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ELSEVIER
SAUNDERS

The Curtis Center
Independence Square West
Philadelphia, Pennsylvania 19106

VASCULAR TRAUMA, SECOND EDITION

ISBN: 0-7216-4071-0

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NOTICE

Surgery is an ever-changing field. Standard safety precautions must be followed, but as new research
and clinical experience broaden our knowledge, changes in treatment and drug therapy may
become necessary or appropriate. Readers are advised to check the most current product
information provided by the manufacturer of each drug to be administered to verify the
recommended dose, the method and duration of administration, and contraindications. It is the
responsibility of the licensed prescriber, relying on experience and knowledge of the patient, to
determine dosages and the best treatment for each individual patient. Neither the publisher nor
the author assumes any liability for any injury and/or damage to persons or property arising from
this publication.

The Publisher

Previous edition copyrighted 1978

International Standard Book Number: 0-7216-4071-0

Printed in the United States of America

Last digit is the print number: 987654321

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To those who serve and have served our
country

— in the military, both at home and in

distant lands

— in our nation's trauma centers

— in the education of surgeons with an

interest in vascular disease

— in the development of new knowledge

— in safety net hospitals

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CONTRIBUTORS

JOHN T. ANDERSON, MD

Assistant Professor

Department of Surgery

Trauma Surgery and Surgical Critical Care

University of California, Davis

Sacramento, California

JUAN A. ASENSIO, MD

Associate Professor

Department of Surgery

University of Southern California Keck School of Medicine

Los Angeles, California

WALTER L. BIFFL, MD

Associate Professor

Department of Surgery

Brown Medical School

Chief, Division of Trauma and Surgical Critical Care

Rhode Island Hospital

Providence, Rhode Island

F. WILLIAM BLAISDELL, MD

Professor

Department of Surgery
University of California, Davis
Sacramento, California

KEVIN M. BRADLEY, MD

Assistant Professor

Department of Surgery

Temple University School of Medicine

Philadelphia, Pennsylvania

ROBERT F. BUCKMAN, MD

Professor

Department of Surgery

Drexel University College of Medicine

Trauma Program Director

Saint Mary Medical Center

Langhorne, Pennsylvania

VI 1

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Vlll CONTRIBUTORS

JON M. BURCH, MD

Professor

Department of Surgery

University of Colorado Health Sciences Center

Denver, Colorado

NEAL S. CAYNE, MD

Assistant Professor

Department of Surgery

New York University School of Medicine

Director of Endovascular Surgery

New York University Medical Center

New York, New York

IRSHAD H. CHAUDRY, PhD

Professor, Departments of Surgery, Microbiology, Physiology, and Biophysics
Vice Chairmen, Department of Surgery
Director, Center for Surgical Research
The University of Alabama at Birmingham
Birmingham, Alabama

RAUL CIOMBRA, MD

Associate Professor

Department of Surgery

Division of Trauma, Surgical Critical Care and Burns

University of California, San Diego School of Medicine

San Diego, California

LORI D. CONKLIN, MD

Surgical Resident

Michael E. DeBakey Department of Surgery

Baylor College of Medicine

Houston, Texas

MICHAEL E. DeBAKEY, MD

Chancellor Emeritus

Distinguished Service Professor

Michael E. DeBakey Department of Surgery

Baylor College of Medicine

Houston, Texas

DEMETRIOS DEMETRIADES, MD, PhD

Professor

Department of Surgery

Division of Trauma and Critical Care

Keck School of Medicine University of Southern California

Los Angeles, California

JAMES W. DENNIS, MD

Professor

Department of Surgery

University of Florida Health Science Center

Chief, Division of Vascular Surgery

Shands Jacksonville Medical Center

Jacksonville, Florida

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CONTRIBUTORS IX

DAVID V. FELICIANO, MD

Professor

Department of Surgery

Emory University School of Medicine

Chief of Surgery

Grady Memorial Hospital

Atlanta, Georgia

ERIC R. FRYKBERG, MD

Professor

Department of Surgery

University of Florida College of Medicine

Chief, Division of General Surgery

Shands Jacksonville Medical Center

Jacksonville, Florida

PRISCILLA J. GARCIA, MD

Resident, Department of Anesthesia
Baylor College of Medicine
Houston, Texas

NICHOLAS J. GARGIULO, III, MD

Assistant Professor

Department of Surgery

The Albert Einstein College of Medicine

Chief of Endovascular Surgery

Jack D. Weiler Hospital

Bronx, New York

THOMAS S. GRANCHI, MD, MBA

Associate Professor

Michael E. DeBakey Department of Surgery

Baylor College of Medicine

Medical Director, Emergency Center

Ben Taub General Hospital

Houston, Texas

ASHER HIRSHBERG, MD

Associate Professor

Michael E. DeBakey Department of Surgery

Baylor College of Medicine

Director of Vascular Surgery

Ben Taub General Hospital

Houston, Texas

DAVID B. HOYT, MD

Professor and Interim Chairman

Department of Surgery

University of California, San Diego

Chief, Division of Trauma, Burns, and SICU

UCSD Medical Center

San Diego, California

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CONTRIBUTORS

RAO R. IVATURY, MD

Professor

Department of Surgery

Virginia Commonwealth University

Chief, Division of Trauma/Critical Care

VCU Medical Center

Richmond, Virginia

DORAID JARRAR, MD

Chief Resident

Department of General Surgery

The University of Alabama at Birmingham

Birmingham, Alabama

KAJ JOHANSEN, MD, PhD

Clinical Professor

Department of Surgery

University of Washington School of Medicine

Director, Peripheral Vascular Services

Swedisky Medical Center

Seattle, Washington

M. MARGARET KNUDSON, MD

Professor

Department of Surgery
University of California
Director, Injury Research Center
San Francisco General Hospital
San Francisco, California

ANNA M. LEDGERWOOD, MD

Professor

Department of Surgery
Wayne State University
Detroit, Michigan

SCOTT A. LeMAIRE, MD

Assistant Professor

Division of Cardiothoracic Surgery

Michael E. DeBakey Department of Surgery

Baylor College of Medicine

Houston, Texas

MICHAEL R. LePORE, MD

Medical Director of Peripheral Vascular Surgery
Sarasota Memorial Hospital
Sarasota, Florida

CHARLES E. LUCAS, MD

Professor

Department of Surgery
Wayne State University
Detroit, Michigan

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CONTRIBUTORS XI

KENNETH L. MATTOX, MD

Professor and Vice Chairman

Michael E. DeBakey Department of Surgery

Baylor College of Medicine

Chief of Staff and Chief of Surgery

Ben Taub General Hospital

Houston, Texas

SAMUEL R. MONEY, MD

Clinical Associate Professor

Department of Surgery

Tulane University

Head, Section of Vascular Surgery

Ochsner Clinic Foundation

New Orleans, Louisiana

ERNEST E. MOORE, MD

Vice Chairman and Professor

Department of Surgery

University of Colorado Health Sciences Center

Chief of Surgery and Trauma

Denver Health

Denver, Colorado

JAMES A. MURRAY, MD

Division of Trauma and Critical Care

Department of Surgery

Keck School of Medicine University of Southern California

Assistant Professor of Surgery

University of Southern California

Los Angeles, CA

TAKAO OHKI, MD, PhD

Associate Professor

Department of Surgery

Albert Einstein College of Medicine

Chief, Vascular and Endovascular Surgery

Montefiore Medical Center

Bronx, New York

ABHIJIT S. PATHAK, MD

Assistant Professor

Department of Surgery

Temple University School of Medicine

Director, Surgical Intensive Care Unit

Temple University Hospital

Philadelphia, Pennsylvania

DAVID C. RICE, MD, MB, BCH

Assistant Professor

Department of Thoracic and Cardiovascular Surgery
University of Texas M.D. Anderson Cancer Center
Houston, Texas

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Xll CONTRIBUTORS

NORMAN M. RICH, MD

Leonard Heaton and David Packard Professor

Chairman, Department of Surgery, USUHS

Chief, Division of Vascular Surgery, Emeritus

F. Edward Herbert School of Medicine

Uniformed Services University of the Health Sciences

Bethesda, Maryland

AURELIO RODRIGUEZ, MD

Professor

Department of Surgery

Drexel University College of Medicine

Director, Division of Trauma Surgery

Allegheny General Hospital Shock Trauma Center

Pittsburgh, Pennsylvania

SALVATORE J.A. SCLAFANI, MD

Professor

Department of Radiology
State University of New York
Director, Department of Radiology
Kings County Hospital Center
Brooklyn, New York

BRADFORD G. SCOTT, MD

Assistant Professor

Michael E. DeBakey Department of Surgery

Baylor College of Medicine

Associate Trauma Medical Director

Ben Taub General Hospital

Houston, Texas

STEVEN R. SHACKFORD, MD

Stanley S. Fieber Professor and Chairman

Department of Surgery

University of Vermont College of Medicine

Surgeon-in-Chief

Fletcher Allen Health Care

Burlington, Vermont

MICHAEL J. SISE, MD

Clinical Professor
Department of Surgery
UCSD School of Medicine
Medical Director
Scripps Mercy Hospital
San Diego, California

ERNESTO SOLTERO, MD

Assistant Professor

Michael E. DeBakey Department of Surgery

Baylor College of Medicine

Chief of Cardiovascular Surgery

Michael E. DeBakey VA Medical Center

Houston, Texas

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CONTRIBUTORS Xlll

MICHAEL C. STONER, MD

Fellow

Division Vascular and Endovascular Surgery

Massachusetts General Hospital

Boston, Massachusetts

FRANK J. VEITH, MD

Professor and Vice Chairman

Department of Surgery

Albert Einstein College of Medicine

The William J. von Liebig Chair in Vascular Surgery

Montefiore Medical Center

Albert Einstein College of Medicine

Bronx, New York

MATTHEW J. WALL, Jr, MD

Professor

Michael E. DeBakey Department of Surgery

Baylor College of Medice

Deputy Chief of Surgery

Chief of Cardiothoracic Surgery

Ben Taub General Hospital

Houston, Texas

PING WANG, MD

Professor and Chief

Division of Surgical Research

Department of Surgery

North Shore-Long Island Jewish Medical Center

Manhasset, New York

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FOREWORD

Nearly 25 years have passed since the first edition of Vascular Trauma
was published, edited by Norman Rich and myself. The first edition
included experiences from both the Korean and Vietnam Con-
flicts. The Korean experiences demonstrated for the first time that arte-
rial repair was imminently feasible in battle casualties without a serious
hazard of infection. As cited by Hughes, a total of 304 arterial injuries
underwent 269 repairs, with a 13% amputation rate as compared to the
dismal 50% amputation rate following ligation in World War II. Our results
in the U.S. Marine Corps were separately reported in the Annals of Surgery
in 1955.

The Korean experience quickly led to widespread adoption of
arterial repair, following which over 7500 such injuries were repaired
in the Vietnam Conflict. These were entered into the Walter Reed
Vascular Registry organized by Norman Rich; 1500 late results were then
evaluated.

Arterial repair became possible primarily from the development of
helicopter evacuation of wounded men. This coincided with the evolu-
tion of techniques of vascular repair, improved resuscitation, and anti-
biotics. Now, it is well established that the majority of arterial injuries can
be effectively repaired if blood flow is restored within 6 to 7 hours after
injury. After 7 to 8 hours, however, there is a rapid rise in the frequency of
irreversible muscle necrosis, depending primarily upon extent of the
associated soft tissue destruction with loss of collateral circulation.

Initially, it was feared that arterial repair would result in a prohibi-
tive degree of wound infection, especially in Korea where the widespread
use of cow manure for fertilizer resulted in gross contamination of virtu-
ally all injuries. Nonetheless, with adequate debridement, antibiotics and
secondary closure, infection was rarely seen.

Several valuable developments have occurred since 1978 that make
vascular repair even more feasible than before. These include the use
of soft tissue pedicle flaps to cover arterial repair after radical debride-
ment, the early detection of the vascular compartment syndrome by
tissue pressure monitoring, and the recent development of endovascular
techniques.

This book is of special importance because vascular injuries are uncom-
mon in civilian trauma though increasing in frequency, primarily from

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XVI FOREWORD

automobile accidents and gunshot wounds. Civilian wounds fortunately
often don't have the severe concomitant soft tissue destruction that often
occurs with injury from high velocity missiles. Hence, extensive debride-
ment and secondary closure are less often needed, but form the basis of
the time-honored fact that the hazard of infection should virtually never
prohibit arterial repair.

The rarity of arterial injuries makes continuing efforts with educa-
tion, training, and referral to specialized vascular centers most important.
Extremities are still lost because the gravity of early crucial symptoms of
limb-threatening ischemia was missed. It has been known for over four
decades that limb-threatening ischemia produces loss of peripheral nerve
function within a few minutes after onset, manifested by numbness and
paralysis in the affected extremity; but this crucial basic physiological fact
is simply unknown to a surprisingly large number of personnel treating
injured patients.

Another fact emphasizing the importance of experience is the fact
that an acute vascular injury can be repaired with a success rate probably
greater than 95% if treated with modern techniques within 6 to 7 hours
after injury. If repair initially fails, however, prompt reoperation similarly
has a success rate over 90%, for the cause of failure is usually thrombosis
of an inadequate repair or thrombi incompletely removed at the first
operation. Both of these preventable complications usually result from
simple lack of experience.

These facts clearly show the importance of this book for all physi-
cians and staff treating injured patients. Strong adherence to the basic
principles described makes arterial repair achievable in the vast majority
of patients. The authors are to be congratulated on their significant
contributions.

Frank Spencer, MD

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FOREWORD

Among traumatic injuries, those affecting the major vessels are of
great importance, since they represent a serious threat to life and
limb. These injuries assume special significance in light of the
increasing number of trauma patients arriving at the hospital as a result
of vehicular accidents, violent crimes, and other hazardous events.

Until relatively recently, therapy for vascular injuries was limited to
lifesaving control of hemorrhage. Even during World War II, surgical
repair of arterial injuries was rarely attempted. The pioneering deve-
lopments in vascular surgery that evolved in the early 1950s and the
successful surgical repair of vascular injuries in the Korean War provided
the basis for effective surgical treatment of this form of trauma. Accord-
ingly, in the care of patients with vascular trauma only, salvage of life
is no longer acceptable; the goal is also rapid restoration of normal
circulatory dynamics.

The authors, Norman Rich, Kenneth Mattox, and Asher Hirshberg,
have had extensive and wide-ranging experience in the development of
the most effective methods of treatment of vascular injuries, including
civilian and military experience, especially during the Korean and Vietnam
Wars. The authors have incorporated in this book a consideration of the
entire subject of vascular injuries, including an interesting historical review
of the topic; the relative frequency, and sites of their occurrence; and the
clinical, anatomical, and surgical technical aspects of this subject. It
will therefore be of immense value and usefulness to both civilian and
military surgeons.

Micheal E. DeBakey, M.D.

Distinguished Service Professor

and Olga Keith Wiess Professor of Surgery

Michael E. DeBakey Department of Surgery

Director, DeBakey Heart Center

Chancellor Emeritus, Baylor College of Medicine

Houston, Texas

xvi 1

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PREFACE

The first edition of this text was published in 1978 as a monograph
written by Drs. Norman Rich and Frank Spencer. It was an exten-
sive treatise on the pathophysiology, diagnosis, and management
of traumatic injuries to blood vessels. It was and still is one of a kind. No
other textbook on vascular trauma has been published before or since.
The first edition was written in the aftermath of the Vietnam War, the
first military conflict where modern principles of vascular surgery were
applied to traumatic injuries of the blood vessels. Many of the lessons and
concepts delineated in the first edition were based on the Vietnam Vas-
cular Registry, an unprecedented effort, led by Dr. Rich, to systematically
collect and analyze the vascular injuries in a large-scale military conflict.
Yet with very few exceptions, most surgeons who performed vascular recon-
structions in Vietnam did so only on a handful of patients.

In the 1980s, as surgeons began to encounter increasing numbers of
major injuries to blood vessels in the civilian population, there was a surge
of interest in vascular trauma and an exponential rise in the number of
publications on the subject. Many of the advances in the field originated
at urban trauma centers, and particularly at the Ben Taub General Hos-
pital in Houston, where the modern concepts of cardiovascular surgery,
pioneered by Drs. Michael E. DeBakey, Stanley Crawford, Arthur Beall
and others at Baylor College of Medicine, were developed into new man-
agement strategies in vascular trauma by Dr. Kenneth L. Mattox and his
team described in more than a hundred publications.

Ten years ago, Dr. Rich enlisted the assistance of Dr. Mattox in writing
the second edition of Vascular Trauma. The objective was to combine the
military and civilian experience into one cohesive text. However, the task
rapidly proved to be a "mission impossible" as the rapid developments in
the fields of trauma systems, care of the injured patient, damage control
surgery, vascular imaging and endovascular intervention constantly
outpaced the revision of the original text. This led to the addition
of Dr. Asher Hirshberg to the editorial team. He represents a new
generation of surgeons formally trained in both trauma and vascular
surgery. The plan for the book has subsequently changed from a mono-
graph to a multi-authored text containing cutting-edge concepts and
information in vascular trauma. At the same time, we wished to keep
some of the original exciting "flavor" from the first edition of Vascular
Trauma, so expertly and lovingly compiled by Drs. Rich and Spencer.

xix

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XX PREFACE

Drs. Rich and Spencer assembled all their references at the end of
the first edition, assuming that many of the references will be used in
more than one chapter. Dr. Rich continued to collect key references during
the next two decades, and his entire treasury of vascular trauma refer-
ences, a unique and extremely valuable resource for any surgeon inter-
ested in the care of patients with injuries to blood vessels, is given at the
end of this book. We have attempted to assure that all citations in each
chapter are in this reference list, but because of the enormity of this project,
it is inevitable that some might have been omitted. It is also inevitable that
some vascular trauma references might have been missed by all three
editors.

The editors are indebted to the numerous authors of this text, each
one with a life-long commitment to the care of the injured. Ms. Mary Allen
was the persistent force that brought the many aspects of this book together.
In addition, we are grateful to the numerous individuals at Elsevier who
contributed to the culmination of this endeavor.

Norman M. Rich, MD
Kenneth L. Mattox, MD
Asher Hirshberg, MD

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Historical and Military
Aspects of Vascular Trauma
(With Lifetime Reflections of
Doctor Norman Rich)

NORMAN M. RICH

HISTORICAL OVERVIEW ON VASCULAR TRAUMA

Control of Hemorrhage from the Time of Antiquity

EARLY DIRECT VASCULAR RECONSTRUCTION

MILITARY VASCULAR TRAUMA EXPERIENCE

Balkin Wars

World War I Experience

World War II Experience

Experiences during the Korean Conflict

Experience in Vietnam

Military Armed Conflicts following Vietnam

CIVILIAN VASCULAR INJURIES

HISTORICAL NOTES ON 20TH CENTURY PROGRESS WITH VENOUS
INJURIES

SPECIAL HISTORIC OBSERVATIONS

Site of Injury

Iatrogenic Injury

Historic Observations on Mechanism of Injury

Fractures

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

Posterior dislocation of the knee

Blunt injury in presence of other vascular pathology

Use of crutches

Athletic injuries

Vascular injury in children

Radiation

Vibratory tools
Historic Classification of Vascular Injury
HISTORY OF BALLISTICS AND VASCULAR INJURY
HISTORICAL REFLECTIONS AND PROJECTIONS

The advances in vascular surgery are typical
of those in other fields of medicine and
surgery. Each step is discovered and
recorded only to be rediscovered by other
individuals who failed to read and profit by
the experience of others.
Carl W. Hughes (1961)

HISTORICAL OVERVIEW ON
VASCULAR TRAUMA

Although the first crude arteriorrhaphy was
performed about 243 years ago, only in the
past 40 years has vascular surgery become
widely practiced with the anticipation of con-
sistently obtaining good results. By the turn
of this century, extensive experimental work
and some early clinical applications had
occurred, employing most of the techniques
of vascular surgery in use today. In retrospect,
it is almost astonishing that it took nearly 50
years before the work of early pioneers such
as Murphy, Goyanes, Carrel, Guthrie, and
Lexer was widely accepted and applied in the
treatment of vascular injuries. Since the days
of Ambroise Pare in the mid-1 6th century,
major advances in the surgery of trauma have
occurred during the times of armed conflict,
when it was necessary to treat large numbers
of severely injured patients often under con-
ditions far from ideal. This has been especially
true with vascular injuries.

Although German surgeons accomplished
a limited number of arterial repairs in the early
part of World War I, it was not until the Korean
Conflict in the early 1950s that ligation of
major arteries was abandoned as the standard
treatment for arterial trauma. The results of
ligation of major arteries following trauma
were clearly recorded in the classic manuscript
by DeBakey and Simeone (1946) , who found
only 81 repairs in 2471 arterial injuries among
U.S. troops in World War II. All but three of
the arterial repairs were performed by lateral
suture. Ligation was followed by gangrene and
amputation in nearly one half of the cases.
The pessimistic conclusion reached by many
was expressed by Sir James Learmonth (1946) ,
who said that there was little place for defin-
itive arterial repair in the combat wound.

Between the end of World War II and the
beginning of the Korean Conflict, advances
in suture, noncrushing clamps, and arteriog-
raphy were emerging. During the Korean
Conflict continuing technology in polymer-
ized material (plastic) added a new opportu-
nity for vascular reconstruction.

The possibility of successfully repairing arte-
rial injuries was established conclusively, stem-
ming particularly from the works of Hughes,
Howard, Jahnke, and Spencer. In 1958,
Hughes emphasized the significance of this
contribution in a review of the Korean expe-
rience, finding that the overall amputation
rate was lowered to about 13%, compared to
the approximately 49% amputation rate that
followed ligation in World War II.

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1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

During the Vietnam hostilities, more than
600 young U.S. surgeons, representing most
of the major surgical training programs in the
United States, treated more than 7500 patients
with vascular injuries. Rich and Hughes (1969)
reported the preliminary statistics from the
Vietnam Vascular Registry, established in
1966 at Walter Reed General Hospital to
document and follow all servicemen who sus-
tained vascular trauma in Vietnam. The
interim Registry report, encompassing 1000
major acute arterial injuries, showed little
change from the overall statistics presented
in the preliminary report (Rich, 1970). Con-
sidering all major extremity arteries, the
amputation rate remained near 13%.
Although high-velocity missiles created more
soft tissue destruction in injuries seen in
Vietnam, the combination of a stable hospi-
tal environment and rapid evacuation of casu-
alties, similar to that in Korea, made successful
repair possible. Injuries of the popliteal artery
remained an enigma, with an amputation rate
remaining near 30%.

In the past 40 years, civilian experience with
vascular trauma has developed rapidly under
conditions much more favorable than those
of warfare. As might be predicted, several
series have reported results that are signifi-
cantly better than those achieved with mili-
tary casualties in Korea and Vietnam. Mattox
(1989) published the epidemiology of the
largest civilian experience in managing vas-
cular trauma in the history of the world.

Control of Hemorrhage from
the Time of Antiquity

The control of hemorrhage following injury
has been of prime concern to humans since
the beginning. Methods have included various
animal and vegetable tissues, hot irons, boiling
pitch, cold instruments, styptics, bandaging,
and compression. These methods were
described in a historical review by Schwartz
in 1958. Ancient methods of hemostasis used
by Egyptians about 1600 bc are described in
the Ebers' papyrus, discovered by Ebers at
Luxor in 1873 (Schwartz, 1958) . Styptics pre-
pared from mineral or vegetable matter were
popular, including lead sulfate, antimony, and

copper sulfate. Several hundred years later,
copper sulfate again became popular during
the Middle Ages in Europe and was known as
the hemostatic "button." In ancient India,
compression, cold elevation, and hot oil were
used to control hemorrhage, while the
Chinese about 1000 bc used tight bandaging
and styptics.

The writings of Celsus provide most of the
knowledge of methods of hemostasis in the
1st and 2nd centuries ad, Celsus was the first
to record an accurate account of the use of
ligature for hemostasis in 25 ad. During the
first three centuries ad, Galen, Heliodorus,
Rufus of Ephesus, and Archigenes advocated
ligation or compression of a bleeding vessel
to control hemorrhage. The prevailing sur-
gical practice when amputation was done for
gangrene was to amputate at the line of
demarcation to prevent hemorrhage. Archi-
genes, in the 1st century ad was apparently
the first to advocate amputating above the line
of demarcation for tumors and gangrene,
using ligature of the artery to control
hemorrhage.

Rufus of Ephesus (1st century ad) noted
that an artery would continue to bleed when
partly severed, but when completely severed,
it would contract and stop bleeding within a
short time. Galen, the leading physician of
Rome in the 2nd century ad, advised placing
a finger on the orifice of a bleeding superfi-
cial vessel for a period to initiate the forma-
tion of a thrombus and the cessation of
bleeding. He noted, however, that if the vessel
were deeper, it was important to determine
whether the bleeding was coming from an
artery or a vein. If a vein, pressure or a styptic
usually sufficed, but ligation with linen was
recommended for arterial injury. Herophilus,
the Greek physician and anatomist of the 3rd
century bc described the difference between
veins and arterial as "veins were weak and thin-
walled, containing only blood, whereas arter-
ies were thick-walled, containing air 'pneuma'
and blood."

Following the initial contributions of Celsus,
Galen, and their contemporaries, the use of
ligature was essentially forgotten for almost
1200 years. Throughout the Middle Ages,
cautery was used almost exclusively to
control hemorrhage. Jerome of Brunswick

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

(Hieronymus Brunschwig) , an Alsatian Army
surgeon, actually preceded Pare in describ-
ing the use of ligatures as the best way to stop
hemorrhage (Schwartz, 1958). His recom-
mendations were recorded in a textbook pub-
lished in 1497 and provided a detailed account
of the treatment of gunshot wounds. Ambroise
Pare, with a wide experience in the surgery
of trauma, especially on the battlefield, estab-
lished firmly the use of ligature for control of
hemorrhage from open blood vessels. In 1 552 ,
he startled the surgical world by amputating
a leg above the line of demarcation, repeat-
ing the demonstration of Archigenes 1400
years earlier. The vessels were ligated with
linen, leaving the ends long. Pare also devel-
oped the "bee de corbin," ancestor of the
modern hemostat, to grasp the vessel before
ligating it (Fig. 1-1). Previously, vessels had
been grasped with hooks, tenaculums, or the
assistant's fingers.

In the 17th century, Harvey's monumental
contribution describing the circulation of the
blood greatly aided the understanding of
vascular injuries. Although Rufus of Ephesus
apparently discussed arteriovenous commu-
nications in the 1 st century ad, it was not until
1757 that William Hunter first described the
arteriovenous fistula as a pathologic entity. The
historical development of the treatment of
arteriovenous fistulas and false aneurysms are
discussed in Chapter 24. Also, similar review
of false aneurysms is included. As early as the
2nd century ad, Antyllus described the phys-
ical findings and management by proximal

■ FIGURE 1-1

Artist's concept of the bee de corbin,
developed by Pare and Scultetus in the mid-
16th century. It was used to grasp the vessel
before ligating it. (From Schwartz AM: Surgery
1958;44:604.) ■

and distal ligation. He was the first to docu-
ment collateral circulation.

The development of the tourniquet was
another advance that played an important role
in the control of hemorrhage. Tight bandages
had been applied since antiquity, but subse-
quent development of the tourniquet was slow.
Finally, in 1674, a military surgeon named
Morel introduced a stick into the bandage and
twisted it until arterial flow stopped (Schwartz,
1958). The screw tourniquet came into use
shortly thereafter. This method of temporary
control of hemorrhage encouraged more fre-
quent use of the ligature, which required time
for its application. In 1873, Freidrich van
Esmarch, a student of Langenbeck, intro-
duced his elastic tourniquet bandage for first
aid use on the battlefield. Previously, it was
thought that such compression would injure
vessels irreversibly. His discovery permitted
surgeons to operate electively on extremities
in a dry, bloodless field.

In addition to the control of hemorrhage
at the time of injury, the second major area
of concern for centuries was the prevention
of secondary hemorrhage occurring days to
weeks later. Because of its great frequency, styp-
tics, compression, and pressure were used for
several centuries after ligation of injured
vessels became possible. Undoubtedly, the
high rate of secondary hemorrhage after
ligation was due to infection of the wound.
Although John Hunter demonstrated the
value of proximal ligation for control of a false
aneurysm in 1 757, failure to control secondary
hemorrhage resulted in the use of ligature only
for secondary bleeding from the amputation
stump. Subsequently, Bell (1801) and Guthrie
(1815) performed ligation both proximal and
distal to the arterial wound with better results
than those previously obtained.

Some of the first clear records of ligation
of major arterial were written in the 19th
century and are of particular interest. The first
successful ligation of the common carotid
artery for hemorrhage was performed in 1 803
by Fleming but was not reported until 14 years
later by Coley (1817), because Fleming died
a short time after the operation was per-
formed. A servant aboard the HMS Tonnant
attempted suicide by slashing his throat.

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1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

When Fleming saw the patient, it appeared
that he had exsanguinated. There was no pulse
at the wrist and the pupils were dilated. It was
possible to ligate two superior thyroid arter-
ies and one internaljugular vein. A laceration
of the outer and muscular layers of the carotid
artery was noted, as well as a laceration of the
trachea between the thyroid and cricoid car-
tilages. This allowed drainage from the wound
to enter the trachea, provoking violent seizures
of coughing. Although the patient seemed to
be improving, approximately 1 week follow-
ing the injury, Flemming recorded that "on
the evening of the 1 7th, during a violent parox-
ysm of coughing, the artery burst, and my
poor patient was, in an instant, deluged with
blood!"

The dilemma of the surgeon is appreciated
by the statement, "In this dreadful situation I
concluded that there was but one step to take,
with any prospect of success; mainly, to cut-
down upon, and tie the carotid artery below
the wound. I had never heard of such an
operation being performed; but conceived
that its effects might be less formidable, in
this case, than in a person not reduced by
hemorrhage."

The wound rapidly healed following liga-
tion of the carotid artery and the patient
recovered.

Ellis (1845) reported the astonishing expe-
rience of successful ligation of both carotid
arteries in a 21-year-old patientwho sustained
a gunshot wound of the neck while he was
setting a trap in the woods on October 21,
1844, near Grand Rapids, Michigan, when he
was unfortunately mistaken for a bear by a
companion. Approximately 1 week later, Ellis
had to ligate the patient's left carotid artery
because of a hemorrhage. An appreciation
of the surgeon's problem can be gained by
Ellis' description of the operation, "We placed
him on a table, and with the assistance of
Doctor Piatt and a student, I ligatured the
left carotid artery, below the omohyoideus
muscle; an operation attended with a good
deal of difficulty, owing to the swollen state
of the parts, the necessity of keeping up pres-
sure, the bad position of the parts owing to
the necessity of keeping the mouth in a certain
position to prevent his being strangulated by

the blood, and the necessity of operating by
candlelight."

There was recurrent hemorrhage on the
11th day after the accident and right carotid
artery pressure helped control the blood loss.
It was, therefore, necessary to ligate also the
right carotid artery 4/ 2 days after the left
carotid artery had been ligated. Ellis (1845)
remarked, "For convenience, we had him in
the sitting posture during the operation;
when we tightened the ligature, no disagree-
able effects followed; no fainting; no bad
feeling about the head; and all the percepti-
ble change was a slight paleness, a cessation
of pulsation in both temporal arteries, and of
the hemorrhage."

The patient recovered rapidly with good
wound healing and returned to normal daily
activity. There was no perceptible pulsation
in either superficial temporal artery.

The importance of collateral circulation in
preserving viability of the limb after ligation
was well understood for centuries. The fact
that time was necessary for establishment of
this collateral circulation was recognized.
Halsted (1912) reported cure of an iliofemoral
aneurysm by application of an aluminum band
to the proximal artery without seriously affect-
ing the circulation or function of the lower
extremity. The importance of asepsis had now
been recognized, and the frequency of sec-
ondary hemorrhage and gangrene following
ligation promptly decreased. Subsequently,
Halsted (1914) demonstrated the roll of col-
lateral circulation by gradually completely
occluding the aorta and other large arteries
in dogs by means of silver or aluminum bands,
which were gradually tightened over a period
of time.

EARLY DIRECT VASCULAR
RECONSTRUCTION

About two centuries after Pare established the
use of the ligature, the first direct repair of
an injured artery was accomplished. This
event, about 243 years ago, is credited as the
first documented vascular repair. Hallowell
(1762) , acting on a suggestion by Lambert in

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

Figure-of-eight suture
Pin

Laceration

Brachial Artery

■ FIGURE 1-2

The first arterial repair performed by Hallowell, acting on a suggestion by Lambert in 1759. The
technique, known as the farrier's (veterinarian's) stitch, was followed in repairing the brachial artery
by placing a pin through the arterial walls and holding the edges in apposition with a suture in a
figure-of-eight fashion about the pin. (From Lambert. Med Obser Inq 1762;30:360.) ■

1759, repaired a wound of the brachial artery
by placing a pin through the arterial walls and
holding the edges in apposition by applying
a suture in a figure-of-eight fashion about the
pin (Fig. 1-2). This technique (known as the
Farrier stitch) had been used by veterinari-
ans but had fallen into disrepute following
unsuccessful experiments. Table 1-1 outlines
early vascular techniques.

Unfortunately, others could not duplicate
Hallowell's successful experience, almost
surely because of the multiple problems of
infection and lack of anesthesia. There was
one report by Broca (1762) of a successful
suture of a longitudinal incision in an artery.
However, according to Shumacker (1969) , an
additional 127 years passed following the
Hallowell-Lambert arterial repair before a
second instance of arterial repair by lateral

TABLE 1-1

VASCULAR REPAIR PRIOR TO 1900

Technique Year

Surgeon

Pin and thread

1759

Hallowell

Small ivory clamps

881

Gluck

Fine needles and silk

889

Jassinowski

Continuous suture

890

Burci

Invagination

896

Murphy

Suture all layers

899

Dorfler

Adapted from Guthrie GC: Blood Vessel Surgery and Its
Application. New York: Longmans, Green, 1912.

suture of an artery in a man was reported by
Postempski in 1886.

With the combined developments of anes-
thesia and asepsis, several reports of attempts
to repair arteries appeared in the latter part
of the 19th century. The work ofjassinowsky,
who is credited in 1889 for experimentally
proving that arterial wounds could be sutured
with preservation of the lumen, was later
judged by Murphy in 1897 as the best exper-
imental work published at that time. In 1865,
Henry Lee of London attempted repair of arte-
rial lacerations with suture (Shumacker, 1969).
Gluck in 1883 reported 19 experiments with
arterial suture, but all experiments failed
because of bleeding from the holes made by
suture needles. He also devised aluminum and
ivory clamps to unite longitudinal incisions
in a vessel, and it was recorded that the ivory
clamps succeeded in one experiment on the
femoral artery of a large dog. Von Horoch of
Vienna reported six experiments, including
one end-to-end union, in 1887, all of which
thrombosed. In 1889, Bruci sutured six lon-
gitudinal arteriotomies in dogs; the procedure
was successful in four. In 1890 Muscatello suc-
cessfully sutured a partial transection of the
abdominal aorta in a dog. In 1894 Heiden-
hain closed by catgut suture, a 1-cm opening
in the axillary artery made accidentally while
removing the adherent carcinomatous glands.
The patient recovered without any circulatory
disturbance. In 1883, Israel, in a discussion of
a paper by Gluck, described closing a lacera-
tion in the common iliac artery created

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1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

during an operation for peri typhli tic abscess.
The closure was accomplished by five silk
sutures. However, Murphy (1897) did not
believe it could be possible from his personal
observations to have success in this type of
arterial repair. In 1896, Sabanyeff successfully
closed small openings in the femoral artery
with sutures.

The classic studies ofjohn B. Murphy (1897)
of Chicago contributed greatly to the devel-
opment of arterial repair and culminated in
the first successful end-to-end anastomosis of
an artery in 1 896. Previously, Murphy had care-
fully reviewed earlier clinical and experi-
mental studies of arterial repair and had
evaluated different techniques extensively in
laboratory studies. Murphy attempted to
determine experimentally how much artery
could be removed and still allow an anasto-
mosis. He found 1 inch of calf's carotid artery
could be removed and the ends still approx-
imated by invagination suture technique
because of the elasticity of the artery. He con-
cluded that arterial repair could be done with
safety when no more than three fourths of an
inch of an a artery had been removed, except
in certain locations such as the popliteal fossa
or the axillary space where the limb could be
moved to relieve tension on the repair. He
also concluded thatwhen more than one half
of the artery was destroyed, it was better to
perform and end-to-end anastomosis by
invagination rather than to attempt repair of
the laceration. This repair was done by intro-
ducing sutures into the proximal artery,
including only the two outer coats, and
using three sutures to invaginate the proxi-
mal artery into the distal one, reinforcing
the closure with an interrupted suture
(Fig. 1-3).

In 1 896 Murphy was unable to find a similar
recorded case involving the suture of an artery
after complete division, and he consequently
reported his experience (1897) in one patient
and then and carried out a number of exper-
iments to determine the feasibility of his pro-
cedure. Murphy's patient was a 19-year-old
male shot twice, with one bullet entering the
femoral triangle. The patientwas admitted to
Cook County Hospital in Chicago on Sep-
tember 19, 1896, approximately 2 hours after
wounding. There was no hemorrhage or

**&

■ FIGURE 1-3

The first successful clinical end-to-end
anastomosis of an artery was performed in
1896. Sutures were placed in the proximal
artery, including only the few outer costs, and
three sutures were used to invaginate the
proximal artery into the distal one; the closure
was reinforced with an interrupted suture.
(From Murphy JB: Exp Clin Res Med Rec
1897;51:73-104.) ■

increased pulsation noted at the time. Murphy
first saw the patient 15 days later, October 4,
1896, and found a large bruit surrounding
the site of the injury. Distal pulses were barely
perceptible. Two days later, when demon-
strating this patient to students, a thrill was
also detected. An operative repair was decided.
Because of the historical significance, the
operation report is quoted:

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

Operation, October 7, 1896. An incision five
inches long was made from Poupart's
ligament along the course of the femoral
artery. The artery was readily exposed about
one inch above Poupart's ligament; it was
separated from its sheath and a provisional
ligature thrown about it but not tied. A careful
dissection was then made down along the
wall of the vessel to the pulsating clot. The
artery was exposed to one inch below the
point and a ligature thrown around it but not
tied; a careful dissection was made upward to
the point of the clot. The artery was then
closed above and below with gentle
compression clamps and was elevated, at
which time there was a profuse hemorrhage
from an opening in the vein. A cavity, about
the size of a filbert, was found posterior to the
artery communicating with its caliber, the
aneurysmal pocket. A small aneurysmal sac
about the same size was found on the
anterior surface of the artery over the point of
perforation. The hemorrhage from the vein
was very profuse and was controlled by
digital compression. It was found that one-
eighth of an inch of the arterial wall on the
outer side of the opening remained, and on
the inner side of the perforation only a band
of one-sixteenth of an inch of adventitia was
intact. The bullet had passed through the
center of the artery, carried away all of its wall
except the strands described above, and
passed downward and backward making a
large hole in the vein in its posterior and
external side just above the junction of the
vena profunda. Great difficulty was
experienced in controlling the hemorrhage
from the vein. After dissecting the vein above
and below the point of laceration and placing
a temporary ligature on the vena profunda,
the hemorrhage was controlled so that the

vein was greatly diminished in size, but when
the clamps were removed it dilated about
one-third the normal diameter or one-third the
diameter of the vein above and below. There
was no bleeding from the vein when the
clamps were removed. Our attention was then
turned to the artery. Two inches of it had been
exposed and freed from all surroundings. The
opening in the artery was three-eighths of an
inch in length; one-half inch was resected
and the proximal was invaginated into the
distal for one-third of an inch with four double
needle threads which penetrated all of the
walls of the artery. The adventitia was peeled
off the invaginated portion for a distance of
one-third of an inch: a row of sutures was
placed around the edge of the overlapping
distal end, the sutures penetrating only the
medial of the proximal portion; the adventitia
was then brought over the end of the union
and sutured. The clamps were removed. Not
a drop of blood escaped at the line of suture.
Pulsation was immediately restored in the
artery below the line of approximation and it
could be felt feebly in the posterior tibial and
dorsalis pedis pulses. The sheath and
connective tissue around the artery were then
approximated at the position of the suture
with catgut, so as to support the wall of the
artery. The whole cavity was washed out with
a five percent solution of carbolic acid and
the edges of the wound were accurately
approximated with silk worm-gut sutures. No
drainage. The time of the operation was
approximately two and one-half hours, most
of the time being consumed in suturing the
vein. The artery was easily secured and
sutured, and the hemorrhage from it readily
controlled. The patient was placed in bed
with the leg elevated and wrapped in
cotton.

The anatomic location of the injuries, the
gross pathology involved and the repair for
Murphy's historically successful arterial anas-
tomosis are shown in Figure 1-4. Murphy men-
tioned that a pulsation could be felt in the
dorsalis pedis artery 4 days following the oper-
ation. The patient had no edema and no

disturbance of his circulation during the
reported 3 months of observation.

Subsequently, Murphy (1897) reviewed the
results of ligature of large arteries before the
turn of the century. He found that the abdom-
inal aorta had been ligated 10 times with only
one patient surviving for 10 days. Lidell

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1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

Femoral artery

Femoral vein

Posterior

Aneurysmal pockets
on the anterior and
posterior surface of
the femoral a.

■ FIGURE 1-4

The first successful end-to-end arterial anastomosis in man by Murphy in 1896. A, The anatomic
location of the injury. B, The close pathology involved. C, Degree of destruction, portion resected
and appearance after invagination of femoral artery. See text for details including venous repair.
(From Murphy JB: Med Rec 1897;51:73-104.) ■

reported only 16 recoveries after ligation of
the common iliac artery 68 times, a mortality
of 77% . Balance and Edmunds reported a 40%
mortality following ligation of afemoral artery
aneurysm in 31 patients. Billroth reported

secondary hemorrhage from 50% of large
arteries ligated in continuity. Wyeth collected
106 cases of carotid artery aneurysms treated
by proximal ligation, with a mortality rate of
35%.

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

In 189 7 Murphy summarized techniques he
considered necessary for arterial suture. They
bear a close resemblance to principles gen-
erally followed today:

1. Complete asepsis

2. Exposure of the vessel with as little injury
as possible

3. Temporary suppression of the blood
current

4. Control of the vessel while applying the
suture

5. Accurate approximation of the walls

6. Perfect hemostasis by pressure after the
clamps are taken off

7. Toilet of the wound

Murphy also reported that Billroth, Schede,
Braun, Schmidt, and others had successfully
sutured wounds in veins. He personally had
used five silk sutures to close an opening
three eighths of an inch in the common
jugular vein. Several significant accomplish-
ments occurred in vascular surgery within
the next few years. Matas (1903) described
his technique with endoaneurysmorrhaphy
for aneurysm, a technique that remained
the standard technique for aneurysms for
more than 40 years. In 1906 Carrel and
Guthrie performed classic experimental
studies over a period with many significant
results. These included direct suture repair
of arteries, vein transplantation, and trans-
plantation of blood vessels, organs, and limbs
(Fig. 1-5).

In 1912 Guthrie independently published
his continuing work on vascular surgery. Fol-
lowing Murphy's successful case in 1896, the
next successful repair of an arterial defect
came 10 years later when Goyanesused a vein
graft to bridge an arterial defect in 1906.
Working in Madrid, Goyanes excised a
popliteal artery aneurysm and used the accom-
panying popliteal vein to restore continuity
(Fig. 1-6).

He used the suture technique, developed
by Carrel and Guthrie, of triangulation of the
arterial orifice with three sutures, followed by
continuous suture between each of the three

■ FIGURE 1-5

The triangulation method of suturing vessels.
Initially conceived in 1902 by Carrel, this
method was used by Carrel and Guthrie in their
monumental contributions in the direct suture
repair of arteries, vein transplants, and
transplantation of blood vessels and organs.
(Courtesy the New York Academy of Medicine
Library.) ■

A year later in Germany, Lexer (1907) first
used the saphenous vein as an arterial sub-
stitute to restore continuity after excision of
an aneurysm of the axillary artery. In his 1969
review, Shumacker commented thatwithin the
first few years of this century, the triangula-
tion stitch of Carrel (1902), the quadrangu-
lation method of Frouin (1908), and the
Mourin modification (1914) (Fig. 1-7) had
developed.

By 1910 Stich reported more than 100 cases
of arterial reconstruction by lateral suture. His
review also included 46 repairs by end-to-end
anastomosis or by insertion of a vein graft
(Nolan, 1968). It is curious with this promis-
ing start that more than 30 years had elapsed
before vascular surgery was widely employed.
A high failure rate, usually by thrombosis,
attended early attempts at repair, and few
surgeons were convinced that repair of an
artery wasworthwhile. Matas (1913) stated that
vascular injuries, particularly arteriovenous
aneurysms, had become a conspicuous feature
of modern military surgery, and he felt that
this class of injury must command the closest
attention of the modern military surgeon:

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1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

Artery

■ FIGURE 1-6

The first successful repair of an arterial defect
utilizing a vein graft. Using the triangulation
technique of Carrel with endothelial coaptation,
a segment of the adjacent popliteal vein was
used to repair the popliteal artery. (From
Goyanes DJ: El Siglo Med 1906;53:546,561 .) ■

A most timely and valuable contribution to the
surgery of blood vessels resulted from
wounds in war. . . . Unusual opportunities for
the observation of vascular wounds inflicted
with modern military weapons . . . based on
material fresh from the field of action, and

fully confirmed the belief that this last war,
waged in closed proximity to well equipped
surgical centers, would also offer an
unusual opportunity for the study of the
most advanced methods of treating injuries
of blood vessels.

MILITARY VASCULAR
TRAUMA EXPERIENCE

Balkin Wars

In 1913 Soubbotitch (Fig. 1-8) described the
experience of Serbian military surgeons
during the Serbo-Turkish and Serbo-Bulgar-
ian Wars. Seventy-seven false aneurysms and
arteriovenous fistulas were treated. There were
45 ligations, but 32 vessels were repaired,
including 19 arteriorrhaphies, 13 venorrha-
phies, and 15 end-to-end anastomoses (11
arteries and 4 veins) . It is impressive that infec-
tion and secondary hemorrhage were avoided.
Matas (1913), in discussing Soubbotitch's
report, emphasized that a notable feature was
the suture (circular and lateral repair) of
blood vessels and the fact that it had been used
more frequently in the Balkan Conflict than
in previous wars. He also noted that judging
by Soubbotitch's statistics, the success obtained
by surgeons in the Serbian Army Hospital in
Belgrade far surpassed that obtained by other
military surgeons in previous wars, with the
exception perhaps of the remarkably favor-
able results in the Japanese Reserve Hospital
reported by Kikuzi during the Russo-
Japanese War (1904/1905). It is ironic that

■ FIGURE 1-7

The original triangulation stitch
of Carrel in 1902 was modified
to a quadrangulation method
by Frouin in 1908. Another
modification, as shown here,
was that of Mourin in 1914.
(From Moure P. Les Greffes
Arterielles, 1914.) ■

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14 I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

■ FIGURE 1-8

Dr. V. Soubbotitch (front-row center), Lt Col., Serbian Army Reserves, is flanked by members of his
staff at the Belgrade State Hospital (circa 1912-1913). The reference provides additional details
regarding the Matas-Soubbotitch connection. (From Rich NM, Clagett GP, Salander JM, Piscevic S:
Surgery 1983;93:17-19.) ■

the vascular experience continued in the
Balkans, in the early 1990s. Additional infor-
mation regarding Soubbotitch came directly
from Geza De Takats (Fig. 1-9) who was in
Belgrade early in World War II. Table 1-2 iden-
tifies the Soubbotitch experience.

World War I Experience

During the early part of World War I, with the
new techniques of vascular surgery well estab-
lished, the German surgeons attempted repair
of acutely injured arteries and were success-
ful in more than 100 cases (Nolan, 1968).
During the first 9 months of World War I, low-
velocity missiles caused arterial trauma of a

TABLE 1-

-2

TREATMENT OF TRAUMATIC

ANEURYSMS FROM THE SERBO-

TURKISH AND SERBO-BULGARIAN

WARS

Partial Circular

Ligation

Suture Suture

Arteries

8 11

Veins

9 4

Modified from Soubbotitch V: Lancet 1913:2:720-721.

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1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

MILITARY SURGICAL HERITAGE

DEPARTMENT OF SURGERY, USUHS

Geza de Takats 1892 - 1985

1st. LT, MC Austro-Hungarian Army
At Funeral of Emperor Franz Joseph 1916
A Dedicated Friend of Military Surgeons
Consultant, Great Lakes Naval Hospital, 1946 -

■ FIGURE 1-9

An internationally acclaimed pioneer
in vascular surgery Geza De Takats is
among the early contributors to our
military surgical heritage. (From Rich
NM: Am J Surg 1993;166:91-96.) ■

limited extent. In 1915, however, the wide-
spread use of high explosives (the high explo-
sive artillery shells replaced the Shrapnel shell
in use since British action in Surinam in 1904)
and high-velocity bullets, combined with mass
casualties and slow evacuation of the wounded,
made arterial repair impractical.

Bernheim (1920) , who had performed vas-
cular research in a Hunterian Laboratory, per-
formed the first vascular repair using
saphenous vein in the United States at Johns
Hopkins University and went to France with
the specific intent of repairing arterial injuries.
Despite extensive prior experience and
equipment, however, he concluded that
attempts atvascular repair were unwise (1920) .
He wrote

Opportunities for carrying out the more
modern procedures for repair or
reconstruction of damaged blood vessels
were conspicuous by their absence during
the recent military activities. . . . Not that
blood vessels were immune from injury; not
that gaping arteries and veins and
vicariously united vessels did not cry out for
relief by fine suture or anastomosis. They
did, most eloquently, and in great numbers,
but he would have been a foolhardy man
who would have essayed sutures of arterial
or venous trunks in the presence of such
infections as were the rule in practically all
of the battle wounded.

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

The great frequency of infection with sec-
ondary hemorrhage virtually precluded arte-
rial repair. In addition, there were inadequate
statistics about the frequency of gangrene fol-
lowing ligation, and initial reports subse-
quently proved to be unduly optimistic. Poole
(1927), in the Medical Department History
of World War I, remarked that if gangrene
was a danger following arterial ligation,
primary suture should be performed and the
patient watched very carefully.

Despite the discouragement of managing
acute arterial injuries in World War I, fairly
frequent repair of false aneurysms and arte-
riovenous fistulas was carried out by many
surgeons. These cases were treated after the
acute period of injury, when collateral circu-
lation had developed with the passage of time
and ensured viability of extremities. Matas
(1921) recorded that most of these repairs
consisted of arteriorrhaphy by lateral or
circular suture, with excision of the sac or
endoaneurysmorrhaphy.

Makins (1919), who served in World
War I as a British surgeon, recommended
ligating the concomitant vein when it was
necessary to ligate a major artery. He
thought that this reduced the frequency of
gangrene. This hypothesis was debated
for more than 20 years before it was finally
abandoned.

Goodman (1918), in describing his expe-
rience at the number 1 (Presbyterian U.S.A.)
General Hospital in France during World War
I, reported a successful closure with continu-
ous silk suture of 5-mm longitudinal openings
in both the popliteal artery and the popliteal
vein in one patient with a shell fragment.
However, the patient was followed for only 9
days before being transferred to the Base
Hospital. Goodman reported, "An attempt to
obtain further information covering the case
is now underway and will be embodied in a
subsequent report."

If there was any further follow-up infor-
mation obtained or reported, it became
obscured in the available literature. At least
this military surgeon recognized the impor-
tance of obtaining long-term follow-up infor-
mation to thoroughly evaluate his method of
managing vascular trauma.

In 1987, Shumacker identified that
Weglowski was a neglected pioneer in vascu-
lar surgery. Weglowski served first in a Russian
Military Hospital and later as Surgeon General
of the Polish Army. Based on his experience
with more than 600 patients, he summarized
his recommendations in 1919 that all arterial
injuries and post-traumatic aneurysms, includ-
ing those of the aorta, carotid, iliac, and sub-
clavian arteries, and the arteries of the
extremities, should be repaired by vascular
suture either immediately after the injury or
after 1 month for pulsating hematomas. In
1924 Weglowski presented the results of 193
personal vascular repairs including 46 by
lateral sutures, 12 by end-to-end anastomosis
and 56 using venous grafts. Ligation was
required in the remaining 79 patients because
of infection and the risk of postoperative
bleeding. His results were surprisingly good.
In 1994, Nunn wrote in detail about Ernst
Jeger, who he called a "forgotten pioneer in
cardiovascular surgery." Jeger's work was
recorded only in the German language. Jeger
described his research in a book, Die Chirgiirie
der Blutgefasse und des Herzens in 1913. He was
drafted as a physician for the German Army
in 1914 and died tragically in a Russian prison
camp in 1915. Jeger did report his operative
experience with 10 soldiers with vascular
injuries. He had success in seven patients using
lateral suture or end-to-end anastomosis.
Based on his successful experience, he rec-
ommended increased use of vascular repair
in war injuries.

World War II Experience

Experiences with vascular surgery in World
War II are well recorded in the classic review
of DeBakey and Simeone (1946), analyzing
2471 arterial injuries. Almost all were treated
by ligation, with a subsequent amputation rate
near 49%. Only 81 repairs were attempted,
78 by lateral suture and 3 by end-to-end anas-
tomosis, with an amputation rate of approxi-
mately 35%. The use of vein grafts was even
more disappointing: They were attempted in
40 patients, with an amputation rate of nearly
58%. Early patency of a venous graft in the

chOl.qxd 4/16/04 3:20PM Page 17

1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

arterial system was demonstrated angio-
graphically. DeBakey (Fig. 1-10) has had the
opportunity to contribute to the development
and progress in vascular surgery over more
than 50 years, from 1946 to 1996.

The controversial question of ligation of the
concomitant vein remained, although few
observers were convinced that the procedure
enhanced circulation. The varying opinions
were summarized by Linton in 1949.

A refreshing exception to the dismal World
War II experience in regard to ligation and
gangrene was the case operated on by Doctor
Allen M. Boyden: an acute arteriovenous
fistula of the femoral vessels repaired shortly
after D-Day in Normandy. The following com-
ments are taken from his field notes about 26

years later Boyden (personal communication,
1970) and emphasize the value of adequate
records, even in military combat:

High explosive wound left groin, 14 June

1944, at 2200 hours. Acute arteriovenous

aneurysm femoral artery
Preoperative blood pressure 140/70; pulse

104
Operation: 16 June 1944, nitrous oxide and

oxygen
Operation: 1910 to 22 hours
One unit blood transfused during the

operation

Continued

MILITARY SURGICAL HERITAGE

Department of Surgery, USUHS

Michael E. DeBakey, MD

Colonel, MC, AUS Third AMEDD Surgical Consultant 1946

Consultant Department of Surgery USUHS, 1977-

Visiting Board Department of Surgery USUHS, 1978-

Advisor, USU Surgical Associates, 1980- President 1990

Michael E. Debakey International Military Surgeon's Award

■ FIGURE 1-10

Doctor DeBakey is recognized for
his numerous and valuable
contributions to surgery, in general,
and specifically to military vascular
surgery. The Michael DeBakey
International Military Surgeons
Award is presented at the Uniformed
Services University Surgical
Associates Day each spring at the
Uniformed Services University of the
Health Sciences, Bethesda,
Maryland. (From Rich NM: Am J
Surg 1993;166:91-96.) ■

chOl.qxd 4/16/04 3:20PM Page 18

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

Arteriovenous aneurysms isolated near

junction with profunda femoris artery
Considerable hemorrhage
Openings in both artery and vein were sutured

with fine silk
Postoperative blood pressure 120/68; pulse

118
Circulation of the extremity remained intact

until evacuation

As this case demonstrated Boyden's inter-
est in vascular surgery, the Consulting Surgeon
for the First Army presented him with one half
of the latter's supply of vascular instruments
and material. This supply consisted of two sets
of Blakemore tubes, two bulldog forceps, and
a 2-mL ampule of heparin!

The conclusion that ligation was the treat-
ment of choice for injured arteries was
summarized by DeBakey and Simeone in 1946,
"It is clear that no procedure other than lig-
ation is applicable to the majority of vascular
injuries which come under the military sur-
geons' observation. It is not a procedure of
choice. It is a procedure of stern necessity, for
the basic purpose of controlling hemorrhage,
as well as because of the location, type, size
and character of most battle injuries of the
arteries."

In retrospect it should be remembered that
the average time lag between wounding and
surgical treatment was more than 10 hours in
World War II, virtually precluding successful
arterial repair in most patients. Of historical
interest is the nonsuture method of arterial
repair used during World War II (Figs. 1-11
and 1-12).

Although considerable time and effort
were expended following World War II in an
attempt to provide additional long-term
follow-up information, the results of this
effort are not generally available. Individual
follow-up has been possible in a random way
for some patients, such is the case of an acute
femoral arteriovenous fistula that was repaired
shortly after D-Day in Normandy on June 16,
1944 (Boyden, 1970) . This was an unusual case
because it involved the successful repair of
both the common femoral artery and the

■ FIGURE 1-11

Completed unsutured vein graft of the popliteal
artery which was complicated by a severe
compound fracture of the tibia. This was
representative of 40 cases utilizing the double-
tube graft technique in World War II as
advocated by Blakemore, Lord and Stefko in
1942. (From DeBakey ME, Simeone FA: Ann
Surg 1946;123:534-579.) ■

common femoral vein in a combat zone at a
time when ligation of vascular injuries was the
accepted principle. Unfortunately, when it was
possible more than 26 years later to obtain
follow-up data on this patient, it was learned
that hemorrhage occurred in the left inguinal
wound after the patient was evacuated to a
General Hospital in England. Ligation of both
the common femoral artery and the common
femoral vein was required. Additional follow-
up was not possible because the patient died
of tuberculosis approximately 16 months
after receiving the wound. Shumacker (1946,
1947a, 1947b, 1948a, 1948b) (Fig. 1-13)
(Table 1-3) made many valuable contribu-
tions to vascular surgery with the U.S. Army,
as did Rob (Fig. 1-14) with the British Army.

Experiences During the
Korean Conflict

The successful repair of arterial injuries in the
Korean Conflict, in pleasant contrast to the
experiences of World War I and World War

chOl.qxd 4/16/04 3:20PM Page 19

1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

Proximal

S^rRubber shod
(Artery c| a m P

Kelly clamp

Distal end of
vein placed into
Distal proximal end of artery
5

■ FIGURE 1-12

The various steps of a nonsuture method
of bridging arterial defects designed
during World War II (1)The Vitallium tube
with its two ridges (sometimes grooves).
(2) The exposed femoral artery and vein
retracted and clamps placed on a
branch. (3) The removed segment of
vein is irrigated with saline solution. (4)
The vein has been pushed through the
inside of the Vitallium tube, and the two
ends everted over the ends of the tube
held in place with one or two ligatures of
fine silk. (5) Distal end of the segment of
vein is placed into the proximal end of
the artery and held there by two ligatures
of fine silk. (6) The snug ligature near the
end of the Vitallium tube is tied to
provide apposition of the artery and vein.
(7) The completed operation, showing
the bridging of a 2-cm gap in the femoral
artery. (From Blakemore AH, Lord JW,
Stefko PL: Surgery 1942;12:488-508.) ■

MILITARY SURGICAL HERITAGE

DEPARTMENT OF SURGERY, USUH8

Harrli B Shumlcktl, Jr.

Captain, 118th General, (Johns Hopkins)

Camp Edwarda, Cap* Cod 1942

Prolasaor of Surgery, USUHS

1 July 1081 -

■ FIGURE 1-13

Doctor Harris Shumacker made
many valuable contributions in World
War II to the early development of
military vascular surgery.
Subsequently, he received
appropriate recognition by being
named the first, and only,
distinguished professor in the
Department of Surgery at the
Uniformed Services University of the
Health Sciences, Bethesda,
Maryland. (From Rich NM: Am J
Surg 1993;166:91-96.) ■

chOl.qxd 4/16/04 3:20PM Page 2

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

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chOl.qxd 4/16/04 3:20PM Page 21

1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

MILITARY SURGICAL HERITAGE

DEPARTMENT OF SURGERY, USUHS

Charla* G. Rob

ilt Royal Amy Mit Tc al Corps

Ti w a ar l , North Africa January 1943

Prof»»«or of Surgery, USUHS

1 July 19B3 -

■ FIGURE 1-14

Doctor Charles Rob has had a
distinguished career, both in the
United Kingdom and in the United
States; he has been recognized for
his international contributions in
vascular surgery. Dr. Rob continues
to serve as professor and senior
advisor at the Uniformed Services
University of the Health Sciences,
Bethesda, Maryland. (From Rich
NM: Am J Surg 1993;166:91-96.) ■

II, was due to several factors. There had been
substantial progress in the techniques of vas-
cular surgery, accompanied by improvements
in anesthesia, angiography, blood transfusion,
and antibiotics. Perhaps of the greatest impor-
tance was rapid evacuation of wounded men
often by helicopter, permitting their transport
from time of wounding to surgical care often
within 1 to 2 hours (Fig. 1-15). In addition,
a thorough understanding of the importance
of debridement, delayed primary closure, and
antibiotics greatly decreased the hazards of
infection.

Initially in the Korean Conflict, attempts at
arterial repair were disappointing. During one
report of experiences at a surgical hospital
for 8 months between September 1951 and

April 1952, only 11 of 40 attempted arterial
repairs were thought to be successful (Hughes,
1959). Only 6 of 29 end-to-end anastomoses
were considered initially successful, and all 6
venous grafts failed. In another report from
a similar period, only 4 of 18 attempted repairs
were considered successful. Warren (1952)
emphasized that an aggressive approach was
needed, with the establishment of a research
team headed by a surgeon experienced in vas-
cular grafting. Surgical research teams were
established in the Army, and there was
improvement in results of vascular repairs in
1952. Significant reports were published by
Jahnke and Seeley (1953), Hughes (1955,
1958), and Inui, Shannon, and Howard
(1955). Hughes (Fig. 1-16) continued his

chOl.qxd 4/16/04 3:20PM Page 22

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

■ FIGURE 1-15

Helicopter evacuation of the wounded during the
Korean Conflict helped reduce the lag time
between injury and definitive surgical care.
Continued improvement in Vietnam in helicopter
evacuation of the wounded allowed some
patients with vascular trauma to reach a
definitive surgical center within 15 to 30 minutes.
(US Army photograph.) ■

MILITARY SURGICAL HERITAGE

DEPARTMENT OF SURGERY, USUHS

■ FIGURE 1-16

Doctor Carl Hughes had a
distinguished military career
providing valuable contribution
during the Korean Conflict and,
subsequently, during the Vietnam
War. He continues to serve as
professor at the Uniformed Services
University of the Health Sciences,
Bethesda, Maryland. (From Rich
NM. Am J Surg 1993;166:91-96.) ■

WS5 HASH, CNH Won ¥■»•», Kor*» 1MS

MG, MC, US* (RET)
Pr o Umr ot lan)MV, USUHS 1M4-1MC
1 twawy, USUHS ISM-

chOl.qxd 4/16/04 3:20PM Page 23

1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

efforts in vascular surgery rising to the rank
of Major General. He continues at the Uni-
formed Services University of the Health Sci-
ences, a Distinguished Professor of Surgery.
Howard reflected in 1998 on his clinical and
research experiences during the Korean Con-
flict. Similar work in the Navy was done with
the U.S. Marines during 1952 and 1953 by
Spencer and Grewe (1955). These surgeons
worked in specialized research groups under
fairly stabilized conditions, considering that
they were in a combat zone (Fig. 1-17).
Spencer reflected on his experiences during
the Korean Conflict during his Presidential
Address to the American Surgical Association
in 1998.

Brigadier General Sam Seeley, who was
Chief of the Department of Surgery at Walter
Reed Army Hospital in 1950, had the fore-
sight to establish Walter Reed Army Hospital
as a vascular surgery center, and this made it
possible for patients with vascular injuries to
be returned there for later study (Fig. 1-18) .
In a total experience with 304 arterial injuries,
269 were repaired and 35 ligated (Hughes,
1958). The overall amputation rate was 13%,
a marked contrast to that of about 49% in
World War II. Because the amputation rate is
only one method of determining ultimate

Rights were not granted to include this figure in electronic media.
Please refer to the printed publication.

■ FIGURE 1-18

An autogenous greater saphenous vein graft
was utilized in 1952 at Walter Reed General
Hospital to repair a traumatized proximal
popliteal artery. Each anastomosis is an
everting type with intima-to-intima held by
everting mattress sutures. (Rich NM, Hughes
CW. Bull Am Coll Surg 1972;57:35.) ■

success or failure in arterial repair, it is impor-
tant to emphasize thatjahnke (1958) revealed
that in addition to the lowered rate of limb
loss, limbs functioned normally when arter-
ial repair was successful. The arteriovenous
fistula experience is expanded on in
Chapter 24.

■ FIGURE 1-17

Postoperative ward in a mobile army surgical
hospital (MASH) shows some of the conditions
at the time of the Korean Conflict when it was
demonstrated that arterial repair could be
successful, even under battlefield conditions.
(Hughes CW. Milit Med 1959;124:30-46.) ■

Experience in Vietnam

In Vietnam the time lag between injury and
treatment was reduced even further by the
almost routine evacuation by helicopter, com-
bined with the widespread availability of sur-
geons experienced in vascular surgery. In one
study of 750 patients with missile wounds in
Vietnam, 95% of the patients reached the hos-
pital by helicopter (Rich, 1968) (Fig. 1-18).
This prompt evacuation, however, similarly
created an adverse effect on the overall
results, for patients with severe injuries from
high-velocity missiles survived only long
enough to reach the hospital. During initial
care, they expired. These patients would
never have reached the hospital alive in pre-
vious military conflicts.

chOl.qxd 4/16/04 3:20PM Page 24

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

In the initial Vietnam studies, between
October 1, 1965,andjune30, 1966, there were
177 known vascular injuries in U.S. casualties,
excluding those with traumatic amputation
(Heaton and colleagues, 1966) . One hundred
sixteen operations were performed on 106
patients with 108 injuries (Table 1-4). These
results included the personal experience of
one of us (N.M.R.) at the Second Surgical Hos-
pital. The results reported included a short-
term follow-up of approximately 7 to 10 days
in Vietnam. In Vietnam, amputations were
required for only 9 of the 108 vascular injuries,
a rate of about 8%. Subsequently, more
detailed analysis from the Vietnam Vascular
Registry (Rich and Hughes, 1969; Rich, 1970)
found the amputation rate of approximately
13%, identical to that of the Korean Conflict.
Almost all amputationswere performed within
the first month after wounding.

The Vietnam Vascular Registry (Figs. 1-19
and 1-20) was established at Walter Reed
General Hospital in 1966 to document and
analyze all vascular injuries treated in Army
Hospitals in Vietnam. A preliminary report

■ FIGURE 1-19

During the war in Vietnam, most patients were
rapidly treated in fixed installations. An early
example is the 2 nd Surgical Hospital at An Khe
in January, 1966. Ninety-five per cent of the
wounded reached a hospital by helicopter.
(Rich NM, Georgiade NG. Plastic and
Maxillo-facial Trauma Symposium. CV Mosby,
St Louis, 1969.) ■

(Rich and Hughes, 1969) involved the com-
plete follow-up of 500 patients who sustained
718 vascular injuries (Table 1-5). Although
vascular repairs on Vietnamese and allied mil-
itary personnel were not included, the Reg-
istry effort was soon expanded to include all
U.S. service personnel, rather than limiting
the effort to soldiers.

Fisher (1967) collected 154 acute arterial
injuries in Vietnam covering the 1965 to 1966
period. There were 108 arterial injuries with
significant information for the initial review
from Army hospitals. In 1967, Chandler and
Knapp reported results in managing acute vas-
cular injuries in the U.S. Navy hospitals in
Vietnam. These patients were not included in
the initial Vietnam Vascular Registry report,
but after 1967, an attempt was made to
include all military personnel sustaining
vascular trauma in Vietnam. This included
active-duty members of the U.S. Armed
Forces treated at approximately 25 Army
hospitals, six Navy hospitals, and one Air Force
hospital.

As with any registry, success of the Vietnam
Vascular Registry has depended on the coop-
eration of hundreds of individuals within the
military and civilian communities. In the initial
report from the Registry, the names of 20 sur-
geons who had done more than five vascular
repairs were included (Rich and Hughes,
1969) . In the first edition of Vascular Trauma,
the names of many more who contributed to
the Vietnam Vascular Registry are included
(Rich and Spencer, 1978).

We would be remiss if we did not gain some-
thing positive from an experience with as many
negative aspects as the U.S. involvement in
Southeast Asia between 1965 and 1972. The
Vietnam Vascular Registry provides a unique
opportunity for long-term follow-up of thou-
sands of young men with vascular repairs. The
challenge remains and the potential is great.
Additional historical details regarding the Reg-
istry activities are included in the first edition
of Vascular Trauma. Unfortunately, the major-
ity in the United States did not want to hear
the word Vietnam for nearly 25 years. Only
recently has the value of the Vietnam Vascu-
lar Registry been appreciated appropriately
and it is hoped that the efforts can be
completed.

chOl.qxd 4/16/04 3:20PM Page 25

1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

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ACUTE ARTE8IAL INJURIES IN VIETNAM

■ a

■ FIGURE 1-20

4, This exhibit representing the management of
acute arterial trauma in Vietnam was presented
from material in the Vietnam Registry to the
Clinical Congress of the American College of
Surgeons in Chicago in 1970. At least 1 10
surgeons who had previously performed arterial
repairs in Vietnam visited the exhibit. B,
Identification card sent to armed forces
personnel who were wounded in Vietnam. This
card was issued in an attempt to identify
participation in the Registry and with the hope
that additional long-term follow-up information
will be generated. (A, From A. F.I. P. photograph;
B, From Walter Reed General Hospital.) ■

VIETNAM VASCULAR REGISTRY

CERTIFY THAT

HAS A HtWMAWtNT FILE AT
B WALTER REED GENERAL HDSPITAL.

TABLE 1-5

MANAGEMENT OF ARTERIAL TRAUMAIN VIETNAM CASUALTIES PRELIMINARY
REPORT FROM THE VIETNAM VASCULAR REGISTRY*

End-to-End

Vein

Lateral

Prosthetic

Artery

Anastomosis

Graft

Suture

Graft

Thrombectomy

Ligation

Common carotid

6(2)

(2)

Internal carotid

Subclavian

Axillary

6(3)

12(3)

2(3)

(3)

(1)

Brachial

57(8)

32(10)

2(1)

1(9)

1(2)

Aorta

3(1)

Renal

Iliac

1(1)

(1)

Common femoral

4(2)

11(1)

4(1)

1(2)

(2)

(4)

Superficial femoral

63(5)

37 (14)

7(7)

(4)

2(6)

(4)

Popliteal

31(5)

28(13)

6(4)

(10)

2(4)

TOTAL

165 (23)

127 (43)

29(17)

2(8)

3(33)

6(16)

'Numbers in parenthesis represent additional procedures performed after the initial repair in Vietnam and repair of major arterial

injuries not initially treated in Vietnam.

Modified from Rich NM, Hughes CE: Vietnam vascular registry: a preliminary report. Surgery 65:218-226, 1969.

chOl.qxd 4/16/04 3:20PM Page 27

1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

TABLE 1-6

LOCATION OF EXTREMITY VENOUS INJURIES IN VIETNAM (1965-1969), ISRAEL
(1 973), LEBANON (1 969-1 982), AND CROATIA (1 991 -1 992)

Vietnam (%)

Israel (%)

Lebanon (%)

Croatia (%)

Vein

= 361)

(n = 26)

= 348)

(n = 41)

Subclavian

—

Axillary

Brachial

—

Iliac

—

Femoral

Popliteal

From Leppaniemi A, Rich NM, Browner BD (eds): Techniques in Orthopaedics, vol 10, pp 265-271, 1995, Philadelphia, JB.
Lippincott.

Military Armed Conflicts
Following Vietnam

From Beruit (1982) to Grenada (1983),
Panama (1989), the GulfWar (1991) , Somalia
(1992), as well as recent experiences in
Croatia, Rwanda, and Haiti (and even the
2001 /2002 War against Terrorism) , no United
States military surgeons have had more than
an antidotal vascular case or two to manage.
The data from Vietnam remain pertinent and
valuable today! Leppaniemi (1995) makes
comparisons between Vietnam and recent
wars in Israel (1973), Lebanon (1969tol982)
and Croatia (1992) (Table 1-6). Roostar
(1995) adds the Soviet experience in
Afghanistan in the early 1980s (Table 1-7).
There are military sources such as Croatia and
Serbia; however, these are generally limited
in coverage considering the large numbers of
casualties. The following report is outlined
because of the information contained. Luetic
and colleagues, at the "Doctor Ozren Novosel"
Clinical Hospital at the University of Zagreb,
has documented experience in the manage-
ment of military vascular injuries in Croatia.
He presented a single center experience in
the recent conflict, documenting results from
April through December 1991. Luetic and col-
leagues (1993) managed 1020 casualties with
76 patients sustaining 120 vascular injuries.
This is a relatively high 7.5% of the casualties
with vascular trauma. Also, patients averaging

TABLE 1-7

LOCATION OF INJURIES IN THE
AFGHANISTAN WAR

Artery

Location

Artery

Vein

and Vein

Total

Carotid

—

Subclavian

Axillary

—

Brachial

—

Radial

—

Iliac

—

Femoral

Popliteal

Tibial

—

TOTAL

156

206

Modified from Roostar L: Treatment plan used for vascular
injuries in the Afghanistan war. Cardiovasc Surg 3:42-45,
1995.

1.58 vascular injuries is a very high percent of
multiple injuries. It is particularly pertinent
to note that the casualties were transported
after initial treatment in forward surgical facil-
ities, reaching the university hospital within
3 to 18 hours, with a mean time of 7 hours.
The most common injuries were to the
popliteal artery (12.5%) and the brachial veins
(10%). There was a relatively high incidence
of concomitant fractures, occurring in 90.4%
of the cases. They routinely employed exter-
nal fixation of the concomitant fractures. They

chOl.qxd 4/16/04 3:20PM Page 28

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

used venous interposition grafts in 45 arter-
ial injuries and 20 venous injuries. Prostheses
were used in only three arterial injuries. They
did have a relatively high incidence of arteri-
ovenous fistulas and pseudoaneurysms, with
the former occurring in seven patients and
the latter in six patients (9.8%) with one
patient having injury to the popliteal artery
and five having injuries to the superficial
femoral artery. Sepsis, deep venous throm-
bosis, and extensive myonecrosis contributed
to the required amputations, with three
patients not receiving definitive surgical repair
until 12 hours after injury. All patients requir-
ing amputations had concomitant injury to
bone, nerve, soft tissue, veins, and arteries.
There was a mortality rate of 3.9%, with three
patients dying.

CIVILIAN VASCULAR INJURIES

Several differences exist between civilian and
military vascular injuries. First, military injuries
are characteristically in young persons without
arterial disease. They frequently result from
high-velocity missiles with extensive soft tissue
destruction, often with injuries of multiple
organ systems and in circumstances in which
surgical treatment is less than ideal. Civilian
injuries, however, are usually from wounds
associated with minimal soft tissue destruction.
Prompt treatment and excellent hospital facil-
ities are usually available. Although young civil-
ians are commonly injured, there is also a
significant percentage of older patients who
often have preexisting arterial disease. In addi-
tion, there are frequent injuries from blunt
trauma, such as automobile or industrial acci-
dents, and fractures of long bones. Finally, an
increasing number of vascular injuries are
being seen as a complication of diagnostic pro-
cedures involving cannulation of peripheral
arteries, as in angiography or cardiac
catheterization.

The frequency of arterial injuries in civil-
ian life has increased greatly in the past decade.
This is due to more automobile accidents, the
appalling increase in gunshot and stab
wounds, and the increasing use of therapeu-
tic and diagnostic techniques involving the
cannulation of major arteries. As recently as
1950, most general surgeons had little expe-
rience or confidence in techniques of arter-
ial repair. The experiences in the Korean
Conflict, combined with the widespread teach-
ing of techniques of vascular surgery in sur-
gical residencies, resulted in a great increase
in frequency of arterial repair between 1950
and 1960.

One of the first large series of civilian arte-
rial trauma was reported by Morris, Creech,
and DeBakey in 1957. They described a series
of 136 patients with acute arterial injuries
treated over 7 years at Baylor University-affil-
iated hospitals in Houston (Fig. 1-21). Sixty-

Currently accepted principles regarding
management of acute vascular injuries is
largely based on military experience.
Theodore Drapanas (1970)

■ FIGURE 1-21

Anatomic locations of arterial injuries in the
civilian experience in Houston. In addition to
the fact that nearly one half of the injuries
involved the brachial and femoral arteries,
exactly 50% of the injuries also involved
arteries supplying the upper extremity. (From
Morris GC Jr, Creech O Jr, DeBakey ME: Am J
Surg 1957;93:565-567.) ■

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1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

TABLE 1-8

THE CIVILIAN EXPERIENCE IN ATLANTA COMPARING TWO CONSECUTIVE 5-YEAR
PERIODS SHOWS THE INCREASE IN INCIDENCE OF INJURY AND THE MARKED
IMPROVEMENT OF SUCCESSFUL REPAIR FROM 36 PERCENT TO 90 PERCENT.
THERE WAS ALSO AN ASSOCIATED REDUCTION IN THE MORTALITY RATE BY ONE-
THIRD AND AMPUTATION RATE BY ONE HALF

100

1950 1951 1952 1953 1954 1955 1956 1957 1958 1959

■ Percentage of cases treated by repair

D Percentage of repairs successful (restoration of distal pulses)

From Ferguson IA, Byrd WM, McAfee DK: Experiences in the management of arterial injuries. Ann Surg 153:980-986, 1961.

eight injuries, one half of the group, involved
the upper extremities, and forty-seven injuries
(about 35%) involved the lower extremities.
There were injuries of either the abdominal
or the thoracic aorta and 11 of the carotid
artery. One hundred twenty of the patients,
88%, were male, and most of the injuries were
caused by acts of violence. Primary arterial
repair was possible in a high percentage of
these patients.

In 1961, Ferguson, Byrd, and McAfee,
reported from Grady Memorial Hospital in
Atlanta, 200 arterial injuries treated over 10
years. The superficial femoral artery was
injured most often, 39 patients, or nearly 20%
of the total group. However, 54 of the 200
patients had injuries of minor arteries such
as the radial or ulnar arteries. The propor-
tion of patients treated by arterial repair
increased from less than 10% in 1950 to more
than 80% in 1959. In the latter part of the
study, ligation was done only for injuries of
minor arteries, such as the radial or ulnar, or
certain visceral arteries. The mortality rate was
reduced by one third and the amputation rate

by one half when two consecutive 5-year
periods were compared. The rate of success
of arterial repair improved from 36% to 90%
(Table 1-8). As in Houston, most resulted
from acts of violence (Table 1-9) . Automo-
bile, industrial, and domestic accidents
accounted for most of the remaining injuries.

TABLE 1-9

TYPE OF ACUTE ARTERIAL INJURIES IN
CIVILIAN PRACTICE, HOUSTON, PRIOR
TO 31 JULY 1956

No.

Transection
Laceration
Contusion
Spasm

TOTAL

136

52.2

41.2

4.4

2.2

100.0

Modified from Morris GC Jr, Creech O Jr, DeBakey ME: Acute
arterial injuries in civilian practice. Am J Surg 93:565-572,
1957.

chOl.qxd 4/16/04 3:20PM Page 3

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

In 1963, Smith, Foran, and Caspar
described experiences with 59 patients with
61 vascular injuries in Detroit, including both
acute and chronic arterial injuries (Table
1-10). They properly emphasized that a
careful distinction must be made between
results with acute and chronic lesions. Col-
lateral circulation has usually developed when
a chronic lesion is treated and the problem
of soft tissue is not present. Acts of violence,
gunshot and stab wounds, caused 18 injuries,
44% of the penetrating lesions (Table 1-11).
Their patients included ten industrial injuries
and eight iatrogenic injuries resulting either
from surgical operations or from diagnostic
procedures. These eight included three
injuries of the external iliac artery during
inguinal herniorrhaphy, three arterial injuries
following diagnostic arterial catheterization,
one injury of the internal iliac artery during
removal of a herniated intravertebral disc, and
one arteriovenous fistula developing after a
mass suture ligature of the renal pedicle
during nephrectomy.

In 1964, Patman, Poulos, and Shires
described experiences with 256 patients, with
a total of 271 arterial injuries, treated at the
Parkland Memorial Hospital in Dallas over 1 2
years starting in July 1949. As in other U.S.
series, most resulted from acts of violence,
and only a few resulted from industrial or
automobile accidents. Multiple arterial
injuries occurred in 6% of the group.
Although chronic lesions from trauma were
included, it was noteworthy that these were
few: only 6 arteriovenous fistulas and 12 false
aneurysms among the entire group of 256
patients.

A somewhat different group of cases was
reported from Europe by Vollmar in 1968. In
an analysis of 85,000 injured patients treated
in the Heidelberg University Surgery Clinic
between 1953 and 1966, there were only 172
arterial lesions, an incidence of 0.3%. In
marked contrast to the U.S. experience, only
1% of the injuries were due to gunshot
wounds. Most patients were injured in indus-
trial accidents (Table 1-12). Approximately

TABLE 1-10

CIVILIAN ARTERIAL TRAUMA IN DETROIT,

61 ARTERIAL INJURIES

Type of Trauma

Laceration

Early

Lesions

Spasm

Transection

Thrombosis

Penetrating injuries
Nonpenetrating injuries

TOTAL

10
_2
12

6
2
8

2
4
6

2
2

Modified from Smith RF, Szilagyi DE, Pfeifer JR: Arterial trauma. Arch Surg 86:825-835, 1963.

TABLE 1-11

ETIOLOGIC FACTORS CAUSING 61 ARTERIAL INJURIES, 59 PATIENTS IN CIVILIAN
SERIES IN DETROIT

42 Penetrating Injuries

Gunshot 13

Industrial 10

Iatrogenic 8

Household 6

Stab 5

21.3

16.4

13.1

9.8

8.2

19 Nonpenetrating Injuries

Industrial 1 1

Auto 4

Athletic 2

Household 2

18.0
6.6
3.3

3.3

Modified from Smith RF, Szilagyi DE, Pfeifer JR: Arterial trauma. Arch Surg 86:825-835, 1963.

