic trauma, 452–453

overview, 397

pelvic fracture fixation, 450–454

primary blast injuries, 65

special wounds, 424–426

surgical wound debridement, 434–438

tendon injury, 424–425

tetanus immunization, 439–441

thigh fasciotomy, 413

tourniquet use, 16, 127–129

upper arm fasciotomy, 413

upper extremity fracture fixation, 447–448

vascular injury, 424–425

wet-to-dry dressing debridement, 433–434

wound closure, 426–431

wound flora, 431

wound management, 423–424

Extremity tourniquets, 127–129, 200

Eye injuries

anterior segment examination, 311–313

assessment of, 268–269

case studies, 333–338

chemical, 331–332

choroidal injuries, 318

closed globe injuries, 315–318

conjunctival lacerations, 328

corneal abrasion, 315

corneal foreign bodies, 315–316

enucleation, 323–325

external ocular examination, 310–311

eyelid lacerations, 326–328

globe repair, 323–324

hyphema, 316

imaging techniques, 314–315

incidence of, 303

intraocular foreign body, 325–326

intraocular pressure measurement, 310

lens subluxation or dislocation, 317

levels of ophthalmic combat casualty care, 304–307

ocular adnexal trauma, 326–328

ocular motility, 309–310

open globe injuries, 318–326

orbital foreign bodies, 330–331

orbital fractures, 331

orbital trauma, 329–331

patient history, 307–308

posterior segment examination, 313

primary blast injuries, 65

pupil examination, 309

retinal injuries, 318

retrobulbar hemorrhage, 329–330

sympathetic ophthalmia, 323

traumatic iritis, 317

traumatic optic neuropathy, 332

visual acuity, 308–309

visual field testing, 310
xxxiv | Combat Casualty Care

vitreous hemorrhage, 317–318

Eyelid lacerations, 326–328

F

Facial injuries

burns, 267–268

facial lacerations, 255–256

facial nerve injury, 254–255

lower face, 274–277

parotid nerve injury, 254–255

soft-tissue injuries, 266–267

Fascial excision, 619–621

Fasciotomy

burn care, 613–615

forearm, 413

hand compartment, 413

Joint Theater Trauma System guidelines, 471–480

lower leg, 412–413

morbidity risk, 410

prophylactic, 409

surgical steps, 411

techniques, 412–414

thigh, 413

traumatic limb amputations, 419–420

upper arm, 413

FAST. See Focused abdominal sonography in trauma

FDA. See Food and Drug Administration

Femoral vasculature injuries, 201

Femur fracture fixation, 449–450

Fentanyl, 364, 617

Fentanyl citrate, oral transmucosal, 103

FFP. See Fresh frozen plasma

Fiberoptic bronchoscopy, 658

Fibrin-impregnated bandages, 129

Fibrinogen, 137

Field care, tactical

acute airway obstruction, 97–98

air medical evacuation considerations, 103

fluid resuscitation, 96–97

hemorrhage control, 95

hemostatic agents, 95

hypothermia prevention and management, 101–102

infection prophylaxis, 102

pain management, 102–103

spinal injury precautions, 99

tension pneumothorax, 98–99

tourniquet use, 95

traumatic brain injuries, 99–101

vascular access, 96–97

ventilatory support, 97–98

FiO2. See Fraction of inspired oxygen

Flail chest, 657

Fluid therapy

acute respiratory distress syndrome, 669

traumatic brain injuries, 100

vascular access, 96–97

Focal traumatic brain injuries, 355

Focused abdominal sonography in trauma, 110, xi
Index | xxxv

Foley catheters, 209

Food and Drug Administration, 27, 103

Forearm fasciotomy, 413

Foreign bodies

corneal, 315–316

orbital, 330–331

Forward Resuscitative Surgical System

function of, 108

transporting casualties, 7

Forward Surgical Teams

facilities, 18–19

situational awareness, 8

transporting casualties, 5, 7, 17

triage issues, 8

Fosphenytoin, 376, 557

Fraction of inspired oxygen, 645, 653, 661, 664, 667

Fractures

acetabular, 454

external fixation, 445–454

extremity injuries, 441–454

femur, 449–450

frontal sinus, 269–270

initial stabilization, 443–444

initial wound management, 443

LeFort fractures, 274

lower extremity, 448–449

mandible, 251–253

naso-orbito-ethmoid region, 270–273

open fracture management, 444–445

open pelvic fractures, 207–208

orbit, 274

orbital, 331

panfacial, 277

pelvis, 450–454

skull, 573–576

stabilization of maxillofacial injuries, 262–263

upper extremity, 447–448

zygoma, 273–274

Fragment wounds, 66–67

Fragmentation landmines, 48–49

Fresh frozen plasma, 26, 136–137

Fresh whole blood

role of, 26–27

transfusions, 137–138

use in damage control resuscitation, 23

Frontal sinus fractures, 269–270

FRSS. See Forward Resuscitative Surgical System

FST. See Forward Surgical Teams

FTSG. See Full-thickness skin grafts

Full-thickness skin grafts, 625

Fundoscopic exam, 313

FWB. See Fresh whole blood G

Gammagraft

®, 619

Gardner-Wells tongs, 509–510

Gastric intramucosal pH, 677

Gastric stress ulcers, 377
xxxvi | Combat Casualty Care

Gastrointestinal bleeding prophylaxis, 695

Gastrointestinal tract injuries, 63

GCS. See Glasgow Coma Scale

Genitalia injuries, 210–211

Genitourinary injuries, 208–210, 453

Gerota’s fascia, 188–190

Glasgow Coma Scale, 14, 134, 351, 353, 567–568, 570

Glucocorticosteroids, 499

Glucose metabolism

pediatric, 542–544

sepsis, 689–690

Granular zeolite, 129

Grenades, rocket-propelled, 50

Grey-Turner’s sign, 203

Guillotine amputation, 481–482

Gunpowder, 45

H

H2-receptor antagonists, 377, 695

Halo ring apparatus, 509–510

Hand compartment fasciotomy, 413

Harriet Lane Handbook, 545

Head injuries. See also Traumatic brain injuries

pediatric, 537–540

Health Services Support, 107–109

HEAT. See High-explosive antitank rounds

Hematomas

epidural, 355–357

retrohepatic, 186

subdural, 355–356

HemConTM dressings, 17, 369

Hemicraniectomy, 374

Hemodilution, 23

Hemorrhage

complications of, 11–13

control adjuncts, 15–17

control techniques, 126–127

damage control resuscitation, 22–27

damage control surgery, 27–28

extradural, 576

gastrointestinal bleeding prophylaxis, 695

intradural, 576

neck injuries, 281–283

pressure points, 17, 126–127

preventable death from, 88–89, 124

tactical field care, 95

tourniquet use, 15, 16, 95, 127–130

traumatic intracerebral, 357–358

vitreous, 317–318

Hemorrhagic chemosis, 311–313

Hemorrhagic shock

pediatric, 551–552

treatment of, 30

Hemostatic agents

hemorrhage control, 17

nonsurgical, 143–144

tactical field care, 95

traumatic brain injury, 369
Index | xxxvii

Hemostatic dressings, 127–130

Heparin, 377

Hepatic parenchymal injuries, 186–187

Herniation syndromes, 358–360, 556

Hetastarch, 96–97

Hextend

®, 96–97

HFOV. See High-frequency oscillation ventilation

HFV. See High-frequency ventilation

HHS. See Health Services Support

High-explosive antitank rounds, 50, 52

High-frequency oscillation ventilation, 553, 668–669

High-frequency ventilation, 653

High-Mobility Multipurpose Wheeled Vehicles, 89, 112

High-order explosives, 45–46

High-pressure lavage devices, 432–433

Hilar clamping, 180

Hip dislocations, 453–454

HMMWVs. See High-Mobility Multipurpose Wheeled Vehicles

HMX. See Cyclotetramethylene tetranitramine

Hollow organ injuries, 63

Host-nation patients, 19

HSS. See Health Services Support

HTS. See Hypertonic saline

Hydrocortisone, 555

Hyperglycemia, 689–690

Hyperkalemia, 138

Hypertension, intracranial, 375

Hypertonic saline, 96–97, 370–373, 556

Hyperventilation, 350, 367–368

Hyphema, 316

Hypocapnia, 350

Hypoglycemia, 544

Hypoperfusion, cerebral, 100, 349

Hypotension

pediatric, 541

permissive, 24, 140–142

sepsis, 685

systemic, 100

traumatic brain injury and, 349, 368

Hypotensive resuscitation, 140–142

Hypothermia

burn care, 616–617

coagulation system effect, 140

damage control resuscitation, 22–23, 124–125

damage control surgery and, 170

induced, 374

prevention and management, 101–102, 130–131

Hypothermia Prevention and Management Kit, 101

Hypotonic fluids, 369

Hypovolemic shock, 673 I

ICP. See Intracranial pressure

ICRC. See International Committee for the Red Cross

ICU. See Intensive care unit

IEDs. See Improvised explosive devices

Immobilization, spinal, 496–497, 507

Implosion, 58
xxxviii | Combat Casualty Care

Improvised explosive devices, 50–52, 353

Improvised tourniquets, 403–405

Incomplete cord syndromes, 504–06

Induced hypothermia, 374

Infection

burn care, 626–627

critical care, 682, 695

diagnosis of, 260–261

epidemiology of wound infection, 260

irrigation, 432–433

management of, 261

negative-pressure wound dressings, 438–441

prophylaxis, 102, 259, 362

sepsis, 682

spinal injuries, 513–514

surgical management, 260

traumatic brain injuries, 362

war wounds, 258–259

wound debridement, 431, 433–438

wound flora, 431

Inferior cantholysis, 329–330

Informed consent, 263

Infrarenal aortic injuries, 185

Infrarenal vena cava injuries, 186

Inhalation injuries, 69–70

Inhaled nitric oxide, 668–669

Injury patterns, 11

Injury Severity Score, 56

Inotropic therapy, 688–689

INR. See International normalized ratio

Insulin, 690

Intensive care unit, 696

International Committee for the Red Cross, 111

International normalized ratio, 22, 134, 688

Intestinal injuries, 192–193, 562–564

Intraabdominal hypertension, 194

Intracerebral hemorrhage, traumatic, 357–358

Intracranial hypertension, 375

Intracranial pressure

monitoring, 572–573

pediatric, 541, 572–573

traumatic brain injury and, 349–350, 364–375

Intradural hemorrhages, 576

Intraocular air, 323

Intraocular foreign body, 325–326

Intraocular pressure measurement, 310

Intrathoracic vascular injury, 175–178

Intravascular volume, 683–684

Intubation

awake endotracheal intubation, 245–246

combat casualty care, 97

confirmation of tube placement, 246–247

crash intubation, 246

displacement, 546–547

orotracheal, 97

pediatric, 535–537, 549–550

preparation, 243–244

rapid sequence, 245, 364–365, 549–550
Index | xxxix

technique, 244–247

IOFB. See Intraocular foreign body

IOP. See Intraocular pressure measurement

Iraq. See also Operation Iraqi Freedom

Combat Support Hospitals, 19

landmine prevalence, 46–47

Iritis, traumatic, 317

Irrigation, wound, 432–433, 483–484

ISS. See Injury Severity Score J

Jaw-thrust maneuver, 239

Jejeunostomy, 187

Joint injuries, open, 425–426

Joint Patient Movement Requirement Center, 698

Joint Patient Tracking Application, 22, 31

Joint Theater Trauma Registry

creation of, 4, 9

injury patterns, 43

maxillofacial injury type, distribution and mechanism, 232–234

physician trauma admitting record, 10

Joint Theater Trauma System

combat injury patterns, 11

creation of, 9

extremity wounds guidelines, 471–480, 483–484

function of, 20

preventable death causes, 11–13

JPMRC. See Joint Patient Movement Requirement Center

JPTA. See Joint Patient Tracking Application

JTTR. See Joint Theater Trauma Registry

JTTS. See Joint Theater Trauma System K

K-wires, 443–444

Kaolin-impregnated gauze, 130

KIA. See Killed in action

Killed in action, rates, 12–13

Kinetic energy rounds, 54 L

Laboratory testing, 134

Lactate, 673–674

Lactated Ringer’s solution, 23, 142, 369, 542–543, 609–611

Lactic acidosis, 690

Landmines

antipersonnel, 46–47

antitank, 54

blast, 47–49

directional fragmentation, 49–50

fragmentation, 48–49

Landstuhl Regional Medical Center, Germany, 19, 697–698

Laparotomy, pediatric, 561

Laryngeal-mask airways, 97

Laryngoscopes, 244

Laryngoscopic orotracheal intubation, 97

Laryngotracheal injuries, 287

Lateral canthotomy, 329–330

Lavage devices, 432–433
xl | Combat Casualty Care

LeFort fractures, 274

Length of hospital stay, 54

Lens subluxation/dislocation, 317

Lethal triad, 22–23, 124–125, 170

Levetiracetam, 376

Lidocaine, 364

Ligament injuries, 424–425

Limb amputations, traumatic, 415–422

Limb compartment syndrome

clinical findings, 407–408

definition, 406

diagnosis, 408–409

fasciotomy techniques, 412–414

forearm fasciotomy, 413

hand compartment fasciotomy, 413

incidence of, 405

Joint Theater Trauma System guidelines, 471–480