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1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

TABLE 1-12

TYPE OF ACCIDENT RESPONSIBLE
FOR 169 PATIENTS WITH ARTERIAL
INJURIES, HEIDELBERG UNIVERSITY
SURGICAL CLINIC 1953-1966

Etiology

No.

Industrial ace

dent

Domestic accident

Suicide

Traffic

Iatrogenic

TOTAL

169

100

Modified from Vollmar J: In Hiertonn T, Rybeck B (eds):
Traumatic arterial lesions. Stockholm: Forsvarets
Forskningsanstalt, 1968.

TABLE 1-13

NATURE OF 197 ARTERIAL LESIONS IN
168 PATIENTS, HEIDELBERG
UNIVERSITY, SURGICAL CLINIC

Type

No.

Sharp penetrating

Blunt

Cut

Stab

Shot

Closed

Open

Modified from Vollmar J: In Hiertonn T, Rybeck B (eds):
Traumatic arterial lesions. Stockholm: Forsvarets
Forskningsanstalt. 1968.

one fourth resulted from simple domestic acci-
dents. Twelve resulted from automobile acci-
dents. It was significant in this group that 41 %
of the total resulted from blunt trauma (Table
1-13).

In 1968, Saletta and Freeark described expe-
riences with 57 patients with partially severed
major peripheral arteries treated in Chicago
(Table 1-14). Most of the injuries resulted
from physical violence from gunshot wounds

TABLE 1-14

LOCATION AND CAUSE OF INJURY IN 57 PATIENTS WITH PARTIALLY
SEVERED ARTERIES

Location and Artery

No.

Gunshot

Knife

Etiology

Glass Blunt

Other

Head and neck

Temporal

Internal carotid

External carotid

Vertebral

Lingual

Upper extremity

Axillary

Brachial

Innominate

Subclavian

Lower extremity

Femoral

Common femoral

Popliteal

External iliac

Deep femoral

Anterior tibial

Posterior tibial

Tibioperoneal

1 (needle)
1 (needle)

1 (tin can)

Modified from Saletta JD, Freeark RJ: The partially severed artery. Arch Surg 97:198-205, 1968.

chOl.qxd 4/16/04 3:20PM Page 32

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

or knives. Also, in 1968 Dillard, Nelson, and
Norman described the treatment of 85 arte-
rial injuries in St. Louis over 8 years begin-
ning in 1958 (Table 1-15). Eighty-one percent
of the injuries involved an extremity. Pene-
trating injuries from knives or glass caused 35
of the injuries, 31 resulted from gunshot
wounds, and 19 were caused by blunt trauma
or crushing injuries (Table 1-16).

Two large series are those of Drapanas and
colleagues (1970) from New Orleans, which
included 226 arterial injuries, and the cumu-
lative report by Perry, Thai, and Shires from
Dallas (1971), which included 508 arterial
injuries. At Charity Hospital in New Orleans,
226 patients with arterial injuries were treated
between 1942 and 1969 (Drapanas and col-
leagues, 1970) (Fig. 1-22). Of 226 patients,
173 had major arterial injuries and 53 had
minor injuries. The most frequently injured
arteries were the brachial (39 injuries) and
the superficial femoral (31 injuries). There
was an unusually large number (23) of aortic
injuries involving the thoracic or abdominal
aorta.

In 1971, Perry Thai, and Shires reported
additional series of 259 arterial injuries from
Dallas. About 55% of these were associated
with gunshot wounds (Table 1-17). Combined
with the 1964 report (Patman, Poulos, and
Shires) , there were a total of 508 injuries
(Table 1-18). These included 442 injuries of

TABLE 1-15

DISTRIBUTION OF ARTERIAL INJURIES,
ST. LOUIS, MISSOURI, 1958-1966

Artery

Axillary artery

7.1

Brachial artery

30.6

Subclavian artery

4.7

Thoracic aorta

9.4

Abdominal aorta and branches

9.4

Iliac artery

2.3

Common femoral artery

8.2

Superficial femoral artery

16.5

Popliteal artery

11.8

TOTAL

100.0

TABLE 1-16

ETIOLOGY AND ANATOMIC
DISTRIBUTION OF 85 ARTERIAL
INJURIES, ST. LOUIS, MISSOURI, 1958-
1966

A. Knife or glass penetrating injuries

Upper extremities

Thoracic aorta

Abdominal aorta and branches

Lower extremities

TOTAL

35(41.2%)

Penetrating gunshot injuries

Upper extremities

Thoracic aorta

Abdominal aorta and branches

Lower extremities

TOTAL

31 (36.5%)

Blunt trauma or crush injuries

Upper extremities

Thoracic aorta

Abdominal aorta and branches

Lower extremities

TOTAL

19(22.3%)

Modified from Dillard BM, Nelson DL, Norman HG Jr: Review
of 85 major traumatic arterial injuries. Surgery 63:391-395,
1968.

arteries in the extremities, representing 87%
of the total. There were also 42 cervical arte-
rial injuries and 24 visceral arterial injuries.
Moore and colleagues in 1971 reported 250
vascular injuries treated in Galveston, 45% of
which occurred in the extremities (Table
1-19) . In this series, 40% of the cases involved
either the chest, the abdomen, or the head
and neck, a percentage higher than that in
other reports. The injuries resulted from
either gunshot or stab wounds in 60% of the
group (Table 1-20) . Thirteen percent resulted
from blunt trauma, and iatrogenic injuries
were responsible for ten percent. Among the
25 iatrogenic injuries, there were 16 acute arte-
rial thromboses resulting from a total of more
than 3000 cardiovascular radiographic
procedures, a frequency of less than 1%
(Table 1-21).

Smith, Elliot, and Hageman (1974)
reported a survey of 268 patients in Detroit
with 285 penetrating wounds of the limbs and
neck. There were 127 peripheral arterial
injuries identified. Kelly and Eiseman (1975)

chOl.qxd 4/16/04 3:20PM Page 33

1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

Sup. mes.~3

S. femoral-31

■ FIGURE 1-22

Distribution of 226 acute civilian arterial injuries
covering a 30-year period in New Orleans
starting in 1942. Eighty percent of the injuries
involve arteries to the extremities. (From
Drapanas T, Hewitt RL, Weichert RF 3rd, Smith
AD: Surg 1970;172:351-360.) ■

reported 43% of 143 patients in Denver with
vascular injuries sustained gunshot wounds.
The brachial artery was injured most often,
37 times. Hardy and colleagues (1975) in
Jackson recorded 192 arterial injuries from
firearms (155 gunshot and 37 shotgun), 91
stab wounds and lacerations, 48 injuries from
blunt trauma, and 20 iatrogenic injuries. The
series included 36 aortic injuries. However,
approximately two thirds involved extremity
vessels. Cheek and colleagues (1975) reviewed
200 operative cases of major vascular injuries
in Memphis, which included 155 arterial
injuries. Bole and colleagues (1976) reported
126 arterial injuries in 122 patients in New
York City from 1968 to 1973.

Reynolds, McDowell, and Diethelm (1979)
documented results in managing 191 con-
secutive patients treated for arterial injuries
during an 8-year period at the University of
Alabama Medical Center starting in 1970. Most
of their patients sustained penetrating
wounds, either gunshot or shotgun; however,
there were also 46 patients, or 24%, who had
blunt trauma associated with their arterial
injuries. Barros D'Sa and colleagues (1980)
from the Queen's University Hospital at
Belfast reviewed their experience with missile-
induced vascular trauma over 7/ 2 years of
serious hostilities involving the civilian pop-
ulation of northern Ireland. They docu-
mented the results in managing 113 patients
with 191 vascular injuries treated at the Royal
Victoria Hospital. It is particularly important
to note that treatment commenced within 1
hour in 87% of the patients. Etiology of the

TABLE 1-17

CAUSE AND TYPE OF INJURY, CIVILIAN ARTERIAL TRAUMA, DALLAS, TEXAS

Cause

No.

Arterial Injury

Gunshot wound

143

55.2

Laceration

133

51.4

Edged instruments

35.5

Transection

38.2

Blunt trauma

9.3

Puncture

6.9

TOTAL

259

100.0

Contusion

2.7

Spasm

0.8

TOTAL

259

100.0

Modified from Perry MO, Thai ER, Shires GT: Management of arterial injuries. Ann Surg 173:403-408, 1971.

chOl.qxd 4/16/04 3:20PM Page 34

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

TABLE 1-18

DISTRIBUTION OF CIVILIAN ARTERIAL INJURIES, DALLAS, TEXAS, 508 ARTERIAL
INJURIES

Extremity (89.0%)

Cervical (8.3%)

Visceral (4.7%)

Aorta

Common carotid

Celiac

Innominate

Internal carotid

Splenic

Subclavian

External carotid

Superior mesenteric

Axillary

Vertebral

Renal

Brachial

TOTAL

Hepatic

Radial

TOTAL

Ulnar

Common iliac

External iliac

Hypogastric

Common femoral

Superficial femoral

Profunda femoral

Popliteal

Tibial

TOTAL

442

Modified from Perry MO, Thai ER, Shires GT: Management of arterial injuries. Ann Surg 173:403-408, 1971.

TABLE 1-19

LOCATION OF VASCULAR TRAUMA IN
250 CIVILIAN INJURIES, GALVESTON,
TEXAS, 1960-1970

TABLE 1-20

LOCATION OF VASCULAR TRAUMA IN
250 CIVILIAN INJURIES, GALVESTON,
TEXAS, 1960-1970

Location

Head and neck
Thoracic outlet
Chest
Abdomen
Extremities

TOTAL

Type

Gunshot

Stab

Blunt

latragenic

Other

100

TOTAL

Modified from Moore CH, Wolma FJ, Brown RW, Derrick JR:
Vascular trauma. A review of 250 cases. Am J Surg 122:576-
578, 1971.

39.0
25.0

13.0

10.0

13.0

100.0

Modified from Moore CH, Wolma FJ, Brown RW, Derrick JR:
Vascular trauma. A review of 250 cases. Am J Surg 122:576-
578, 1971.

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1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

TABLE 1-21

25 CASES OF IATROGENIC VASCULAR INJURIES, GALVESTON, TEXAS, 1960-1970

Procedure

Injury

Treatment

No.

Central venous catheterization

Thrombosis

Thrombectomy

Lumbar laminectomy

Arteriovenous fistula

Repair of fistula

Osteotomy of hip

Arteriovenous fistula

Repair of fistula

Renal hemodialysis

False aneurysm

Resection of aneurysm

arteriovenous shunts

Pelvic irradiation

Femoral artery rupture

Aortofemoral bypass

Fracture of humerus

Volkmann's ischemia

Open reduction; free

closed reduction

artery and fasciotomy

Subclavian catheterization

Arteriovenous fistula

Repair of fistula

TOTAL

Modified from Moore CH, Wolma FJ, Brown RW, Derrick JR: Vascular trauma. A review of 250 cases. Am J Surg 122:576-578,
1971.

injuries is outlined in Table 1-22. A special
group of 38 patients had "knee capping" con-
tributed to most of the popliteal vascular
injuries.

Koivunen (1982) documented the experi-
ence in managing vascular trauma in a rural
population in Missouri. During a 10-year
period, they identified 89 cases of vascular
trauma. Recognizing that the considerable
delay in abdominal vasculature accounted for
33.7% of the injuries. Multiple injuries were
common, with 1057 patients having two or
more concurrent vascular injuries. There
were three patients who had four or more sep-
arate vascular injuries. The increasing inci-

TABLE 1-22

INCIDENCE OF VASCULAR INJURIES
RELATED TO TYPE

Wounding Missile

Patien

No.

Bullet

Low velocity

42.5

High velocity

24.8

Uncertain velocity

19.5

= ragments from explosions

13.2

TOTAL

113

From Barros D, Sa AA, Hassard TH, Livingston RH, et al:
Missile-induced vascular trauma. Injury 12:13-30, 1980.

dence of vascular trauma in urban centers is
emphasized by the marked increase from an
average of 27 patients per year in the early
1960s to nearly a tenfold increase to the
current average of 213 patients peryear. These
data can be compared and contrasted to other
civilian and military experience, as noted in
Table 1-23.

Feliciano and colleagues (1984) reported
a 1-year experience with 456 vascular and
cardiac injuries among 312 patients during
1982 at the Ben Taub Hospital in Houston.
More than 87% of the injuries were pene-
trating, as identified in Table 1-24. Specifi-
cally, there were 408 vascular injuries and 48
cardiac injuries. Thirty-four percent of the
patients had two or more vascular or cardiac
injuries. The majority were penetrating, with
more than 87% secondary to gunshotwounds,
stab wounds, or shotgun wounds. The largest
number of injuries occurred in the extremi-
ties, 39.9%, with the brachial artery being the
most common arterial injury. There was a rel-
atively large number of abdominal vascular
injuries, accountingfor 31.9% of the total. The
most common venous injury occurred in the
internal jugular vein in 26 patients.

Mattox and colleagues (1989) detailed a
unique epidemiologic evolutionary profile
from the civilian trauma registry at Baylor
College of Medicine in Houston. During a 30-
year period from 1958 to 1987, where con-
sistent evaluation and treatment philosophy

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

TABLE 1-23

LOCATION OF REPORTED VASCULAR INJURIES IN MAJOR WARS

Neck

Chest Abdomen Upper Extremity Lower Extremity Total

Makins (WWI 4 )

176

—

367

648

1202

DeBakey(WWII 2 )

—

871

1517

2471

Hughes (Korea 3 )

—

109

304

Rich (Vietnam 7 )

354

416

840

1377

TOTAL

300

421

1763

3179

5667

LOCATION OF CARDIOVASCULAR INJURIES IN CIVILIAN EPIDEMIOLOGIC
VASCULAR TRAUMA REPORTS

Author

City

Year

Neck

Chest

Abdomen

Upper
Extremities

Lower
Extremities

Total

Morris 19

Houston

1957

136

Ferguson 13

Atlanta

1961

200

Smith 23

Detroit

1962

Treiman 24

Los Angeles

1966

233

Dilard 10

St. Louis

1968

Drapanas 11

New Orleans

1970

226

Perry 21

Dallas

1971

213

141

508

Moore 16

Galveston

1971

250

Cheek 9

Memphis

1975

200

Kelly 15

Denver

1975

—

175

Hardy 16

Jackson

1975

116

360

Bole 8

New York

1976

126

Sirinek 22

San Antonio

1983

218

—

270

TOTAL

315

206

725

850

763

2859

From Mattox KL, Feliciano DV, Burch J, et al: Five thousand seven hundred sixty cardiovascular injuries in 4459 patients.
Epidemiologic evolution, 1958 to 1987. Ann Surg 209:698-707, 1989.

TABLE 1-24

MECHANISMS OF INJURY; ALL
VASCULAR AND CARDIAC INJURIES

Mechanism

Gunshot wound
Stab wound
Shotgun wound
Laceration
Iatrogenic
Blunt

TOTAL

No.

166(53.2%)
88 (28.2%)
18(5.8%)
17 (5.4%)
14(4.5%)
9 (2.9%)

312 (100%)

87.2%

From Feliciano DV, Bitando CG, Mattox KL, et al: Civilian
trauma in the 1980s. A 1-year experience with 456 vascular
and cardiac injuries. Ann Surg 199:717-724, 1984.

existed, they treated 5760 cardiovascular
injuries in 4459 patients. Eighty-six percent
of the patients were male, with an average age
of 30years. Penetrating trauma accounted for
more than 90.0% of the injuries, with 51.1%
resulting from gunshot wounds, 31.1% from
stab wounds, and 6.8% from shotgun wounds
(Table 1-25). The remaining injuries were
iatrogenic or secondary to blunt trauma. Table
1-26 outlines the specific cardiovascular
injuries by etiology and grouped by body
region. Of particular interest and note, and
in marked contrast with military experience
and many previous civilian series, truncal
injuries, including the neck, accounted for
66% of all injuries treated. The lower extrem-
ities, including the groin, accounted for only
19% of the injuries, specifically, injuries to the
six patients. In the decade of the 1980s, there
was marked increase in the number of

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1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

TABLE 1-25

ETIOLOGY OF PATIENT CARDIOVASCULAR INJURIES PER 5-YEAR TIME INTERVAL

Etiology

1958-1963 1964-1968 1969-1973 1974-1978 1979-1983 1984-1988 Total

Gunshot wound

236

436

501

625

456

2296

Stab/laoeration

110

161

229

362

463

1389

Blunt trauma

304

Shotgun wound

214

Iatrogenic

Other/unknowns

111

225

TOTAL

163

399

811

900

1117

1069

4459

From Mattox KL, Feliciano DV, Burch J, et al: Five thousand seven hundred sixty cardiovascular injuries in 4459 patients:
Epidemiologic evolution 1958 to 1987. Ann Surg 209:698-707, 1989.

manuscripts devoted to the management of
civilian vascular trauma culminated by the
extensive review of Mattox and colleagues.

During the 1990s, there continued to be a
significant number of reports of the man-
agement of civilian arterial injuries. Oiler and
colleagues (1992) established a State Trauma
Registry that had an early report of 1148 vas-
cular injuries suffered by 9 78 patients in North
Carolina over 39 months (October 1987 to
January 1991) (Table 1-27). Whether human
made or natural, there will continue to be
trauma patients with associated vascular
injuries. Internationally Kurtoglu and col-
leagues (1991) described treating 115 periph-
eral arterial injuries in Istanbul (Table 1-28) .
There will be additional details throughout
the text emphasizing the recent experience
of the past decade. The following, however,
identifies areas of historical significance
related to specific considerations involving
vascular injuries.

HISTORICAL NOTES ON 20th
CENTURY PROGRESS WITH
VENOUS INJURIES

It could be recorded in history that
outstanding contributions based on
experience of managing Vietnam casualties
by American military surgeons did as much
to stimulate and direct interest and success

in repair of venous injuries as was
established during the Korean Conflict with
repair of arterial injuries. Vietnam Vascular
Registry, Rich (1977)

Several excellent historic reviews of the
development of venous trauma have been pub-
lished (Haimovici, 1963; Shumacker, 1969;
Rob, 1972). Two earlier outstanding refer-
ences are Guthrie (1912) andMurphy (1897).
As early as 1816, Travers supposedly closed a
small wound in a femoral vein. In 1830,
Guthrie reported more precisely that he
closed a laceration of the internaljugular vein
by placing a tenaculum through the cut
edges, after which he tied a suture around the
tenaculum to constitute a lateral ligature. In
1878, Agnew used lateral sutures to close
venous wounds. Only a year earlier, Eck had
performed the first vascular anastomosis by
suturing the portal vein to the inferior
vena cava. Schede in 1882 in Germany is
generally given credit for performing the
first successful lateral suture repair of a lac-
eration in a vein in clinical practice, and he
advocated repair ofwounds of the femoral vein
in man.

In the late 19th century, other surgeons who
with apparent success sutured wounds of veins
include Billroth, Braun of Koenigsberg, and
Schmidt. In his experimental laboratory,
Hirsch in 1881 successfully repaired divided
veins in dogs. When Dorfler in 1889 outlined
his method of arterial repair, he recom-
mended the same technique for repairing

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

TABLE 1-26

SPECIFIC CARDIOVASCULAR INJURIES BY ETIOLOGY AND GROUPED BY
BODY REGION

Gunshot Stab wound/
wound laceration

Blunt Shotgun Unknown/

trauma wound lateogenic Other

Total

Carotid artery

115

—

190

Jugular vein

116

154

—

296

Vertebral artery

—

Subclavian vessel

—

168

Heart

220

261

539

Coronary artery

—

Ascending aorta

—

Innominate artery

—

Pulmonary artery

—

Desc thorac aorta

—

Aortic arch

—

Thorac vena cava

—

Innominate vein

—

Pulmonary vein

—

Azygous vein

—

Thoracic duct

—

Int mammary artery

—

Intercostal artery

—

Abdominal aorta

180

249

Inf vena cava

353

100

—

535

Mesentric artrey

136

—

216

Portal venous

116

—

189

Iliac artery

172

232

Iliac vein

224

289

Renal vessel

—

163

Epigastric artery

—

Hepatic veins

—

Axillary vessel

143

Brachial artery

184

163

446

Radial/ulnar art

169

261

Cephalic/basilic vein

—

Femoral artery

316

500

Femoral vein

184

—

280

Popliteal artery

—

156

Popliteal vein

—

Tibial artery

—

Tibial vein

—

Saphenous vein

—

TOTAL

3134

1543

385

341

293

5760

From Mattox KL, Feliciano DV, Burch J, et al: Five thousand seven hundred sixty cardiovascular injuries in 4459 patients:
Epidemiologic evolution 1958 to 1987. Ann Surg 209(6):698-707, 1989.

veins. Haimovici (1963) described Dorfler's
method, "The essential features of this method
consisted of the use of fine, round needles
and fine silk and his suture was continuous,
embracing all of the coats of the vessel. From

his experience, although limited to 16 cases,
he concluded that aseptic silk thread in the
lumen of the vessel does not necessarily lead
to thrombosis and, therefore, the penetration
of the intima was not contraindicated."

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1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

TABLE 1-27

VASCULAR INJURIES IN A RURAL
STATE: A REVIEW OF 978 PATIENTS
FROM A STATE TRAUMA REGISTRY

Vessels Injured by Region

Head carotid and neck

Common

Internal

External

Unspecified

Jugular internal

Other vessels of neck
Thorax

Aorta

Innominate/subclavian A & V

Pulmonary vessels

Intercostals, mammary, superior
vena cava, other, unspecified
Abdomen/pelvis

Aorta

Interior vena cava

Celiac and mesenteric artery

Porta and splenic vessel

Renal vessel

Iliac vessels

Ovarian, other, unspecified
Upper extremity

Axillary vessels

Brachial vessels

Radial artery

Ulnar artery

Digital

Other, unspecified
Lower extremity

Common femoral artery

Superficial femoral artery

Femoral vessel

Popliteal artery

Popliteal vein

Popliteal vessels

Tibital vessels

Plantar, other, unspecified

No. (%)

133(9.9)

17
9

63
166(12.4)

211 (15.7)

30
361 (26.9)

22
271 (20.2)

From Oiler DW, Rutledge R, Clancy T, et al: Vascular injuries
in a rural state: a review of 978 patients from a state trauma
registry. J Trauma 32:740-746, 1992.

In 1889, Kummel performed the first clin-
ical end-to-end anastomosis of a femoral vein.
In 1901, Clermont successfully reunited the
ends of a divided vena cava with a continuous
fine silk suture. A month later, the lumen of
the vena cava was found to be smooth and
unobstructed at the site of the anastomosis.
Jensen in 1903 was successful in four of seven

TABLE 1-28

ETIOLOGIC FACTORS MANAGEMENT
OF VASCULAR INJURIES OF THE
EXTREMITIES (115 CASES)

Etiologic Factors Number of Cases

Penetrating trauma
Stab wounds
Traffic accidents
Gunshot injury
Industrial accidents
Failing from heights
latragenic

50
25
22
9
5
2
2

43
21
19
8
5
2
2

From Kurtoglu M, Ertekin C, Bulut T, et al: Management of
vascular injuries of the extremities: 1 15 cases, Int Angiol
10:95-99, 1991.

operations in anastomosing transected veins,
using a continuous suture technique.

In World War I the clinical use of lateral
suture repair of venous lacerations was
reported by Goodman (1918). He reported
experiences with five patients with vascular
injuries in whom a lateral suture repair of
venous lacerations was done in four, involv-
ing two popliteal and two superficial femoral
veins. The defects ranged from 5 to 20 mm in
length. The results are unknown because there
was no follow-up evaluation.

The importance of venous repair was min-
imized by the proposal of Makins in 1917,
which was that the concomitant vein should
be ligated when an arterial injury was treated
by ligation. The results reported by Makins to
support this hypothesis were later found to
have no statistical significance (Table 1-29) .
The influence persisted even until World
War II. Data from World War II showed no
benefit from ligation of the concomitant
vein, however (DeBakey and Simeone,
1946). During the Korean Conflict, repair
of injuries of major veins was again under-
taken in selected patients (Hughes, 1959).
This was expanded in Vietnam (Rich, 1970 to
1995).

One of the most bizarre recommendations
in the history of vascular surgery is the mid-
19th century recommendation that ligation
of the concomitant uninjured artery should
be done when a venous injury was treated by

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

TABLE 1-29

A COMPARISON OF THE RESULTS OF LIGATIONS OF THE ARTERY ALONE WITH
THOSE OF SIMULTANEOUS LIGATIONS OF ARTERY AND VEIN

Artery

Alone

Artery

and Vein

No. of

Good

Percent

No. of

Good

Percent

Cases

Result

angrene

Gangrene*

Cases

Result

Gangrene

Gangrene*

Subclavian

25.0

—

0.0

Axillary

16.6

—

0.0

Brachial

23.0

—

0.0

= emoral

25.0

21.0

Popliteal

41.6

21.4

Tibial

—

0.0

—

0.0

Carotid

3.3

25.0

TOTAL

101

28.0

19.7

*AII the percentages were added to the table by the author, except the total percentages, which appear in Makins' original table
Modified from Montgomery ML: Arch Surg 1932;24:1016-1027.

ligation (Rich and Rob, 1996) . Apparently this
astonishing recommendation was first made
by Gensoul in 1883, who feared the hazards
of venous engorgement if the vein alone was
ligated. Other surgeons (Dupuytren, 1839;
Chassaignac, 1855; Langenbeck, 1861; Pilch er,
1886) made similar recommendations,
although these were intended primarily to
minimize hemorrhage with venous injuries
(Simeone, Grillo, and Rundle, 1951).

Moreover, during the Korean Conflict,
there was a renewal of interest in repair of the
involved vein during the elective repair of
arteriovenous fistulas that usually was per-
formed several months after the initial injury.
Traditionally such fistulas were treated by lig-
ation of both the artery and the vein. The tech-
nique of repair gradually evolved to include
repair of the artery and often repair of the
concomitant vein. Successful results in such
patients generated some enthusiasm for repair
of acute venous injuries (Hughes, 1958):

. . noted 63 percent major vein injuries
accompanying major artery injuries. A
number of other vein injuries were treated in
which there was no arterial involvement.
Most of these veins were treated by ligation,
but in some, ligations resulted in various

degrees of venous stasis. On rare occasion,
massive venous stasis resulted in
amputation of the extremity. To eliminate this
complication two investigators . . . [sic]
Hughes and Spencer independently . . .
began the repair of major veins. They
reported 20 major veins repaired, all by
lateral suture except one which was
repaired by direct anastomosis. Some of
these are known to have thrombosed later
without complications. No embolic
complications resulted.

A review concerned primarily with the
management of venous injuries in civilian
practice was published by Caspar and Treiman
in 1960; it described injuries of 52 major veins
in 51 patients. Venous reconstruction when
performed was usually by lateral suture.

During the Vietnam Conflict, with the
interest and experience resulting from the
necessity of treating thousands of vascular
injuries, there was a significant effort to
perform venous repairs in the last 5 years of
the conflict (from 1968 to 1972). In a sym-
posium on venous surgery in the lower extrem-
ities atWalter Reed Army Institute of Research,
the combined experiences of both civilian and
military surgeons were summarized (Swan and

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1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

colleagues, 1975) . Venous Trauma, by Hobson,
Rich, and Wright (1983) , reviews civilian and
military experience with venous injuries.

Venous injuries are unimportant to many
surgeons, so the true frequency is not docu-
mented accurately. This is particularly true in
the case of combined arterial and venous
injuries. Analysis of the Vietnam experience
found numerous cases in which venous trauma
was not documented in the records. The first
major interest in the frequency of venous
injuries in military trauma was during the
Korean Conflict. In analysis of 180 acute vas-
cular injuries (Table 1-30), Hughes (1954)
found nearly as many injuries in major veins
(71) as there were in major arteries (79). Sim-
ilarly, in civilian practice, the frequency of
venous trauma was documented only occa-

TABLE 1-30

INCIDENCE OF ACUTE VASCULAR
TRAUMA IN KOREAN CASUALTIES

Vessel

No.

Major

arteries

43.9

Major

veins

39.4

Minor

arteries

16.7

TOTAL

180

100.0

Modified from Hughes CW: Acute vascular trauma in Korean
casualties: analysis of 180 cases. Surg Gynecol Obstet
99:91-100, 1954.

sionally, most reports describing only arterial
trauma until 1980. There are numerous large
series of arterial injuries reported thatgive no
details regarding venous trauma and this con-
tinues through 1996. The report by Caspar
and Treiman (1960) is one of the first to have
a detailed analysis of venous injuries alone.
In a group of 228 patients with vascular injuries
at the Los Angeles County General Hospital
over a period of 10 years, about 22% (51
patients) had venous injuries. The superficial
femoral vein was most commonly injured
(nine times) . The inferior vena cava and the
internal jugular vein were each injured eight
times, and the brachial veins seven. In 1966
40 patients were added to the original series
in a supplementary report by Treiman. The
frequency of venous injury in the different
locations is shown in Table 1-31. Mullins,
Lucas, and Ledgerwood (1980) published a
large series of civilian venous injuries from
Detroit.

In the preliminary Vietnam Vascular Reg-
istry report, approximately one fourth of the
patients had venous trauma (Table 1-32)
(Rich and Hughes, 1969). There were only
28 injuries of isolated veins, and most of the
venous injuries were combined with arterial
trauma. The increased incidence of venous
trauma when associated with arterial trauma
was emphasized in an interim Registry report,
which documented concomitant venous
injuries in 37.7% of cases with acute major
arterial trauma (Table 1-33) (Rich, 1970).

TABLE 1-31

INCIDENCE OF VENOUS INJURIES

No.

Total

Vein

1948-1958

1958-1963

1948-1963

Axillary brachial

14.1

Innominate subclavian

8.7

Superior vena cava

1.1

Inferior vena cava

13.0

Iliac

12.0

Femoral

18.5

Other

32.6

TOTAL

100.0

Modified from Treiman RL, Doty D, Gaspar MR: Acute vascular trauma a fifteen year study. Am Surg 1 11:469-473, 1966.

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

TABLE 1-32

INCIDENCE OF VENOUS TRAUMA;
PRELIMINARY VIETNAM VASCULAR
REGISTRY REPORT (500 PATIENTS)

Total vascular injuries

718

Venous injuries

194

(27.0%)

Isolation

(14.4%)

Combined

166

(85.6%)

Modified from Rich NM, Hughes CW: Vietnam vascular
registry: a preliminary report. Surgery 65:218-226, 1969.

TABLE 1-33

CONCOMITANT VENOUS TRAUMA
ASSOCIATED WITH ACUTE ARTERIAL
TRAUMA

Cases
Venous injuries

1000
377

(37.7%)

Modified from Rich NM, Baugh JH, Hughes CW: Acute
arterial injuries in Vietnam: 1000 cases. J Trauma
1970;10:359-369.

■ FIGURE 1-23

Clinical success is demonstrated
angiographically by the patent compilation vein
graft used to repair an injured common femoral
vein. (Courtesy Dr. William G. Sullivan.) ■

Combat situations provide fertile opportuni-
ties for young surgeons to learn by managing
many similar injuries in a short period under
similar circumstances and this has been
emphasized repeatedly. Over an 8-year period
in Vietnam (from 1965 to 1972), this oppor-
tunity was provided for approximately 600
young U.S. surgeons. The consensus devel-
oped toward an increased emphasis for repair
of major lower extremity veins that were
injured with a particular emphasis for repair
of the popliteal vein. Valid statistical data are
still badly needed to determine the best
method of venous repair, especially when end-
to-end venous anastomosis or vein grafts are
required. Only by such long-term evaluation
can the reliability of different types of venous
reconstruction be determined. Figure 1-23
demonstrates patency of a compilation graft
of autogenous greater saphenous vein used
successfully to repair a defect in the left
common femoral vein. Although this repair
was successful in the immediate postoperative

period, it is also important to know whether
long-term patency can be anticipated. The
second important area in which long-term
data are needed is the frequency of signifi-
cant venous insufficiency following ligation.
Because venous insufficiency may not develop
for several years, often after repeated episodes
of phlebitis induced by stasis from the origi-
nal vein ligation, long periods of observation
are necessary. Another consideration is the
possibility of delayed venous reconstruction
in some patients with chronic venous insuffi-
ciency following ligation. In such patients,
serial venography may be useful. This is
shown in a report by Rich and Sullivan (1972)
of a patient with recanalization of an autoge-
nous vein graft in the popliteal vein (Figs.
1-24 and 1-25). Early recanalization can be
seen in Figure 1-26. Additional phlebograms
area needed in the extended follow-up, and
some findings have been encouraging, such
as the long-term patency %/ % years after lateral
suture repair (Fig. 1-27).

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1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

■ FIGURE 1-24

This venogram was performed 72 hours
postoperatively at the 12th Evacuation Hospital
in the Republic of Vietnam. It revealed
thrombosis of the autogenous cephalic vein
graft placed in the right popliteal vein. (From
Rich NM, Sullivan WG: J Trauma 1972;12:919-
920.) ■

The importance of repair of the popliteal
vein when associated with injuries of the
popliteal artery is discussed in further detail
in Chapter 18. Recently, additional experience
has been accumulated regarding the use of
adjunctive measures. Schramek and Hash-
monai (1974) and Schramek and colleagues
(1975) in Israel have used a branch of the pro-
funda femoris artery to reconstruct a distal
arteriovenous fistula with an autogenous vein
graft for repair of the femoral in three patients
(Fig. 1-28).

A study from the Vietnam Vascular Registry
(Rich and colleagues, 1976) evaluates the man-
agement and long-term follow-up of 110
patients with isolated popliteal venous trauma.
Nearly an equal number were repaired and
ligated. Thrombophlebitis and pulmonary
embolism were not significant complications
in this series. The only pulmonary embolus
occurred after ligation of an injured popliteal
vein. However, therewas a significant increase

■ FIGURE 1-25

An additional venogram was performed at
Walter Reed General Hospital approximately
4 1 / 2 months following a venogram performed in
Vietnam (see Fig. 1-24). Note recanalization of
the 3-cm cephalic vein graft in the right
popliteal vein. (From Rich NM, Sullivan WG: J
Trauma 1972:12:919-920.) ■

in edema in the involved extremity following
ligation of the popliteal vein (Table 1-34) .
Rich (1977) also provided a 10-year follow-up
of 51 Vietnam casualties who had lower
extremity venous injuries repaired using au-
togenous interposition venous grafts. Only
onepatient (2%) developed thrombophlebitis
in the postoperative period and this was tran-
sitory in nature (Table 1-35) .

Although repair rather than ligation of arte-
rial injuries has been widely and enthusiasti-
cally accepted for the past 40 years, the same
approach has not developed for venous

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

■ FIGURE 1-26

The venogram shows minimal recanalization of
a segment of the left greater saphenous vein,
which was used to repair the right popliteal vein
2 1 / 2 months earlier in Vietnam. Also note some
of the remaining collateral venous
development. Interestingly, the patient had no
distal edema. (From Rich NM, Hobson RW: In
Swan KE, et al. [eds]: Venous Surgery in the
Lower Extremity. St. Louis: Warren H. Green
Publishers, Inc., 1975.) ■

■ FIGURE 1-27

Venogram demonstrating patency of the
popliteal vein at its junction with the superficial
femoral vein. Note the metallic fragments that
caused the injury. The vein was repaired by
lateral suture 3 1 / 2 years earlier in Vietnam.
Repair of concomitant venous injuries is
advocated as one of the methods that will help
lower the relatively high amputation rate
associated with popliteal artery trauma. (From
Rich NM, Jarstfer BS, Geer TM: J Cardiovasc
Surg 1974;15:340-351.) ■

injuries (Fig. 1-29) . In many instances, these
have been simply treated by ligation. There
are several reasons for this paucity of interest
in repair. First, many veins can be ligated and
little or no disability follows. Even when very
large veins are ligated, the extremity may not
be threatened, although months or years later
venous insufficiency may appear. Second, the
effectiveness of repair of many venous injuries
is uncertain. With the low pressure in the
venous system, thrombosis is much more
common than it is after repair of arterial

injuries. Acquisition of data to show the effec-
tiveness of repair is particularly difficult
because there is no simple method for patency
of a venous reconstruction; with arterial
repair, simple palpation of a peripheral pulse
is usually adequate.

The degree of disability from chronic
venous insufficiency is not recognized by
many, because it may become evident only
months or years after injury. A clinical example
of disability including venous stasis, edema,
skin pigmentation, and ulceration following

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1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

■ FIGURE 1-28

Operative photograph showing the H-type
arteriovenous fistula, which measures
approximately 1 cm in length and 8 mm in
diameter (arrow), constructed approximately 2
to 3 cm distal to the suture line of the vein graft
(between two vascular forceps) in the femoral
vein of the canine model. Patency of the
autogenous vein graft in the venous system
was enhanced by the adjuvant distal
arteriovenous fistula. (From Rich NM, Levin PM,
Hutton JE Jr: In Swan KE, et al. Venous Surgery
in the Lower Extremity. St. Louis: Warren H.
Green Publishers, Inc., 1975.) ■

TABLE 1-34

INCIDENCE OF EDEMA FOLLOWING
LIGATION AND REPAIR OF INJURED
POPLITEAL VEINS

Management

No.

Ligation
Repair

57
53

With
Edema

29
7

50.9
13.2

Modified from Rich NM, Hobson RW, Collins GJ Jr, Anderson
CA: The effect of acute popliteal venous interruption. Ann
Surg 183:365-368, 1976.

TABLE 1-35

COMPLICATIONS OF VENOUS REPAIR
USING AUTOGENOUS VENOUS
GRAFTS

Complication

Thrombophlebitis

2.0

Pulmonary embolism

0.0

Amputation

0.0

Death

0.0

Edema

None
Early
Residual

TOTAL

66.6

21.6

11.8

100.0

From Rich NM, Collins GJ, Andersen CA, McDonald PT:
Autogenous venous interposition grafts in repair of major
venous injuries. J Trauma 17:512-520, 1977.

ligation of the superficial femoral and greater
saphenous veins is shown in Figure 1-30.
Because of the uncertainty of the importance
and the effectiveness of repair of venous
injuries, an analysis and a preliminary report
from the Vietnam Vascular Registry were pre-
pared in 1970; this report encouraged the
repair of major veins in the lower extremities
(Rich, 1970). Although data thus far are
meager and the effectiveness of some types
of venous reconstruction is yet unproved,
certain clinical guidelines are now well
established.

Venous trauma remains a continuing chal-
lenge with controversy regarding appropriate
management. Selective references (1980-
1996) emphasize experience from an expand-
ing literature. Ironically, John B. Murphy
emphasized in 1987 in Chicago that injured
veins, like injured arteries, should be repaired.
Including all medium and large-caliber veins
in a general description might add to the exist-
ing confusion. There is a considerable dif-
ference in injury to the inferior or superior
vena cava compared and contrasted to the axil-
lary or superficial femoral veins, with the latter
two being duplicated more frequently. Addi-
tional controversial exchanges have centered
on the management of injured veins by liga-
tion or repair particularly in larger caliber

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46 I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

■ FIGURE 1-29

This exhibit, entitled "Management of Venous Injuries: Clinical and Experimental Evaluation," has
been used to stimulate an increased interest in the repair of venous injuries. Although repair of
arterial injuries has been accepted during the past 20 years, all too often the repair of venous
injuries has been treated with minimal interest and even disdain. (A. F.I. P. photograph.) ■

lower extremity veins. It has been widely rec-
ognized that most patients can tolerate liga-
tion of injured veins, although the contest has
been in identifying the challenge to determine
which patients will not tolerate the ligation of
medium and larger veins, again, particularly
in the lower extremities. General agreement
emphasizes that the patient's overall condi-
tion must be considered primarily, and the
requirement to save a patient's life when mul-
tiple injuries are present may necessitate lig-
ation of injured veins. Prevention of long-
term disability, particularly from lower extrem-
ity swelling, on the other hand, should be
considered and this is what has emphasized
the importance to place a priority on the
repair of major lower extremity veins when
possible.

Venous repair may be important in at least
three circumstances. First, when popliteal
injuries, repair of the vein may be necessary
to prevent loss of the leg despite successful
arterial reconstruction. This observation was
first made during the Korean Conflict and has
been confirmed repeatedly since that time
(Hobson and Rich, 1995; Rich, 1995). Amajor
factor in this decision is the anatomy of the
popliteal space, where an injury often criti-
cally impedes venous return from the lower
extremity. Second, venous repair may be nec-

essary in the presence of massive soft tissue
injury in the extremities, where the wide-
spread loss of soft tissue interrupts venous
return to a crucial degree. Third, repair should
be routinely considered with large veins,
especially when the damage is proximal to the
profunda femoris, to prevent chronic venous
insufficiency. This includes the common
femoral, and the external and common iliac
veins.

For a long time, a natural concern with
repair of venous injuries was the fear of pro-
ducing venous thrombosis and pulmonary
embolization. Though an apparently likely
hazard, this dangerous sequence has been sur-
prisingly absent. Conceivably, small emboli
may not be recognized clinically, but the
absence of clinically detectable pulmonary
emboli has been uniformly documented in
both the Vietnam Vascular Registry and in civil-
ian reports (1980 to 1995).

There have been an increasing number of
reports from the civilian community in the
United States and from a variety of locations
around the world since the documented
experience from U.S. surgeons in Vietnam.
Confirming and conflicting military and civil-
ian experiences have been reported. Civilian
reports have identified that ligation of injured
veins, including those in the lower extremi-

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1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

■ FIGURE 1-30

Chronic venous insufficiency has been seen in
the Registry with increasing frequency in
patients who had lower extremity venous
ligation in Vietnam. In addition to edema, other
changes similar to the postphlebitic syndrome
have been evident, including venous stasis
changes in the skin and even some superficial
ulcerations. Some of these changes are
present in the right lower extremity of this
patient, who had ligation of his superficial
femoral vein. (Walter Reed General Hospital
1969. Vietnam Vascular Registry #225,
NMR.) ■

ties, did notresultin significantmorbidity. Rec-
ognizing that civilian and military wounds are
considerably different, this should not be a
surprise. Civilian wounds had in general less
soft tissue destruction, less interruption of lym-
phatics, and less interruption of venous col-
laterals with fewer associated fractures with
wounds resulting more often from knives or
low-velocity handguns in contrast to the more
massive military wounds, which lead to increas-

ing morbidity with ligation of major caliber
veins, particularly in the lower extremities.
Ideally, determination of patients injeopardy
for complications would be desired. Nonin-
vasive examinations, ambulatory venous pres-
sures, and phlebography can all be of
assistance. These studies are, however, often
impractical. Also, it is important to empha-
size the inconsistency in venous anatomy. It
would be helpful to know the anatomy before
making claims regarding success or failure of
management whether by ligation or repair.
In summation, it is important to emphasize
the difference in wounds in civilian and mil-
itary experiences around the world recog-
nizing that many civilian wounds have become
more military in nature in recent years. This
latter fact emphasizes the validity of continu-
ing to analyze the military experiences. Long-
term follow-up remains a major requirement.
Nevertheless, it is becoming increasingly
obvious that there are patients who suffer life-
long disability from ligation of medium and
larger caliber lower extremity veins. Many
studies have evaluated the pathophysiology of
acute interruption of major caliberveins. Cor-
relation with clinical experiences and long-
term follow-up are part of the remaining
challenge.

SPECIAL HISTORIC
OBSERVATIONS

Site of Injury

The specific site of arterial injury is impor-
tant. All of the cited series, except that of
Mattox in 1989, emphasize the predomi-
nance of extremity arterial injuries. On the
other hand, arterial injuries in the thorax or
abdomen may be more difficult to diagnose
or may present additional problems in man-
agement. There has been a relatively high mor-
tality rate associated with arterial injuries at
the base of the neck as a result of uncontrol-
lable hemorrhage and cerebral ischemia. In
1964, Pate and Wilson described experiences
with 21 patients with arterial injuries at the
base of the neck treated at the City of Memphis
Hospital over a 12 year period. As would be

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

expected, there was a significant percentage
of permanent crippling neurologic injuries.
The interesting observation was made that
93% of the patients who were stabbed were
injured on the left side, suggesting that most
of the assailants were right handed.

Until the past 20 years, little had been pub-
lished about intra-abdominal vascular injuries,
perhaps because most victims died of exsan-
guinating hemorrhage. In 1968, Perdue and
Smith reported a group of 90 patients with
126 separate injuries treated in Atlanta over
a period of 10 years beginning in 1956. Most
injuries resulted from low-velocity bullet
wounds. Five were injured with a shotgun and
fourteen were stab wounds. Mattox's epi-
demiologic study reported in 1989 empha-
sized the increasing number of truncal
vascular injuries from civilian vascular expe-
rience in contrast to the military vascular expe-
rience where extremity arteries are involved
predominantly.

Iatrogenic Injury

Of historical interest is the fact that one of
the first hospital-incurred vascular injuries
(iatrogenic injuries) was described approxi-
mately lOOyears ago. Murphy (1897) reported
that Heidenhain used a catgut suture to
close a 1-cm laceration of the axillary artery,
accidentally injured during removal of
adherent carcinomatous glands on May 28,
1894. The patient made a good recovery with
no disturbance of the circulation in the
extremity.

Several reports have described arterial
injuries complicating the removal of a herni-
ated nucleus pulposus; usually the injury
involves the common iliac artery. One of the
first detailed reports of this complication was
made by Seeley (1954). The injury resulted
from the anatomic location of the iliac vessels
on the anterior surface of the lumbar verte-
brae, especially at the intervertebral spaces
between the fourth and fifth lumbar vertebrae
and between the fifth lumbar and first sacral
ribs. In addition to the anatomic susceptibil-
ity to injury, the use of a pituitary rongeur for
removal of the intervertebral discs was found
to predispose to this type of injury (Fig. 1-31) .

Common Iliac Vs. Rt. Common Iliac A.

■ FIGURE 1-31

Manner in which the common iliac artery can
be injured while using an angled pituitary
rongeur at the intervertebral space between L4
and L5 during removal of a herniated nucleus
pulposus. (From Seeley SF, Hughes CW,
Jahnke EJ Jr: Surgery 1954;35:421-429.) ■

At least eight such cases have been seen at
Walter Reed General Hospital over a period
of 25 years, including the report by Jarstfer
and Rich (1976). Salander and colleagues
(1984) expanded the Walter Reed Army
Medical Center report to six patients oper-
ated on from 1949 to 1982 for vascular injury
following lumbar disc surgery. All six patients
had common iliac artery injuries.

Arteriovenous fistulas have occurred at
numerous sites after ligation in continuity of
an artery and a vein, such as a renal artery
and vein following nephrectomy, the splenic
artery and vein following splenectomy, or the
superior thyroid artery and vein following
thyroid lobectomy. Pritchard and colleagues
(1977) reported an interesting case of trau-
matic popliteal arteriovenous fistula follow-
ing meniscectomy treated at the Mayo Clinic.
Jimenez and colleagues (1988) presented an
interesting case of a popliteal artery and
venous aneurysm as a complication of arthro-
scopic meniscectomy. There was an associated
arteriovenous fistula. It was emphasized that

chOl.qxd 4/16/04 3:20PM Page 4 9

1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

this is a rare finding following open surgical
techniques.

In 1968, Dillard, Nelson, and Norman
described an arterial injury developing from
a Kirschner wire placed through the popliteal
artery while applying skeletal traction for a
femoral fracture. Saletta and Freeark (1972)
described injury of the profunda femoris
artery caused by a drill point during an ortho-
pedic procedure. Injuries of the femoral
artery and vein have occurred during inguinal
herniorrhaphy, especially during attempts to
control hemorrhage with deep, blindly
inserted sutures. A series of 11 iatrogenic
injuries were reported by Lord and colleagues
in 1958 (Table 1-36). Although retrograde
dissection of an iliac artery and the aorta
have been uncommon, Kay, Dykstra, and Tsuji
(1966) have emphasized this catastrophic
complication of cannulation and perfusion
of the common femoral artery in open
heart surgery. Aust, Bredenberg, and Murray
(1981) reported five cases of arterial compli-
cations associated with total hip replacement.
All five injuries resulted from intraoperative
injury.

Kozloff and colleagues (1980) presented a
report of eight patients seen over 18 months
who had significant iliofemoral arterial com-
prise secondary to cannulation for car-
diopulmonary bypass or intra-aortic balloon
pumping. Perler and colleagues (1983) doc-
umented an incidence of vascular complica-
tions of 8.8 percent utilizing the intra-aortic
balloon pump in 794 patients at the Massa-
chusetts General Hospital in Boston. Eighty-
seven major vascular complications occurred
in 70 patients. Specifically, 36 patients had a
limb ischemia and arterial trauma occurred
in 20. No limbswere lost. Todd and colleagues
(1983) identified vascular complications
related to percutaneous intra-aortic balloon
pump inserted in 112 patients (Table 1-37).
While six patients had reversal of ischemic
signs following removal of the device, nine
patients required exploration of the femoral
artery for thrombectomy, femoral laceration
repair, or false aneurysm repair.

Vascular injuries following angiographic
procedures have increased in number with the
rapid development of precise techniques of
angiography. The actual incidence of these

injuries has decreased somewhat with the avail-
ability of skilled vascular radiologists, specifi-
cally trained for angiography, but the
increasing utilization of such diagnostic tech-
niques has resulted in an overall increase in
the number of cases seen. Complications
include hemorrhage, hematoma formation,
false aneurysm, arteriovenous fistula, subin-
timal dissection (with and without thrombus),
distal embolization of thrombi material, and
breakage of a guidewire or catheter.

In 1971, Bolasny and Killen reviewed the
frequency and management of arterial injuries
following angiography at Vanderbilt Univer-
sity over a period of 2/2 years, starting in
January 1968. Almost 4000 angiographic pro-
cedures were performed, following which
there were 33 vascular injuries requiring
surgical intervention (0.8%) (Table 1-38).
Twenty-six of thirty-three complications were
thrombosis at the site of catheterization.
Sixteen involved the femoral artery, three the
axillary, and five the brachial. In three
instances, there was extensive dissection of the
intima in association with thrombosis (Fig.
1-32).

Two patients developed arteriovenous fis-
tulas and one had a distal embolus from the
puncture site in the femoral artery. Almost
none of the arterial injuries resulted simply
from the needle puncture, in only one case
did the injury occur from uncomplicated
passage of a single arterial catheter. Most
injuries occurred when manipulation of the
catheter was "difficult" or multiple catheters
were inserted. Complications were more
common with arteries with atherosclerotic
plaques. Spasm alone did not cause serious
problems in any patient. Among numerous
other recent papers describing complications
associated with angiographic procedures is the
1973 report by Brener and Couch from
Boston. They reported a thrombosis rate of
13% in using the brachial route for angio-
cardiographic catheterization (Table 1-39) .
Their overall complication rate was 6% when
the femoral route was used, and 28% when
the brachial route was used.

Rich, Hobson, and Fedde (1974) described
the Walter Reed Hospital experience with hos-
pital-incurred vascular trauma. This was
updated by Youkey and colleagues in 1983

chOl.qxd 4/16/04 3:20PM Page 50

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

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chOl.qxd 4/16/04 3:20PM Page 51

1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

TABLE 1-37

INCIDENCE OF VASCULAR

COMPLICATIONS

No.

(%) of

Complications

Survivors

Until

Total

Balloon

Group

Removal

(N =102)

(N =67)

Total no. of clinically

15(14.7)

15(22.4)

evident vascular

complications

Limb ischemia

6(5.9)

6(8.9)

responding to

balloon removal

Limb ischemia requiring

6(5.9)

6 (8.9)

thrombectomy

Hemorrhage requiring

3(2.9)

3(4.5)

operation

From Todd GJ, Bregman D, Voorhees AB, Reemtsma K:
Vascular complications associated with percutaneous intra-
acute balloon pumping. Arch Surg 118:963-964, 1983.

TABLE 1-38

ARTERIAL INJURY RESULTING FROM
3934 ANGIOGRAPHIC PROCEDURES:
0.8% INCIDENCE, VANDERBILT
UNIVERSITY MEDICAL CENTER, 1
JANUARY, 1968-1 JULY 1977

Cases

78.8

Complications

Thrombosis at site of entry

Femoral 18

Axillary 3

Brachial 5

Intimal dissection with occlusion
Arteriovenous fistula
Embolus from puncture site
Perforation with hemorrhage

TOTAL

Modified from Bolasny BL, Killen DA: Surgical management
of arterial injuries secondary to angiography. Ann Surg
174:962-964, 1971.

■ FIGURE 1-32

Arch aortogram in a patient with angiographic
dissection of the subclavian artery shows an
intimal dissection caused by transfemoral
selective arteriography. View is of the origin of
the arch vessels. Arrow indicates intimal
"septum" in the first portion of the left
subclavian artery. (From Bolasny BL, Killen DA:
Ann Surg 1971;174:962-964.) ■

TABLE 1-39

INCIDENCE OF ANGIOGRAPHIC
CATHETER COMPLICATIONS

9.1
6.1
3.0
3.0
100.0

Complications

Femoral
(223 Patients)

Brachial
(96 Patients)

3
2

Thrombosis
Stenosis
Embolus
False aneurysm

TOTAL

2 (1%)

7 (3%)

4 (2%)

13(6%)

12(13%)
14(15%)

26 (28%)

Modified from Brener BJ, Couch MP: Surgical arterial
complications of left heart catheterization and their
management. Am J Surg 125:521-526, 1973.

chOl.qxd 4/16/04 3:20PM Page 52

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

noting many similarities. Natali and Ben-
hemori (1979) reviewed an interesting group
of 125 cases of iatrogenic vascular injuries
excluding angiographic injuries from Paris.
Included were three cases in which there was
inadvertent arterial stripping during a vein
stripping operation.

Alpert and colleagues (1980) presented
five patients who sustained limb ischemia
in neonates after umbilical artery catheteri-
zation. Gangrene developed in three patients
and two patients died from primary illness,
with the third patient surviving after leg
amputation. In the remaining two infants
who had advanced ischemia, there was a favor-
able response to catheter removal and
heparinization.

Cronenwett, Walsh, and Garrett (1988)
identified an unusual case of multiple tibial
artery pseudoaneurysms that appeared 4
years after balloon catheter embolectomy.
They reviewed the literature and found 46
cases of balloon catheter injuries reported,
including arterial disruption (29), intimal
rupture (12),orcathetermalfunction (5). The
injuries resulted in hemorrhage (13), arteri-
ovenous fistula (12), pseudoaneurysm (4),
thrombosis (3) , dissection (5) , accelerated ath-
erosclerosis (4), and catheter fragment
embolism (5). Only 41% of these complica-
tions were recognized during the initial
operation.

Gurri and Johnson (1980) reviewed oper-
ative management of 42 patients who sus-
tained brachial arterial injury following
cardiac catheterization at the University of
North Carolina at Chapel Hill.

Adar, Bass, and Walden (1982) reviewed a
University Hospital experience with iatrogenic
vascular complications. They emphasized that
a concerted effort to study these injuries can
lead to a decrease in incidence.

Orcutt and colleagues (1985) reviewed 46
patients who were treated for iatrogenic vas-
cular injuries at the University of Texas Health
Science Center in San Antonio during a 6-
year period ending in December 1982. Diag-
nostic procedures led to 24 injuries and
therapeutic procedures were responsible for
22 vascular injuries.

Flanigan and colleagues (1983) docu-
mented a 32-month period involving iatro-

genic pediatric vascular injuries in 79 extrem-
ities in 76 children in Chicago. They empha-
sized that iatrogenic pediatric vascular injuries
are common and can result in significant limb
growth impairment.

Historic Observations on
Mechanism of Injury

FRACTURES

Although an arterial injury can occur with
almost any type of fracture or dislocation, it
is surprising that such an injury does not occur
more often. The usual injury is confusion with
spasm and subsequent thrombosis, rather than
laceration or transection (Collins andjacobs,
1961; Makins, Howard, and Green, 1966).
Such injuries commonly have been over-
looked in the past, confusing the signs of acute
arterial insufficiency with soft tissue trauma,
hemorrhage, and "arterial spasm." The avail-
ability of angiography has greatly facilitated
the management of such problems; the ques-
tion of arterial injury in a patient with a frac-
ture can be resolved simply by performing an
angiogram. Fractures of the midshaft of the
femur may lacerate the superficial femoral
artery (Kirkup, 1963), whereas fractures of the
distal tibia and fibula may lacerate the poste-
rior and anterior tibial arteries (Miller, 1957) .
Pelvic fractures have traumatized the iliac
arteries, whereas medial angulation of the
radial fragments of a fracture of the neck of
the humerus may lacerate the axillary or
brachial artery (Hughes, 1958) .

POSTERIOR DISLOCATION OF
THE KNEE

Dislocation of the knee has frequently been
associated with injury of the popliteal artery,
often leading to amputation. In one series of
22 dislocated knees, the popliteal artery was
injured in 13 patients, an incidence of nearly
60% (Kennedy, 1959). Similarly, Hoover,
reporting from the Mayo Clinic in 1961, found
9 popliteal artery occlusions associated with
14 knee dislocations. Less commonly, dislo-
cation of the elbow has injured the brachial

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1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

or radial arteries. Anterior dislocation of the
shoulder has injured the axillary artery
(McKenzie and Sinclair, 1958) . Trauma to the
axillary artery may be compounded by trauma
to the subscapular and humeral circumflex
branches; this may make the injury more
serious by destroying important collateral
pathways for arterial flow to the upper extrem-
ity. Fractures or the clavicle may injury the
subclavian artery, the subclavian vein and the
brachial plexus.

BLUNT INJURY IN PRESENCE OF
OTHER VASCULAR PATHOLOGY

The types of blunt trauma that may in unusual
instances injure an artery are almost endless.
Gibson (1962) described injury from direct
blunt force. Instances of intimal dissection,
prolapse, and eventual thrombosis were
reported by Elliott in 1956 and Moore in 1958.
Ngu and Konstam (1965) reported the case
of a woman who developed traumatic dissec-
tion of the abdominal aorta following blunt
trauma from a surfboard.

USE OF CRUTCHES

Lesions of the axillary artery have resulted
from long-term use of crutches (Rob and
Standeven, 1956). In 1973, Abbott and Darling
added eight cases of axillary artery aneurysm
secondary to crutch trauma from the Massa-
chusetts General Hospital between 1965 and
1971 to a review of the English literature that
contained only 11 cases of arterial thrombo-
sis and 2 cases of arterial aneurysms. Ettien
(1980) reported the case of a crutch-induced
aneurysm of the axillary artery, which resulted
in distal embolism.

marked, amputations have not been necessary.
In baseball pitchers, thrombosis of the axil-
lary artery has developed apparently as a result
of the motion of the throwing arm from a
position of exaggerated hyperabduction
through a wide downward arc with great
force. The two possibilities of injury are a
tear of the intima from repeated stretching
or twisting and compression from hypertro-
phy of the pectoralis minor tendon, causing
repetitive trauma to the artery (Whelan and
Baugh, 1967). The importance of complete
angiography in these unusual instances of
arterial trauma has recently been emphasized.
Aneurysms of the ulnar artery in the wrist
or palm, which without angiographic inves-
tigation would have gone undetected, have
been found to be responsible for distal
emboli.

VASCULAR INJURY IN CHILDREN

Meagher and colleagues (1979) performed a
retrospective evaluation of vascular trauma in
infants and children in Houston. They iden-
tified 53 cases of blunt and penetrating vas-
cular injuries in pediatric patients. The
brachial artery, superficial femoral artery, and
inferior vena cava were the vessels most often
involved. There were 41 major arterial and 32
major venous injuries.

Richardson and colleagues (1981) reviewed
the management of arterial injuries in 29
children treated at the University of Louisville.
Blunt trauma was responsible for 1 1 injuries,
gunshot wounds for 9, penetrating injuries
by sharp objects for 5 injuries, and angio-
graphic-related injury occurred in the remain-
ing 4. The femoral artery was most often
injured.

ATHLETIC INJURIES

In baseball players, effort thrombosis of the
subclavian artery and vein has been described.
In addition, the syndrome has developed in
the index finger of the catching hand, where
the major force of the baseball is received.
Although signs of ischemia may become

RADIATION

The extent of arterial trauma secondary to
radiation therapy is not completely under-
stood. However, it is generally believed that
only smaller vessels are usually affected. Fre-
quent observations have been made that there
seems to be an increase in the friable nature
of the vena cava during a retroperitoneal node

chOl.qxd 4/16/04 3:20PM Page 54

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

dissection following radiation for pelvic
carcinoma.

VIBRATORY TOOLS

Chronic use of vibratory tools such as an air
hammer has caused thrombosis of the distal
arteries (Barker and Hines, 1944; De Takats,
1959).

Historic Classification of
Vascular Injury

The types of arterial injury that can occur can
be conveniently divided into five groups, as
follows: lacerations, transections, contusions,
spasm, and arteriovenous fistulas (Fig. 1-33) .
In almost every series reported, laceration or
transection accounts for 85% to 90% of the
total injuries seen.

A laceration varies from a simple puncture
wound to almost complete transection of

the arterial wall. Transection varies from
simple division of the artery to actual loss of
substance from a high velocity bullet, often
with injury of the ends of the divided artery.
Contusion ranges from a trivial hematoma in
the adventitia to diffuse fragmentation and
hematomas throughout the arterial wall. In
the most severe form, there is fracture of the
intima, subsequent prolapse into the lumen
and eventual thrombosis. Spasm is a definite
entity that can occur in the absence of any
organic injury, but it is extremely rare. It can
be demonstrated simply in the laboratory
by repetitively stretching an artery. This ini-
tiates a sustained contraction of "spasm" of
the concentric bands of smooth muscle in the
media of the arterial wall. When it occurs, it
is important to appreciate that spasm is a
mechanical myogenic response and not a
neurogenic response that is typically see in
smaller arterial tributaries under the influence
of the sympathetic nervous system. Arteri-
ovenous fistulas classically occur with a for-
tuitous injury of concomitant artery and

Laceration

Transection

Incomplete
Transection

Contusion and
Segmental Spasm

'■";S'.<*?"

Contusion and
Thrombosis

Contusion and
True Aneurysm

Pulsating Hematoma
or False Aneurysm

External
Compression

Arteriovenous Fistula

■ FIGURE 1-33

Common types of arterial trauma. Lacerations and transections account for the vast majority of
arterial injuries. Transections may be associated with avulsions with missing segments of artery.
External compression can be caused by displaced bone from comminuted fractures. ■

chOl.qxd 4/16/04 3:20PM Page 55

1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

vein, but the overall frequency of their occur-
rence is small. False aneurysms evolve from
lacerations of an artery temporarily sealed by
blood clot. Eventually the thrombosis lique-
fies and the lesion begins to expand. Often
only after the appearance of an expanding
lesion is the presence of an arterial injury first
recognized.

HISTORY OF BALLISTICS AND
VASCULAR INJURY

Primary damage and wounding results from
direct crushing of tissue in front of the
moving missile and from stretching and
tearing in a wide range around the missile
path. The stretching results from the
formation of a large temporary cavity behind
the missile which leaves a region of
extravasated blood on collapse. The cavity
formation is explosive in character and a
comparison is drawn between a shot into
tissue and an underwater explosion.
Harvey (1947)

arteries. This can be demonstrated best exper-
imentally. The effort is warranted in view of
an alarming increase in the number of
gunshot wounds, including those involving
arterial trauma, even in civilian experience.
The mechanical disruption of arteries by high-
velocity missiles has presented additional
problems in arterial repair. Controversy
regarding the extent of arterial trauma and
the significance of this trauma to the even-
tual success of the arterial repair stimulated
additional experimental work based on clin-
ical impressions from both the Korean and
Vietnam experiences. Many misconceptions
regarding wound ballistics have been cor-
rected through experimental research. Even
a lower velocity missile creates a temporary
cavity, as shown in Figure 1-34. Nevertheless,
the wounding power of high-velocity missiles,
in comparison to that of lower velocity mis-
siles, is greatly accentuated by the additional
energy in the larger temporary cavity. Within
microseconds after impact, the missile trans-
fers energy to the tissues struck. Herget
(1956) emphasized that high internal pres-
sures and Shockwaves as high as 100 atmos-
pheres (1500 pounds per square inch) exist
in the temporary cavity as the tissue along the

Primary damage and wounding results
from direct crushing of tissue in front of the
moving missile and from stretching and
tearing in a wide range around the missile
path. The stretching results from the forma-
tion of a large temporary cavity behind the
missile, which leaves a region of extravasated
blood on collapse. The cavity formation is
explosive in character and a comparison is
drawn between a shot into tissue and an under-
water explosion (Harvey, 1947) .

Experimental effort has been expended by
a small number of individuals in an attempt
to better understand the wounding power of
missiles, particularly during the last 50 years.
This knowledge is of paramount importance
before one can gain a full appreciation of the
various etiologies of arterial trauma and
the resultant degree of damage. As stated in
the aforementioned quote, the temporary cav-
itational affect of a missile has an extremely
important adverse effect on tissues, including

■ FIGURE 1-34

A 16-grain sphere traveling at 1000 feet per
second through the suspended hindlimb of a
canine model demonstrates that there is even a
small temporary cavity formed in muscle by a
low velocity missile. (From Amato JJ, Billy LJ,
Lawson NS, Rich NM: High velocity missile
injury. An experimental study of the retentive
forces of tissue. Am J Surg 1974;127:454-
459.) ■

chOl.qxd 4/16/04 3:20PM Page 56

56 I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

■ FIGURE 1-35

These angiograms of a canine model, started 10 minutes after missile wounding (the entrance
wound is marked), show the marked increase in arterial flow in the injured leg on the dog's left side,
compared to the contralateral side, as judged by the rapid transit of contrast media. Note in C the
earlier venous filling. (From Rybeck B: Acta Chir Scand Suppl 1974;450:1.) ■

wound tract expands after the high-velocity
missile passes through it.

Under the auspices of the International
Commission of the Red Cross, a series of meet-
ings have been held by many interested
nations to discuss the possibility of prohibi-
tion of certain weapons used in warfare (Rich,
1975). Included in the weapons systems that
have been criticized are those that fire high-
velocity bullets. In 1974 in Sweden, Rybeck
conducted an interesting series of five exper-
iments to determine the hemodynamic effects
if energy absorption following missile wound-
ing. Among their results is a graphic demon-
stration of the increased arterial flow in the
injured limb compared to that in the oppo-
site uninjured limb (Fig. 1-35).

Experimental vascular trauma continues to
challenge the interested investigator. Some
might say this is only a problem for military
medicine. However, with the increasing
number of gunshot wounds in our cities,
including those caused by high-velocity mis-
siles, this information also has practical value
in our civilian community. Despite the inter-
national prohibition at the turn of the century,
the "dum-dum" bullet is again being used. It
is no longer used on the battlefield; however,
numerous law enforcement agencies in the
United States have reinstituted or are con-
sidering reinstitution of its use. Yet very little
is understood regarding either the experi-
mental or the clinical aspects of the wound-
ing power of this missile.

Additional international symposia on
wound ballistics has been conducted. The
interested reader is referred to the 1988 and
1996 supplements from the Journal of Trauma,
where additional detailed studies are reported
from numerous investigators around the
world. Additional material from individuals
investigators is available from the Sixth Inter-
national Symposium in Wound Ballistics held
in November 1988 in Chongqing, Peoples
Republic of China and in St. Petersburg, Russia
in September 2 through 7, 1994.

With the rapidly expanding increase in the
management of civilian vascular trauma, it is
equally important that long-term follow-up be
obtained to evaluate the true success of
various acceptable procedures and to develop
new techniques that will help continue to
improve the results of managing patients with
vascular trauma.

HISTORICAL REFLECTIONS
AND PROJECTIONS

We should not rest content with the work of our
predecessors, or assume that it has proved
everything conclusively, on the contrary it
should serve only as a stimulus to further
investigation. Ambroise Pare (sixteenth
century)

chOl.qxd 4/16/04 3:20PM Page 57

1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

This quote from the translated review by Bill-
roth (1931) on studies on the nature and treat-
ment of gunshot wounds emphasizes the
historical development and current status of
vascular surgery. Although some might say that
all the principles of vascular surgery are estab-
lished and accepted by the vast majority of
surgeons, we must not lose sight of the need
for continued analysis of results and contin-
ued investigation to solve the problems that
remain.

As a prime example, the "ideal conduit" still
has not been discovered, appreciating the pio-
neering work of Voohrees reported first in
1952. A substitute for both the arterial and
the venous system is greatly needed. A conduit
of varied size in diameter and length that
would be an acceptable biologic substitute will
always be needed in the repair of traumatized
arteries and veins. Although some might
argue that the ravages of atherosclerosis can
be greatly helped by drug therapy and other
conservative medical regimens in the future,
the increasing incidence of injured arteries
and veins in civil life (urban violence) and on
the battlefield accentuates the importance of
the need for a substitute vascular conduit.
Many materials have been investigated, both
clinically and under laboratory conditions. At
Walter Reed Army Institute of Research, an
assortment of grafts and prostheses have been
used in the venous system without universal
success. The problem remains more signifi-
cant in the repair of injured veins than of
injured arteries. Considering that the Nobel
Prize in Medicine was awarded to Carrel in
1912 based in part on his contributions to vas-
cular surgery, including the reconstruction of
arteries and veins, this might be an additional
stimulus to the serious investigator in search
of the "ideal conduit."

The first vascular surgery procedures were
described in patients with vascular trauma. For
almost two centuries, the treatment of vascu-
lar conditions was basically a very early history
of the evaluation and treatment of injured
vessels. The observations in the patients with
injured arteries and veins led to innumerable
concepts and laboratory experiments that
made significant contributions to the field of
surgery. It was the concomitant availability of
angiography, antibiotics, plastics, vascular

instruments developed through metallurgy,
and synthetic monofilament suture that
allowed the explosion of vascular surgery
development during the 1950s and 1960s.
Ironically, the principles established in treat-
ment of wounded arteries and veins were
immediately available and adaptable to the
receptive new vascular surgeons eager to
develop new imaginative horizons. Con-
comitantwith this new composite technology
and surgical vision, three major campaigns
allowed for the field testing of many of the
emerging concepts and instrumentation.
Ironically, the types of lessons learned in Korea
and Vietnam became adaptable to the third
major warfare in the urban hospitals of
America. There was a paradigm shift from the
military vascular injury where over 90% were
in the extremities to the civilian vascular
trauma arena where over 60% were in the
trunk. It is also ironic that this epidemic con-
tinued through the writing of the second
edition of this book. It is further ironic that
during the military conflicts in Grenada
(1983), Panama (1989), and the Persian
Gulf (1991) and Somalia (1992), as well as
"peace keeping" in Haiti (1994 to 1996) and
Bosnia (1996 to 1999), that no single surgeon
handled more than two or three vascular
injuries.

Continuing technology, at the time of the
writing of the second edition of this book,
innumerable controversies, and advance-
ments are dynamically evolving. These include
the areas of imaging, noninvasive evaluation,
use of the intravascular technology, changing
roles of the surgeon and interventional radi-
ologists, improvements in substitute conduits
and suture material, and changing adjuncts
in autotransfusion and extracorporeal bypass
and various shunts. There are also changes in
hospital and specialty credentialing and
recognition, as well as an explosion of spe-
cialty organizations with interests in vascular
surgery and in trauma. The areas of infection
and thrombosis continue to plague the vas-
cular surgical investigator. In the interim
between the writing of the first two editions
of this book, the viral infections of hepatitis
B and C, human immunodeficiency virus, and
others create challenges, paranoia, and ethical
issues for the patient and the clinician alike.

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

Finally, the issue of training, role models, and
the practice of vascular trauma has consider-
able problems in the arena of managed care,
health maintenance organizations, trauma
center development, and specialty drift. The
push for increased numbers of primary care
physicians and primary surgeons will increase
to the detriment to not only the vascular
surgery specialists, but individuals who choose
to enter the field of trauma care. Furthermore,
the current regulatory and medical/legal
climate and the perceptions of potential liti-
gation involving the patient with a vascular
injury may cause the patient who literally
needs the care of an advanced specialist the
most to not be able to find one during their
moment of greatest need.

A major factor in this remaining problem
in vascular surgery has been the obvious
paucity of long-term follow-up studies of vas-
cular repairs. The importance of long-term
follow-up of patients with vascular injuries
cannot be overemphasized. This would be
true of both patients who have had success-
ful repair and those in whom repair failed or
was not possible. In the former group, peri-
odic evaluation of the function of the repair
should be carried out. There is early docu-
mentation of the value of providing details of
vascular cases with appropriate follow-up
information. Although arterial aneurysms
previously had been treated by proximal lig-
ation, excision, or the Matas repair from within
the sac, Pringle (1913) developed a modifi-
cation of the method used by Carrel and
Guthrie in excising an aneurysm of the
popliteal artery and reestablishing continu-
ity with an autogenous saphenous vein graft.
Both the resected popliteal aneurysm and the
vein graft specimen were obtained years later
postmortem, and the findings are shown in
Figure 1-36.

Goodman (1918), in describing his expe-
rience at the number 1 (Presbyterian U.S.A.)
General Hospital in France during World War
I, reported a successful closure with continu-
ous silk suture of 5-mm longitudinal openings
in both the popliteal artery and vein in one
patient with a shall fragment. However, the
patient was followed only 9 days before being
transferred to the Base Hospital. Goodman
reported that "an attempt to obtain further

■ FIGURE 1-36

The value of adequate documentation and
follow-up of vascular cases was demonstrated
early by Pringle. A, An excised popliteal
aneurysm is shown, and B, the vein specimen
obtained years later at postmortem. Pringle
reported his work in 1913, when he modified
the method of Carrel and Guthrie in excising an
aneurysm of the popliteal artery by
reestablishing continuity with an autogenous
saphenous vein graft. (Photograph obtained
from and used with permission of the Royal
College of Surgeons of Edinburgh.) ■

information covering the case is now under-
way and will be embodied in a subsequent
report."

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1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

In the classic report by DeBakey and
Simeone (1946) from the U.S. experience in
World War II, early patency of venous graft in
the arterial system was demonstrated angio-
graphically (Fig. 1-37). Although consider-
able time and effort were expended following
World War II in an attempt to provide addi-
tional long-term follow-up information, the
results of this effort are not generally avail-
able. Individual follow-up has been possible
in a random way for some patients, such as in
the case of an acute, femoral arteriovenous
fistula, mentioned earlier, which was repaired
shortly after D-Day in Normandy on June 16,
1944 (Boyden, personal communication,
1970). Rob (1985) had a 10-year follow-up of
a patient from World War II (Fig. 1-38).

The importance of a well-documented past
medical history covering previous vascular
trauma was emphasized in the long-term
follow-up of a 50-year-old former United
States Army Officer who entered the Periph-
eral Vascular Surgery Clinic at Walter Reed
General Hospital for evaluation to rule out
cerebrovascular ischemia. The patient had
complained of several episodes of visual dis-
turbance and weakness of his left hand during
the past year. The patient knew that he had a

ligation of "some of the arteries in his neck"
during World War II. An angiogram of the
aortic arch and its major branches was
obtained to determine the amount of arter-
ial flow to the brain. The study demonstrated
no identifiable right common carotid artery
or its branches, and there was no late retro-
grade filling of the right internal carotid
artery. A copy of part of his old military medical
records was finally obtained and it was revealed
that he had sustained a fragment wound on
the right side of the neck on January 19, 1945,
on Saipan when an ammunition dump
exploded. Although only debridement was
necessary at first, approximately 6 months later
ligation of the right common internal and
external carotid arteries was necessary. In sub-
sequent follow-up through the Vascular Clinic,
the patient had no significant problems.
Jackson, Brengman, and Rich (1997) have
added the latest long-term delayed vascular
injury from Walter Reed Hospital. The patient
was a World War II casualty who developed a
false aneurysm of the brachial arterial branch
about 50 years after injury (Fig. 1-39) .

Murray (1952) stated approximately 45
years ago that the fate of venous grafts in the
arterial system had been under considerable

m FIGURE 1-37

A, This arteriogram was performed
there and one-half weeks after a
nonsuture anastomosis of the
superficial femoral artery. There is
patency of the anastomosis and no
evidence of undue ballooning of the
vein segment. The operation was
performed at the 8th Evacuation
Hospital during World War II. B, This
roentgenogram of a successful
nonsuture anastomosis of the
superficial femoral artery shows the
extent of the defect bridged by the
position of the Vitallium tubes. (From
DeBakey ME, Simeone FA: Ann
Surg 1946;123:534-579.) ■

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

■ FIGURE 1-38

This follow-up angiogram was obtained by
Professor Charles G. Rob at St. Mary's Hospital
in London in 1954, which was 10 years after
successful repair of a popliteal arteriovenous
fistula during World War II. Although patency
was maintained, aneurysmal dilation occurred
at the site where a portion of the sac had been
included in the repair. This was replaced with a
vein graph. (From Rob CG: JR Army Med
Corps 1986;132:11-15.) ■

discussion. However, he felt that the saphe-
nous grafts would continue to function
without complications for a long period of
time. He reported that he had removed a
venous graft that had functioned in the
carotid artery of a dog for nine years. Although
the graft was slightly larger than the adjacent
artery and there was some arteriosclerotic
change in one area, it continued to function
well. There are some reports of good results
with aneurysmal formation in utilizing an
adjacent vein, such as the femoral vein next
to the common femoral artery as documented
by Murray (1952) , but the greater saphenous

vein still appears to be the best arterial sub-
stitute, particularly for major arteries of the
extremities.

The outstanding documentation of the U.S.
experience during the Korean Conflict by
Hughes, Jahnke, Spencer, and others has pro-
vided an opportunity for long-term follow-up.
Figure 1-40 is an angiogram of a patient fol-
lowed up after 19 years with a patent inter-
position greater saphenous vein in the
proximal right superficial femoral artery.
The establishment of a Vascular Registry and
Blood How Laboratory at Walter Reed General
Hospital in 1966 provided an opportunity for
long-term follow-up of former combat casu-
alties who sustained vascular injuries. In the
early efforts of the Vietnam Vascular Registry,
the problems of obtaining long-term follow-
up of patients who had vascular injuries in
Vietnam were illustrated by an attempt to
follow those listed in Fisher's report (1967)
of 108 vascular injuries. After intensive inves-
tigation at the time of organization of statis-
tics for the preliminary report for the Vietnam
Vascular Registry, it was possible to find only
60 of his patients whose postoperative period
and convalescence could be completely eval-
uated. This represents slightly more than 50%
of the patients of the original study. In sub-
sequent years, however, the long-term follow-
up percentage continued to improve.

What is the long-term fate of the autoge-
nous greater saphenous vein used as an inter-
posed segmental graft in the arterial system?
Most surgeons continue to believe that the
long-term patency is excellent. However, few
recognize the development of aneurysmal
changes in these grafts. The long-term follow-
up effort in the Vietnam Vascular Registry has
continued to demonstrate an increasing
number of patients with these changes. The
true significance and the actual percentage
of these changes remain unknown. This does,
however, emphasize the great need for con-
tinued long-term follow-up studies. This com-
plication of fusiform aneurysmal dilation of
an autogenous greater saphenous interposi-
tion segment used for repair of an injured
artery was first brought to our attention by
Carrasquilla and Weaver (1972) when they
reported on the follow-up of a 22-year-old
Marine who had originally been wounded and

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1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

■ FIGURE 1-39

Angiogram demonstrates a false aneurysm of a branch of the brachial artery diagnosed 49 years
after the original injury in World War II. Successful treatment was carried out at Walter Reed Army
Medical Center. (From Jackson MR, Brengman ML, Rich NM: J Trauma 1997;43:159-616.) ■

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

■ FIGURE 1-40

This long-term follow-up femoral angiogram
demonstrates patency of an interposition
autogenous greater saphenous vein used to
repair the proximal right superficial femoral
artery. The follow-up period extended from
1953 until the patient was evaluated at Walter
Reed General Hospital in 1972 (19 years). This
is one of the longest known follow-ups and
represents the continued effort to provide this
type of data for former combat casualties from
the Korean Conflict. (From Rich WR: General
Hospital, 1978.) ■

this manner. B-mode ultrasonography has
been tested to augment this information;
however, data remain fragmentary and unsat-
isfactory. Color-flow duplex offers good eval-
uations of many arteries and veins, although
the equipment is expensive (Fig. 1^13).

The continuing challenge that remains in
the management of patients with vascular
injuries is exemplified by the questions and
problems involving the search for the "ideal
conduit" for segmental replacement of injured
arteries and veins. There are also many other
aspects of the management of injured patients
with vascular injuries that could be expanded.
The management of concomitant fractures
associated with vascular injuries, the use of
fasciotomy, the use of fasciotomy in extremi-
ties with vascular injuries, and other associ-
ated considerations are among these factors.
Moreover, there are a multitude of profes-
sional challenges that exist in unusual situa-
tions involving vascular trauma. The following
is cited as an example. Kapp, Gielchinsky,
and Jelsma (1973) stated that they could
find only four cases of intravascular metallic
fragment embolization to the cerebral circu-
lation. To their surgical review they added the
report of two patients who were treated by the
24th Evacuation Hospital in the Republic of
South Vietnam. Because of the unusual
problem, some details of one of these cases
follow:

treated in Vietnam. Figure 1-41 demonstrates
the findings. With the accumulation of
approximately 250 follow-up angiograms of
Vietnam casualties, with the range in time from
months to years, the number of recognized
aneurysmal dilation of these venous interpo-
sition grafts is in the range of 6%.

It is often not practical or economically fea-
sible to routinely obtain follow-up angiograms,
particularly in asymptomatic patients. The
long-term follow-up through the Vietnam Vas-
cular Registry relies to a great extent on the
noninvasive approach through the Blood
Flow Laboratory. Figure 1-42 demonstrates
this type of follow-up, using the measurement
of wrist pressures and obtaining tracings with
the Doppler ultrasound method. Unfortu-
nately, aneurysmal changes in venous grafts
in the arterial system cannot be detected in

A 19-year-old American soldier received a
fragment wound of the right side of the neck
from a grenade explosion, associated with
immediate onset of weakness of the left side
of his body. An exploration of his neck was
carried out and showed no evidence of
vascular trauma. Three days after
wounding, the patient was transferred to the
24th Evacuation Hospital where he showed
slight improvement in his left-sided
weakness.