lower leg fasciotomy, 412–413

mechanisms, 406

overview, 405

recurrent, 408

risk, 406

thigh fasciotomy, 413

treatment, 409–414

upper arm fasciotomy, 413

Liver injuries, pediatric, 562

LMA. See Laryngeal-mask airways

Local rotational tissue transfer, 428

Lorazepam, 556

LOS. See Length of hospital stay

Low-order explosives, 45

Lower extremities

fasciotomy, 412–413

fracture fixation, 448–449

Lower face injuries, 274–277

Lund-Browder chart, 606

Lung injuries

acute lung injury, 661

damage control surgery, 178–180

primary blast injuries, 60–63

pulmonary contusion, 655–661

M

M16A2 landmine, 49

MACE. See Military Acute Concussion Evaluation

Magnetic resonance imaging

maxillofacial wound infection diagnosis, 260–261

ocular injuries, 314–315

spinal injuries, 501–503

traumatic brain injuries, 351

Malnutrition, pediatric, 543–544

Mandible fractures, 251–253

Mandibular reconstruction, 275–276

Mannitol, 69, 370–372, 556

Manometry, 408

MAP. See Mean arterial pressure

Marcus Gunn pupil, 268, 309

Marine Corps. See Forward Resuscitative Surgical System
Index | xli

Mass-casualty-incident management, 109–111

Massive transfusions

coagulopathy, 138–140

complications, 138–140

defined, 125

electrolyte disorders, 138

predicting need for, 132–135

preventing need for, 126–131

Maxillofacial injuries. See also Neck injuries

airway control, 237–242

awake endotracheal intubation, 245–246

breathing support, 237–242

cervical spine protection and control, 242–243

confirmation of endotracheal tube placement, 246–247

crash endotracheal intubation, 246

cricothyroidotomy, 247–250

definitive management, 261–266

dental injury, 253–254

difficult airways, 250–251

endotracheal intubation preparation, 243–244

endotracheal intubation technique, 244–247

evaluation of, 262

facial burns, 267–268

facial injury, 254–256

facial lacerations, 255–256

facial nerve injury, 254–255

facial soft-tissue injuries, 266–267

fracture stabilization, 262–263

frontal sinus fractures, 269–270

infection prevention and management, 258–261

initial airway control, 251–256

initial management, 257

LeFort fractures, 274

lower face injuries, 274–277

mandible fractures, 251–253

nasal airway, 241–242

naso-orbito-ethmoid region fractures, 270–273

ocular assessment, 268–269

oral airway, 241–242

orbit fractures, 274

overview, 229–236, 256–257

panfacial fractures, 277

parotid nerve injury, 254–255

percutaneous transtracheal ventilation, 250

radiographic imaging, 262

rapid sequence intubation, 245

surgery informed consent, 263

surgical airway management, 247–250

surgical principles, 264–266

timing of surgery, 263–264

treatment planning, 262

wound care, 257–258

zygoma fractures, 273–274

Mean arterial pressure, 350, 369

Mechanical ventilation

atelectotrauma, 646

barotrauma, 646

biotrauma, 647–648
xlii | Combat Casualty Care

key concepts, 643–645

ventilator-induced lung injury, 646–648

volutrauma, 646

MEDEVAC units, 20–21, 103–107, 112

Medical Emergency Triage Tags, 110

Medical evacuation. See Patient evacuation

Medical Treatment Facilities, 7

Meloxicam, 103

Meshed skin grafts, 623–625

Metabolic acidosis, 546

METTAG. See Medical Emergency Triage Tags

METT-TC information, 105

MFST. See Mobile Field Surgical Teams

Microporous crystalline aluminosilicate, 129

Midazolam, 364

Military Acute Concussion Evaluation, 64–65

Military casualties

explosive-related injuries, 54–55

Milrinone, 555

Mine-resistant ambush protected vehicles, 50, 52

Mixed venous oxygen saturation, 676–677

Mobile Field Surgical Teams

function of, 108

transporting casualties, 7

Modified Brooke Formula, 609–611

MODS. See Multiple organ dysfunction syndrome

Molotov cocktails, 45

Morphine, 617

MRAP. See Mine-resistant ambush protected vehicles

MRI. See Magnetic resonance imaging

MTF. See Medical Treatment Facilities

Multiple organ dysfunction syndrome, 24

Muscle injuries, 424–425

Myoglobinuria, 68–69

N

Narrow complex tachycardia, 560

Nasal airway, 241–242

Naso-orbito-ethmoid region fractures, 270–273

Nasoduodenal tubes, 543

Nasopharyngeal airway, 241–242

National Acute Spinal Cord Injury Study, 540

National Heart Lung and Blood Institute, 664

National Naval Medical Center Bethesda, 19

National Training Center, 13

NATO. See North Atlantic Treaty Organization

Naval Special Warfare Command, 92

Navy

Casualty Receiving and Treatment Ships, 7

combat health support, 109

Near infrared spectroscopy, 678

Neck injuries. See also Maxillofacial injuries

airway assessment and management, 281

bleeding assessment and management, 281–283

damage control surgery, 181–183

esophageal injury, 286–287

hard signs mandating immediate exploration, 182

imaging, 283
Index | xliii

immediate hemorrhage control, 283

laryngotracheal injury, 287

neck anatomy, 279

neck zones, 279–280, 284–286

operative indications, 283

overview, 229–234

penetrating wounds, 278–288

Needle cricothyroidotomy, 250

Needle thoracostomy, 15

Negative-pressure ventilation, 643

Negative-pressure wound dressings, 438–439, 618

Nephrectomies, 190

Nerve repair, 426

Nerve root syndromes, spinal, 506

Neurogenic shock, 499

Neuroimaging, 362–363

Neurosurgical interventions, 565–576

NICE-SUGAR study. See Normoglycemia in Intensive Care Evaluation-Survival Using Glucose Algorithm Regulation

NIPPV. See Noninvasive positive-pressure ventilation

NIRS. See Near infrared spectroscopy

Nitric oxide, inhaled, 668–669

Nitrocellulose, 45

Nitroglycerin, 45

NOE region. See Naso-orbito-ethmoid region fractures

Nondepolarizing neuromuscular blocking agents, 365

Noninvasive positive-pressure ventilation, 657–658, 659

Nonsteroidal antiinflammatory drugs, 103

Nonsurgical hemostatic agents, 143–144

Norepinephrine, 369

Normal saline, 23, 142

Normoglycemia in Intensive Care Evaluation-Survival Using Glucose Algorithm Regulation, 689–690

North Atlantic Treaty Organization

burn triage criteria, 598

mass-casualty-incident management, 109–111

nine-line MEDEVAC request, 106

Roles of Care, 109

NovaLung®, 669

NPV. See Negative-pressure ventilation

NSAIDs. See Nonsteroidal antiinflammatory drugs

NTC. See National Training Center

Nutritional goals

acute respiratory distress syndrome, 671

burn care, 627–628

pediatric, 543–544

sepsis, 691

O

Ocular adnexal trauma, 326–328

Ocular injuries

anterior segment examination, 311–313

assessment of, 268–269

case studies, 333–338

chemical eye injuries, 331–332

choroidal injuries, 318

closed globe injuries, 315–318

conjunctival lacerations, 328

corneal abrasion, 315

corneal foreign bodies, 315–316
xliv | Combat Casualty Care

enucleation, 323–325

external ocular examination, 310–311

eyelid lacerations, 326–328

globe repair, 323–324

hyphema, 316

imaging techniques, 314–315

incidence of, 303

intraocular foreign body, 325–326

intraocular pressure measurement, 310

lens subluxation or dislocation, 317

levels of ophthalmic combat casualty care, 304–307

ocular adnexal trauma, 326–328

ocular motility, 309–310

open globe injuries, 318–326

orbital foreign bodies, 330–331

orbital fractures, 331

orbital trauma, 329–331

patient history, 307–308

posterior segment examination, 313

primary blast injuries, 65

pupil examination, 309

retinal injuries, 318

retrobulbar hemorrhage, 329–330

sympathetic ophthalmia, 323

traumatic iritis, 317

traumatic optic neuropathy, 332

visual acuity, 308–309

visual field testing, 310

vitreous hemorrhage, 317–318

Ocular motility, 309–310

Ocular Trauma Score, 319

OEF. See Operation Enduring Freedom

OIF. See Operation Iraqi Freedom

Omental packing, 187

Open globe injuries, 318–326

Open joint injuries, 425–426

Open pelvic fractures, 207–208

Open pelvic trauma, 452–453

Operation Enduring Freedom

damage control resuscitation components, 125–126

injury patterns, 43

killed in action rates, 13

mortality and survival rates, 4

use of temporary vascular shunts, 196–200

Operation Iraqi Freedom

damage control resuscitation components, 125–126

injury patterns, 43

killed in action rates, 13

mortality and survival rates, 4

use of temporary vascular shunts, 196–200

Opioid analgesics, 103

Optic neuropathy, traumatic, 332

Oral airway, 241–242

Oral transmucosal fentanyl citrate, 103

Orbit fractures, 274

Orbital foreign bodies, 330–331

Orbital fractures, 331

Orchiectomy, 211
Index | xlv

Organizational innovations, 17–22

Oropharyngeal airway, 239, 241

Orotracheal intubation, 97

Osteomyelitis, 260–261

OTFC. See Oral transmucosal fentanyl citrate

Otolaryngology, 60

Out-of-hospital care

case study, 89–91, 111–112

combat and civil sector care, 91–92

Oxygen saturation, 676–678

Oxygen toxicity, 647–648

Oxygenation, 367 P

Packed red blood cells, 22–23

PaCO

2

. See Partial pressure of carbon dioxide in arterial blood

Pain management, 102–103, 617

PALS. See Pediatric Advanced Life Support

Pancreatic injuries, 187–188

Pancreaticoduodenectomy, 187–188

Pancuronium, 365

Panfacial fractures, 277

Panoramic tomography, 262

Panorex, 262

PaO

2

. See Partial pressure of oxygen in arterial blood

Paradoxical brain herniation, 360

Parotid nerve injuries, 254–255

Partial pressure of carbon dioxide, 547

Partial pressure of carbon dioxide in arterial blood, 645

Partial pressure of oxygen in arterial blood, 661

Patient evacuation. See also Patient transportation

aeromedical evacuation system, 21

air medical evacuation considerations, 103

burn care, 628–629

Critical Care Air Transport Teams, 20–21, 172, 377, 697–700

echelons of care, 17–20, 104

en-route nursing care, 21

evacuation chain for combat casualties, 17

Joint Patient Tracking Application, 22

MEDEVAC units, 20–21, 103–107, 112

spinal injuries, 507

Tactical Combat Casualty Care, 103–107

tactical evacuation, 199

times, 5–6

traumatic brain injuries, 376–377

Patient information

Joint Patient Tracking Application, 22

Patient transportation, 5, 7, 17. See also Patient evacuation

PCV. See Pressure-control ventilation

PCWP. See Pulmonary capillary wedge pressure

Pediatric Advanced Life Support, 549, 558

Pediatric trauma

abdominal interventions, 561–564

acute respiratory distress syndrome, 553

airway, 534–537, 548–550

anatomic considerations, 534–547

asystole, 558

blood product transfusion, 553
xlvi | Combat Casualty Care

body surface area, 540

bradycardia with poor perfusion, 559

burn care, 564

cardiac rhythm disturbances, 558–560

cerebral herniation syndromes, 556

circulation, 551–553

electrolytes, 542–544

end-of-life care, 580

epidemiology, 533

extradural hemorrhage, 576

fluid requirements, 542–544

glucose metabolism, 542–544

head, 537–540, 566

initial assessment, 566–568

intracranial pressure monitoring, 572–573

intradural hemorrhage, 576

narrow complex tachycardia, 560

neurosurgical interventions, 565–576

nutrition, 542–544

patient monitoring, 546–547

Pediatric Advanced Life Support, 549, 558

pharmacology, 545–546

physiology, 541–547

pulseless electrical activity, 558

pulseless ventricular tachycardia, 559

rapid sequence intubation, 549–550

respiratory system, 544–545

resuscitation, 548–553

scalp injuries, 568–572

seizure management, 556–557

septic shock, 553–556

severe sepsis, 553–556

skeleton, 540

skull fractures, 573–576

spinal cord, 537–540, 576–580

thoracic interventions, 560–561

triage, 566–568

vascular access, 550–551

ventricular fibrillation, 559

vital signs, 541–542

weight-based dosing, 567

wide complex tachycardia, 560

PEEP. See Positive end-expiratory pressure

Pelvic injuries

acute management, 205–207

angiography, 205

background, 202

bladder injury, 208–210

computed tomography imaging, 204–205

fracture fixation, 450–454

genitalia injury, 210–211

open pelvic fractures, 207–208

open pelvic trauma, 452–453

physical examination, 203

radiographic examination, 203–205

urethral injury, 208–210

Penetrating wounds

neck injuries, 278–288
Index | xlvii

spinal injuries, 510–514, 580

traumatic brain injuries, 361–363

Penile injuries, 210–211

Pentaerythritol tetranitrate, 45

Pentobarbital, 373

Percutaneous transtracheal ventilation, 250, 536–537

Perihepatic vascular injuries, 186

Peripheral vascular injuries

arterial injury, 195–200

extremity tourniquets, 200

femoral vasculature injury, 201

popliteal vasculature injury, 201

proximity to great vessel injury, 200

temporary vascular shunts, 196–200

tibial vasculature injury, 210

upper extremity arterial injury, 201

venous injury, 200

Permissive hypotension, 24, 140–142

Person-borne devices, 51

PETN. See Pentaerythritol tetranitrate

pH

blood, 23, 142

gastric intramucosal, 677

Phenobarbital, 376, 557

Phenylephrine, 369

Phenytoin, 375–376, 556–557

Photopsias, 318

Physician trauma admitting record, 10

Ping-pong fractures, 574

Pipe bombs, 45

PIRO staging system, 680

Plasma transfusion ratios, 25

Platelets

transfusion, 137

transfusion ratios, 25

Pneumonectomy, 178–179

Pneumonia, combat-associated, 692–694

Pneumothorax, tension

air medical evacuation considerations, 103

preventable death from, 88–89

tactical field care, 98–99

treatment of, 14, 15

Popliteal vasculature injuries, 201

Positive end-expiratory pressure, 62, 659, 664–667

Positive-pressure ventilation

airway pressure release ventilation, 652

assist-control, 649

blast lung injuries, 62

high-frequency ventilation, 653

overview, 648–649

pressure-control ventilation, 650–651

pressure-regulated volume control, 652–653

pressure-support ventilation, 651–652

pulmonary contusion, 659

synchronized intermittent mandatory ventilation, 649–650

Post-traumatic stress disorder, 64, 354

Potentiators, 56–57

PPV. See Positive-pressure ventilation
xlviii | Combat Casualty Care

Pressure-control ventilation, 650–651

Pressure differentials, 58

Pressure points, 17, 126–127

Pressure-regulated volume control, 652–653

Pressure-support ventilation, 651–652

Preventable death causes, 11–13, 88–89, 124

Primary amputation, 417

Primary blast injuries

brain, 63–65

ears, 58–60

extremities, 65

eyes, 65

hollow organs, 63

injury effects based on distance from open-space explosion, 68

lungs, 60–63

mechanism of injury, 57

solid organs, 63

Pringle maneuver, 186

Prone positioning, 670–671

Prophylactic antibiotic therapy, 102, 259, 362, 440

Propofol, 373, 545–546

Propofol infusion syndrome, 373, 546

Proton-pump inhibitors, 377, 695

PROWESS trial. See Recombinant Human Activated Protein C Worldwide Evaluation in Severe Sepsis