Roentgenograms of the skull showed a
small, jagged, metallic fragment, and an arte-
riogram revealed that the fragment was lodged
at the origin of the middle cerebral artery,
completely occluding the middle cerebral
artery and projecting into the carotid artery
(Fig. 1-44).

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1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

Rights were not granted to include this figure in electronic media.
Please refer to the printed publication.

■ FIGURE 1-41

A, Fusiform aneurysmal dilation of an autogenous greater saphenous vein segment used as an
interposition graft in the right common carotid artery of a Vietnam casualty is demonstrated
angiographically. B, The operative photograph demonstrates the dilated segment of saphenous
vein. C, Arterial reconstruction was completed with a Dacron prosthesis. (From Carrasquilla C,
Weaver AW: Aneurysm of the saphenous graft to the common carotid artery. Vase Surg 1 972;6:66-
68.) ■

It was also thought that there was throm-
bus formation around the fragment. Six days
following injury, the right internal carotid
artery, the anterior cerebral artery and the
middle cerebral artery were exposed through
a right front temporal craniotomy. After
applying temporary vascular clamps, the frag-
ment was removed without difficulty through
a longitudinal arteriotomy in the internal
carotid artery. A thrombus was also extracted

from the middle cerebral artery. An arterior-
rhaphy was performed, with some initial
spasm at the repair site. In the postoperative
period the patient's neurologic status
improved. An arteriogram performed on the
25th postoperative day revealed that the
carotid artery was patent and without steno-
sis or aneurysmal formation (Fig. 1-45) . The
middle cerebral artery was thrombosed at
its origin, but its branches filled readily via

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

■ FIGURE 1-42

The long-term follow-up through
the Vietnam Vascular Registry
includes the recording of wrist
pressures and Doppler
ultrasonicgraphic tracings. The
two tracings at the top show the
comparison of the right side and
the abnormal left side, where
occlusion of the repair of the left
brachial artery with a saphenous
vein graft had occurred in 1969.
The two lower tracings show the
change after reconstruction of
the left brachial artery with a new
segment autogenous greater
saphenous vein. There is
considerable improvement in the
wrist pressure and Doppler
tracing on the left. (From NM.
Walter Reed General Hospital,
1978.) ■

Left

Wrist Pressure 150

Pre-op

Wrist Pressure 88

Post-op

Wrist Pressure 150

:;::

■ '■■■■

a ■
m :

: ::

: SL

- :::

IfeiJi

•MS

liMi!!

! -

. 1 i

Wrist Pressure 140

■ FIGURE 1-43

Color-flow duplex sonogram of axillary vein valve transfer 1 year postoperatively. No venous reflux is
found when the patient performs a Valsalva maneuver, indicating that the valve remains competent.
(From Goff JM, Gillespie DL, Rich NM: J Trauma 1998;44:209-211.) ■

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1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

■ FIGURE 1-44

A, Reports of migration of intravascular metallic
fragments have been rare. This right carotid
angiogram demonstrates an intra-arterial metal
fragment at the intracranial bifurcation of the
carotid explosion. B, This operative photograph
taken at the 24th Evacuation Hospital in
Vietnam shows an intra-arterial fragment with
extreme thinning of the wall of the artery
overlying the fragment at the origin of the
middle cerebral artery. (From Kapp JP,
Gielchinsky I, Jelssma R: J Trauma
1973;13:256-261.) ■

collateral channels with a large patent right
anterior cerebral artery.

The authors outlined the possible problems
that might occur when a metallic fragment
lodges in a cerebral vessel:

1. Neurologic defect secondary to arterial
occlusion and infarction

■ FIGURE 1-45

This angiogram performed 25 days after
removal of the intra-arterial metallic fragment
shown in Figure 1-44 A and B demonstrates
patency of the carotid artery, a patent anterior
cerebral artery that is larger than normal, and
thrombosis of the origin of the middle cerebral
artery. (From Kapp JP, Gielchinsky I, Jelssma
R: J Trauma 1973;13:256-261.) ■

2. Proximal and distal propagation of throm-
bus, which could extend the infarcted area

3. Erosion with hemorrhage

4. Infection, arteritis, and then abscess for-
mation or meningitis

5. Infection with mycotic aneurysm formation
and probable subsequent rupture

They emphasized that one of their main
concerns was the possibility of erosion through
the small, thin-walled artery caused by pul-
satile motion of the fragment. They also
stressed the importance of maintaining a high
index of suspicion in patients with neurologic
symptoms who have wounds of the neck and
chest.

International exchange of information is
important in the treatment of patients with
vascular trauma. In some parts of the world,

chOl.qxd 4/16/04 3:21PM Page 6 6

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

■ FIGURE 1-46

Temporary intraluminal arterial shunts have been used in Munich, Germany, to reduce the ischemic
time, to diminish thrombosis in the peripheral venous system, and to allow repair of concomitant
lacerated veins for major arterial repair. This use of the temporary intraluminal arterial shunt in the
management of acute arterial injuries is somewhat unique in that it was not documented in the
United States during the same period between 1965 and 1970. (From Mack D, Scherer H, Maurer P:
Mschr Unfallheilk 1973;76:217-224.) ■

specific vascular trauma, such as avulsion of
the femoral vessels by a bull's horn in the bull-
ring in Mexico or in Spain, may be unique to
a certain region or country. Nevertheless, the
common goal of all surgeons to provide the
best medical care possible creates a desirable
situation for exchange of data and experience
among surgeons in all parts of the world who
have an interest in the management of vas-
cular injuries. Language difficulties can often
be overcome through personal exchange and
translation of scientific articles. An example
of this is the personal exchange that took place
with Doctor Peter Mauer in Munich in 1973.
Mack, Scherer, and Maurer (1973) described
the treatment of 154 patients with vascular
injuries in Munich betweenjanuary 1965 and
December 1971. They found that 80% of 129
of their patients had suffered additional
trauma, including fractures, trauma to the
head, and rupture abdominal organs. Also,
60% of their patients had vascular injuries in
association with concomitant fractures. They
found angiography to be of great value in diag-
nosing the vascular injury. One relatively
unique aspect of their management, in con-
trast to the management of arterial injuries
in the United States during the same time,
was reestablishing arterial flow by temporary
intraluminal shunts (Fig. 1-46) . They felt that

this reduced ischemic time, diminished throm-
bosis in the peripheral venous system, and
allowed repair of lacerated veins before arte-
rial repair was instituted. They were success-
ful in restoring circulation in 75.8% of their
patients; 12.6% showed remaining symptoms
secondary to complications associated with
vascular injuries, and their amputation rate
was4.2%.BarrosD'Sa (1990) champions intra-
luminal shunts in northern Ireland.

In the United States, Weinstein and Golding
(1975) used temporary external Silastic arte-
rial and venous shunts in replanting a trau-
matically amputated upper extremity in a
10-year-old boy who was involved in an auto-
mobile accident (Fig. 1-47). The level of the
incomplete traumatic amputation was at the
upper third of the arm, with only a posterior
skin bridge intact. These authors emphasized
that early arterial perfusion decreased the total
anoxic time. The challenge persists with
unusual and complex injuries such as this, and
the varied and unique additions to the
surgeon's armamentarium that might assist
in obtaining satisfactory results should be
known and understood.

The following quote by Carleton Mathew-
son, Jr., (Fig. 1-48) in the discussion of the
paper by Morris, Creech, andDeBakey (1957)
is most apropos:

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1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

Venous shunt
Arterial shunt-

■ FIGURE 1-47

This diagrammatic drawing demonstrates the use
of temporary external Silastic arterial an venous
shunts during replantation of a traumatically
amputated upper extremity in a 10-year-old boy
involved in an automobile accident. The shunts,
which were 20cm long and 2.5mm in internal
diameter, reduced the anoxic time during
replantation of the upper extremity. (From
Weinstein MH, Golding AL: J Trauma
1975:15:912-915.) ■

MILITARY SURGICAL HERITAGE

DEPARTMENT OF SURGERY, USUHS

CarMon Malhawtoit, Jr.

Chlnf of Surgery (COL) 59th Evac Hoso 1942 - 1946

Organized first Military Surgery Residency Program 1040

Consultant Le tier man Army Hospital 1046 -

visiting Board of Surgery, USUHS 1977 -

■ FIGURE 1-48

Doctor Carleton Mathewson (1902-
1 989) as professor of surgery at
Stanford, and subsequently at the
University of California, provided
leadership in establishing residency
programs in surgery in the military
following World War II. He served on
the Visiting Board at the Uniformed
Services University of the Health
Sciences, (Bethesda, Maryland) with
other senior surgeons identified in
this manuscript. ■

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

Unfortunately in many quarters these lessons
so well emphasized during the stress of
world conflict have been neglected in the
complacency of civilian life. It is important,
therefore, that we re-emphasize the
seriousness of vascular injury and, where
possible, stress the favorable
circumstances that present themselves in
civilian life with the successful primary
repair of injured vessels.

Endovascular procedures offer a new and
alternative consideration to the more tradi-
tional suture repair of injured arteries and
veins in the 1990s. Parodi (1990) in Buenos
Aires championed this approach. In collabo-
ration with Marin and Veith in New York City
(1994) endovascular approaches have been
used for primary repairs of arteriovenous fis-
tulas and false aneurysms in most cases (Fig.
1-49) . Durability and ultimate success await
needed follow-up.

Exciting challenges remain. From the
microbiology research, we know of a con-

* * 1

BAU.OMV I

■ FIGURE 1-49

Angiographic images of a patient who
sustained a gunshot wound to the right chest.
A, Prograde arteriogram showing subclavian
artery and active bleeding in the region. B,
Image after proximal balloon occlusion, which
stopped the bleeding. C, Retrograde brachial
arteriogram showing extent of injury. D,
Completion arteriogram after successful repair.
(From Patel AV, Marin MD, Veith FJ, et al. J
EndovascSurg 1996;3:382-388.) ■

nection between P-55 receptor site alterations
and complications of vascular manipulation
to include thrombosis and possible stenosis.
Nevertheless, while basic research continues
so does daily examples of man's inhumanity
to man resulting in vascular trauma now in
regional conflicts and in urban violence.

REFERENCES

Abbott WM, Darling RC: Axillary artery aneurysms
secondary to crutch trauma. Am J Surg 1973;
125:515-520.

Adar R, Bass A, Walden R: Five years' experience
in general and vascular surgery in a university
hospital. Ann Surg 1982;196:725-729.

Agnew D II: The Principles and Practice of Surgery.
Philadelphia, JB Lippincott Co, 1978.

Alpert J, O'Donnell JA, Parsonnet V, et al: Clini-
cally recognized limb ischemia in the neonate
after umbilical artery catheterization. Am J Surg
1980;140:413-418.

AustJC, Bredenberg CE, Murray DG: Mechanisms
of arterial injuries associated with total hip
replacement. Arch Surg 1981;116:345-349.

Barker NW, Hines EAJr: Arterial occlusion in the
hands and fingers associated with repeated
occupational trauma. Proc Staff Meet Mayo Clin
1944;19:345-349.

Barros D'Sa AAB, Hassard TH, Livingston RH,
Irwin JW: Missile-induced vascular trauma. Injury
1980;12:13-30.

Bell J: Principles of surgery. Discourse 1801;9:4.

Bernheim BM: Bloodvessel surgery in the war. Surg
Gynecol Obstet 1920;30:564-567.

Billroth T: Historical studies on the nature and treat-
ment of gunshot wounds from the 15th century
to the present time. Yale J Biol Med 1931;4:16-
36.

Bolasny BL, Killen DA: Surgical management of
arterial injuries secondary to angiography. Ann
Surg 1971;174:962-964.

Bole PV, Purdy RT, Munda RT, et al: Civilian arte-
rial injuries. Ann Surg 1976;183:13-23.

Boyden AM: Personal communication, 1970.

Brener BJ, Couch N: Peripheral arterial compli-
cations of left heart catheterization and their
management. Am J Surg 1973;125:521-526.

Carrasquilla C, Weaver AW: Aneurysm of the saphe-
nous graft to the common carotid artery. Vase
Surg 1972;6:66-68.

chOl.qxd 4/16/04 3:21PM Page S 9

1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

Carrel A: La technique operatoriesdes anastomoses
vasculaires e t la tran splan tation de s viscere s. Lyon
Medical 1902;98:859.

Carrel A, Guthrie CC: Uniterminal and bitermi-
nal venous transplantations. Surg Gynecol Obstet
1906;2:266-286.

Chandler JG, RnappRW: Early definitive treatment
of vascular injuries in the Vietnam conflict. JAMA
1967;202:960-966.

Cheek RC, Pope JC, Smith HF, etal: Diagnosis and
management of major vascular injuries: A review
of 200 operative cases. Am Surg 1 975;41 :755-760.

Clermont G: Suture laterale et circulaire des
veines. Presse Med 1901;1:229.

Coley RW. Case of rupture of the carotid artery
and wound of several of its branches successfully
treated by tying off the common trunk of the
carotid itself. Med Chir J (Lond) 1817;3:2.

Collins HA, Jacobs JK Acute arterial injuries due
to blunt trauma. J Bone Joint Surg 1 961 ;43A: 193-
197.

CronenwettJL, Walsh DB, Garrett HE: Tibial artery
pseudoaneurysms: delayed complication of
balloon catheter embolectomy. J Vase Surg
1988;8:483-488.

DeBakey ME, Simeone FA: Battle injuries of the
arteries in World War II: An analysis of 2,471 cases.
Ann Surg 1946;123:534-579.

De Takats G: Vascular Surgery. Philadelphia, WB
Saunders, 1959.

Dillard BM, Nelson DL, Norman HG: Review of 85
major traumatic arterial injuries. Surgery
1968;63:391-395.

Dorfler J: Uber arteriennaht. Beitr Klin Chir
1889;25:781.

Drapanas T, Hewitt RL, WeichertRF III, Smith AD:
Civilian vascular injuries: A critical appraisal of
three decades of management. Ann Surg
1970;172:351-360.

Eck NV: K. voprosu o perevyazkie vorotnois veni.
Predvaritelnoye soobshtshjenye (Ligature of the
portal vein). Voen Med J 2001;130:1-2.

ElliotJA: Acute arterial occlusion: an unusual cause.
Surgery 1956;39:825-827.

Ellis J: Case of gunshot wound, attended with sec-
ondary hemorrhage in which both carotid arter-
ies were tied at an interval of four and a half
days. N YJ Med 1845;5:187.

Ettien JT: Crutch-induced aneurysms of the axil-
lary artery. Am Surg 1980;46:267-269.

Feliciano DV, Bitondo CG, Mattox KL, et al: Civil-
ian trauma in 1 980s: A one-year experience with

456 vascular and cardiac injuries. Ann Surg
1984;199:717-724.

Ferguson IA, Byrd WM, McAfee DK: Experiences
in the management of arterial injuries. Ann Surg
1961;153:980-986.

Fisher GW: Acute arterial injuries treated by the
United States Army Medical Service in Vietnam,
1965-1966. J Trauma 1967;7:844-855.

Flanigan DP, Keifer TJ, Schuler JJ, et al: Experi-
ence with iatrogenic pediatric vascular injuries:
Incidence, etiology, management, and results.
Ann Surg 1983;198:430-442.

Caspar MR, Treiman RL: The management of
injuries to major veins. AmJ Surg 1960;100:l7l-

175.

Gensoul: Note sur les Bless es recus a l'Hotel Dieu
de Lyon, pendant les troubles de 1831 . Gaz Med
Paris 1883;297.

Gibson JMC: Rupture of axillary artery. J Bone Joint
Surgl962;44B:114-115.

Gliick T: Uber zwei falle von aortenaneurysmen
nebst bemerkungen uber die naht der blutge-
fasse. Arch Klin Chir 1883;28:548.

Goodman C: Suture of blood vessel from projec-
tiles of war. Surg Gynecol Obstet 1918;27:528.

Goyanes J: Neuvos trabajos de chirurgial vascular:
substitution plastica de las the arterias por las
venas, o arterio-plastia venosa, aplicado, como
neuvo metodo, al traitamiento de los aneuris-
mas. El Siglo Med 1906;53:546-561.

GurriJA, Johnson G Jr: Management of brachial
artery occlusion after cardiac catheterization. Am
Surg 1980;46:233-235.

Guthrie GJ: Disease and injuries of arteries.
1830.

Haimovici H: History of arterial grafting. J Cardiac
Surg 1963;4:152-174.

Hallowell. Extract of a letter from Mr. Lambert,
surgeon at Newcastle upon Tyne, to Dr. Hunter,
giving an account of new method of treating an
aneurysm. Med Obser Inq 1762;30:360.

Halsted WS: The effect of ligation of the common
iliac artery on the circulation and function of
lower extremity. Report of a cure of iliofemoral
aneurysm by their application of an aluminum
band to the vessel. Bull Johns Hopkins Hosp
1912;23:191-220.

Hardy JD, Raju S, Neely WA, Berry DW: Aortic and
other arterial injuries. Ann Surg 1975;181:640-
653.

Heaton LD, Hughes CW, Rosegay H, et al: Military
surgical practices of the United States Army in

chOl.qxd 4/16/04 3:21PM Page 70

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

Vietnam. In Current Problems in Surgery.
Chicago, Year Book Medical Publishers,
1966.

Herget CH: Wound ballistics. In Bowers WB (ed) :
Surgery of Trauma. Philadelphia, JB Lippincott
Co, 1956.

Hobson RW II, Rich NM: Traumatismes veineux
des membres inferieurs. In Kieffer E (ed) : Trau-
matismes Arteriels. Paris, AERCV, 1995.

Hobson RW II, Rich NM, Wright CB: Venous
Trauma: Pathophysiology, Diagnosis and Surgi-
cal Management. Mt. Kisco, NY, Futura Pub-
lishing, 1983.

Hoover NW: Injuries of the popliteal artery asso-
ciated with fractures and dislocations. Surg Clin
North Am 1961;41:1099-1112.

Hughes CW: Acute vascular trauma in Korean War
casualties: An analysis of 180 cases. Surg Gynec
Obstet 1954;99:91-100.

Hughes CW: The primary repair ofwounds of major
arteries: An analysis of experience in Korea in
1953. Ann Surg 1955;141:297-303.

Hughes CW: Arterial repair during the Korean War.
Ann Surg 1958;147:555-561.

Hughes CW: Vascular surgery in the armed forces.
Milit Med 1959;124:30-46.

Hunter W: The history of an aneurysm of the aorta,
with some remarks on aneurysms in general. Med
Obs Soc Phys Lond 1757;1:323.

Inui FK, Shannon J, Howard JM: Arterial injuries
in the Korean conflict: Experiences with 111 con-
secutive injuries. Surgery 1955;37:850-857.

Jackson MR, Brengman ML, Rich NM: Delayed pre-
sentation of 50 years after a World War 2 vascu-
lar injury with intraoperative localization by
duplex ultrasound of a traumatic false aneurysm.
J Trauma 1 997;43: 1 59-1 61 .

Jahnke EJJr: Late structural and functional results
of arterial injuries primarily repaired. Surgery
1958;43:175-183.

Jahnke EJJr, Seeley SF: Acute vascular injuries in
the Korean War: An analysis of 77 consecutive
cases. Ann Surg 1953;138:158-177.

Jarstfer BS, Rich NM: The challenge of arteriove-
nous fistula formation following disk surgery: A
collective review. J Trauma 1976;16:726-733.

Jassinowsky A: Die arteriennhat: Eine experi-
mentelle studie. Inaug Diss Dorpat 1889.

Jensen: Ueber circulare gefassutur. Arch Klin Chir
1903;69:938-998.

Jimenez F, Utrilla A, Cuesta C, etal: Popliteal artery
and venous aneurysm as a complication of

arthroscopic meniscectomy. J Trauma 1988;28:
1404-1405.

Kapp JP, Gielchinsky I, Jelsma R: Metallic fragment
embolization to the cerebral circulation. J
Trauma 1973;13:256-261.

Kay JK Dykstra PC, Tsuji HK: Retrograde ilioaor-
tic dissection. A complication of common
femoral artery perfusion during open-heart
surgery. Am J Surgery 1966;111:464-468.

Kelly GL, Eiseman B: Civilian vascular injuries.
J Trauma 1975;15:507-514.

Kennedy JC: Complete dislocations of the knee.
J Bone Joint Surg 1959;41:878.

Kozloff L, Rich NM, Brott WH, et al: Vascular
trauma secondary to diagnostic and therapeu-
tic procedures: Cardiopulmonary bypass and
intra-aortic balloon assist. Am Surg

1980;140:302-305.

Kummel: Uber circulare naht der gefasse. Munch
Med Wschr 1899;46:1398.

KirkupJR: Major arterial injury complicating frac-
ture of the femoral shaft. J Bone Joint Surg
1963;45:337-343.

Kurtoglu M, Ertekin C,BulutT, etal: Management
of vascular injuries of the extremities. One
hundred and fifteen cases. Int Angiol 1991;
10:95.

Langenbeck B: Beitrage zur chirurgischen patholo-
gie der venen. Arch Klin Chir 1861 ;1:1.

Learmonth J: Vascular injuries in war. Royal Soc
Med 1946;39:488.

Lexer E: Die ideale operation des arteriellen und
des arte riell-venosen aneurysma. Arch Klin Chir
1907;83:459-477.

Linton R: Injuries to major arteries and their treat-
ment. N YJ Med 1949;49:2039.

Lord JW, Stone P, Clouthier W, Breidenbach L:
Major blood vessel injury during elective surgery.
Arch Surg 1958;77:282.

Luetic V, Sosa T, Tonkovic I, et al: Military vascu-
lar injuries in Croatia. Cardiovasc Surg 1993;1 :3-
6.

Makins G: Gunshot injuries to the blood vessels.
Bristol, England, John Wright and Sons,
1919.

Makins G, Howard JM, Green R: Arterial injuries
complicating fractures and dislocations: The
necessity for a more aggressive approach. Surgery
1966;59:203-209.

Matas R: An operation for radical cure of aneurysm
based on arteriography. Ann Surg 1903;37:161-
196.

chOl.qxd 4/16/04 3:21PM Page 71

1 • HISTORICAL AND MILITARY ASPECTS OF VASCULAR TRAUMA

Matas R: Military Surgery of the Vascular System.
Philadelphia, WB Saunders, 1921.

Mattox KL: Approaches to trauma involving the
major vessels of the thorax. Surg Clin North Am
1989;69:77-92.

Mattox KL, Feliciano DV, Burch J, et al: Five thou-
sand seven hundred sixty cardiovascular injuries
in 4459 patients: epidemiologic evolution 1958
to 1987. Ann Surg 1989;209:698-707.

McKenzie A, Sinclair A: Axillary artery occlusion
complicating shoulder dislocation: a report of
two cases. Ann Surg 1958;148:139-144.

Meagher DJ, Defore W, Mattox KL, Harberg F: Vas-
cular trauma in infants and children. J Trauma
1979;19:532-536.

Miller D: Gangrene from arterial injuries associ-
ated with fractures and dislocations of the leg in
the young and in adults with normal circulation.
Am J Surg 1957;93:367-375.

Moore T: Acute arterial obstruction due to the trau-
matic circumferential intimal fracture. Ann Surg
1958;148:111-114.

Moore C, Wolma F, Brown R, Derrick J: Vascular
trauma: A review of 250 cases. Am J Surg
1971;122:576-578.

Morris GCJr, Creech OJr, DeBakey ME: Acute arte-
rial injuries in civilian practice. Am J Surg
1957;93:565-572.

Mullins R, Lucas C, Ledgerwood A: The natural
history following venous ligation for civilian
injuries. J Trauma 1980;20:737-743.

Murphy J: Resection of arteries and veins injured
in continuity end-to-end suture. Exp Clin Res
Med Rec 1897;51:73-104.

Murray G: Surgical repair of injuries to main arter-
ies. Am J Surg 1952;83:480.

Natali J, Benhemori AC: Iatrogenic vascular
injuries. J Cardiovasc Surg 1979;20:169-176.

Ngu V, Konstam PG: Traumatic dissecting
aneurysm of the abdominal aorta. Br J Surg
1965;52:981-982.

Nolan B: Vascular injuries. J Royal Coll Surg
1968;13:72.

Oiler D, Rutledge R, Clancey T, et al: Vascular
injuries in a rural state: A review of 978 patients
from a state trauma registry. J Trauma 1992;32:
740-746.

Orcutt M, Levine B, Gaskill H III, Sirinek K Iatro-
genic vascular injury: A reducible problem. Arch
Surg 1985;120:384-385.

Pate J, Wilson H: Arterial injuries of the base of
the neck. Arch Surg 1964;89:1106-1110.

Patman R, Poulos E, Shires G: The management
of civilian arterial injuries. Surg Gynecol Obstet
1964;118:725-738.

Perdue GJ, Smith RI: Intra-abdominal vascular
injury Surgery 1968;64:562-568.

Perler B, McCabe C, Abbott WM, Buckley MJ: Vas-
cular complications of in tra-aortic balloon coun-
terpulsation . Arch Surg 1983;118:957-962.

Perry MO, Thai E, Shires G: Management of arte-
rial injuries. Ann Surg 1971;173:403-408.

Postempski P: La sutura dei vasi sanguigni. Arch
Soc Ital Chir Roma 1886;3:391.

Pritchard D, MaloneyJ, Barnhorst DA, Spittel JJ:
Traumatic popliteal arteriovenous fistulas. Arch
Surg 1977;112:849-852.

Reynolds R, McDowell H, Diethelm A: The surgi-
cal treatment of arterial injuries in the civilian
population. Am Surg 1979;189:700-708.

Rich NM: Vietnam missile wounds evaluated in 750
patients. Milit Med 1968;133:9-22.

Rich NM: Vascular trauma in Vietnam. J Cardio-
vasc Surg 1970;11:368-377.

Rich NM: Venous injuries. In Sabiston DJ (ed) : Text-
book of Surgery. Philadelphia, WB Saunders,
1995.

Rich NM, Hobson RW II, Collins GJ Jr, Anderson
CA: The effect of acute popliteal venous inter-
ruption. Ann Surg 1976;183:365-368.

Rich NM, Hobson RW II, Fedde C: Vascular trauma
secondary to diagnostic and therapeutic proce-
dures. Am J Surg 1974;128:715-721.

Rich NM, Hughes CW: Vietnam Vascular Registry:
A preliminary report. Surgery 1969;65:218-226.

Rich NM, Spencer FC: Vascular Trauma. Philadel-
phia, WB Saunders, 1978.

Rich NM, Sullivan W: Clinical recanalization of an
autogenous vein graft in the popliteal vein. J
Trauma 1972;12:919-920.

Richardson JD, Fallat M, Nagaraj H, et al: Arterial
injuries in children. Arch Surg 1981 ;1 16:685-690.

Rob CG: A history of arterial surgery. Arch Surg
1972;105:821-823.

Rob CG, Standeven A: Closed traumatic lesions of
the axillary and brachial arteries. Lancet
1956;1:597-599.

Rybeck B: Missile wounding and hemodynamic
effects of energy absorption. Acta Chir Scand
1974;450:1.

Salander J, YoukeyJ, Rich NM, e t al: Vascular injury
related to lumbar disk surgery. J Trauma
1984;24:628-631.

chOl.qxd 4/16/04 3:21PM Page 72

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

Saletta J, Freeark R: The partially severed artery.
Arch Surg 1968;97:198-205.

Saletta J, Freeark R: Injuries to the profunda femoris
artery. J Trauma 1972;1 2:778.

Schede M: Zur frage von der jodoformvergiftung.
Zentralb Chir Beil 1882;9:33-38.

Schramek A, Hashmonai M: Distal arteriovenous
fistula for the prevention of occlusion of venous
interposition grafts to veins. J Cardiovasc Surg
1974;15:392-395.

Schramek A, Hashmonai M, Farbstein J, Adler O:
Reconstructive surgery in major vein injuries in
the extremities. J Trauma 1975;15:816-822.

Schwartz A: The historical development of methods
of hemostasis. Surgery 1958;44:604.

Seeley S: Vascular surgery at Walter Reed Army Hos-
pital. US Armed Forces Med J 1954;8.

Shumacker HBJr: Incisions in surgery of aneurysm:
With special reference to explorations in the
antecubital and popliteal fossae. Ann Surg
1946;124:586-598.

Shumacker HB Jr: Surgical cure of innominate
aneurysm; report of a case with comments on
applicability of surgical measures. Surgery
1947a;22:729-739.

Shumacker HBJr: Resection of the clavicle with
particular reference to the use of bone chips in
the periosteal bed. Surg Gynecol Obstet
1947b;84:245-248.

Shumacker HBJr: Problem of maintaining the con-
tinuity of artery in surgery of aneurysms and arte-
riovenous fistulae; notes on the development and
clinical application of methods of arterial suture.
Ann Surg 1948a;l 27:207-230.

Shumacker HBJr: Operative exposure of the blood
vessels in the superior anterior mediastinum. Am
Surg 1948b;l 27:464-475.

Shumacker HBJr: Arterial suture techniques and
grafts: Past, present and future. Surgery
1969;66:419-433.

Simeone F, Grillo H, Rundle F: On the question
of ligation of the concomitant vein when a major
artery is interrupted. Surgery 1951;29:932-951.

Smith R, Elliot J, Hageman J: Acute penetrating
arterial injuries of the neck and limbs. Arch Surg
1974;109:198-205.

Smith L, Foran R, Caspar MR: Acute arterial injuries
of the upper extremity. Am J Surg 1963;106:144-

151.

Soubbotitch V: Military experiences of traumatic
aneurysms. Lancet 1913;2:720-721.

Spencer FC, Grewe R: The management of acute
arterial injuries in battle casualties. Ann Surg
1955;141:304-313.

Stich R: Ueber gefaess und organ transplantatio-
nen mittelst gefaessnaht. Ergeon Chir Orth
1910;1:1.

Swan KG, Hobson RWII, Reynolds D, et al: Venous
surgery in the lower extremities. In Swan KG,
Hobson R, Reynolds D, et al (eds): St Louis,
Warren H Green Publishers, 1975.

Todd G, Bregman D, Voorhees A, Reemtsma K Vas-
cular complications associated with percuta-
neous intra-aortic balloon pumping. Arch Surg
1983;118:963-964.

Vollmar J: Surgical experience with 197 traumatic
arterial lesions (1953-66) . In Hiertonn T,Rybeck
B (eds) : Traumatic Arterial Lesions. Stockholm,
Forsvarets Forskningsanstalt, 1968.

Warren R: Report to the Surgeon General. Wash-
ington, DC, Department of the Army, 1952.

Weinstein M, Golding A: Temporary external
shunt bypass in the traumatically amputated
upper extremity. J Trauma 1975;15:912-915.

Whelan TJ, Baugh JH: Non-Atherosclerotic Arter-
ial Lesions and Their Management. Current
Problems in Surgery. Chicago, "Vfear Book Medical
Publishers, 1967.

\bukeyj, Clagett GP, Rich NM, et al: Vascular trauma
secondary to diagnostic and therapeutic proce-
dures: 1974 through 1982. Am J Surg 1983;146:
788-791.

ch02.qxd 4/16/04 3:19 PM Page 73

Ischemia and
Reperfusion Injury

IRSHAD H. CHAUDRY
PING WANG
DORAID JARRAR

O INTRODUCTION

O ISCHEMIA-REPERFUSION INJURY

O ROLE OF ENDOTHELIAL CELLS FOLLOWING ISCHEMIA-REPERFUSION

O LEUKOCYTE-ENDOTHELIAL CELL INTERACTION FOLLOWING
ISCHEMIA-REPERFUSION

O ROLE OF PLATELETS AND COMPLEMENT SYSTEM

O DIVERGENT EFFECTS OF NITRIC OXIDE AND SUPEROXIDE
FOLLOWING ISCHEMIA-REPERFUSION

O CONFOUNDINGCOMORBIDITIESFOLLOWING ISCHEMIA-REPERFUSION

O SYSTEMIC LEVELS OF INFLAMMATORY MEDIATORS AND REMOTE
ORGAN INJURY

O SIGNIFICANCE OF ISCHEMIC PRECONDITIONING

O MODIFYING FACTORS DETERMINING ISCHEMIA-REPERFUSION INJURY

O TREATMENT OF ISCHEMIA-REPERFUSION INJURY: ROLE OF
PHARMACOLOGIC ADJUNCTS

O SUMMARY

ch02.qxd 4/16/04 3:19 PM Page 74

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

INTRODUCTION

The original Greek words ischein and haima
mean to hold and blood. In the modern
medical field, this means the lack of circula-
tion or perfusion. In this chapter, the patho-
physiology of ischemia and the clinical
implications for the clinician are outlined.
Specific attention is devoted to ischemia
caused by vascular injury, as well as the
potential therapeutic options under those
conditions (Bickwell and colleagues, 1989;
Burch and colleagues, 1990; Bickell and
colleagues, 1994; de Guzman and colleagues,
1999). Vascular injury is present in approxi-
mately 20% of all trauma admissions to a ter-
tiary care center. Besides obvious vascular
trauma with the threat of immediate exsan-
guination, vascular compromise with subtle
changes in perfusion and subsequent
ischemia is an important issue in the sec-
ondary survey of the traumatized host. A thor-
ough physical examination of the patient is,
therefore, mandatory to identify vascular
compromise and possible ischemia of the
dependent organ or system.

With the evolution of multicellular organ-
isms, the development of the cardiovascular
system was essential, because the exchange of
nutrients and oxygen is limited by diffusion
and, therefore, is feasible only for single-cell
organisms. In an adult human, thousands
of miles of vessels of various size, shape, and
capacity provide the body with oxygen and
nutrients. This complex system also is respon-
sible for the clearance of waste products and
serves as the transport medium for hormones
to reach their target sites. With the depen-
dence of virtually all organs on aerobic metab-
olism, a stasis or even a reduction of blood
flow will inevitably result in tissue damage or
death, unless the collateral blood flow is
sufficient to meet the metabolic demands of
the affected organ bed.

The terms ischemia and hypoxia have been
used indiscriminately. In view of this, differen-
tiation between these two terms is important.
In this chapter, ischemia refers to a total lack of
oxygen, whereas hypoxia refers to decreased
oxygen availability. Furthermore, whereas
ischemia, that is, stasis of blood flow, inevitably
leads to hypoxia of the dependent organ or

organ system, hypoxia can occur in the pres-
ence of normal blood flow. Moreover, it
appears that the detrimental effects of
ischemia are not only due to the lack of oxygen,
but also to the role of blood both to preserve
tissue homeostasis and to deliver oxygen.

Clinical decision making is highly depen-
dent on whether the ischemic event occurred
acutely or has evolved over a prolonged time.
If there has been a slow onset of decreased
blood flow, leading ultimately to ischemia, col-
lateral blood supply may have developed.
However, in the case of traumatic vascular
injury to an extremity, revascularization must
be accomplished within 6 hours, because
warm ischemia time for striated muscle results
in irreversible damage after 6 to 8 hours.

With the re-establishment of blood flow to
a previous ischemic organ or limb, reperfu-
sion is initiated, that is, ischemia-reperfusion
(I/R) . This event also marks the onset of
reperfusion injury, a complex event that
involves many cellular and hormonal com-
ponents including oxygen radicals, neu-
trophils, and complement activation.
Reperfusion of an ischemic vascular bed not
only produces local injury but also could
produce distant organ injury.

The clinical hallmarks of ischemia are the
five Ps: pain, pulselessness, paresthesia, pallor,
and paralysis. In the event of acute ischemia,
pain and pulselessness are the leading clini-
cal symptoms. Nevertheless, it should be kept
in mind that in the multi-injured or uncon-
scious patients, the clinical diagnosis may be
difficult, and an appropriate vascular exami-
nation including Doppler flow ultrasound is
mandated if vascular injury or compromise is
suspected. If vascular trauma is present, the
therapeutic goal should be restoration of func-
tion to the preinjury level (Burch and col-
leagues, 1990; Bickell and colleagues, 1994).
In case of extremity trauma, warm ischemia
time should not exceed 6 hours to ensure com-
plete recovery of the extremity.

ISCHEMIA-REPERFUSION
INJURY

Ischemia caused by conditions such as hem-
orrhagic shock, vascular trauma, and cardiac

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2 • ISCHEMIA AND REPERFUSION INJURY

arrest, followed by reperfusion of the tissues
with oxygenated blood, can compromise
microvascular and cellular integrity (Massberg
and Messmer, 1998; Ikeda and colleagues,
2000; Lefer, 1999; Lefer, 1994). The patho-
physiologic mechanisms causing the so-called
I/R injury are quite complex and involve a
variety of cell populations including endothe-
lial cells, leukocytes, hormones, up-regulation
of cell surface proteins, and activation of the
complement system. Part of the I/R injury is
attributable to the phenomenon of slow reflow
or no reflow, which is characterized by reduced
blood flow despite the restoration of adequate
perfusion pressure (Menger and colleagues,
1992). Although this phenomenon is still
poorly understood, apparently, leukocytes, at
least partially, mediate postischemic microvas-
cular compromise (Schlag and colleagues,
2001; Kadambi and Skalak, 2000; Menger and
colleagues, 1997; Waxman, 1996; Nolte and
colleagues, 1991; Lehr and colleagues, 1991) .
Leukocyte adhesion to the endothelium is
significantly enhanced following I/R injury,
which is mediated by several adhesion mole-
cules on the surface of leukocytes and/or
endothelial cells such as immunoglobulin-like
receptors (intercellular adhesion molecule-1
[ICAM-1], platelet endothelial cell adhesion
molecule-1 [PECAM-1 ] , vascular cell adhesion
molecule-1 [VCAM-1]), integrins (CD11/
CD18) , and selectins (E-, P-, L-selectin) (Nolte
and colleagues, 1994; Thorlacius and col-
leagues, 1998; Jaeschke, 1998; Weiser and col-
leagues, 1996; Farhood and colleagues, 1995) .
The endothelium now has been recognized
not just to be a lining of the vascular conduit,
but also to play a key role in the multistep
process of leukocyte accumulation and emi-
gration (Ikeda and colleagues, 2000). More-
over, soluble mediators, which are released
after reperfusion, such as proinflammatory
cytokines (tumor necrosis factor-a [TNF-a],
interleukins, platelet-activating factor [PAF] ) ,
and leukotrienes, contribute to postischemic
endothelial edema formation and perfusion
dysfunction (Lefer, 1999; Jarrar and col-
leagues, 1999; Wang and colleagues, 1995;
Jarras and colleagues, 2001; Linden, 2001).
Moreover, radicals generated during reper-
fusion with oxygen-rich blood are factors that
cause membrane damage and microvascular
dysfunction.

The depletion of energy-rich phosphates
such as adenosine triphosphate (ATP) dimin-
ishes the ability of the endothelial cell to main-
tain a transmembrane gradient of cations and
anions as during normal homeostasis and
leads to cell swelling and impairs cell integrity,
causing extravasation of macromolecules, the
so-called leakage (Wang and colleagues, 1999;
Chaudry, 1983; Chaudry, 1990; Wang and col-
leagues, 1995; Wang and colleagues, 1994;
Clemens and colleagues, 1985; Chaudry,
1989). The bioavailability of nitric oxide
(NO) under those conditions is also markedly
reduced (Ikeda and colleagues, 2000; Kim and
Hwan, 2001; Hierholzer and colleagues, 2001;
Uhlmann and colleagues, 2000; Traber, 2000) .
NO plays an important role in maintaining
vascular tone and has antiadhesive properties
(Wang and colleagues, 1995; Carden and
Granger, 2000; Zhou and colleagues, 1997,
Wang and colleagues, 1995; Wang and col-
leagues, 1994) . With the advances in molec-
ular biology techniques and knowledge, it has
been shown that the proinflammatory milieu
and generation of oxygen radicals trigger the
activation of intracellular signaling pathways,
leading to translocation of nuclear transcrip-
tion factors and induction of stress genes and
de novo protein synthesis (Okubo and col-
leagues, 2000; McDonald and colleagues,
2001; Jarrar and colleagues, 2000; Massberg
and colleagues).

The key role of leukocytes in the manifesta-
tion of I/R injury has been documented using
anti-adhesion molecule strategies, for example,
monoclonal antibodies or antineutrophil
serum. Through polymorphonuclear (PMN)
leukocytes accumulation and leukocyte-capil-
lary plugging, reperfusion is further impaired,
enhancing the vicious cycle of no- reflow under
those conditions (Massberg and Messmer,
1998; Lefer, 1999; Schlag and colleagues, 2001;
Yamaguchi and colleagues, 1999).

The gut has been proposed as the motor
for initiating multiorgan dysfunction follow-
ing trauma and I/R. Although endotoxin and
bacteria translocation may play a role in induc-
ing cell and organ dysfunction following I/R,
mediators that are released to the portal blood
or lymph can activate neutrophils and Kupffer
cells to release proinflammatory mediators,
causing organ dysfunction. Characterization
of the role of gut-derived mediators and/or

ch02.qxd 4/16/04 3:19 PM Page 76

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

factors during I/Rwill provide further insight
into the mechanism responsible for cell and
organ dysfunction following I/R.

ROLE OF ENDOTHELIAL CELLS
FOLLOWING ISCHEMIA-
REPERFUSION

Unstressed endothelial cells express a distinct
set of genes that produce a nonthrombogenic
lining of the blood vessels (Linden, 2001 ; Boyle
and colleagues, 1999) . This minimizes inter-
action between the endothelial lining and cir-
culating blood cells and platelets. Moreover,
during homeostasis, antithrombotic and pro-
coagulatory mechanisms are balanced. This
includes the production of thrombomodulin
and vasoactive molecules such as NO and
prostacyclin, which promote vasodilation and
inhibition of smooth muscle cell contraction
(Boyle and colleagues, 1999; Massberg and
colleagues, 1999; Lefer and Lefer, 1993). Fol-
lowing I/R, genes favoring an inflammatory
milieu are preferentially induced. This leads
to the increased production of E-selectin,
ICAM, VCAM, and in terleukin-8 (IL-8) , which
promote leukocyte rolling, aggregation, sub-
sequent adhesion and trans-endothelial cell
migration (Massberg and Messmer, 1998;
Schlag and colleagues, 2001; Massberg and
colleagues, 1999; Boyle and colleagues, 1999) .
Moreover, the production of the vasoactive
molecule NO by constitutive NO synthetase
(NOS) is diminished, whereas superoxide pro-
duction is increased. Experimental data have
shown that following I/R, endothelium-
dependent vasodilation in arterioles is
reduced because NO is not available in
sufficient quantities to serve as a second mes-
senger in response to endogenous vasodila-
tors such as acetylcholine (Farhood and
colleagues, 1995; Lefer and Leafer, 1993).
Arteriolar smooth muscle cell responsiveness,
however, is maintained under those condi-
tions. At a molecular level, studies have shown
that the transcription factor NF-kB plays a key
in the phenotypic changes of the endothelial
cell lining toward an inflammatory phenotype.
NF-kB is activated by oxidative stress, and upon
degradation of its inhibitory molecule IkBoc,
NF-kB is translocated to the nucleus where it

binds to specific deoxyribonucleic acid (DNA)
binding sequences, commonly the promoter
region of inflammatory proteins and adhe-
sion molecules, thereby increasing their rate
of gene transcription. This includes E-selectin,
VCAM, ICAM, IL-8, TNF-a, and the inter-
leukins. Moreover, PAF receptor, tissue factor,
and plasminogen activator are regulated by
NF-kB and are induced following I/R, leading
to microthrombosis, reduced blood flow, and
leukocyte activation (McDonald and col-
leagues, 2001).

LEUKOCYTE-ENDOTHELIAL
CELL INTERACTION
FOLLOWING ISCHEMIA-
REPERFUSION

Leukocyte trafficking through the microcir-
culation of tissues is essential for immune sur-
veillance of tissues and early detection of
pathologic conditions. Leukocyte recruit-
ment is tightly regulated not only by the neu-
trophils, but also by the endothelial cell and
adjacent tissue cells such as monocytes and
mast cells. Several distinct steps regulate the
recruitment of leukocytes into the extravas-
cular space following inflammatory stimuli as
observed after I/R (Fig. 2-1). The first step
in this process is the rolling of leukocytes
along the microvascular endothelium. Under
normal flow conditions, leukocytes travel
along an axial stream, whereas rolling allows
contact of the blood cells with the endothe-
lium. P-selectin, an adhesion glycoprotein, pri-
marily regulates this process. In the second
step, which is mediated via the expression of
CD11/CD18, a member of the (3 2 -integrins,
on the surface of leukocytes and ICAM-1,
a member of the immunoglobulin super-
family, on the apical site of endothelial cells,
the rolling leukocyte adheres firmly to the
endothelium (Massberg and colleagues, 1998;
Becker and colleagues, 1994; Menger and col-
leagues, 1994; Menger and colleagues, 1997;
Pickelmann and colleagues, 1998; Steinbauer
and colleagues, 1998; Kaeffer and colleagues,
1997). Finally, transendothelial migration
occurs, requiring PECAM-1. The primary
target sites for the aforementioned process

ch02.qxd 4/16/04 3:19 PM Page 77

Proinflammatory milieu: E-selectin, P-selectin, IL-6, IL-8

2 • ISCHEMIA AND REPERFUSION INJURY 77
Oxidative stress Procoagulant

Free flowing

C3a, C5aa, Histamine,
Bradykinin, Serotonin

■ FIGURE 2-1

This figure shows the leukocyte-endothelium cell interactions following ischemia-reperfusion. Under
normal conditions, the cellular components of the blood are separated from the endothelium by a
rim of plasma. Following adverse circulatory conditions such as ischemia-reperfusion, the leukocyte
gets in proximity to the endothelial wall by rolling along the wall. Up-regulation of adhesion
molecules such as intercellular adhesion molecule-1 on the endothelial surface and the CD1 1/CD18
complex on polymorphonuclear (PMN) leukocytes then promotes sticking of the leukocytes to the
venules. Subsequently, transendothelial migration of PMN is enhanced by tissue mast cells and the
release of inflammatory meditators. Together with activation of platelets, this leads to the no-reflow
phenomenon in postcapillary venules following ischemia-reperfusion. ■

are the postcapillary venules. This multistep
process is markedly enhanced by local oxida-
tive stress. Although initially the endothelium
via xanthine oxidase serves as a production
site of superoxide and hydrogen peroxide, the
adherent leukocyte then amplifies this event
and accounts for the substantially greater
amount of radicals produced. Reperfusion
and reintroduction of molecular oxygen add
significantly to oxidative stress in the post-
capillary venules. Furthermore, this results in
an imbalance in the production of NO and
superoxide, accounting for microvascular
dysfunction and the no-reflow phenomenon.
The lack of sufficient NO by the endothelial
NOS leads to the unavailability of NO to serve
as a second messenger and to effectively
scavenge superoxide. Studies by Massberg
and Messmer (1998) have demonstrated that

leukocyte-endothelial cell interaction pre-
cedes capillary perfusion failure and is the
primary step responsible for the pathophysi-
ologic sequelae following I/R (Fig. 2-2).

ROLE OF PLATELETS AND
COMPLEMENT SYSTEM

Other than PMN cells and the endothelium,
other blood components such as the anuclear
platelets play an important role in I/R injury.
Platelets are a source of oxygen radicals,
release inflammatory mediators including
thromboxane A 2 , leukotrienes, serotonin,
and platelet factor-4. Recruitment of platelets
early following I/R to the postischemic vas-
culature leads to luminal narrowing and local

ch02.qxd 4/16/04 3:19 PM Page 78

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

-| Ischemia/Reperfusion [

Leukocytes |

NF-kB, MAPK

Calpain/HSP/Antisense
oligonucleotides

CD11/CD18

Endothelium

| Inflammatory milieu

NF-kB, MAPK

Adhesion molecules:
ICAM-1, ICAM-2

] P-selectin

Anti-selectin Ab ,

\ Decreased ATP

ATP-MgCl2 ,

^Leukotrienes

NF-kB, MAPK

TNF-a, IL-6, Reactive oxygen species

-^Scavengers, Receptor antagonists

Decreased nitric oxide

L-Arginine/Allopurinol r

■ Increased superoxide

^ Platelet-activating factor receptor

| Tissue/plasminogen factor

] Activation of complement system |

Prostaglandin E1 ,

-i Calcium blocker: Diltiazem .

m FIGURE 2-2

This schema shows the pathophysiologic changes occurring following ischemia-reperfusion and
possible therapeutic interventions. Activation of intracellular stress signaling pathways are the key
event on a molecular level. The inflammatory milieu then results in a vicious cycle on the level of the
microcirculation. The potential therapeutic strategies are highlighted in dashed boxes. ■

thrombosis. Concomitantly, fibrinogen is
deposited at the endothelium, which displays
a procoagulant phenotype under those
conditions (Massberg and colleagues, 1997;
Massberg and colleagues, 1999). This is
dependent on the expression of ICAM-1.

DIVERGENT EFFECTS OF
NITRIC OXIDE AND
SUPEROXIDE FOLLOWING
ISCHEMIA-REPERFUSION

NO plays a critical role in I/R injury. As men-
tioned earlier in this chapter, this is partially
due to the role of NO to scavenge superox-
ide, which is produced by xanthine oxidase.
The substrate of xanthine oxidase, hypoxan-
thine, accumulates as the ATP stores are
depleted. The imbalance between reduced
availability of NO and the enhanced produc-
tion of toxic radicals increases leukocyte

accumulation and impairs microvascular per-
fusion. The role of xanthine oxidase as a con-
tributor to I/R injury has been demonstrated
using inhibitors of this enzyme such as allop-
urinol. Experimental data support the notion
that xanthine oxidase-derived oxidants act as
a chemoattractant that regulates leukocyte
trafficking in the microvasculature. The
studies of Suzuki and colleagues (1991) have
shown that exposure of postcapillary venules
to oxidative stress increases leukocyte accu-
mulation. The precise contribution of NO to
I/R injury, however, is complicated because
depending on the enzymatic source, NO may
have beneficial or deleterious effects on tissue
perfusion. Both constitutive and inducible
forms of the enzyme NOS accountfor the pro-
duction of NO. Constitutive Ca 2+ -dependent
production by constitutive NOS (cNOS)
(endothelial and neuronal NOS) is present
before the injury and is thought to be
beneficial. The Ca 2+ -independent, inducible
isoform (inducible NOS [iNOS], NOS-2)

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2 • ISCHEMIA AND REPERFUSION INJURY

accounts for the detrimental effects of NO,
including the production of peroxynitrate.
Insight into the complicated role of NOS fol-
lowing I/R has been gained using mice with
targeted disruption of the iNOS (NOS-2)
isoform (Kozlov and colleagues, 2001).
Deficiency in iNOS-derived NO resulted in a
significant reduction of skeletal muscle necro-
sis following hind-limb ischemia and reper-
fusion. Moreover, L-arginine supplementation
during I/R prevents microvascular perfusion
dysfunction by providing substrate for cNOS
and maintaining tissue NO levels while con-
comitantly decreasing superoxide production
(Ikeda and colleagues, 2000; Uhlmann and
colleagues, 2000; Traber, 2000; Carden and
Granger, 2000; Suzuki and colleagues, 1991;
Rahat and colleagues, 2001). These findings
not only underscore the significance of NO
in maintaining microvascular integrity and
perfusion under normal and pathologic con-
ditions but also imply that L-arginine may be
a useful therapeutic agent under those
conditions.

CONFOUNDING
COMORBIDITIES FOLLOWING
ISCHEMIA-REPERFUSION

Although most trauma patients are in the
younger population with no prior medical
history, the consequences of I/R injury sec-
ondary to vascular trauma and/or compro-
mise require special attention in comorbid
patients. Comorbidities such as diabetes niel-
li tus, hypertension, and hypercholesterolemia
are all associated with arteriosclerotic disease
and preexisting microvascular compromise
(Huk and colleagues, 2000; Tailor and Granger,
2000; Hoshida and colleagues, 2000; Salas and
colleagues, 1999; Bouchard and Lamontagne,
1998; Panes and colleagues, 1996). It is very
conceivable and proven experimentally using
animal strains expressing the aforementioned
diseases that these confounding factors
further aggravate I/R injury following vascu-
lar trauma and successful revascularization.
This should be kept in mind when taking care
of elderly patients, because the window for
successful therapeutic interventions is even
narrower under those conditions.

SYSTEMIC LEVELS OF
INFLAMMATORY MEDIATORS
AND REMOTE ORGAN INJURY

Following ischemia and reperfusion, local pro-
duction and release of inflammatory media-
tors such cytokines, oxygen radicals, and
vasoactive peptides are markedly enhanced.
As discussed earlier in this chapter, this local
inflammatory milieu contributes to PMN
and platelet adhesion and ultimately to the
no-reflow phenomenon. However, following
I/R, this is not contained to the affected organ
or organ system and leads to significant
increased levels of mediator in the systemic
circulation. For example, even simple laparo-
tomy increased TNF-a messenger ribonucleic
acid (mRNA) production in lung tissues,
which was even further enhanced after
remote, that is, intestinal, I/R. Circulating
levels of xanthine oxidase are markedly ele-
vated following I/R and accounted for acti-
vation of Kupffer cells and elevated liver
enzyme release following hind-limb ischemia.
Moreover, similar results were obtained
by the administration of exogenous xanthine
oxidase. From experimental and clinical data,
it appears that the lungs are the most sus-
ceptible organ to low-flow conditions includ-
ing ischemic events. The acute respiratory
distress syndrome (ARDS) is a threaded event
following adverse circulatory conditions, with
a high mortality once fully developed. Appar-
ently, once the initial I/R insult has been severe
enough to lead to the systemic inflammatory
response syndrome, circulating neutrophils
are activated, leading to leukocyte-
endothelial cell interaction in multiple vas-
cular beds. The radiologic hallmark of ARDS,
bilateral infiltrates, are caused by leukocyte
influx, interstitial edema, and alveolar wall
thickening. The development of respiratory
insufficiency usually begins within 24 to 72
hours after the initiating ischemic event. As
outlined earlier, the risk of developing ARDS
corresponds to the length of the ischemic time
and is markedly increased in the elderly
comorbid patient.

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

SIGNIFICANCE OF ISCHEMIC
PRECONDITIONING

Preconditioning refers to the phenomenon in
which the exposure of cells, tissues, or organ
systems to brief periods of ischemia protects
them from the deleterious effects of sub-
sequent prolonged ischemia. Although pre-
conditioning, for obvious reasons, is not
available in the acute setting of vascular
trauma and because of the need for subse-
quent immediate revascularization, it should
be discussed because important insights into
the mechanism ofl/R injury have been gained
from this phenomenon. Preconditioning
blunts the impairment of endothelium-
dependent relaxation to acetylcholine,
capillary plugging, leukocyte adhesion, and
the no-reflow phenomenon usually observed
following I/R. Among other mechanisms, a
distinct set of genes the family of heat shock
proteins (HSPs) confers protection against
adverse circulatory events. HSPs maintain cel-
lular survivability by preserving metabolic and
structural integrity of cells. Recent data suggest
that via the adenosine A[ receptor and acti-
vation of protein kinase C, as well as tyrosine
kinases, HSP27 is phosphorylated, thereby
conferring protection against a subsequent
lethal insult (Davies and Hagen, 1993;
Speechly-Dick and colleagues, 1995) . Sum-
marizing ongoing efforts, it appears that
selective induction of the HSPs might become
a therapeutic modality.

MODIFYING FACTORS
DETERMINING ISCHEMIA-
REPERFUSION INJURY

Several factors modify the consequences, that
is, the extent of tissue injury following
I/R. Ambient temperature is well known to
modulate the extent of necrosis. These lessons
are learned from transplantation of solid
organs, a classic example of I/R injury.
Decreasing the temperature of the storage
solution to 4°C can accomplish later re-
establishment of the venous and arterial
blood flow with complete return of organ func-

tion. In the case of extremity trauma with com-
plete amputation, the recommendations are
that the severed limb be stored in ice water
until the patient is transported to an appro-
priate center with expertise in vascular surgery.

TREATMENT OF ISCHEMIA-
REPERFUSION INJURY: ROLE
OF PHARMACOLOGIC
ADJUNCTS

A key event during ischemia is the decrease
in the cellular levels of energy-rich phosphates,
such as ATP. In view of this, studies have used
the approach of administrating ATP-MgCl 2
after I/R, and such studies have shown that
endothelial cell function can be restored fol-
lowing adverse circulatory conditions (Wang
and colleagues, 1999; Wang and colleagues,
1995; Dana and colleagues, 2000; Gaudio and
colleagues, 1982; Chaudry and colleagues,
1983; Ohkawa and colleagues, 1983; Chaudry
and colleagues, 1984) . Moreover, monoclonal
antibodies against adhesion molecules such
as CD 11 /CD 18 or the P-selectin family have
also been beneficial in preventing I/R injury
(Ohkawa and colleagues, 1984).

Improvement of blood flow using rheologic
agents such as dextran are also effective in
improving capillary reflow following I/R
(Sharar and colleagues, 1991; Schott and
colleagues, 1998). Administration of pro-
staglandin Ex following I/R normalized NO
and superoxide release and thus improved
microvascular blood flowwith reduced adher-
ence of leukocytes (Berglund and colleagues,
1981).

Although all the aforementioned agents
have been shown to reduce I/R injury in
experimental models, they have not been used
clinically to improve outcome in patients
following vascular trauma and subsequent
ischemic events. Only the intraoperative
administration of heparin following vascular
extremity injury has been shown to signifi-
cantly improve the rate of limb salvage (Forrest
and colleagues, 1991; Melton and colleagues,
1997; Wang and colleagues, 1990; Rana and
colleagues, 1992; Wang and colleagues, 1993;
Wang and colleagues, 1994; Zellweger, 1995) .

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2 • ISCHEMIA AND REPERFUSION INJURY

SUMMARY

This chapter has covered pathophysiology of
ischemia and reperfusion injury, including the
consequences of re-establishment of blood
flow following a variable period of cessation
of perfusion with oxygenated blood (Wang
and colleagues, 1996; Wall and colleagues,
1996) . Apparently, I/R injury is due not only
to the lack of oxygen as seen during ischemia,
but also to the absence of whole blood with
its scavenging properties. Generally speaking,
I/Rinjury is the most common cause of death
in the Western Hemisphere because of the
prevalence of arteriosclerotic disease includ-
ing the coronary arteries (Shin and col-
leagues, 2000; Beebe and colleagues, 1996;
Brengman and colleagues, 2000; Eifert and
colleagues, 2000). The key pathophysiologic
events following I/R have been investigated
in depth. In this regard, the leukocyte-
endothelial cell interactions appear to be a
key element, which results in the phenome-
non of no reflow following adverse circula-
tory conditions, secondary to enhanced PMN
leukocyte recruitment to the postcapillary
venules. Using intravital microscopy, it has
been shown that an orderly sequence of events
takes place including leukocyte rolling, stick-
ing, and adherence, followed by transendothe-
lial migration. These processes are modified
by the inflammatory milieu generated fol-
lowing I/R injury. Reactive oxygen species,
proinflammatory cytokines, superoxide, and
other paracrine messengers all intensify
the leukocyte-endothelial cell interaction,
leading to microvascular perfusion failure.
Paradoxically, most of the damage occurs
during the reperfusion period and to a lesser
extent during the actual ischemic time.

The probably most significant independent
factor determining injury following vascular
injury and subsequent ischemia of an organ
or limb is time until re-establishment of blood
flow. Modifying factors, however, include
ambient temperature and preexisting comor-
bidities. Although a variety of therapeutic
agents have been effectively used in experi-
mental studies, this has notyet been translated
into an accepted modality in clinical practice.
Of note, the decrease in hematocrit during

vascular injury caused by blood loss has bene-
ficial effects on the rheology of the microvas-
culature but does mandate immediate blood
transfusion.

With the use of molecular biology tools, the
changes on the cellular mRNA and protein
level have also been characterized following
I/R. A distinct set of stress response genes and
signaling pathways appear activated, leading
to a change in the phenotype of leukocytes
and endothelial cells. This propagates the local
inflammatory milieu, resulting in the up-
regulation of adhesion molecules and the no
reflow following ischemia and reperfusion.
With the advances in our understanding of
the molecular mechanisms of I/R injury, selec-
tive modulation of the aforementioned phe-
notypic changes in leukocytes and endothelial
cells should be forthcoming.

REFERENCES

Barker JE, Knight KR, Romeo R, et al: Targeted
disruption of the nitric oxide synthase 2 gene
protects against ischemia/ reperfusion injury to
skeletal muscle. J Pathol 2001;194:10-115.

Becker M, Menger MD, Lehr HA: Heparin-re leased
superoxide dismutase inhibits postischemic
leukocyte adhesion to venular endothelium. Am
J Physiol 1994;267:H925-H930.

Beebe HG, Bergan JJ, Bergqvist D, et al:
Classification and grading of chronic venous
disease in the lower limbs. A consensus statement.
EurJ Vase Endovasc Surg, 1996;12:487-492.

Berglund B, Swanbeck G, Hedin H: Low molecu-
lar weight dextran therapy for digital ischemia
due to collagen vascular disease. Dermatologica
1981;163:353-357.

Bickell WH, Shaftan GW, Mattox KL: Intravenous
fluid administration and uncontrolled hemor-
rhage . J Trauma 1989;29:409.

Bickell WH, Wall MJ Jr, Pepe PE, et al: Immediate
versus delayed fluid resuscitation for hypoten-
sive patients with penetrating torso injuries. N
Engl Med 1994;331:1105-1109.

Bouchard JF, Lamontagne D: Protection afforded
by preconditioning to the diabetic heart against
ischemic injury. Cardiovasc Res 1998;37:82-
90.

Boyle EM Jr, Canty TG Jr, Morgan EN, et al: Treat-
ing myocardial ischemia-reperfusion injury by

ch02.qxd 4/16/04 3:19 PM Page 82

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

targeting endothelial cell transcription. Ann
Thorac Surg 1999;68:1949-1953.

Brengman ML, O'Donnell SD, Mullenix P, et al:
The fate of a patent carotid artery contralateral
to an occlusion. Ann Vase Surg 2000;14:77-81.

Burch JM, Richardson RJ, Martin RR, Mattox KL:
Penetrating iliac vascular injuries: recent expe-
rience with 233 consecutive patients. J Trauma
1990;30:1450-1459.

Carden DL, Granger DN: Pathophysiology of
ischemia-reperfusion injury. J Pathol 2000;190:
255-266.

Chaudry IH: Cellular mechanisms in shock and
ischemia and their correction. Am J Physiol
1983;245:R117-R134.

Chaudry IH: ATP-MgCL and liver blood flow fol-
lowing shock and ischemia. Prog Clin Biol Res
1989;299:19-31.

Chaudry IH: The use of ATP following shock and
ischemia. Ann N Y Acad Sci 1990;603:
130-141.

Chaudry IH, Ohkawa M, Clemens MG: Improved
mitochondrial function following ischemia and
reflow by ATP-MgCl,. Am J Physiol 1984;246:
R799-R804.

Chaudry IH, Ohkawa M, Clemens MG, Baue AE:
Alterations in electron transport and cellular
metabolism with shock and trauma. Prog Clin
Biol Res 1983;111:67-88.

Clemens MG, McDonah PF, Chaudry IH, Baue AE:
Hepatic microcirculatory failure after ischemia
and reperfusion: Improvement with ATP-MgCL
treatment. AmJPhysiol 1985;248:H804-H811.

Dana A, Skarli M, Papakrivopoulou J, Yellon DM:
Adenosine A(l) receptor induced delayed
preconditioning in rabbits: Induction of p38
mitogen-activated protein kinase activation and
Hsp27 phosphorylation via a tyrosine kinase —
and protein kinase C-dependent mechanism.
Circ Res 2000;86:989-997.

Davies MG, Hagen PO: The vascular endothelium.
A new horizon. Ann Surg 1993;218:593-609.

de Guzman E, Shankar MN, Mattox KL: Limited
volume resuscitation in penetrating thoracoab-
dominal trauma. AACN Clin Issues 1999;10:61-
68.

Eifert S, VillavicencioJL, Kao TC, et al: Prevalence
of deep venous anomalies in congenital vascu-
lar malformations of venous predominance.
J Vase Surg 2000;31 :462-471 .

Farhood A, McGuire GM, Manning AM, et al:
Intercellular adhesion molecule 1 (ICAM-1)
expression and its role in neutrophil-induced

ischemia-reperfusion injury in rat liver. J Leukoc
Biol 1995;57:368-374.

Forrest CR, Pang CY, Zhong AG, Kreidstein ML:
Efficacy of intravenous infusion of prostacyclin
(PG12) or prostaglandin Ei (PGE]) in augmen-
tation of skin flap blood flow and viability in the
pig. Prostaglandins 1991;41:537-558.

Gaudio KM, Taylor MR, Chaudry IH, et al: Accel-
erated recovery of single nephron function by
the postischemic infusion of ATP-MgCL. Kidney
Int 1982;22:13-20.

Geller DA, Chia SH, Takahashi Y, et al: Protective
role of the L-arginine-nitric oxide synthase
pathway on preservation injury after rat liver
transplantation. J Patenter Enter Nutr 2001;
25:142-147.

Hierholzer C, Harbrecht BG, Billiar TR, Tweardy
DJ: Hypoxia-inducible factor-1 activation
and cyclo-oxygenase-2 induction are early
reperfusion-independent inflammatory events
in hemorrhagic shock. Arch Orthop Trauma
Surg 2001;121:219-222.

Hoshida S, Yamashita N, Otsu K, et al: Cholesterol
feeding exacerbates myocardial injury in Zucker
diabe tic fatty rats. Am J Physiol Heart Circ Physiol
2000;278:H256-H262.

Huk I, Brovkovych V, Nanobashvili J, et al:
Prostaglandin E] reduces ischemia/reperfusion
injury by normalizing nitric oxide and super-
oxide release. Shock 2000;14:234-242.

Ikeda Y, Young LH, Scalia R, Lefer AM: Cardio-
protective effects of citrulline in ischemia/
reperfusion injury via a non-nitric oxide-
mediated mechanism. Methods Find Exp Clin
Pharmacol 2000;22:563-571.

Jaeschke H: Mechanisms of reperfusion injury after
warm ischemia of the liver. J Hepatobiliary
Pancreat Surg 1998;5:402-408.

Jarrar D, Chaudry IH, Wang P: Organ dysfunction
following hemorrhage and sepsis: Mechanisms
and therapeutic approaches [Review] . Int J Mol
Med 1999;4:575-583.

Jarrar D, Wang P, Chaudry IH: Hepatocellular
dysfunction: Basic considerations. In Holzheimer
RG, Mannick JA (eds): Surgical Treatment:
Evidence-Based and Problem-Oriented. Munich,
Germany, Zuckschwerdt Verglad, 2001 : 763-767.

Jarrar D, Wang P, Song GY, et al: Inhibition of tyro-
sine kinase signaling after trauma-hemorrhage:
A novel approach for improving organ function
and decreasing susceptibility to subsequent
sepsis. Ann Surg 2000;231:399-407.

ch02.qxd 4/16/04 3:19 PM Page 83

2 • ISCHEMIA AND REPERFUSION INJURY

Kadambi A, Shalak TC: Role of leukocytes and
tissue-derived oxidants in short-term skeletal
muscle ischemia-reperfusion injury. Am J Physiol
Heart Circ Physiol 2000;278:H435-H443.

Kaeffer N, Richard V, Thuillez C: Delayed
coronary endothelial protection 24 hours after
preconditioning: Role of free radicals. Circula-
tion 1997;96:2311-2316.

Kim H, Hwan KK: Role of nitric oxide and mucus
in ischemia/ reperfusion-induced gastric muco-
sal injury in rats. Pharmacology 2001;62:200-207.

Kozlov AV, Sobhian B, Duvigneau C, et al: Organ
specific formation of nitrosyl complexes under
intestinal ischemia/reperfusion in rats involves
NOS-independent mechanism (s). Shock 2001;
15:366-371.

Lefer AM: Endotoxin, cytokines, and nitric oxide
in shock. Shock 1994;1:79-80.

Lefer AM: Role of the beta2-integrins and
immunoglobulin superfamily members in
myocardial ischemia-reperfusion. Ann Thorac
Surg 1999;68:1920-1923.

Lefer AM, Lefer DJ: Pharmacology of the endothe-
lium in ischemia-reperfusion and circulatory
shock. ArmRev Pharmacol Toxicol 1993;33:71-90.

Lehr HA, Guhlman A, Nolte D, et al: Leukotrienes
as mediators in ischemic-reperfusion injury in
a microcirculation model in the hamster. J Clin
Invest 1991;87:2036-2041.

Linden J: Molecular approach to adenosine recep-
tors: Receptor-mediated mechanisms of tissue
protection. Ann Rev Pharmacol Toxicol 2001;
41:775-787.

Massberg S, Enders G, Matos FC, et al: Fibrinogen
deposition at the postischemic vessel wall pro-
motes platelet adhesion during ischemia-reper-
fusion in vivo. Blood 1999;94:3829-3838.

Massberg S, Messmer K: The nature of ischemia/
reperfusion injury. Transplant Proc 1998;30:
4217-4223.

Massberg S, Sausbier M, Klatt P, et al: Increased
adhesion and aggregation of platelets lacking
cyclic guanosine 3',5'-monophosphate kinase I.
J Exp Med 1999;189:1255-1264.

McDonald MC, Mota-Filipe H, Paul A, et al:
Calpain inhibitor I reduces the activation of
nuclear factor-kappaB and organ injury/
dysfunction in hemorrhagic shock. FASEB J
2001;15:171-186.

Melton SM, Croce MA, Patton JHJr, et al: Popliteal
artery trauma. Systemic anticoagulation and
intraoperative thrombolysis improves limb
salvage. Ann Surg 1997;225:518-527.

Menger MD, Kerger H, Geisweid A, et al:
Leukocyte-endothelium interaction in the
microvasculature of postischemic striated
muscle. Adv Exp Med Biol 1994;361:541-545.

Menger MD, Pelikan S, Steiner D, Messmer K;
Microvascular ischemia-reperfusion injury in stri-
ated muscle: significance of reflow paradox. Am
J Physiol 1992;263:H1901-H1906.

Menger MD, Rucker M, Vollmar B: Capillary dys-
function in striated muscle ischemia/
reperfusion: on the mechanisms of capillary
no-reflow. Shock 1997;8:2-7.

Menger MD, Volmmar B: In vivo analysis of
microvascular reperfusion injury in striated
muscle and skin. Microsurgery 1994;15:383-389.

Nolte D, Hecht R, Schmid P, et al: Role of Mac-1
and ICAM-1 in ischemia-reperfusion injury in a
microcirculation model of BALB/C mice. Am J
Physiol 1994;267:H1320-H1328.

Nolte D, Lehr HA, Messmer K: Adenosine inhibits
postischemic leukocyte-endothelium interac-
tion in postcapillary venules of the hamster. Am
J Physiol 1991;261:H651-H655.

Ohkawa M, Chaudry IH, Clemens MG, Baue AE:
ATP-MgCL produces sustained improvement in
hepatic mitochondrial function and blood flow
after hepatic ischemia. J Surg Res 1984;37:226-
234.

Ohkawa M, Clemens MG, Chaudry IH: Studies on
the mechanism of beneficial effects of ATP-MgCL
following hepatic ischemia. Am J Physiol 1983;
244:R695-R702.

Okubo S, Bernardo NL, Elliott GT, et al: Tyrosine
kinase signaling in action potential shortening
and expression of HSP72 in late precondition-
ing. Am J Physiol Heart Circ Physiol 2000;279:
H2269-H2276.

PanesJ, Kurose I, Rodriguez-Vaca D, et al: Diabetes
exacerbates inflammatory responses to ischemia-
reperfusion. Circulation 1996;93:161-167.

Pickelmann S, Nolte D, Leiderer R, et al: Attenu-
ation of postischemic reperfusion injury in stri-
ated skin muscle by diaspirin-cross-linked
Hb. Am J Physiol 1998;275:H361-H368.

Rahat MA, Lahat N, Smollar J, et al: Divergent
effects of ischemia/reperfusion and nitric oxide
donor on TNF-alpha mRNA accumulation in rat
organs. Shock 2001;15:312-317.

RanaMW, Singh G, WangP, etal: Protective effects
of preheparinization on the microvasculature
during and after hemorrhagic shock. J Trauma
1992;32:420-426.

Salas A, PanesJ, Rosenbloom CL, et al: Differen-
tial effects of a nitric oxide donor on

ch02.qxd 4/16/04 3:19 PM Page 84

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

reperfusion-induced microvascular dysfunction
in diabetic and non-diabetic rats. Diabetologia
1999;42:1350-1358.

Schlag MG, Harris KA, Potter RF: Role of leuko-
cyte accumulation and oxygen radicals in
ischemia-reperfusion-induced injury in skeletal
muscle. Am J Physiol Heart Circ Physiol 2001;
280:H1716-H1721.

Schott U, Lindbom LO, Sjostrand U: Hemody-
namic effects of colloid concentration in exper-
imental hemorrhage: A comparison of Ringer's
acetate, 3% dextran-60, and 6% dextran-70. Crit
Care Med 1998;16:346-352.

Sharar SR, Winn RK, Murry CE, e t al: A CD1 8 mon-
oclonal antibody increases the incidence and
severity of subcutaneous abscess formation after
high-dose Staphylococcus aureus injection in
rabbits. Surgery 1991;110:213-220.

Shin DD, Wall MJ Jr, Mattox KL: Combined pene-
trating injury of the innominate artery, left
common carotid artery, trachea, and esophagus.
J Trauma 2000;49:780-783.

Speechly-Dick ME, Grover GJ, Yellon DM: Does
ischemic preconditioning in the human involve
protein kinase C and the ATP-dependent K +
channel? Studies of contractile function after
simulated ischemia in an atrial in vitro model.
Circ Res 1995;77:1030-1035.

Steinbauer M, Harris AG, Leiderer R, et al:
Impact of dextran on microvascular distur-
bances and tissue injury following ischemia/
reperfusion in striated muscle. Shock 1998;9:
345-351.

Tailor A, Granger DN: Role of adhesion molecules
in vascular regulation and damage. Curr Hyper-
tens Rep 2000;2:78-83.

Thorlacius H, Vollmar B, Westermann S, et al:
Effects of local cooling on microvascular hemo-
dynamics and leukocyte adhesion in the striated
muscle of hamsters. J Trauma 1998;45:715-
719.

Traber DL: Nitric oxide synthase and tissue injury.
Shock 2000;14:243-244.

Uhlmann D, Uhlmann S, Spiegel HU: Endothe-
lin/nitric oxide balance influences hepatic
ischemia-reperfusion injury. J Cardiovasc Phar-
macol 2000;36:S212-S214.

Wall MJ Jr, Granchi T, Liscum K, Mattox KL: Pen-
etrating thoracic vascular injuries. Surg Clin
North Am 1996;76:749-761.

Wang P, Ba ZF, Chaudry IH: Endothelial cell dys-
function occurs after hemorrhage in nonhep-
arinized bvit not in preheparinized models. J Surg
Res 1993;54:499-506.

Wang P, Ba ZF, Chaudry IH: Chemically modified
heparin improves hepatocellular function,
cardiac output, and microcirculation after
trauma-hemorrhage and resuscitation. Surgery
1994;116:169-175.

Wang P, Ba ZF, Chaudry IH: Nitric oxide. To block
or enhance its production during sepsis? Arch
Surg 1994;129:1137-1142.

Wang P, Ba ZF, Chaudry IH: ATP-MgCL restores
depressed endothelial cell function after hem-
orrhagic shock and resuscitation. Am J Physiol
1995;268:H1390-H1396.

Wang P, Ba ZF, Chaudry IH: Endothelium-
dependent relaxation is depressed at the macro-
and microcirculatory levels during sepsis.
Am J Physiol 1995;269:R988-R994.

Wang P, Ba ZF, Reich SS, et al: Effects of nonanti-
coagulant heparin on cardiovascular and hepa-
tocellular function after hemorrhagic shock. Am
J Physiol 1996;270:HI294-HI302.

Wang P, Ba ZF, Stepp KJ, Chaudry IH: Pentoxify-
line attenuates the depressed endothelial cell
function and vascular muscle contractility fol-
lowing trauma and hemorrhagic shock. J Trauma
1995;39:121-126.

Wang P, Singh G, Rana MW, et al: Prehepariniza-
tion improves organ function after hemorrhage
and resuscitation. Am J Physiol 1990;259:R645-
R650.

Wang P, Tait SM, Ba ZF, Chaudry IH: ATP-MgCL
administration normalizes macrophage cAMP
and beta-adrenergic receptors after hemorrhage
and resuscitation. Am J Physiol 1994;267:G52-
G58.

Waxman K: Shock: ischemia, reperfusion, and
inflammation. New Horiz 1996;4:153-160.

Weiser MR, Gibbs SA, Valeri CR, et al: An ti-se lectin
therapy modifies skeletal muscle ischemia and
reperfusion injury. Shock 1996;5:402-407.

Yamaguchi Y, Matsumura F, Liang J, et al: Neu-
trophil elastase and oxygen radicals enhance
monocyte chemoattractant protein-expression
after ischemia/ reperfusion in rat liver. Trans-
plantation 1999;68:1459-1468.

Zellweger R, Ayala A, Zhu XL, e t al: A novel nonan-
ticoagulant heparin improves splenocyte and
peritoneal macrophage immune function after
trauma-hemorrhage and resuscitation.J Surg Res
1995;59:211-218.

Zhou M, Wang P, Chaudry IH: Endothelial nitric
oxide synthase is downregulated during hyper-
dynamic sepsis. Biochim Biophys Acta 1997;
1335:182-190.

ch03.qxd 4/16/04 3:21PM Page 85

Minimal Vascular Injuries

JAMES W. DENNIS

O DEFINITION

O HISTORY OF THE MANAGEMENT OF MINIMAL INJURIES

O DEFINING THE NATURAL HISTORY OF MINIMAL INJURIES

O APPLICATION TO PENETRATING PROXIMITY EXTREMITY TRAUMA

O APPLICATION TO PENETRATING NECK INJURIES

O APPLICATION TO HIGH-RISK ORTHOPEDIC INJURIES

O SUMMARY

Arterial injuries come in various
shapes and sizes. Regardless of the
etiology, complete transections,
occlusions, bleeding lacerations, and large
pseudoaneurysms almost universally require
immediate surgical intervention or the patient
faces the loss of life or limb. These types of
arterial injuries make up the vast majority
(80% to 90%) of cases (Hardy and colleagues,
1975) . Since the earliest times, surgeons have
recognized that the type of injury can have a
profound effect on the ultimate outcome. A
special class of injuries has been recognized
over the past 15 years that can be called
"minimal injuries." This small select group
appears to have a unique natural history and

must be considered in this light. By under-
standing this natural history, management
plans for patients presenting with certain types
of injuries can be formulated so that they
ensure proper and safe treatment in the acute
setting.

DEFINITION

Minimal injuries are generally defined as
identifiable damage to a blood vessel, usually
by arteriography or ultrasound, with no clin-
ical signs of that injury. By definition, hard
signs of vascular trauma including pulse

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

■ FIGURE 3-1

A, Short segmental narrowing and intimal irregularity after a gunshot wound to the right brachial
artery. B, Complete resolution of injury 6 weeks later. (From Dennis JW, Frykberg ER, Crump JM, et
al: New perspectives on the management of penetrating trauma in proximity to major limb arteries. J
Vase Surg 1990;11:84-93.) ■

deficit, active hemorrhage, expanding
hematoma, distal ischemia, and bruit or thrill
are absent. Soft signs such as a history of bleed-
ing, stable hematoma, associated nerve deficit,
or unexplained hypotension may or may not
be present and have no direct relationship to
these injuries. Minimal injuries will also reg-
ularly demonstrate prograde flow of contrast
on arteriography or flow on ultrasound. In
addition, no gross, uncontained extravasation
of blood or contrast is seen outside the
normal lumen of the vessel involved.

Studies have identified four basic types of
minimal injuries, of which two dominate. The
first major type is focal segmental narrowing
or constriction that is characteristically smooth
in nature with tapering at both ends (Figs. 3-
1A and 3-2A). Arteries can demonstrate this
abnormality secondary to external compres-
sion, intramural hematoma (contusion), or

reactive spasm. Spasm is due to the myogenic
response of blood vessels to the blast effect of
penetrating missiles or direct effects of blunt
forces. Blood flow can be demonstrated
throughout this narrowed segment, which can
vary in length from just a few millimeters to
several centimeters.

The second predominant type of minimal
injury is that of the intimal flap or irregular-
ity (Fig. 3-3A) . This is usually seen as a luminal
surface abnormality in which the intimal layer
has a raised portion extending into the lumen.
Flaps may be lifted in either a proximal or a
distal orientation. It may also appear as a focal,
roughened area of the luminal surface. In both
forms, flow is present within the lumen and
there is no extravasation outside of it.

Small pseudoaneurysms and arteriovenous
(AV) fistulas make up the other two
smaller categories of minimal injuries.

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3 • MINIMAL VASCULAR INJURIES

■ FIGURE 3-2

A, Long smooth area of narrowing of the left brachial artery after a gunshot wound. B, Complete
resolution after 1 week. (From Dennis JW, Frykberg ER, Crump JM, et al: New perspectives on
the management of penetrating trauma in proximity to major limb arteries. J Vase Surg 1 990;
11:84-93.) ■

Pseudoaneurysms areformed when there is an
incomplete laceration of an artery with the
resultant hemorrhage contained by the sur-
rounding tissue (Fig. 3-4A) . These lesions are
easily seen by arteriography or ultrasound and
will appear as contained extravasation of con-
trast or blood outside the normal arterial
lumen. AVfistulas develop when an arterial lac-
eration and simultaneous laceration or tear
occurs in the adjacentvein causing flow to enter
into the low-pressure venous channel. This is
also clearly identified by arteriography or ultra-
sound as a direct passage of contrast or blood
from an artery into a vein without passing
through a capillary system.

In each of these minimal injuries, distal
pulses usually remain intact. In patients with
a pseudoaneurysm or AV fistula, an audible
bruit or thrill may be present on physical exam-
ination, indicating the need for further

evaluation to determine the nature and extent
of these injuries.