PRVC. See Pressure-regulated volume control

Pseudo Jefferson fracture, 548

PSV. See Pressure-support ventilation

Ptosis, 310–311

PTSD. See Post-traumatic stress disorder

PTTV. See Percutaneous transtracheal ventilation

Pulmonary artery pressure, 645

Pulmonary capillary wedge pressure, 661

Pulmonary contusion

adjunctive strategies, 659–661

airway protection, 657–658

basic concepts, 655–657

management, 657–661

positive-pressure ventilation, 659

pulmonary toilet, 657–658

Pulmonary injuries, 178–180

Pulse oximetry, 100, 246

Pulseless electrical activity, 558

Pulseless ventricular tachycardia, 559

Pupil examination, 309

Q

QRS complex, 558, 560

Quaternary blast injuries

explosive-related injuries, 69–70

mechanism of injury, 57

QuikClot® dressings, 17, 129, 369

Quinary blast injuries

explosive-related injuries, 70–72

mechanism of injury, 57

R

Radiographic imaging

maxillofacial injuries, 262
Index | xlix

ocular injuries, 314–315

pelvic injuries, 203–205

spinal injuries, 501–503

Radionuclide scanning, 260–261

Randomized Evaluation of Surgery with Craniectomy for Uncontrollable Elevation of Intra-Cranial Pressure, 374

Rapid sequence intubation, 245, 364–365, 549–550

RDX. See Cyclotrimethylene trinitramine

REACH. See Registry of Emergency Airways at Combat Hospitals

Recombinant factor VIIa

role in hemorrhage control, 27, 143–144

use in damage control resuscitation, 23

Recombinant human activated protein C, 689

Recombinant Human Activated Protein C Worldwide Evaluation in Severe Sepsis, 689

Rectal injuries, 193

Red blood cells

lifespan, 26

massive transfusions, 125

packed, 22–23

transfusion ratios, 25

transfusions, 135

Red reflex, 313

Registry of Emergency Airways at Combat Hospitals, 97

Rehabilitation, traumatic limb amputations, 422

Renal injuries, 188–190

Reperfusion injury, 199

RESCUEicp, 374

Respiratory system, pediatric, 544–545

Resuscitation

base deficit, 674–675

basic concepts, 672–673

central venous oxygen saturation, 676–677

critical care, 672–678

damage control, 22–27

endpoints, 672–679

gastric intramucosal pH, 677

lactate, 673–674

mixed venous oxygen saturation, 676–677

pediatric, 548–553

sepsis, 682–683

spinal, 498–499

sublingual PCO2, 677–678

supraphysiologic oxygen delivery attainment, 675

tissue carbon dioxide and oxygen assessment, 678

Resuscitative thoracotomies, 560–561

Retinal injuries, 318

Retrobulbar hemorrhage, 329–330

Retrohepatic hematomas, 186

Retroperitoneal injuries, 192, 562

Revised Trauma Score, 134

rFVIIa. See Recombinant factor VIIa

Rhabdomyolysis, traumatic, 68, 612

Ringer’s solution, lactated, 23, 142, 369, 542–543, 609–611

Rocket-propelled grenades, 50, 89–90

Rocuronium, 545–546

Roux-en-Y jejeunostomy, 187

RPGs. See Rocket-propelled grenades

RTS. See Revised Trauma Score
l | Combat Casualty Care

S

Saline solution, 23, 542–543, 556

SALT. See Triage/Treat/Transport system

SAM® SPLINTS, 5780

SAPS II. See Simplified acute physiology score

SBP. See Systolic blood pressure

Scalp injuries, 568–572

Schiotz tonometer, 310

SCIWORA. See Spinal cord injury without radiographic abnormality

Scrotal injuries, 210–211

Sea-Air-Land special warfare corpsmen

Tactical Combat Casualty Care training, 93

SEALs, 93

Second impact syndrome, 354–355

Secondary blast injuries

fragment physics, 66

fragment range, 67–68

fragment wounds, 66–67

injury effects based on distance from open-space explosion, 68

mechanism of injury, 57

primary and secondary fragments, 65–66

Secretary of Defense for Health Affairs, Office of, xi

Seidel’s sign, 312–313

Seizure management, 556–557

Sepsis

bicarbonate therapy, 690–691

blood product transfusion, 687–688

corticosteroids use, 685–686

critical care, 679–691

definition, 679–680

hyperglycemia, 689–690

infection source control, 682

inotropic therapy, 688–689

intravascular volume, 683–684

management, 680–691

nutritional goals, 691

oxygen delivery adequacy assessment, 686–687

pathophysiology, 680

prognosis, 680

recombinant human activated protein C, 689

resuscitation goals, 682–683

vasopressors use, 684–685

Septic shock, 553–556, 679

Severe sepsis, 553–556, 679–680

Shaped-charges, 52–54

Shear injuries, 58

Sheet explosives, 45

Shock Trauma Platoons, 30, 108

SIADH. See Syndrome of inappropriate secretion of antidiuretic hormone

Silver-impregnated dressings, 268

Simple Triage and Rapid Treatment, 111

Simplified acute physiology score, 670

SIMV. See Synchronized intermittent mandatory ventilation

SIRS. See Systemic inflammatory response syndrome

Skin grafting, 621–625

Skull fractures, 573–576

Small arms casualties, 44

Small Business Innovative Research Program, xi
Index | li

Smectite, 130

SOF. See Special Operations Forces

Soft-tissue injuries

facial, 266–267

large wounds, 192

Solid organ injuries, 63

Sort, Assess, Lifesaving Interventions, 111

Space of Retzius, 202, 207

Spalling, 58

Special Operations Forces, 13

Spermatic cord injuries, 210–211

Spinal cord injury without radiographic abnormality, 506, 537, 539–540

Spinal injuries

anatomy, 500–501

anterior cord syndrome, 504–505

assessment of, 500–506

axial traction, 508–510

Brown-Séquard syndrome, 505–506

cauda equina syndrome, 506

central cord syndrome, 504–506

cerebrospinal fluid fistulae, 512–513

cervical spine protection and control, 242–243

closed, 576–580

complete cord syndrome, 503–504

emergency management, 493–497

epidemiology, 490

glucocorticosteroids use, 499

incomplete cord syndromes, 504–06

infection control, 511–512

infections, 513–514

levels of combat casualty care, 490–493

management considerations, 507––516

mechanical stability, 510–511

neurogenic shock, 499

overview, 489–490

pediatric, 537–540, 576–580

penetrating, 580

penetrating injury, 510–514

precautions, 99

projectiles in disc space, 514–515

projectiles in spinal canal, 515–

radiographic considerations, 501–503

restoring alignment, 499

spinal cord injury patterns, 503–506

spinal cord injury without radiographic abnormality, 506

spinal immobilization, 496–497, 507

spinal nerve root syndromes, 506