HISTORY OF THE
MANAGEMENT OF MINIMAL
INJURIES

Early information concerning vascular
trauma was the result of military experience
inWorldWarsIandll (DeBakeyandSimeone,
1946). Direct vascular repair of injuries was
not performed on a widespread basis, however,
until the 1950s in both the Korean conflict
and civilian settings (Hughes, 1958; Ferguson,
Byrd, and McAfee, 1961). The decision to
operate was initially based on physical exam-
ination alone, as there was no other available
or reliable means to diagnose vascular injuries.

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

■ FIGURE 3-3

A, Intimal irregularity or flap in the superficial femoral artery after a through-and-through gunshot
wound of the right thigh. 6, Complete resolution of the injury after 1 week. (From Dennis JW,
Frykberg ER, Crump JM, et al: New perspectives on the management of penetrating trauma in
proximity to major limb arteries. J Vase Surg 1990;11:84-93.) ■

Penetrating wounds in proximity to major
arteries began to be routinely explored to
determine the presence or absence of a
vascular injury. This policy continued into the
1970s when arteriography began to be widely
used to evaluate patients for vascular trauma
and avoid unnecessary surgery.

Multiple studies were published in the late
1970s and early 1980s that showed arteriog-
raphy to be as accurate as surgical exploration
for detecting any type of vascular injury fol-
lowing penetrating trauma to the extremities
(Synder and colleagues, 1978; Sirinek and
colleagues, 1981). These studies consistently
showed a more than 95% chance of having a
significant arterial injury when hard signs were
present on physical examination. In addition,
there was a 10% to 20% risk of an arterio-
graphic abnormality found even in the face
of normal physical examination results (Table
3-1). This new use of arteriography first
demonstrated the presence of these minimal
arterial injuries that had not been seen before

its use. Because no data existed about their
clinical significance, surgeons erred on the
side of operating on any abnormalities found.
This approach was based on the fear of
missing an injury that needed repair even in
the absence of any clinical findings. Univer-
sal recommendations resulting from these
series were to either surgically explore or
obtain an arteriogram on every patient with
penetrating trauma to the extremities. If any
abnormalities were seen on arteriography,
they required immediate exploration and
repair if needed.

DEFINING THE NATURAL
HISTORY OF MINIMAL
INJURIES

The first evidence that minimal vascular
injuries might have the potential to

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3 • MINIMAL VASCULAR INJURIES

■ FIGURE 3-4

A, Small pseudoaneurysm of
the left distal axillary artery
after a gunshot wound to the
shoulder. B, Pseudoaneurysm
10 months later — essentially
unchanged with possibly slight
improvement. (From Dennis
JW, Frykberg ER, Crump JM, et
al: New perspectives on the
management of penetrating
trauma in proximity to major
limb arteries. J Vase Surg
1990;11:84-93.) ■

TABLE 3-1

MECHANISM OF PENETRATING PROXIMITY EXTREMITY TRAUMA AND ULTIMATE

OUTCOME

Injury

Total (No.)

No. Arterial Injuries

No. Requiring Surgery (%)

Gunshot

247

24(9.7)

2 (0.8)*

Stab

5 (9.3)

2(3.7)

Shotgun

3(17.6)

2(11.8)*

Total

318

32(10.0)

6(1.8)

*One operated on immediately.

From Dennis JW, Frykberg ER, Crump JM, et al: New perspectives on the management of penetrating trauma in proximity to

major limb arteries. J Vase Surg 1990;11:84-93.

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

TABLE 3-2

RESULTS OF NONOPERATIVE OBSERVATION OF 29 CLINICALLY OCCULT ARTERIAL
INJURIES ACCORDING TO MORPHOLOGY

Total No.

Repeat Arteriogram (No.)
RES IMP UNC

WOR

Clinical
Follow-up (No.)

UNC

WOR

Narrowing

Intimal flap

Pseudoaneurysm

Total

'Underwent surgical repair.

IMP, improved; RES, resolved; UNC, unchanged; WOR, worsened.

From Dennis JW, Frykberg ER, Crump JM, et al: New perspectives on the management of penetrating trauma in proximity to

major limb arteries. J Vase Surg 1990;11:84-93.

spontaneously heal was work done by Glover
in 1986. He induced intimal tears in rat arter-
ies and harvested them for up to 1 year later.
All vessels remained patent and the endothe-
lial injury was consistently healed by 8 weeks
with no long-term sequelae (Glover, 1986) .
Clinical studies suggesting this might hold true
in humans began to appear soon (Stain and
colleagues, 1989; Kestenberg, 1990). These
scientific studies began to look at the natural
history of this unique class of injuries. The
first prospective series on penetrating extrem-
ity injuries was performed by Frykberg and
colleagues in 1989. This landmark article
detailed the potential healing properties of
this new class of minimal injuries when
followed with nonoperative management and
serial arteriograms. This new approach
revealed the natural history to be somewhat
benign in that the vast majority (up to 89%)
would either resolve spontaneously or remain
unchanged. Approximately 11% would dete-
riorate and require surgical repair, but this
could be done safely and with no increase in
morbidity or limb loss when performed on a
delayed basis. Alarger series published almost
2 years later confirmed the earlier results, by
showing 87% of minimal injuries would
heal if treated conservatively (Dennis and
colleagues, 1990) (Table 3-2). Other trauma
centers soon reported similar experiences
when nonoperative management of these
minimal injuries was employed (Francis and
colleagues, 1991; Itani, 1991; Trooskin, 1993;

Gahtan, 1994). The ability to resolve these
minimal injuries in nonextremity arteries was
also first demonstrated by Frykberg and
colleagues (1991) in a series that included
injuries of the torso and neck.

The data consistently illustrated that dif-
ferent types of minimal injuries behaved dif-
ferently over time. Smooth arterial narrowings
would almost uniformly resolve on their own
and are the most benign of the minimal
injuries (Figs. 3-l_B and 3-2-B). Intimal flaps
or irregularities would deteriorate into pseu-
doaneurysms approximately 10% of the time.
The morphology of the intimal disruption did
not reliably predict the possibility of it wors-
ening. Even the fact that a flap might be large
or directed "upstream " into the prograde flow
of blood did not seem to be a particularly
ominous sign (Fig. 3-3_B). Also, cases in which
there appeared to be little intimal damage
were later found to worsen into pseudo-
aneurysms. The long held view that these types
of injuries would soon lead to acute arterial
occlusions was also proven to be false. To date,
there have been no documented cases of these
types of minimal injuries ever deteriorating
in such a fashion. Of note, no heparin or any
type of antiplatelet agent was ever used in these
studies.

Small (<2-cm) pseudoaneurysms are
much less common, and as a result, a much
smaller number of these lesions have been
followed. Older series had demonstrated
their potential to thrombose, embolize,

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3 • MINIMAL VASCULAR INJURIES

become infected, and even rupture (Linde-
nauer, Thompson, and Kraft, 1969; Bole,
Munda, and Purdy, 1976). More current
studies have also shown them to be more
likely to worsen over time if watched expec-
tantly than smooth narrowings or intimal
flaps (Dennis and colleagues, 1990).
Approximately 40% will eventually require
surgical repair, and the remaining 60% will
either remain stable or improve (Fig. 3-4U) .
Even those pseudoaneurysms diagnosed on
a delayed diagnosis basis carry an amputa-
tion rate reported to be zero (Feliciano and
colleagues, 1987; Richardson, Vitale, and
Flint, 1987) . This indicates a more flexible
approach is possible than mandatory repair.

Small AV fistulas are the rarest of the
minimal injuries and similarly may or may not
resolve over time. Smaller AV fistulas tend to
close spontaneously, and larger ones will
more often remain patent and become symp-
tomatic (Shumacker and Waysson, 1950; Fryk-
berg and colleagues, 1991). Due to the small
numbers involved, the exact chance of
resolution is difficult to determine. Initial
observation of small fistulas has proven to be
benign and late repair can also be undertaken
with no increase in morbidity.

Over the past decade, no center has been
able to demonstrate any conclusive data con-
trary to these studies. Anecdotal reports have
described cases of delayed presentations of
arterial injuries (Perry, 1993; Tufaro, 1994).
These reports generally lack detailed accounts
of the initial presentation, initial management,
overall incidence, and consistent follow-up by
an experienced surgeon. Despite this lack of
any substantial conflicting evidence, many
surgeons expressed concern that over the
long-term follow-up of these patients, some
of these minimal injuries would eventually lead
to vascular-related problems. This argument
was put to rest with a 5- to 1 0-year study showing
no negative long-term sequelae (Dennis and
colleagues, 1998) . Two groups of patients were
studied. The first group of 39 patients had doc-
umented minimal injuries on arteriograms
between the years 1986 and 1989. Twenty-
three of these patients (58%) were re-
evaluated by history, physical examination,
and ultrasound at a mean follow-up interval
of 9.1 years (range, 8.6 to 11.1 years). All were

asymptomatic, all had normal physical exam-
ination results, and only one had a residual
mild narrowing by ultrasound. A second
much larger group of 287 patients with
penetrating proximity injuries who were
seen between the years 1989 and 1991 and
not evaluated by arteriography was also con-
sidered. Four had required delayed surgery,
all within the first week of the injury. Seventy-
eight patients representing 90 injuries (29%)
could be contacted. All patients within this
group reported no long-term complications
from any missed injury that later developed
into a significant vascular problem. No patient
at this institution (including those outside this
study) has been found to have any deteriora-
tion after 3 months following the initial
trauma if they are compliant with follow-up.
Based on these long-term data, it appears that
nonoperative management can now be con-
sidered the standard of care of these minimal
injuries when identified by arteriography or
ultrasound. Follow-up of these patients is
extremely important both within the initial
hospitalization and for up to 3 months
after the injury. This component of the man-
agement may limit the application of this
approach in small nondesignated trauma
centers with limited personnel and resources.

APPLICATION TO
PENETRATING PROXIMITY
EXTREMITY TRAUMA

The rationale behind obtaining arteri-
ograms in all penetrating trauma to the
extremities in which the penetrating agent or
missile trajectory was determined to be in
proximity to major arteries was the 10% to
20% chance of a clinically occult injury that
would otherwise escape detection by physical
examination. The new emerging data that
documented these minimal injuries had a
benign clinical course led to the next step of
no longer obtaining arteriograms, because
their detection would not alter any manage-
ment decisions. A summary of 1 5 studies using
this approach documents the overall missed
injury rate to be 1.4% (Table 3-3). This rate
is not significantly different than the 0.3% to

ch03.qxd 4/16/04 3:21PM Page 92

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

TABLE 3-3

PROFILE OF ASYMPTOMATIC PENETRATING INJURIES IN PROXIMITY TO
EXTREMITY ARTERIES*

No. of

No. of Occult

Proximity

Vascular Injuries

Author

Wounds

(%)

Requiring Surgery (%)*

Dennis and colleagues, 1990*

254

25(10)

2 (0.8)

= rancis and colleagues, 1991*

160

17(11)

7 (4.4)

Gahtan, 1994

394

37 (9.4)

7(1.8)

Gomez and colleagues, 1986

17(24)

1 (1.4)

Hartling and colleagues, 1987

5(14)

Itani and colleagues, 1992

1712

216(14)

28(1.6)

Kauffman, 1992*

22 (24)

Lipchik, 1987

3(5)

1(1.7)

McCorkell and colleagues, 1985

7(12)

McDonald, Goodman, and Weinstock, 1975

5(6)

Rose and Moore, 1988

Not Given

Smyth, 1991

2(3)

1(1.5)

Tohmeh, 1990

1(1.7)

Trooskin, 1993*

153

7 (4.6)

1(1.3)

Weaver and colleagues, 1990*

157

17(11)

1 (0.6)

Total

3451

381 (11)

50(1.4)

'Including only published cases in the extremity proper, excluding shotgun and thoracic outlet injuries.

♦Percentage of all proximity wounds, excluding negative explorations.

♦Prospective study.

From Dennis JW, Frykberg ER, Veldenz HC, et al: Validation of nonoperative management of occult vascular injuries and

accuracy of physical examination alone in penetrating extremity trauma: 5-10 year follow-up. J Trauma 1998;44:243-253.

6% missed injury rate reported for arteriog-
raphy (Sclafani and colleagues, 1986; Feli-
ciano, 1987). In addition, arteriography
carries the small but real risk of contrast allergy
and local complication such as hemorrhage,
pseudoaneurysms, and thrombosis. Depend-
ing on the location and extent of the exami-
nation, the cost of arteriography will approach
$2000 to $3000 per patient. The time involved
in obtaining any imaging study may also delay
the definitive treatment of other serious asso-
ciated injuries.

Some trauma centers, however, have been
reluctant to base treatment on physical exam-
ination results alone and have advocated
duplex ultrasound or Doppler pressure mea-
surements as alternatives (Bynoe, 1991;
Johansen and colleagues, 1991; Knudson and
colleagues, 1993). Though accurate, these
tests require time, equipment, and skilled per-
sonnel. In addition, no study has ever demon-
strated them to be significantly more accurate
than physical examination alone. Again,
emphasis must be placed on the importance

of close observation of these patients to iden-
tify the small group that will eventually dete-
riorate and require surgery. This should be
done for the first 24 hours after the injury and
for the first 3 months after discharge. Careful
instructions must be given to patients con-
cerning the possible development of
significant vascular symptoms and the need
to return immediately to the hospital should
they develop at home. The current manage-
ment algorithm for penetrating extremity
injuries at the University of Florida, Jack-
sonville, is shown in Figure 3-5 (Dennis and
colleagues, 1998).

APPLICATION TO
PENETRATING NECK INJURIES

Early military and civilian experience first
led surgeons to adopt the practice of
mandatory neck exploration for any pene-
trating injury deep to the platysma (Hughes,

ch03.qxd 4/16/04 3:21PM Page 93

3 • MINIMAL VASCULAR INJURIES

Penetrating Mechanism
INJURED EXTREMITY

Resuscitation

PHYSICAL EXAMINATION

Hard Signs

Severe Bone Fracture
Chronic Vascular Disease
Soft Tissue Injury
Shotgun Wound
Thoracic Outlet Location
Missile Parallels Vessel

SURGICAL «-
EXPLORATION

No Hard Signs

Yes

Positive (Occlusion
or Extravasation)

Arteriography

Negative or "Minimal" —
Nonocclusive Arterial Injury

NONOPERATIVE
OBSERVATION

■ FIGURE 3-5

Algorithm for evaluation and
management of penetrating
extremity trauma used at
University of Florida,
Jacksonville. (From Dennis JW,
Frykberg ER, Veldenz HC, et al:
Validation of nonoperative
management of occult vascular
injuries and accuracy of
physical examination alone in
penetrating extremity trauma:
5-10 year follow-up. J Trauma
1998:44:243-253.) ■

1954; Fogelman, 1956). Penetrating neck
injuries were later divided and classified in the
1960s according to anatomic zones, and man-
agement was based on the zone in which the
injury occurred (Monson, Saletta, and
Freeark, 1969). Patients with penetrating
injuries to zones 1 and 3 were recommended
to undergo arteriography because of their
difficult exposure, and patients with zone 2
injuries would continue to be explored,
regardless of the physical findings.

Similar to the history of managing pene-
trating extremity trauma, the high number of
negative explorations led surgeons to consider
arteriography as an alternative. An extended
review by Merion in 1981 analyzed 27 articles
in the literature concerning this topic and
found no significant difference in the mor-
bidity or mortality rates between the two treat-
ment groups (Merion, 1981). These results
subsequently led most trauma centers to
replace routine exploration with arteriogra-
phy (Massac, 1983; Hiatt, Busuttil, andWilson,
1984; Carducci, 1986) . As experience grew, it
was soon noted that similar to extremity
arteriography, cervical arteriography began
to identify minimal injuries in the carotid and
vertebral arteries. Initially, surgical dogma
stated that any abnormality seen on arteri-
ogram required surgical repair. In the late
1980s and early 1990s, however, having
observed the benign natural history of these
minimal injuries in the extremities, some

centers began challenging the need to obtain
any imaging study (Rivers, 1988; Menawatand
colleagues, 1992). Careful analysis revealed
that minimal injuries of the cervical arteries
occurred in approximately 5% of the patients
in this situation and could be safely observed.
This was particularly helpful in zone 3 and
vertebral arteries, because of their difficult sur-
gical access. Also noted were other abnor-
malities such as asymptomatic vertebral artery
occlusions, which did not need to be treated
either. Mean follow-up time was 6 months for
the entire study group.

These retrospective studies formed the
basis on which prospective studies could be
performed (Atteberry and colleagues, 1994;
Biffl and colleagues, 1997; Sekharan and
colleagues, 2000) . The rationale was similar
to that in the extremities: If minimal injuries
do not have to be treated, then arteriography
is not needed to identify them. It then follows
that physical examination alone is adequate
to determine whether a patient needs surgi-
cal repair after penetrating trauma to zone 2,
which is amenable to it. Prospective studies
appear to support this hypothesis (Table 3-
4). The combined false-negative or missed
injury rate using this approach is 0.6%, which
is equal to or better than that of arteriogra-
phy or ultrasound without the added time and
cost (Table 3-5) . Some reluctance still appears
to linger by surgeons to accept this manage-
ment approach to zone 2 neck injuries. Many

ch03.qxd 4/16/04 3:21PM Page 94

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

TABLE 3-4

PENETRATING NECK TRAUMA: MANAGEMENT BY MECHANISM AND LOCATION OF
INJURY

Observed

Explored

Missed
Injury (%)

Negative
Exploration (%)

Significant
Injury (%)

Zone 1

GSW

Zone 2

GSW

109

0.9

Zone 3

GSW

Total

37
206

0.5

8
88

29
29

GSW, gunshot wound; SW, stab wound.

From Biff I WL, Moore EE, Rehse DH, et al: Selective management of penetrating neck trauma based on cervical level of injury.

Am J Surg 1997;174:678-682.

trauma centers still obtain arteriograms or
ultrasounds in these patients (Demetriades,
1995; Ginzburg, 1996). This is probably
because of a persistentyet unfounded concern
over causing a stroke by missing a significant
injury, a complication considered more
serious than a missed injury of the extremity.
Published long-term follow-up data are some-
what lacking at this time also.

APPLICATION TO HIGH-RISK
ORTHOPEDIC INJURIES

Generally, much less evidence is known con-
cerning minimal arterial injuries and blunt
trauma. Although the overall risk of arterial
injury with bone fractures is between 0.3%
and 6.4% (depending on the definition),

TABLE 3-5

STUDIES RECOMMENDING PHYSICAL EXAMINATION ALONE IN THE MANAGEMENT
OF PENETRATING ZONE 2 NECK INJURIES

No. of

Penetrating Zone 2 Injuries

With Hard Signs

With No

No. of Missed

Study

Total

or Explored

Hard Signs

Injuries (%)

Biffl and colleagues, 1997*

208

128

1 (0.9)

Beitsch, 1994

178

136

1 (0.7)

Jarvik, 1995

111

Demetriades, 1993*

335

269

2 (0.7)

Gerst, 1990

110

Byers, 1990

106

Rivers, 1988

Sekharan and colleagues, 2000*

145

114

1 (0.8)

Totals

1216

379

837

5 (0.6)

'Prospective study.

From Sekharan J, Dennis JW, Veldenz JC, et al: Continued experience with physical examination alone for evaluation and

management of penetrating zone 2 neck injuries: Results of 145 cases. J Vase Surg 2000;32:483-489.

ch03.qxd 4/16/04 3:21PM Page 95

3 • MINIMAL VASCULAR INJURIES

several orthopedic injuries have been well
documented to carry an increased risk up to
20% of the time (Lange and colleagues, 1985;
Bassett, 1986; Cone, 1989). These include
posterior knee dislocations, supracondylar
humerus fractures, first rib fractures, and prox-
imal tibia and distal femur fractures. The
devastating consequences of a missed arter-
ial injury in these cases (limb loss risk up to
60%) have led many surgeons to obtain
arteriograms in all patients with these frac-
tures or dislocations. This practice would iden-
tify minimal arterial injuries on approximately
15% to 30% of the arteriograms obtained
in the patients with no clinical signs, a rate
somewhat higher than that seen in pene-
trating proximity injuries (Dennis, 1993;
Atteberry and colleagues, 1996). Further-
more, despite having a different etiology of
these minimal injuries, the little information
to date indicates these to have a similar benign
natural history.

Particularly ominous has been arterial
injuries associated with knee dislocations.
This is due to results of early series in which
the incidence of limb loss was over 50%,
although more recently this risk has been
reduced to less than 5% (Bishara and
colleagues, 1986). The question whether
minimal injuries found in the popliteal
artery following knee dislocation could be
watched was answered in two studies in 1992
and 1993 (Treiman and colleagues, 1992;
Dennis, 1993). These are the two largest
studies reported, and when their data are
combined, 16 minimal injuries (all intimal
irregularities and smooth narrowings) were
observed nonoperatively without a single
adverse outcome. Strict follow-up immedi-
ately after any orthopedic manipulation and
for several weeks after an injury is essential
for this type of management to be successful.

The use of physical examination alone to
determine whether immediate significantvas-
cular injury has occurred with these high-risk
types of orthopedic injuries has been advo-
cated (Treiman and colleagues, 1992;
Atteberry and colleagues, 1996) . The presence
of hard signs of vascular injury mandates
surgery or arteriography, depending on the
exact type of clinical picture. Patients with
a bruit or thrill, distal ischemia, active

hemorrhage, or absent pulses are generally
treated with immediate exploration. Those with
non-life-threatening bleeding or expanding
hematomas should undergo arteriography,
because up to 70% of these cases will not have
significant arterial injury requiring repair.
Often, single hand-injected arteriograms in
the operating room before the orthopedic
manipulation are the simplest and most expe-
ditious means to evaluate the arterial status.
Arteriograms are essential if there are multi-
ple sites of potential arterial injury because
of more than one orthopedic injury. If
minimal injuries are detected, they may be
safely observed with careful follow-up. Recent
analysis has shown this approach to be both
safe and accurate when evaluating patients
with knee dislocations (Miranda, 2001).

SUMMARY

Information gathered to date indicates
minimal injuries tend to follow a similar
natural history regardless of the trauma
etiology. Smooth narrowings are extremely
benign and can be watched with the assur-
ance that almost all will resolve spontaneously.
Intimal irregularities or flaps will also gener-
ally heal, although it must be recognized that
10% to 15% will deteriorate and require
definitive treatment. This change will almost
always occur within the first 3 months after
an injury, and patients should always be fol-
lowed for this amount of time as a minimum.
Those injuries that deteriorate may be
repaired on a delayed basis with no proven
adverse effect on morbidity or mortality.
Careful instructions must be given to patients
upon discharge, to help them recognize if
their particular arterial injury is worsening.
Small pseudoaneurysms (<2cm) may also be
safely watched buthave a far greater tendency
to progress to needing direct repair. This prob-
ably happens 40% to 50% of the time. In addi-
tion, small AV fistulas need not always be fixed
immediately unless symptomatic. Evidence
shows that clinical follow-up is adequate in
most instances; however, duplex ultrasound
can be an adjunct in some difficult or partic-
ularly worrisome injuries.

ch03.qxd 4/16/04 3:21PM Page 96

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

Knowing this natural history allows physi-
cians treating trauma patients to use physical
examination as the definitive basis on which
to manage penetrating injuries to the extrem-
ities and neck, as well as knee dislocations from
blunt trauma. The algorithm in Figure 3-4
may be used in these situations. The only dif-
ference in using this approach with neck
injuries is that distal ischemia may be mani-
fested by focal neurologic deficits such as a
stroke or transient ischemic attack.

Once patients are identified as to having a
deteriorating minimal injury, they can usually
be repaired on an urgent, elective basis
dependent on the presenting symptoms. Stan-
dard surgical techniques may be used in almost
all cases. Depending on the experience and
expertise of the treating surgeons, endovas-
cular techniques are also proving to be very
useful in these situations (Marin, Veith, and
Panetta, 1994; Weiss and Chaikoff, 1999) . The
placement of a stent graft across these lesions
on a planned basis either in the operating
room or in the endovascular suite has become
standard treatment in some trauma centers.
Long-term studies will be needed to ensure
the durability of endovascular repair in these
situations and compare their outcome with
proven surgical techniques.

REFERENCES

Penetrating extremity trauma and minimal
arterial injuries

Dennis JW, Frykberg ER, Crump JM, et al: New
perspectives on the management of penetrating
trauma in proximity to major limb arteries. J Vase
Surg 1990;11:84-93.

Dennis JW, Frykberg ER, Veldenz HC, et al: Vali-
dation of nonoperative management of occult

vascular injuries and accuracy of physical exam-
ination alone in penetrating extremity trauma:
5-10 year follow-up. J Trauma 1998;44:243-253.

Frykberg ER, Crump JM, Dennis JW, et al: Non-
operative observation of clinically occult arter-
ial injuries: A prospective evaluation. Surgery
1991;109:85-96.

Frykberg ER, Crump JM, Vines FS, et al: A reassess-
ment of the role of arteriography in penetrat-
ing extremity trauma: A prospective study.
J Trauma 1989;29:1041-1052.

Weiss VJ, Chaikof EL: Endovascular treatment of
arterial injuries. Surg Clin North Am
1999;79:653-665.

Penetrating neck injuries and minimal
arterial injuries

Biffl WL, Moore EE, Rehse DH, et al: Selective man-
agement of penetrating neck trauma based on
cervical level of injury. AmJ Surg 1997;174:678-
682.

MenawatSS,DennisJW, Laneve LM, etal: Are arte-
riograms necessary in penetrating zone II neck
injuries? J Vase Surg 1992;16:397-401.

Sekharan J, Dennis JW, Veldenz JC, et al: Contin-
ued experience with physical examination alone
for evaluation and management of penetrating
zone 2 neck injuries: Results of 145 cases. J Vase
Surg 2000;32:483-489.

Orthopedic injuries and minimal
arterial injuries

Atte berry LR, Dennis JW, Russo-Alesi F, et al: Chang-
ing patterns of arterial injuries associated with
fractures and dislocations. J Am Coll Surg
1996;183:377-383.

Bishara RA, Pasch AR, Lim LT, et al: Improved
results in the treatment of civilian vascular
injuries associated with fractures and disloca-
tions. J Vase Surg 1986;3:707-711.

ch04.qxd 4/16/04 3:22 PM Page 97

Initial Care, Operative Care
and Postoperative Care

DAVID B. HOYT

RAU

L COIMBRA

INTRODUCTION

GENERAL GUIDELINES- INITIAL CARE -C

Primary Survey

Secondary Survey

NECK VASCULAR INJURIES

THORACIC VASCULAR INJURIES

ABDOMINAL VASCULAR INJURIES

EXTREMITY INJURIES

COMPLEX ISSUES WITH CONCOMITANT INJURIES

Blunt Trauma
Penetrating Trauma

PERIOPERATIVE CARE

Initial Anesthesia and Intraoperative Monitoring
Volume Therapy
Hypothermia
Damage Control

POSTOPERATIVE PRIORITIES

Hemodynamic Monitoring and Transfusion in the Postoperative
Phase

Coagulation Monitoring

Complications Following Mass Blood Transfusion

ch04.qxd 4/16/04 3:22 PM Page 98

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

Mechanical Ventilation

Antibiotics

Assessment and Determination of Take Back

Bleeding

Vascular patency

Abdominal compartment syndrome

Extremity compartment syndrome following
prolonged ischemia

O SUMMARY

INTRODUCTION

The prehospital and the initial in-hospital
management of trauma patients with vascu-
lar injuries remain a challenge. Specific
maneuvers or techniques can be used in the
prehospital setting to control external
hemorrhage, but rapid transport to a trauma
center is of utmost importance.

Vascular injuries following blunt trauma are
considered a marker of severe trauma and
as such should be treated in the context of
multisystem trauma. Penetrating mechanisms
cause vascular injuries more often than blunt
trauma, and depending on the injury loca-
tion, patients may present with external
hemorrhage, internal hemorrhage, ischemia,
or more rarely, a pulsating hematoma or a trau-
matic arterio-venous fistula.

GENERAL GUIDELINES:
INITIAL CARE

The initial evaluation and management of
patients with vascular injuries follow the
guidelines established by the advanced trauma
life support (ATLS) course of the American
College of Surgeons-Committee on Trauma
(ACS-COT) .

The history should include details about the
mechanism of injury (e.g., blunt vs. pene-
trating, position of the patient at the time of
injury, position of the extremity observed by
prehospital providers, blood loss at the scene,
and previous injuries) .

Primary Survey

The assessment of airway is the first priority
even with evidence of obvious hemorrhage.
Penetrating wounds of the face, neck, and
chest may be accompanied by airway obstruc-
tion from bleeding or hematomas. The airway
should be controlled as soon as possible in
this circumstance and may require direct trans-
port to the operating room for definitive
control with access to complete instrumen-
tation, excellent light, and anesthesia.

Many penetrating vascular wounds may
present with entrance wounds at the lower
neck or upper abdomen. The wound trajec-
tory may be such that the chest is involved.
There may be a pneumothorax, hemathorax,
or tension pneumothorax, which will present
as difficulty with breathing and will require
appropriate diagnosis and decompression
with a chest tube. This may often be difficult
to distinguish from airway obstruction or may
present with airway obstruction in the same
patient. Systematic evaluation and treatment
is the best course.

The occasional patient will present with
difficulty breathing caused by hypovolemic
shock. Control of the airway before assessment
and treatment of the circulation remains the
priority, even in this circumstance.

After assessment of the airway and breath-
ing and definitive airway control, the hemo-
dynamic status is assessed. Initially, palpation
of pulse gives a rapid assessment. The pres-
ence of a radial pulse correlates with a blood
pressure of at least 90mmHg. The absence
of radial pulse with the pressure of a carotid

ch04.qxd 4/16/04 3:22 PM Page 99

4 • INITIAL CARE, OPERATIVE CARE AND POSTOPERATIVE CARE

pulse suggests a blood pressure of 60 mm Hg.
Overall hemodynamic assessment should
include direct blood pressure measurement,
but caution should be exercised in the patient
with a "stable blood pressure." Systolic blood
pressure can be maintained in the normal
range until almost 30% of circulating blood
volume is lost (class I and II hemorrhage).
Reliance on blood pressure alone can over-
look a patient with significant hypovolemia.
As such, measurement of the base deficit will
also give an initial estimate of the total volume
of hemorrhage and guide subsequent volume
resuscitation and assessment of response to
resuscitation (Table 4-1).

Recent changes in the ATLS protocols have
suggested that bleeding control is a priority
when evaluating the circulation, before fluid
resuscitation. This is important in patients with
vascular injuries, because they may present
with external hemorrhage, for which external
compression should suffice to control bleed-
ing. They may also present with intracavitary
hemorrhage in the chest or abdomen, requir-
ing an operation to control active hemorrhage,
as part of the resuscitation phase of care. Always
keeping control of bleeding as an early pri-
ority will shift priorities to early operation. This
is best for vascular injuries.

Although the ideal fluid therapy (type of
solution, volume given, and timing of infu-
sion) for the bleeding patient still remains a
matter of controversy, it seems reasonable to
avoid over-resuscitation, particularly in the
subgroup of patients in whom the index of
suspicion for the presence of a major vascu-
lar injury is high.

The two major goals in the management of
traumatic shock during initial assessment and
resuscitation are to arrest hemorrhage and to
restore blood volume to provide adequate
tissue oxygen delivery. Delayed resuscitation
has been proposed to avoid rapid increases
in blood pressure, clot dislodgement, and con-
sequently, increased hemorrhage. Avoidance
of over-resuscitation before surgical control
is obtained is certainly prudent. However,
whether all trauma victims would benefit from
delayed fluid resuscitation is not clear.

Rapid cannulation of large veins is essen-
tial for adequate fluid therapy. Care should
be taken when cannulating upper or lower
extremity veins in patients with proximal
penetrating injuries. To achieve adequate fluid
resuscitation, one should use large-bore
tubing. Warmed fluids should be infused to
prevent or minimize heat loss and subsequent
hypothermia. Rapid infusion systems (such as
the level I) have the ability to infuse large
volumes of warmed solutions per minute. Most
practitioners agree that the initial resuscita-
tion should be with crystalloids (Ringer's
lactate or normal saline) ; however, a small but
very important subset of patients will also
require blood transfusion. This will be true if
the estimated blood loss is greater than 30%
of the total circulating blood volume. Avail-
ability of type-specific or O-negative blood is
an essential component of the resuscitation
of the severely injured patient.

Resuscitative or emergency department
(ED) thoracotomy can be used as an adjunct
to resuscitation in the severely injured patient.
However, not all patients are candidates for

TABLE 4-1

QUANTIFICATION OF BLOOD LOSS (ATLS, 1993)

Class I

Class II

Class III

Class IV

Blood loss (ml_)

<750

750-1500

1500-2000

>2000

Blood loss (%)

<15

15-30

30-40

>40

Heart rate

<100

>100

>120

>140

Respiratory rate

14-20

20-30

30-40

>35

Urinary output

>30

20-30

5-15

Absent

Level of consciousness

Anxious

Agitated

Confused

Confused/lethargic

Blood pressure

Normal

Decreased

ch04.qxd 4/16/04 3:22PM Page 100

100

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

this procedure. In general, survival rates are
higher for patients presenting with vital signs
than for patients presenting only with signs
of life. Victims of penetrating trauma benefit
more than patients with blunt trauma.

In general, ED thoracotomy is indicated in
patients with penetrating wounds to the chest
who develop sudden cardiac arrest or loss
of vital signs during transport, persistent
hypotension with signs of cardiac tamponade,
or intrathoracic hemorrhage. Patients with
penetrating injuries to the abdomen and
refractory hypotension may benefit from ED
thoracotomy and aortic cross clamping before
exploratory laparotomy is performed;
however, this is often a matter of individual
preference. Blunt trauma victims with car-
diopulmonary resuscitation (CPR) in progress
and no cardiac electrical activity upon arrival
are not candidates for this procedure.

A rapid neurologic assessment should be
done. A depressed level of consciousness may
be due to shock, associated blunt head injury,
drugs or alcohol, or occasionally direct injury
to the carotid artery. Abnormal or asymmet-
rical motor function should raise suspicion of
an intracranial mass lesion and consideration
of evaluation with a computed tomographic
(CT) scan should be an early priority.

Particularly in victims of penetrating
trauma, it is also important to examine the
whole body surface area, undressing the
patient completely because small gunshot or
stab wounds may be hidden between the but-
tocks, gluteal folds, in the back, in the axilla,
or in the folds of the neck. With complete
exposure, the ongoing concern for hypother-
mia should be initiated and the patient ade-
quately covered with warm blankets while
keeping the ambient temperature warm as
well.

Secondary Survey

The secondary survey should include a
detailed examination of the vascular system
in the extremities. The documentation of
distal pulses is important and will guide
further investigations and the use of specific
diagnostic tools. The presence of a distal pulse,

TABLE 4-2

HARD AND SOFT SIGNS OF
ARTERIAL INJURY

Hard Signs

Signs of ischemia

Pallor

Pain

Pulselessness

Paresthesia

Paralysis
Poikilothermia
Pulsatile bleeding
Palpable thrill/audible bruit
Expanding hematoma

Soft Signs

Diminished distal

pulses
Penetrating injury in the

proximity of major

artery
Fracture in the

proximity of major

artery
History of external

bleeding at the scene
Peripheral neurologic

deficit

however, does not rule out a proximal arter-
ial injury. On the other hand, bilateral absence
of distal pulses in a patient in shock with poor
tissue perfusion does not indicate an arterial
injury.

Clinical signs of arterial injury are divided
into "hard" and "soft" (Table 4-2). According
to the physical examination findings, patients
can be stratified according to the risk of
having an arterial injury. Patients with hard
signs have high-risk injuries, those with soft
signs have intermediate-risk injuries, and
those with no soft or hard signs have low-risk
injuries. Accuracy of this classification system
for the lower extremities is improved when the
ankle-brachial index (ABI) is added.

A thorough and ongoing neurologic
evaluation of the victim with penetrating
extremity trauma is mandatory. Changes in
the neurologic examination results may indi-
cate aggravation of ischemia or a developing
compartment syndrome, and changes in pri-
orities and management might be necessary
in these circumstances.

The diagnosis of a vascular injury in the
multi-injured patient depends on the mech-
anism, clinical signs at presentation, and the
type of arterial injury (Fig. 4-1).

ch04.qxd 4/17/04 2:48 PM Page 101

4 • INITIAL CARE, OPERATIVE CARE AND POSTOPERATIVE CARE 101

ETIOLOGY, INCIDENCE AND CLINICAL PATHOLOGY

Laceration

Transection

•

Incomplete
Transection

Contusion and
Segmental Spasm

^;m.<^-'

Contusion and
Thrombosis

Pulsating Hematoma
or False Aneurysm

Arteriovenous Fistula

Contusion and
True Aneurysm

External
Compression

■ FIGURE 4-1

Common types of arterial injury. (From Rich NM, Spencer FC: Vascular Trauma. Philadelphia, WB
Saunders, 1979.) ■

NECK VASCULAR INJURIES

Penetrating neck injuries generally pre-
sent with external bleeding, a significant
hematoma, or airway obstruction. Surgical
access is limited and determined by surface
landmarks that correlate with surgical acces-
sibility. Monson's zones define the limits of
surgical exposure. Zone III injuries (above the
angle of the mandible) may not be surgically
accessible and angiography can help define
this possibility with a suspicious wound or
hematoma. Zone II wounds (between the
angle of the mandible and the cricoid carti-
lage) are directly accessible through the stan-
dard sternocleidomastoid approach. Zone II
wounds (below the cricoid cartilage or adja-
cent to the thoracic inlet) may require tho-
racic exposure, and hemodynamically stable

patients should undergo angiography to allow
surgical planning.

Blunt carotid or vertebral injuries may be
suspected because of neurologic abnormali-
ties detected, but not confirmed, on CT scan.
Generally a mechanism of extension and
external rotation can be elicited. Any suspi-
cion or evidence of blunt neck trauma should
raise the possibility of carotid injury and
duplex scanning will screen for this
possibility.

THORACIC VASCULAR
INJURIES

Penetrating thoracic vascular injuries usually
present with hemothorax or ischemia. Chest
tube output will determine whether a

ch04.qxd 4/16/04 3:22PM Page 102

102

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

thoracotomy is necessary for bleeding control
and definitive repair of the arterial injury. If
upper extremity or cerebral ischemia is the
predominant clinical sign, a preoperative
angiogram will help operative planning in the
hemodynamically stable patient. Recent expe-
rience with thoracic wounds that traverse the
chest has used fine-cut CT scans to define
superficial wounds in hemodynamically stable
patients. Further experience is needed to
better define the indications.

The aorta or its thoracic branches may be
injured after blunt thoracic injuries. Most
patients who bleed from these injuries die at
the scene or during transport. The majority
of patients with blunt thoracic aortic injury
will present to the ED hemodynamically stable
and will have a widened mediastinum on initial
chest x-ray films. The predominant sign
accompanying injuries to the thoracic aortic
main branches is upper extremity or cerebral
ischemia. The diagnosis is confirmed by
angiography or high-quality helical CT scans.
Patients with isolated bluntinjuries to the tho-
racic aorta should undergo operative repair.
However, many of these patients have associ-
ated closed head injuries, and the manage-
ment of the aortic tear (operative vs.
nonoperative) will depend on the severity of
the head injury.

ABDOMINAL VASCULAR
INJURIES

EXTREMITY INJURIES

Blunt abdominal vascular injuries are rare.
The astute physician should suspect a major
intra-abdominal injury secondary to pene-
trating trauma when the patient does not
respond to initial fluid resuscitation. These
patients should be quickly transported to the
operating room, and the diagnosis is usually
made intraoperatively. Line placement in the
lower extremity should be avoided in patients
with a high index of suspicion for major intra-
abdominal vascular, particularly inferior vena
caval injuries.

In general, patients presenting with significant
external hemorrhage or limb ischemia caused
by an isolated penetrating injury to the
extremity do not pose any difficulty in the diag-
nosis and management. These patients
require no additional diagnostic tests and
should be promptly transported to the oper-
ating room. Patients with multiple penetrat-
ing injuries to the extremity presenting with
ischemia also should be promptly operated
on; however, a preoperative angiogram may
be useful in determining the exact location
of the most proximal injury, thus helping with
operative planning.

Angiography is the "gold standard" test to
evaluate the arterial tree. In some instances,
hemodynamic instability, associated life-
threatening injuries, or the need to perform
other surgical procedures, moving the patient
to the angiography suite is not feasible. In cases
of prolonged ischemia or in which the deci-
sion to perform "damage-control" surgery on
the injured extremity by placement of an
intravascular shunt is necessary, an intraop-
erative on-table angiogram can be obtained.

Trauma surgeons should be familiar with
this procedure, because it may save enormous
amounts of time and may expedite reperfu-
sion of an ischemic limb. For the lower
extremity, an 18-gauge needle is inserted into
the femoral artery, below the inguinal liga-
ment. An x-ray plate is placed under the thigh
and 20 mL of contrast is injected under
pressure. Compression of the femoral artery
above the needle site will limit contrast dilu-
tion, and the dye should be injected as rapidly
as possible. Flow through the Luer lock con-
nector will prevent injecting too rapidly. The
initial film will give the surgeon an idea when
to expose the film to x-ray after the end of the
injection to demonstrate the vessels in the area
of interest. Subsequent films are obtained
distally.

For the upper extremity, on-table
angiograms are useful if one wants to evalu-
ate the proximal axillary artery and the sub-
clavian artery. This can be done by inserting
an 18-gauge needle in the brachial artery and
inflating the cuff of a blood pressure manome-

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4 • INITIAL CARE, OPERATIVE CARE AND POSTOPERATIVE CARE

103

ter over the forearm. An x-ray plate is posi-
tioned under the upper extremity and upper
chest, and 20 mL of contrast is injected under
pressure. Further films are obtained depend-
ing on the area of the arterial tree to be
studied.

Blunt arterial injuries are usually caused by
significant forces applied to the extremities,
also leading to fractures or dislocations. The
classic fracture or dislocation sites associated
with arterial injuries are listed in Box 4—1.
Alignment and immobilization of fractures is
mandatory to decrease bleeding, avoid further
injury to soft tissues, and eventually restore
distal flow.

In general, vascular injuries are just one
component of a multitude of injuries, and
adherence to the priorities set forth by
the ATLS will facilitate initial management
and diagnosis. The management of life-
threatening injuries takes precedence over
limb-threatening injuries. In the presence of
multiple injuries, the management of periph-
eral vascular injuriesmay be delayed, although
trauma surgeons should keep in mind that
duration of ischemia greater than 6 hours is,
in general, associated with poor functional
outcome and should be avoided.

COMPLEX ISSUES WITH
CONCOMITANT INJURIES

Blunt Trauma

In patients with concomitant blunt thoracic
or abdominal trauma and peripheral vascu-
lar injuries with ischemia, the initial priority
is to stop the bleeding in the chest (chest tube
placement and eventually thoracotomy) or
abdomen (exploratory laparotomy) . If the
anticipated ischemia time is greater than 6
hours, consideration should be given to con-
comitant operations (exploratory laparotomy
and/or thoracotomy and vascular explo-
ration) by two separate surgical teams, as well
as fasciotomy and use of temporary antra-
arterial shunts.

For patients with peripheral vascular
injuries and associated long bone fractures or
dislocations, best care is provided by a com-
bined approach, taking into account the
duration of ischemia. Usually the vascular
injury can be approached first and the deci-
sion to use an antra-arterial shunt and perform
orthopedic fixation followed by definitive
repair of the vascular injury versus primary

NLY ASSOCIATED WITH

■

ORTHOPEDIC INJURIES COMMO
VASCULAR TRAUMA

UPPER EXTREMITIES
FRACTURE

ASSOCIATED VASCULAR
INJURIES

O Supracondylar fracture of

the humerus
O Clavicular fracture
O Shoulder dislocation
O First rib fracture

O Brachial artery
O Subclavian artery
O Axillary artery
O Aorta, carotid

LOWER EXTREMITIES
FRACTURE

O Posterior knee dislocation

O Popliteal artery

O Distal femur

O Femoral artery

O Proximal tibia

O Popliteal trifurcation

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

repair of the vascular injury followed by
orthopedic fixation is made intraoperatively
based on objective assessment of the duration
of ischemia and the degree of bony instabil-
ity. Adequate communication between the
surgeon and orthopedist is key to a success-
ful management of these complex patients.

Penetrating Trauma

The decision-making process in patients with
penetrating injuries in multiple body areas is
far less complicated than in blunt trauma. The
principles of management, however, remain
the same.

In patients with penetrating thoracic and
abdominal injuries, the priority is to treat tho-
racic conditions first (hemothorax or pneu-
mothorax), because in the ABCs breathing
(orU) comes before circulation (or G). As with
blunt chest trauma, most patients with pene-
trating chest injuries will not require a tho-
racotomy and tube thoracentesis will suffice.
Once pleural problems have been addressed,
abdominal bleeding should then be addressed
by means of an exploratory laparotomy.

In patients with penetrating neck and
abdominal wounds, the initial priority is to
obtain a patent airway. If there is active bleed-
ing from the neck wound, a two-team
approach should be considered in the
hypotensive patient, and a concomitant neck
and abdominal exploration should be per-
formed. If that is not feasible, then applying
gentle pressure to the neck wound, opening
the abdomen, and packing to control major
bleeding should be done before the formal
neck exploration is performed, because the
likelihood of one dying from exsanguination
is higher with abdominal bleeding than cer-
vical bleeding. The same principles (ABCs)
apply to penetrating neck, thoracic, and
abdominal injuries.

In patients with chest or abdominal injuries
and extremity vascular injuries, the priority
is to rule out intrathoracic hemorrhage,
pneumothorax, and cardiac tamponade.
Then, attention is paid to the abdomen. Most
patients will require an exploratory laparo-
tomy. Lower extremity vascular injuries are the
last priority in this scenario. Depending on

the necessity, an on-table angiogram to deter-
mine the location of the arterial injury, and
eventually, intra-arterial shunt placement can
be done as described previously. Patients with
multiple penetrating injuries of the extrem-
ity and signs of ischemia should undergo an
angiography to help with surgical planning,
and this can be done in the operating room.

PERIOPERATIVE CARE

Initial Anesthesia and
Intraoperative Monitoring

The multi-injured patient with a vascular
injury usually presents with hypovolemia
caused by hemorrhage. Two factors are of
utmost importance when initially assessing
such patients and while in the operating room :
the evaluation of the circulating blood volume
deficit and the prediction of additional losses.

Oxygenation and ventilation, maintenance
of an adequate perfusion pressure, infusion
of warm fluids, and serial monitoring of
urinary output, temperature, hematocrit,
blood gases, base deficit, and coagulation
studies are the intraoperative priorities in the
multi-injured patient. More sophisticated and
invasive monitoring techniques may not be
feasible during the resuscitative and opera-
tive phases of care but should be implemented
during the critical care phase.

Ketamine or etomidate are appropriate
for induction of anesthesia in hypotensive,
hypovolemic patients. Fentanyl and nitrous
oxide are also adequate for anesthesia and
analgesia, but care should be taken when
hypovolemia is profound. Volatile agents,
benzodiazepines, and barbiturates should be
avoided.

All patients receive antibiotics preopera-
tively. Antibiotics should be chosen to achieve
broad coverage but limit toxic side effects,
particularly when aggravated by associated
shock. A second-generation cephalosporin is
ideal.

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105

Volume Therapy

One of the main goals of perioperative care
is to achieve hemodynamic stability. After trau-
matic hemorrhage has been controlled, other
factors may interfere with hemodynamic sta-
bility. Hemostasis is impaired by the devel-
opment of hypothermia coagulopathy and
acidosis.

Initially, maintenance of adequate intravas-
cular volume is achieved by fluid resuscitation
(with crystalloid and blood) during the oper-
ative phase and extended into the initial crit-
ical care phase. Although more sophisticated
devices may be available for intraoperative
monitoring of the cardiovascular system,
large-bore intravenous (IV) lines, a central line
(internal jugular or subclavian), and an arte-
rial line will generally be adequate.

Following massive bleeding and shock, pro-
found acidosis can be concerning because of
the perceived risk of low pH level. Acidosis
will resolve with control of bleeding and ade-
quate volume resuscitation. Use of NaHCO a
should be limited because rapid formation of
increased C0 2 can cause precipitation of intra-
cellular acidosis and make things worse. The
overuse of bicarbonate can lead to diminished
oxygen delivery by shifting the oxygen disas-
sociation curve so that oxygen is more tightly
bound. Acidosis should never be treated with
HC0 3 unless the pH level is less than 7.1 to
7.2. The bicarbonate deficit should be calcu-
lated and only 50% should be replaced until
it can be reassessed. Calculation of the HCO a
deficit is according to the formula: base
deficit X body weight X 0.2. The space of dis-
tribution of HC0 3 is considered to be 20% of
the total body.

A great deal of confusion and controversy
regarding the indications for urgent or
emergent blood transfusion in the severely
injured patient exists. Several factors should
be considered before the decision to trans-
fuse is made, including degree of hemorrhage,
hemoglobin level, intravascular volume status,
and chronic diseases. The goal of blood trans-
fusion is to enhance oxygen delivery to the
tissues.

Communication between the surgery team
and the anesthesiologist is important to avoid
over-transfusion and under-transfusion intra-

operatively. Similarly, the use of too much crys-
talloid can occur particularly if one is not
watching simple parameters. It can be easy to
over-resuscitate with crystalloid if the patient
initially has no urine output because of shock-
induced acute tubular necrosis (ATN). Con-
tinuous surveillance of the correction of the
base deficit should be a reliable guide to
volume resuscitation in this circumstance, and
pushing fluid until urine output returns will
overload the patient.

Uncross-matched type O blood is immedi-
ately available for patients with blood loss
greater than 30% to 40% of total circulating
blood volume with hypotension. If the
patient's blood type is known, transfusion
of type-specific uncross-matched blood is
appropriate. If time is not a cause for concern,
type-specific cross-matched blood should be
used. In an emergency situation, there is often
not enough time to perform all compatibil-
ity testing.

Autotransfusion is an excellent alternative
or adjunct to massive blood transfusion in the
hypotensive trauma patient. It is primarily
useful in patients with a large hemothorax.
The blood accumulated in the reservoir con-
nected to the chest tube can be transfused.
Intraoperative blood salvage using cell-saver
devices is effective in reducing transfusion of
stored autologous blood, even in the presence
of bacterial contamination, because the red
blood cells are washed before transfusion.
Most people will not use contaminated blood
however. Complications of autotransfusion
include coagulopathy resulting from excessive
amounts of anticoagulants or infusion of acti-
vated products of coagulation and fibrinoly-
sis leading to disseminated intravascular
coagulation (DIC).

The use of heparin in the acute setting of
vascular trauma is controversial. Because of a
multitude of injuries and in view of massive
fluid and blood resuscitation, heparin should
primarily be used locally in vascular trauma,
and systemic heparinization should be avoided
until the patient is in the intensive care unit
(ICU) . After 24 hours when hypothermia and
coagulopathy have been corrected, and if no
brain or spinal cord injury has been identified,
if needed, systemic heparin might be appro-
priate.

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

Platelets are used when the platelet count
drops to less than 50,000 cells/mm 3 associ-
ated with microvascular bleeding. Prophylactic
platelet administration after massive transfu-
sion is not indicated. Fresh frozen plasma
(FFP) contains all coagulation factors and is
used in the severely injured patient who has
continuous bleeding after transfusion of
approximately one blood volume or when an
intraoperative coagulopathy is identified as
measured by a partial thromboplastic time
(PTT) of more than 1.5. FFP should not be
used as a volume expander during the resus-
citation phase and is not indicated for general
coagulopathy prophylaxis after massive
transfusion.

Cryoprecipitate contains fibrinogen, factor
VIII, factor XIII, and von Willebrand's factor.
In the acute setting, it is indicated only in
severe fibrinogen deficiency, or when the
serum fibrogen level is less than 100 mg%.

Hypothermia

metabolism, decreased intestinal motility,
hyperglycemia, and increased affinity of hemo-
globin for oxygen.

Rewarming can be passive or active. Passive
external rewarming is indicated for mild
hypothermia and is achieved by increasing
room temperature and using blanket cover-
age to prevent further heat loss. Complica-
tions associated with passive rewarming may
include metabolic acidosis and increased
lactic acid production. Active external rewarm-
ing includes the use of heating or convective
air blankets and radiant warmers. Active core
rewarming is indicated for hypothermic
patients with severe vasoconstriction. Methods
include warmed IVfluids, body-cavity (pleural,
peritoneal) lavage with warm fluids, airway
rewarming, and extracorporeal circulatory
rewarming (cardiopulmonary bypass). The
latter is the most effective rewarming method.
Prevention by avoiding transfusion of
unwarmed crystalloid and refrigerated blood
is important, to avoid the problem during the
first several hours after injury.

Hypothermia in the severely injured massively
resuscitated trauma patient is multifactorial
and may occur at any phase of care. In patients
experiencing hypoperfusion and shock, heat
production is decreased. Rapid infusion of
large amounts of unwarmed crystalloid and
stored blood also contributes to hypothermia.

Normal production is 315 kj per day and
normal loss is about the same. Body temper-
ature drops by l°Cfor each additional 315 kj
lost. Each liter of crystalloid at 21 °C can cause
67.2 kj of heat loss and each unit of 4°C blood
can cause 30°C heat loss. Even with modest
resuscitation, this compounded heat loss can
rapidly cause significant hypothermia.

Hypothermia affects coagulation by
decreasing platelet function, altering enzy-
matic kinetics in the coagulation cascade, and
increasing fibrinolysis. Oxygen consumption
and cardiovascular oxygen demand are
increased in mild hypothermia, and moder-
ate to severe hypothermia can lead to arrhyth-
mias, hypotension, and sudden cardiac arrest.
Other effects of hypothermia include depres-
sion of the respiratory center, bronchospasm,
decreased cerebral blood flow, altered level
of consciousness, fluid shifts, prolonged drug

Damage Control

The surgical management of the severely
injured massively bleeding trauma patient has
changed dramatically in the last decade. The
concept of staged laparotomy or damage-
control operation has emerged from the
observation that prolonged operations to
repair all injuries will lead to physiologic
exhaustion, associated with hypothermia,
acidosis, coagulopathy, and death.

By definition, it is a phased approach to the
critically injured patient. The indications
include patients with hypothermia (tempera-
ture <35°C), nonmechanical bleeding,
pH level less than 7.15, and significant
retroperitoneal and visceral swelling due to
massive fluid resuscitation. Eligible patients
are those with major solid organ injury, pelvic
fractures, major abdominal vascular injury,
bleeding injuries in more than one body area,
or multiple competing injuries. The goal of
the initial operation is to control bleeding and
gross contamination of the peritoneal cavity
with intestinal contents. This can be achieved
by shunting or ligating injured vessels, packing

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107

solid organs (particularly the liver), and
closing or resecting bowel injuries en bloc,
using staplers.

The definitive reconstruction is left to a
second operation while performing a tempo-
rary closure of the abdomen. The second
phase or stage occurs in the critical care unit,
where the patient will continue to be resusci-
tated and rewarmed and will receive coagula-
tion factors to correct coagulopathy. The goal
of this phase is to restore some of the patient's
physiologic reserve by correcting the base
deficit, restoring intravascular volume, and
achieving adequate oxygenation. Once stable
(i.e., mechanical bleeding stopped, the base
deficit corrected, and the body temperature
near normal) , the patient is taken back to the
operating room for definitive repair of all
injuries. This is an approach described for
abdominal trauma but has been extended to
chest and pelvic and/or extremity injuries asso-
ciated with other competing injuries.

If the abdomen is closed during the first or
second operation, continuous surveillance is
necessary to identify an early complication
associated with this approach abdominal
hypertension, and its most severe form, the
abdominal compartment syndrome.

POSTOPERATIVE PRIORITIES

Hemodynamic Monitoring and
Transfusion in the
Postoperative Phase

Postoperative placement of a Swan-Ganz
catheter to monitor cardiac output and pul-
monary capillary pressure in persistently
unstable patients or in patients with preex-
isting illnesses in the ICU is appropriate.
Nonetheless, it has been ours and others
experience that analysis of base-deficit trends
is as helpful as more sophisticated methods
to monitor effectiveness of resuscitation. If
used, physiologic parameters should not
replace the use of metabolic endpoints such
as base deficit.

Postoperatively, the decision to transfuse is
not as simple, because clear guidelines do not
exist and the "10/30 rule" (lOg/dL of hemo-

globin or 0.30 hematocrit) is no longer widely
accepted. The young adult trauma patient
without comorbid conditions and with a near-
normal intravascular volume usually tolerates
a hematocrit level as low as 0.20. Elderly
patients with limited cardiopulmonary reserve
may need blood transfusion to maintain a
hematocrit level of more than 0.25, but no
good data are available to define this endpoint.

Recently, signs and symptoms of anemia and
oxygen delivery measurements have been
used as transfusion triggers; however, in the
immediate post-traumatic or postoperative
period, most trauma patients will be sedated
and intubated in the ICU, making it difficult
to evaluate symptoms of anemia. Tachycardia
and hypotension may reflect anemia but may
also occur secondarily to inflammatory medi-
ator release and the systemic inflammatory
response and are, therefore, not relatable
transfusion endpoints.

Measurements of oxygen delivery and con-
sumption are probably more reliable in pre-
dicting transfusion requirements. It seems
reasonable to transfuse blood to patients with
a hemoglobin concentration of 7 g/dL or less,
provided the intravascular volume is normal
and there are no associated chronic illnesses.
It is also common practice to transfuse blood
to patients with hemoglobin concentrations
between 7 and 10 g/dL who have coronary
artery disease, are older than 60 years, and
have congestive heart failure.

Recent National Institutes of Health (NIH)
recommendations for perioperative blood
transfusion state that no single criterion for
transfusion such as a hemoglobin concentra-
tion less than 1 g/dL should be used and that
clinical judgment cannot be replaced by any
single measurement. Perioperative transfu-
sion of homologous blood carries docu-
mented risk of infectious and immune
changes. Recent availability of alternatives to
autologous blood transfusion should be care-
fully evaluated.

Coagulation Monitoring

As in the operating room, functional evalua-
tion of coagulation includes platelet number
and function, activity of coagulation factors,
and clot breakdown.

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

Procoagulant activity is evaluated by quan-
tifying the prothrombin time (PT) and the
activated partial thromboplastin time (APTT) .
In the operating room, the time required to
perform these test may limit their usefulness,
but postoperatively this should not be a
problem. Platelet function is evaluated by the
bleeding time and can be used at the bedside
to indicate efficacy of coagulation therapy.
Thromboelastography is a measure of whole
blood coagulation, and it seems to correlate
well with other tests of platelet function. It has
been shown to be useful in the operating room
to make the diagnosis of factor deficiency, DIC,
platelet dysfunction, and others, although its
use is not widespread.

In the ICU setting, serial monitoring of PT,
PTT, fibrinogen, fibrin degradation products,
and platelet count should be done in the
severely injured patient who has received
significant amounts of blood products intra-
operatively or in patients in whom temporary
hemostatic measures (e.g., packing) were used
because of diffuse bleeding associated with
hypothermia, acidosis, and intraoperative
coagulopathy. Transfusion of clotting factors
and platelets, treatment of underlying shock
and hypothermia, and adequate oxygenation
constitute the basis of therapy in patients with
post-traumatic coagulopathy. This must be
done by a constant effort, with both nurses
and physicians collaborating until the goal is
accomplished. Less than a full effortwill often
be met with failure.

Complications following
Massive Blood Transfusion

Citrate intoxication may induce refractory
hypotension, particularly following massive
transfusion or continuous infusion at high
rates. Acute lung injury (ALI) is rare but may
be eventually seen in the postoperative period
as a result of complement activation induced
by the presence donor antibodies interacting
with recipient granulocytes. Coagulopathy
following massive transfusion is usually due
to dilution of platelets and consumption of
coagulation factors. Microvascular bleeding
in the setting of massive transfusion and major
blood loss occurs when platelet counts drop
to less than 50,000 cells/mm", and fibrinogen
level is less than 100 mg%. DIC may develop
postoperatively, secondary to prolonged
shock, acidosis, and hypoxia. Treatment of
DIC should focus on the underlying cause and
replacement of coagulation factors and
platelets.

After massive transfusion of citrated blood,
hypocalcemia may develop. Hypocalcemia
may lead to cardiac dysfunction and hypoten-
sion; however, coagulopathy rarely occurs,
unless serum calcium levels are less than 0.2
mg/dL. Mobilization of Ca 2+ is usually ade-
quate after infusion of large amounts of citrate.
Calcium replacement should be based
on measured levels and should not given
prophylactically.

Patients with normal liver function should
not receive empirical calcium supplementa-
tion. Iatrogenic hypercalcemia leads to
arrhythmias and hypotension. The only
patients who should receive supplemental
calcium following massive transfusion are
those with severe liver disease.

Box 4-2 lists the most common complications
after multiple blood transfusions. The inci-
dence of these complications varies with the
amount of blood units transfused. Metabolic
abnormalities are common following trans-
fusion. Hyperkalemia may be due to potas-
sium being released from destroyed red blood
cells. Acidosis may occur as a result of the accu-
mulation of lactic and pyruvic acids in stored
blood; however, metabolic alkalosis occurs
more commonly, because of the conversion
of citrate to bicarbonate in the liver.

Mechanical Ventilation

The routine management of ventilation has
changed significantly over the last decade. For
the uncomplicated patient who undergoes
surgery with no anticipated postoperative
problems, weaning and extubation should
follow a standard protocol relying on the rapid
shallow breathing index as an indicator for
extubation success.

A considerable number of severely injured
patients will develop ALI and acute respira-

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109

TRANSFUSION TRANSMITTED DISEASES

O Hepatitis

O Human immunodeficiency virus

O Bacterial infections

O Viral infections

HYPOTHERMIA

COAGULATION DYSFUNCTION

O Factor dilution

O Disseminated intravascular coagulation

O Thrombocytopenia

ACID-BASE IMBALANCE

ELECTROLYTE IMBALANCE

HEMOLYTIC REACTIONS

ALLERGIC (NONHEMOLYTIC) REACTIONS

TRANSFUSION-RELATED ACUTE LUNG INJURY

CITRATE INTOXICATION

tory distress syndrome (ARDS) . Early
ALI/ARDS usually follows massive fluid resus-
citation and its occurrence depends at least
on the injury severity and hyper-inflammation
in the post-traumatic period. Late ARDS is
usually caused or accompanied by sepsis.

New mechanical ventilation strategies have
recently been developed to provide adequate
oxygenation and to decrease the risk of baro-
trauma and ventilator-induced lung injury. A
protective strategy can be defined as low tidal
volumes and the elimination of inspiratory
plateau pressure while maintaining positive
end-expiratory pressure (PEEP) above the
lower inflection point of the pressure-volume
compliance curve. This can be done with a
volume ventilator or a pressure ventilator, and
the recent use of pressure-control ventilation
has gained popularity because of the relative
ease in achieving this protective strategy.

The use of permissive hypercapnia often
becomes a necessary by-product of this pro-
tective strategy and has become acceptable
practice. Multiple studies have suggested this
strategy is associated with lower mortality.
Recently, several studies evaluated protective
strategies and compared them to traditional
strategies in the treatment of ARDS. Taken
together, a lung protective strategy including
lower tidal volumes, permissive hypercapnia,
and the use of PEEP above the inferior
inflection point while limiting inspiratory
plateau pressure seems preferable and prob-
ably is associated with improved survival.
Because an actual increase in oxygenation
does not explain the difference in outcome,
the reduction in sheer stress and inflamma-
tion accompanies a lung protective strategy
could conceivably account for the observed
effect. Those who follow an evidence-based

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

strategy in caring for their patients should con-
sider the routine use of a protective strategy.
In general, most patients will do well if they
are placed on initial tidal volume of 4 to 8
mL/kg, with plateau pressures not to exceed
35mLH,0.

Another technique used to improve
oxygenation is called prone ventilation. The
rationale for prone ventilation is to decrease
the volume loss that accompanies patients
lying on their back and thereby correct
ventilation/perfusion mismatch. Most believe
that recruitment of previously atelectatic
areas induced by altered gravitational forces
accounts for redistribution of blood flow and
improvement in ventilation/perfusion and
oxygenation. Although the evidence is still
being assessed, this remains an important
adjunct to patients who are difficult to venti-
late. Several techniques that allow this to be
done safely in most patients have emerged,
including turning devices and protective
padding.

Once a patient's ALI or ARDS is resolved,
all patients must go through a weaning
process; recent studies suggest that using a
strategy of a once-daily trial of spontaneous
breathing is associated with more rapid extu-
bation than intermittent mechanical ventila-
tion (IMV) or pressure support weaning. Most
importantly, a consistent protocol, if used by
physicians, nurses, and respiratory therapists
together, seems to be critical to rapid suc-
cessful weaning.

Antibiotics

The use of antibiotics should be guided by
the general principles of the use of antibiotics
in trauma patients. In general, these should
be limited to a preoperative dose and 24 hours
of postoperative antibiotics. No good data exist
about whether prolonged antibiotics in
patients in whom a vascular graft is placed
reduces the incidence of postoperative infec-
tion; however, many practitioners will extend
antibiotic coverage for several days. When
there is gross contamination and a vascular
graft needs to be placed (a colon injury and
iliac artery injury), trying to cover the graft
or route the graft through uncontaminated

tissue is best, thereby trying to avoid the
problem altogether. The use of antibiotics in
this situation will be user dependent, and even
here, prolonged antibiotics have some atten-
dant risks.

Antibiotics should be limited to second-
generation cephalosporins and the use of
multiple antibiotics and in particular amino
glycosides should be avoided. Recently sur-
veillance data have documented dramatic
increases in the incidence in infections caused
by Staphylococcus aureus, coagulase-negative S.
aureus, Streptococcus pneumoniae, and Entero-
coccus. These organisms are associated with a
rapid increase in resistance to many available
antimicrobial agents, and prolonged use of
antibiotics in the initial phase of treatment
will select out resistant organisms and subse-
quently cause resistant infection, which may
be ultimately untreatable.

Equally important to antibiotics is the pro-
vision of good graft and anastomosis cover-
age with local tissue. The use of adjacent
muscle, omentum, or even the rotation of a
nonadjacent muscle to get adequate coverage
and sealing of a graft is essential for avoiding
infection.

Once in the postinjury period, antibiotics
should be targeted to a specific diagnosis, and
if started for empirical therapy, they should
be stopped as soon as cultures direct specific
therapy or indicate that therapy is not needed.
The length of treatment should be restricted
to a defined period and the antibiotics
stopped. Patients should be re-cultured if they
develop new symptoms. Recent strategies to
overcome antibiotic resistance include the use
of rotation of various antibiotics for empiri-
cal therapy. This avoids the "antibiotic pres-
sure" that allows resistant organisms to
emerge. This may be a useful strategy, but it
will require further study.

Assessment and Determination
of Take Back

Ongoing assessment of vascular injuries
involves the evaluation of bleeding, assessment
of peripheral pulses, and the development of
compartment syndromes of the abdomen and
extremity.

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BLEEDING

Following massive bleeding and coagulopa-
thy, the assessment of bleeding involves criti-
cal judgment. On the one hand, until the
coagulopathy has been reversed and the
patient warmed, reoperation for bleeding may
be unsuccessful. Similarly, in the presence of
profound shock, primary hemostasis may
have prevented small vessels from bleeding,
thereby avoiding surgical hemostasis only to
subsequently vasodilate and bleed in the ICU.
This dilemma is solved only by careful bedside
surveillance, concerted correction with coag-
ulation factors, and continuous monitoring
of output (e.g., chest tube and drains) , abdom-
inal distention, hematocrit, and coagulation
indicators.

Once a reasonable attempt and success with
rewarming and factors and platelet repletion
has occurred, one has to decide whether the
possibility of unchecked bleeding exists. If
there is concern and the rate of drain output
or hematocrit is falling, or if ongoing blood
replacement does not seem better or contin-
ually gets worse, then returning to the oper-
ating room and re-exploration is the most
appropriate course of action. Reapplication
of damage control and temporary closure may
also be appropriate after re-exploration.

VASCULAR PATENCY

After vascular repair or reconstruction, par-
ticularly if accompanied by shock, assessment
of peripheral pulses may be difficult in the
cold vasoconstricted patient. The initial pres-
ence of adequate perfusion can be reassur-
ing and the presence of symmetrical pulses
detectable by Doppler flow studies will provide
initial evidence of patency. With warming,
distal perfusion should progressively improve
with brisk capillary refill and good venous
filling. As resuscitation improves, pulses
should return or suspicion should be raised
that there is a problem. Use of segmental
Doppler flow studies may help, but if there is
any question about thrombosis, re-explo-
ration or angiography should be immediately
pursued.

ABDOMINAL COMPARTMENT
SYNDROME

The abdominal compartment syndrome
usually occurs in patients undergoing damage-
control operations, intra-abdominal packing,
massive fluid resuscitation, and visceral
swelling. It is characterized by the presence
of a distended tense abdomen, hypoxia,
carbon dioxide retention, oliguria, hypoten-
sion, and high peak inspiratory pressures. The
diagnosis is suspected on the basis of physical
findings and is confirmed by measurement of
intra-abdominal pressure indirectly as bladder
pressure. Patients with a bladder pressure
higher than 25 to 30 cm H 2 should return
to the operating room for decompression and
the abdomen should be left open.

EXTREMITY COMPARTMENT
SYNDROME FOLLOWING
PROLONGED ISCHEMIA

Extremity compartment syndrome is the
result of trauma or reperfusion following
severe prolonged ischemia, leading to
increased swelling within a closed fascial com-
partment. It may also occur after massive fluid
resuscitation, and continuous surveillance is
required to avoid delays in diagnosis. This con-
tained swelling results in an elevation in tissue
pressure up to the point that blood flow is
compromised and no longer provides enough
oxygen to the cells. If left untreated or undi-
agnosed, itwill resultin myonecrosis and limb
dysfunction or limb loss.

The most commonly involved areas are the
anterior compartment in the lower leg and
the volar compartment in the forearm.
Because nerve tissue is more susceptible to
ischemia than other tissues in the extremity
(e.g., muscle, bone, and tendons) , initial symp-
toms are paresthesia and pain. On palpation,
the muscles are tense, and if the patient is
awake and able to cooperate with physical
examination, pain may be severe and even-
tually increased with passive movement of the
extremity and contraction of the involved
muscles. Pulses are usually palpable, even in
advanced stages, and its presence does not rule
out this diagnosis. The diagnosis is based on

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

physical findings, although a high index of
suspicion is necessary in the subgroup of
patients with associated injuries in other body
areas with competing pain or those sedated
on mechanical ventilation. Once the diagno-
sis of compartment syndrome is suspected,
compartment pressure should be measured.
Fasciotomy is generally indicated when com-
partmental pressure is greater than 30 mm Hg.

SUMMARY

The management of vascular injuries can be
one of the most challenging injuries in the
severely injured patient. They will often be
accompanied by airway obstruction or trou-
bled breathing caused by penetrating adjacent
wounds and will often present in hypov-
olemic shock. As such, decision making and
prioritization, decision making in the oper-
ating room, and limiting operative surgery ini-
tially and staging it subsequently are complex
decisions that when made correctly will save
lives.

Because of the nature of these injuries, these
patients are at the highest risk for postoper-
ative/post-traumatic complications includ-
ing aspiration, ARDS, renal failure, and
coagulopathy. The trauma surgeon must be
equipped to anticipate each of these problems
and stay ahead of their subsequent deterio-
ration by aggressive management.

REFERENCES

Battistella FD: Ventilation in the trauma and sur-
gical patient. Crit Care Clin 1998;14:731-742.

Cosgriff N, Moore EE, Sauaia A, et al: Predicting
life-threatening coagulopathy in the massively
transfused trauma patient: Hypothermia and aci-
dosis revisited. J Trauma 1997;42:857-862.

Davis JW, Parks SN, Kaups KL, et al: Admission base
deficit predicts transfusion requirements and risk
of complications. J Trauma 1996;41:769-774.

Gentilello LM, Pierson DJ: Trauma critical care.
Am J Respir Crit Care Med 2001;163:604-607.

Ham AA, Coveler LA: Anesthetic considerations
in damage control surgery. Surg Clin North Am
1997;77:909-919.

Hirshberg A, Mattox KL: Planned reoperation for
severe trauma. Ann Surg 1995;222:3-8.

Ivatury RR, Diebel L, Porter JM, et al: Intraab-
dominal hypertension and the abdominal com-
partment syndrome. Surg Clin North Am
1997;77:783-800.

Jurkovich GJ, Greiser WB, Luterman A, et al:
Hypothermia in trauma victims: An ominous pre-
dictor of survival. J Trauma 1987;27:1019-1024.

McFarland JG: Perioperative blood transfusions:
Indications and options. Chest 1 999;1 15:11 3-121 .

Price JA, Rizk NW: Postoperative ventilatory man-
agement. Chest 1999;115:130-142.

Rotondo MF, Zonies DH: The damage control
sequence and underlying logic. Surg Clin North
Am 1997;77:761-777.

Shackford SR, Rich NH: Peripheral vascular injury.
In Mattox KL, Feliciano DV, Moore EE (eds):
Trauma. New York, McGraw Hill, 2000.

ch05.qxd 4/16/04 3:25 PM Page 113

Diagnosis of
Vascular Trauma

JOHN T. ANDERSON
F. WILLIAM BLAISDELL

PATHOPHYSIOLOGY

Classification

Mechanism

Ischemia

Reperfusion Injury

Compartment Syndrome

DIAGNOSIS

History

Physical Examination

Hard and Soft Signs of Vascular Injury

Ancillary Tests

SUMMARY

Diagnosis and management of vascular
injury has evolved dramatically over
the past century. Early experience
during combat demonstrated that prompt
identification and repair of injured arteries

resulted in improved functional outcome
and decreased rates of amputation. Military
experience supported routine operative
exploration of gunshot wounds of the extrem-
ities because of a high incidence of vascular

113

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114

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

injury following high-velocity gunshot wounds
in proximity to major vessels. Application of
these principles to civilian trauma that typi-
cally involves low-velocity gunshot wounds,
shotgun wounds, or stab wounds resulted in
unacceptably high rates of negative explo-
rations. Arteriography was promulgated as
an alternative to mandatory exploration in
patients without obvious vascular injury (i.e.,
no findings of pulselessness, arterial bleeding,
or expanding and/or pulsatile hematoma) .
However, the yield of routine application of
arteriography, especially for proximity alone,
is also low. Further, not all arterial injuries iden-
tified by arteriography require surgical treat-
ment. Recently, the goal has shifted toward
the identification of those injuries that require
operative intervention. To this end, algorithms
varying from use of physical examination
alone or in combination with duplex ultra-
sonography and/or selective arteriography
have been promoted. The ideal diagnostic
approach that will maximize accurate detec-
tion of vascular injury while minimizing mor-
bidity and cost is still a matter of debate and
active research.

PATHOPHYSIOLOGY
Classification

Although a wide variety of individual injury
types may result from trauma (see Fig. 4-1),
they essentially fall into three basic categories.
The arterial wall can be completely transected,
partially transected, or injured without tran-
section. The patient with a completely tran-
sected artery will frequently have a history of
initial active bleeding but present without
overt hemorrhage. The media of the normal
artery is capable of significant vasoconstric-
tion that promotes clot formation and hemo-
stasis. If the involved artery is a conduit vessel,
distal pulses will be absent. In certain cir-
cumstances, hemostasis may not be achieved.
Iliac and intercostal arteries may continue
to bleed as tethering of the vessels by sur-
rounding structures prevents retraction. Also,
in older patients and those with diseased

vessels due to atherosclerosis, the artery may
be incapable of adequate vasoconstriction and
bleeding may continue unabated.

Partial transection of an artery limits vaso-
constriction and the injured area tends to gape
open. Active external bleeding will continue
if not contained by surrounding tissues. A
pseudoaneurysm will form if the tissues
prevent active external bleeding. Acutely, this
may be manifest as a pulsatile hematoma at
the site of injury. Pulses may continue to be
palpable distal to the site of injury. At times,
the initial arterial injury is not apparent
and an expanding pseudoaneurysm may later
present with pain, a pulsatile mass, or symp-
toms of nerve impingement. Veins run in prox-
imity to arteries and are frequently injured
along with the artery. An arteriovenous (AV)
fistula may result as blood decompresses from
a partially transected artery into an adjacent
injured vein. The AV fistula often is not ap-
parent on initial presentation. Typically, the
fistula enlarges over time and may ultimately
result in high-output cardiac failure or chronic
arterial or venous insufficiency.

Finally, the arterial wall can be injured
without full-thickness transection. The in tima
of the artery is relatively inelastic in compar-
ison to the media and the adventitia. Stretch
or compression of an artery may disrupt the
in tima and tunica interna of the media while
leaving the tunica externa of the media and
the adventitia of the artery intact. Throm-
bosis of the artery may result from clot
formation following exposure of the highly
thrombogenic media or from a mechanical
obstruction as a result of an intimal flap. Alter-
natively, small clot fragments may form and
embolize distally. More severe degrees of
stretch or compression may weaken or disrupt
an additional layer of the arterial wall so that
a pseudoaneurysm may form; extreme
degrees of stretch will result in complete dis-
ruption. The use of the term spasm is men-
tioned only to be discarded. True arterial
spasm, defined as constriction of the media
in an otherwise uninjured vessel, is rarely
present. Spasm identified on arteriography
invariably represents an intimal injury or
embolic clot from a more proximal arterial
injury.

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5 • DIAGNOSIS OF VASCULAR TRAUMA

115

Mechanism

Penetrating mechanisms are responsible for
most vascular injuries, even in rural centers
that generally care for a predominately blunt
trauma population. Civilian penetrating
trauma is almost exclusively from low-
velocity mechanisms such as handgun, knife,
or shotgun injuries. Less common injuries
can occur from penetration by sharp objects
such as glass, metal, or wood splinters. These
mechanisms typically cause partial or com-
plete transection of the artery as a result of
direct trauma. Occasionally, the vessel is indi-
rectly injured as a result of an associated frac-
ture. High-velocity (>2500 feet per second)
gunshot wounds can directly and indirectly
injure arteries. Even a trajectory in proximity
to a major artery may cause arterial damage
as the kinetic energy of the high-velocity pro-
jectile is transferred to the tissues. Extensive

Disrupted
media

Lateral geniculate
collateral flow

■ FIGURE 5-1

Mechanism of popliteal artery injury following
posterior knee dislocation. (Redrawn from
American College of Surgeons: ACS Surgery:
Principles and Practice. New York: WebMD,
2003.) ■

soft tissue and skeletal damage and collateral
circulation disruption also occur.

Blunt trauma generally causes vascular
injury as a result of stretch or compression.
Usually, arterial thrombosis results. The arter-
ies are particularly susceptible to injury at sites
of arterial fixation and around joints, for
example, the popliteal artery, which may be
injured following knee dislocation (Fig. 5-1).
At times, bony fragments can puncture the
vessel directly, as with a supracondylar femur
fracture (Fig. 5-2) .

Associated injuries, many of which are life
threatening and require immediate inter-

■ FIGURE 5-2

Injury to the distal superficial femoral artery
associated with a supracondylar femur
fracture. ■

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

vention, are frequently present in combina-
tion with penetrating and blunt vascular
injuries. Damage due to penetrating trauma
is generally confined to the area of the tra-
jectory of the penetrating object, although
multiple injury sites are common. Blunt
trauma results in a wider distribution of
affected structures. Overall, mortality and
amputation are more common following
blunt trauma.

Ischemia

As a general rule, re-establishing perfusion
within a "golden period" of 6 hours from the
time of injury is a desirable goal to ensure
optimal functional outcome. Warm ischemia
less than 4 hours generally will not lead to
muscle necrosis, whereas delays beyond 6
hours may be associated with significant
muscle damage. Clinical decisions should not
be made with strict adherence to these time
limit guidelines because some degree of
collateral circulation is often present and
reperfusion even beyond 6 hours following
injury may result in successful functional
outcome. In blunt trauma, associated tissue
trauma may interrupt collaterals to a greater
extent then penetrating trauma and likely
accounts in part for the increased severity of
ischemia and the higher rate of amputation
following blunt trauma. An exception to this
generalization may be seen with high-velocity
bullet wounds in which associated soft tissue
injury and collateral disruption may be
significant.

The peripheral nerves are especially sus-
ceptible to ischemia. This is the consequence
of a high basal metabolic rate and a general
lack of significant glycogen stores. Dysfunc-
tion of the nerves due to ischemia results in
a "stocking-glove" distribution sensory deficit.
This finding portends progression to gan-
grene if perfusion is not re-established
promptly. This should be distinguished from
direct peripheral nerve injury that will present
with a neurologic deficit in the distribution
of the nerve. Paralysis associated with an anes-
thetic limb carries a bad prognosis. Restora-
tion of blood flow in such a limb, even within

the golden period cited earlier, may result in
limb loss.

Reperfusion Injury

"Reperfusion injury" is the damage caused
locally (i.e., to skeletal muscle and peripheral
nerves) and systemically following re-
establishment of blood flow to an ischemic
body region. Ischemia sets into process a
number of biochemical alterations that cumu-
late in cellular damage following reperfusion.
The severity of the reperfusion injury is cor-
related with the volume of ischemic tissue (i.e.,
lower limb vs. upper limb) and duration of
ischemia. A variety of substances are released
including superoxide anion, a highly reactive
free radical. Reperfusion results in microvas-
cular endothelial membrane damage, neu-
trophil activation, platelet aggregation, and
decreased nitric oxide production. Ultimately,
microvascular perfusion is compromised
resulting in progression of the original
ischemic injury. Release of metabolic prod-
ucts into the systemic circulation may cause
hyperkalemia, acidosis, and myoglobulinemia.
Additionally, the inflammatory and coagula-
tion systems are activated. Cardiac arrhyth-
mias, acute respiratory distress syndrome,
renal failure, multiorgan failure, and death
may follow if not identified and aggressively
treated. Reperfusion of the entire lower limb
may be life threatening. Reperfusion of
the lower leg is less morbid but can still have
life-threatening consequences in the older
patient.