spinal reduction interventions, 508–510

spinal resuscitation, 498–499

spinal shock, 496

spinal stability determination, 503

tactical combat casualty care, 497–498

timing of surgical interventions, 507–508

transport considerations, 507

vascular injuries, 514

Spinal nerve root syndromes, 506

Splenic injuries, 190–192

Split-thickness skin graft, 622–623
lii | Combat Casualty Care

SSTP. See Surgical Shock Trauma Platoon

START®. See Simple Triage and Rapid Treatment

Static landmines, 47–48

Steroids, 686

STP. See Shock Trauma Platoons

Stress gastritis, 695

Stryker frame, 670

STSG. See Split-thickness skin graft

Subdural hematomas, 355–356

Subfalcine brain herniation, 358–360

Sublingual PCO2, 677–678

Succinylcholine, 365, 545–546

Suicide bombs, 51

Sulfamyalont®, 625

Supraphysiologic oxygen delivery attainment, 675

Suprarenal aorta injuries, 185

Suprarenal vena cava injuries, 186

Supraventricular tachycardia, 560

Surgery. See Damage control surgery; specific injury type

Surgery informed consent, 263

Surgical Shock Trauma Platoon, 108

Surgical wound debridement, 434–438

Surviving Sepsis Campaign 2008, 682, 685

Sympathetic ophthalmia, 323

Synchronized intermittent mandatory ventilation, 649–650

Syndrome of inappropriate secretion of antidiuretic hormone, 612

Systemic hypotension, 100

Systemic inflammatory response syndrome, 673, 679

Systolic blood pressure, 134

T

TACC. See Tanker Airlift Control Center

TACEVAC. See Tactical evacuation

Tactical combat casualty care

acute airway obstruction, 97–98

advancements in, 13–14

air medical evacuation considerations, 103

care-under-fire issues, 93–94

evacuation care, 103–107

field care, 95–103

fluid resuscitation, 96–98

Health Services Support, 107–109

hemorrhage control, 95

hemostatic agents, 95

hypothermia prevention and management, 101–102

infection prophylaxis, 102

mass-casualty-incident management, 109–111

pain management, 102–103

phases of, 93

program development, 92–93

spinal injuries, 497–498

spinal injury precautions, 99

tension pneumothorax, 98–99

tourniquet use, 95

traumatic brain injuries, 99–101

treatment measures, 93

vascular access, 96–98

ventilatory support, 97–98
Index | liii

Tactical evacuation, 199

Tangential excision, 619

Tanker Airlift Control Center, 698

TBI. See Traumatic brain injuries

TBSA. See Total body surface area

TCCC. See Tactical combat casualty care

Telemedicine, 696

TELFATM, 621

Temporary vascular shunts, 196–200

Tendon injuries, 424–425

Tension pneumothorax

air medical evacuation considerations, 103

preventable death from, 88–89

tactical field care, 98–99

treatment of, 14, 15

Tertiary blast injuries

explosive-related injuries, 68–69

mechanism of injury, 57

Testicular injuries, 210–211

Tetanus immunization, 439–441

Thermal Angel

®, 130

Thigh fasciotomy, 413

Thiopental, 373

Thoracic injuries

emergency thoracotomy, 173–175

esophageal injury, 180–181

intrathoracic vascular injury, 175–178

pediatric, 560–561

pulmonary injury, 178–180

rates of, 15

tracheobronchial injury, 178–180

Thoracostomies, needle, 15

Thoracotomies

emergency, 173–175

resuscitative, 560–561

Thromboelastography, 139

Tibial vasculature injuries, 210

Tidal volume, 654, 663–665, 719

TNT. See 2,4,6-Trinitrotoluene

Tonic-clonic seizures, 556–557

Tono-Pen

®, 310

Tonsillar brain herniation, 360

Topical sealants, 143

Total body surface area, 597–598, 606, 610

Total parenteral nutrition, 674

Tourniquets

advancements in, 15–16

Combat Application Tourniquets, 128, 404–405, 469–470

damage control resuscitation, 127–130

extremity injuries, 16, 127–129, 200, 403–405

improvised, 403–405

tactical field care, 95

Toxic gases, 54–55

Tracheal injuries, 287

Tracheobronchial injuries, 178–180

Tractotomy, pulmonary, 178–179

Training advancements, 13–14

Tranexamic acid, 144
liv | Combat Casualty Care

Transcranial herniation, 360

Transcutaneous oxygen content, 678

Transfusion Requirements in Critical Care, 687

Transfusions

blood product ratios, 24–26

fibrinogen, 137

fresh frozen plasma, 136–137

fresh whole blood, 137–138

massive, 125–135

pediatric, 553

platelets, 137

ratios, 24–26

red blood cells, 135

sepsis, 687–688

Transient nerve palsy, 16

Translational blast injuries, 54–55

Transportation. See Patient transportation

Traumatic brain injuries. See also Head injuries

air evacuation, 376–377

airway and breathing management, 363–365, 367

anticonvulsants use, 375–377

blast injury, 353–354

central herniation, 358–360

cerebrospinal fluid leaks, 362

Clinical Practice Guidelines, 64

closed head injury, 351

combat casualty care, 99–101

critical care, 376–377

decompressive craniectomy, 374–377

diffuse, 355

effects of, 64

epidural hematomas, 355–357

external ventricular drains, 369–370

focal, 355

head positioning, 366

hemodynamic management, 368–369

herniation syndromes, 358–360

hypertonic saline, 370–373

hyperventilation, 367–368

induced hypothermia, 374

infection, 362

initial management, 363–367

intracranial pressure, 349–350, 364–375

intractable intracranial hypertension, 375

management considerations, 363–378

mannitol use, 370–372

mild injury, 351–360

moderate injury, 351–360

neuroimaging, 362–363

overview, 347–348

paradoxical herniation, 360

pathophysiology of, 348–351

penetrating, 361–363

pharmacologic agents to reduce intracranial pressure, 373–375

prevalence of, 63

prevention of, 65

second impact syndrome, 354–355

secondary survey, 366–367
Index | lv

severe injury, 351–360

subdural hematomas, 355–356

subfalcine herniation, 358–360

tonsillar herniation, 360

transcranial herniation, 360

traumatic intracerebral hemorrhage, 357–358

uncal herniation, 358–360

upward herniation, 360

ventilation, 367

Traumatic Data Coma Bank Classification Scale, 568

Traumatic iritis, 317

Traumatic limb amputations

degree of, 481

delayed amputation, 420–421

fasciotomy, 419–420

initial assessment, 415–416

initial resuscitation, 417–421

mechanism of, 481

number of limbs, 481

primary amputation, 417

rehabilitation, 422

surgical amputation, 420–421

surgical technique, 481–482

timing of, 481

wound care, 420–421

wound debridement, 417–419

Traumatic optic neuropathy, 332

Traumatic rhabdomyolysis, 68, 612

Triage Officers responsibilities, 8

Triage systems

mass-casualty-incident management, 109–111

Triage/Treat/Transport system, 111

TRICC. See Transfusion Requirements in Critical Care

2,4,6-Trinitrotoluene, 45

Tromethamine, 690–691

TXP

®, 629

Tympanic membranes, 59–60 U

Ultrasonography

intravascular volume, 683

maxillofacial wound infection diagnosis, 260

ocular injuries, 314–315

traumatic brain injuries, 363

Uncal brain herniation, 358–360

Unexploded ordnances

embedded, 72–73

injuries from, 46–47

United States mass-casualty-incident management, 109–111

Upper extremities

fasciotomy, 413

fracture fixation, 447–448

Upper thigh wounds, 437–438

Upward brain herniation, 360

Ureteral injuries, 190–191

Urethral injuries, 208–210

US Army Institute of Surgical Research, 69, 130, 609–610, 628–629

US Marine Corps
lvi | Combat Casualty Care

combat health support, 109

en-route nursing care, 21

US Special Operations Command, 13, 92

USAISR. See US Army Institute of Surgical Research

USSOCOM. See US Special Operations Command

UXOs. See Unexploded ordnances

V

Valproate, 376

VAP. See Ventilator-associated pneumonia

Vascular access, 96–97, 550–551

Vascular injuries

arterial injury, 195–200

extremity tourniquets, 200

femoral vasculature injury, 201

intrathoracic, 175–178

perihepatic, 186

peripheral, 195–201, 210

popliteal vasculature injury, 201

proximity to great vessel injury, 200

spinal, 514

temporary vascular shunts, 195–200

tibial vasculature injury, 210

upper extremity arterial injury, 201

venous injury, 200

wound care, 424–425

Vascular shunts, 196–200

Vasoactive agents, 143

Vasopressin, 143

Vasopressin and Septic Shock Trial, 685

Vasopressors, 684–685

VASST. See Vasopressin and Septic Shock Trial

VDR-4t®, 629

Vecuronium, 365

Vehicle-borne devices, 51

Venous injuries, 200

Venous thromboembolism, 377

Ventilation, positive-pressure. See Positive-pressure ventilation

Ventilator-associated pneumonia, 692

Ventilator-induced lung injury

atelectotrauma, 646

barotrauma, 646

biotrauma, 647–648

volutrauma, 646

Ventilators

procedures, 719

settings for normal lungs, 653–655

Volumetric Diffusive Respiration ventilators, 629

Ventilatory compromise, 88–89

Ventilatory support, 97–98, 367

Ventricular drains, external, 369–370

Ventricular fibrillation, 559

Ventricular tachycardia, 560

Victim-actuated devices, 51

Video-based laryngoscopic devices, 97

Vietnam War

Wound Data and Munitions Effectiveness Team, 12

VILI. See Ventilator-induced lung injury
Index | lvii

Visual acuity, 308–309

Visual field testing, 310

Vital signs, pediatric, 541–542

Vitreous hemorrhage, 317–318

Volumetric Diffusive Respiration ventilator, 629

Volutrauma, 646

W

Walter Reed Army Medical Center, 19

Warm shock, 555

WDMET. See Wound Data and Munitions Effectiveness Team

Weapons effects

explosive-related injuries, 54–73

explosives, 44–54

small arms, 44

weapons, 44

Wet-to-dry dressing debridement, 433–434

Whipple procedure, 187

White phosphorus injuries, 419, 600–601

Whole blood, fresh

role in transfusion, 26–27

use in damage control resuscitation, 23

Wide complex tachycardia, 560

Windlass tourniquets, 403–405

Woods lamp, 601

Wound closure

overview, 426

techniques, 427–430

timing of, 427

wound coverage, 430

Wound Data and Munitions Effectiveness Team, 12, 88

Wound debridement, 259, 261, 417–419

Wound flora, 431

Wound irrigation

additives, 432

irrigants, 432

irrigation devices, 432–433

timing of, 432

WoundStatTM granules, 17, 130

X

Xylocaine®, 571

Z

Zygoma fractures, 273–274
lviii | Combat Casualty Care