Compartment Syndrome

Compartment syndrome results from swelling
of soft tissues enclosed within a relatively rigid
fascial space. As pressure increases within
the compartment, microvascular perfusion is
limited, and ultimately, tissue necrosis results.
Most commonly, compartment syndrome
occurs in the lower leg or forearm, however,
additional locations can be involved. Swelling
may result from hemorrhage into the soft
tissues, from tissue edema as a result of
venous occlusion, from ischemic or dying

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5 • DIAGNOSIS OF VASCULAR TRAUMA

117

muscle, or from external causes such as tight
casts or circumferential burn eschars.

The diagnosis of compartment syndrome
is clinical and based on clinical findings of the
four Ps: pressure, pain, paresthesia, and intact
pulses. Increased pressure is manifested as a
tense compartment to palpation and can be
confirmed by direct pressure measurement.
Pain is out of proportion to that expected from
the extremity injury. Also, passive stretching
of the ischemic muscle aggravates the pain.
Paresthesia, which may progress to complete
anesthesia and paralysis, is a late finding in
compartment syndrome. Distal pulses are
often intact, a finding that when present serves
to distinguish compartment syndrome from
arterial insufficiency.

Compartment pressures are readily mea-
sured with either handheld devices (e.g.,
Stryker pressure monitor) or with a side-port
catheter attached to an arterial pressure trans-
ducer. Blood flow to muscle is cut off when
compartment pressures exceed venous pres-
sure. Criteria based on an absolute compart-
ment pressure value are of limited utility
in hypotensive patients. Several investigators
have advocated calculation of a gradient
between the measured compartment pressure
and either the mean arterial pressure or the
arterial diastolic pressure. A gradient of less
than 10 to 30mmHg below the diastolic or
less than 30 to 40mmHg below the mean
arterial pressure has improved specificity in
the diagnosis of extremity compartment syn-
drome. Of note, patients with venous injury
or obstruction are particularly susceptible to
subsequent compartment syndrome and
should be closely monitored.

An effort should be made to determine the
cause of the compartment syndrome. The
ultimate functional outcome of fasciotomy
depends on the etiology of the compartment
syndrome and the extent of muscle necrosis.
Increased compartment pressures due to
either hemorrhage into the compartment or
venous obstruction, especially with underly-
ing viable muscle, are clear-cut indications of
the need for fasciotomy. Controversy regard-
ing the utility of fasciotomy arises in patients
who have compartment syndrome on the basis
of ischemia alone (e.g., compartment syn-
drome of the calf following prolonged femoral

artery occlusion). Release of the fascial enve-
lope will not result in recovery of necrotic
muscle. Subsequent infection, nonhealing,
and need for amputation generally result.
These patients are best served without fas-
ciotomy. The muscle will become fibrotic;
however, the patient may be left with a func-
tional limb.

DIAGNOSIS

Identification and management of life-
threatening injuries and treatment of shock
should be the first priority. Advanced Trauma
Life Support (ATLS) guidelines should be fol-
lowed. Initial treatment and evaluation should
proceed simultaneously. It is important to rec-
ognize and control external hemorrhage.
Generally, direct pressure is effective. Patients
should be promptly resuscitated as the pres-
ence of shock itself may lead to diminished
pulses in the extremities and confusion about
the presence of vascular injury. Associated frac-
tures and dislocations may compromise vas-
cular patency and should be reduced.
Frequently, there are associated injuries to the
abdomen, chest, or head that require imme-
diate intervention. Prompt resuscitation and
identification and management of vascular
injuries should be the goals to limit warm
ischemia and ensure optimal functional
outcome.

History

The patient and prehospital personnel should
be questioned about the mechanism of injury.
With penetrating trauma, information such
as the length of the knife, the number and
direction of bullets fired, and the body posi-
tion at the time of injury should be sought.
With blunt trauma, the severity of the injury
mechanism (e.g., distance of fall, vehicle
speed, and damage) and evidence of fracture,
dislocation, or altered perfusion of extremi-
ties should be elucidated. Further, certain
mechanisms such as "car bumper" injuries or
posterior knee dislocations may be associated
with vascular injury and their occurrence
should be sought. The amount and charac-

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

ter of blood loss should be ascertained. Bright
red pulsatile bleeding is suggestive of an
arterial injury, whereas dark blood suggests
a venous origin. Evidence of shock must be
soughtfrom the prehospital personnel, aswell
as the volume of fluid administered. The use
of a tourniquet and duration of its applica-
tion should be determined. Information
about neurologic symptoms including sensory
and motor deficits should be obtained. Also,
the patient should be questioned regarding
a history of peripheral vascular disease, dia-
betes, or other conditions such as coronary
artery disease that carry a high incidence of
associated vascular disease.

Physical Examination

The patient should be adequately exposed and
thoroughly examined. Deformity due to frac-
ture or dislocation should be identified.
Careful attention should be directed to skin-
folds in the axilla or perineum and buttocks
that may hide wounds due to penetrating
trauma. In the case of penetrating trauma, the
trajectory of the wounding object should be
estimated, particularly with reference to major
arteries. Wounds should be inspected for
evidence of active bleeding or hematoma
formation. The character of the bleeding,
pulsatile bright red blood, or a steady ooze
of dark blood should be noted. A tense or
expanding hematoma indicates the presence
of an arterial injury with bleeding contained
by surrounding soft tissues. Finally, the oppo-
site uninjured extremity should be inspected
for evidence of chronic peripheral vascular
disease. Absent pulses in the non-injured leg
markedly decreases the likelihood of vascu-
lar injury in the traumatized extremity.

The pulse examination should include pal-
pation of pulses proximal and distal to the
injury. Skin temperature and capillary refill
distal to the injury should also be assessed as
indexes of perfusion. A difference in the char-
acter of the pulse or skin perfusion should
prompt additional workup. Of note, pulses
may be palpable and normal in up to one third
of patients with avascular injury. Comparison
of skin perfusion and pulses of the injured
extremity to that of the non-injured extrem-

ity is very helpful. Hypoperfusion and dimin-
ished peripheral pulses due solely to shock
will be similar on both sides. Further, dimin-
ished or absent pulses as a result of periph-
eral vascular disease are generally symmetrical
between the extremities. Occasionally, patients
may have a congenital absence of the dorsalis
pedis pulse.

AV fistulas may be identified by ausculta-
tion of a bruit over the involved arterial
segment; a thrill, palpable evidence of an AV
fistula, is rarely present in acute injury. Aglove
should be placed over the bell of the stetho-
scope to keep the stethoscope free of blood
when there is an open injury. Thrills and bruits
may not be obvious, particularly early after
injury. AVfistulas generally progress over time
and bruits that were not initially present may
appear the next day.

Complete preoperative evaluation and doc-
umentation of neurologic function is impor-
tant, as ultimate functional outcome largely
depends on intact sensory and motor func-
tion. As mentioned, a "stocking-glove" distri-
bution sensory deficit indicates neurologic
dysfunction due to ischemia. Development
of gangrene will ensue if flow is not promptly
re-established.

Hard and Soft Signs of
Vascular Injury

Findings identified on history and physical
examination may be divided into two cate-
gories, hard signs and soft signs, each with a
varying degree of association with arterial
injury (Table 5-1 ) . Hard signs are strong pre-
dictors of the presence of an arterial injury
and the need for operative intervention.
Obvious examples are pulsatile bleeding
or an expanding hematoma. Evidence of
ischemia manifested with the six Ps: Pulse-
lessness, pallor, pain, paralysis, paresthesia,
and poikilothermia are further strong evi-
dence of arterial injury. A thrill, palpable evi-
dence of an AV fistula, is not as commonly
noted as is a bruit. An arterial pressure index
(API) of less than 0.90 is included as a hard
sign. The API is determined by dividing the
systolic pressure of the injured limb by the
systolic pressure of the non-injured limb.

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5 • DIAGNOSIS OF VASCULAR TRAUMA

119

TABLE 5-1

HARD VERSUS SOFT SIGNS OF
VASCULAR INJURY

Hard Signs

Active arterial bleeding

Pulselessness/evidence

of ischemia
Expanding pulsatile

hematoma
Bruit or thrill
Arterial pressure index

< 0.90 pulse deficit

Soft Signs

Neurologic injury in
proximity to vessel

Small to moderate-sized
hematoma

Unexplained hypotension

Large blood loss at scene

Injury (due to penetrating

mechanism, fracture, or

dislocation) in proximity

to major vessel

trauma to look for foreign bodies or evidence
of fracture or dislocation. Radiopaque
markers should be placed on all penetrating
wounds for identification on subsequent radi-
ographs. The number of bullets visualized
should be correlated with the number of
wounds. The sum of the number of bullets
and the number of wounds should equal an
even number. If the sum results in an odd
number, the possibility of a missile embolism
should be entertained. The bullet may travel
within the vascular system to the heart and
pulmonary system if the bullet gains access to
the venous system (Figs. 5-3 and 5-4) or the
distal artery if the bullet gains access to the
arterial system. Additional x-ray films, includ-
ing fluoroscopy, should be obtained and the

Johansen and colleagues (1991) found that
an API of less than 0.90 had 95% sensitivity
and 97% specificity for identification of occult
arterial injury. Further, an API of more than
0.90 had a 99% negative predictive value for
an arterial injury. However, an API may be
normal in patients who have injuries to non-
conduit vessels such as the femoris profunda.
Also, API can be unreliable in the evaluation
of penetrating injuries in the region of the
groin. Nonetheless, the API is readily obtained
at bedside and is a useful extension of the phys-
ical examination, particularly when the pulse
strength is questionably diminished.

Soft signs are suggestive of an arterial
injury, though with a much decreased sensi-
tivity and specificity than hard signs (see Table
5-1). The incidence of arterial injury varies
with the specific finding. When proximity is
the only indicator of possible vascular injury,
evaluation with arteriography generally finds
identifiable injuries in fewer than 10% of
patients, and many do not require additional
specific treatment other than observation
alone. Much of the controversy of vascular
trauma evaluation centers on the workup of
patients with soft signs.

Ancillary Tests

Plain x-rays of the injured extremity should
be obtained in both penetrating and blunt

■ FIGURE 5-3

Bullet embolism to pulmonary artery from iliac
vein injury. (From What's Your Diagnosis:
Photographic Case Studies in General Surgery.
Greenwich, Conn: Cliggott Publishing, 1994.) ■

■ FIGURE 5-4

Extraction of bullet embolism to right pulmonary
artery. (From What's Your Diagnosis:
Photographic Case Studies in General Surgery.
Greenwich, Conn: Cliggott Publishing, 1994.) ■

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

patient re-examined until the discrepancy is
resolved. Occasionally, folds in the axilla and
perineum may hide additional wounds.
Finally, the foreign body image should be scru-
tinized. Blurring of the edges of the bullet sug-
gests movement that could be the result of an
intimate relationship with a pulsatile artery.

Application of routine operative explo-
ration of penetrating extremity trauma to civil-
ian trauma proved to result in a large number
of negative explorations. In a landmark paper,
Snyder and colleagues (1978) validated the
use of arteriography to accurately detect vas-
cular lesions. They evaluated 177 patients with
183 penetrating extremity injuries using arte-
riography and subsequent operative explo-
ration. They identified 1 false-negative and 14
false-positive arteriograms. Arteriography is
generally not required in patients with obvious
arterial injury (e.g., active arterial bleeding,
pulselessness, and/or expanding hematoma) .
However, arteriography is invaluable in
patients in whom the diagnosis is less clear or
the extent or location of vascular injury is not
readily apparent (Table 5-2) . Arteriography
is generally well tolerated. Complications can
occur in 2% to 4% of patients. Usually, these
are minor, most frequently limited groin
hematomas. Major complications such as
iatrogenic pseudoaneurysms, AV fistulas, or
embolic occlusion are uncommon. In part,
this may reflect the younger population typical
for trauma.

Patients who require urgent operation
either for an obvious vascular injury or for
life-threatening associated injuries should
have any necessary arteriograms performed
in the operating room to minimize warm

TABLE 5-2

INDICATIONS FOR ARTERIOGRAPHY:
EXTREMITY TRAUMA

Unclear location or extent of vascular injury

Extensive soft tissue injury

Fracture or dislocation

Trajectory parallel to an artery

Multiple wounds

Shotgun injuries

Peripheral vascular disease

ischemia time. Arteriograms are obtained with
percutaneous cannulization of the artery
proximal to the site of suspected injury. Con-
trast is then injected into the artery, and plain
films are obtained. Fluoroscopy can be used
as an alternative to plain radiographs to min-
imize the amount of contrast required and to
aid with timing of the contrast injection. If
visualization of the axillary artery is necessary,
outflow occlusion with a cuff can be per-
formed to allow filling of the axillary artery
proximal to the site of contrast injection as
described by O'Gorman and colleagues
(1984). Of note, O'Gorman and colleagues
(1984) described the use of surgeon-per-
formed angiography in the emergency room
to exclude significant vascular injury. They
were subsequently able to discharge some
patients from the emergency room.

Duplex ultrasonographic scanning has been
shown by several investigators to have a sen-
sitivity and specificity approaching 100% for
the investigation of penetrating extremity
trauma. The modality combines real-time
two-dimensional imaging with guided Dop-
pler insonation. Flow to or from the point of
Doppler investigation can be represented on
a color scale. Duplex ultrasonography is more
sensitive than an API evaluation. Further, non-
conduit arterial injuries, which do not alter
the API, can be evaluated.

Evaluation of the patient with penetrating
extremity trauma who presents with only soft
signs of arterial injury continues to be a subject
of debate. Routine use of arteriography on
patients with proximity injuries will identify
abnormalities in up to 10% of cases. Several
series report the need for vascular repair in
between 0.6% and 4.4% of patients with prox-
imity penetrating injuries (Dennis, 1998) .
Dennis, Frykberg, and colleagues (1998) has
championed physical examination alone in
this group, arguing that patients those patients
who need operative intervention will ulti-
mately develop identifiable hard signs. A
number of investigators have promulgated
duplex ultrasonography as a noninvasive alter-
native between routine arteriography and
physical examination alone. The lesions
missed on initial physical examination that
ultimately require operative intervention are

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5 • DIAGNOSIS OF VASCULAR TRAUMA

121

injuries to the profunda femoris artery,
pseudoaneurysms, and AV fistulas. Both of
these lesions progress with time and delayed
operative repair is technically more chal-
lenging. Further, many investigators have
documented the poor follow-up possible in
the trauma population. Duplex ultrasonog-
raphy is capable of detecting these lesions at
the time of initial presentation. The major lim-
itations are that the modality is technician
dependent and often not readily available
during off-hours when most patients are
injured. However, even proponents of physi-
cal examination alone advocate admission and
observation for 24 hours. Moreover, more than
43% of patients with proximity penetrating
extremity trauma at University of California-
Davis required physical therapy, and 46%
required complex wound care. Thus, admis-
sion during which duplex ultrasonography
can be obtained is easilyjustified. Ultimately,
the choice is a balance between the need to
promptly diagnose all arterial injuries requir-
ing treatment and prevent unnecessary
morbidity on the one hand and the cost,
availability, and morbidity of diagnostic modal-
ities on the other hand.

Patients with suspected vascular injury fall
into three basic priorities: (1) Patients with
evidence of pulselessness/ischemia, active
bleeding, or a pulsatile hematoma, (2) patients
with hard signs and a palpable pulse, and (3)
patients with soft signs or an injury known to
be associated with vascular injury. In all
patients, life-threatening injuries take prior-
ity and should be addressed immediately. The
patient should be resuscitated and shock
managed appropriately. Fractures and dislo-
cations should be reduced and the pulse exam-
ination and skin perfusion evaluated. Hard
and soft signs should be specifically elicited
(Fig. 5-5).

Patients who are pulseless or show evidence
of ischemia or those who have active bleed-
ing manifested with either external bleeding
or an expanding pulsatile hematoma should
be taken promptly to the operating room.
Often, the location of the injury can be
identified from the history and physical
examination and operative intervention can
proceed directly. However, in certain cir-

cumstances, the exact location or extent of
injury may be unclear (see Table 5-2). In these
patients, on-table arteriography, performed
in the operating room, is used to assess vas-
cular injury and minimize warm ischemia
time.

Patients who have hard signs but have a pal-
pable pulse and no evidence of ischemia can
generally undergo a more deliberate workup.
Usually information required to guide inter-
vention is obtained from formal arteriogra-
phy in the radiology suite. In general, the
quality of formal arteriograms is better than
that of those obtained in the operating room.
Additionally, therapeutic endovascular pro-
cedures such as embolization of bleeding
muscular branches, pseudoaneurysms, or AV
fistulas can be performed in the radiology
suite. Occasionally urgent operation is
required for associated injuries, such as intra-
abdominal injury. In these patients, on-table
arteriography provides a means to promptly
identify arterial injuries to guide subsequent
operative or nonoperative management.

Patients who have soft signs or who have a
mechanism suggestive of an arterial injury,
such as a posterior knee dislocation, can be
evaluated in various ways. Viable options, each
with their ardent advocates and literature
support, include routine arteriography or
duplex ultrasonography and/or serial physical
examination. Vascular abnormalities identi-
fied by duplex ultrasonography are subse-
quently evaluated with arteriography as a
diagnostic and possibly therapeutic inter-
vention. Development of hard signs in patients
followed by physical examination is generally
evaluated by formal arteriography.

Patients with injury in the region of the
groin, thoracic outlet, or neck should undergo
arteriography. Duplex ultrasonography of
the subclavian, axillary, and iliac vessels is
limited. Further, consequences of missed
injuries in these areas, such as exsanguination
from intrapleural hemorrhage, may be cata-
strophic. At times, the vascular lesion may
be amenable to treatment with endovascular
techniques.

Once arterial injuries are identified and
delineated, management proceeds as
appropriate.

ch05.qxd 4/16/04 3:25 PM Page 122

122

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

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5 • DIAGNOSIS OF VASCULAR TRAUMA

123

SUMMARY

Diagnostic modalities and algorithms have
evolved as treatment paradigms have pro-
gressed over the past century from expectant
management, to repair of all arterial injuries,
to the repair of selected arterial injuries prac-
ticed today. Continued refinements are to be
expected with ongoing clinical research and
patient follow-up.

REFERENCES

Dennis JW, Frykberg ER, Veldenz HC, et al:
Validation of nonoperative management of
occult vascular injurie s and accuracy of physical
examination alone in penetrating extremity
trauma: 5- to 10-year follow-up. J Trauma 1998;
44(2):242-252.

The authors present long-term outcome data to
validate safety and efficacy of physical examina-
tion alone to determine the treatment of pene-
trating extremity trauma. Two groups of patients
are presented, the first during a period of liberal
use of arteriography, and the second with the
use of physical examination alone. Group 1 had
43 patients with 44 clinically occult injuries sub-
sequently demonstrated on angiography. Four
(9%) had deterioration within a month and
required operative repair. Follow-up, with a mean
of 9.1 years, was possible in 58% of the remain-
ingpatients; all were asymptomatic. Group 2 had
287 patients with 309 asymptomatic proximity
injurie s evaluated by physical examination alone .
Four (1.3%) deteriorated and required surgery.
Follow-up, with a mean of 5.4 years, was possi-
ble in 29%; no patient reported vascular
symptoms.

Fry WR, Smith RS, Sayers DV, et al: The success of
duplex ultrasonographic scanning in diagnosis
of extremity vascular proximity trauma [see Com-
ments] . Arch Surg 1993;128(12):1368-1372.

Study of the use of duplex ultrasonographic scan-
ning in the evaluation of penetrating extremity
vascular trauma. Two-hundred patients with 225
penetrating extremity injuries were evaluated
with duplex ultrasonography for either vascular
proximity injury or diminished pulse strength.
Arteriograms were obtained in the first 50
patients. The sensitivity and specificity were both
100% in this initial cohort. Duplex ultrasonog-
raphy was used in the remaining 175 injuries.

Eighteen injuries were identified, seventeen of
which were confirmed by either arteriography
or operative exploration. The remaining patient
had spasm of the superficial femoral artery on
arteriography, which did not require treat-
ment. Seven unsuspected venous injuries were
identified.

Johansen K, Lynch K, Paun M, Copass M: Non-
invasive vascular tests reliably exclude occult
arterial trauma in injured extremities. J Trauma
1991;31(4):515-522.

Follow-up study to validate the use of arterial pres-
sure index (API) to exclude significant arterial
damage in patients with extremity trauma.
Overall, a value of 0.90 was found to have a sen-
sitivity and specificity of 95% and 97%, respec-
tively, for the presence of significant arterial
injury. A value of more than 0.90 had a negative
predictive value of 99% . Arteriography was advo-
cated for those limbs with an API of less than
0.90. The authors argue the API is safe, accu-
rate, and cost-effective in the evaluation of
extremity vascular trauma.

O'Gorman RB, Feliciano DV, Bitondo CG, et al:
Emergency center arteriography in the evalua-
tion of suspected peripheral vascular injuries.
Arch Surg 1984;119(5):568-573.

Description of a surgeon-performed arteriog-
raphy in a group of 488 patients with suspected
vascular injuries. The majority of arteriograms
were obtained for proximity (353/488) ; 76 arte-
riograms were performed for a diminished
pulse. Overall, 20% of the patients were found
to have a vascular injury requiring subsequent
operative intervention. Only one false-normal
and four false-abnormal arteriograms were
reported. The authors conclude that the method
is simple, sensitive, and cost-effective in patients
with potential peripheral vascular injuries.

Richardson JD, Vitale GC, Flint LM Jr: Penetrat-
ing arterial trauma. Analysis of missed vascular
injuries. Arch Surg 1987;122(6):678-683.

Classic article describing an experience of 677
patients with penetrating wounds to the upper
and lower extremity and neck with suspected
vascular injury. Patients were evaluated with a
combination of surgical exploration and/or
arteriography. Long-term follow-up for an
average of 5.1 years was obtained in 33% of the
patients. Missed vascular injurieswere identified
in patients undergoing either surgical explo-
ration alone or arteriography alone. No missed
injuries were identified in patients who
underwent both arteriography and surgical
exploration.

ch05.qxd 4/16/04 3:25 PM Page 124

124 I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

Snyder WH III, Thai ER, Bridges RA, et al: The raphy and subsequent operative exploration,

validity of normal arteriography in penetrating Compared to operative exploration, arteriogra-

trauma. Arch Surg 1978;1 13(4) :424-426. phy had 36 true positives, 132 true negatives, 14

Landmark paper comparing arteriography to false positives, and 1 false negative. The authors

operative vessel exploration. One hundred conclude that arteriography is sensitive enough

seventy-seven patients with 183 penetrating to exclude arterial injury in patients with

extremity wounds were evaluated with arteriog- equivocal clinical signs of vascular injury.

ch06.qxd 4/16/04 3:28 PM Page 125

Vascular Diagnostic Options in
Extremity and Cervical Trauma

KAJ JOHANSEN

O INTRODUCTION

O PENETRATING AND BLUNT TRAUMA TO THE EXTREMITIES

A Historical Perspective

Noninvasive Physiologic Vascular Tests

Limb Swelling and Pain following Extremity Revascularization

O PENETRATING OR BLUNT INJURIES TO THE BRACHIOCEPHALIC
VESSELS

Physical Examination

O SUMMARY

INTRODUCTION

Sometimes the diagnosis of extremity arter-
ial trauma is straightforward: Torrential hem-
orrhage, acute limb ischemia, a pulsatile
hematoma, or other such urgent problems
generally require little attention to dia-
gnostic maneuvers other than immediate
operation. However, a large proportion of
peripheral vascular injuries may not be imme-
diately apparent, presenting in subtle, con-
fusing, or obscure fashion. Alternatively,
vascular injuries may be entirely silent,

discovered only during a general diagnostic
survey of the trauma patient. This chapter elu-
cidates currently accepted "best practices"
for the diagnosis of extremity and cervical
vascular trauma.

PENETRATING AND BLUNT
TRAUMA TO THE EXTREMITIES

Injury to the major arteries of the extremities
may result in severe bleeding or in immedi-
ate or delayed ischemia — in either case, a

125

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126

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

"SEVEN Ps" OF ACUTE ARTERIAL INSUFFICIENCY

Pain

Paresthesia

Pulselessness

Pallor

Poikilothermia (or Polar)

Paralysis

(Past midnight!)

threat to limb viability. Further, as is noted later,
technically successful revascularization of the
traumatized extremity may threaten extrem-
ity viability anew by producing an ischemia-
reperfusion phenomenon, manifested
clinically by compartment syndrome.

Patients with substantial ongoing external
bleeding, rapidly expanding hematoma,
evidence for acute arterial insufficiency — the
"Seven Ps" (Box 6-1) — or other less common
objective signs of major arterial injury (e.g.,
the presence of a large arteriovenous [AV]
fistula) almost always warrant immediate
operation as the first diagnostic test. Other
diagnostic tests such as arteriography are dila-
tory and rarely add useful decision-making
information (occasional patients, such as
those with shotgun injuries or with extremity
fractures at multiple levels, may require
imaging studies preoperatively to define the
precise anatomic site of arterial disruption) .
The need for immediate operation is obvious
in patients with exsanguinating hemorrhage,
and equivalent urgency is present in patients
with acute arterial insufficiency, in whom
experimental and clinical data as well as long-
established clinical observation document at
most a 6-hour "grace period" to restore per-
fusion before a substantially increased likeli-
hood of postoperative tissue infarction and
limb loss can be anticipated. This acceptable
"golden period" may be even shorter if shock,
crush injury, or other comorbidities compli-
cate the clinical picture.

Unfortunately, most patients with extrem-
ity trauma do not have "hard" signs of

vascular injury but only "soft" indications that
arterial or venous injury has occurred. Alter-
natively, they may have no evidence to support
the possibility that a vascular injury is present,
but only clinical suspicion based on the mecha-
nism of injury or on proximity of the injury
tract to important vessels.

A Historical Perspective

The "gold standard" for making the diag-
nosis of occult extremity injury has changed
substantially during the professional lifetime
of many still-active clinicians. Wound explo-
ration was the norm in the 1950s and 1960s
and had even been mandated in the battle-
field setting. However, the morbidity of this
approach (including the extremely low yield
of mandatory wound exploration) became
clear and resulted in a switch to the use of
contrast arteriography (usually by a trans-
femoral arterial approach) in the 1970s and
1980s. This approach was fueled by the
general belief (promoted by experienced
trauma surgeons at several major trauma
centers) that physical examination is inade-
quately accurate for the assessment of vascu-
lar status in injured extremities (Perry, Thai,
and Shires, 1971). Contrast arteriography
proved relatively rapid and extremely sensi-
tive and specific for the identification of arte-
rial disruption in trauma victims; several
studies documented false-positive and false-
negative rates of less than 2% in contrast
arteriography performed to rule out arterial

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6 • VASCULAR DIAGNOSTIC OPTIONS IN EXTREMITY AND CERVICAL TRAUMA

127

injury in the extremities (Snyder and col-
leagues, 1978; Rose and Moore, 1988).

However, contrast arteriography generally
requires transfer of the patient out of the emer-
gency department (ED) to a site in which
ongoing surveillance, volume resuscitation,
and management of secondary injuries are
difficult to conduct. Contrast arteriography
is invasive and expensive and has a small but
definite risk of contrast dye reactions or arte-
rial puncture-site complications. Most impor-
tantly, it became clear that the real clinical
yield of contrast arteriography, when per-
formed as the screening technique of choice
in injured extremities, is extremely low. In
several series, fewer than 5% of patients actu-
ally required operative intervention for arte-
rial injuries discovered by means of contrast
arteriography (Frykberg and colleagues, 1989;
Anderson and colleagues, 1990).

Noninvasive Physiologic
Vascular Tests

In the 1980s, some clinicians began to use
several noninvasive diagnostic techniques in
the acute setting, which had previously been
found to be of major diagnostic value in the
assessment of chronic arterial occlusive
disease. These included measurement of
Doppler-derived arterial pressure indexes
(APIs) and the use of duplex sonography.
These two techniques have proven extremely
useful as initial screening tests for patients
thought potentially to harbor an occult
extremity arterial injury.

Lynch andjohansen (1991) initially demon-
strated that among 100 injured limbs in 93
patients, in whom both Doppler APIs and con-
trast arteriography were carried out, a Doppler
API of 0.90 had a sensitivity of 87% and a speci-
ficity of 95% for arterial injury. Because two
(2%) of the contrast arteriograms were actu-
ally falsely positive in circumstances in which
the ultimate outcome had been accurately pre-
dicted by the Doppler API, the sensitivity and
specificity of the Doppler API technique was
actually even higher — 95% and 97% — when
clinical outcome was used as the comparison
standard. The negative predictive value for an
API of more than 0.90 was 99%.

In a subsequent study, Johansen and
colleagues (1991) evaluated 100 consecutive
limbs in 96 vascular trauma victims by screen-
ing Doppler API; arteriography was reserved
for patients in whom Doppler API was less than
0.90. In this series, 83 limbs had a normal API
(>0.90) and 17 limbs had an abnormal API
and underwent contrast arteriography. The
patients with a normal Doppler API were fol-
lowed up clinically and by duplex sonography;
none required further vascular intervention,
and all (except for two patients who under-
went normal arteriograms as a protocol
violation) had been spared contrast
arteriography. Among the 17 limbs undergo-
ing contrast arteriography, 16 (94%) arterial
abnormalities were found and seven under-
went operative intervention.

These studies demonstrated that use of
Doppler API could substantially reduce the
number of "exclusion" contrast arteriograms
performed in our trauma center (an 80%
reduction compared with the 12-month
period before the trial, P<.01), markedly
increase the diagnostic "yield" when contrast
arteriography was required, facilitate the
overall management of most patients not
requiring contrast arteriogram, and save a sub-
stantial sum in hospital charges (Lynch and
Johansen, 1991; Johansen and colleagues,
1991).

Many of the trauma victims in the studies
in which Doppler API was validated were the
victims of penetrating trauma. For this
reason, some trauma specialists — especially
orthopedic surgeons — were reluctant to
accept Doppler API as a screening test for
proximal extremity injuries in blunt trauma —
fractures, dislocations, and crush injuries.
Accordingly, Cole and colleagues (1999)
recently conducted a study of 70 trauma
victims (75 limbs) who had suffered fractures
and dislocations around the knee. Among
these patients, Doppler API was normal in 57
limbs and abnormal in 18. By clinical outcome
(including duplex scan in about one third of
the patients) , no late abnormalitieswere iden-
tified in the individuals who had an initially
normal Doppler API. In those with a Doppler
API of less than 0.90, contrast arteriography
was performed in 16 (88%) and was positive
in 14 (87% of arteriograms) ; operative repair

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128

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

was performed in 6 (33%). The negative pre-
dictive value of a normal Doppler API in these
bluntly traumatized lower extremities was
100% (Cole and colleagues, in press), sug-
gesting that Doppler API is as accurate and
useful a screening tool in blunt extremity
trauma as it is for penetrating injury.

Studies from other trauma centers regard-
ing the utility of Doppler API in screening
through the extremities for a potential arte-
rial injury came to similar conclusions
(Schwartz and colleagues, 1993; Frykberg,
1995). Schwartz and colleagues (1993) use a
higher threshold Doppler API of 1.0, thereby
slightly increasing sensitivity at the expense
of a substantially higher number of negative
contrast arteriograms.

The limitations of Doppler API as a screen-
ing tool for occult arterial injury in the
extremities must also be made clear. The tech-
nique does not accurately diagnose damage
in branch arteries (e.g., the profunda femoris
or profunda brachii arteries) , cannot accu-
rately detect small intimal flaps, AV fistulas or
pseudoaneurysms, and will not, of course,
discover significant venous injuries. This diag-
nostic technique is clearly much less accurate
in the interrogation of arteries proximal to
the inguinal or axillary crease, for example,
the iliac or subclavian/axillary arteries; such
vessels are best evaluated by contrast arteri-
ography. The Doppler API technique can be
"fooled" (as can contrast arteriography) by
arterial spasm and may not detect arterial
lacerations.

Accordingly, Doppler API has been vali-
dated as an accurate, rapid, inexpensive, and
noninvasive bedside screening examination
for the purposes of initial screening of a bluntly
or sharply injured extremity for occult arter-
ial injury.

The excellent diagnostic capabilities of
duplex sonography — pulsed wave Doppler
ultrasound — became clear in the mid 1980s,
again in the evaluation of carotid (and other
types of) atherosclerosis. This technology has
been thoroughly assessed as being portable,
rapid, and noninvasive in the evaluation of
trauma victims.

Panetta and colleagues (1992) demon-
strated, in a carefully performed compara-
tive study of duplex sonography and

arteriography among different types of exper-
imental arterial injuries, that when evaluated
by blinded observers, duplex sonography was
overall more accurate than contrast arteriog-
raphy in diagnosing arterial disruption
(P< .02), especially for arterial lacerations
CP<.001).

Among 89 patients with 93 sites of extrem-
ity or cervical trauma, Meissner, Paun, and
Johansen (1991) demonstrated that duplex
sonography resulted in only four false posi-
tives and no false negatives for significant
arterial injury. A similar study in 198 trauma
patients by Bynoe and colleagues (1991)
from the University of South Carolina found
only two false-positive and one false-negative
study. In this study, sensitivity was 95% and
specificity was 99% for arterial injury.

These studies might appropriately be crit-
icized because arteriography control was not
consistently carried out. Fry and colleagues
(1993) conducted a trial in patients with
extremity trauma in which the first 50 sub-
jects who were studied by Doppler ultra-
sound also underwent contrast arteriography
(or operative exploration). When perfect
agreement was discovered between ultra-
sonographic and arteriographic diagnostic
modalities in these patients, a subsequent 1 75
patients were studied by duplex scan alone,
with arteriography reserved for patients with
an abnormal ultrasonographic study. This trial
of duplex scan showed 100% sensitivity and
97% specificity for major arterial trauma; only
one false-positive study resulted. In addition,
the investigators reported discovery of seven
major venous injuries by means of duplex
sonography, which they asserted would not
have been identified had only contrast arte-
riography been performed as a diagnostic tool
(Fry and colleagues, 1993).

The advantages of duplex scanning as a
screening examination for arterial injury in
a patient with extremity trauma are obvious;
it can be brought to the bedside in the ED
and is noninvasive, rapid, easily repeated, and
inexpensive. In addition, certain injuries not
readily identified by other means — for
example, major venous disruptions — may
potentially be identified by this technique.

The limitations of duplex sonography must
also be emphasized. These include potentially

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6 • VASCULAR DIAGNOSTIC OPTIONS IN EXTREMITY AND CERVICAL TRAUMA

129

reduced access because of open wounds, dress-
ings, splints, or casts; relatively lesser accuracy
in identifying truncal vascular injury; and a
substantial "learning curve "for technologists
and interpreting physicians. In addition, at a
time of continued economic retrenchment by
urban trauma hospitals, it has become increas-
ingly difficult to sustain night/weekend
vascular laboratory coverage, obligatory for
evaluation of trauma victims in the ED.

Do all arterial injuries need to be repaired?
Although some continue to adhere to the
traditional tenet that any arterial disruption
warrants operative exploration (Stain and
colleagues, 1993), more contemporary
studies, based on the excellent natural history
data which can be accumulated from repeated
duplex ultrasonograms of various arterial
injuries, have suggested that many "minor"
arterial injuries — small intimal flaps, pseu-
doaneurysms, and AV fistulas — resolve on
their own without intervention. The obser-
vation that most intimal injuries that result
from catheter arteriography go on to "heal"
without operation certainly predicts such a
conclusion. Stain and colleagues (1993)
observed 80 "minimal" pseudoaneurysms,
intimal flaps or dissections, and AVfistulas with
serial duplex ultrasound examinations; at the
end of 12 months, only 4 (5%) of the lesions
had required operative repair.

Thus, the noninvasive vascular physiologic
examinations of Doppler API measurement
and duplex sonography can be employed with
accuracy and cost-effectiveness in the evolu-
tion of extremity arterial injuries. We have
developed an algorithm (Fig. 6-1) that incor-
porates these modalities.

Limb Swelling and Pain
following Extremity
Revascularization

The unwary clinician may ignore the fact
(or fail to recall) that prolonged or severe limb
ischemia followed by successful revasculari-
zation can result in the ischemia-reperfusion
phenomenon, manifested clinically as com-
partment syndrome. This may be seen par-
ticularly after crush injuries, combined arterial
and venous trauma, closed fractures of the

Significant bleeding or ischemia, or shotgun wound?

Yes

Doppler pressure
measurement

APK0.90 API > 0.90

Arteriogram
(or operation)

Observation

(serial exams, ?

noninvasive imaging?)

■ FIGURE 6-1

Algorithm for diagnostic management of
patients potentially harboring an extremity
vascular injury. ■

extremity, and ischemia complicated by sys-
temic hypotension or shock. Compartment
syndrome, if not recognized and treated in a
timely fashion, is associated with a substantial
risk of myonecrosis and limb loss.

In the otherwise uncomplicated trauma
victim, the diagnosis of compartment syn-
drome is usually straightforward. Such
patients have pain out of proportion to what
would be expected, as well as inexorably wors-
ening neurologic dysfunction of the extrem-
ity as characterized by both numbness and
extensor weakness. Calf or forearm muscles
(for practical purposes, the only two sites
where compartment syndrome normally pre-
sents) will be unnaturally tight, swollen, and
tender. Thus, the diagnosis of compartment
syndrome is not difficult, given the appro-
priate clinical scenario and the symptoms and
signs noted earlier.

However, relevant symptoms and signs may
be obscured by one or more of a constella-
tion of comorbid conditions. These may
include intoxication with alcohol or other
drugs, closed head injury, general or neuraxial
anesthesia, spinal cord injury resulting in para-
plegia or quadriplegia, or obscuration of the
examination by casts, splints, or dressings. In
such patients, the diagnosis of compartment
syndrome may be obscured or ignored until
muscle necrosis has already occurred.

One approach, espoused by many, is to
adopt a liberal posture toward the

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I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

performance of prophylactic fasciotomy when
even the possibility of compartment syn-
drome is contemplated. I am a proponent of
such a view. However, in certain clinical set-
tings, such an approach might be imprudent
or unwarranted, and alternative dependable
means of making the diagnosis of compart-
ment tissue hypertension are required.

The time-honored technique is that of tissue
manometry, using various commercially avail-
able devices to transduce tissue pressure after
insertion of a needle into a given compart-
ment of the calf or forearm. This technique,
in use since the mid 1970s (Whiteside and col-
leagues, 1975; Matsen, 1978) is both sensitive
and specific for compartmental hypertension;
its only drawbacks are its invasive nature (thus
making it difficult to do repeat studies) and
the fact that devices for measuring may occa-
sionally be unavailable, out of commission, or
unfamiliar to the clinician. Tissue pressures
higher than 40mmHg or higher than
30 mm Hg for longer than 3 hours have been
considered diagnostic of compartmental
hypertension and are an indication for imme-
diate fasciotomy (Matsen, 1978). A more
contemporary understanding of the patho-
physiology of compartmental hypertension
compares the measured compartment pres-
sure to either the diastolic or the calculated
mean arterial pressure, with compartmental
hypertension being characterized by a pres-
sure differential of less than 30 mm Hg
(Matava and colleagues, 1994).

Other techniques, such as the measurement
of somatosensory evoked potentials (Present
and colleagues, 1993), the use of near-infrared
spectrophotometry (Giannotti and col-
leagues, 2000), and the objective measure-
ment of tissue hardness (Steinberg and
Gelberman, 1994) have been assessed.

A clever conceptual leap by Jones, Perry,
and Bush (1989), experimentally validated by
Ombrellaro and colleagues (1996), permits
the assessment of effects of tissue pressure on
calf or forearm venous hemodynamics by use
of venous duplex scanning. Arterial pressures
and flows should clearly be only minimally (if
at all) impacted by changes in ambient tissue
pressure. However, venous hemodynamics
should be exquisitely sensitive to local tissue
pressure: Normal venous pressures in the calf

and forearm are virtually identical to tissue
pressures (5 to 10 mmHg). Whereas the sen-
sitivity of duplex scanning of the calf or
forearm veins for compartment syndrome may
not be particularly high (i.e., abnormal venous
hemodynamics might be due to crush injury,
hematoma, splints or dressings, or compart-
mental hypertension) , the specificity of exam-
ination should be quite close to 100% (i.e.,
normal tibial venous respiratory variation and
phasi city in a particular calf compartment indi-
cate that compartmental hypertension cannot
be present). Duplex scanning of tibial or
forearm veins is the screening test of choice
at my medical center in patients in whom
the diagnosis of compartment syndrome is
entertained.

PENETRATING OR BLUNT
INJURIES TO THE
BRACHIOCEPHALIC VESSELS

Among many other complications of
trauma to the head, neck, and upper chest is
the possibility of injury to the large arteries
and veins of the head and upper extremities.
Not only is early or delayed exsanguination a
risk, but the late implications of arterial
thrombosis or embolization secondary to
dissection, intimal flap, or pseudoaneurysm
include the risk of disabling or even lethal
stroke. An ongoing controversy attends the
question of the proper diagnostic pathway to
be followed in patients with penetrating cer-
vical trauma — mandatory exploration or selec-
tive operation based on the results of a panel
of diagnostic tests (arteriography, triple
endoscopy, barium swallow). This dispute
remains undecided despite careful ongoing
evaluation over the last 4 decades.

As for other anatomic sites in the body, signs
of significant hemorrhage (pulsatile external
or oropharyngeal bleeding, expanding/
pulsatile hematoma) mandate immediate
operation. In addition, it has become increas-
ingly clear that cervical vascular injury asso-
ciated with any degree of neurologic deficit
warrants emergency extracranial carotid (or
vertebral) arterial reconstruction as well
(Richardson and colleagues, 1992). Although

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6 • VASCULAR DIAGNOSTIC OPTIONS IN EXTREMITY AND CERVICAL TRAUMA

131

the results of such surgical repair in patients
with carotid artery injury associated with coma
are generally dismal, case reports suggest that
even in this desperate setting, occasional cere-
bral salvage can occur by timely carotid arte-
rial repair (Robbs and colleagues, 1983) .

As elsewhere, much more major controversy
attends the management of patients with "soft"
signs of cervical carotid (or vertebral) arter-
ial injury or in whom there is concern about
an occult arterial injury based on the sound-
ing mechanism or the location of the injury
tract. Because such wounds potentially also
involve the airway or (as seriously) the esoph-
agus or the oropharynx, either routine opera-
tive exploration as the first diagnostic test or
a series of radiographic, endoscopic, and arte-
riographic studies is obligatory in this setting.
As noted already, no clear consensus has been
achieved in defining the superiority of one
diagnostic approach over the other.

Detection of occult cervical arterial injuries
is assisted by now well-established means of
categorizing such potential injuries by
anatomic site. It is generally agreed that
injuries below the sternal notch (zone 1) will
likely require median sternotomy or thora-
cotomy for management; accordingly, pre-
operative contrast arteriography is generally
considered necessary. Injuries above the angle
of the jaw (zone 3), because they are surgi-
cally remote, may require craniotomy or
(potentially) even more complex vascular
exposure; contrast arteriography is thus indi-
cated in this setting as well. Arteriography for
lesions in zone 3 also occasionally identifies
lesions surgically inaccessible enough (e.g.,
in the carotid siphon) so that treatment by
catheter-directed means (e.g., coil emboliza-
tion of carotid artery-cavernous sinus fistula)
is the preferred therapeutic choice.

In zone 2 penetrating injuries to the neck,
duplex sonography has been found to play a
highly dependable diagnostic role. Fry and
colleagues (1994), using control arteriogra-
phy "run-in"for the first 15 patients in a series
of 100 patients, demonstrated equivalent
100% sensitivities and specificities for duplex
sonography in examining cervical carotid
injuries. Demetriades and colleagues (1995)
compared contrast arteriography, duplex
sonography, and simple serial physical

examination in 82 patients with penetrating
neck trauma. As previously demonstrated with
peripheral arterial injuries in the extremities,
contrast arteriography was "hypersensitive "for
arterial injuries; 11 arterial disruptions were
discovered, but only 2 required operation.
Physical examination was accurate for all clin-
ically significant injuries but missed six minor
vascular injuries. Duplex sonography found
10 of the 1 1 injuries detected by contrast arte-
riography, and sensitivity and specificity for
clinically relevant injuries were 91 % and 99%,
respectively.

Blunt cervical arterial injuries are even more
complicated to diagnose, because unlike pen-
etrating trauma (which usually involves the
common carotid artery), blunt trauma more
commonly involves the internal carotid artery.
Closed head injury, basilar skull fractures,
various forms of deceleration motor-vehicle
accidents resulting in injuries to the head and
neck, and the increased use of shoulder-lap
restraints have resulted in a sharply increased
recent incidence of blunt carotid injury
(Kerwin and colleagues, 2001 ) . Because these
patients frequently present without initial
symptoms only later developing neurologic
deficits related to thrombosis or dissection of
the internal carotid artery, a screening tech-
nique that is accurate and rapid would clearly
be of use in this clinical scenario.

Duplex sonography may play a substantive
role as a screening tool in this setting. As
demonstrated in the landmark animal studies
by Panetta and colleagues (1992) , duplex scan-
ning is as accurate as contrast arteriography
in the diagnosis of dissections, intimal flaps,
and arterial lacerations. In a large series of
patients with blunt cervical trauma, Fabian
and colleagues (1996) demonstrated the diag-
nostic value of duplex sonography in detect-
ing occult arterial injuries. Because logistic
regression analysis of the data in this study
demonstrated independent survival benefit
associated with heparinization in those
patients not requiring operation, the value of
early diagnosis of such initially silent injuries
(either by sonography or by contrast arteri-
ography) is abundantly clear.

Contrast-enhanced cervical computed
tomographic (CT) scanning with fine cuts at
the cervical level was demonstrated by Zeman

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132

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

and colleagues (1995) at the University of
Vermont to be more accurate even than ultra-
sonography or arteriography in determining
whether a bluntly traumatized or dissected
carotid artery is patent or not. Indeed, because
many such patients undergo head CT scans
to rule out concurrent cerebral injuries, an
effective strategy might potentially be to con-
tinue the scan down to the level of the carotid
bifurcation, thereby demonstrating in a few
extra minutes whether the internal carotid
arteries are intact and obviate the need to
perform either duplex sonography or four-
vessel cerebral arteriography.

Transcranial Doppler (TCD) studies have
been used only rarely in the trauma setting.
However, conceptually this technology may
play a useful role in selected patients with
actual or potential cerebrovascular trauma,
on either a blunt or a penetrating basis
(Rae-Grant and colleagues, 1996). For
example, TCD studies can demonstrate the
adequacy of intracranial arterial flow and can
contribute to a decision about whether
extracranial carotid (or vertebral) revascular-
ization needs to be performed. In addition,
information regarding whether temporary
carotid shunting during arterial reconstruc-
tion should be used can be derived from TCD
studies. Finally, in patients with devastating
head injuries (or in whom irreversible brain
injury is suspected) , TCD is an acknowledged
means of demonstrating (based on intracra-
nial arterial flow arrest) that the patient is brain
dead (Wejdiecks ejection fraction, 2001).

Physical Examination

The simplest diagnostic tool is a careful phys-
ical examination. As previously intimated, the
adequacy of physical examination in the diag-
nosis of vascular trauma has been heavily
debated over the past 3 to 4 decades. Experi-
enced trauma surgeons at Parkland Hospital
in Dallas, in a series of reports in the 1970s,
suggested the relative inaccuracy (or at least
inadequacy) of physical examination alone in
patients potentially harboring an arterial
injury and were in the vanguard of those pro-
moting the use of routine "exclusion" arteri-
ography in patients with extremity trauma

(Perry, Thai, and Shires, 1971; Snyder and
colleagues, 1978).

However, it has subsequently become clear
that physical examination has an important
role to play, at least as a screening tool for
various forms of penetrating and blunt extrem-
ity and cervical trauma. I consider measure-
ment of Doppler arterial pressure in injured
extremities and calculation of Doppler API
to be a simple extension of palpation and other
aspects of the physical examination; Doppler
API has been found, in studies in which I as
well as others have participated, to be highly
sensitive and specific in the diagnosis of
important forms of flow-limiting lesions of
extremity arteries (Lynch an djohansen, 1991;
Johansen and colleagues, 1991; Cole and
colleagues, in press; Schwartz and colleagues,
1993; Frykberg, 1995).

Physical examination has also been found
to be accurate for important extracranial
carotid artery injuries in a controlled trial
comparing serial physical examination with
duplex sonography and contrast arteriogra-
phy (Demetriades and colleagues, 1995).
Coming full circle, Francis and colleagues
( 199 1 ) from Parkland Hospital confirmed the
validity of serial physical examination by an
experienced surgeon in ruling in or out
extremity vascular injury.

SUMMARY

The morbidity and mortality associated with
major central or peripheral vascular injury
mandate diagnostic measures that are rapid
(or at least timely) and accurate. Because of
the invasiveness and morbidity of contrast
arteriography and operative exploration, such
diagnostic maneuvers are optimally rapid,
portable, noninvasive, repeatable, and inex-
pensive.

Contrast arteriography continues to be the
"gold standard" for establishing the presence
and anatomic location of arterial injuries
within the chest or abdomen and in zones 1
and 3 for penetrating neck trauma. However,
widespread use of contrast arteriography in
the diagnosis of vascular injury is hampered
by its invasiveness, expense, the time taken to

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6 • VASCULAR DIAGNOSTIC OPTIONS IN EXTREMITY AND CERVICAL TRAUMA

133

perform such studies, and the necessity in most
cases to carry such studies out in a site remote
from the ED or the operating room.

Prospective studies in trauma victims have
demonstrated the validity of Doppler arterial
pressure measurement as a sensitive and
specific screening tool for both penetrating
and blunt arterial injuries that are axial and
flow limiting. Duplex sonography subse-
quently has been found to be as accurate as
contrast arteriography in the diagnosis of
extremity arterial injury, and the technique
has the additional benefit of being able to diag-
nose major venous injuries of the extremities.
Duplex ultrasonography has been demon-
strated to have diagnostic accuracy equivalent
to that of contrast arteriography in penetrat-
ing zone 2 injuries of the neck and has equiv-
alently excellent diagnostic accuracy in blunt
trauma to the extracranial carotid and verte-
bral arteries. Detection of patency of the inter-
nal carotid artery following blunt trauma
and subsequent dissection is accurately made
with contrast-enhanced cervical CT scanning,
a more accurate means of assessing flow
than either contrast arteriography or duplex
sonography.

Although compartment syndrome may be
best averted by adoption of a liberal policy of
prophylactic fasciotomy in trauma victims at
significant risk of developing this compli-
cation, alternative diagnostic methods may
include a series of minimally invasive or
noninvasive techniques measuring tissue pres-
sure or hardness, neurologic function, or com-
partment venous hemodynamics.

Finally, after being long discounted as a valid
means of diagnosing occult arterial injury,
serial physical examination has been resur-
rected as an accurate diagnostic technique by
well-performed prospective clinical trials.

REFERENCES

Abou-Sayed H, Berger DL: Blunt lower-extremity
trauma and popliteal artery injuries: Revisiting
the case for selective arteriography. Arch Surg
2002;137(5):585-589.

Anderson RJ, Hobson RW, Padberg FT, et al:
Reduced dependency on arteriography for pen-
etrating extremity trauma (PET): Influence of
wound location and non-invasive vascular studies.
J Trauma 1990;30:1059-1065.

Barnes CJ, Pietrobon R, Higgins LD: Does the pulse
examination in patients with traumatic knee dis-
location predict a surgical arterial injury? A meta-
analysis. J Trauma 2002;53(6):1109-1114.

Bynoe RP, Miles WS, Bell RM, et al: Noninvasive
diagnosis of vascular trauma by duplex ultra-
sonography. J Vase Surg 1991;14:346-350.

Cole P, Campbell R, Swiontkowski M, Johansen K:
Doppler arterial pressures reliably exclude occult
arterial injury in blunt lower extremity trauma.
J Orthop Trauma (in press).

Demetriades D, Theodorou D, Cornwell E, et al:
Penetrating injuries of the neck in patients in
stable condition: Physical examination, angiog-
raphy or color flow Doppler imaging. Arch Surg
1995;130:971-975.

Fabian TC, Patton JH Jr, Croce MA, et al: Blunt
carotid injury: Importance of early diagnosis and
anticoagulant therapy. Ann Surg 1996;223:513-
522.

Francis H III, Thai ER, Weigelt JA, Rodman HC:
Vascular proximity: Is it a valid indication for arte-
riography in asymptomatic patients? J Trauma
1991;31:512-514.

FryWR, DortJA, Smith RS, etal: Duplex scanning
replaces arteriography and operative explo-
ration in the diagnosis of potential cervical
vascular injury. Am J Surg 1994;168:693-695.

Fry WR, Smith RS, Sayers DV, et al: The success of
duplex ultrasonographic scanning in the diag-
nosis of extremity vascular proximity trauma.
Arch Surg 1993;128:1368-1372.

Frykberg EP: Advances in the diagnosis and treat-
ment of extremity vascular trauma. Surg Clin
North Am 1995;75:207-215.

Frykberg ER, Crump JM, Vines FS, et al: A reassess-
ment of the role of arteriography in assessing
acute vascular injuries. J Trauma 1989;29:1041-
1052.

Giannotti G, Cohn SM, Brown M, et al: Utility of
near-infrared spectroscopy in the diagnosis of
lower extremity compartment syndrome.
J Trauma 2000;48:397-399.

Johansen K, Lynch K, Paun M, Copass MK:
Non-invasive vascular tests reliably exclude occult
arterial trauma in injured extremities. J Trauma
1991;31:515-522.

Jones WG II, Perry MO, Bush HL Jr: Changes in
tibial blood flow in the evolving compartment
syndrome. Arch Surg 1989;124:801-804.

Kerwin AJ, Bynoe RP, Murray J, et al: Liberalized
screening for blunt carotid and vertebral artery
injuries is justified. J Trauma 2001;51:308-314.

ch06.qxd 4/16/04 3:28 PM Page 134

134

I • GENERAL PRINCIPLES OF VASCULAR TRAUMA

Lynch K,Johansen KH: Can Doppler pressure mea-
surements replace "exclusion" arteriography in
extremity trauma? Ann Surg 1991;214:737-
741.

Matava MJ, Whiteside TE Jr, Seiler JG III, et al:
Determination of the compartment pressure
threshold of muscle ischemia in a canine model.
J Trauma 1994;37:50-58.

Matsen FA III: Compartmental syndrome : a unified
concept. Clin Orthop 1978;113:8-13.

Meissner M, Paun M, Johansen K: Duplex scanning
for arterial trauma. AmJ Surg 1991 ;161 :552-555.

Ombrellaro MP, Stevens SL, Freeman ML, et al:
Ultrasound characteristics of lower extremity
venous flow for the early diagnosis of compart-
ment syndrome: An experimental study. J Vase
Technol 1996;20:71-75.

Panetta TF, Hunt JP, Buechter KJ, et al: Duplex
ultrasonography versus arteriography in the
diagnosis of arterial injury: An experimental
study. J Trauma 1992;33:627-635.

Perry MO: Complications of missed arterial injuries.
J Vase Surg 1993;17:399-403.

Perry MO, Thai ER, Shires GT: Management of
arterial injuries. Ann Surg 1971;173:403-408.

Present DA, Nainzedeh NK, Ben-Yishay A, Mazzara
JT: The evaluation of compartmental syndromes
using somatosensory evoked potentials in
monkeys. Clin Orthop 1993;287:376-285.

Rae-Grant AD, Eckert N, Barbourt PJ, et al:
Outcome of severe brain injury: A multimodal-
ity neurophysiologic study. J Trauma 1996;40:401-
407.

Richardson R, Obeid FN, Richardson JD, et al: Cere-
brovascular injury: Neurologic consequences.
J Trauma 1992;32:755-760.

Robbs JV, Human RR, Rajaruthnam P, et al: Neu-
rological deficit and injuries involving the neck
arteries. Br J Surg 1983;70:220-222.

Rose SC, Moore EE: Trauma angiography: The use
of clinical findings to improve patient selection
and care preparation. JTrauma 1988;28:240-245.

Schwartz MR, Weaver FA, Yellin AE, et al: Refining
the indications for arteriography in penetrating
extremity trauma: A prospective analysis. J Vase
Surg 1993;17:166-170.

Snyder WH III, Thai ER, Bridges RA, et al: The
validity of normal arteriography in penetrating
trauma. Arch Surg 1978;113:424-426.

Stain SC, Yellin AE,WeaverFA,etal: Selective man-
agement of nonocclusive arterial injuries. Arch
Surg 1989;124:1136-1140.

Steinberg BD, Gelberman RH: Evaluation of limb
compartments with suspected increased inter-
stitial pressure: A non-invasive method for deter-
mining quantitative hardness. Clin Orthop
1994;300:248-253.

Wejdiecks EF: The diagnosis of brain death. N Engl
J Med 2001;344:1215-1221.

Whiteside TE Jr, Haney TC, Morimoto K, Harada
H: Tissue pressure measurements as a determi-
nant for the need of fasciotomy. Clin Orthop
1975;113:43-51.

Zeman RK, Silverman PM, Vieco PT, Costello P:
CT angiography. AJR Am J Roentgenol 1995;
165:1079-1088.

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Access, Control and Repair

Techniques

KENNETH L. MATTOX
ASHER HIRSHBERG

O POSITIONING

O INITIAL HEMORRHAGE CONTROL

General Principles of Vascular Control
Adjuncts to Hemorrhage Control
O EXPOSURE AND CONTROL OF SPECIFIC INJURIES
Neck

Thoracic Outlet
Chest

Upper Extremity
Axillary Artery
Brachial Artery
Abdomen and Pelvis
Lower Extremity
Groin

Distal Superficial Femoral Artery
Popliteal Artery and Branches
O REPAIR PRINCIPLES AND TECHNIQUES
O SUMMARY

137

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138

II • PRINCIPLES OF OPERATIVE CARE

The repair of vascular injuries is one of
the most challenging aspects of trauma
for the surgeon. In the massively bleed-
ing patient with a major vascular injury, rapid
and effective exposure and control of the
bleeding vessel often mark the difference
between a spectacular save and on-table death
from exsanguination. Despite recent advances
in trauma systems, prehospital care, operative
techniques, and critical care, many critically
injured patients still die in the operating room
(OR) from uncontrolled hemorrhage from
major vessels. Vascular trauma is especially
demanding also because there is a very narrow
margin for technical and judgment errors.
Compared with gastrointestinal injuries,
for example, vascular repairs are much less
forgiving and less tolerant of technical
imperfection.

The operative sequence in vascular trauma
consists of access, exposure, control, and
repair. While the specific techniques used in
addressing individual injuries are described
in other chapters in this book, this chapter
addresses the general principles underlying
the operative approach to injuries to blood
vessels. Our purpose is therefore to provide,
in one location, a single comprehensive

reference to operative principles in vascular
trauma, with special emphasis on universal
considerations that form the foundation for
the control and repair of vascular injuries.

POSITIONING

Correct positioning of the injured patient on
the operating table and an accurate definition
of the operative field are the keys to a smooth
operative procedure. Incorrect positioning
can turn a straightforward operation into a
technical nightmare, severely limits the
surgeon's options, and reflects lack of under-
standing of the ramifications and potential sce-
narios into which the procedure may evolve.
The "generic" position of the trauma patient
in the OR is in the supine position, with both
armsfully extended (Fig. 7-1). One of the car-
dinal principles in trauma surgery is that the
surgeon must be prepared to rapidly shift his
or her attention to another visceral cavity, so
the potential operative field for truncal trauma
extends from the chin to below the knees and
as far laterally as the posterior axillary lines
on both sides, even if the initial procedure is

■ FIGURE 7-1

Drawing depicting supine
and right decubitus (left chest
up) positions. ■

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7 • ACCESS, CONTROL AND REPAIR TECHNIQUES

139

focused on the abdomen or the chest. When
the operative procedure is limited to an
extremity, the surgeon must still be prepared
for an unexpected deterioration that may
require access to the chest (for chest tube
placement) or the groin (for insertion of a
line). Thus, for example, it would be a bad
mistake to attempt to use the posterior
approach to the popliteal artery in the trauma
patient, because with the patient in the prone
position, the surgeon's options for interven-
tions in other anatomic locations are severely
limited.

A left posterolateral thoracotomy, which is
performed with the patient in a right lateral
decubitus position, is a notable exception.
Because gaining access to the posterior medi-
astinal structures (such as the descending
thoracic aorta or the esophagus) through an
anterolateral thoracotomy is difficult, it may
occasionally be necessary to place the injured
patient in the right lateral decubitus position,
thus limiting access not only to the con-
tralateral chest but also to the abdomen or
the extremities. Choosing the right lateral
decubitus position in the trauma patient is
therefore a calculated risk that is typically
undertaken only after injuries to other visceral
compartments have been ruled out.

When positioning the patient for a periph-
eral vascular repair, the surgeon must keep in
mind several important principles: The poten-
tial operative field extends at least one joint
above and below the injured segment. An
uninjured lower limb must be included in the
field to enable rapid harvesting of the saphe-
nous vein. For injuries in proximity to the
groin or axilla, considerations of proximal
control dictate that the abdomen or chest,
respectively, be included in the operative field.
Lastly, full mobility of the injured extremity
within the operative field is mandatory to
enable the surgeon to adjust the position of
the relevant vascular segments as the opera-
tion unfolds.

In summary, when positioning the patient
with vascular trauma, it is a good general
principle to always consider the "worst-case
scenario." This means not only optimizing
exposure of the relevant anatomic area but
also being fully prepared either for a large
extension of the incision or for an urgent

intervention in another visceral compart-
ment (Box 7-1).

INITIAL HEMORRHAGE
CONTROL

Initial control of external hemorrhage,
whether in the field, emergency department,
or OR, is one of the first priorities addressed
during the primary survey of the injured
patient according to Advanced Trauma Life
Support principles. Control of external hem-
orrhage (typically from an injured extremity)
is usually achieved by simple digital or manual
compression, which will almost invariably
control bleeding without damaging adjacent
elements of the neurovascular bundle. In
unusual circumstances, such as combat trauma
care or a mass casualty scenario, an arterial
tourniquet may be lifesaving, albeit at the price
of compromising both the collateral circula-
tion and venous drainage from the injured
extremity.

The classic error in temporary control of
external hemorrhage is an attempt to use sur-
gical instruments (such ashemostats) instead
of digital pressure to obtain control in the
field or in the emergency department. Blind
groping withhemostats in the face of ongoing
torrential hemorrhage is not only ineffective
but also likely to result in iatrogenic damage
to the adjacent structures of the neurovascu-
lar bundle and convert a simple partial injury
into a complete transection with a crushed
arterial wall.

Manual compression of the bleeding site
(usually by a member of the trauma team other
than the surgeon) should be continuously
maintained into the OR, until proper proxi-
mal and distal control is obtained. The com-
pressing hand should then be prepared in the
operative field. While the surgeon makes the
incision to obtain proximal and distal control
and expose the injured vessel, the first assis-
tant should maintain external manual pres-
sure. Selective clamping of the vessel should
thus be performed under optimal conditions
in the OR, away from the site of injury and
using appropriate vascular instruments and
technique.

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140

II • PRINCIPLES OF OPERATIVE CARE

INCISIONS USED FOR CONTROL, EXPOSURE, AND REPAIR OF
VASCULAR INJURY

Anterior neck, anterior to the sternocleidomastoid muscle

Supraclavicular

Infraclavicular

Combined supraclavicular/infraclavicular

Axillary

Inner arm

Antecubital fossa

Forearm

Anterior left second interspace

Left fourth or fifth posterolateral thoracotomy

Median sternotomy with anterior cervical or supraclavicular extension

Midline laparotomy

Low transverse lateral abdominal (kidney transplant incision)

Groin incision

Medial distal thigh

Medial proximal calf

Fasciotomy incisions of the extremity

Balloon catheter tamponade is a very useful
adjunct to initial control of external hemor-
rhage, especially for penetrating injuries to
the groin, clavicular fossa, and axilla, where
manual pressure is not as effective and a
tourniquet cannot be applied. A Foley balloon
catheter is rapidly inserted into the actively
bleeding tract of a bullet or a stab wound and
then is inflated. This simple maneuver creates
local extraluminal compression of the injured
vessel, which temporarily controls hemor-
rhage and frees the compressing hand of the
assistant (Fig. 7-2).

General Principles of
Vascular Control

Definitive control of a major vascular injury
is the accurate placement of vascular clamps
on both the inflow and the outflow tract of
the injured vessel. This cardinal principle of
obtaining proximal and distal control before
approaching the injured segment is one of

the fundamentals of surgery for vascular
trauma, and its importance cannot be
overstated.

Most vascular injuries exhibit some degree
of tamponade, be it from a hemostatic plug,
surrounding tissues, local pressure, spasm of
the injured vessel, or a combination thereof.
Entering the hematoma without first obtain-
ing proximal and distal control away from the
site of injury is the worst mistake a surgeon
can commit, a mistake that often leads to
unnecessary blood loss, a disorganized
attempt to regain control, and sometimes
exsanguination and death.

Proximal control is obtained outside the
hematoma surrounding the injured segment.
This frequently requires extension of the sur-
gical incision and dissection through virgin
tissue planes. An important principle in
obtaining proximal control is to try and go
beyond an anatomic structure that serves as
a natural barrier to the expansion of the
hematoma. For example, dissection in the
groin to gain control of an injured common

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7 • ACCESS, CONTROL AND REPAIR TECHNIQUES

141

Kenneth L. Matlcs, M.D.

■ FIGURE 7-2

Drawing depicting the insertion
of a balloon catheter through
the site of a lower neck
penetrating wound to control
hemorrhage. ■

femoral artery is difficult and fraught with
danger. If the surgeon extends the incision
cranially and dissects above the inguinal lig-
ament, he or she discovers that the ligament
serves as a natural barrier to the expansion
of the hematoma, and the tissue planes above
it are much easier to identify. Similarly, the
pericardium is a barrier to the extension of a
mediastinal hematoma from an innominate
artery injury, and the parietal pleura is a
barrier to the extension of an axillary
hematoma.

Occasionally, precise definition of the
injured vessel is impossible and vigorous
bleeding presents an immediate and grave
danger to the patient's life. Under these cir-
cumstances, an alternative "last-resort" tech-
nique is application of a large noncrushing
vascular clamp to the total gross area of active
hemorrhage, including adjacent structures.
Once "global" proximal and distal vascular
control has been achieved, the clamp can
either be removed or be gradually advanced

toward the site of the specific injury as dis-
section proceeds in a relatively bloodless
field.

Another important adjunct is the use of
intraluminal Fogarty balloon catheters. When
the proximal or distal segment of the injured
vessel is inaccessible to direct clamping (e.g.,
deep in the pelvis), a useful alternative is the
insertion of a Fogarty balloon catheter con-
nected to a three-way stopcock into the orifice
of the bleeding vessel. Inflation of the balloon
inside the vessel lumen achieves direct intra-
luminal hemostasis and obviates the need for
time-consuming and difficult dissection to
define the vessel from the outside.

ADJUNCTS TO
HEMORRHAGE CONTROL

An important aspect of hemorrhage control
is fluid resuscitation. The trauma team
must direct the resuscitative efforts toward

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II • PRINCIPLES OF OPERATIVE CARE

controlled rather than overaggressive fluid
administration. A crucial part of initial hem-
orrhage control is creation of a hemostatic
plug, a soft clot that is formed at the site
of injury by the hemostatic mechanisms of
the body. Dislodgment of this clot is now
presumed to occur at a lower systemic blood
pressure than previously appreciated. The
resuscitating team should therefore avoid
attempts to achieve a blood pressure at
"normal" preinjury levels and remember that
a systolic pressure in the range of 80 mm Hg
is actually in the bleeding patient's best inter-
est. Aggressive resuscitation that leads to
rebleeding and the need for additional fluids
(the so-called "cyclic hyper-resuscitation")
creates a dilutional coagulopathy, activates
inflammatory mediators, and promotes
further bleeding. Avoiding hypothermia and
dilution, both of which directly contribute
to a coagulopathy state, is also very impor-
tant in enabling effective hemostasis by the
coagulation cascade.

The surgeon may elect to use an intravas-
cular temporary shunt (see Chapter 8)
as a hemorrhage control technique. When
inserted into an injured vessel and held in
place proximally and distally, the shunt effec-
tively controls hemorrhage while preserving
distal flow. Topical hemostasis has been an aid
to hemorrhage throughout history using a
wide variety of hemostatic agents ranging from
cellulose, thrombin-like products, and fibrin
glue. The common denominator of all these
topical measures is reliance on the body's phys-
iologic hemostatic mechanisms. The benefit
of the topical device is not always clear, and
in the context of vascular trauma, it is never
a substitute for a carefully placed vascular
suture. It may however serve as a hemostatic
adjunct near avascular repair, to help control
oozing from the suture line or from adjacent
raw surfaces. During the last decade, topically
applied "fibrin glue" has been used in liver,
spleen, and raw surface bleeding. A dry fibrin
dressing technology, based on thrombin
powder, is under development, which has
shown promise in the laboratory as being
able to stop bleeding even from medium-size
arteries and veins.

Recent research focuses on enhancing the
body's physiologic clotting mechanism in

areas of endothelial disruption. Recombinant
activated factor Vila, a hemostatic product
used in the treatment of hemophilia, recently
has been successful in treating coagulopathic
bleeding in critically injured patients. Several
case reports have led to laboratory studies
in animal models. If proven effective in con-
trolled clinical trials, this agent may represent
a paradigm shift from external control to
initiating focused clotting "from within."

EXPOSURE AND CONTROL
OF SPECIFIC INJURIES

Gaining access and exposure to perform
precise reconstruction is a surgical art form
made possible by a detailed knowledge of
surgical anatomy, experience, andjudgment,
as well as an intuitive ability to rapidly access
difficult areas without adding iatrogenic
injury. In vascular trauma, there are times
when aggressive blunt dissection is necessary
to achieve access and control, while other
situations demand the most delicate touch
in dissecting, exposing, and repairing a
complex injury. Nowhere else in surgery is
this dichotomy of the surgical craft more
obvious than in a patient with a vascular
injury. Some injuries pose special problems
of access and hemorrhage control, primarily
because the injury is not in a body area com-
monly operated on and familiar to the surgeon
(Box 7-2) .

Incisions for vascular trauma are selected
with the goal of control, exposure, and repair.
Some incisions are those routinely used for
elective vascular reconstruction, and others
have been specifically adapted for vascular
trauma. Over the years, some incisions have
declined in use or become obsolete. For
example, the "trapdoor" incision (whereby a
left supraclavicular incision is connected to
an anterolateral thoracotomy incision by
means of a partial median sternotomy) was
found to add very little to the exposure of a
vascular injury in the thoracic outlet while
leading to significant chronic causalgia-like
pain. The anterior thoracoabdominal incision
was found to be too time consuming in the
trauma setting, did not allow for adequate

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143

LIST OF INJURIES THAT POSE SPECIAL DIFFICULT ACCESS AND
HEMORRHAGE CONTROL CHALLANGES

High carotid injury
Vertebral artery hemorrhage
Thoracic outlet vascular injury
Azygous vein
Axillary artery injury
Proximal abdominal aorta
Intrathoracic inferior vena cava
Suprarenal inferior vena cava
Deep pelvic iliac vascular injury
Complex groin vascular injury
Distal popliteal/tibial vascular injury

exposure of the thoracic aorta or other
thoracic vasculature, and had significant long-
term healing complications (Box 7-3).

Neck

Access to virtually all vascular injuries in the
neck is accomplished via an incision along the
anterior border of the sternocleidomastoid
muscle. The patient is positioned with the
head rotated as much as possible away from

the operated side and extended, with the
shoulders supported. The operative field
always includes the anterior chest and an
uninjured lower extremity.

A typical incision for neck exploration for
trauma extends from the suprasternal notch
upward toward the ear lobe. Slightly curving
the upper part of the incision away from the
jaw will prevent inadvertent damage to the
marginal mandibular branch of the facial
nerve. During an exploration for penetrating
trauma, and particularly in the presence of

INCISIONS THAT ARE INFREQUENTLY OR NO LONGER USED FOR
VASCULAR TRAUMA

Collar neck incision

Across the clavicle incision

"Trapdoor" or "book" thoracotomy

Anterior thoracoabdominal

Posterior thoracoabdominal

Combined midline abdominal extending across the groin

Posterior popliteal

Transverse abdominal

Abdominal paramedian

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II • PRINCIPLES OF OPERATIVE CARE

active hemorrhage, many anatomic land-
marks in the neck are obscured or distorted,
and the surgeon has to rely on rapid
identification of three key landmarks: the ante-
rior border of the sternocleidomastoid, the
internal jugular vein immediately behind it,
and the facial vein.

After division of the platysma the incision
"opens up," allowing identification of the
anterior border of the sternocleidomastoid.
Lateral retraction of the muscle and further
dissection in the middle cervical fascia exposes
the jugular vein (Fig. 7-3). Dissection along
the anterior border of the jugular vein allows
the surgeon to identify, isolate, and divide the
common facial vein between ligatures. This
vein, a major branch of the internal jugular,
is the "gateway to the neck" because free access
and exposure of the common carotid artery
and its bifurcation hinges upon division of the
facial vein. Furthermore, the facial vein is fre-
quently at the level of the carotid bifurcation.

The sequence of dissection in the neck
depends on the operative findings. In most
cases, the focus of interest is the content of
the carotid sheath, in which case dissection
proceeds medial to the internal jugular vein,
with special care being taken to identify and

protect the vagus nerve. However, when arte-
rial bleeding emanates lateral to the carotid
sheath, the entire neurovascular bundle
(including the internal jugular vein, the
carotid artery, and the vagus) should be
retracted medially, and dissection lateral to
this anatomic compartment will allow access
to the transverse processes of the cervical
vertebrae and hence to the vertebral artery,
an uncommon but life-threatening source of
hemorrhage.

The cardinal principle of obtaining proxi-
mal and distal control before entering the
injured segment applies in the neck. Occa-
sionally, this will entail extending the neck
incision into a median sternotomy to gain
proximal control at the thoracic outlet for
injuries to the proximal common carotid
artery (zone 1 ). On rare occasions with simul-
taneous bilateral injury, especially with a
bullet across the neck ("transcervical" trajec-
tory) , a U- or //-shaped incision coming across
the trachea caudally to the thyroid cartilage
facilitates bilateral neck exploration or expo-
sure of both carotid sheaths and the anterior
airway.

GKerawth [.. Maltov, M.D.

■ FIGURE 7-3

Drawing depicting a "standard" neck incision,
anterior to the sternocleidomastoid muscle with

division of the anterior facial vein. ■

THORACIC OUTLET

The thoracic outlet is a transitional anatomic
area between the neck and the chest, where
vascular injuries are difficult to access. Most
surgeons infrequently operate in this area;
therefore, deciding on the correct incision can
be problematic.

A patient with a thoracic outlet injury may
be hemodynamically stable, thus allowing a
precise angiographic localization of the injury.
Under these circumstances, the location of
the injury dictates the incision and the oper-
ative approach. However, when the patient is
actively bleeding from a vascular injury in the
thoracic outlet, the decision has to rely on the
clinical presentation. A penetrating injury
around the distal clavicle that is bleeding exter-
nally can initially be controlled with a Foley
balloon tamponade inserted into the missile
tract (Fig. 7-2) . An incision above and paral-
lel to the clavicle will expose the injured vessel
(see later discussion). On the other hand, a

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145

hemothorax is usually associated with a more
medial injury, which may require proximal
control of the subclavian artery through a high
anterolateral thoracotomy on the left, or a
median sternotomy on the right. For a patient
with a thoracic outlet hematoma evident on
the chest radiograph and without supra-
clavicular or neck hematoma, a median
sternotomy is the incision of choice.

Access to the innominate artery, proximal
left carotid, intrathoracic superior vena cava,
and innominate vein is via a median ster-
notomy. The key landmarks to performing
a safe median sternotomy is to identify the
sternal notch, the xiphoid, and the sternal
midline, extending the incision a few cen-
timeters below the xiphoid and opening the
linea alba. A probing finger bluntly develops
the space under the sternum both from below
and from above behind the manubrium. One
should be careful with the use of electro-
cautery at the manubrial notch when divid-
ing the retrosternal ligament attachment to
the anterior neck fascia, because iatrogenic
injury to the innominate artery and carotid
may occur. This blunt dissection just beneath
the sternum is relatively easy and proceeds in
a bloodless plane. The sternal saw divides the
sternum from the xiphoid to the manubrium,
taking care to always stay in the midline. A
partial sternotomy usually does not yield
appropriate exposure and should therefore
be avoided. Bleeding from the edge of the
sternum can be impeded by the use of elec-
trocautery. Only in the coagulopathic patient
will bone wax be required for hemostasis from
the marrow of the sternum. The sternal
retractor is gradually opened as dissection con-
tinues. If one immediately opens the sternal
retractor to its full extent, an area of vascular
injury can be "opened" more widely during
forceful retraction of the sternum. In addi-
tion, excessive and over-retraction of the
sternum can create rib fractures, sternal frac-
ture, and stretch injury to the brachial plexus.
The pericardium is sharply entered in the
midline and the dissection is carried cepha-
lad to the area of an injury or to the innomi-
nate vein that crosses in front of the aortic
arch. This opening of the pericardium allows
for the sternal retractor to be opened more
widely for more exposure.

Access to the extrathoracic left subclavian
artery may be difficult, especially if the arm
is extended. It is best achieved with the arm
prepared free and initially placed at the
patient's side. Exposure of the extrathoracic
portion of the subclavian artery requires an
incision about one fingerbreadth above and
parallel to the clavicle from the sternal notch
extending laterally. After division of the
platysma muscle, the clavicular portion of the
sternocleidomastoid is either retracted medi-
ally or more conveniently divided. The scalene
fat pad is encountered and removed, expos-
ing the clavicular head of the sternocleido-
mastoid muscle and the anterior scalene
muscle. The phrenic nerve crosses in front of
the anterior scalene muscle and must be iso-
lated and carefully preserved. The more pos-
teriorly located brachial plexus should also
be protected while dividing the anterior
scalene muscle. It is at this point that the sub-
clavian artery first comes into view. It can now
be carefully dissected and exposed. Care must
be taken, because this is one of the most fyrigile
arteries in the body. Only on rare occasions
where the injury is proximal to the insertion
of the scalene anticus muscle will the head
of the clavicle need to be removed.

In the presence of an expanding hematoma
in the supraclavicular area, often it is difficult
to define the anatomic landmarks. Under
these circumstances, the artery can be rapidly
exposed through the bed of the clavicle. The
incision is made along the clavicle itself,
and the bone is rapidly exposed. A periosteal
elevator is used to peel off the periosteum
around the clavicle and thus separate the bone
from the adjacent muscles. The bone is
rapidly divided as laterally as possible, lifted
from its bed by grasping it with a towel clip,
and the head is separated from the stern-
oclavicular joint and removed. The subclav-
ius muscle is sharply divided along the bed of
the clavicle, providing access to the anterior
scalene muscle and the phrenic nerve.

For an extrathoracic left subclavian artery
injury, a short anterior thoracotomy above
the nipple (in the left second or third inter-
space) may facilitate looping of the intratho-
racic portion of the left subclavian artery
proximal to the injury (Fig. 7-4) . A clamp or
a snare tourniquet is then applied, which can

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146

II • PRINCIPLES OF OPERATIVE CARE

be tightened as the subclavian injury is
exposed through a separate clavicular incision.
Because of rich collateral circulation, this
mode of proximal control does not stop bleed-
ing completely but does help to make the
situation more amenable to repair.

An innominate artery injury may present
intraoperatively as a large superior mediasti-
nal hematoma. Blind dissection in such a
hematoma is fraught with danger, because vas-
cular structures (e.g., the innominate vein)
are difficult to identify. Under these circum-
stances, it is often prudent to deliberately enter
the pericardium, which serves as a natural
barrier to the extension of the hematoma. The
vessels can be identified and controlled prox-
imally, and a bypass graft can be inserted
before dissection within the hematoma itself
is undertaken (Fig. 7-5).

Chest

The chest is composed of three separate vis-
ceral compartments, each accessible through
different incisions. In the presence of massive

■ FIGURE 7-4

Drawing depicting an extrathoracic hematoma
around the left subclavian artery and a left
second interspace anterolateral thoracotomy,
picking up the proximal left subclavian artery,
encircling it with a ligature tourniquet (snare), to
be used if necessary for vascular control when
the hematoma is entered from a supraclavicular
approach. ■

hemothorax, the utility incision is an antero-
lateral thoracotomy, because it is and easy to
perform and it does not require special posi-
tioning. An anterolateral thoracotomy is per-
formed in the fourth or fifth intercostal space
on the side of the presumed injury, that is,
below the nipple in the male patient or the
manually retracted breast in the female
patient. The incision extends from just lateral
to the sternum to the midaxillary line. In the
female patient, it is made in the inframam-
mary crease. The pectoralis muscle is divided
by dissection and the ribs are exposed. The
intercostal muscles are divided along the
upper aspect of the rib to avoid the neu-
rovascular bundle, and the pleura is entered.
A rib spreader is inserted with the handle
pointing toward the axilla. Once inside the
pleural cavity, the surgeon's first act is to mobi-
lize the lung by dividing the pulmonary liga-
ment up to the level of the inferior pulmonary
vein. The lung is retracted anteriorly and the
posterior mediastinum is thus exposed. In the
left hemithorax, this incision provides good
exposure of the descending thoracic aorta,
left subclavian artery, left pulmonary artery,
and pulmonary veins. In the right side of the
chest, the intrathoracic inferior vena cava
(IVC), right pulmonary artery, azygous vein,
and superior vena cava can be seen. Atransster-
nal bilateral anterolateral incision (clamshell)
is accomplished by joining left and right
anterolateral thoracostomies across the
sternum using a Gigli saw, large-bone cutters,
or an electric saw. Care must be taken to make
the transsternal incision in the midportion
of the body of the sternum, and not at the
xiphoid, so a firm osseous closure will be pos-
sible at the end of the operation. Care must
also be taken to identify and ligate the divided
internal mammary arteries. This clamshell
incision is the only one that provides access
to all three thoracic cavities, albeit at the cost
of slight increased morbidity.

A patient with precordial penetration who
is not in extremis and whose bullet trajectory
appears to be through the mid upper medi-
astinum is best approached via a median ster-
notomy. With some difficulty, this incision
affords access also to the azygous vein, right
main pulmonary artery, and left proximal sub-
clavian artery.

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7 • ACCESS, CONTROL AND REPAIR TECHNIQUES

147

& Konnoth ].. VI alto*, M.D.

■ FIGURE 7-5

Drawing of a hematoma
around the innominate artery
and proximal left carotid artery
with a median sternotomy and
ligation of the innominate vein
covering this area. Also shown
is a "bypass" technique from
the ascending aorta (end to
side) to the distal innominate
artery (end to end), with
oversewing of the stump of the
innominate artery at the aortic
arch. ■

Although a resuscitative thoracotomy is
usually performed via an anterolateral tho-
racotomy, when a descending thoracic aortic
repair is planned, a posterolateral thoraco-
tomy is preferable. In either case, the poste-
rior mediastinum is exposed by rotating the
lung anteriorly (Fig. 7-6) . Division of the pari-
etal pleura over the posterior mediastinum
and mobilization of the hilum of the lung will
assist in this exposure. The esophagus is
locatedjust anterior to the aorta and the recur-
rent laryngeal nerve recurs around the liga-
mentum arteriosum. It is important not to
injure these structures during access, expo-
sure, or reconstruction.

If the surgeon performs an anterolateral
thoracotomy and discovers a posterior injury
(e.g., to the esophagus or the descending
aorta) , he or she is better advised to close the
anterior incision and put the patient into a
right lateral decubitus position. A left pos-

terolateral fourth interspace incision is per-
formed and the chest entered.

Approaching a thoracic aortic injury in its
usual location just distal to the ligamentum
arteriosum, the lung is retracted anteriorly.
The distal thoracic aorta, well away from the
hematoma is encircled first, followed by the
subclavian artery as it exits the chest. At this
point, the transverse arch is dissected free from
the pulmonary artery and the aortic arch
between the left carotid artery and the left
subclavian artery is encircled. This "control"
is achieved well away from the undisturbed
hematoma. If the surgeon elects to use car-
diopulmonary bypass or active shunting, the
cannula for this adjunct can be inserted at this
point.

An injury to the azygous vein is usually
serendipitously discovered at emergency
thoracotomy. Anterior incisions make
exposure and ligation of a bleeding azygous

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II • PRINCIPLES OF OPERATIVE CARE

Kvnnulhl.. Mattox,M.D.

■ FIGURE 7-6

Exposure of the proximal descending thoracic
aorta, by rotating the lung anteriorly and
demonstrating that the esophagus is anterior to
the aorta. Vascular clamp on the descending
thoracic aorta as a temporary attempt to
impede the rate of distal hemorrhage. ■

vein very difficult, contributing to the high
mortality of this injury. Using an extra long
needle holder and approaching the injury
from the left side of the operating table pro-
vides the surgeon with the greatest chance for
achieving suture ligation of a bleeding azygous
vein.

The thoracic IVC is entirely within the
pericardium and very difficult to expose. The
surgeon may encounter an injury to this
structure, digitally control the bleeding deep
within the right lower pericardium, and then
have great difficulty exposing the area for
repair. Should bleeding be controlled, the
trauma surgeon should call for a thoracic
surgeon for assistance before attempting
to proceed, because repair is exceedingly

difficult and may require cardiopulmonary
bypass, with double caval cannulation and
repair of the caval injury from within the
opened right atrium.

Upper Extremity

AXILLARY ARTERY

The first and second parts of the axillary artery
are approached through an infraclavicular
incision that extends from the mid-clavicle
to the deltopectoral groove. The fibers of
the pectoralis major are separated bluntly,
revealing the clavipectoral fascia medial to
the pectoralis minor muscle. Opening the
clavipectoral fascia and dissection in the axil-
lary fat reveals first the axillary vein and then
deep and superior to it, the axillary artery with
the adjacent elements of the brachial plexus.
The second part of the axillary artery is
exposed by hooking up and then taking down
the insertion of the pectoralis minor muscle
as close as possible to the coracoid process
using the electrocautery (Fig. 7-7) . In the pres-
ence of an axillary hematoma, itmay be advis-
able to first obtain proximal control on the
subclavian artery through a supraclavicular
incision and then perform a separate axillary
incision or alternatively transect the clavicle
to join the incisions.

Other axillary exposures that are sometimes
used in elective situations are rarely if ever
used in the trauma situation. These include
a lateral approach to the distal artery through
a vertical incision along the lateral border of
the pectoralis major or the deltopectoral
groove approach. Lastly, endovascular control
is possible when active extravasation is noted
from the subclavian-axillary complex at
angiography. A pair of occluding balloons,
proximal and distal to the site of injury, will
provide temporary control and minimize
blood loss.

BRACHIAL ARTERY

The proximal brachial artery is usually
approached via a medial upper arm incision
placed in the groove between the biceps and

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7 • ACCESS, CONTROL AND REPAIR TECHNIQUES

149

3**' O Kenneth L. Mattos, M.D.

■ FIGURE 7-7

Drawing of exposure of the
axillary artery by division of the
muscle fibers between the
clavicular and pectoral
portions of the pectoralis major
muscle and detachment of the
insertion of the pectoralis minor
on the coracoid process of the
scapula. ■

triceps muscles. Care should be taken in an
arm with a large hematoma, as the neurovas-
cular bundle is closer to the surface than one
might expect and iatrogenic injury is to be
avoided. Care must also be taken to identify
any concomitant injury to the brachial vein
and adjacent nerves. Dissection in the groove
between the triceps and biceps muscles reveals
the neurovascular bundle, and the first struc-
ture that is encountered is the median nerve,
which should be carefully preserved.

A distal brachial artery injury often requires
exposure at the antebrachial fossa, through
a sigmoid incision that avoids crossing in the
antecubital skin crease. The artery is located
immediately below the biceps tendon, which
can be divided with impunity. The sigmoid
incision may be carried upward along the
medial part of the upper arm or distally to
expose the brachial artery bifurcation.

Access to vascular injuries in the extremi-
ties is based on the Henry principle of exten-
sile exposure. Every incision can be extended
proximally or distally or joined with an inci-
sion exposing a more proximal or distal
vessel. Thus, the subclavian and axillary expo-
sures can be joined by dividing the clavicle.
The axillary and brachial incisions can be
joined by extending the former in the del-
topectoral groove across the shoulder.

Abdomen and Pelvis

Abdominal vascular injuries account for
the majority of truncal vascular trauma
seen in a civilian practice. These injuries are
approached via a midline laparotomy incision,
one of the most commonly used incisions
in trauma. After incision of the skin and

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II • PRINCIPLES OF OPERATIVE CARE

subcutaneous tissue using the xiphoid process
and umbilicus as markers, the linea alba is
gained by identifying the midline decussation
of the fibers of the anterior rectus sheaths on
both sides. In a trauma laparotomy, time is
typically not wasted on superficial hemostasis
and the entire incision is rapidly performed
with a scalpel. The peritoneum is typically
entered immediately above the umbilicus,
where rapid atraumatic penetration of the
peritoneum is usually possible. Very rarely will
the surgeon choose a different incision. In a
patient who is in shock and has had multiple
previous operations through a midline inci-
sion, it may be wise to avoid the dense and
time-consuming adhesions by rapidly per-
forming a subcostal ("chevron" or "rooftop")
incision instead.

When considering definitive control and
repair of intraabdominal vascular injury, the
surgeon has several distinct patterns of
retroperitoneal hematoma to guide him or
her to specific vascular injuries. An upper
abdomen (supramesocolic) midline retrope-
ritoneal hematoma is associated with injury
to the suprarenal aorta, celiac axis, and the
superior mesenteric artery. The midabdomi-
nal midline retroperitoneal (inframesocolic)
hematoma is associated with proximal renal
artery and infrarenal aortic or vena cava injury.
A perinephric hematoma may be associated
with renal or renal vascular injury. A pelvic

midline hematoma is most often associated
with a pelvic fracture or bladder injury, and
a large or expanding lateral pelvic hematoma
is associated with iliac vascular injury. A right
lateral retroperitoneal hematoma suggests an
IVC injury that may be infrarenal or retro-
hepatic. Finally, a hematoma presenting in the
porta hepatis indicates an injury to the portal
venous system.

Currently, initial vascular control of
intraabdominal hemorrhage is achieved in the
abdomen alone, initially by using laparotomy
pads or manual/digital pressure.

Rapid evisceration of the small bowel will
allow the surgeon to define the area of major
hemorrhage. In the presence of profuse
bleeding from a midline retroperitoneal
hematoma, the first assistant digitally occludes
the aorta at the esophageal hiatus. Use of
various aortic occluding instruments is much
less effective than simple digital occlusion.
Virtually all abdominal venous bleeding can
initially be controlled by pressure packs.

Temporary control of gross bleeding in the
area of the celiac trunk often presents a
difficult technical situation to the surgeon
because visibility in this area is very limited
without elaborate dissection. Hemostasis
can sometimes be achieved with a large gross
ligature, using rather large suture material,
such as 1 or suture on a large needle
(Fig. 7-8) . Although intended as a temporary

■ FIGURE 7-8

Drawing depicting a gross
ligature of an area of gross
bleeding such as in the area of
the celiac axis. This suture
should be rather large suture
material, such as 1 or suture
on a large needle. This is a
temporary tactic and might be
removed later after other
control techniques. ■

9KcEinclhLMatlc<, U.D.

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7 • ACCESS, CONTROL AND REPAIR TECHNIQUES

151

hemostatic maneuver, if the maneuver is
effective and the surgeon is satisfied that
mesenteric and hepatic injuries have not
resulted from this "blind" suturing, this
temporary suture may be left in place
permanently.

Cross clamping of the aorta has tradition-
ally been viewed as an important maneuver
in trauma surgery. Such clamping is per-
formed both to control exsanguinating hem-
orrhage in the abdomen or pelvis and as a
resuscitative maneuver. Historically, this has
been done by cross clamping the descending
thoracic aorta in the chest, away from the site
of intraabdominal bleeding (Fig. 7-6). Unfor-
tunately, this addition of a thoracic incision
in a patient with a complex abdominal injury
who is already coagulopathy, acidotic, and
hypothermic serves only to aggravate this often
fatal triad and should therefore be avoided.
The aortic cross-clamp maneuver is per-
formed for several reasons, the most common
one being to preserve the residual blood
volume for vital perfusion of the heart, brain,
and lungs during resuscitative emergency
department thoracotomy. However, when
performed for proximal control of an injury
to the abdominal aorta or its visceral branches,
the inexperienced surgeon rapidly discovers
that because of very rich collateral circulation,
this does not dry up the operative field.
However, digital occlusion of the abdominal
aorta at the esophageal hiatus will markedly
reduce bleeding (Fig. 7-9). Numerous com-
plications have occurred after thoracic or
abdominal aortic cross clamping, especially
when the procedure is performed by an
inexperienced surgeon. If clamping of the
supraceliac aorta is required, the safest tech-
nique is either to take down the left triangu-
lar ligament of the liver or to bluntly enter
the lesser omentum and then perform a blunt
digital separation of the fibers of the diaphrag-
matic crus immediately above and behind the
origin of the abdominal aorta, as described
by Veith, Gupta, and Daly (1980). The
surgeon's index finger is then insinuated
through the diaphragmatic crus on each side
of the aorta, to create just enough space for
the clamp on both sides of what is in fact the
lowermost part of the thoracic aorta. Using
this technique, the surgeon avoids the

S Kenneth L. Mdttox. VI. D.

■ FIGURE 7-9

Drawing depicting the right hand of the first
assistant (left-hand side of the patient's body),
compressing the abdominal aorta, with a
hematoma around the aorta at the level of the
mesenteric vessels and achieving vascular
control. ■

hazardous and frustrating dissection in the
thick periaortic tissue that surrounds the first
part of the visceral aortic segment.

Access to the injured suprarenal aorta is
one of the greatest operative challenges in
abdominal trauma. An anterior approach
would require the stomach and pancreas to
be either retracted or transected, and the
dense periaortic nerve and fibrous tissue make
dissection in this area difficult. A medial rota-
tion of all the intraabdominal viscera to the
patient's right from a dissection plane lateral
to the left colon and going behind the spleen,
kidney, and tail of the pancreas allows a lateral
and relatively easy approach to the aorta. This
intraoperative maneuver has been called the
"Mattox maneuver" for the past 2 decades
(Fig. 7-10). This dissection plane is on top of
the psoas muscle and can be rapidly achieved
by rapid blunt dissection that begins with the
peritoneal reflection lateral to the distal
descending colon and is carried upward

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152

II • PRINCIPLES OF OPERATIVE CARE

■ FIGURE 7-10

Rightward visceral rotation
from the left side from the
diaphragm to the iliac arteries
("Mattox maneuver"). ■

4*r

D Konni'lli L. U.illos, Ml)

lateral to the spleen and up toward the
diaphragmatic hiatus, rotating all left-sided
abdominal viscera medially and exposing the
abdominal aorta from the esophageal hiatus
to where the external iliac arteries exit the
abdomen to the groin. In most situations
where this maneuver is needed, the retroperi-
toneal hematoma itself already achieves a
significant separation of the relevant dissec-
tion planes, thus greatly facilitating the
maneuver. The left lateral diaphragmatic
crux can be divided and a lateral incision in
the diaphragm can further expose the distal
thoracic aorta for proximal control even as
high as the T6 vertebra without having to open
the chest. A thick fascial layer separates the
aorta from the dissection plane and must be
carefully incised to cleanly define the aortic
wall in preparation for clamping. In the pres-
ence of proximal vascular control, the aorta
loses its pulse and is a flaccid tube that is not
always easy to identify in a large hematoma.
As soon as the aorta is exposed, vascular clamps
are then precisely placed on the injured vessel
for control and reconstruction.

The infrarenal aorta is exposed by eviscer-
ating the small bowel to the patient's right and
upward, mobilizing the ligament of Treitz, and
then longitudinally dividing the posterior
peritoneum between the duodenum and the
inferior mesenteric vein. The pitfall in this
exposure is failure to identify the left renal

vein in the presence of a large infrarenal
hematoma, which may lead to an iatrogenic
injury and additional blood loss.

The most complete and extensive access to
the mid and lower retroperitoneal structures
is by performing the Cattell-Braasch maneu-
ver, an extensive mobilization of the peritoneal
structures off the aorta, vena cava, and their
major branches (including the renal and iliac
vessels) (Fig. 7-11). This maneuver involves
division of the peritoneal attachments of the
duodenum, right colon, and mesentery of the
small bowel from the posterior abdominal
wall. The line of incision is a triangle that
begins at the lateral edge of the hepatoduo-
denal ligament (adjacent to the common bile
duct) , is carried downward to the cecum, and
then upward along the insertion of the small
bowel mesentery to the ligament of Treitz. This
allows full rotation of the midgut from the
duodenum to the transverse colon with its
accompanying mesentery, up onto the ante-
rior chest. The extended Kocher maneuver
is mobilization of the duodenum and right
colon only, a limited version of the full Cattell-
Braasch maneuver that is often sufficient to
expose vena cava injuries.

The renal vessels can be controlled either
proximally ("midline looping") or by mobi-
lizing the kidney itself and clamping across
the renal hilum. Midline looping conforms
to the principle of proximal control and

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7 • ACCESS, CONTROL AND REPAIR TECHNIQUES

153

Kciuuth L. Matto*, M.D.

■ FIGURE 7-1 1

Drawing depicting the
combined Kocher and Cattell-
Braasch maneuvers showing
that the movement of the
duodenum, small bowel, and
right colon to the left exposes
the entire inferior vena cava,
right renal vessels, and the
right iliac vessels. ■

involves identification and isolation of the left
renal vein as it crosses the aorta, and then
identification and looping of the right or left
renal artery as it comes off the aorta. In the
presence of an actively bleeding perinephric
hematoma, it is sometimes quicker to simply
mobilize the entire kidney from its bed in a
manner akin to a splenectomy and place a vas-
cular noncrushing clamp en masse across the
entire hilum.

Control of the portal vein between the top
of the pancreas and the liver is aided by a
Pringle maneuver, which consists of placing
a vascular clamp across all of the structures
of the porta hepatis. Under rare conditions,
a "double Pringle" maneuver is performed by
placing vascular clamps on either side of an
injury in the hepatoduodenal ligament.

The control of portal venous injuries behind
the pancreas is often challenging and can be
aided by deliberate division of the neck of the
pancreas (Fig. 7-12. Control by direct pres-
sure or application of large vascular clamps
is accomplished preparatory to this division.
Dissection in the hepatoduodenal ligament
and identification and division of the gastro-
duodenal artery is the most time-consuming
part of this elaborate (but sometimes lifesav-
ing) maneuver. This procedure is the only
practical way to gain access to the confluence
of the splenic and superior mesenteric veins
to form the portal vein.

The suprarenal retrohepatic IVC is another
area of difficult exposure. A contained
hematoma in this location is best left undis-
turbed because there are no major retro-
hepatic arterial structures, so the injury is
invariably venous and can often be controlled
with local pressure. If free bleeding from this

■ FIGURE 7-1 2

Drawing depicting exposure of the portal vein
and proximal superior mesenteric vein, by
dividing the mesenteric root and deliberately
dividing the neck of the pancreas, showing the
confluence of the superior mesenteric vein, and
splenic vein to form the portal vein. ■

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II • PRINCIPLES OF OPERATIVE CARE

area is encountered, containment with laparo-
tomy packs is the goal, with atrial caval shunts
reserved for uncontrolled hemorrhage from
the retrohepatic IVC.

Injury to the iliac vasculature, either at the
confluence of the iliac veins to the IVC or at
the inguinal ligament, poses several exposure
and control challenges (Fig. 7-13). After
opening the abdomen and discovering a
hematoma in the pelvic retroperitoneum,
hemorrhage control might require initially
local pressure using folded sponges on a
"sponge stick." This is mainly because "blind"
clamping of the iliac arteries in a hematoma
is likely to result in injury to the immediately
underlying iliac veins or the overlying ureters.
On rare occasions, large vascular occluding
clamps are required to gain control en masse
of both the iliac artery and the iliac vein.

A careful technique for gaining control of
an iliac vascular injury in a gradual fashion
has been described by Burch and colleagues
(1990). Initially, the distal aorta and vena
cava are clamped away from the pelvic
hematoma, and the distal external iliac artery
is controlled by "towing in"with a large Deaver
retractor over the lower edge of the abdomi-
nal incision, thus globally compressing the
external iliac vessels against the pelvic brim.
As dissection proceeds into the pelvis, the

KluhiUi I.. MattOX. Mil.

■ FIGURE 7-13

Drawing depicting a lateral lower abdominal
hematoma suggesting an injury to the iliac
vasculature. ■

upper clamps are gradually advanced distally
to selectively control the injured arterial or
venous segment of the iliac vasculature, a
technique called "walking the clamps." On
very rare occasions, the groin must be opened
to gain control of backflow by occluding
the common femoral artery and the deep
femoral vein.

Lower Extremity

Three areas in the lower extremity are the
focus of the surgeon considering a vascular
injury: the groin, distal thigh, and proximal
calf. At the groin, access is achieved via a
routine groin incision, exposing the common
femoral artery and its branches. The distal
superficial femoral and proximal popliteal
arteries are approached via a distal medial
thigh incision.

GROIN

In the emergency department, active bleed-
ing from the groin is often controlled by
direct pressure. This challenging bleeding
can also be controlled by balloon tamponade.
The dilemma is whether to go into the
abdomen for proximal control or to approach
the injury directly in the groin. If a pene-
trating wound such as a gunshot injury also
obviously enters the abdomen, then rapid
proximal control in the abdomen is indicated
because there is an independent indication
for laparotomy. However, if the injury appears
to be limited to the groin, options are either
to do a vertical utility incision over thefemoral
triangle with an extension unto the inguinal
ligament and then divide the ligament and
gain proximal control or to first gain proxi-
mal control through an oblique incision
above and parallel to the inguinal ligament
and expose the external iliac vessels in this
extraperitoneal location. In our experience,
it is almost always possible to gain proximal
control of femoral injuries in the groin. A
useful trick is to identify the inguinal ligament
and instead of incising it to just separate the
fibers of the ligament approximately 1 to
2 cm above its shelving edge, and thus bluntly

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7 • ACCESS, CONTROL AND REPAIR TECHNIQUES

155

"penetrate" through the ligament into the
retroperitoneum. This small opening is usually
enough to insert a narrow and deep retrac-
tor, to feel the external iliac pulse, and to clamp
the artery safely.

The technical key to a safe dissection in the
groin in the presence of a vascular injury is
to identify the common, superficial, and deep
femoral arteries and their accompanying
veins before clamping, to avoid troublesome
back bleeding and to preserve the deep
femoral artery. The lateral circumflex iliac vein
crosses the deep femoral artery very close to
its origin and is easily injured when looping
of the profunda femoris is attempted in the
presence of a large hematoma and hostile
groin anatomy. The specific location of the
injury to the femoral vessels has profound
implications on the repair options. Often the
surgeon must extend the initial incision to
create a broader exposure than was initial
thought to be sufficient.

DISTAL SUPERFICIAL
FEMORAL ARTERY

A medial distal thigh incision is the "utility"
approach to the distal superficial femoral
artery, deep femoral vein, and proximal
popliteal artery. The sartorius muscle is
reflected upward or downward and Hunter's
canal is opened. Proximal control can be
achieved by a proximal tourniquet, proximally
occluding the distal femoral artery, or control
from a groin incision with exposure of the
proximal superficial femoral artery. Care
should be taken not to iatrogenically injure
the saphenous vein or its accompanying nerve
that in the thigh travels in proximity to the
superficial femoral artery.

POPLITEAL ARTERY AND BRANCHES

A difficult area for vascular access is the
popliteal artery. Injuries at the popliteal bifur-
cation are best exposed by a liberal incision
below the knee, which in the presence of a
large hematoma, fractures, or soft tissue
destruction may begin proximal to the knee
in an uninjured area and extend distally

according to the principle of extensile
exposure. Often adj acent nerves and veins are
also injured. Although it is acceptable to cut
across the pes anserinus at the medial aspect
of the knee, it is less morbid to make two inci-
sions (one above the knee and the other below
the knee) if the popliteal artery injury is in
the proximal or mid segment of this artery. A
pneumatic tourniquet in place at the groin
may assist access to the proximal tibial
arteries during dissection and identification
of the injured vessels.

Care must be taken to wo£injure the greater
saphenous vein at the time of the skin inci-
sion so that it can serve as a collateral venous
outflow tract should the popliteal vein require
ligation. The contralateral leg is prepared and
draped so that this uninjured site can be used
for a substitute conduit if necessary.

As a useful general guideline, the major
neurovascular bundles of the lower extrem-
ity are always located immediately behind the
bone. This is especially important to remem-
ber in the presence of hematoma and gross
anatomic distortion. Thus the distal superficial
femoral artery and the popliteal artery will be
found immediately behind the femur, and the
popliteal bifurcation and tibioperoneal trunk
will be found immediately behind the tibia.
One often encounters the accompanying
vein before the artery during the dissection.

The incision to expose the tibioperoneal
trunk and its branches is made just posterior
to the medial edge of the tibia. It is carried
down to the medial head of the gastrocnemius
muscle that is sharply divided off the tibia (Fig.
7-14) . Often the attachments of the soleus
muscle must also be detached to expose the
posterior tibial and peroneal vessels. In the
presence of a hematoma, it is often advisable
to begin the dissection far proximally,
identify and isolate the uninjured proximal
popliteal segment, and then gradually advance
distally toward the injury.

The medial approach affords only proxi-
mal control of the origin of the anterior tibial
artery. The vessel itself is best exposed through
an anterolateral incision placed approxi-
mately two fingerbreadths lateral to the ante-
rior edge of the tibia and carried past the fascia
and between the tibialis anterior and the
extensor hallucis longus muscles.

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II • PRINCIPLES OF OPERATIVE CARE

■ FIGURE 7-14

Drawing depicting a long below the knee
medial incision, division of the medial head of
the gastrocnemius muscle to expose the distal
popliteal and tibial vessels. ■

Assess the extent of the injury or injuries.

Decide whether "vascular damage control" is
required.

Determine the amount of debridement
required.

Determine the type of repair required.

Set up the vessels for evaluation and repair by
placement of "stay sutures."

Pass Fogarty catheters to ensure the proximal
and distal clot has been removed.

Instill local heparin into the open vessels.

Apply local vascular occluding devices.

Perform the suture line.

Flush proximally and distally before comple-
tion of the suture line.

Complete the suture line.

Remove the clamps.

Assess the distal circulation.

Consider the need for fasciotomy.

Determine special post-repair requirements.

REPAIR PRINCIPLES
AND TECHNIQUES

For both vascular trauma and elective vascu-
lar reconstruction, a number of basic princi-
ples apply to all areas of vascular surgery. These
principles especially apply to the injured
vessel that may be surrounded by a hematoma,
may be actively bleeding, or may be in an area
of disrupted or "hostile" anatomy. Before any
vascular procedure, the surgeon should ascer-
tain the availability of any special instruments,
equipment, assistants, imaging devices, or
other devices that might be required during
the procedure. After making the decision to
explore an area, gaining access and control,
and then discovering a vascular injury, the pro-
gression through repair is as follows:

Ensure proximal and distal control.

Explore the injury.

Carefully enter the hematoma.

Each of these steps are not covered in detail,
but the major points of interest to the trauma
surgeon are covered.

1. Ensure proximal and distal control.

To enter a hematoma without the ability
to have proximal and distal control will
cause the trauma surgeon to have con-
siderable difficulty with the vascular injury
and add to the potential for additional
iatrogenic injury.

2. Explore the injury.

The area of the hematoma or the trajec-
tory of a wounding agent is evaluated
and explored. Associated injuries are
tabulated and the surgeon determines
priorities. Because of the potential for
exsanguinating hemorrhage and distal
ischemia, vascular injury usually takes the
highest priority.

3. Carefully enter the hematoma.

Anatomy is often distorted following
trauma. The surgeon enters the area of

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7 • ACCESS, CONTROL AND REPAIR TECHNIQUES

157

specific vascular injury and assesses the
extent of the vascular injury. Although
proximal and distal control has been
obtained, local control is often required,
by direct digital pressure, movement of
vascular clamps closer to the vascular
wound, application of a partially occlud-
ing vascular clamp, and/or the use of
intraluminal balloons.

4. Decide whether "vascular damage
control" is required.

The patient with a vascular injury presents
in a hemodynamically unstable condi-
tion, often acidotic, coagulopathic, and
hypothermic, thus differing considerably
from the patient requiring elective vas-
cular surgery. It is at this point that the
surgeon should consider options for
"vascular damage control." This might
include ligation of this specific vascular
injury for local hemorrhage control and
performing an extra-anatomic bypass for
distal perfusion. Vascular damage control
might also entail the insertion of a tem-
porary intraluminal shunt. Finally, a
damage control tactic of ligation might
become the final procedure if hemor-
rhage is controlled and distal circulation
is intact.

5. Determine the amount of debridement
required.

The extent of an "adequate" debridement
of an injured vessel is a matter of judg-
ment. With simple lacerations and
penetrations from low-velocity missiles,
debridement should be to the extent to
demonstrate a normal-appearing intima.
With extensive arterial destruction, such
as with high-velocity gunshot wounds,
blast injury, and crush injury, more
extensive debridement is necessary.
Detection of a normal-appearing arter-
ial wall, including an intact intima, is
usually satisfactory evidence of suffi-
cient debridement. The surgeon should
closely observe the quality of both inflow
and outflow because this gives some
indication of problems proximal to the
repair and on the adequacy of collateral
circulation.

6. Determine the type of repair required.

It is at this point that the surgeon deter-
mines whether the injury can be repaired
by simple lateral repair, apply a patch
angioplasty, perform an end-to-end anas-
tomosis, or insert a substitute conduit.
This decision might require another
member of the operative team to obtain
a saphenous vein from the previously
prepared leg donor site.

7 . Set up the vessels for evaluation and repair
by placement of "stay sutures."

The vessel to be repaired is "set up" for
the reconstruction. This often entails the
application of lateral stay sutures and
establishment of a new clean operative
field.

8. Pass Fogarty catheters to ensure the prox-
imal and distal clot has been removed.

A surgeon who uses Fogarty catheters only
occasionally should be reminded of a
number of caveats (Box 7-4) . Over-
inflation of the balloon will cause it to
rupture and potentially cause intimal
injury at the site of rupture. In addition,
there is a risk of remote perforation of
the vessel and an increased risk to the
intima with each repeated pass of the
catheter. Much of the art form of using
Fogarty balloon catheters is in the feel and
touch of pressure or resistance felt by
the surgeon at the time of advancing the
catheter, inflation of the balloon, and
extraction of the catheter. At least two
"clean" passes should be made before
declaring that an artery is free from distal
clots. The operating surgeon should
control three items simultaneously: the
pressure on the syringe connected to the
Fogarty balloon catheter, the pull of
the catheter extracting any clots, and the
orifice of the vessel. Many surgeons will
infuse a small amount of heparinized
saline after the final pass of the catheter
as the clamp is reapplied to the vessel.

9. Instill local heparin into the open
vessels.

Systemic anticoagulation is rarely used in
patients with acute trauma, especially with

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II • PRINCIPLES OF OPERATIVE CARE

CAVEATS IN THE USE OF FOGARTY CATHETERS
IN VASCULAR TRAUMA

Choose the smallest balloon that will accomplish the task required.

Estimate the size of the most distal site to which the balloon is to be inserted
in determining the size of the balloon to be used.

Always read the volume of liquid required to inflate the balloon.

Put only the volume of liquid required to inflate the balloon in the syringe
used for inflation.

Test the balloon inflation before insertion into the artery to ensure that the
balloon is functional and to see the diameter of the inflated balloon.

Always advance the ballooned catheter with the balloon deflated.

Always advance the balloon with the surgeon's fingers, not an instrument.

Should resistance be met, further advancement should not be attempted.

Remember that the Fogarty catheter can perforate an artery if forced.

The surgeon who advances the catheter should inflate the balloon, and if
resistance is met, the balloon should not be inflated further.

With the balloon inflated, the catheter should be withdrawn. During the
withdrawal if the surgeon meets resistance, the balloon should be allowed
to deflate slightly before beginning the withdrawal anew.

Remember that an overinflated Fogarty balloon can tear the intima of an
artery and forcibly extract long segments of intima, denuding the inte-
rior of the artery.

Should clot be removed, a second pass should be accomplished.

Passes to the distal artery should continue until no clot remains to be
removed.

multisystem acute trauma. The trauma
and/or vascular surgeon is always con-
cerned about coagulopathies and worried
that with systemic heparinization, hem-
orrhage at the sites of injury will com-
pound those injuries, especially the head
and orthopedic trauma. Furthermore,
many trauma patients often are already
somewhat, if not frankly, coagulopathy
by the time they get to the OR. Aggres-
sive crystalloid fluid resuscitation of as
little as 750 mL of fluid results in a statis-
tically difference in the clotting studies
compared with matched patients who
received little or no resuscitative fluid. The
first concern of a trauma surgeon is that
no new factors are introduced that would
contribute to a coagulopathy. Hypother-

mia, dilution of clotting factors, and
addition of drugs that alter clotting all
contribute to a coagulopathy.

Except for patients who are placed on
total cardiopulmonary bypass, systemic
anticoagulation is avoided acutely in the
trauma patient. However, under certain
circumstances, systemic heparinization
may be in the patient's best interest. When
the arterial injury is the result of a single
penetrating injury (such as a stab wound
to the brachial artery), the risk of bleed-
ing is minimal, and in a teaching situa-
tion or when the reconstruction is very
time consuming, systemic heparinization
may be considered. Similarly, in the pres-
ence of severe and prolonged distal
ischemia (e.g.,whenafirstreconstruction

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7 • ACCESS, CONTROL AND REPAIR TECHNIQUES

159

is unsatisfactory and an immediate redo
is required) , when there is concern about
clotting of the microcirculation and irre-
versible damage, again systemic heparin
may be considered provided that no
other injuries are likely to bleed.

Most patients with vascular injury
undergo operation in this acute period.
Many trauma patients with vascular
trauma have undergone a series of arte-
riograms in the angiographic suite, where
repeated aliquots of heparin have been
administered. Should an early operation
follow, the surgeon would be well served
to determine the level of anticoagulation
by an intraoperative determination of the
activated clotting time.

Many surgeons will consider the admin-
istration of heparin to patients with an
acute, totally occluded artery, to preserve
distal function, with the theory being that
collaterals and venous return are pre-
venting from thrombosing. Whether
this is true for trauma patients, who
are already relatively coagulopathic, is
unknown. Because many of the coagula-
tion profiles available in many hospitals
report a result at least 1 to 2 hours after
the blood was obtained and the patient's
coagulation status may have changed
considerably in that period, tests that
demonstrate concurrent status are pre-
ferred. Most trauma centers also have
either cardiac or vascular surgical capa-
bility and have equipment to measure
an activated clotting time available in
the ORs; this test is preferred. The acti-
vated clotting time is well recognized by
cardiac surgeons to be an excellent deter-
minant of the effect of heparin on clot-
ting activity.

Many surgeons elect to inject through
the open ends of an injured vessel prox-
imally and distally small aliquots of
heparinized saline. These solutions
contain a variable number of units of
heparin, depending on the local recipe.
Often these "local" injections result in a
"systemic" heparinization dose, which
literally occurs within minutes of the
infusion.

10. Apply local vascular occluding devices.

The locally applied vascular occluding
device should be noncrushing and gentle
to the vessel. A vascular clamp should not
be maximally applied but closed only to
the extent required to prevent bleeding
from the open ends of the vessel. In some
locations, a customized snare tourniquet
allows for the occlusion to be complete
but keeps the instruments out of the
operative field. In other instances, intra-
luminal balloon catheters serve as the
occluding device.

11. Perform the suture line.

Anastomoses must be tension free and
carefully constructed to create an everted,
smoothly coapted layer of intact and
healthy intima. The surgeon should wear
magnifying loupes if necessary, espe-
cially for small vascular reconstructions.
Several options exist for vascular trauma
reconstruction.

a. Simple vascular repair techniques

Any vascular reconstruction in vascu-
lar trauma should be tailored to both
the patient's condition and the par-
ticular injury encountered. There is
no single "practice guideline" that is
applicable to every injury. A large
number of acceptable standards of
practice exist. For instance, for an
unstable patientwith extensive truncal
injury, an extremity arterial injury may
be left unreconstructed to focus on a
critical life-threatening truncal injury.
In such an omission or delay, an ampu-
tation might be the ultimate outcome
in a patient who is now alive because
the truncal and cerebral injuries were
addressed. Several simple approaches
to vascular reconstruction exist.

A "simple" vascular repair tech-
nique is a lateral venorrhaphy or
arteriorrhaphy. Should lateral arteri-
orrhaphy or venorrhaphy be accom-
plished without narrowing the vessel
and without tension on the suture line,
this technique is the preferred ap-
proach over more complex vascular

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II • PRINCIPLES OF OPERATIVE CARE

repair techniques. Lateral repair is
sometimes performed in a linear and
at other times in a horizontal manner.
In principle, the axis of the suture line
should be oriented perpendicular to
the axis of the vessel, to avoid nar-
rowing. However, in special circum-
stances when the vessel is large (such
as the IVC) and a perpendicular repair
is impossible, a suture line parallel to
the axis of the vessel is an acceptable
second-best approach.

The choice relates to the size of the
vessel and the surgeon's preference.
Surgeons choose the smallest suture
material possible to accomplish the
closure safely, most often using poly-
propylene suture material.

Ligation of a bleeding vessel has
been a form ofvascular control/repair,
because the word suture was used in
the Edwin Smith Surgical Papyrus. The
ancient and modern literature aptly
demonstrates the natural history
following ligation (or thrombosis) of
major arteries and some major veins,
that being distal ischemia and loss of
the distal organ, often expressed as
an amputation. Ligation is an option
in almost all venous injuries and in a
number of arterial injuries when the
patient's condition and overall trauma
burden preclude a reconstruction.
Examples of arteries that can be ligated
include subclavian, internal iliac,
superficial femoral, one of the tree
distal vessels in the lower arm or calf.
In other instances, ligation (e.g.,
external iliac artery) may be required
for hemorrhage control in a very
complex injury, where a secondary
reconstruction outside the major
injury is accomplished (a femoral-
femoral arterial crossover graft) .
Ligation of one of paired arteries
(brachial and ulnar arteries, anterior
and posterior tibial arteries) is toler-
ated provided distal crossover collat-
eral circulation exists (as in the case
of an intact palmar arterial arch). If
ligation is used as a procedure of
choice for vascular hemorrhage

control, the surgeon must early and
frequently assess the viability and func-
tion of the circulation distal to the lig-
ature and make a decision if secondary
procedures are indicated.

b. End-to-end repair

If a lateral arteriorrhaphy or venor-
rhaphy is not possible, an end-to-end
repair is preferable if possible. Such
an anastomosis must be tension free.
When debridement has occurred, it
may be very difficult to bring the vessel
ends together into a tension-free anas-
tomosis. Mobilization of an artery by
tying off branches in order to "gain
length" is time consuming and often
leads to the need for revision. Our pref-
erence is, when an artery is completely
transected and debrided, to consider
the insertion of a substitute conduit.
Often a microscope or magnifying
loupes are used for very small vessels.
For very small vessel anastomoses, an
interrupted suture line has greater
long-term patency. Precision in the
performance of a vascular anastomo-
sis is paramount to immediate and
long-term patency. The smaller the
vessel, the more unforgiving of lack
of precision and attention to detail.
As with the use of Fogarty balloons, a
number of principles exist relating to
the performance of a vascular anas-
tomosis (Box 7-5). With an exercise
of precision and abiding by these prin-
ciples, the surgeon should expect a
high degree of success from the vas-
cular anastomosis. Reasons for failure
include lack of distal flow, lack of
inflow, narrowed anastomosis, pres-
ence of distal clot, and kinking of the
conduit, among others.

For a continuous anastomosis, the
surgeon should use "triangulation" or
lateral "stay" suture techniques to
ensure that the anastomosis is not nar-
rowed. The first assistant must be vig-
ilant to ensure that the continuous
anastomosis is not "purse stringed" by
the assistant pulling to tightly on the
suture as he or she follows for the

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161

PRINCIPLES RELATING TO THE PERFORMANCE OF
A VASCULAR ANASTOMOSIS

The anastomosis must be tension free.

Consideration must be given to the various positions of the adjacent and
distal anatomy after repair.

Consideration should be made for redundancy to allow for full extension
of an extremity after reconstruction.

Consideration must be made regarding coverage of the repair.

The suture material must be nonabsorbable.

The finest suture material to accomplish a permanent anastomosis should
be selected.

The needle size and shape should be chosen to maximize an ideal
anastomosis.

The needle must enter the vessel at a right angle.

The rotation on the needle should follow the curve of the needle.

The needle should be grasped with the needle driver somewhere between
the middle of the curve and the tip.

The suture material should not be used to "pull" the anastomosis together
but lie together without tension.

surgeon. Another consideration is to
spatulate the anastomosis to make the
anastomosis actually larger than the
repaired vessel. Some end-to-end
anastomoses are accomplished using
vascular staples. Some appropriately
chosen techniques should be used to
determine the adequacy of the anas-
tomosis at the completion of the
procedure. Some surgeons choose
Doppler ultrasound, and others will
use arteriography, depending on the
size of the vessel.

Insertion of a substitute conduit

A substitute interposition conduit has
been used extensively in vascular
trauma. An interposition (end-to-end,
end-to-side, or side-to-side) conduit is
used when extensive destruction exists
and one of the other reconstruction
options does not exist. Considerable
discussion, debate, and research have
focused on the synthetic versus auto-
genous conduits. This concern basi-

cally comes down to a consideration
in only two locations, the superficial
femoral and the subclavian arteries. In
the trunk, use of PTFE or Dacron pros-
theses are an issue of size match and
durability. Long-term favorable results
have been extensively reported. In the
neck, distal extremities, and smaller
truncal arteries, the size match of
currently available prostheses is
unacceptable and use of the scavenged
saphenous vein is most appropriate.
Currently, for vessels 5 mm or smaller,
the use of the saphenous vein is the
preferred conduit.

Debate has also occurred regarding
which graft material to use in the
presence of potential infection. One
option would be to use ligation and
extra-anatomic routing around the
area of infection when potential or real
infection occurs. In some instances,
such as reconstruction of an injured
abdominal aorta, it is virtually im-
possible to avoid reconstruction in an

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II • PRINCIPLES OF OPERATIVE CARE

area of potential infection. In other
instances, infection is not a consider-
ation until a graft is later exposed, or
a secondary infection or abscess occurs
in an area of infection. Another argu-
ment has been whether venous or
arterial autografts are "living" at the
time that the conduit is scavenged and
repositioned elsewhere, devoid of its
vasovasorium. A case can be made that
this (foreign body) collagen tube
becomes "living" after it has become
re-endothelized at a later date. If this
is correct, all substitute conduits —
regardless of being autologous,
homologous, frozen, xenographic, or
manufactured — the infectious risk
should be similar. Despite the use of
Dacron substitute conduits in the
injured abdominal aorta for almost all
reported successfully managed cases
and a high rate of enteric contamina-
tion at the time of implantation, no
infected aortic grafts in these cases
have been documented in the litera-
ture. Other synthetic grafts, such as
those constructed with PTFE, have
been percutaneously punctured and
yet have a suggested "resistance to
infection." More than 30 laboratory
studies have been reported in which
purposeful infections have been
created around grafts, comparing
synthetic with autogenous material.
The infectivity is almost identical, but
the complications are different, both
in the laboratory and in people.
With synthetic conduits, perigraft
infections result in either suture line
aneurysms, thrombosis of the graft, or
occasionally sepsis from chronic graft
infection. With "autogenous" con-
duits, periconduit infections result
in dissolution of the collagen tube,
distal embolization, and often exsan-
guinating hemorrhage, sometimes
uncontrollable.

Although end-to-end anastomoses
are often used at both ends of the sub-
stitute conduit, consideration for an
end-to-side reconstruction at either
end or both ends of the conduit war-

rants consideration. In some instances,
such as injury to the popliteal artery,
immediately behind the knee, this
variation offers an additional option
with long-term favorable results.

d. Patch angioplasty

Patch angioplasty using autogenous
venous material is actually used very
infrequently in vascular trauma. When
it is used, it is often as a secondary
procedure to correct a narrowing at a
previous reconstruction. With current
technology, a catheter-based inter-
ventional dilation and stenting would
precede a secondary open procedure
to widen a previously constructed vas-
cular repair.

1 2 . Flush proximally and distally before com-
pletion of the suture line.

Before the completion of the suture
line, the proximal and distal clamps are
temporally removed to ensure that pro-
grade and retrograde back bleeding
occurs. If there is no back bleeding from
the distal suture line, one might
consider another pass of the Fogarty
catheter.

1 3. Complete the suture line/clamp removal.

When the surgeon is ensured that
inflow and outflow are adequate, the
suture line is completed and the clamps
are removed.

14. Assess the distal circulation.

After completion of a vascular recon-
struction, the surgeon must evaluate the
adequacy of the anastomosis for any
stenosis, kinking of the prosthesis, and
patency of the distal outflow tract. This is
best accomplished using completion arte-
riography, which despite the availability
of Doppler and ultrasound technologies
still remains the "gold standard."
However, in the critically injured patient,
there may not be time for a completion
study. When dealing with large arteries,
such as the iliac, subclavian, and femoral
vessels, a good distal pulse and a normal
triphasic Doppler signal are often taken

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7 • ACCESS, CONTROL AND REPAIR TECHNIQUES

163

as evidence of a technically satisfactory
repair. The best time to accomplish any
needed re-reconstruction is at the time
of the first operation.

15. Consider the need for fasciotomy.

Fasciotomy and compartment syndromes
are addressed in Chapter 23. In cases of
an ischemic limb for more than 4 hours,
the surgeon is well advised to consider per-
forming a fasciotomy before a vascular
reconstruction. In cases of ligation of an
outflow vein, especially the iliac, axillary,
deep femoral, or popliteal veins, apostre-
pair fasciotomy is strongly encouraged. If
there be any concern for the performance
of a fasciotomy, compartment pressures
can be measured. Although debate exists
concerning the exact pressures where a
fasciotomy must be performed, com-
partment pressures of more than 30 cm
H 2 should cause the surgeon to strongly
consider the procedure.

16. Ensure appropriate coverage.

A cardinal principle in vascular trauma
is that a vascular reconstruction must
always be covered with viable soft tissue;
otherwise, failure with catastrophic bleed-
ing is all but certain. Coverage can be
achieved using various techniques, but in
the presence of massive soft tissue destruc-
tion, covering an arterial graft with viable
soft tissue can be both challenging and
time consuming. Most often, coverage is
with the tissue within the operative field,
which in the normal closure adequately
covers the vascular repair. On occasion,
special flaps will be necessary to bring vas-
cularized pedicles over the reconstruc-
tion. In extremely rare situations, use of
porcine xenograft or homograft mater-
ial might be neces-sary to temporarily
cover a vascular reconstruction.

The trauma surgeon undertaking avas-
cular reconstruction must keep in mind
the importance of soft tissue coverage
because occasionally an unusual or
unorthodox extra-anatomic route will be
selected for the graftjust because the con-
ventional anatomic route is exposed or
will present a cover problem.

SUMMARY

This chapter is intended to communicate
the fundamentals required by a general
surgeon approaching a patient with a sus-
pected or proven vascular injury upon
arrival in the OR. The principle of initial
control of external hemorrhage is followed
by considerations for positioning on the
OR table and determination of incision
placement.

Fundamental in approaching a vascular
injury is initially obtaining access and control
away from the area of suspected injury so no
additional injury ensues as the area of specific
injury and hemorrhage is dissected. An area-
by-area review of some general access and
control suggestions is provided for specific
injuries.

Finally, some general repair techniques
are presented, which are standard for the
reconstruction of any vascular injury.

REFERENCES

Buckman RF, Miraliakbari R, Badellino MM:
Juxtahepatic venous injuries: A critical review
of reported management strategies. J Trauma
2000;48:978-983.

Burch JM, Richardson RJ, Martin RR, Mattox KL:
Penetrating iliac vascular injuries: Recent expe-
rience with 233 consecutive patients. J Trauma
1990;30:1450-1459.

Feliciano DV, Burch JM, Mattox KL, et al: Balloon
catheter tamponade in cardiovascular wounds.
Am J Surg 1990;160:583-587.

Henry AK: Extensile Exposure, 2nd ed. Baltimore:
Williams & Wilkins, 1957.

Hoyt DB, Coimbra R, Potenza BM, Rappold JF:
Anatomic exposures for vascular injuries. Surg
Clin North Am 2001 Dec;81(6):1299-1330.

Martin RR, Barcia PJ, Johnson EA: Making
matters worse: Complications of initial evalua-
tion, treatment and delayed diagnosis. In Mattox
KL (ed) : Complications of Trauma. New \brk,
Churchill Livingstone, 1994, pp 139-154.

Mattox KL: Red River anthology. J Trauma 1997;
42:353-368.

Mattox KL, Hirshberg A: Vascular trauma in vas-
cular surgery. In Haimovici H, Ascer E, Hollier
LH, et al (eds) : Haimovici's Vascular Surgery —

ch07.qxd 4/16/04 3:30PM Page 164

164

II • PRINCIPLES OF OPERATIVE CARE

Principles and Techniques, 4th ed. Cambridge,
Mass, Blackwell Scientific, 1995.

Mattox KL, McCollum WB, Jordan GL Jr, et al:
Management of penetrating injuries of the
suprarenal aorta. J Trauma 1975;15:808-815.

Rutherford RB: Atlas of Vascular Surgery. Basic
Techniques and Exposures. Philadelphia,
Harcourt Brace Jovanovich, 1993.

Surgical exposure of vessels. In Haimovici H,
Ascer E, Hollier LH, et al (eds): Haimovici's

Vascular Surgery — Principles and Techniques,
4th ed. Cambridge, Mass, Blackwell Scientific,
1995, pp 351-420.

Veith FJ, Gupta S, Daly V: Technique for oc-
cluding the surpaceliac aorta through the
abdomen. Surg Gynecol Obstet 1980;151(3):
426-428.

Wind GG, Valentine RJ: Anatomic Exposures in
Vascular Surgery. Baltimore, Williams &Wilkins,
1991.

ch08.qxd 4/16/04 3:31PM Page 165

Damage Control for
Vascular Trauma

ASHER HIRSHBERG
BRADFORD G. SCOTT

INTRODUCTION

EVOLUTION OF THE DAMAGE-CONTROL CONCEPT

The Physiologic Envelope

Practical Application of "Damage Control"

VASCULAR REPAIR TECHNIQUES

TEMPORARY SHUNTS

POSTOPERATIVE LIMB ISCHEMIA

PLANNED REOPERATION

INTRODUCTION

"Damage control" is a surgical strategy for the
staged management of multivisceral trauma
that represents a major paradigm shift in
trauma surgery. With this approach, the tra-
ditional single definitive operation is replaced
by a staged repair, whereby a rapid "bailout"
operation (to control hemorrhage and
spillage) is followed by a delayed reconstruc-
tion after the patient's physiology has been
stabilized. In the last decade, this approach
has become part of the standard repertoire

of trauma surgeons when operating on their
most critically wounded patients.

Major vascular trauma is often part of the
injury complex in patients with exsanguinat-
ing hemorrhage in whom the damage-control
approach is the patient's only hope. There-
fore, a detailed acquaintance with this strat-
egy and its application to the management of
arterial and venous injuries is mandatory for
every surgeon involved in trauma care.

Damage control for vascular injuries is par-
ticularly challenging because of the inherent
conflict between the need for a precise and
time-consuming vascular reconstruction on

165

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II • PRINCIPLES OF OPERATIVE CARE

the one hand and the urgency of an abbrevi-
ated procedure on the other. However, the
futility of attempting a complex arterial repair
in the presence of diffuse coagulopathy should
be quite obvious even to a surgeon who is unac-
quainted with the damage-control strategy.

The concept of staged repair in emergen-
cies is not new to vascular surgeons. For
example, the current operative management
of infected intra-abdominal aortic grafts often
consists of a two-stage operation whereby an
extra-anatomic bypass is inserted first, and
removal of the infected graft is delayed for a
subsequent procedure. The reason for this is
not technical, but it is the desire to avoid a
huge physiologic insult in a compromised
patient. Similarly, a staged repair of a bleed-
ing aortoduodenal fistula (the first operation
consisting of temporary control of bleeding
and of the duodenal perforation much like
in a damage-control procedure) has been
advocated as a more effective approach than
the traditional one-stage operation because
the results of the latter carry a prohibitive
mortality.

This chapter presents the general philoso-
phy of damage control and the underlying
physiologic considerations that form the ratio-
nale for employing the strategy. This will then
serve as a background for a discussion of the
application of damage-control principles to
the modern management of vascular trauma,
and a detailed description of specific "bailout"
techniques for the management of major arte-
rial and venous injuries.

EVOLUTION OF THE DAMAGE-
CONTROL CONCEPT

During the past 2 decades, civilian trauma sur-
geons have encountered new wounding pat-
terns characterized by high-energy transfers
(from automaticweaponsandfastmotorvehi-
cles) causing extensive damage to multiple
organs and massive blood loss. These exsan-
guinating patients, who previously would have
died before reaching the hospital, are now
rapidly transferred to trauma centers by
efficient prehospital systems, presenting sur-
geons with an unusual array of challenges. The

conventional operative sequence for trauma,
consisting of rapid access, bleeding control,
and reconstruction, is inappropriate in these
exsanguinating patients. Such definitive repair
usually requires lengthy and complex proce-
dures, which these critically ill patients will
not tolerate. The result of heroic attempts at
definitive repairs has typically been early post-
operative death due to "irreversible shock,"
diffuse coagulopathy bleeding or multiple
organ system failure. These considerations
have led to the development of the damage-
control approach, a modified operative
sequence whereby only immediately life-
threatening visceral injuries are addressed
using rapid temporary lifesaving measures.
The patient is then transferred to the surgi-
cal intensive care unit (ICU) for rewarming
and resuscitation, and definitive repair of the
injuries is postponed until reoperation can be
performed on a nonbleeding, stable patient
with restituted physiologic parameters (see
Table 8-1).

Damage control represents a profound
change in the way trauma surgeons view their
role in the operating room. The center of
attention has shifted from reconstruction
of the anatomy to restitution of the injured
patient's physiologic reserves. In other words,
the completeness of the anatomic repair is
temporarily sacrificed to address the physio-
logic insult before it becomes irreversible.
Herein lies the fundamental difference
between the traditional approach of a single
definitive procedure and the damage-control
approach of a staged repair.

Trauma surgeons were slow to adopt this
unconventional strategy because abrupt
termination of an "unfinished" operation and
acceptance of a temporary and anatomically
incomplete repair seemed to contrast with tra-
ditional surgical values. This is why almost a
decade passed between the original descrip-
tion of the strategy in patients with coagu-
lopathy by Stone, Strom, and Mullins in 1983
and the publication of the first large series in
the early 1990s. Gradual adoption of damage
control as a valid alternative to the traditional
definitive operation evolved slowly (see Table
8-1). In the mid-1990s, the new approach was
expanded to the management of urologic, tho-
racic, vascular, and even limb injuries.

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8 • DAMAGE CONTROL FOR VASCULAR TRAUMA

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TABLE 8-1

THE EVOLUTION OF "DAMAGE CONTROL"

Period

1983
1982-1990

1991

1992

1992-1994

1994-1997

1997-Present

Key Development

Staged approach to coagulopathy

Sporadic technical reports
Balloon catheter tamponade

Largest series (200 patients) and
philosophy explained

"Damage control" coined

New concept gains acceptance

Extension outside abdomen

Attempts to define physiological
envelope

References

Stone, Strom, and Mullins
Feliciano and colleagues (1990)

Burch and colleagues (1992)

Rotondo and colleagues (1993)

Morris and colleagues (1993)

Hirshberg et al (7)
Wall and colleagues (1994)
Porter and colleagues (1997)
Scalea and colleagues (1994)

Cosgriff and colleagues (1997)
Cushman and colleagues (1997)
Garrison and colleagues (1996)

The Physiologic Envelope

The concept of the "physiologic envelope" is
key to understanding the rationale of damage
control. Despite technologic advances, the
operating room remains a physiologically
unfavorable environment for the severely
wounded patient. Extensive peritoneal expo-
sure during a trauma laparotomy results in
accelerated heat loss, which is further aggra-
vated by massive transfusion. Hypothermia in
turn impairs blood clotting and thus con-
tributes to ongoing hemorrhage. Shock leads
to metabolic acidosis and a subsequent need
for further transfusion. The most obvious
manifestation of the injured patient's physi-
ologic derangement is, therefore, the triad of
hypothermia coagulopathy and acidosis.
Together these derangements create a self-
propagating vicious cycle that eventually leads
to an irreversible physiologic insult. This irre-
versibility may present intraoperatively as
diffuse bleeding that cannot be controlled sur-
gically, followed by refractory ventricular
arrhythmias and death. More commonly, the
patient survives the operation only to exhibit
a refractory systolic blood pressure of 60 to
80mmHg, oliguria, peripheral vasocon-
striction, massive swelling, progressive

hypoxemia, and diffuse oozing from every inci-
sion and vascular access site. Death almost
invariably ensues within the first few postop-
erative hours.

Thus, the triad of hypothermia, coagu-
lopathy, and acidosis defines the patient's
physiologic envelope, a set of physiologic
parameters that together mark the boundary
between a survivable physiologic insult and
an irreversible derangement. Termination of
the operative procedure before this physio-
logic envelope is breached is the essence of
damage control.

Hypothermiahas emerged as a central patho-
physiologic event in exsanguinating trauma
patients. Shocked patients with penetrating
torso injuries lose body heat to a mean tem-
perature of 34.5°C by the time they reach the
operating room. The ambient temperature in
the operating room is around 22°C, and rapid
infusion of crystalloids or blood without a
warming device contributes to the fast devel-
opment of hypothermia. The open peri-
toneal cavity itself is also a major source of
accelerated heat loss. It has been clearly shown
that in the severely injured patient, hypother-
mia is harmful and adversely affects survival
independent of injury severity. Of the three
components of the physiologic envelope,

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II • PRINCIPLES OF OPERATIVE CARE

hypothermia is the only one for which there
is a well-defined threshold value. In 1987,
Jurkovich and colleagues convincingly demon-
strated that in severely wounded patients
undergoing laparotomy, a core temperature
less than 32°C is associated with 100% mor-
tality. Based on this observation, a mathe-
matical model of intraoperative heat loss
during laparotomy for exsanguinating hem-
orrhage predicts a window of opportunity of
no more than 60 to 90 minutes before this
threshold is reached.

Coagulopathy typically presents as diffuse
oozing inside and outside the operative field.
Attention has focused on hypothermia as the
cause of coagulopathy in trauma. Hypother-
mia affects clotting through alteration of
platelet function and inhibition of the coag-
ulation cascade. In the hypothermic patient,
platelets are sequestered in the liver and spleen
and exhibit marked morphologic changes.
Platelet activation is inhibited resulting in pro-
longation of the bleeding time and other
abnormal platelet function test results. The
enzymes of the coagulation cascade are tem-
perature sensitive and therefore are inhibited
during hypothermia. However, both platelet
dysfunction and enzyme inhibition become
clinically important only when the core tem-
perature drops to less than 32°C, which is well
below the usual range seen in the severely
injured.

Hemodilution is another important cause
of coagulopathy in exsanguinating patients.
Extensive blood loss and massive replacement
with packed cells and crystalloids combine
to produce rapid "washout" of platelets and
clotting factors. Because many of the pa-
tients undergoing damage-control operations
require massive transfusion, and because the
actual blood volume of these patients changes
rapidly and is difficult to quantify, dilution is
probably an underestimated contributor to
coagulopathy. Hypothermia and dilution also
have been clearly shown to have an additive
effect in causing clotting abnormalities.

Coagulopathy in the critically injured
patient is a clinical and not a laboratory diag-
nosis. Standard coagulation tests often fail to
reflect the full magnitude of the clotting dis-
order in these patients because they are rou-
tinely conducted at 37°C and often take too

long to be useful guides for real-time replace-
ment of clotting factors in the exsanguinat-
ing patient.

Lactic acidosis is the result of anaerobic gly-
colysis and reflects inadequate tissue perfu-
sion. Acidosis adversely affects myocardial
contractility and cardiac output in animal
models, but the full scope of its physiologic
and metabolic effects remains unclear. Aci-
dosis is a useful measure of the severity of shock
and a reliable predictor of survival. Serum
lactate levels, base deficit, and the time inter-
val to normalization of the serum lactate have
all been shown to closely correlate with mor-
tality from severe trauma in both animal
and clinical studies. However, no well-defined
threshold value for lactic acidosis can serve
as a marker of irreversible shock.

Several attempts were made to better define
the physiologic envelope. Cosgriff and
colleagues (1997) analyzed prospectively col-
lected physiologic data from 58 injured
patients who received massive transfusions,
and they identified four significant risk factors
that predict the onset of coagulopathy: pH <
7.10, temperature <34°C, Injury Severity Score
>25, and systolic blood pressure <70mmHg.
About one in four severely injured patients
requiring massive transfusion developed coag-
ulopathy, but when all four risk factors were
present, the probability of developing coag-
ulopathywas98%. In another study, Cushman
and colleagues (1997) attempted to quantify
the physiologic envelope in a series of 53
patients with iliac vascular injuries. Their study
showed that an initial pH level of less than
7.1 and a final operating room temperature
of less than 35 °C were the best predictors
of imminent death.

Practical Application of
"Damage Control"

The damage-control sequence consists of
three phases: initial operation, surgical ICU
resuscitation, and planned reoperation. The
initial operation is typically a rapid "bailout"
procedure in which the surgeon does only
the absolute minimum necessary to save the
patient's life. Rapid temporary techniques are
used to control bleeding, prevent spillage of

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8 • DAMAGE CONTROL FOR VASCULAR TRAUMA

169

intestinal content or urine, restore blood
flow to vital vascular beds, and achieve rapid
closure of the abdomen or chest. Time-
consuming formal resections and recon-
structions are deliberately avoided.

Bleeding from solid organs (such as the
liver) or diffusely oozing cavities (such as
the retroperitoneum) is controlled by packing.
Spillage of intestinal content is controlled by
ligation or stapling of bowel injuries without
resection, or by external tube drainage of
duodenal, pancreatic, and common bile duct
injuries. Similar spillage-control techniques
have been applied to injuries of the urinary
tract. In the chest, stapled nonanatomic lung
resection and laying open a bullet tract
through the lung parenchyma to control
bleeding (instead of resection) enable rapid
termination of the operative procedure in
accordance with damage-control principles.

Closure of the injured cavity is performed
rapidly using temporary measures, such as
skin-only closure by a running monofilament
suture. In the presence of massive visceral
edema that precludes skin closure without
tension, plastic silos or absorbable mesh is used
to temporarily accommodate and protect the
edematous viscera.

The second phase of the sequence is re-
suscitation in the surgical ICU. Aggressive
correction of hypothermia is the most impor-
tant consideration in the early postoperative
period. This can usually be achieved using vig-
orous external rewarming, but arteriovenous
rewarming can greatly expedite the process
in severely hypothermic patients. Empirical
replacement of blood, plasma, and platelets
is equally important to restore normal hemo-
stasis. Support of the cardiovascular system
focuses initially on volume replacement. The
early use of invasive cardiovascular monitor-
ing (a soon as the patient's coagulopathy is
corrected) may be a useful adjunct. To achieve
a favorable outcome, these patients require a
direct and massive investment of bedside time
and continuous direct involvement of the
trauma team in the early postoperative period.

Not uncommonly, patients may require an
urgent (unplanned) reoperation during the
second phase of the damage-control sequence.
The main indication for urgent reoperation
is ongoing hemorrhage. This is usually the

result of either failed hemostasis during
the "bailout" procedure, a missed injury, or
an iatrogenic trauma. Other indications for
an urgent reoperation are intra-abdominal
hypertension and limb ischemia distal to an
indwelling temporary intraluminal shunt.

Planned reoperation is undertaken in a
stable patient, usually within 2 to 3 days of the
initial "bailout" procedure. The aims at this
stage are to perform a definitive repair of the
injuries and to accomplish formal closure of
the visceral cavity.

Although most trauma cases are effectively
managed using the traditional approach of a
single definitive operation, the damage-
control approach is indicated only in a small
group of the most critically injured patients,
and one of the major problems facing the
surgeon is deciding when to employ it.

Formally stated, damage controlh indicated
when the magnitude of the visceral damage
is such that definitive repair of all injuries
is likely to exceed the patient's physiologic
limits. However, this is a simplified definition
of a complex and multidimensional dilemma.
Making the decision early, within a few minutes
of entering the injured cavity, is one of the
keys to successful damage control. Garrison
and colleagues (1996) have shown that an
early decision to perform packing is an impor-
tant determinant of survival in abdominal
trauma, because deterioration in coagulation,
low pH level, and long duration of hypoten-
sion are all associated with a decreased chance
of survival.

Because no good qualitative definition of
the point at which the physiologic insult
becomes irreversible is available, an early deci-
sion to "bail out" must rely on recognition of
typical injury patterns that require damage
control rather than on physiologic parame-
ters. The combination of a major intra-abdom-
inal vascular injury with hollow or solid-organ
damage is a class injury pattern in which an
early decision to "bail out" is often lifesaving.
However, isolated major vascular injuries can
usually undergo a definitive repair even in a
patient who has sustained a massive amount
of blood loss because bleeding is controlled,
resuscitation can be accomplished intraop-
eratively, and the definitive repair can
be accomplished relatively quickly. Other

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II • PRINCIPLES OF OPERATIVE CARE

patterns include destruction of the pancre-
aticoduodenal complex, a high-grade hepatic
injury, retroperitoneal or pelvic bleeding, and
injuries to multiple visceral compartments.

VASCULAR REPAIR
TECHNIQUES

The application of damage-control principles
to vascular trauma hinges on a clear distinc-
tion between two categories of vascular repairs:
simple and complex. Simple repairs are rapid
and straightforward and include lateral repair,
ligation, and temporary intraluminal shunt
insertion. These techniques are not time con-
suming, do not create long suture lines, and
can be used even in the presence of diffuse
coagulopathic bleeding or unfavorable phys-
iology. Complex repairs include vascular
reconstructions such as end-to-end anasto-
mosis, patch angioplasty, and graft interposi-
tion. These techniques are usually poor
options in the hypothermic coagulopathic
patient not only because they result in ongoing
oozing from the suture lines but also because
they are time consuming and significantly
prolong the "bailout" procedure. This
unorthodox approach represents a sharp
deviation from the standard principles of vas-
cular reconstruction but is eminently applic-
able to the damage-control scenario, in which
not everything that is technically possible is
in the patient's best interest.

Lateral repair is feasible in the absence of
complete transection or extensive destruction
of the arterial wall. It is important to main-
tain the orientation of the repair perpendic-
ular to the axis of the vessel, to avoid stenosis.

Ligation is an underused option in the
severely injured patient, especially when the
injured vessel is relatively inaccessible or a
complex repair is required. All limb veins can
be ligated with impunity, and certainly in the
context of damage control, reconstructing a
peripheral vein is unjustified. The subclavian
and iliac veins and the inferior vena cava can
be rapidly ligated with the acceptable price
of postoperative limb edema. Ligation of the
portal and superior mesenteric veins is a valid
option in the patient in extremis, but this results

in massive third spacing that requires very
aggressive fluid resuscitation in the post-
operative phase.

Many injured arteries can also be ligated
with impunity. The external carotid artery is
an obvious example. In the context of pene-
trating trauma, injury to the inaccessible retro-
mandibular part of the internal carotid artery
(in zone 3) is managed by ligation or balloon
tamponade, with the calculated risk of a
neurologic deficit weighted against the neces-
sity of obtaining rapid hemostasis. In most
patients, ligation of the subclavian artery does
not result in critical ischemia of the upper
extremity because of the ample collateral cir-
culation around the shoulder. The amputa-
tion rates following ligation of the femoral
arteries were 81% for the common femoral
and 55% for the superficial femoral artery,
based on data from World War II (before the
advent of fasciotomy). When a major limb
artery is ligated during a damage — control
procedure, it is usually prudent to proceed
with an immediate fasciotomy.

Ligation of the proximal suprapancreatic
superior mesenteric artery has been reported
as a valid technical alternative in critically
injured patients who are unlikely to tolerate
a lengthy reconstruction because the rich col-
lateral blood supply from the inferior mesen-
teric and celiac arteries will maintain midgut
viability. The celiac axis can be ligated with
impunity, and complex repair of renal artery
injury in the exsanguinating patient with
multiple injuries should not be attempted.

An effective alternative to ligation in inac-
cessible sites is balloon catheter tamponade,
a simple and effective vascular damage-control
technique. A Foley or large Fogarty balloon
catheter is inserted into the tract of the injur-
ing missile, and the balloon is inflated until
hemorrhage is controlled. Balloon tampon-
ade can be either a temporary hemostatic
maneuver or even a definitive management
of an inaccessible injury (Fig. 8-1). Balloons
have been successfully used to control bleed-
ing from the carotid artery high in the neck,
from inaccessible pelvic vessels, or from a trans-
fixing liver injury.

Another useful hemostatic technique is
packing. Although traditionally employed to
achieve hemostasis from high-grade liver

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8 • DAMAGE CONTROL FOR VASCULAR TRAUMA

171

■ FIGURE 8-1

Balloon catheter tamponade of the distal internal carotid artery in zone 3 of the neck.

injuries, packing is a very useful adjunct in a
coagulopathy patient with a limb injury and
ongoing hemorrhage from multiple muscu-
lar bleeders that cannot be controlled directly.

TEMPORARY SHUNTS

Intraluminal shunts are prosthetic conduits
placed within the vessel lumen across an
injured segment to temporarily reestablish
blood flow until a definitive vascular recon-
struction can be performed. Vascular surgeons
have used temporary shunts for at least
3 decades. In 1971, Eger and colleagues
described the use of a shunt in a series of
popliteal artery injuries to maintain limb per-
fusion while the bones are aligned before vas-
cular repair. This series was the first modern
report of the use of shunts in vascular trauma.
It has recently been shown in an experimen-
tal study that a temporary shunt provides
approximately half the blood flow of the intact
vessel and that increased oxygen extraction
compensates for the lower flow.

The choice of shunt material is a matter of
personal preference, because any rigid smooth
synthetic tube of appropriate caliber can serve
as a temporary vascular conduit. The original
description by Eger and colleagues (1971) was
of a polyethylene tube with a side port. The
side port facilitates access for monitoring of
flow or flushing of the lumen. Others have
used commercially available carotid shunts
(such as ajavid or a Sundt shunt) or a heparin-
bonded catheter or have improvised with a
segment of a suction catheter or small Ar gyle's
catheter cut to the appropriate length.

Temporary shunts remained functional for
as long as 24 hours in an animal model. In
clinical practice, temporary shunts remain
functional for many hours, and patency as late
as 36 hours after insertion has been observed.
The presence of coagulopathy in the critically
injured usually prevents clotting of the shunt
during the first postoperative hours, so early
postoperative failure is usually the result of a
technical error during insertion. Temporary
shunt insertion is an excellent damage-control
option because it is rapid, controls hemor-
rhage from the injured vessel, and preserves

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172

II • PRINCIPLES OF OPERATIVE CARE

■ FIGURE 8-2

A temporary intraluminal shunt (Argyle's tube)
maintaining flow across a transected brachial
artery. ■

distal flow while keeping all future recon-
structive options open for the surgeon
(Fig. 8-2).

Shunts are also used in the surgical repair
of combined orthopedic and vascular injuries.
Here the preferred sequence would be to
achieve bone alignment before arterial recon-
struction, but often the extremity is grossly
ischemic and requires immediate restoration
of distal flow. Shunt insertion allows fracture
fixation to proceed and allows a subsequent
vascular reconstruction once the bones are
properly aligned.

Temporary shunts have been used in the
management of brachial, iliac, femoral, and
popliteal arterial injuries. A single case of
the successful use of a temporary shunt for
superior mesenteric artery injury has been
reported. Several attempts have been made
to use an Argyle chest tube as a temporary
shunt across an injury to the abdominal aorta
in patients in extremis, none of whom survived
beyond the immediate postoperative period.

Insertion of a temporary intraluminal shunt
begins with proximal and distal control of the
injured segment. Typically, the injured artery
will be completely or almost completely tran-
sected. The injury should be carefully assessed

and the inflow and outflow tracts to the
damaged segment should be cleared by a
Fogarty balloon thrombectomy. A shunt of the
appropriate diameter is then gently inserted
distally, flushed retrograde, and then inserted
proximally. Special care is taken to avoid
raising an intimal flap or causing additional
injury to the vessel. The shunt can be secured
in place either with heavy silk ligatures or vessel
loops held in place by a Rummel tourniquet.
The former technique is simpler but more
traumatic to the arterial wall. A central heavy
silk ligature placed around the mid-body of
the shunt is helpful for manipulation and
serves as a marker for proximal or distal migra-
tion of the conduit. Once the shunt is in place,
distal perfusion should be confirmed by pal-
pation of a distal pulse or obtaining a Doppler
signal distal to the injured segment. Systemic
heparin is not administered.

The two major postoperative concerns are
shunt dislodgment and thrombosis. Dislodg-
ment of the shunt is rare and usually results
from inadequate fixation of the shunt in place.
There is sudden gross swelling of the involved
extremity with oozing between the skin
sutures, indicating the presence of a rapidly
expanding hematoma. Immediate reexplo-
ration is indicated to obtain hemostasis and
reinsert the shunt.

Early shunt failure is usually caused by a
technical problem, and much like with early
postoperative failures of arterial reconstruc-
tions, the cause is poor inflow, a problem with
the shunt itself, or inadequate outflow. Poor
inflow or outflow can be the result of an intimal
flap, a more proximal or distal injury, or a
residual thrombus (proximal or distal to the
shunt). The shunt itself can also be occluded
by tying the ligatures that fix it in place too
tightly, by angulation from excessive length,
or by migration of the shunt into a distal arte-
rial branch.

POSTOPERATIVE LIMB
ISCHEMIA

Limb ischemia is the major concern after
damage-control procedures that include a vas-
cular component. Ischemia may be the result

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8 • DAMAGE CONTROL FOR VASCULAR TRAUMA

173

of intentional ligation of the injured artery, a
clotted temporary shunt, a failed repair, or a
missed injury. The major considerations in the
management of limb ischemia in the damage-
control context are the same regardless of the
etiology. The first obvious step is the diagno-
sis of limb ischemia. Normal peripheral pulses
are rarely palpable in these patients, even in
the absence of an arterial injury. Hypotension,
hypothermia, peripheral vasoconstriction,
and edema of the injured extremity all
combine to make the diagnosis of limb
ischemia quite difficult in the critically
wounded. Therefore, it is vital to establish
reliable vascular follow-up parameters in
the injured extremity immediately upon the
patient's arrival in the surgical ICU.

Such a parameter can be a Doppler signal,
the presence of capillary refill, or even a pulse
oximeter that is applied to a toe in the rele-
vant extremity. The diagnosis of acute post-
operative ischemia is based on a change in
this follow-up parameter and on a difference
between the perfusion of the two extremities
that gradually becomes apparent as the
patient's hypothermia and hypovolemia is
corrected.

Because an ischemic extremity is not an
imminent threat to life, immediate reopera-
tion is usually not undertaken. Instead, the
surgeon should assess the patient's overall
physiology, clinical trajectory, and the feasi-
bility of a vascular repair, and then formulate
a plan of action. For example, undertaking a
vascular reconstruction in the presence of clin-
ically obvious coagulopathy is futile and often
leads to further deterioration in the patient's
already precarious condition. When the
circumstances are unfavorable for an urgent
complex arterial reconstruction, acceptable
options may include watchful waiting to see
whether the collateral circulation sustains
limb viability, performing a fasciotomy at the
bedside, or thrombectomy with reinsertion of
a temporary shunt until the patient is stable
enough to undergo a definitive arterial recon-
struction. Late (>12 hours) occlusion of the
shunt usually indicates that the patient's coag-
ulopathy has been corrected and that it is time
for a definitive repair.

On rare occasions, an urgent reconstruc-
tion is required for limb salvage in a patient

■ FIGURE 8-3

Bedside surgery in the surgical intensive care
unit. An urgent vascular reconstruction can
occasionally be undertaken at the bedside in
unstable patients with limb-threatening
ischemia following damage-control surgery. ■

whose physiology is so unstable that making
a trip to the operating room is extremely risky.
Under these unusual circumstances, simple
peripheral arterial reconstruction can be
undertaken at the bedside in the surgical ICU.
This entails a serious logistic effort to mobi-
lize operating room technology and create an
appropriate sterile work environment at the
bedside (Fig. 8-3). However, in the critically
ill patient on high-dose inotropic support and
severe acute respiratory distress syndrome
on a nonconventional ventilatory mode, this
may be the safer option. A classic example is
a bedside crossover femorofemoral bypass in
a critical patient whose iliac artery has been
ligated or whose iliac shunt has clotted off.

PLANNED REOPERATION

The vascular damage-control sequence ends
with a planned reoperation in which defini-
tive reconstruction of the injuries is under-
taken. The timing of a planned reoperation
depends on the clinical circumstances, but in
general the patient should be stable, warm,
and with normal coagulation. If possible, a
planned repeated laparotomy should be post-
poned until the patient has attained a nega-
tive fluid balance because the presence of

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II • PRINCIPLES OF OPERATIVE CARE

swollen edematous bowel and a noncompli-
ant abdominal wall typically precludes defin-
itive abdominal closure. If the required
vascular reconstruction is in the abdomen, it
is undertaken before depacking of solid
organs because the removal of packs may result
in rebleeding and the need for repacking and
rapid "bailout."

Peripheral arterial reconstructions are
performed in the standard fashion. The
extreme circumstances of patients undergo-
ing damage-control procedures often pre-
clude formal angiographic imaging of
the injured arterial tree before reoperation,
and the surgeon may, therefore, elect to
begin the vascular reoperation with an on-
table angiogram to precisely delineate the
anatomic conditions before reconstruction
and to ascertain that there are no missed
injuries proximally or distally. If a temporary
intraluminal shunt is in place, the shunt is
removed and a Fogarty balloon catheter is
passed proximally and distally. The arterial wall
is then trimmed so the sites of the ligatures
or Rummel tourniquets securing the shunt in
place are not incorporated into the suture line
because the arterial wall is presumed to be
compromised. The injury is carefully assessed
and dEbrided, and a decision is made regard-
ing the optimal reconstructive technique. In
the femoral segment, the choice of conduit
for definitive reconstruction (either vein or
PTFE) is a matter of controversy, and despite
concerns about an increased risk of infection
following reoperation in the same site, there
are no data to support preference of one
option over the other. Fasciotomy, if not pre-
viously performed, should be considered
under these circumstances, because it extends
the tolerance of the limb to ischemia and pro-
tects against the swelling that occurs with
reperfusion after a prolonged ischemic insult.

The definitive vascular repair is often per-
formed in conjunction with operative proce-
dures in other visceral compartments. If the
various planned repairs are performed in a
serial fashion, the operative time is prolonged
in a patient who is still critically ill. Thus, every
effort should be made to shorten the opera-
tive time by planning a multiteam simultane-
ous operation. With correct planning of the

operative sequence, the vascular team can
work in parallel with other teams addressing
abdominal, thoracic, or head injuries.

REFERENCES

Accola KD, Feliciano DV, Mattox KL, et al: Man-
agement of injuries to the superior mesenteric
artery. J Trauma 1986;26(4):313-319.

Aucar JA, Hirshberg A: Damage control for vas-
cular injuries. Surg Clin North Am 1997;77:853-
862.

Bickell WH, Wall MJJr, Pepe PE, et al: Immediate
versus delayed fluid resuscitation for hypoten-
sive patients with penetrating torso injuries. N
EnglJ Med 1994;331:1105-1109.

Ballard RB, Salomone JP, Rozycki GS, et al: "Damage
control" in vascular trauma: A new use for
intravascular shunts. Paper presented at the
Twenty-Eighth Annual Meeting of the Western
Trauma Association, Feb 22-28, 1998, Lake
Louise, Alberta, Canada.

Burch JM, Ortiz VB, Richardson RJ, et al: Abbre-
viated laparotomy and planned reoperation for
critically injured patients. Ann Surg
1992;215:476-484.

Coburn M: Damage control for urologic injuries.
Surg Clin North Am 1997;77:821-834.

Cosgriff N, Moore EE, Sauaia A, et al: Predicting
life-threatening coagulopathy in the massively
transfused trauma patient: Hypothermia and aci-
doses revisited. J Trauma 1997;42:857-862.

Cushman JG, Feliciano DV, Renz BM, et al: Iliac
vessel injury: Operative physiology related to
outcome. J Trauma 1997;42:1033-1040.

Dawson DL, Putnam AT, Light JT, et al: Tempo-
rary arterial shunts to maintain limb perfusion
after arterial injury: An animal study. J Trauma
1999;47:64-71.

DeBakey ME, Simeone FA: Battle injuries of the
arteries in World War II. Ann Surg 1 946;1 23:534-
579.

Eger M, Golcman L, Goldstein A, Hirsch M: The
use of a temporary shunt in the management of
arterial vascular injuries. Surg Gynecol Obstet
197l;132(l):67-70.

Feliciano DV, Burch JM, Mattox KL, et al: Balloon
catheter tamponade in cardiovascular wounds.
Am J Surg 1990;160:583-587.

Garrison JR, Richardson JD, Hilakos AS, et al:
Predicting the need to pack early for severe intra-

ch08.qxd 4/16/04 3:31PM Page 175

8 • DAMAGE CONTROL FOR VASCULAR TRAUMA

175

abdominal hemorrhage. J Trauma 1996;40:923-
929.

Gentiello LM, Jurkovich GJ, Stark MS, et al: Is
hypothermia in the victim of major trauma pro-
tective or harmful? A randomized, prospective
study. Ann Surg 1997;226:439-447.

Gubler KD, Gentiello LM, Hassantash Maier RV:
The impact of hypothermia on dilutional coag-
ulopathy. J Trauma 1994;36(6):847-851.

Hirshberg A, Mattox KL: "Damage control" in
trauma surgery. Br J Surg 1993;80:1501-
1502.

Hirshberg A, Mattox KL: Planned reoperation for
severe trauma. Ann Surg 1995;222:3-8.

Hirshberg A, Sheffer N, Barnea O: Computer sim-
ulation of hypothermia during "damage control"
laparotomy. World J Surg 1999;23:960-965.

Hirshberg A, Stein M, Adar R: Reoperation:
Planned and unplanned. Surg Clin North Am
1996;77:897-907.

Hirshberg A, Walden R: Damage control for
abdominal trauma. Surg Clin North Am 1997;
77:813-820.

Hirshberg A, Wall MJJr, Mattox KL: Planned reop-
eration for trauma: A two year experience with
124 consecutive patients. J Trauma 1994;37:365-
369.

Hirshberg A, Wall MJJr, Ramchandani MK, Mattox
KL: Reoperation for bleeding in trauma. Arch
Surg 1993;128:1163-1167.

Husain AK, Khandeparker JMS, Tendolkar AG,
e t al: Temporary intravascular shunts for periph-
eral vascular trauma. J Postgrad Med 1992;38:68-
69.

Johansen K Bandyk D, Thiele B, Hanser STJr: Tem-
porary intraluminal shunts: Resolution of a man-
agement dilemma in complex vascular injuries.
J Trauma 1982;22(5) :395-402.

Jurkovich GF, Greiser WB, Luterman A, Curreri
PW: Hypothermia in trauma victims: An ominous
predictor of survival. J Trauma 1987;27:1019-
1024.

Majeski JA, Gauto A: Management of peripheral
arterial vascular injuries with a Javid shunt. Am
J Surg 1979;138:324-325.

Mattox KL, Hirshberg A: Vascular trauma. In
Haimovici's Vascular Surgery: Principles and
Techniques, 4th ed. Cambridge: Blackwell
Science, Inc, 1996.

Michelson AD, MacGregor H, Barnard MR, et al:
Reversible inhibition of human platelet activa-

tion by hypothermia in vivoand in vitro. Thromb
Haemost 1994;71 (5):633-640.

MorrisJAJr, Eddy VA, Blinman TA, etal: The staged
celiotomy for trauma. Issues in unpacking and
reconstruction. Ann Surg 1993;217:576-586.

Patt A, McCroskey BL, Moore E: Hypothermia-
induced coagulopathies in trauma. Surg Clin
North Am 1988;68:775-785.

Porter JM, Ivatury RR: In search of the optimal end
points of resuscitation in trauma patients: a
review. J Trauma 1998;44:908-914.

PorterJM, Ivatury RR, Nassoura ZE: Extending the
horizons of "damage control" in unstable trauma
patients beyond the abdomen and gastroin-
testinal tract. J Trauma 1997;42(3):559-561.

Pourmoghadam KK, Fogler RJ, Shaftan GW: Lig-
ation: An alternative for control of exsanguina-
tion in major vascular injuries. J Trauma 1997;
43:126-130.

Reed RL II, Johnson TD, Hudson JD, Fischer RP:
The disparity between hypothermic coagulopathy
and clotting studies. J Trauma 1992;33:465-470.

Reilly PM, Rotondo MF, Carpenter JP, et al: Tem-
porary vascular continuity during damage
control: Intraluminal shunting for proximal
superior mesenteric artery injury. J Trauma
1995;39:757-760.

Rohrer MJ, Natale AM: Effect of hypothermia on
the coagulation cascade. Crit Care Med
1992;20:1402-1405.

Rotondo MF, Schwab CW, Gonigal MD, et al:
"Damage control": An approach for improved
survival in exsanguinating penetrating abdom-
inal injury. J Trauma 1993;35:375-383.

Rotondo MF, Zonies DH: The damage control
sequence and underlying logic. Surg Clin North
Am 1997;77:761-777.

Scalea TM, Mann R, Austin R, Hirschowitz M:
Staged procedures for exsanguinating lower
extremity trauma: An extension of a technique
[case report] J Trauma 1994;36:291-293.

Sriussadaporn S, Pak-art R: Temporary intravas-
cular shunt in complex extremity vascular
injuries. J Trauma 2002 Jun;52(6):1129-1133.

Stone HH, Febian TC, Turkleson ML: Wounds of
the portal venous system. World J Surg 1966;6:
335-341.

Stone HH, Strom PR, Mullins RJ: Management of
the major coagulopathy with onset laparotomy.
Ann Surg 1983;197:532-535.

Walker AJ, Mellor SG, Cooper GJ: Experimental
experience with a temporary intraluminal
heparin-bondedpolyure thane arterial shunt. Br
J Surg 1994;81:195-198.

ch08.qxd 4/16/04 3:31PM Page 176

176

II • PRINCIPLES OF OPERATIVE CARE

Wall MJ Jr, Hirshberg A, Mattox KL: Pulmonary
tractotomy with selective vascular ligation for pen-
etrating injuries to the lung. Am J Surg 1994;1 68:
665-669.

Wall MJ Jr, Soltero E: Damage control for thoracic
injuries. Surg Clin North Am 1997;77:863-878.

Watts DD, Trask A, Soeken K, et al: Hypothermic
coagulopathy in trauma: Effect of varying levels
of hypothermia on enzyme speed, platelet
function, and fibrinolytic activity. J Trauma
1998:44:846-854.

chlO.qxd 4/16/04 3:34PM Page 207

Endovascular Grafts for
Traumatic Vascular Lesions

NICHOLAS J. GARGIULO, III
TAKAO OHKI
NEAL S. CAYNE
FRANK J. VEITH

O INTRODUCTION

O COIL EMBOLIZATION, INTRAVASCULAR STENTS, AND OTHER
ENDOVASCULAR TECHNIQUES

O ENDOVASCULAR GRAFTS FOR ARTERIAL TRAUMA: BACKGROUND

The Montefiore Experience with Endovascular Grafts for
Arterial Trauma

Technique and Devices

Results
O SUMMARY
O ACKNOWLEDGMENTS

INTRODUCTION

The advent of endovascular grafting to
treat abdominal aortic aneurysms (AAAs)
by Parodi, Palmaz, and Barone (1991) has
expanded to include arterial occlusive disease,
occluded grafts, peripheral aneurysms, and
traumatic arterial lesions (Marin and col-
leagues, 1995a, 1995b; Parodi, 1995) . The past

decade has marked a new enthusiasm for the
endovascular repair of AAAs. However, the
value and long-term outcome have yet to be
proven. Endoleaks, arterial injury, and late
graft deterioration continue to complicate
endovascular graft repair of AAAs. Since stan-
dard open aneurysm repair remains a safe and
reliable procedure with good long-term out-
comes, the role of endovascular graft repair
in low-risk patients remains to be determined.

207

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208

III • DIAGNOSTIC AND INTERVENTIONAL RADIOLOGY

On the other hand, the role of endovascu-
lar grafts for traumatic arterial injuries appears
to be more easily defensible, especially when
large central vessels are involved. Vascular
trauma within the thorax or abdomen com-
plicates the surgical approach to a vascular
injury. Distorted anatomy due to a large
hematoma or false aneurysm and venous
hypertension secondary to an arteriovenous
fistula are just a few of the problems encoun-
tered during an open repair of injured vessels.
Endovascular repair is more appealing
because it can be performed from a remote
site and does not require direct surgical expo-
sure of the injury site, thus reducing the mor-
bidity and mortality rates that accompany
open repair. Furthermore, endovascular
repair is most beneficial for those patients who
are critically ill from other injuries or medical
comorbidities.

The main endovascular techniques used
in the treatment of vascular trauma include
coil embolization, intravascular stents, and
endovascular stented grafts. Traumatic vas-
cular lesions usually have normal, healthy,
proximal, and distal arterial segments or graft
fixation zones for endovascular graft deploy-
ment. This is in contrast to the complex necks
and iliac tortuosity of AAAs. As a result, high
technical success rates and low rates of endo-
graft migration or leakage have been reported
after endovascular grafting for traumatic vas-
cular lesions.

This chapter describes endovascular tech-
niques that may prove helpful in vascular
trauma and reviews our experience with
endovascular grafts for traumatic lesions at
Montefiore Medical Center in New York. We
also discuss the role of endovascular grafts for
thoracic aortic vascular injuries.

COIL EMBOLIZATION,
INTRAVASCULAR STENTS, AND
OTHER ENDOVASCULAR
TECHNIQUES

Embolization coils have been used to treat
relatively small traumatic arteriovenous fistu-
las and pseudoaneurysms involving nones-
sential vessels, such as a lumbar artery, the

internal mammary artery, or the branches of
the hypogastric or deep femoral arteries
(Rosch, Dotter, and Brown, 1972; Panetta and
colleagues, 1985) . Long-term follow-up results
of the use of these coil-treated lesions have
proven favorable. Placement of intravascular
stents is useful for the repair of intimal flaps.
Because of their porous nature, however,
uncovered stents are not indicated for treat-
ing arteriovenous fistulas or pseudoaneurysms
of large vessels. Although coils and stents
have proved to be effective in selected cases,
most patients with vascular trauma are not
amenable to such therapy.

A novel method for obtaining intraluminal
balloon control of arteries in difficult cir-
cumstances has been previously described by
our group (Veith, Sanchez, and Ohki, 1998).
This technique is particularly useful when
bleeding, scarring, or infection makes dis-
section of proximal arteries difficult or dan-
gerous. Through an arterial puncture distal
to the site where proximal control is required,
an 18-gauge needle is inserted into a normal
artery. A guidewire is inserted through the
needle. Over the guidewire, a 6- or 7-Fr hemo-
static sheath and dilator is inserted. Under
fluoroscopic guidance, a standard balloon
catheter is passed through the hemostatic
sheath. Radiopaque contrast is then injected
to confirm optimal placement of the balloon
catheter for proximal occlusion within the
arterial tree. The sheath may then be
retracted, and the balloon inflated until arte-
rial inflow is occluded. Alternatively, double-
lumen balloon catheters may be passed over
a guidewire and angiographic techniques can
be used to facilitate proximal balloon control.

ENDOVASCULAR GRAFTS FOR
ARTERIAL TRAUMA:
BACKGROUND

Endovascular grafts have significantly
extended the potential of endovascular
therapy for vascular trauma. The concept of
endovascular grafting for traumatic arterial
lesions was initially proposed by Dotter (1969).
Volodos and colleagues (1991) were the first
to clinically apply this technology by placing

chlO.qxd 4/16/04 3:34PM Page 209

10 • ENDOVASCULAR GRAFTS FOR TRAUMATIC VASCULAR LESIONS

209

III!

III

■ FIGURE 10-1

Endovascular stented graft. A
Palmaz stent is sewn to an
expanded PTFE graft. (From
Ohki T, Veith FJ, Marin ML, et
al: Endovascular approaches
for traumatic arterial lesions.
Semin Vase Surg 1997;10:272-
285.) ■

a Dacron graft and a self-expanding stent to
treat a thoracic aortic pseudoaneurysm in
1986.

Endovascular grafts have been used to treat
almost every kind of injury at various locations
in the body. Some patients treated with
endovascular grafts have been hemodynami-
cally stable. However, some of these grafts have
also been used to treat life-threatening acute
hemorrhage (Becker and colleagues, 1991;
Patel and colleagues, 1996). The types of
devices that have been reported are pre-
dominantly a combination of a Palmaz stent
and an expanded PTFE (ePTFE) graft (Fig.
10-1) (Marin and colleagues, 1993, 1994;
Becker and colleagues, 1995; Terry and col-
leagues, 1995; Zajiko and colleagues, 1995;
Gomez-Jorge and colleagues, 1996; Criado
and colleagues, 1997; Dorros and Joseph,
1997) . The use of a vein graft in combination

with a Palmaz stent has also been reported,
since the traumatized field is often contami-
nated. More recently, industry made devices
such as the Corvita endovascular graft, the
AneuRx graft and the Wallstent graft have
become commercially available in the United
States. AneuRx grafts have been approved by
the Food and Drug Administration for the
treatment of AAAs, and the Wallstent for
obstructive biliary lesions. Components of the
AneuRx include the bifurcated graft and the
proximal and distal extension cuffs. Though
not approved for the use in traumatic lesions,
these grafts have been used in the "off-label"
fashion.

The lesion, location, characteristics, site of
arterial access, technical success rate, and the
outcome of endovascular grafts in the treat-
ment of vascular trauma are summarized in
Table 10-1. These results have been encour-

TABLE 10-1

ENDOVASCULAR GRAFTS FOR ARTERIAL TRAUMA

Type

Combination of Palmaz
Stent and Various Grafts

Cragg Endopro

Corvita Graft

Stent Palmaz stent Nitinol Self-expanding braided stent

Graft material PTFE Dacron Vein Silicone Ultrathin woven polyester Polycarbonate urethane

fabric

Arterial access 1 or 2 2 2 1 or 2 2 2

1, open arteriotomy; 2, percutaneous.

From Ohki T, Marin ML, Veith FJ: Use of endovascular grafts to treat non-aneurysmal arterial disease. Ann Vase Surg

1997:11:200-205.

chlO.qxd 4/16/04 3:34PM Page 210

210

III • DIAGNOSTIC AND INTERVENTIONAL RADIOLOGY

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10 • ENDOVASCULAR GRAFTS FOR TRAUMATIC VASCULAR LESIONS 211

■ FIGURE 10-2

A, Schematic drawing of an endovascular stented graft or covered stent. A segment of expanded
PTFE is attached to a Palmaz stent (St) using two 5-0 Prolene U stitches (S). B, Schematic drawing
of a double-stent endovascular stented graft. The proximal stent (St) is sutured to the graft as
described in (A). The distal end of the graft is marked with gold markers (G) for visualization under
the fluoroscope. C, The stent graft (SG) is mounted on an angioplasty balloon (B) and placed into a
sheath (C) before insertion. Note the presence of a dilator tip (D) at the end of the balloon catheter,
which provides a smooth taper within the catheter. W, guidewire. (From Ohki T, Veith FJ, Marin ML,
et al: Endovascular approaches for traumatic arterial lesions. Semin Vase Surg 1997;10:272-285.) ■

aging with a high technical success rate (94%
to 100%) and a complication rate of 0% to
7% (Table 10-2), especially when we consider
the difficulties that could be encountered in
treating these lesions by a direct surgical repair.
In addition, the minimal invasiveness and
the potential for cost-effectiveness of such
endovascular techniques are apparent from
the short length of stay (3.3 to 3.5 days) (Table
10-2) . Most endovascular grafts are deployed
in nonatherosclerotic central vessels of a
large caliber and have excellent durability.
Mean follow-up at 16 months revealed excel-
lent mid-term patency rates ranging from 85 %
to 100% depending on where deployment
occurred.

The Montefiore Experience
with Endovascular Grafts for
Arterial Trauma

TECHNIQUE AND DEVICES

At Montefiore Medical Center, we have

mainly used the Palmaz stent (Cordis
[Johnson &Johnson Company, Warren, NJ] )
in combination with a thin-walled ePTFE graft
(Fig. 10-1) covering to perform arterial repairs
of pseudoaneurysms and arteriovenous fistu-
las (Marin and colleagues, 1993, 1994, 1995a) .
Depending on the length of the lesion, either
a single stent device or a doubly stented device
was used. The stents varied between 2 and
3 cm in length (Palmaz P-204, 294, 308) and
were fixed inside 6 mm Gore-Tex grafts (W.L.
Gore and Associates, Flagstaff, Ariz) by two U
stitches. The stented graft was then mounted
on a balloon angioplasty catheter, which had
a tapered dilator tip firmly attached to its end
(Fig. 10-2). The entire device was contained
within a 10- to 12-Fr delivery system for over-
the-wire insertion either percutaneously or
through an open arteriotomy.

Alternative devices included the Corvita
stent graft (Corvita Corporation, Miami, Fla) ,
and the Wallgraft, both of which are fabricated
from a self-expanding stent or braided wire.
The Corvita stent graft is covered with poly-
carbonate elastomer fibers, and the Wallgraft
is covered with Dacron. The Corvita stent graft

chlO.qxd 4/16/04 3:34PM Page 212

212

III • DIAGNOSTIC AND INTERVENTIONAL RADIOLOGY

may be cut to the desired length in the
operating room using a wire-cutting scissors
and then loaded into a specially designed
delivery sheath. This sheath has a central
"pusher" catheter, which is used for main-
taining the graft in position while the outer
sheath is being retrieved. TheWallgraft comes
in various diameters up to 14 mm and lengths
up to 7 cm.

RESULTS

Each procedure was performed in the
operating room under fluoroscopic (OEC
9800, OEC/GE, Salt Lake City, Utah; Philips,
BV 212, Netherlands) guidance. Most cases
were performed under local or epidural anes-
thesia with two cases requiring general anes-
thesia. A total of 17 stented grafts were used
to treat 17 patients with traumatic arterial
lesions (Table 10-3). The etiology for these
lesions is described in Table 10-3, with the
majority comprising gunshot wounds (Figs.
10-3 and 10-4) and iatrogenic injuries (Figs.
10-5 and 10-6).

All injuries except for one were associated
with an adjacent pseudoaneurysm (Fig. 10-5) .
Five patients had an arteriovenous fistula (Fig.
10-6) , and eight patients had other associated
injuries (Table 10-3).

Procedural complications were limited
to one distal embolus, which was treated
with suction embolectomy, and one wound
hematoma, which resolved without further
intervention. Graftpatencywas 100% with no
early or late graft occlusions (mean follow-up
was 30 months [range, 6 to 46 months]).

One patient with a left axillary subclavian
stent graft developed compression of the stent
at 12 months and was treated with balloon
angioplasty. This recurred 3 months later but
did not require any intervention. At 3-year
follow-up, the graft was patent. A second
patient developed stenosis at either end of his
stent graft and was successfully treated with
additional balloon dilation and Palmaz stent
placement (Fig. 10-4). A third patient with
an axillary pseudoaneurysm repaired with a
stent graft required a vein patch to close a small
brachial artery insertion site.

Immediate repair of blunt thoracic aortic

injuries to prevent rupture of the contained
hematoma as previously described may no
longer be necessary based on studies by Camp
and Shackford (1997) and Maggisano and col-
leagues (1995). These authors suggest that
delayed repair of hemodynamically stable tho-
racic aortic injuries reduces morbidity and
mortality. Delayed repair allows the trauma
team to surgically optimize the multi-injured
patient before a major surgical insult. These
studies have significantly influenced the role
of endovascular grafting in the treatment
of thoracic aortic injuries. Myriad unique
endovascular techniques and grafts have been
employed and reported to treat these injuries
(White and colleagues, 1997; Lobato and col-
leagues, 2000; Fontaine and colleagues, 2001;
Ruchat and colleagues, 2001).

Endovascular grafting has been employed
in blunt and penetrating injuries of the
abdominal aorta (White and colleagues, 1997;
Fontaine and colleagues, 2001 ) . These include
successful exclusion of a posterior aortic
pseudoaneurysm between the superior
mesenteric artery and the right renal artery
following a gunshot wound. A Cooley VeriSoft
vascular graft attached to the outer surface of
an extra-large Palmaz stent was successfully
deployed across the aortic pseudoaneurysm
3 weeks after the initial injury.

In addition to these homemade devices,
industry-made devices recently became avail-
able. These include the Talent thoracic
endovascular graft (World Medical Corpora-
tion, Medtronic) , the Thoracic Excluder graft
(W.L. Gore, Flagstaff, Ariz) and the AneuRx
graft (Fontaine and colleagues, 2001; Ruchat
and colleagues, 2001). Neither of these has
been approved by the FDA for commercial-
ization in the United States; however, some
investigators have successfully used these
grafts to treat life-threatening thoracic aortic
injuries on a compassionate basis. These
industry-made devices, especially the Excluder
graft, are much more flexible and have a lower
insertion profile.

Delayed repair has been reported from 1
week to a mean of 5.4 months after the initial
accident. There has been no evidence of
endoleak or rupture at approximately 1-year
follow-up. Furthermore, although the number

Text continued on p. 218

chlO.qxd 4/16/04 3:34PM Page 213

10 • ENDOVASCULAR GRAFTS FOR TRAUMATIC VASCULAR LESIONS

213

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214

III • DIAGNOSTIC AND INTERVENTIONAL RADIOLOGY

UK\I III \1

■ FIGURE 10-3

Angiographic images of a
patient who sustained a
gunshot wound to the right
chest. A, An angiogram
performed via a femoral artery
puncture shows occlusion of
the right subclavian artery and
active bleeding. B, An
occlusion balloon was placed
to achieve hemostasis. C,
Following hemostasis, the
patient was taken to the
operating room. A guidewire
was successfully passed
across the injured artery and
was repaired by the insertion of
a stented graft of
polytetrafluoroethylene
(expanded PTFE and Palmaz
stent). (From Patel AV, Marin
ML, Veith FJ, et al:
Endovascular graft repair of
penetrating subclavian artery
injuries. J Endovasc Surg
1996;3:382-388.) ■

■^ ^^H

OCCLUSION
BALLOON

chlO.qxd 4/16/04 3:34PM Page 215

10 • ENDOVASCULAR GRAFTS FOR TRAUMATIC VASCULAR LESIONS

215

■ FIGURE 10-4

The patient is a 19-year-old man status post a gunshot wound to the chest that traversed the
mediastinum from right to left, injuring his esophagus, trachea, and left subclavian artery. A, The
initial angiogram shows occlusion of the left vertebral artery and a small pseudoaneurysm (p) at
that site. He was transferred to our institution for endovascular treatment following placement of a
covered esophageal stent to repair his tracheoesophageal fistula. B, A Corvita endoluminal graft
was placed across the lesion and there was excellent flow through it. Continued

chlO.qxd 4/16/04 3:34PM Page 216

216 III • DIAGNOSTIC AND INTERVENTIONAL RADIOLOGY

■ FIGURE 10-4

cont'd C, A plain x-ray film demonstrates the esophageal stent and the Corvita graft in the left
subclavian artery. D, At 4 months after graft insertion, his left radial pulse was diminished, although
he remained asymptomatic. An angiogram was taken that revealed intimal hyperplasia throughout
the graft, more prominent at both ends of the graft (arrows). These lesions were angioplastied and a
Palmaz stent was placed. After the procedure, the patient had a strong radial pulse. (From Ohki T,
Veith FJ, Kraas C, et al: Endovascular therapy for upper extremity injury. Semin Vase Surg
1998;11:106-115.) ■

chlO.qxd 4/16/04 3:34PM Page 217

10 • ENDOVASCULAR GRAFTS FOR TRAUMATIC VASCULAR LESIONS 217

■ FIGURE 10-5

A, This arteriogram shows a large pseudoaneurysm of the subclavian artery (arrow) just distal to the
right vertebral artery that occurred after an attempted subclavian vein catheter insertion. B, Following
stented graft (expanded PTFE and Palmaz stent) placement through the right brachial artery, the
pseudoaneurysm was excluded. Vertebral artery flow was maintained (V). (From Marin ML, Veith FJ,
Panetta TF, et al: Transluminal^ placed endovascular stented graft repair for arterial trauma. J Vase
Surg 1994;20:466-473.) ■

chlO.qxd 4/16/04 3:34PM Page 218

218

III • DIAGNOSTIC AND INTERVENTIONAL RADIOLOGY

■ FIGURE 10-6

A, Preoperative angiogram of an iatrogenic arteriovenous fistula (AVF) following lumbar disk
surgery. The patient presented with severe swelling of the left lower extremity. The left common iliac
vein (C) is dilated secondary to the fistula. B, Completion angiogram. A PTFE graft was fixed
proximally (p) and distally (d) with a Palmaz stent to exclude the fistula from the arterial circulation.
Coil embolization of the internal iliac artery was performed before stent-graft insertion. (From Ohki T,
Veith FJ: Endovascular techniques in the treatment of penetrating arterial trauma. In Yao JST,
Pearce WH [eds]. Practical Vascular Surgery, 1st ed. Stamford, Conn, Appleton & Lange, 1999,
pp 409-423.) ■

of reported cases is small, there has been no
mention of postoperative paraplegia. These
limited experiences suggest that endovascu-
lar graft techniques will be better than more
traditional open techniques of thoracic aortic
repair requiring either bypass or the clamp-
and-sew technique, which report postopera-
tive paraplegia rates of 4.5% to 16.4%,
respectively (Fabian and colleagues, 1997).

SUMMARY

Endovascular grafting for traumatic arterial
lesions has become an additional tool for
the vascular surgeon. Complex open surgical
repair of thoracic or intra-abdominal vascu-

lar injuries may be approached with minimally
invasive endovascular techniques. Large
hematomas, false aneurysms, and arteriove-
nous fistulas that often obscure the open
surgical field have minimal impact on
endovascular repair. This can be performed
by accessing vascular lesions from remote sites
so that embolization coils, stents, or endovas-
cular grafts may be deployed.

Few vascular injuries may be amenable
to coil embolization or stent placement.
However, endovascular grafts have greatly
expanded endovascular therapy for vascular
trauma. These grafts have been used to treat
myriad vascular injuries at various locations
in the body.

Endovascular grafts have a low morbidity
rate, high success rate, reduced anesthetic

chlO.qxd 4/16/04 3:34PM Page 219

10 • ENDOVASCULAR GRAFTS FOR TRAUMATIC VASCULAR LESIONS

219

requirements, and a minimal dissection
requirement in the traumatized field. These
qualities are particularly advantageous for
patients with central arteriovenous fistulas or
false aneurysms, especially those critically ill
from other coexisting injuries or medical
comorbidities.

Endovascular grafts and techniques will con-
tinue to evolve and complement traditional
open techniques in vascular trauma. Future
development of smaller delivery systems,
better endografts, operating rooms equipped
with improved angiographic imaging systems,
and a supply of endovascular equipment will
increasingly help vascular surgeons of the
future to manage patients with vascular trauma
better.

ACKNOWLEDGMENTS

This work was supported by grants from the
U.S. Public Health Service (HL 02990), the
Manning Foundation, the Anna S. Brown
Trust, the New York Institute for Vascular
Studies, and the William J. von Liebig
Foundation.

REFERENCES

Becker GJ, Benenati JF, Zemel G, et al: Percuta-
neous placement of a balloon-expandable intra-
luminal graft for life-threatening subclavian
arterial hemorrhage. JVTR 1991;2:225-229.

Becker GJ, Katzen BT, Benenati JF, et al: Endografts
for the treatmen t of aneurysm and traumatic vas-
cular lesions: MVI experience. J Endovasc Surg
1995;2:380-382.

Brandt MM, Kazanjian S, Wahl WL: The utility of
endovascular stents in the treatment of blunt arte-
rial injuries. J Trauma 2001;51(5):901-905.

Camp PC, Shackford SR: Outcome after blunt trau-
matic thoracic aortic laceration: Identification
of a high-risk cohort. Western Trauma Associa-
tion Multicenter Study Group. J Trauma 1997;
43:413-422.

Criado E, Marston WA, Ligush J, et al: Endovas-
cular repair of peripheral aneurysms, pseudo-
aneurysms, and arteriovenous fistulas. Ann Vase
Surg 1997;11:256-263.

Dorros G, Joseph G: Closure of a popliteal arteri-
ovenous fistula using an autologous vein-covered

Palmaz stent. J Endovasc Surg 1995;2:177-
181.

Dotter CT: Transluminally-placed coilspring endar-
terial tube grafts: Long-term patency in canine
popliteal artery. Invest Radiol 1969;4:329-332.

Fabian TC, Richardson JD, Croce MA, et al:
Prospective study of blunt aortic injury: Multi-
center trial of the American Association for the
Surgery of Trauma. J Trauma 1997;42:374-380.

Fontaine AB, Nicholls SC, Borsa JJ, et al: Seat belt
aorta: Endovascular management with a stent-
graft. J Endovasc Ther 2001;8:83-86.

Gomez-Jorge JT, Guerra JJ, Scagnelli T, et al:
Endovascular management of a traumatic sub-
clavian arteriovenous fistula. JVIR 1996;7:599-
602.

Lobato AC, Quick RC, Phillips B, et al: Immediate
endovascular repair for descending thoracic
aortic transection secondary to blunt trauma. J
Endovasc Ther 2000;7:16-20.

Maggisano R, Nathens A, Alexandrova NA, et al:
Traumatic rupture of the thoracic aorta: Should
one always operate immediately? Ann Vase Surg
1995;9:44-52.

Marin ML, Veith FJ, Cynamon J, et al: Initial expe-
rience with transluminally placed endovascular
grafts for the treatment of complex vascular
lesions. Ann Surg 1995a;222:449-469.

Marin ML, Veith FJ, Lyon RT, et al: Transfemoral
endovascular repair of iliac artery aneurysms.
Am J Surg 1995b;170:l79-182.

Marin ML, Veith FJ, PanettaTF, etal: Percutaneous
transfemoral insertion of a stented graft to repair
a traumatic femoral arteriovenous fistula. J Vase
Surg 1993;18:229-302.

Marin ML, Veith FJ, Panetta TF, et al: Translumi-
nally placed endovascular stented graft repair
for arterial trauma. J Vase Surg 1994;20:466-473.

Marty-Ane CH, Berthet JP, Branchereau P, et al:
Endovascular repair for acute traumatic rupture
of the thoracic aorta. Ann Thorac Surg 2003
Jun;75(6):1803-1807.

Orend KH, Pamler R, Kapfer X, et al: Endovascu-
lar repair of traumatic descending aortic tran-
section. JEndovasc Ther 2002 Oct;9 (5) :573-578.

Panetta TF, Sclafani SJA, Goldstein AS, et al: Per-
cutaneous transcatheter embolization for arte-
rial trauma. J Vase Surg 1985;2:54-64.

ParodiJC: Endovascular repair of abdominal aortic
aneurysms and other arterial lesions. J Vase Surg
1995;21:549-557.

ParodiJC, Palmaz JC, Barone HD: Transfemoral
intraluminal graft implantation for abdominal
aortic aneurysms. Ann Vase Surg 1991 ;5:491-499.

chlO.qxd 4/16/04 3:34PM Page 220

220

III • DIAGNOSTIC AND INTERVENTIONAL RADIOLOGY

Patel AV, Marin ML, Veith FJ, et al: Endovascular
graft repair of penetrating subclavian artery
injuries. J Endovasc Surg 1996;3:382-388.

Rosch J, Dotter CT, Brown MJ: Selective arterial
embolization. Anew method for control of acute
gastrointestinal bleeding. Radiology 1972;102:
303-306.

Ruchat P, Capasso P, Chollet-Rivier M, et al:
Endovascular treatment of aortic rupture by
bluntchest trauma.J Cardiovasc Surg 2001 ;42:77-
81.

Terry PJ, Houser EE, Rivera FJ, et al: Percutaneous
aortic stent placement for life-threatening aortic
rupture due to metastatic germ cell tumor. J Urol
1995;153:1631-1634.

Thompson CS, Rodriguez JA, Ramaiah VG, et al:
Acute traumatic rupture of the thoracic aorta
treated with endoluminal stent grafts. J Trauma
2002 Jun;52(6) :1 1 73-1 1 77.

Veith FJ, Sanchez LA, Ohki T: Technique for obtain-
ing proximal intraluminal control when arter-
ies are inaccessible or unclampable because of
disease or calcification. J Vase Surg 1998;27:582-
586.

Volodos NL, Karpovich IP, Troyan VI, et al: Clini-
cal experience of the use of self-fixing synthetic
prostheses for remote endoprosthetics of the tho-
racic and the abdominal aorta and iliac arteries
through the femoral artery and as intraopera-
tive endoprosthesis for aorta reconstruction . Vasa
1991;33(suppl):93-95.

White R, Donayre C, Walot I, e t al: Endograft repair
of an aortic pseudoaneurysm following gunshot
wound injury: Impact of imaging on diagnosis
and planning of intervention. J Endovasc Ther
1997;4:344-351.

Zajiko AB, Little AF, Steed DL, et al: Endovascular
stent-graft repair of common iliac artery-to-
inferior vena cava fistula. JVIR 1995;6:803-806.

chll.qxd 4/16/04 3:36 PM Page 223

Penetrating Cervical
Vascular Injury

RAO R. IVATURY
MICHAEL C. STONER

O SURGICAL ANATOMY

O INCIDENCE AND ETIOLOGY OF CIVILIAN INJURIES

O INCIDENCE AND ETIOLOGY OF MILITARY INJURIES

O PATHOLOGY

O INITIAL EVALUATION AND MANAGEMENT

O DIAGNOSIS OF VASCULAR INJURIES: ZONES OF NECK AND THE ROLE
OF PHYSICAL EXAMINATION

Angiography

Color Flow Doppler

Computed Tomographic Angiography and Magnetic Resonance
Angiography

O TREATMENT

Innominate and Subclavian Vessel Injuries

Carotid Artery Injuries

Surgical treatment

Surgical Treatment of Carotid Artery Injury in Patients with
Neurologic Deficits

Vertebral Artery Injuries

Venous Injuries

O SUMMARY

223

chll.qxd 4/16/04 3:36 PM Page 224

224

IV • SPECIFIC VASCULAR INJURIES

Injuries to the arteries of the neck are rel-
atively uncommon but are of paramount
importance to the trauma and vascular
surgeon because of their end organ. The inci-
dence of arterial injury in patients with pen-
etrating neck wounds is 12% to 13%, whereas
the incidence of venous injury is 18% to 19%
(Asensio and colleagues, 1991, 2001). Mor-
tality attributable to cervical vascular injury
has been cited to be as high as 11%. Because
of the relatively low overall incidence, it is dif-
ficult for any one surgeon to gain extensive
experience in the repair and management of
these injuries. This underscores the impor-
tance of multicenter and registry reviews when
determining the proper treatment of these
trauma patients. Most of these injuries, and
certainly the most significant, are carotid
artery injuries.

Ambrose Pare is credited with the first
recorded attempt to surgically treat a carotid
artery injury more than 400years ago (Watson
and Silverstone, 1939) . Pare ligated the carotid
artery of a French soldier, saving his life but
leaving him with a profound neurologic
deficit consisting of left-sided hemiplegia
and aphasia. Mr. Flemming (1817), 250
years later, successfully ligated the common
carotid artery of a patient aboard the H.M.S.
Tonnant. The operation was successful in
controlling hemorrhage without neurologic
consequences.

Simple ligation dominated surgical decision
until the last 50 years. The devastating
outcome of stroke or death following ligation
of the carotid artery led surgeons to adopt
a conservative approach to these injuries.
Surgery was proposed for those patients with
severe hemorrhage, enlarging hematoma,
airway compromise, or pseudoaneurysm.

As with most penetrating trauma, military
conflicts have provided the bulk of informa-
tion about penetrating carotid artery injuries.
In World War I, Makins (1919) reported that
one third of 128 cases of carotid artery injury
treated by ligation resulted in irreversible neu-
rologic deficit. During World War II and the
Korean conflict, there were a handful of
reports of carotid artery repair (Lawrence and
colleagues, 1948; Huhges, 1958).

The Vietnam conflict provided a wealth
of information about carotid artery trauma.

By this time, improved diagnosis, vascular
operative techniques, and instrumentation
yielded significantly improved morbidity and
mortality. The Vietnam Vascular Registry, a
massive project, was instrumental in shaping
the modern approach to cervical vascular
trauma.

The unfortunate rise in civilian penetrat-
ing trauma has been documented in various
series. Several factors have led to improved
management, probably the most significant
of which is expeditious intervention. Fogel-
man and Stewart (1956) demonstrated a
35% mortality rate in patients with delayed
surgical exploration versus 6% for those
undergoing immediate operation. The
authors advocated prompt exploration of all
wounds penetrating the platysma, and this
soon became a standard of care. This aggres-
sive approach led to a high rate of negative
explorations and caused many surgeons to
reconsider the indications for operation. This
controversy continues today and is outlined
in further detail within this chapter.

SURGICAL ANATOMY

The key landmark to exploration of the neck
is the sternocleidomastoid muscle, which
defines the anterior and posterior triangles
and is invested by the deep cervical fascia. Inci-
sion over the anterior aspect of the muscle
is the preferred route of exposure for most
carotid injuries. Thoracic and cranial exten-
sions are easily adapted to this incision as
warranted.

The most superficial layer of the neck mus-
culature is the platysma, a thin confluence of
muscle arising from the upper portion of pec-
torals and inserting onto the skin and subcu-
taneous tissue of the lower face. As described
earlier in this chapter, the platysma is an impor-
tant landmark of historical significance defin-
ing superficial from deep penetrating cervical
wounds. The external jugular vein is the only
vascular structure between this layer and the
deep cervical fascia.

Emerging from the jugular foramen at
the base of the skull, the internal jugular vein
courses downward within the carotid sheath,

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11 • PENETRATING CERVICAL VASCULAR INJURY

225

along with the carotid artery and vagus nerve.
Each component of the carotid sheath is encir-
cled in its own connective tissue investment
throughout the cervical region. Because of
the considerable distensibility of these con-
nective tissue layers, the carotid sheath tends
to be attenuated over the jugular vein. The
internal jugular ends at the clavicle where
it joins with the subclavian vein to form the
brachiocephalic vein. On the left side, an
important posterior anatomic relationship is
the thoracic duct, which eventually inserts at
the confluence of the jugular and subclavian
veins.

In most patients, the right carotid arises
from the brachiocephalic artery, and the
left from the aortic arch. Each artery passes
upward to the level of the thyroid cartilage
and divides into internal and external
branches. Prior to this point, the common
carotid is without branches except for the rare
anomalous superior thyroid artery or ascend-
ing pharyngeal branch. At the bifurcation, the
artery dilates, and this region is known as the
carotid bulb. The carotid bifurcation can be
difficult to identify in the presence of an
extensive hematoma. An important land-
mark in identifying the bifurcation is the loca-
tion of the facial vein and the medial portion
of the ansa cervicalis. At their origin, the
common carotid arteries are relatively close,
separated only by the trachea. As they ascend,
thyroid, larynx, and then pharynx intervene
between the two arteries. Sternocleidomastoid
covers the common carotid artery, the inter-
nal carotid artery (ICA) , and the external
carotid artery throughout their course except
for a small window between its anterior border
and digastric muscle at the base of the skull
(Fig. 11-1).

The ICA is typically larger than the exter-
nal and supplies the anterior part of the brain
and the eye and sends branches to the face
and nose. At the origin of the ICA is a pressor
receptor, the carotid sinus, stimulation of
which results in hypotension and bradycardia.
Along the posterior aspect of the artery runs
the sympathetic trunk, and the spinal mus-
culature behind that. The esophagus is medial
and is of paramount importance when assess-
ing for digestive injury. The hypoglossal nerve
courses over the anterolateral aspect and is

an important surgical landmark. A series of
important relationships are essential in dif-
ferentiating the ICA from the external carotid
artery: (1) In the vast majority of patients, the
ICA has no cervical branches; (2) the ICA
usually lies posterolateral to external carotid;
and (3) asitascends, the ICA moves to a medial
position relative to external carotid artery
(Fig. 11-2).

The external carotid artery, termed exter-
nal because if its extracranial distribution,
extends upward to the mandibular neck
where it divides into its two terminal branches:
the superficial temporal artery and the max-
illary artery. The main trunk of the external
carotid quickly gives rise to a series of branches:
superior thyroid, ascending pharyngeal,
lingual, facial, occipital, and posterior auric-
ular. Of note, a portion of the external carotid
is encompassed by the parotid salivary gland,
an important consideration in exposure and
repair.

The vertebral artery is the first and largest
branches of the subclavian artery. It ascends
behind the common carotid artery to enter
the vertebral foramen at the transverse process
of the sixth cervical vertebrae. Before enter-
ing the base of the skull, the vertebral artery
passes behind the lateral aspect of the atlas,
in an almost horizontal plane. Once entering
the skull through the foramen magnum, the
paired vertebral arteries converge, giving rise
to the basilar artery and proceed to the circle
of Willis as their termination (Fig. 11-3).

It is important for the surgeon to keep in
mind the many potential collaterals between
the internal and external system, because
these collaterals may be able to sustain blood
flow after ICA or external carotid artery injury.
One significant collateral is between the
ophthalmic branch of internal carotid and
the facial branch of external carotid artery.
Second, the thyrocervical trunk rises up the
neck between thejugular vein and the antero-
medial boarder of sternocleidomastoid. It is
a potential source of collateral flow to the
external carotid artery. Perhaps the most
important and often misrepresented collat-
eral circulation is the circle of Willis (see Fig.
11-3). Historical autopsy data suggest that
up to one half of patients will have "nonstan-
dard" circulation here (Puchades-Orts and

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226

IV • SPECIFIC VASCULAR INJURIES

Post, communicating a

Post, cerebral a.
Int. carotid a
Basilar a
Vertebral aa

Superf. temporal a.
Basilar a

Int. carotid a

Occipital a

Ascend,
pharyngeal a.

Vertebral a

Ext. carotid a.
Facial a.
gual a.
Superior thyroid a.

Common carotid a.

■ FIGURE 11-1

Except for the intrathoracic portion of the left common carotid artery, the cervical anatomy of the
carotid arteries and the vertebral arteries is bilaterally similar. ■

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11 • PENETRATING CERVICAL VASCULAR INJURY

227

Rights were not granted to include this figure in electronic media.
Please refer to the printed publication.

■ FIGURE 1 1-2

The close proximity of important contiguous structures, such as the internal jugular vein and the
vagus nerve, is emphasized. The cross section shows the contents of the carotid sheath and the
associated surrounding structures. ■

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228

IV • SPECIFIC VASCULAR INJURIES

Ant. cerebral a.
Ant. communicating a.

Middle cerebral a.

Post communicating a

Post, cerebral a

=k Basilar a.

m FIGURE 11-3

The standard model of the circle of Willis.
Although normal variations within the circle are
common, hypoplasia of various segments may
be particularly significant with interruption of
either internal carotid artery. This may result in
an inadequate collateral flow. (From Strandness
DE Jr. Collateral Circulation in Clinical Surgery.
Philadelphia: WB Saunders, 1969.) ■

colleagues, 1976). Because of the redun-
dancy, hypoplasia of an individual component
of the circle is rarely a problem, unless carotid
flow is interrupted and the segments of the
circle are unable to sustain adequate flow. A
recent magnetic resonance angiographic
study supports this high rate of variance
(Krabbe-Hartkamp and colleagues, 1998) .
The authors noted that only 42% of randomly
selected adults had complete circles, with pos-
terior variations being the most common.
Other minor collateral circulations exist such
as vertebral to vertebral muscular branches,
external carotid to external carotid, and ver-
tebral occipital branches.

INCIDENCE AND ETIOLOGY OF
CIVILIAN INJURIES

The incidence of carotid artery injuries in
civilian series ranges from 12% to 17% of
total penetrating neck injuries. Information
about the precise anatomic distribution of

these injuries is sometimes limited by the
presentation of data within a particular study
and the lack of a standardized grading system
and registry database specific for vascular
injury. Recently, Mittal and colleagues (2000)
have suggested a grading system to standard-
ize the assessment and reporting of cervical
vascular injuries. Compared to military
injuries, civilian carotid injury tends to be
blunt or stabbing. This must be considered
when comparing outcome data between these
groups.

INCIDENCE AND ETIOLOGY OF
MILITARY INJURIES

Historic military data report that carotid
artery injuries represent approximately 5 % of
all arterial injuries. The most recent and exten-
sive database for modern military traumatic
cervical vascular injury is the Vietnam Vascu-
lar Registry (Rich and colleagues, 1970) . Data
from this experience indicate that fragment
wounds (projectiles from explosive ordinance,
shrapnel, or debris) accountfor the vastmajor-
ity of wounds. Gunshot wounds were found
to be much less common (especially as com-
pared to civilian trauma) because military
weaponry tends to be of high velocity and
therefore more likely to be fatal.

The incidence of carotid arterial injury in
wartime, based on a total number of arterial
injuries, was reported to be highest in a World
War I study by Makins (1919) and lowest in a
World War II study by De Bakey and Simeone
(1946), as indicated in Table 11—1. The
Vietnam conflict data indicate that common
carotid injury is a more common occurrence
than either internal or external carotid injury.
Obviously, the vast majority of these injuries
are penetrating, because of the nature of
weaponry involved.

PATHOLOGY

The patient who survives penetrating neck vas-
cular injury and reaches a surgeon most likely
has a laceration or perforation. Complete

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11 • PENETRATING CERVICAL VASCULAR INJURY

229

TABLE 1 1-1

COMPILATION OF WARTIME DATA ILLUSTRATING THE INCIDENCE OF
CAROTID ARTERY INJURY EXPRESSED AS A PERCENTAGE OF TOTAL ARTERIAL
INJURIES REPORTED

Study

Makins, 1919 (World War I)
De Bakey and Simeone,

1946 (World War II)
Hughes, 1958 (Korean)
Rich and colleagues,

1970 (Vietnam)

Total Arterial

Common

Internal

Injuries

Carotid

Total Carotid

Percentage

120

128

10.7

247

0.4

304

3.6

100

5.0

disruptions of the carotid artery are almost
always fatal, although reports exist demon-
strating viable patients with completely tran-
sected carotid arteries, with thrombus
formation at the severed ends, thus alleviat-
ing the hemorrhage (Rich and colleagues,
1970; Harris and colleagues, 1985).

Cerebral vasospasm appears to be an impor-
tant factor in the pathophysiology of cervical
vascular injury. Acute spasm of the cerebral
arteries can occur almost immediately after
cervical arterial injury and can severely exac-
erbate ischemia. For the most part, however,
spasm seems to play a late role in the poten-
tial pathology of carotid or vertebral artery
injury, with the peak incidence occurring 5
to 10 days after injury (Kordestani and col-
leagues, 1997). Acute arteriovenous fistula is
an important entity that if improperly iden-
tified, will have a high propensity to recur
(Marks and colleagues, 1984). Early diagno-
sis can be difficult on physical examination
alone, as the classic murmur may not be
audible for several days. Some patients may
have a substantial thrill that is palpable along
the course of the fistula. Missile trajectory
or pattern is very important when one
attempts to predict possible fistulas. A report
from our own institution described an acute
carotid to cavernous sinus fistula after shotgun
blast (Fields and colleagues, 2000). Diagnos-
tic modalities for the workup of fistulas and
other pathology associated with cervical vas-
cular injury are discussed in the following
section.

INITIAL EVALUATION
AND MANAGEMENT

A careful history and physical examination
should be undertaken. Weapon characteris-
tics are important in predicting the extent of
injury, especially for high-velocity missile
injury. Trajectory should be assessed from
entrance and exit wounds, especially in trans-
cervical wounds because of the high inci-
dence of vital structure damage (Hirshberg
and colleagues, 1994). Obvious signs of vas-
cular injury include external hemorrhage,
expanding or pulsate hematoma, decreased
pulses, and avascular bruit or thrill. So-called
"soft signs" of vascular injury include dimin-
ished temporal or facial arterial pulses, signs
of hemothorax, or pharyngeal bleeding.
Patients with hard signs of vascular injury
require emergent neck exploration. A thor-
ough neurologic examination is an integral
part of the patient's evaluation. Care should
be taken to ascertain for signs of cord injury
such as paralysis, paresthesia, and hyper-
reflexia. Likewise, severe cerebral vascular
insufficiency from carotid injury may result
in contralateral hemiparesis. Evidence of
cerebral infarct is important. This is discussed
later in this chapter in the context of vascu-
lar repair in a patient with preexisting neu-
rologic deficit.

Initial clinical management begins in the
prehospital phase of trauma care. For the
patient with penetrating cervical injury,

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IV • SPECIFIC VASCULAR INJURIES

prompt transport to the nearest trauma
center with skilled personnel is paramount.
Because airway establishment is fraught with
a variety of potential problems, patients
should probably be intubated only if unre-
sponsive or if their situation is deteriorating
and a long transport time is anticipated. Exter-
nal bleeding should be controlled with direct
pressure.

When the patient presents to the trauma
bay with a penetrating neck injury, airway
control should be the foremost concern. Most
early deaths in these patients result from either
airway compromise or external hemorrhage,
both of which can be addressed with fastidi-
ous care. The airway management algorithm
is straightforward for the unresponsive patient
or those presenting in extremis (Rao and
colleagues, 1993): rapid establishment of
orotracheal or surgical airway. The difficult
patient is the agitated patient with obvious
severe cervical injury. Establishment of
orotracheal or nasotracheal airway may be
problematic because of blood or secretions
in the oropharynx or the patient's general
status.

These patients need the most experienced
personnel in the most optimal place possible
in the most expeditious way. In our opinion,
these patients, if at all possible, should be
rushed to the operating room where the most
experienced anesthesiologist and surgeon can
together manage the airway by carefully indi-
vidualized interventions: conscious intubation
or sedation and a rapid surgical airway.

Once the patient's airway is evaluated and
steps are taken to ensure definitive tracheal
intubation as required, massive external bleed-
ing needs to be controlled. Precise digital
pressure should be applied to any bleeding
sites. Nasopharyngeal or oropharyngeal
packing may be necessary as a temporary
hemostatic aid. During this time, paired large-
bore intravenous access should be obtained
and secured. Anteroposterior and lateral
cervical roentgenograms and chest radi-
ograms are obtained to assess for retained pro-
jectile, bony injury, and thoracic or pleural
violation.

Outside the context of this chapter, con-
current injury must be assessed and dealt with.
The high incidence of aerodigestive tract

injury with penetrating neck trauma has been
well described and may require rapid diag-
nosis and treatment. Severe tracheal injury
may complicate the establishment of a defin-
itive airway in these patients and can prove
fatal. Delay to diagnosis of esophageal or
pharyngeal injury is directly related to poor
outcome and must be assessed fastidiously
(Asensio and colleagues, 2001).

DIAGNOSIS OF VASCULAR
INJURIES: ZONES OF NECK
AND THE ROLE OF
PHYSICAL EXAMINATION

In a landmark 1969 article, Monson and col-
leagues (1969) arbitrarily divided the neck into
three clinical zones (Fig. 11-4). Zone 1 is
defined as being below to sternal notch, zone
3 above the angle of the mandible, and zone
2 is the intervening region. This system has
become a standard for discussing the diag-
nostic approach to penetrating neck vascular
trauma because of the clinical relevance of
injuries to anatomic locations. Zone 2 injuries
are accessible via standard cervical approaches
and should not present difficulty in obtain-
ing proximal and distal vascular control.
Zone 1 injuries by definition involve the tho-
racic inlet, and proximal control may require
thoracotomy or supraclavicular incisions in
addition to a cervical dissection. Zone 3
injuries are problematic because of the poten-
tial difficulty in obtaining distal control. The
widely accepted practice is thatzone 2 injuries
are explored in the operating room, whereas
zone 1 and 3 injuries require angiography
because of the more extensive surgical
approaches and potential complications.

Surgical access and exposure for sympto-
matic vascular injuries is relatively easy, and
the morbidity from surgical exploration of
zone 2 is very low. In addition, several studies
have suggested that because zone 2 of the neck
is amenable to physical examination, signifi-
cant vascular injuries in this location are rarely
occult. Sekharan and colleagues (2000)
reviewed 145 patients with neck penetration;
in 30 of these patients, the penetrating tra-
jectory also traversed zone 1 or 3. Thirty-one

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11 • PENETRATING CERVICAL VASCULAR INJURY 231
ZONES OF NECK FOR TRAUMA

■ FIGURE 1 1-4

Zones of the neck. ■

patients (21%) had hard signs of vascular
injury (active bleeding, expanding hematoma,
bruit/ thrill, pulse deficit, central neurologic
deficit) and were taken immediately to the
operatingroom;28 (90%) of these 30 patients
had either major arterial or venous injuries
requiring operative repair (the false-positive
rate for physical examination thus being
10%). Of the 114 patients with no hard signs,
23 underwent arteriography because of prox-
imity of the injury to the vertebral arteries or
because the trajectory included another zone.
Of these 23 arteriograms, three showed
abnormalities, but only one required opera-
tive repair. This case had no complications
relating to the initial delay. The remaining 91
patients with no hard signs were observed
without imaging or surgery for a minimum
of 23 hours, and none had any evidence of
vascular injury during hospitalization or
during the initial 2-week follow-up period
(1/114; false-negative rate for physical

examination, 0.9%) . Based on these data, the
authors confirmed that patients with zone
2 penetrating neck wounds can be safely
and accurately evaluated by physical exami-
nation alone to confirm or exclude vascular
injury.

Angiography

Four-vessel cervical angiography is the gold
standard by which all other modalities are
judged. The goal of angiography is to define
the exact arterial injury and it anatomic rela-
tions, to identify any collateral flow, to look
for any arteriovenous communications, and
to stratify injuries in the patient with multiple
vascular injuries. As angiography became
readily available in the last 30 years, this system
has become useful to define which injuries
require arteriography. The precise indications
for arteriography in stable patients, however,

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IV • SPECIFIC VASCULAR INJURIES

remain controversial. Preoperative arteriog-
raphy is recommended in all patients with
zone 1 penetration if they are hemodynamically
stable and do not have evidence of active hemor-
rhage. It is recommended because these
injuries are frequently clinically occult and
their exposure technically challenging.
Angiography appears to be essential in zone 3
neck wounds because of the potential inacces-
sibility of distal vascular injuries. The role of
angiography in identifying injuries in zone 2
is more controversial, as discussed earlier in
this chapter.

Arteriography is more likely to be helpful
in low-velocity gunshot wounds than in
stab wounds, but recommendations to eliminate
arteriography from a selective management proto-
col in stab wounds of the neck must await further
studies. High-velocity bullet wounds, shrapnel
injuries, and close-range shotgun wounds
all have exceptionally high incidences of
significant organ injury, and arteriography
in the stable patient without exsanguinating
hemorrhage may be of considerable
assistance.

Azuaje and colleagues (2002) studied 216
patients with penetrating neck injuries (from
1992 to 2001). Excluding 48 emergent explo-
rations and 16 shotgun wounds, the remain-
ing 152 patients had injuries in zone 1 (45
patients), zone 2 (83 patients), and zone
3 (23 patients); 63 patients had a positive
physical examination (e.g., hematoma, bruit,
thrill, and bleeding) and 40 (68%) also had
a positive angiogram. Twenty of these required
operative repair. Of the 89 patients with a neg-
ative physical examination, only 3 had a pos-
itive angiogram and none of these required
operative repair. Physical examination had
93% sensitivity and a 97% negative predictive
value for predicting the results of angiogram.
The authors concluded that with careful phys-
ical examination, angiography may not be
necessary irrespective of zone of injury.

Color Flow Doppler

Recently, color flow Doppler has become an
alternative to angiography in the diagnostic
workup of vascular trauma. It has been studied
to some extent in peripheral arterial injuries,

although its use in cervical trauma is ill
defined. A study by Fry and colleagues (1994)
demonstrated the feasibility of ultrasound
for the assessment of vascular injury. A pilot
study with 15 patients receiving duplex ultra-
sonography and concomitant angiography
demonstrated equal accuracy of the two tech-
niques. With these pilot data, the study was
extended to an additional 85 patients in whom
ultrasound was the primary imaging modal-
ity. The authors reported that ultrasound was
as effective as operative exploration or angiog-
raphy in their hands. A smaller study in 1996
demonstrated the success of ultrasonography
as a screening modality for vascular trauma,
with all major injuries being detected by the
sonogram (Montalvo and colleagues, 1996) .
These findings were confirmed by Demetri-
ades and colleagues (1995) in their study of
82 patients. They demonstrated that Doppler
imaging identified 10 of the 11 injuries, for a
sensitivity of 91% and a specificity of 98.6%.
It appears that careful examination coupled
with the experienced use of ultrasonography
provides results comparable to angiography.
Pitfalls with Doppler do exist though, impor-
tantly, the difficulty in establishing the exact
anatomic relationship with the resolution
available to angiography and the difficulty
in securing readily available equipment, an
experienced technologist, and skilled
interpreter.

Computed Tomographic
Angiography and Magnetic
Resonance Angiography

Currently attracting increasing attention,
computed tomographic angiography (CTA)
should still be considered unproven. One
study looked at 16 patients with suspected
traumatic carotid artery injury who underwent
CTA. Twelve of these patients had penetrat-
ing injuries and four had blunt injuries to the
neck. All the CTAs were diagnostic. Positive
findings included one complete tear of the
right common carotid artery (confirmed by
surgery) from a penetrating injury and one
bilateral ICA thrombosis after blunt injury to
the neck. Negative findings on CTA were con-

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11 • PENETRATING CERVICAL VASCULAR INJURY

233

firmed by surgical exploration (Ofer and
colleagues, 2001). In a prospective study of
146 arteries (77 carotid, 69 vertebral) studied
by means of conventional angiography and
helical CTA, conventional angiograms showed
arterial injuries in 10 (17%) of 60 patients.
These included arterial occlusion ( n = 4) , arte-
riovenous fistula (w=2), pseudoaneurysm
(n= 3), pseudoaneurysm with arteriovenous
fistula (n= 1), and normal arteries (n= 136).
Nine of ten arterial injuries and all normal
arteries were depicted adequately at helical
CTA. The sensitivity of helical CTA was 90%,
specificity was 100%, positive predictive value
was 100%, and negative predictive value was
98%. The sensitivity and specificity of helical
CTA, therefore, seem high for detection of
major carotid and vertebral arterial injuries
resulting from penetrating trauma (Munera
and colleagues, 2000), at least in experienced
hands.

Magnetic resonance angiography has been
described as an imaging modality in this
context as well, but experience with pene-
trating neck trauma, technical considera-
tions, and limited experience make it difficult
to recommend its use (Prabhu and colleagues,
1994; Friedman and colleagues, 1995).

TREATMENT

Innominate and Subclavian
Vessel Injuries

subclavian are best approached by an incision
along the clavicle with extension along the
sternocleidomastoid, if necessary. Subpe-
riosteal resection of the mid or medial one
third of the clavicle will allow excellent expo-
sure. Most of these vascular injuries may be
managed by simple closure or end-to-end anas-
tomosis. Occasionally, a saphenous vein graft
may be necessary. In stable patients with sub-
clavian pseudoaneurysm or intimal injuries,
endovascular stent grafts are an evolving
option.

Carotid Artery Injuries

The general consensus now is that injuries to
the carotid arteries are best approached by
surgical intervention and repair, either by end-
to-end anastomosis or graft techniques, espe-
cially in the accessible portions of the carotid
artery (Figs. 11-5 and 11-6). For selected
intracranial injuries high in zone 1, endovas-
cular stents are being used with increasing fre-
quency, as discussed later in this chapter.

SURGICAL TREATMENT

The patient should be placed in a prone posi-
tion with both arms tucked in if possible. As
long as there is no concurrent spine injury, a
shoulder roll should be placed to extend the
neck and the table placed in a semi-Fowler

Operative exposure of zone 1 vascular injuries
are outside the scope of this chapter and are
only briefly mentioned for completion. If the
patient is hemodynamically unstable with a
large hemothorax or excessive bleeding from
the chest tube, an anterolateral thoracotomy
(high in the third or fourth intercostal space)
in the emergency center will allow apical
packing and tamponade the bleeding from
innominate or proximal subclavian vessels. In
the operating room, a median sternotomy will
expose the innominate. For the left subcla-
vian artery, the incision maybe extended along
the sternocleidomastoid or the clavicle. This
approach is superior to the "trap-door" inci-
sion. The second and third portions of the

■ FIGURE 1 1-5

Gunshot wound of the neck. Angiogram reveals
internal carotid cutoff just distal to its origin. ■

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234 IV • SPECIFIC VASCULAR INJURIES
I

■ FIGURE 1 1-6

A and B, Carotid artery injury at operation
repaired by a saphenous vein interposition
graft. ■

position to aid in the operative exposure. The
entire thorax and abdomen should be pre-
pared in case of zone 1 injury for accessing
the abdomen for potential multicavitary
injuries. The groin and both thighs are pre-
pared and draped for possible saphenous vein
harvest. Carotid exposure is obtained via a skin
incision made along the anterior border of
the sternocleidomastoid muscle. The carotid
sheath and its contents are readily identifiable.
The venous and lymphatic structures are
retracted in a lateral direction. Proximal and
distal exposure of the carotid arteries is
obtained after identifying the ansa cervicalis
and twelfth cranial nerve. Digital pressure or
a side-biting vascular clamp can be used to
control hemorrhage while obtaining control.
Proximal injury to the carotid at its aortic or
subclavian origin requires more extensive
exposure than the simple neck incision.

Median sternotomy is the most commonly
employed approach. A supraclavicular inci-
sion is useful for exposure in some cases, and
dislocation or resection of the clavicle may
improve the exposure, as detailed elsewhere
in this text.

High zone 3 injuries resulting in distal inter-
nal carotid laceration or disruption can prove
very problematic in exposure and control.
Anterior subluxation of the mandible can
improve exposure, but only by about 2 cm.
Osteotomy of the mandibular ramus may
provide better exposure and mobility. Place-
ment of a Fogarty balloon catheter to provide
distal vascular control can be lifesaving during
these maneuvers. The carotid artery may
require ligation. Depending on the surgeon's
experience in operating around the base of
the skull, intraoperative assistance from either
a maxillofacial surgeon or a neurosurgeon
is advisable in difficult cases. A recent series
illustrated the management and outcomes of
four consecutive patients, two with pseudo-
aneurysms and two with acute occlusions, after
injury to the distal cervical/petrous ICA from
gunshot wounds. Preoperative assessment
determined intracranial collateral flow pat-
terns and established the patency of the distal
portion of the petrous ICA. Two patients
underwent cervical-to-petrous ICA vein bypass
grafts without neurologic complications. Both
grafts remained patent without evidence of
emboli at 2 years and 3 months. The two
patients who were managed conservatively
died, one from a massive cerebral infarction
and the other from intracerebral hemorrhage.
These authors concluded that the cervical-
to-petrous ICA vein bypass graft is a valuable
management option that can reduce the
potential morbidity and mortality from acute
ischemic or delayed embolic or hemorrhagic
infarcts (Romily, Newell, and Grady, 2001).
This approach, however, may be of limited
value in the management of the bleeding
patient with a difficult surgical exposure.
In this setting, ligation of the ICA may be
lifesaving.

Once proximal and distal control are
secured, a Fogarty balloon catheter is care-
fully passed to remove any thrombus and
both proximal and distal ends are flushed
with heparinized saline. A monofilament

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11 • PENETRATING CERVICAL VASCULAR INJURY

235

polypropylene suture of 5-0 or 6-0 size is used
for the repair and handled with appropriate
vascular technique. Except for tangential
lacerations, primary repair is often difficult,
because the transected ends of the artery
retract. For a simple, small laceration, inter-
rupted lateral repair is usually possible. Larger
lacerations require a running repair, with two
separate sutures, each originating in an apex
of the injury and is approximated in the
middle. Care must be taken to inspect for and
repair any intimal flap at this time. This can
often be done by incorporating the intimal
defect into the laceration repair by using a
series of interrupted sutures. Also, the lumen
of the artery must not be narrowed by this
primary repair; otherwise, vein patch or inter-
position graft will be required.

Stab wounds or low-velocity missile injuries
often result in simple lacerations with minimal
devitalized tissue. Most of these arteriotomies
can be repaired with simple suture plication
or minimal mobilization and primary repair.
If there is a considerable destruction of the
carotid artery, resection of devitalized tissue
may preclude a tension-free primary repair.
In these cases, interposition grafting is war-
ranted, preferably using autologous tissue.
Saphenous vein is generally accepted to be
the ideal conduit. If adequate autologous
conduit is not available, synthetic material may
be used. The choice between woven Dacron
and ethyl polytetrafluoroethylene is based on
surgeon's preference, because neither rep-
resents an ideal substitute for a vein graft. If
anatomy permits, the external carotid artery
can be divided at a distal location and trans-
posed to the ICA. The thyroidal and pharyn-
geal branches should be ligated to provide
mobility. The use of a shunt is not mandated
by the available data. The Vietnam experience
established the safety of carotid artery repair
without the use of shunts, even with arterial
occlusion lasting up to 60 minutes. In many
series, stump pressures (pressure measured
in the distal portion of carotid artery after
ligation or resection) failed to predict post-
operative neurologic deficits after carotid
endarterectomy. Even though similar data are
not available in civilian trauma series, the use
of a shunt or stump pressures is a matter of
personal choice.

Recently, percutaneous transluminal
placement of endovascular devices has
become an alternative option to surgical
repair. One series evaluated the potential for
using flexible self-expanding uncovered stents
with or without coiling to treat post-traumatic
pseudoaneurysms involving the extracranial
ICA, the subclavian artery, and other periph-
eral artery (Assali and colleagues, 2001).
Three patients with post-traumatic pseudo-
aneurysms of the carotid (one patient) and
subclavian (two patients) were treated by stent
deployment (Fig. 11-7). Angiography demon-
strated complete occlusion of the pseudo-

■ FIGURE 11-7

A and B, Subclavian artery injury just proximal
to its origin by a gunshot wound in a patient
with severe associated brain injury. This was
managed by a stented graft placed by the
interventional radiologist. (Courtesy T. Marrone
and J. Tisnado.) ■

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IV • SPECIFIC VASCULAR INJURIES

aneurysms. At long-term follow-up (6 to 9
months), all patients were asymptomatic
without flow into the aneurysm cavity by
Duplex ultrasound.

Much like in the extremities, minimal
injuries to the carotid artery (small pseudo-
aneurysms or intimal flaps) probably have a
benign course, and may not necessarily require
operative repair. The natural course of many
intimal flap injuries is unknown. Considering
the nature and importance of the carotid cir-
culation, however, the most judicious course
of action may be a serial objective evaluation
via duplex color flow ultrasonography or
angiography. In a recent experimental study,
only up to one third of all intimal injuries
resolved without complication, and this figure
underscores the need for diligent follow-up
(Panetta and colleagues, 1992). There is no
definitive information from the literature that
elucidates the role of anticoagulation or
antiplatelet agents in carotid artery injuries.
Some authors, based on elective carotid
endarterectomy data, advocate the use of low-
dose aspirin or intravenous low-molecular-
weight dextran to provide prophylaxis
against thrombosis (Robless and colleagues,
1999).

Surgical Treatment of Carotid Artery
Injury in Patients with Neurologic Deficits

Bradley in 1973 and Thai and colleagues in
1974 challenged the concept of repairing the
carotid artery in the face of an established cere-
bral infarct and suggested that the repair and
establishment of carotid flow may convert an
anemic infarct into a hemorrhagic infarct.
This concept, however, was refuted by a col-
lective series of 223 patients by Liekwig and
Greenfield (1978). Similar data were pre-
sented by Unger, Jorgensen, and Hoffman
(1990), Lawrence and colleagues (1948),
Ledgerwood, Mullins, and Lucas (1980), and
Weaver and colleagues (1988) . Many of these
studies concluded that the outcome was
dismal regardless of the type of therapy in the
patient with a fixed profound neurologic
deficit, but that the patients did better with
repair than ligation. It is advisable, therefore,
to repair the injury as long as the patient's
clinical condition permits.

The prognosis for penetrating carotid artery
injuries depends on the neurologic status on
admission (Lawrence and colleagues, 1948;
Ledgerwood, Mullins, and Lucas, 1980; Deme-
triades and Stewart, 1985; Asensio and col-
leagues, 1991; Demetriades and colleagues,
1996a). The mortality rates range from 6.6%
to 33%, with an average of 17% (Asensio
and colleagues, 1991), mostly related to
neurodeficits.

Vertebral Artery Injuries

Vertebral artery injuries fortunately are not
common. The first clinical review of vertebral
artery injuries is attributed to Rudolph Matas
of New Orleans in 1893. In his landmark
article, Matas elegantly described the difficulty
in diagnosing and surgically managing verte-
bral artery injuries, "A glance at the surgical
anatomy of this vessel as it lies deeply hidden
in the skeleton of the neck, only escaping
at short intervals from its osseous canal, to
become immediately invested by the very
important and vital cervical nerves as they issue
from the spinal foramina, will at once remind
us of the magnitude of the purely technical
difficulties in the way of its atypical ligation,
and of the errors of diagnosis that must
be incurred" (Yee and colleagues, 1995).
Reported injuries to the vertebral artery have
been exceedingly rare during major conflicts
involving the United States. Although three
vertebral artery injuries were reported in
World War I, none were reported in either
World War II, the Korean War, or the Vietnam
War (De Bakey and Simeone, 1946).

If identification and exposure of the ver-
tebral artery injury are uncomplicated during
neck exploration, proximal and distal surgi-
cal ligation of the injured vessel is performed.
If encountered at neck exploration, the fol-
lowing steps are indicated: (1) gauze packing
at the site of bleeding, (2) exposure of the
subclavian artery by dividing the origin of ster-
nomastoid from the clavicle, and (3) proxi-
mal control of the origin of the subclavian
artery. The neck incision is carried posterior
to the ear with division of the attachment of
sternomastoid and splenitis capitis muscle.
Distal ligation may be performed by dividing

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11 • PENETRATING CERVICAL VASCULAR INJURY

237

the splenitis capitis and sternomastoid attach-
ments to the mastoid, palpation of the trans-
verse process of the atlas, and exposing the
vertebral artery between the axis and atlas.
Bone wax or other hemostatic agents can be
used to pack and compress this area, or "blind "
application of surgical clips deep into the
wound may staunch the bleeding.

Because of the anatomic difficulties in
vascular control of the vertebral artery, angio-
graphic embolization represents an accept-
able alternative. If the injured vertebral artery
is discovered in the initial evaluation by
angiography, the surgeon has a "road map"
in planning the operative approach. Addi-
tionally, preoperative angiography allows for
selection of patients who may not require lig-
ation, specifically those with vertebral artery
narrowing or occlusions. The approach to
patients with pseudoaneurysms, dissections,
arteriovenous fistulas, or extravasations will
depend on the skill and judgment of the
trauma surgeon, as well as the availability of
experienced neuroradiologists.

Some series (Reid andWeigelt, 1970) noted
several cases in which a disrupted artery, as
seen operatively, had been diagnosed inac-
curately as an occlusion by preoperative
angiography. As a result, they recommended
neck exploration for all angiographically
diagnosed vertebral artery injuries unless
deemed minimal. In the recent series from
San Francisco (Yee and colleagues, 1995) , five
of six patients with vertebral artery occlusion
were treated by clinical observation, whereas
one underwent embolization. No adverse
symptoms or neurologic sequelae were seen
in these five patients. In addition, three
patients with angiographic narrowing were
treated by observation without complication,
which are findings consistent with those
reported by others. In the series reported
by Demetriades and colleagues (1996b), 22
patients with vertebral artery injuries were
reviewed. Only four patients required an emer-
gency operation. Most of the injuries (13/22)
were successfully managed by observation.
Five patients were managed by angiographic
embolization, which was successful in three.
In three patients with an aneurysm and arte-
riovenous fistula, proximal embolization of the
vascular lesion was not adequate and a sub-

occipital craniectomy was required for distal
ligation. Neurologic sequela from vertebral
embolization is very uncommon (Demetri-
ades and Stewart, 1985). These data support
the conclusion that most vertebral artery
injuries can safely be managed without an
operation or by angiographic embolization
(Fig. 11-8). Surgical intervention should be
reserved for patients with severe bleeding or
in whom embolization has failed (Demetri-
ades and colleagues, 1989).

Venous Injuries

Injuries to the innominate, subclavian, axil-
lary, or internaljugular vein may be the source
of severe hemorrhage. All of these veins can
be ligated if the destruction is severe. In stable
patients, they may be repaired. In a recent
series of 49 consecutive patients with cervical
and thoracic venous injuries (Nair, Robbs, and
Muckart, 2000) , the vessels involved were inter-
nal jugular in 25, subclavian in 15, brachio-
cephalic in 6, and superior vena cava in 3.
Injured veins were ligated in 25 patients and
repaired by lateral suture in 22. No complex
repairs were performed. There were eight
perioperative deaths and five cases of transient
postoperative edema (Makins, 1919). In the
case of severe bilateral jugular venous injury,
ligation will carry significant clinical conse-
quences. In this setting, reconstruction with
autologous conduit is advisable.

SUMMARY

The escalating civilian violence of modern
times is contributing to increasing frequency
of vascular injuries in the neck. Early deaths
are related to airway compromise or exsan-
guinating hemorrhage. If the patient arrives
stable to the hospital, an orderly assessment
and diagnosis may be made and the wounds
successfully managed. Late deaths are from
neurodeficits secondary to cerebral hypoxia.
Advances in the management of penetrating
vascular injuries on the horizon include non-
invasive diagnostic testing and nonoperative
radiologic procedures of endovascular

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IV • SPECIFIC VASCULAR INJURIES

■ FIGURE 1 1-8

A, Lateral view of a patient with a gunshot wound of the neck with active bleeding from the wound.
The injury to the cervical vertebra is evident. B and C, Angiography reveals injury to the vertebral
artery. After confirming a complete circle of Willis, this was embolized successfully. (Courtesy T.
Marrone and J. Tisnado.) ■

stenting and grafting. All of this progress is
directly attributable to the early foundations
laid down by the Vietnam Vascular Registry.

REFERENCES

Asensio JA, Chahwan S, et al: Penetrating
esophageal injuries: multicenter study of the
American Association for the Surgery of Trauma.
J Trauma 2001;50(2) :289-296.

Asensio JA, Valenziano CP, et al: Management of
penetrating neck injuries. The controversy
surrounding zone II injuries. Surg Clin North
Aml991;71(2):267-296.

Assali AR, Sdringola S, Moustapha A, etal: Endovas-
cular repair of traumatic pseudoaneurysm by
uncovered self-expandable stenting with or
without trans stent coiling of the aneurysm cavity.
Cathet Cardiovasc Interv 2001;53:253-258.

Azuaje RE, Jacobson LE, Glover J, et al: Reliability
of physical examination as a predictor of vascu-
lar injury following penetrating neck trauma.
Paper presented at the 15th Scientific Assembly
of EAST; Orlando; January 15-19, 2002.

Bradley EL: Management of penetrating carotid
artery injuries. An alternative approach. J
Trauma 1973;13:248-255.

De Bakey ME, Simeone FA: Battle injuries of arter-
ies in World War II: an analysis of 2471 cases.
Ann Surg 1946;123:534-579.

chll.qxd 4/16/04 3:36 PH Page 239

11 • PENETRATING CERVICAL VASCULAR INJURY

239

Demetriades D, Asensio JA, et al: Complex prob-
lems in penetrating neck trauma. Surg Clin
North Am 1996a;76:661-683.

Demetriades D, Skakkides J, Fofianos C, et al:
Carotid artery injuries (1989): experience with
124 cases. J Trauma 1989;29:91-94.

Demetriades D, Stewart M: Penetrating injuries of
the neck. Ann R Coll Surg Engl 1985;67:71-74.

Demetriades D, Theodorou D, et al: Penetrating
injuries of the neck in patients in stable condi-
tion. Physical examination, angiography, or
color flow Doppler imaging. Arch Surg
1995;130:971-975.

Demetriades D, Theodorou D.AsensioJ, etal: Man-
agement options in vertebral artery injuries. Br
J Surg 1996b;83:83-86.

Fields CE, Cassano AD, et al: Indirect carotid-
cavernous sinus fistula after shotgun injury.
J Trauma 2000;48 (2) :338-341 .

Flemming D. Case of rupture of the carotid artery
and wounds of several of its branches treated by
tying the common trunk of the carotid itself. Med
ChirJRevl817;3:2.

Fogelman MJ, Stewart RD: Penetrating wounds of
the neck. Am J Surg 1956;91:581.

Friedman D, Flanders A, et al: Vertebral artery
injury after acute cervical spine trauma: rate of
occurrence as detected by MR angiography and
assessment of clinical consequences. AJR Am J
Roentgenol 1995;164:443-447.

Fry WR, Dort JA, et al: Duplex scanning replaces
arteriography and operative exploration in the
diagnosis of potential cervical vascular injury. Am
J Surg 1994;168:693-695.

Golueke PJ, Goldstein AS, etal: Routine versus selec-
tive exploration of penetrating neck injuries. A
randomized, prospective study. J Trauma 1984;
24:1010.

Harris JP, Anterasian G, et al: Management of
carotid artery transection resulting from a stab
wound to the ear. Laryngoscope 1985;95(7, pt
l):782-785.

Hirshberg A, Wall MJ, et al: Transcervical gunshot
injuries. Am J Surg 1994;167(3):309-312.

Huhges CW: Arterial repair during the Korean War.
Ann Surg 1958;147:555.

Kordestani RK, Counelis GJ, et al: Cerebral arter-
ial spasm after penetrating craniocerebral
gunshot wounds: transcranial Doppler and
cerebral blood flow findings. Neurosurgery
1997;41:351-359.

Krabbe-Hartkamp MJ, van der Grond J, et al:
Circle of Willis: morphologic variation on three-

dimensional time-of- flight MR angiograms.
Radiology 1998;207:103-111.

Lawrence KB, Sheffts LM, et al: Wounds of the
common carotid arteries. Reports of seventeen
cases from World War II. Am J Surg 1948;76:29.

LeBlang SD, Nunez DBJr: Helical CT of cervical
spine and soft tissue injuries of the neck. Radiol
Clin North Am 1999;37:515-532.

Ledgerwood AM: Neck: vascular injuries. In:
Ivatury RR, Cayten CG, eds. The textbook of
penetrating trauma. Philadelphia: Williams &
Wilkins, 1996.

Ledgerwood AM, Mullins RJ, Lucas CE: Primary
repair vs. ligation for carotid artery injuries. Arch
Surg 1980;115:488-493.

LiekwigWGJr, Greenfield LJ: Management of pen-
etrating carotid artery injury. Ann Surg
1978;188:587.

Makins GH: Gunshot injuries to the blood vessels.
Bristol: John Wright and Sons, Ltd, 1919.

Marks MW, Argenta LC, et al: Traumatic arteri-
ovenous malformation of the external carotid
arterial system. Head Neck Surg 1984;6:1054-
1058.

Mittal VK, Paulson TJ, et al: Carotid artery injuries
and their management. J Cardiovasc Surg
(Torino) 2000;41:423-431.

Monson DO, Saletta JD, et al: Carotid vertebral
trauma. J Trauma 1969;9:987-999.

Montalvo BM, LeBlang SD, et al: Color Doppler
sonography in penetrating injuries of the neck.
AJNR Am J Neuroradiol 1996;17:943-951.

Munera F, Soto JA, Palacio D, et al: Diagnosis of
arterial injuries caused by penetrating trauma
to the neck: comparison of helical CT angiog-
raphy and conventional angiography. Radiology
2000;216:356-362.

Nair R, Robbs JV, Muckart DJ: Management of
penetrating cervicomediastinal venous trauma.
Eur J Vase Endovasc Surg 2000;19(l):65-69.

Ofer A, Nitecki SS, BraunJ, et al: CT angiography
of the carotid arteries in trauma to the neck. Eur
J Vase Endovasc Surg 2001;21:401-407.

Panetta TF, Sales CM, et al: Natural history, duplex
characteristics, and histopathologic correlation
of arterial injuries in a canine model. J Vase Surg
1992;16:867-874.

Prabhu VC, Patil AA, et al: Magnetic resonance
angiography in the diagnosis of traumatic ver-
tebrobasilar complications: a report of two cases.
Surg Neurol 1994;42:245-248.

Puchades-Orts A, Nombela-Gomez M, et al: Varia-
tion in form of circle of Willis: some anatomical

chll.qxd 4/16/04 3:36 PH Page 240

240

IV • SPECIFIC VASCULAR INJURIES

and embryological considerations. Anat Rec
1976;185:119-123.

Rao PM, Ivatury RR, Sharma P, et al: Cervical vas-
cular injuries: a trauma center experience.
Surgery 1993;114(3):527-531.

ReidJD, Weigelt JA: Forty-three cases of vertebral
artery trauma. J Trauma 1988;28:1007-1012.

Rich NM, Baugh JH, et al: Acute arterial injuries
in Vietnam: 1,000 cases. J Trauma 1970;
10(5):359-369.

Robless P, Okonko D, et al: Vascular surgical society
of great Britain and Ireland: platelet function
during carotid endarterectomy and the
antiplatelet effect of dextran 40. Br J Surg
1999;86(5):709.

Romily RC, Newell DW, Grady MS, et al: Gunshot
wounds of the internal carotid artery at the skull
base: management with vein bypass grafts and a
review of the literature .J Vase Surg 2001 ;33:1001-
1007.

Sekharan J, Dennis JW, Veldenz H, et al: Contin-
ued experience with physical examination alone
for evaluation and management of penetrating
zone 2 neck injuries: results of 145 cases. J Vase
Surg 2000;32:483.

Thai ER, Snyder WH III, et al: Management of
carotid artery injuries. Surgery 1974;76:955-962.

Unger S,Jorgensen J, Hoffman M: Carotid artery
trauma. Surgery 1990;87:47740.

Watson WL, Silverstone SM: Ligature of the
common carotid artery in cancer of the head
and neck. Ann Surg 1939;109:1.

Weaver FA, "Vellin AE, et al: The role of arterial
reconstruction in penetrating carotid artery
injuries. Arch Surg 1988;123:1106-1111.

Yee LF, Olcott EW, Knudson MM, et al: Extralu-
minal, transluminal, and observational treatment
for vertebral artery injuries. J Trauma 1995;
39:480-486.

chl2.qxd 4/16/04 3:37PM Page 241

Blunt Cervical Vascular Injury

WALTER L. BIFFL
ERNEST E. MOORE
JON M. BURCH

O ANATOMIC CONSIDERATIONS

O MECHANISMS OF INJURY

O PATHOPHYSIOLOGY

O CLINICAL PRESENTATION

O SCREENING AND THE INCIDENCE OF BLUNT CERVICAL VASCULAR
INJURIES

Screening for Blunt Cerebrovascular Injuries

Identifying the Patient at Risk
O DIAGNOSTIC EVALUATION
O INJURY GRADING
O TREATMENT AND OUTCOME
O SUMMARY AND GUIDELINES

Blunt cervical vascular injuries (BCVIs) ,
those to the extracranial carotid and
vertebral arteries (VAs), have histori-
cally been considered rare, yet they are rec-
ognized as potentially devastating events.
Given the dearth of experience with BCVIs,
even in busy trauma centers, there is essen-
tially no class I literature to guide their man-
agement. Furthermore, BCVIs present a
unique set of challenges because (1) they often
occur in the setting of multisystem trauma,

particularly head injuries, and symptoms may
be masked by depressed consciousness or
attributed to intracranial injury; (2) they are
typically not diagnosed until after cerebral
ischemic injury, making it difficult to achieve
a good outcome; (3) they may occur follow-
ing relatively minor neck "trauma," and so
even with a high index of awareness of BCVIs,
patients might not be considered at risk until
they manifest cerebral ischemia; (4) the only
reliable diagnostic test is invasive, resource

241

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IV • SPECIFIC VASCULAR INJURIES

intensive, and associated with its own risks,
and alternative noninvasive diagnostic tests
may miss early subtle lesions; (5) the natural
history of various injury types is unknown, and
thus, it must be presumed that all injuries
should be treated; and (6) treatments are
potentially risky, there is no consensus on the
optimal treatment for various lesions, and effi-
cacy of treatment is largely unproven. In sum,
BCVIs present dilemmas in risk assessment,
screening, diagnosis, and treatment.

ANATOMIC CONSIDERATIONS

The left common carotid artery (CCA) orig-
inates from the aortic arch within the thorax,
whereas the right CCA is a terminal branch
of the innominate artery behind the stern-
oclavicular joint. There are no significant
arterial branches from the CCA. It generally
divides into the internal carotid artery (ICA)
and external carotid artery (ECA) at the level
of the C3-C4 disc space, corresponding to the
superior border of the thyroid cartilage. The
ECA does not directly supply circulation to
the brain; thus, traumatic injuries to the ECA
are usually well tolerated neurologically unless
there is preexisting cerebrovascular disease.
On the other hand, in the presence of carotid
or VA occlusive disease, the ECA branches may
provide critical collateral flow. The ICA can
be separated anatomically into four segments:
cervical, petrous, cavernous, and cerebral
(supraclinoid) . The cervical portion has no
named branches because it ascends ventral to
the transverse processes of the C1-C3 verte-
bral bodies (a relationship that is pivotal
in the pathophysiology of many injuries, as
described later in this chapter) . The petrous
segment traverses the carotid canal in the
petrous portion of the temporal bone; here,
it is at risk of laceration in the setting of a basilar
skull fracture. The cavernous portion (also
called the carotid siphon because of its gentle
S shape) is the first part of the ICA within the
cranial vault. It is suspended between the layers
of the dura matter that form the cavernous
sinus. At the anterior clinoid process, the ICA
perforates the dura and becomes the supra-
clinoid, or cerebral, segment. The ICA divides

terminally into the anterior and middle
cerebral arteries.

The VAs originate from the subclavian arter-
ies, enter the cervical vertebral foramina at
the level of C6, exit the transverse foramen of
C2, and merge intradurally to form the basilar
artery. There is considerable asymmetry to the
point of agenesis (2% of right and 3% of left
VAs) . The circle of Willis connects the ante-
rior and posterior circulation but is intact and
symmetric injust 20% of individuals. The fre-
quency of variations in collateral circulatory
routes may explain unusual clinical presen-
tations of arterial injuries and underscores the
need to image the entire cerebral circulation
in cases of BCVI.

MECHANISMS OF INJURY

There are four fundamental mechanisms of
carotid injuries. The most common is associ-
ated with hyperextension and rotation of the
head and neck. The lateral articular processes
and pedicles of the upper three cervical ver-
tebrae (C1-C3) project more anteriorly than
those of C4-C7; thus, the overlying distal cer-
vical ICA is prone to stretch injury during
cervical hyperextension. Rotation at the
atlantoaxial joint may result in anterior move-
ment of the contralateral CI lateral mass,
further exacerbating the stretch (Fig. 12-1).
A direct blow to the neck may crush the artery,
or it may be compressed between the mandible
and the vertebral prominences in acute cer-
vical hyperflexion injuries. Intraoral trauma
may injure the ICA, typically seen in children
who have fallen with a hard object (such as a
pencil) in their mouth. Finally, basilar skull
fractures that involve the sphenoid or petrous
bones may result in laceration of the artery.

The third segment of the VA, which extends
from the level of C2 to the dura, is most com-
monly injured by blunt trauma because of the
increased degree of stretching and compres-
sion (Fig. 12-2) ; the relationship between the
VA and the cervical bodies puts the VA at risk
when the vertebral body — particularly the
foramen transversarium — is fractured.

Of note, numerous case reports in the
literature have documented BCVI following

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12 • BLUNT CERVICAL VASCULAR INJURY

243

"trivial trauma." These include virtually any
athletic endeavor, chiropractic manipulation,
visiting the hairdresser, "head banging" to
music, "bottoms-up" drinking, rapid head
turning, and everyday activities such as cough-
ing, shaving, vomiting, nose blowing, and
scolding a child. This is in contradistinction
to "spontaneous" carotid dissection, which by
definition occurs in the absence of trauma.
Reported risk factors for spontaneous dis-
section include hypertension, Marfan's
syndrome, fibromuscular dysplasia, syphilis,
arteriopathies, and Erdheim's cystic medial
necrosis. It is the contention of some that truly
spontaneous dissections are rare, but that such
risk factors simply predispose patients to
BCVI following trivial trauma. The absence
of trauma from an individual's history does
not exclude it as an etiology, because patients
often consider events too insignificant (or
embarrassing) to relate.

PATHOPHYSIOLOGY

■ FIGURE 1 2-1

Rotation at the atlantoaxial joint may result
in anterior movement of the contralateral
C1 lateral mass, further exacerbating the
stretch. ■

Regardless of the underlying mechanism of
injury, the final common pathway of BCVI in
most cases is intimal disruption. This exposes
thrombogenic subendothelial collagen, pro-
moting platelet aggregation with subsequent
embolization, partial thrombosis with low flow,
or complete thrombosis. In addition, the
intimal tear offers a portal of egress for a
dissecting column of blood. Dissection may
result in progressive luminal narrowing and
subsequent occlusion. Whether caused by
thromboembolism or occlusion, the end
result, particularly in the setting of multisystem
trauma with hypotension, is cerebral ischemia.
Less commonly, partial or complete transec-
tion of the artery occurs, resulting in pseudoa-
neurysm formation or free rupture. The
former may increase in size to compress and
occlude the vessel lumen; it may be the source
of platelet thromboembolism; or it may
rupture. Rupture may result in hemorrhage
or arteriovenous fistula formation.

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244 IV • SPECIFIC VASCULAR INJURIES

■ FIGURE 1 2-2

The third segment of the vertebral artery, which extends from the C2 level to the dura, is most
commonly injured by blunt trauma because of the increased degree of stretching, which occurs at
the atlantoaxial and atlanto-occipital joints during head rotation. ■

CLINICAL PRESENTATION

The clinical manifestations of BCVI depend
on the type of injury, the involved artery, and
collateral circulation. Premonitory signs and
symptoms associated with the vessel injury may
suggest the presence of BCVI before mani-
festations of cerebral ischemia. Pain (neck,
ear, face, or periorbital) can be present in up
to 60% of patients and is believed to reflect
mural hemorrhage or dissection of the vessel
wall. Complaints of such pain are often diffi-
cult to elicit in the multi-injured patient and
may be attributed to other injuries; however,
BCVI must be considered in the differential
diagnosis of post-traumatic neck pain and
headache. Horner's syndrome or oculosym-
pathetic paresis (partial Horner's syndrome)
may result from disruption of the periarter-
ial sympathetic plexus. Pupillary asymmetry
can have several etiologies in the injured
patient. However, if the larger of the pupils is
reactive and the smaller pupil is not, carotid
injury should be suspected on the side of the
smaller pupil.

Systematic neurologic examination will
help localize the distribution of cerebral
ischemia; however, cerebral ischemic signs or
symptoms may be absent in the acute setting,

because of (1) the presence of collateral cir-
culatory pathways and (2) a characteristic
latent period between the time of injury and
the appearance of clinical manifestations.
Unless the vessel is immediately occluded, time
is required for a platelet plug to form and
either limit flow or embolize. In various
series, 23% to 50% of patients first developed
signs or symptoms of BCVI more than 12 hours
after the traumatic event. In our experience,
42% of symptomatic patients manifested
more than 18 hours after injury and two exhib-
ited symptoms 7 days later. Delayed recogni-
tion may also occur in the face of multisystem
trauma, with critical injuries demanding
immediate attention, or head injury, which
may preclude a meaningful neurologic exam-
ination. To make the early diagnosis of BCVI,
the surgeon must recognize the signs and
symptoms in a trauma patient. These include
(1) hemorrhage — from mouth, nose, ears
or wound — of potential arterial origin; (2)
expanding cervical hematoma; (3) cervical
bruit in a patient 50 years old or younger; (4)
evidence of cerebral infarction on computed
tomographic (CT) scan; or (5) unexplained
or incongruous central or lateralizing neu-
rologic deficit, transient ischemic attack (TIA) ,
amaurosis fugax, or Horner's syndrome.

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12 • BLUNT CERVICAL VASCULAR INJURY

245

SCREENING AND THE
INCIDENCE OF BLUNT
CEREBROVASCULAR INJURIES

The incidence of BCVI is difficult to quantify
because many remain asymptomatic or
symptoms may be attributed to associated
brain (or other) injury. However, the inci-
dence of BCVI among blunt trauma victims
seems to be increasing. Early multicenter
reviews identified an incidence of BCVI of
0.08% to 0.17% among patients admitted to
trauma centers following blunt trauma, but
more recent series have reported incidences
of 0.24% to 0.44%. The argument that the
incidence actually is increasing is supported
by the fact that nearly all the patients in the
series published through 1997 were sympto-
matic at the time of diagnosis. A number of
factors could account for this explosion of
BCVI at our center, including (1) higher
highway speed limits in Colorado, (2) more
widespread use of shoulder restraints and
airbags, and (3) our role as a regional trauma
center in the Statewide Trauma System, with
increasing numbers of individuals being trans-
ferred to us following major mechanism
injuries. However, without question, screen-
ing has identified injuries that would other-
wise have been overlooked. In fact, two-thirds
of patients diagnosed with BCVI at our center
in the 1990s were asymptomatic.

Screening for Blunt
Cerebrovascular Injuries

In 1996, Fabian and colleagues suggested that
blunt carotid injuries (BCI) were being under-
diagnosed. This had been suspected based on
the Western Trauma Association multicenter
study and demonstrated in a preliminary
prospective study of screening at our center.
Recognizing the potential to improve neuro-
logic outcome by identifying and treating
carotid injuries before occurrence of cerebral
ischemia, we instituted an aggressive policy of
screening and recently reported an epidemic
of BCI. Between January 1990 and June 1996,
before screening, our incidence of BCI was
0.1% of blunt trauma admissions — similar to

multicenter reports. During 4.5 years with a
formal screening protocol, the incidence of
BCVI has approached 1% of all blunt trauma
admission to our center. In Memphis, a high
index of suspicion and increasingly liberal
screening resulted in an incidence of carotid
injuries of 0.5%.

Identifying the Patient at Risk

Although the Louisville group has asserted
that BCVI cannot be predicted based on
clinical grounds, a number of groups have
reported higher incidences of BCVI when
diagnostic testing is employed for specific
injury patterns and mechanisms. We formu-
lated our screening criteria based on a knowl-
edge of injury mechanisms and anatomic
considerations. The screening criteria include
(1) an injury mechanism compatible with
several cervical hyperextension/rotation or
hyperflexion, particularly if associated with dis-
placed or complex midface or mandibular
fracture, or closed head injury consistentwith
diffuse axonal injury of the brain; (2) near
hanging resulting in cerebral anoxia; (3) seat-
belt abrasion or other soft tissue injury of the
anterior neck resulting in significant cervical
swelling or altered mental status; (4) basilar
skull fracture involving the carotid canal:
and (5) cervical vertebral body fracture or
distraction injury, excluding isolated spinous
process fracture. This widespread screening
approach requires a tremendous commitment
of resources. In an attempt to allocate
resources more effectively, we critically eval-
uated our screening criteria, analyzing the
injury mechanisms and patterns of all the
patients who underwent arteriography to
exclude BCVI over a 9-year period, to iden-
tify independent predictors of BCVI. By mul-
tivariate analysis, Glasgow Coma Scale score
less than 6, petrous bone fracture, diffuse
axonal brain injury, and Le Fort II or II frac-
ture were identified as risk factors for carotid
injuries. The only independent predictor of
VA injury was cervical spine injury. In 4.5 years
of screening, we have performed screening
cerebral arteriography on 390 patients; of
these, 131 (33%) have had BCVI. More than
two thirds were asymptomatic at diagnosis. On

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246

IV • SPECIFIC VASCULAR INJURIES

the other hand, a handful of patients have
been transferred from remote facilities who
became symptomatic from BCVI following
"trivial trauma," who would not have met cri-
teria for screening. We believe these criteria
represent a starting point; however, the ques-
tion of optimal criteria will ultimately require
a multicenter collaborative effort.

DIAGNOSTIC EVALUATION

The discovery of signs or symptoms sugges-
tive of BCVI mandates emergent diagnostic
evaluation. The gold standard for diagnosis
of BCVI is four-vessel biplanar cerebral arte-
riography. Unfortunately, it is invasive and
resource intensive. Its risks include compli-
cations related to catheter insertion (1% to
2% hematoma, potential arterial pseudoa-
neurysm), contrast administration (1% to 2%
renal dysfunction, potential allergic reac-
tion), and stroke (<1%). Noninvasive diag-
nostic alternatives are available for screening
asymptomatic patients for BCVI; however, one
must recognize that diagnostic sensitivity is
compromised in avoiding invasive testing.
Duplex ultrasonography is widely considered
the modality of choice for imaging the carotid
arteries; however, experience in diagnosing
BCVI is limited. In the Western Trauma Asso-
ciation multicenter review, duplex scanning
had 86% sensitivity for ICA injury. In that
series, the lesions missed by duplex were
located at the base of the skull. Because most
ICA injuries involve the artery at or near the
base of the skull, this is a major potential weak-
ness. Furthermore, although duplex scanning
can provide indirect evidence of injuries by
detecting turbulence and other flow distur-
bances, these findings are not reliable in the
presence of stenoses of less than 60%. Unfor-
tunately, we have witnessed the potential for
innocuous-appearing luminal irregularities to
cause devastating cerebrovascular accidents
and thus do not believe duplex scanning is
adequate for BCVI screening. CT angiogra-
phy (CTA) is attractive because most multi-
system trauma patients have indications for
CT scanning. However, our experience has
shown that CTA has a sensitivity no better than

that of duplex ultrasonography. To image the
cerebral vessels in their entirety with a slice
thickness and pitch adequate for sufficiently
sensitive reconstruction is not practical; in
addition, bony artifact is in the carotid canal,
potentially obscuring injuries. Of all the non-
invasive screening modalities, magnetic reso-
nance angiography (MRA) holds the greatest
promise to reliably supplant cerebral arteri-
ography. Advantages of MRA include the capa-
bility to simultaneously image the remainder
of the head and neck and detect cerebral
infraction earlier than CT scanning while
avoiding contrast administration. Major
impediments include a lack of timely avail-
ability at many institutions and incompatibil-
ity of ventilatory and orthopedic fixation
equipment with the magnet. Recent prospec-
tive trials have reported suboptimal accuracy
of MRA as well as CTA. Until more rigorous
evaluation, arteriography remains the gold
standard.

INJURY GRADING

Carotid artery and VA injuries are a hetero-
geneous mix of lesions. Several groups have
suggested that different types of injuries
might be managed differently; the absence
of a formal BCVI grading scale, however,
has been a major impediment to formulating
sound practice guidelines. We hypothesized
that different injury types had distinct impli-
cations in terms of response to therapy and
ultimate neurologic outcome. Thus, we devel-
oped a grading scale based on the literature
and our collective experience with 109 carotid
injuries (Table 12-1 ) . We reported that stroke
incidence increased with injury grade. In con-
trast, recent analysis of our experience with
VA injuries revealed no similar correlation
between injury grade and posterior circula-
tion stroke (Table 12-2).

TREATMENT AND OUTCOME

The optimal management of BCVI remains
controversial. The three primary choices for

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12 • BLUNT CERVICAL VASCULAR INJURY

247

TABLE 12-1

BLUNT CAROTID AND VERTEBRAL ARTERY INJURY GRADING SCALE

Injury Grade

IV
V

Description

Luminal irregularity or dissection with <25%

luminal narrowing
Dissection or intramural hematoma with >25%

luminal narrowing, intraluminal thrombus, or

raised intimal flap
Pseudoaneurysm
Occlusion
Transection with free extravasation

AIS90

ICD-9*

Intracranial

Cervicar

900.03

900.3

900.03
900.03

900.03

3
4

3
3

'Internal carotid artery injury; ICD-9 code for common carotid artery injury is 900.01.

+ Add 1 if neurologic deficit (stroke) is not related to head injury.

AIS-90, Abbreviated Injury Scale, 1990 revision; ICD-9, International Classification of Diseases, 9th revision.

TABLE 12-2

STROKE RATE AND MORTALITY OF BLUNT CAROTID AND VERTEBRAL ARTERY
INJURIES, STRATIFIED BY INJURY GRADE

BCAI (%)

BVAI (%)

Worst Injury Grade

Stroke

Mortality

Stroke

Mortality

II
III

3
11
33
44

100

11
11
11
22

100

19
40
13
33

13
11

BCAI, blunt carotid artery injury; BVAI, blunt vertebral artery injury.

management include observation, surgical
therapy, and nonsurgical therapy (e.g., anti-
coagulation and endovascular techniques) . In
determining the treatment for an individual,
one must consider the location and grade of
the injury, as well as symptomatology.

Observation cannot be considered optimal
therapy, given the natural history of sympto-
matic BCVI; early reports established mor-
bidity and mortality rates of 58% and 28%,
respectively. Extrapolating from penetrating
trauma literature, wherein neurologic mor-
bidity and mortality were better in those under-
going operation, early series recommended
surgery in the absence of completed hemi-
plegic deficits. However, most blunt injuries
involve the ICA at or above the base of the

skull. Thus, inaccessibility precludes direct sur-
gical repair. Extracranial-intracranial bypass
has been successfully employed in select
patients, but this remains a controversial
concept.

In 1996, Fabian and colleagues reported a
large single-institution experience with carotid
artery injuries. Anticoagulation improved
neurologic outcome of patients presenting
with minor and major neurologic deficits. In
fact, logistic regression analysis identified
heparin as the only factor independently asso-
ciated with improved neurologic outcome. We
similarly found that symptomatic patients who
are anticoagulated showed a trend toward
greater neurologic improvement at the time
of discharge compared with those who were

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248

IV • SPECIFIC VASCULAR INJURIES

not anticoagulated (Table 12-3). An impor-
tant finding of our series was that identifica-
tion and treatment of carotid injuries before
the onset of symptoms appear critical in
improving neurologic outcome. In our analy-
sis of outcomes following VAinjuries, we again
found that heparin improves neurologic out-
comes (Table 12-4). Neurologic outcomes
were better in the group as a whole, as well as
in the subgroup suffering stroke. In addition,
anticoagulation resulted in favorable trends
including (1) preventing progression of
lesions to higher injury grades (Table 12-5);
(2) preventing neurologic deterioration from
diagnosis to discharge; and (3) preventing
stroke.

Obviously, bleeding complications are a
concern in patients with multisystem injuries.
We have experienced a 10% incidence of
bleeding complications with our anticoagu-
lation protocol. Presently, we are exploring

an alternative in lower risk patients. Specifi-
cally, we are prospectively comparing the safety
and efficacy of antiplatelet therapy versus sys-
temic heparinization in the treatment of
asymptomatic grade I BCVI (intimal irregu-
larity without luminal stenosis, intraluminal
thrombus, or a visible intimal flap).

Deployment of endovascular stents is
gaining increasing favor in the treatment of
vascular lesions. We deploy stents to treat per-
sistent traumatic pseudoaneurysms (grade III
BCVI) , in an attempt to tack down the intima
and exclude the pseudoaneurysm from the
circulation. In addition, we stent grade II
stenoses that threaten to occlude the vessel.
Given the risk of stroke during manipulation
of devices in an acutely injured artery, we rec-
ommend waiting 7 days, if possible, before
attempting stent placement. Until more data
are available, we recommend full anticoagu-
lation after stenting for BCVI. It must be

TABLE 12-3

NEUROLOGIC OUTCOME OF BLUNT CAROTID ARTERY INJURIES, STRATIFIED BY
TREATMENT; COMBINED EXPERIENCE FROM DENVER AND MEMPHIS

Outcome

Neurologic improvement, diagnosis to discharge
Neurologic deterioration, diagnosis to discharge
Good neurologic outcome
Poor neurologic outcome

Systemic

Heparin (%)

PValu

<.05

<c.05

<.05

TABLE 12-4

NEUROLOGIC OUTCOME OF BLUNT VERTEBRAL ARTERY INJURIES, STRATIFIED
BY TREATMENT

Outcome

Poor neurologic function (all BVAI patients)

Poor neurologic function (stroke victims)

Progression of injury grade

Neurologic deterioration, diagnosis to discharge

Stroke

Systemic
Heparin (%)

6
17
25
19

Systemic

Heparin (%)

60
100
60
60
35

P Value

<.05
<.05

.18

.11

.13

BVAI, blunt vertebral artery injury.

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12 • BLUNT CERVICAL VASCULAR INJURY

249

TABLE 12-5

ARTERIOGRAPHY OUTCOME OF GRADED CAROTID ARTERIAL LESIONS

Initial
Injury Grade

Treatment

Healed (5)

Final Injury Grade (%)

Heparin

16(70)

6(26)

—

1(4)

—

No heparin

12 (67)

4(22)

1(6)

—

Heparin

1(10)

6(60)

1(10)

No heparin

—

Heparin

1(8)

—

1 1 (85)

1(8)

No heparin

—

3(100)

—

Heparin

—

1 (100)

No heparin

—

1 (100)

emphasized that these devices are not
approved for these indications, and their use
should be restricted to research protocols.

Angiographic embolization has been
employed widely for maxillofacial arterial
injuries, but ICA embolization has not been
supported because of concern of brain in-
farction. Our experience with attempted
embolization in the ICA distribution has been
confined to grade V injuries; in each instance,
embolization has proven futile. On the other
hand, angiographic embolization has been
promoted as an alternative to surgical ligation
in the management ofVAinjuries. Experience
with this technique is still limited. Another
alternative to surgical ligation of the VA is
endovascular balloon occlusion.

SUMMARY AND GUIDELINES

BCVIs are infrequently diagnosed but may be
overlooked in many patients. Symptoms may
be masked by central nervous system injuries,
but the large majority are asymptomatic at the
time of presentation. Early diagnosis and insti-
tution of treatment appear to improve out-
comes. Thus, the following guidelines have
been adopted by our center.

Emergent cerebral arteriography should be
performed to exclude BCVI in the presence
of the following signs or symptoms: (1)
hemorrhage — from mouth, nose, ears, or
wounds — of potential arterial origin; (2)

expanding cervical hematoma; (3) cervical
bruit in a patient younger than 50 years; (4)
evidence of cerebral infarction on CT scan;
(5) unexplained or incongruous central or
lateralizing neurologic deficit, TIA, amauro-
sis fugax, or Horner's syndrome.

Consideration should be given to screen-
ing individuals with injury mechanisms or
patterns consistent with BCVI. These include
(1) an injury mechanism compatible with
severe cervical hyperextension/rotation or
hyperflexion, particularly if associated with dis-
placed or complex midface or mandibular
fracture, or closed head injury consistentwith
diffuse axonal injury of the brain; (2) near-
hanging resulting in cerebral anoxia; (3) seat-
belt abrasion or other soft tissue injury of the
anterior neck resulting in significant cervical
swelling or altered mental status; (4) basilar
skull fracture involving the carotid canal; and
(5) cervical vertebral body fracture or dis-
traction injury, excluding isolated spinous
process fracture.

Our current diagnostic standard remains
four-vessel cervical arteriography. All BCVIs
are treated. Surgically accessible grade II, III,
IV, and V injuries are repaired. Symptomatic
patients with BCVI should receive some form
of antithrombotic therapy, unless absolutely
contraindicated by central nervous system
injury. In asymptomatic patients with cerebral
intraparenchymal hemorrhage or fractures in
regions with the potential to develop an under-
lying epidural hematoma, anticoagulation is
not initiated until follow-up CT scan in 24

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250

IV • SPECIFIC VASCULAR INJURIES

hours excludes a significant change of the
lesion. If there has been progression of the
brain injury, anticoagulation is held until CT
scans are stable at 24-hour intervals. Anti-
coagulation is not withheld for punctate
intraparenchymal, small subarachnoid, or
intraventricular hemorrhages. Our anticoag-
ulation protocol is to begin a heparin infu-
sion at 15U/kg/hr, without an initial bolus
dose. The partial thromboplastin time (PTT)
is measured 6 hours after therapy is started,
and the infusion rate is adjusted to maintain
the PTT at 40 to 50 seconds. Follow-up arte-
riography is performed 7 to 10 days after
injury. Healing of the injury allows discon-
tinuation of therapy, whereas persistence
warrants 3 months of warfarin (Coumadin)
therapy. Progression of the lesion prompts
alteration in therapy, including endovascular
stent placement or a change in the anticoag-
ulant regimen, as well as additional follow-up
imaging. Patients undergo arteriography
again after 3 months, to determine the need
for further treatment.

REFERENCES

Biffl WL, Moore EE, Ellicott JP, et al: The devas-
tating potential of blunt vertebral arterial
injuries. Ann Surg 2000;231:672-681.

Biffl WL, Moore EE, Offner PJ, et al: Optimizing
screening for blunt cerebrovascular injuries. Am
J Surg 1999;178:517-522.

Biffl WL, Moore EE, Offner PJ, et al: Blunt carotid
arterial injuries: Implications of a new grading
scale. J Trauma 1999;47:845-853.

Biffl WL, Moore EE, Ryu RK, et al: The unrecog-
nized epidemic of blunt carotid arterial injuries:
Early diagnosis improves neurologic outcome.
Ann Surg 1998;228:462-470.

Biffl WL, Ray, CE, Moore EE, et al: Noninvasive
diagnosis of blunt cerebrovascular injuries: A pre-
liminary report. J Trauma 2002;53:850-856.

Carrillo EH, Osborne DL, Spain DA, et al: Blunt
carotid artery injuries: Difficulties with the diag-
nosis prior to neurologic event. J Trauma
1999;46:1120-1125.

Eachempati SR, Vaslef SN, Sebastian MW, Reed RL
II: Blunt vascular injuries of the head and neck:
Is heparinization necessary? J Trauma 1998;
45:997-1004.

Fabian TC, Patton JH Jr, Croce MA ,et al: Blunt
carotid injury: Importance of early diagnosis and
anticoagulant therapy. Ann Surg 1996;223:513-
525.

Giacobetti FB, Vaccaro AR, Bos-Giacobetti MA, et
al: Vertebral artery occlusion associated with cer-
vical spine trauma: A prospective analysis. Spine
1997;22:188-192.

Miller PR, Fabian TC, Croce MA, et al: Prospective
screeing for blunt cerebrovascular injuries:
Analysis of diagnostic modalities and outcomes.
Ann Surg 2002;236:386-395.

Rogers FB, Baker EF, Osier TM, et al: Computed
tomographic angiography as a screening modal-
ity for blunt cervical arterial injuries: Prelimi-
nary results. J Trauma 1999;46:380-385.

chl3.qxd 4/16/04 3:41PM Page 251

Penetrating Thoracic
Vascular Injury

SCOTT A. LEMAIRE
LORI D. CONKLIN
MATTHEW J. WALL, JR.

INITIAL EVALUATION AND MANAGEMENT
Prehospital Management

EMERGENCY CENTER EVALUATION AND MANAGEMENT
Primary Survey and Resuscitation

History

Initial examination

Intravenous access and fluid administration

Tube thoracostomy

Pericardiocentesis

Emergency center thoracotomy
Secondary Survey
DIAGNOSTIC STUDIES
Catheter Arteriography
Computed Tomography
TREATMENT OPTIONS
Endovascular Stenting
Surgical Repair

Preoperative considerations

Damage control

251

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252

IV • SPECIFIC VASCULAR INJURIES

SPECIFIC INJURIES
Thoracic Inlet

Subclavian artery and vein

Innominate artery and vein

Left common carotid artery
Thoracic Aorta

Ascending aorta

Transverse aortic arch

Descending thoracic aorta
Other Major Intrathoracic Vessels

Pulmonary artery and vein

Thoracic vena cava

Azygos vein

Internal thoracic and intercostal arteries
SPECIAL PROBLEMS
Mediastinal Traverse Injuries
Thoracic Duct Injury
Systemic Air Embolism
Foreign Body Embolism
POSTOPERATIVE MANAGEMENT

The lethality of penetrating chest
wounds has been well recognized
throughout history. More than 90% of
the penetrating thoracic wounds described in
Homer's Iliad and Virgil's Aeneid were fatal.
The first successful repair of a penetrating tho-
racic vascular injury did not occur until
October 1913, when a 30-year-old Russian
surgeon named Yustin Djanelidze closed an
8-mm stab wound to the ascending aorta with
three interrupted sutures.

Currently, nearly 4% of patients with pen-
etrating chest wounds have an injury involv-
ing the thoracic great vessels: the aorta and
its brachiocephalic branches, the pulmonary
arteries and veins, the superior and intratho-
racic inferior venae cavae, and the innomi-
nate and azygos veins. The incidence of great
vessel injury is substantially higher following
gunshotwounds (5%) than after stab wounds
(2%).

INITIAL EVALUATION AND
MANAGEMENT

Prehospital Management

Patients sustaining penetrating thoracic
trauma should be immediately transported to
the nearest trauma center capable of manag-
ing thoracic vascular injuries. Intravenous
access should be avoided in the upper extrem-
ities, particularly on the side of injury, because
the central venous structures may be tran-
sected or thrombosed. Allowing mild hypoten-
sion is preferable to aggressive attempts to
increase blood pressure with fluid boluses,
military antishock trousers (MAST suits) , or
pressors. Even transient increases in blood
pressure may dislodge a soft clot and increase
bleeding. In a randomized trial of patients
with penetrating truncal trauma, Bickell and

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13 • PENETRATING THORACIC VASCULAR INJURY

253

colleagues (1994) compared standard fluid
resuscitation with no preoperative fluid resus-
citation and demonstrated a significant sur-
vival advantage in patients who had delayed
resuscitation. Similarly, the use of MAST suits
in hypotensive patients sustaining penetrat-
ing thoracic trauma is associated with
increased mortality. These pneumatic com-
pression devices elevate blood pressure by
increasing afterload and are equivalent to
placing a cross clamp distal to avascular injury,
a clearly counterproductive maneuver.

EMERGENCY CENTER
EVALUATION AND
MANAGEMENT

Patient presentation can range from minimal
symptoms to cardiac arrest necessitating resus-
citative thoracotomy. Penetrating vascular
injuries may produce intraluminal intimal
flaps or thrombosis, arteriovenous fistulas, and
pseudoaneurysms. The resulting clinical
manifestations include external bleeding,
hemothorax, cardiac tamponade, medias-
tinal hematoma, stroke, and limb ischemia.
The diagnosis and treatment of the life-
threatening manifestations occur con-
comitantly during the primary survey and
resuscitation phase.

Primary Survey and
Resuscitation

of hemorrhage at the accident scene and
hemodynamic instability during transport.

INITIAL EXAMINATION

The primary survey addresses the most life-
threatening manifestations of intrathoracic
vascular injury by including focused attention
to airway obstruction, massive hemothorax,
and pericardial tamponade. As always, estab-
lishing satisfactory airway, breathing, and cer-
vical spine protection are the first concerns.
An expanding upper mediastinal hematoma
can cause stridor due to airway compression.
The subsequent circulation assessment
increases the focus on potential thoracic vas-
cular injuries. Hypotension immediately raises
the suspicion for a great vessel injury; the crit-
ical distinction is whether the hypotension is
due to hypovolemia or tamponade from an
intrapericardial injury. Tracheal deviation
away from the side of injury may indicate medi-
astinal shift due to a massive hemothorax.
Among the classic signs of tamponade (e.g.,
distended neck veins, pulsus paradoxus
exceeding lOmmHg, and muffled heart
sounds) , venous engorgement is an important
early sign of pericardial tamponade. Tam-
ponade should be considered in the setting
of progressive hypotension without evidence
of ongoing blood loss. In many trauma centers,
immediate ultrasonography can be performed
at the bedside in the emergency department
to rapidly determine whether a hemoperi-
cardium is present; this is a standard compo-
nent of the Focused Abdominal Sonography
for Trauma examination.

HISTORY

The history may provide the first clues sug-
gesting a thoracic vascular injury. Information
regarding the length of a knife, the firearm
type and number of rounds fired, and the
patient's distance from the firearm — though
not always reliable — is important to obtain
from the patient or accompanying persons.
In addition to information involving the
mechanism of injury, the emergency transport
personnel can provide medical information
important in evaluating the potential for a tho-
racic great vessel injury, such as the amount

INTRAVENOUS ACCESS AND
FLUID ADMINISTRATION

As a general rule, patients with suspected
injuries to the major thoracic venous branches
should have large-bore intravenous access
established in the lower extremities whenever
possible. The saphenous vein can be cannu-
lated percutaneously or via saphenous vein
cutdown at the ankle or in the groin; when
placing the catheter through a cutdown,
sterile intravenous extension tubing can be

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IV • SPECIFIC VASCULAR INJURIES

inserted directly in the vein. If an upper
extremity or subclavian venous catheter is
required in a patient with a potential subcla-
vian vascular injury, the contralateral side
should be used for cannulation.

The treatment of severe shock should
include blood transfusion. However, in
patients with mild hypotension, rapid infu-
sions of either blood or crystalloid should be
avoided before operation because they may
increase the blood pressure to a point that a
protective soft perivascular clot is "blown out"
and fatal hemorrhage ensues.

TUBE THORACOSTOMY

By evacuating the initial hemothorax, place-
ment of an appropriately sized chest tube
(Table 13-1) restores effective breathing and
allows an assessment regarding ongoing hem-
orrhage. The tube is usually placed in the
fourth or fifth intercostal space (near nipple
level) at the anterior to mid-axillary line.
Intrapleural blood loss that results in hypoten-
sion is termed massive hemothorax. If a massive
hemothorax is suspected, based either on clin-
ical findings or on the chest radiograph find-
ings, a repository that allows autotransfusion
can be connected to the chest tube before
insertion. Indications for urgent thoraco-
tomy include (1) large initial chest tube output
(>1500mL in adults and >20% of estimated
blood volume in children), (2) significant
ongoing hemorrhage (>200 to 250 mL per
hour in adults and >1 to 2mL/kg per hour

TABLE 13-1

APPROPRIATE CHEST TUBE SIZES IN
PATIENTS WITH TRAUMATIC
HEMOTHORAX

Age

Newborn

Infants

School age children

Adolescents

Adult

Chest Tube Size

12-16 French
16-18 French
18-24 French
28-32 French
36 French

in children), and (3) a significant increase in
bleeding.

PERICARDIOCENTESIS

If hemopericardium is present and the patient
is hemodynamically unstable, a subxiphoid
pericardial catheter should be placed in the
emergency center. Intermittent removal of
pericardial blood may prevent sudden hemo-
dynamic deterioration while preparing the
patient for surgery. Therefore, after insertion,
the catheter is secured in position to allow
repeated drainage as needed during transport
to the operating room and induction of
anesthesia.

EMERGENCY CENTER THORACOTOMY

Emergency center thoracotomy in patients
presenting with signs of life and hemodynamic
collapse may reveal injuries to major thoracic
vessels. In this setting, the thoracotomy allows
rapid resuscitation and temporary control of
bleeding in preparation for subsequent trans-
fer to the operating room and definitive repair.
A pericardiotomy anterior to the phrenic
nerve is performed to relieve pericardial tam-
ponade and allow effective cardiac compres-
sions. Bleeding from subclavian vessels can be
temporized by tightly packing the thoracic
apex or by inserting large balloon catheters
through the wounds. Either cross clamping
the entire hilum or twisting the lung 180
degrees after releasing the inferior pulmonary
ligament can control major hemorrhage from
the pulmonary hilum.

Secondary Survey

The secondary survey includes a search for
more subtle signs of vascular injury. Each
region of the body is thoroughly examined.
All penetrating wounds are noted and marked
with radiopaque markers. Substantial exter-
nal bleeding is more common after stab
wounds than gunshot wounds. Because vas-
cular thrombosis or an intimal flap may

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TABLE 13-2

CLUES TO PENETRATING THORACIC VASCULAR INJURY

Physical Examination

Shock

Superior vena cava syndrome

Pulse or pressure disparity between right and left

upper extremities
Pulse or pressure disparity between upper and

lower extremities
Intrascapular murmur
Hematoma at base of neck
Signs of pericardial tamponade:

Elevated venous pressure

Muffled heart sounds

Pulsus paradoxus

Chest Radiography

Large hemothorax

Foreign bodies (bullets or shrapnel) or their trajectories in

proximity to the great vessels
A foreign body out of focus with respect to the remaining

radiograph, which may indicate its intracardiac location
A trajectory with a confusing course, which may indicate a

migrating intravascular bullet
"Missing" missile in a patient with a gunshot wound to the

chest, suggesting distal embolization

completely occlude an injured vessel, the
absence of significant bleeding does not rule
out a major vascular injury. Examination of
the chest may reveal an expanding hematoma
at the thoracic inlet or an intrascapular
murmur. Thrills or bruits near the clavicles
may indicate the presence of an arteriovenous
fistula, which most commonly involves the
innominate or subclavian vessels. During
assessment of extremity circulation, the pres-
ence of a distal pulse does not rule out a prox-
imal injury because blood flow can continue
while the surrounding hematoma is contained
by perivascular tissue. Loss of an extremity
pulse may indicate intravascular embolization
of a bullet from an aortic injury. Unequal
blood pressures or pulses in the upper extrem-
ities suggest an innominate or subclavian
artery injury. An injury involving the descend-
ing thoracic aorta may cause pseudocoarcta-
tion syndrome with upper extremity
hypertension and diminished lower extrem-
ity pulses and pressures. Clinical signs indica-
tive of penetrating thoracic great vessel injuries
are summarized in Table 13-2.

As part of the secondary survey, a supine
anteroposterior chest radiograph is per-
formed in the emergency center after placing
radiopaque markers on all entrance and exit
wounds; findings that suggest an intrathoracic
vascular injury are listed in Table 13-2. In
many cases, the radiographic findings are suf-

ficient to warrant immediate arteriography or
direct transport to the operating room.

DIAGNOSTIC STUDIES

Unlike penetrating abdominal vascular
trauma, the operative approach to intratho-
racic vascular injuries varies substantially and
depends on the location of the injury (Table
13-3) . Therefore, imaging studies play a crit-
ical role in diagnosing and localizing the injury
so that the optimal approach can be planned.

Catheter Arteriography

In stable patients with penetrating thoracic
trauma, catheter angiography is indicated for
suspected innominate, carotid, or subclavian
arterial injuries. Different thoracic incisions
are required for proximal and distal control
of each the brachiocephalic vessels. Arteri-
ography, therefore, is essential for localizing
the injury and planning the appropriate inci-
sion. Proximity of a missile trajectory to the
brachiocephalic vessels, even without any
physical findings of vascular injury, is an indi-
cation for arteriography.

Although aortography may also be useful
in hemodynamically stable patients with

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IV • SPECIFIC VASCULAR INJURIES

TABLE 13-3

RECOMMENDED INCISIONS FOR THORACIC VASCULAR INJURIES

Injured Vessel

Uncertain injury (hemodynamically unstable)

Ascending aorta
Transverse aortic arch

Descending thoracic aorta
Innominate artery
Right subclavian artery or vein
Left common carotid artery
Left subclavian artery or vein

Pulmonary artery
Main/intrapericardial
Right or left hilar

Pulmonary vein

Innominate vein

Intrathoracic vena cava

Incision

Left anterolateral thoracotomy

± transverse sternotomy

± right anterolateral thoracotomy (clamshell)

Median sternotomy

± neck extension

Left posterolateral thoracotomy (fourth intercostal space)

Median sternotomy with right cervical extension

Median sternotomy with left cervical extension

Left anterolateral thoracotomy (third or fourth intercostal space)

with separate left supraclavicular incision
± connecting vertical sternotomy ("book" thoracotomy)

Median sternotomy

Ipsilateral posterolateral thoracotomy

Median sternotomy

suspected penetrating aortic injuries, its lim-
itations in this setting must be recognized. If
the laceration has temporarily "sealed off," or
if the column of aortic contrast overlies a small
area of extravasation, the resulting "negative"
aortogram may foster a false sense of security.
To maximize sensitivity, therefore, an effort
must be made to obtain views that are tan-
gential to possible injuries (Figs. 13-1 and
13-2).

Computed Tomography

Until recently, conventional computed tomog-
raphy (CT) had a limited role in evaluating
vascular injuries. Although CT could demon-
strate hemomediastinum and other sugges-
tive signs, it did not provide the diagnostic
capability of standard aortography. However,
newer helical CT equipment is much faster,
uses advanced computer analysis, and per-
forms techniques different from first- or
second-generation CT scanners. Not only is
the resolution much greater than in former
models, but the current machines also allow
for computerized anatomic reconstruction,
which was not available earlier. Compared to

catheter arteriography, CT angiography
(CTA) is faster and less expensive, and it
eliminates complications related to arterial
catheterization. Data regarding its reliability
in evaluating acute injuries, however, are
limited and few trauma centers are equipped
for its routine use. Although prospective trials
will be required to verify its accuracy, CTA
with three-dimensional reconstruction is
rapidly evolving and may replace catheter
arteriography as the study of choice in the
future. Although magnetic resonance angiog-
raphy can generate similarly detailed infor-
mation, its application in these potentially
unstable trauma patients is not currently
practical.

TREATMENT OPTIONS
Endovascular Stenting

Evolving techniques in endovascular stenting
are providing new options for the treatment
of vascular trauma. Endovascular grafts can
seal vascular lacerations from within the
lumen without compromising blood flow. In

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13 • PENETRATING THORACIC VASCULAR INJURY

257

■ FIGURE 13-1

Missed injury by aortography. Chest radiograph (A) of a patient with a tiny puncture wound from a
Philips screwdriver in the left second intercostal space at the sternal border. The patient arrived in
the emergency room 30 minutes after being wounded and had stable vital signs for the following
48 hours. Anteroposterior (B), left anterior oblique (C), and near-lateral (D) projections of the
aortogram were each interpreted by staff radiologist as showing no injury. Subtraction aortography
in the lateral projection (E) demonstrates tiny outpouching of the thoracic aorta anteriorly at the
base of the innominate artery and posteriorly on the undersurface of the transverse aortic arch.
Penetrating injury of the transverse aortic arch was confirmed intraoperatively. (From Mattox KL:
Approaches to trauma involving the major vessels of the thorax. Surg Clin North Am 1989;69:83.) ■

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258 IV • SPECIFIC VASCULAR INJURIES

FIGURE 13-1, cont'd

principle, several aspects of vascular trauma
make it well suited for transcatheter repair.
These injuries occur predominately in rela-
tively young patients without peripheral vas-
cular occlusive disease. Furthermore, remote
access can minimize the morbidity and tech-
nical difficulty often associated with direct sur-
gical repair, particularly when the traumatic
lesion occurs in the presence of a large
hematoma, pseudoaneurysm, or arteriove-
nous fistula. Although direct vascular repair
is generally successful, the wide surgical expo-
sure that is often required can cause persis-
tent pain and various degrees of disability. For
example, the need for clavicular resection
increases the morbidity of subclavian vascu-
lar repairs. Despite the advantages of a less
invasive approach, many trauma patients, such
as those who are hemodynamically unstable
or those with heavily contaminated wounds,
will not be suitable candidates for endovas-
cular repairs.

Despite these caveats, endovascular tech-
niques are being successfully applied with
increasing frequency. Parodi and colleagues
(1999) reported a series of 29 patients who

■ FIGURE 13-2

Plain chest radiograph (A)oi a patient with a penetrating chest wound. 6, The aortogram
demonstrates no apparent injury in the anteroposterior projection but reveals a defect in the anterior
aortic wall on the left anterior oblique projection. (From Mattox KL, Wall MJ Jr, LeMaire SA: Injury to
the thoracic great vessels. In: Mattox KL, Feliciano DV, Moore EE, eds, Trauma, 4th ed. New York:
McGraw-Hill, 2000.) ■

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259

underwent endovascular stent placement for
post-traumatic false aneurysms (10 patients)
and arteriovenous fistulas (19 patients).
Twenty-two of these injuries were located in
thoracic or neck vessels, that is, the subcla-
vian artery (9 injuries), axillary artery (3
injuries), aorta (2 injuries), common carotid
artery (5 injuries) , and internal carotid artery
(3 injuries). The false aneurysms or arteri-
ovenous fistulas were closed completely by one
or more stent-graft devices in 28 of 29 patients.
One patient died 1 month after the stent-graft
false aneurysm closure. Twenty-three of
twenty-nine patients continued to demon-
strate stent-graft patency and remained asymp-
tomatic after 24 months mean follow-up.
Event-free survival at 3yearswas 83%. In 2000,
du Toit and colleagues published a series of
10 patients who qualified for stent-graft place-
ment. The vessels involved were subclavian
artery (in 7 patients), carotid artery (2
patients), and axillary artery (1 patients).
Seven had arteriovenous fistulas and three pre-
sented with pseudoaneurysms. On average
follow-up of 7months, no complicationswere
encountered.

Surgical Repair

Whenever possible, imaging studies are used
to establish the diagnosis and plan the surgi-
cal approach. Clinical deterioration before
obtaining these studies requires immediate
transfer to the operating room for thoraco-
tomy; indications for urgent operation include
hemodynamic instability, hemopericardium,
major hemorrhage from chest tubes, and radi-
ographic evidence of a rapidly expanding
mediastinal hematoma.

PREOPERATIVE CONSIDERATIONS

It is important to inform patients and their
families of the potential for neurologic com-
plications, such as paraplegia, stroke, and
brachial plexus injuries, following surgical
reconstruction of the thoracic great vessels.
Careful documentation of preoperative neu-
rologic status is critical. With any suspicion of
vascular injury, prophylactic antibiotics are

administered preoperatively. In hemody-
namically stable patients, fluid administration
is limited until vascular control is achieved in
the operating room. An autotransfusion
device should be prepared. During the induc-
tion of anesthesia, wide swings in blood pres-
sure are avoided; although profound
hypotension is clearly undesirable, hyperten-
sive episodes can have equally devastating
consequences.

The operative approach to great vessel
injury varies depending on both the overall
patient assessment and the specific injury. The
initial steps of patient positioning and inci-
sion selection (see Table 13-2) are particu-
larly important in surgery for thoracic vascular
injuries, as adequate exposure is mandatory
for proximal and distal control. Preparing and
draping the patient should provide access
from the neck to the knees to allow manage-
ment of all contingencies. For the hypoten-
sive patient with an undiagnosed injury, the
mainstay of thoracic trauma surgery is the left
anterolateral thoracotomy with the patient in
the supine position. In stable patients, pre-
operative arteriography may dictate an oper-
ative approach by another incision.

Appropriate graft materials should be avail-
able. Although an infected prosthetic graft
may form a pseudoaneurysm, a saphenous
vein graft is a devitalized collagen tube sus-
ceptible to bacterial collagenase, which can
cause graft dissolution leading to acute
rupture and uncontrolled hemorrhage.
Therefore, for vessels larger than 5mm, pros-
thetic graft material is the conduit of choice,
especially in potentially contaminated
wounds. However, because of patency con-
siderations, a saphenous vein graft may need
to be used when smaller grafts are required.
For soft vessels, such as the subclavian artery
and the aorta in young people, a soft knitted
Dacron graft is useful. Antibiotic irrigation of
the graft material may help prevent subse-
quent infection.

DAMAGE CONTROL

Patients with severely compromised physio-
logic reserve, including those in extremis and
those with massive or multiple complex tho-

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260

IV • SPECIFIC VASCULAR INJURIES

racic injuries, often require damage control
injury management to achieve survival. The
two approaches to thoracic damage control
are (1) definitive repair of injuries using quick
and simple techniques that restore survivable
physiology during a single operation and (2)
abbreviated thoracotomy that restores sur-
vivable physiology and requires a planned sub-
sequent operation for definitive repairs.
Performing a pneumonectomy using stapling
devices can quickly control severe hilar vas-
cular injuries. Temporary vessel ligation or
placement of intravascular shunts can control
bleeding until subsequent correction of aci-
dosis, hypothermia, and coagulopathy allows
the patient to be returned to the operating
room. En mass closure of a thoracotomy with
a continuous heavy suture is more hemosta-
tic than towel-clip closure. A plastic "Bogota
bag" can be used as a temporary closure of a
median sternotomy in cases with associated
cardiac dysfunction.

SPECIFIC INJURIES

Thoracic Inlet

SUBCLAVIAN ARTERY AND VEIN

Penetrating trauma to the periclavicular
region with injury to the innominate, sub-

clavian, and axillary vessels continues to pose
a challenging problem for the surgeon
because of the significant morbidity and mor-
tality that occurs following damage to these
vessels. The subclavian vessels are the most
commonly injured great thoracic vessels: 21%
of thoracic greatvessel injuries involve the sub-
clavian arteries and 13% involve the subcla-
vian veins. Venous injuries have a significantly
higher mortality than arterial injuries; in a
series of 228 penetrating subclavian vessel
injuries reported by Demetriades (1987), the
overall mortality was 82% and 60%, respec-
tively (P< .01). Approximately 61% of patients
sustaining injuries to the subclavian vessels
are dead on arrival to the emergency center.
Of those who reach the hospital alive, most
require operative intervention, with an oper-
ative mortality of up to 16% and substantial
surgical morbidity. External or intrathoracic
bleeding from the subclavian vessels may be
difficult to control with direct pressure given
their anatomic position behind the clavicle.
In the presence of a supraclavicular wound,
balloon tamponade using one or two Foley
catheters placed through the wound may
control bleeding until the patient arrives in
the operating room (Fig. 13-3).

Patients with injury to the subclavian vessels
may present with hard signs of vascular injury,
such as absent distal pulses, expanding or pul-
satile hematomas, or massive external hem-
orrhage. However, a subset of patients will not

■ FIGURE 13-3

Balloon tamponade of subclavian
vascular bleeding. A Foley catheter
is inserted into the supraclavicular
wound and is advanced as far as it
can go. The balloon is then inflated
and firm traction is applied to the
catheter. The balloon compresses
the subclavian vessels against the
clavicle and the first rib. If there is
persistent external bleeding, a
second catheter is inserted and the
balloon is inflated inside the wound
tract, superficial to the first balloon.
(Modifed from Demetriades D.
Penetrating injuries to the thoracic
great vessels. J Card Surg
1997;12:173-180.) ■

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261

exhibit any of these findings, and their injury
may be found on angiograms obtained solely
on the basis of location of injury or chest radi-
ograph findings.

One pitfall in subclavian injuries is failure
to anticipate the exposure necessary for prox-
imal control. When approaching the sub-
clavian artery via a supraclavicular incision
without proximal control, exsanguination
may occur. A median sternotomy with a cer-
vical extension is employed for exposure of
right-sided subclavian injuries. For left sub-
clavian artery injuries, proximal control is
obtained through an anterolateral thoraco-
tomy (above the nipple, third or fourth inter-
costal space) , while a separate supraclavicular
incision provides distal control. In the
extremely difficult left-sided subclavian artery
injury, a formal "book" thoracotomy incision
may be required. This approach is associated
with a high incidence of postoperative "causal-
gia" type of neurologic complications; there-
fore, its use should be limited. Although this
carries significant morbidity, resection of the
clavicle may also aid in obtaining proximal
control. Alternatively, for distal injuries, a com-
bination of supraclavicular and infraclavicu-
lar incisions may be used to avoid the
morbidity of clavicular resection. In obtain-
ing exposure, it is important to avoid injur-
ing the phrenic nerve, which is located
anterior to the scalenus anticus muscle, and
the brachial plexus. Many patients with sub-
clavian injuries will present with associated
brachial plexus injuries, so careful docu-
mentation of preoperative neurologic status
is important.

In most instances, repair of the subclavian
artery requires either lateral arteriorrhaphy
or graft interposition. A primary end-to-end
anastomosis is usually not possible because of
the fragility of the artery and limited mobi-
lization. Associated injuries to the lung should
be managed with stapled wedge resection or
pulmonary tractotomy.

Achievement of adequate surgical exposure
can be difficult and may be associated with
postoperative neurologic complications;
therefore, certain patients sustaining pene-
trating injuries to the subclavian vessels may
benefit from stent-graft treatment. The success
of stent-graft treatment for traumatic lesions

depends largely on patient selection. Patients
must be hemodynamically stable, and it must
be possible to traverse the damaged segment
with aguidewire. To avoid endoleakswith this
technique, the proximal-distal lumen dis-
crepancy must not be too large, and in the
case of injuries to the subclavian artery, all side-
branches, which potentially participate in the
lesion, must be embolized before stent
deployment (Fig. 13-4).

INNOMINATE ARTERY AND VEIN

The innominate artery is injured in approx-
imately 9% of patients sustaining penetrating
thoracic vascular trauma. Injuries to the left
innominate vein are three times more
common than those to the shorter right
innominate vein. These injuries are
approached through a median sternotomy
with a right- or left-sided extension into the
neck. Isolated venous injuries can be managed
with primary repair or ligation. Division or
ligation of the innominate vein can also be
used to enhance exposure of the underlying
artery.

In selected patients with only partial tears,
the innominate artery may be primarily
repaired using 4-0 polypropylene suture.
More often, injuries to this vessel require
repair via the bypass exclusion technique,
which does not require cardiopulmonary
bypass, hypothermia, systemic anticoagula-
tion, or shunting. Bypass grafting is per-
formed from the ascending aorta to the distal
innominate artery using a Dacron tube graft
(usually a 10-mm graft in adults) . The area of
injury is carefully avoided until the bypass is
completed. The proximal anastomosis con-
nects the graft to the ascending aorta away
from the innominate artery origin; this is
accomplished using a partial occluding, "side-
biting" clamp on the ascending aorta. The
distal anastomosis requires proximal and
distal control of the innominate artery. If the
proximal portion of the artery is injured, a
partial occluding clamp can be placed across
the adjacent aorta. For distal control, a vas-
cular clamp is placed proximal to the bifur-
cation of the innominate artery to allow
collateral flow from the right subclavian artery

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262 IV • SPECIFIC VASCULAR INJURIES

■ FIGURE 13-4

Treatment of a pseudoaneurysm of the left subclavian artery. A, Selective left subclavian artery
arteriogram demonstrating the pseudoaneurysm; B, complete exclusion of the lesion after stent-
graft deployment. (From du Toit DF, Strauss DC, Blaszczyk M: Endovascular treatment of
penetrating thoracic outlet arterial injuries. Eur J Vase Endovasc Surg 2000;19:489-495.) ■

to perfuse the right carotid artery. After the
bypass is completed, the aorta is controlled
with a partial occluding clamp and is oversewn.
If concomitantly injured or previously divided,
the innominate vein may be ligated with
impunity. Alternatively, in stable patients, the
vein can be reanastomosed. If the vein remains
intact, a pedicled pericardial flap can be posi-
tioned between the vein and overlying graft
to prevent erosion. With the bypass principle,
reconstruction of innominate vascular injury
carries an extremely low mortality rate and
minimal morbidity, except in patients with pre-
operative neurologic injury or complex asso-
ciated injuries.

LEFT COMMON CAROTID ARTERY

than 50% of these patients require urgent
or semiurgent intubation because of the
expanding hematoma. Tracheostomy is
avoided because it may disrupt an underlying
hematoma and cause severe bleeding. A base-
line neurologic examination should be doc-
umented. Intraoperative endoscopy should be
considered to rule out associated tracheal or
esophageal injuries. The operative approach
for injuries of the left carotid artery mirrors
that used for an innominate artery injury: a
median sternotomy with a left cervical exten-
sion added when necessary. As with other great
vessel injuries, the use of shunts or pumps
is unnecessary. If the artery is transected
near its origin, repair with the bypass princi-
ple is preferred over a primary end-to-end
anastomosis.

Injuries to the left common carotid artery are
relatively uncommon when compared with
other sites, especially since penetrating tho-
racic outlet injuries account for less than
5% of all civilian vascular trauma. The early
management of these patients is critical
and cannot be overemphasized. Immediate
airway control is a priority because more

Thoracic Aorta

ASCENDING AORTA

Although penetrating injuries involving the
ascending aorta (see Fig. 13-2) are uncom-
mon, they do occur more often than blunt

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263

ascending aortic injuries. Survival rates
approach 50% for patients having stable vital
signs on arrival at a trauma center.

Although primary repair of anterior lacer-
ations can be accomplished without adjuncts,
cardiopulmonary bypass may be required if
there is an additional posterior injury. The
possibility of a peripheral bullet embolus must
always be considered in these patients.

TRANSVERSE AORTIC ARCH

Penetrating aortic arch injuries are increas-
ing in frequency because of the escalating use
of firearms; however, the overall incidence of
these injuries remains small, perhaps because
of its short length and restricted location. The
dominant clinical presentation is a penetrat-
ing thoracic wound with intrathoracic hem-
orrhage and shock.

When approaching an injury to the trans-
verse aortic arch, extension of the median ster-
notomy to the neck is important to obtain
complete exposure of the arch and brachio-
cephalic branches. If necessary, exposure can
be further enhanced by division of the innom-
inate vein. When hemorrhage limits exposure,
the use of balloon tamponade is useful as a
temporary measure. Simple lacerations may
be repaired by lateral aortorrhaphy. With dif-
ficult lesions, such as posterior lacerations
or those with concomitant pulmonary artery
injuries, cardiopulmonary bypass is recom-
mended. As with injuries to the ascending
thoracic aorta, survival rates approaching
50% are possible.

DESCENDING THORACIC AORTA

Penetrating injury to the descending thoracic
aorta occurs in 21 % of patients presenting with
wounds to the thoracic vasculature and is often
accompanied by other organ injuries, such as
the esophagus and heart. Patients may present
to the emergency center with exsanguination,
enlarging hemothorax, or bullet embolism to
the lower extremity.

Injuries to the descending thoracic aorta
are ideally approached via a posterolateral tho-
racotomy through the fourth intercostal space.

However, these are often found during emer-
gent exploration via anterolateral thora-
cotomy. Although lateral aortorrhaphy is
usually possible, the surgeon must also be pre-
pared to perform patch graft aortoplasty or
interposition grafting.

While gaining proximal control at the
upper descending thoracic aorta, care must
be taken to avoid injuring the left recurrent
laryngeal nerve. If itis suspected that the injury
extends to the aortic arch or ascending aorta,
cardiopulmonary bypass should be available
in the operating room. If the patient has had
previous coronary artery bypass surgery with
use of the left internal mammary artery as
a conduit, repair may require profound
hypothermic circulatory arrest.

The most feared complication of descend-
ing thoracic aortic injury is paraplegia, which
has been associated with perioperative
hypotension, injury or ligation of the inter-
costal arteries, and the complexity of the
injury. We have advocated simple clamp and
repair for injuries to the descending thoracic
aorta (without the use of systemic anticoagu-
lation or shunts), a technique that continues
to be used with excellent results.

Other Major Intrathoracic
Vessels

PULMONARY ARTERY AND VEIN

The pulmonary artery is damaged in 16% of
patients presenting to the emergency center
with penetrating trauma to the thoracic
vessels, while the pulmonary veins are injured
in 9% . These injuries are associated with mor-
tality rates that approach 70%. The most
common presenting manifestation of pul-
monary artery injuries is hypotension or
shock in association with either massive hemo-
thorax or hemoptysis.

Distal pulmonary artery injuries are ideally
approached through an ipsilateral postero-
lateral thoracotomy. These injuries are often
identified during an emergent exploration via
anterolateral thoracotomy. If a major injury
to the hilum is present, rapid pneumonectomy
may be a lifesaving maneuver. The use of a
large balloon catheter may control exsan-

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IV • SPECIFIC VASCULAR INJURIES

guinating hemorrhage. The intrapericardial
pulmonary arteries are approached via
median sternotomy. When this approach is
used, minimal dissection is needed to expose
the main and proximal left pulmonary arter-
ies. Exposure of the intrapericardial right pul-
monary artery is achieved by dissecting
between the superior vena cava and ascend-
ing aorta. Although anterior injuries can be
repaired primarily without adjuncts, repair of
a posterior injury usually requires cardiopul-
monary bypass. If ligation of the right or left
pulmonary artery is required, a pneumonec-
tomy is performed.

Injury to the pulmonary veins is difficult
to manage through an anterior incision. With
major hemorrhage, temporary occlusion of
the entire hilum may be necessary. If a pul-
monary vein must be ligated, the appropriate
lobe needs to be resected. Pulmonary vein
injuries are often associated with concomitant
injuries to the heart, pulmonary artery, aorta,
and esophagus.

AZYGOS VEIN

The azygos vein is not usually classified as a
thoracic great vessel, but because of its size
and high flow, azygos vein injuries must be
considered potentially fatal. Penetrating
wounds of the chest can produce combina-
tions of injuries involving the azygos vein,
innominate artery, trachea or bronchus, and
superior vena cava. These complex injuries
have a very high mortality rate and are par-
ticularly difficult to control if approached
through an anterior incision. Combined inci-
sions and approaches are often needed for
successful repair. When injured, the azygous
vein is best managed by suture ligature on both
sides of the injury. Concomitant injury to the
esophagus and bronchus should be consid-
ered and ruled out with a combination of
direct exploration, esophagoscopy, and bron-
choscopy before the patient leaves the oper-
ating room.

THORACIC VENA CAVA

INTERNAL THORACIC AND
INTERCOSTAL ARTERIES

Isolated injury to the suprahepatic or supe-
rior vena cava is infrequently reported. Injury
at either location has a high incidence of asso-
ciated organ trauma and carries a mortality
rate greater than 60%. Intrathoracic inferior
vena cava injury produces hemopericardium
and cardiac tamponade. Exposure of the pos-
terior thoracic inferior vena cava is extremely
difficult unless the patient is placed on total
cardiopulmonary bypass with the inferior
cannula inserted via the groin to the abdom-
inal inferior vena cava. Repair is accom-
plished by a right atriotomy and intracaval
balloon occlusion to prevent air entering the
venous cannula and limit blood return to
the heart. The injury is repaired from inside
the cava via the right atrium. Superior vena
cava injuries are repaired by lateral venor-
rhaphy. At times, an intracaval shunt is nec-
essary. For complex injuries patch angioplasty
or an interposition tube graft (Dacron or
ringed polytetrafluoroethylene) can be used
safely and is more expedient than the time-
consuming construction of saphenous vein
panel grafts.

Injury to the internal thoracic (i.e., the inter-
nal mammary) artery in a young patient can
produce extensive hemothorax or even peri-
cardial tamponade, simulating a cardiac
injury. Such injuries are usually serendipi-
tously discovered at the time of thoracotomy
for suspected great vessel or heart injury. Per-
sistent hemothorax can be caused by simple
lacerations of the intercostal arteries. Because
of difficulty in exposure, precise ligature can
be difficult. Rapid control is best achieved by
circumferential ligatures around the rib on
either side of the intercostal vessel injury.
These injuries are often missed during the
initial operation because of arterial spasm;
bleeding ensues later when the spasm resolves.

SPECIAL PROBLEMS

Mediastinal Traverse Injuries

Because penetrating injuries that traverse the
mediastinum are classically felt to have a high

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265

probability of injury to the thoracic great
vessels and other critical structures, manda-
tory exploration remains a justifiable
approach. The evaluation of stable patients
using less invasive means, such as combined
aortography, bronchoscopy, echocardiogra-
phy, and esophagoscopy, is gaining propo-
nents. Thoracoscopic evaluation of the
mediastinal structures is another potential
alternative that warrants investigation.

Thoracic Duct Injury

Injuries to the thoracic great vessels may be
complicated by concomitant thoracic duct
injury, which if unrecognized may produce
devastating morbidity because of marked
nutritional depletion. Diagnosed by chylous
material draining from the chest tube, this
condition is usually treated medically. Con-
tinued chest tube drainage, coupled with a
diet devoid of long-chain fatty acids, usually
results in spontaneous closure in less than 1
month. Prolonged hyperalimentation beyond
3 weeks has not consistently resulted in spon-
taneous closure of thoracic duct fistula. If
thoracotomy is required, a heavy fatty meal to
increase the chylous flow and facilitate iden-
tification of the fistula is given to the patient
a few hours before surgery. The fistula is simply
ligated.

Foreign Body Embolism

Because of their central location, the thoracic
great vessels may serve as both an entry site
and a final resting place for intravascular bullet
emboli. These migratory foreign bodies
present a diagnostic and therapeutic dilemma.
As the result of intravascular embolization,
bullets may produce infection, ischemia, or
injury to organs distant from the site of trauma.
Bullets and catheters can embolize to the
pulmonary vasculature; 25% of migratory
bullets finally lodge in the pulmonary arter-
ies. Although small fragments, such as those
the size of a BB, can probably be left in place
without causing problems, larger bullet emboli
should be removed to prevent pulmonary
thrombosis, sepsis, or other complications.
Nonoperative management of foreign bodies
located in the left side of the heart should be
performed only in selected asymptomatic
patients, such as those presenting long after
the initial injury and in whom imaging studies
confirm that the foreign body is encapsulated
by fibrous tissue. Percutaneous retrieval of
the foreign body using transvenous catheters
and fluoroscopic guidance may obviate the
need for thoracotomy. Intraoperative imaging
is necessary to rule out unsuspected migra-
tion of the foreign body during patient
positioning.

Systemic Air Embolism

A fistula between a pulmonary vein and bron-
chiole due to a penetrating lung injury may
result in a systemic air embolism (Fig. 13-5) .
The fistula allows air bubbles to enter the left
heart and embolize to the systemic circula-
tion, including the coronary and cerebral
arteries. Intrabronchial pressure of more
than 60 mm Hg increases the incidence of this
complication. Manifestations include seizures
and cardiac arrest. Resuscitation requires
thoracotomy, clamping of the pulmonary
hilum to prevent further air embolization, and
aspiration of air from the left ventricle and
ascending aorta. Cardiopulmonary bypass
can be considered , but very few survivors have
been reported.

POSTOPERATIVE
MANAGEMENT

A significant portion of the in-hospital
mortality associated with great vessel injury
is secondary to the nature of the multisystem
trauma in this group of patients. The oper-
ating surgeon is best qualified to direct
postoperative management. Careful hemo-
dynamic monitoring, with avoidance of both
hypertension and hypotension, is critical.
Although urinary output is a generally a good
indicator of cardiac function, for the patient
with massive injuries, Swan-Ganz monitoring
is often necessary to optimize hemodynamic
parameters and manage fluids, pressors, and
vasodilators.

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IV • SPECIFIC VASCULAR INJURIES

Bronchiole

Alveolus

m FIGURE 13-5

Drawing depicting the mechanism of systemic air embolism following a penetrating lung injury.
(From Baylor College of Medicine, Houston, Texas.) ■

Various pulmonary problems, including
atelectasis, respiratory insufficiency, pneu-
monia, and acute respiratory distress syn-
drome, represent the primary postoperative
complications in this group of patients, neces-
sitating careful fluid administration. Associ-
ated pulmonary contusions also contribute to
respiratory problems. Positive end-expiratory
pressure can be provided to hemodynamically
stable intubated patients, to minimize atelec-
tasis. Patient mobility is important, and ade-
quate medication for pain relief results in
fewer pulmonary complications. For the man-
agement of pain related to a thoracotomy or
multiple rib fractures, postoperative thoracic
epidural anesthesia should be considered in
stable patients without spinal injuries; alter-
natively, intercostal nerve blocks can be

performed intraoperatively and repeated in
the intensive care unit.

Postoperative hemorrhage may be due to
a technical problem but is often the result of
coagulopathy related to hypothermia, acido-
sis, and massive blood transfusion. Coagula-
tion studies must be carefully monitored and
corrected with administration of appropriate
blood products. Blood draining via chest tubes
can be collected and autotransfused.

The presence of a prosthetic vascular graft
requires special attention aimed at avoiding
bacteremia. During the initial resuscitation of
these critically injured patients, various
intravascular lines are often rapidly placed at
the expense of strict sterile technique; such
lines should be replaced after the patient
has stabilized in the intensive care unit.

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267

Antibiotic therapy should be continued into
the postoperative period until potential
sources of infection are eliminated. Patients
are counseled regarding the necessity of
antibiotic prophylaxis during invasive proce-
dures, including dental manipulations.

Most late complications are related to infec-
tions or sequelae from other injuries. Long-
term complications specifically related to the
vascular repair, including stenosis, thrombo-
sis, arteriovenous fistula, graft infection, and
pseudoaneurysm formation, are uncommon.

REFERENCES

Bickell WH, Wall MJ Jr, Pepe PE, et al: Immediate
versus delayed fluid resuscitation for hypoten-
sive patients with penetrating torso injuries. N
Engl J Med 1994;331:1105-1109.

Demetriades D: Penetrating injuries to the thoracic
great vessels. J Card Surg 1997;12:173-180.

du Toit DF, Strauss DC, Blaszcyk M, et al: Endovas-
cular treatment of penetrating thoracic outlet

arterial injuries. Eur J Endovasc Surg 2000;
19:489-495.

Demetriades D, Rabinowitc B, Pezikis A, et al:
Subclavian vascular injuries. Br J Surg 1987;74:
1001-1003.

Feliciano DV: Trauma to the aorta and major
vessels. Chest Surg Clin North Am 1997;7(2):305-
323.

Mattox KL, Wall MJ: Trauma of the chest: newer
diagnostic measures and emergency manage-
ment. Chest Surg Clin North Am 1997;7(2):213-
226.

Parodi JC, Schonholz C, Ferreira LM, Bergan J:
Endovascular stent-graft treatment of traumatic
arterial lesions. Ann Vase Surg 1999;13(2):121-
129.

Richardson JD, Miller FB, Carrillo EH, Spain DA:
Complex thoracic injuries. Surg Clin North Am
1996;76(4):725-748.

Wall MJ, Granchi T, Liscum KR, Mattox KL: Pen-
etrating thoracic vascular injuries. Surg Clin
North Am 1996;76(4):749-761.

chl4.qxd 4/16/04 3:39PM Page 269

Blunt Thoracic
Vascular Injury

AURELIO ROC

RIGUEZ

DAV

ID C. ELL

OTT

BLUNT THORACIC VASCULAR TRAUMA

DEMOGRAPHICS AND PATTERN OF INJURY

PRESENTATION

DIAGNOSIS

Aortogram

Chest X-ray

Computed Tomography

Transesophageal Echocardiography

PREOPERATIVE MANAGEMENT

SURGICAL TECHNIQUE

BLUNT INJURY TO OTHER THORACIC VESSELS
Innominate Artery
Subclavian Artery

Vena Cava

Pulmonary Artery and Vein

SUMMARY

269

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IV • SPECIFIC VASCULAR INJURIES

BLUNT THORACIC
VASCULAR TRAUMA

A 30-year-old man is ejected from his pickup
truck after falling asleep at the wheel and strik-
ing an embankment. Brought rapidly by heli-
copter to a level I trauma center, he is found
by expeditious evaluation to have sustained a
mild closed head injury, a stable pelvic frac-
ture, and multiple rib fractures. Of more
concern, his diagnostic peritoneal lavage
returns grossly positive and his supine chest
radiograph reveals a widened mediastinum
with distortion of the aortic knob.

How will the diagnostic evaluation proceed
from here? Will aortography precede or
follow laparotomy? If a ruptured thoracic aorta
is found, will a Gott shunt, a Bio-Medicus
pump, or a "clamp-and-sew" strategy be
pursued? Will you perform a primary repair
of the injured aorta or place a synthetic graft?
What perioperative measures can you employ
to minimize postoperative complications such
as paraplegia? These are a few of the often
controversial questions surrounding evalua-
tion and treatment of the patient with trau-
matic rupture of the thoracic aorta, which we
attempt to address in this chapter. In addi-
tion, the less commonly seen blunt injuries
to other thoracic vascular structures are also
reviewed.

Blunt thoracic aortic injury (BTAI) is a
major cause of morbidity and mortality in the
United States, with one fifth of motor vehicle
accident deaths attributable thereto. Despite
advances in surgical technique and post-
operative care, survival has not changed much
since 1958, when Parmley and colleagues from
the Armed Forces Institute of Pathology and
Walter Reed U.S. Army Hospital provided the
classic pathophysiologic and epidemiologic
description of BTAI. In their series of 275
patients, 86% died at the scene. Of those who
initially survived, only 26% were alive at 2
weeks. More recent series report comparable
figures for death at the scene, whereas for
those who survived transport to a trauma
center, survival to discharge rates of 50% to
75% are reported. Except those presenting
to the emergency department in extremis or
who have obviously ruptured, injured patients

with BTAI who are stable enough to undergo
thoracotomy and repair have a chance of
survival of 85%.

DEMOGRAPHICS AND
PATTERN OF INJURY

BTAI classically occurs at the aortic isthmus
1 cm distal to the left subclavian artery (at the
site of the ligamentum arteriosum). In the
series by Parmley and colleagues (1958), 45%
of all aortic injuries and 63% of those in early
survivors were at this site, which agrees well
with results from more recent autopsy series.
Other sites of injury, such as ascending,
descending, and abdominal aorta, are less
common and are often associated with spine
fractures. Injury to other great vessels in the
chest, such as the innominate artery and the
subclavian artery and vein, comprises 5% or
less of all blunt thoracic vascular trauma.

One prospective study of 1500 patients sus-
taining significant blunt chest trauma found
that using multivariate logistic regression
analysis, BTAI was associated with high-speed
collisions (>60 miles per hour) and higher
Injury Severity Scores (ISSs), but not direc-
tion of impact, ejection from the vehicle,
sudden deceleration, or other fatalities in the
vehicle. A second recent study assessing direc-
tion of impact found that half of BTAI victims
(48 of 97) sustained lateral impact collisions,
and 83% of these were wearing restraints. As
in motor vehicle collisions, BTAI has also been
found to be a common cause of death among
pedestrians struck by motor vehicles, respon-
sible in one series for 13% of pedestrian
deaths, with a mortality rate of 93% overall.
In the single largest prospective, multi-
institutional study of BTAI (274 patients) , the
mean ISS was 42, the Glasgow Coma Scale
(GCS) score was 12, 93% of injuries were at
the aortic isthmus, and 46 patients (17%)
arrived to the hospital in extremis or exsan-
guinated from free rupture soon thereafter.
Multiple injuries were commonplace and
included head injury (51%), rib fractures
(46% ) , pelvic and long bone fractures (34%) ,
and abdominal injuries (22%). Traumatic
rupture of the aorta rarely (<30% of all cases)

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14 • BLUNT THORACIC VASCULAR INJURY

271

TABLE 14-1

ASSOCIATED INJURIES TRAUMATIC RUPTURE OF THE AORTA

Closed

Head

Pulmonary

Pelvic

Patients

Injury

Abdominal

Contusion

Fracture

Study

in)

(%)

Injury (%)

(%)

Duhaylongsod, Glower, and Wolfe (1992)
Hilgenberg and colleagues (1992)
Hunt and colleagues (1996)
Kieny and Charpentier (1991)
Fabian and colleagues (1998)
Szwerc and colleagues (1999)

144

274

Associated injuries recorded as percent of patients afflicted.

occurs without significant associated injuries.
Table 14-1 lists nine recent series of patients
with BTAI and commonly associated injuries.
In four series, the ISS was calculated, and the
average excluding the aortic component was
18.

Although free rupture of the aorta is imme-
diately lethal, the circumferential extent of
contained tears is not clearly associated with
increased mortality. In the Parmley and col-
leagues (1958) series, 24% of early survivors
had complete circumferential tears. Again,
this finding has been reproduced in more
recent series. Patients with partial-thickness
tears who survive without surgical repair
develop a fibrous pseudoaneurysm. These may
be discovered incidentally on routine chest x-
ray films years after the inciting injury. Alter-
natively, these pseudoaneurysms may become
symptomatic or result in delayed rupture in
one third of patients. Therefore, it is recom-
mended that pseudoaneurysms of the thoracic
aorta are repaired whenever found. Death
from BTAI appears to follow a bimodal dis-
tribution, with early deaths (<4 hours) being
due to free rupture of the aorta and exsan-
guination and late deaths uncommonly due
to bleeding, but due to associated injuries and
resultant multiorgan failure.

PRESENTATION

Despite the dire nature of the injury, the diag-
nosis of BTAI is often subtle because history

and physical examination after blunt thoracic
trauma are neither sensitive nor specific for
aortic injury. Certain clues should, however,
raise the index of suspicion: appropriately
severe mechanism (high-speed motor vehicle
collision, pedestrian struck, or a fall from great
height); dyspnea; dysphagia; interscapular
pain; significant chest wall trauma (multiple
rib fractures or steering-wheel imprint) ; new
cardiac or interscapular murmur; left-sided
hemothorax; left supraclavicular hematoma;
and pseudocoarctation (relative upper extre-
mity hypertension). In particular, left-
sided hemothorax greater than 500 mL, left
supraclavicular hematoma, and pseudo-
coarctation may be signs of imminent free
rupture.

DIAGNOSIS
Aortogram

The gold standard for the diagnosis of BTAI
has been the aortogram. Not only is conven-
tional aortography highly sensitive and spe-
cific for aortic injury, but it also provides
precise anatomic localization of the injury,
which may help guide surgical repair (Fig. 14-
1) . Conversely, aortography is expensive, inva-
sive, and time and resource intensive, requires
patient transport away from the trauma bay,
and has a morbidity rate of up to 10%, making
it unsuitable as a general screening exami-
nation. Digital subtraction angiography may

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IV • SPECIFIC VASCULAR INJURIES

■ FIGURE 14-1

Digital subtraction aortogram demonstrating a
pseudoaneurysm of the proximal descending
thoracic aorta. (Courtesy S. Mirvis.) ■

improve diagnostic accuracy while decreasing
contrast loads.

Chest X-ray

Because of the limitations of aortography and
the lack of sensitivity and/or specificity of the
clinical presentation, all patients with blunt
trauma should undergo an initial supine
anteroposterior chest x-ray. The purpose of
this study is to detect indirect evidence of BTAI
such as mediastinal hemorrhage or bony
fractures indicating high-energy transfer. Fre-
quently cited signs suggestive of BTAI are listed
in Box 14-1.

Many of the signs listed in Box 14-1 are tech-
nique dependent and repeated evaluation in
the upright position or standard posteroan-
terior projection is advocated if there is no
clinical contraindication (Fig. 14-2). Using the
presence of any of the aforementioned signs
as a trigger for further evaluation, some aortic
injuries will still be missed. In a review of the
radiologic literature, Woodring and Dillon
(1984) found that of 656 cases of BTAI, 7.3%

CHEST X-RAY SIGNS SUGGESTIVE OF AORTIC RUPTURE

Mediastinal widening > 8cm

Mediastinal-to-chest width ratio > 0.25

Abnormal aortic contour

Loss of the aorticopulmonary window

Shift of the trachea to the right

Shift of the orogastric/nasogastric tube to the right

Left apical cap

Widening of the paraspinal lines

Depression of the left mainstem bronchus

Left pleural effusion

Scapular fracture

Sternal fracture

Thoracic spine fracture

First or second rib fracture

Multiple rib fractures

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14 • BLUNT THORACIC VASCULAR INJURY

273

Rights were not granted to include this figure in electronic media.
Please refer to the printed publication.

■ FIGURE 14-2

Anteroposterior "true erect" chest radiograph showing a widened mediastinum, loss of aortic
contour, tracheal deviation, loss of the aorticopulmonary window, and a widened left paraspinal line.
The patient sustained an aortic rupture. (Courtesy S. Mirvis). ■

had none of the standard radiologic criteria
for mediastinal hemorrhage. Other recent
series also report a significant incidence of
normal chest x-ray film among patients with
BTAI. Select patients, with compelling mech-
anism of injury, should therefore undergo
further evaluation despite a normal screen-
ing chest x-ray film (Fig. 14-3) .

Computed Tomography

The role of computed tomography (CT) in
the evaluation of blunt thoracic trauma is con-
tested: Does it supplement or possibly replace
the role of chest x-ray and aortography, or is
it merely a waste of time and resources? Over
the last 10 years, CT has evolved from an
adjunct to an inadequate or equivocal chest
radiograph to an all-purpose screening and
diagnostic tool, potentially supplanting both
chest x-ray and aortography. Many earlier
series have documented that standard chest
CT with intravenous contrast can consistently

document mediastinal hemorrhage associated
with BTAI, reporting a zero false-negative rate
and conclude that chest CT can safely decrease
the need for aortography by greater than 50 % .
The latest generation of spiral and helical
CT scanners have greatly increased the accu-
racy of making a diagnosis of BTAI through
noninvasive means. Used with a dynamic bolus
of contrast and three-dimensional recon-
struction algorithms, CT aortography can
perhaps obviate the need for most conven-
tional aortograms. A recent series by Gavant
and colleagues applied this technique to
1518 patients with blunt chest trauma over an
11-month period. Of these, 127 patients had
abnormal CT scans and subsequently under-
went conventional aortography. CT sensitiv-
ity for BTAI was 100% versus 94% for
conventional aortography, and specificity was
82% for the CT versus 96% for conventional
aortography. A follow-up study with 38 tho-
racic aortic and great-vessel injuries demon-
strated that CT aortography can not only
accurately diagnose BTAI but also provide

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IV • SPECIFIC VASCULAR INJURIES

1. High speed collision (>60mph), ejection from vehicle, airplane crash,
fall (>2 stories), multiple severe injuries

■ FIGURE 1 4-3

Suggested algorithm for radiographic evaluation of patients sustaining significant blunt thoracic
trauma. ■

sufficient anatomic detail (previously only
available through conventional aortography)
to guide management. In our hands, CT was
superior to angiography in the diagnosis of
BTAI. Mirvis and colleagues have also docu-
mented the steady progress made with tho-
racic CT in the diagnosis of BTAI, in an earlier
series showing thatnonhelical CT can reliably
(100% sensitivity and negative predictive
value) pick up the presence of mediastinal
hematoma, but in the latest series showing the
same reliability and accuracy with helical CT
in demonstrating the actual aortic injury,
precluding the need for aortography. Three
prospective series similarly add to the growing
body of evidence that helical CT is equal
or superior to aortography in the diagnosis
of BTAI, that this technology represents a
significant improvement over previous non-

helical CT, and that up to 95% of angiogra-
phy scans can be obviated through use of CT
(Fig. 14-4).

The preceding discussions on the merits of
CT and aortography in the diagnosis of BTAI
must be viewed in light of their major draw-
back: Both require transport away from the
trauma bay and therefore are only useful in
a hemodynamically stable patient. Fabian and
colleagues point out that CT has the advan-
tage in this regard; compared to aortography,
helical CT is faster, easier, more available, and
less invasive. Nonetheless, like any other tech-
nologic imaging innovation, results depend
on user experience. The near-perfect diag-
nostic accuracy cited may not be universally
reproducible at facilities where the volume of
trauma patients is insufficient to allow ade-
quate experience with this technique to

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14 • BLUNT THORACIC VASCULAR INJURY

275

■ FIGURE 14-4

Axial dynamic thoracic computed
tomogram revealing a mediastinal
hematoma anteriorly and an aortic
intimal flap. The patient had
sustained an aortic rupture.
(Courtesy S. Mirvis). ■

■ FIGURE 14-5

Transesophageal echocardiogram
revealing an intimal flap of disrupted
descending thoracic aorta. (From
Brooks SW, Young JC, Cmolik B, et al:
J Trauma 1992:32:761-766.) ■

accrue. In such situations, the time-tested
modality of aortography may represent the
diagnostic test of choice.

Transesophageal
Echocardiography

Since its introduction in the early 1980s, trans-
esophageal echocardiography (TEE) has
become the study of choice for various cardiac
diseases and is increasingly used for the
evaluation of the thoracic aorta. TEE is well
suited for this role because of the close
anatomic proximity between the esophagus
and the thoracic aorta.

In a representative study by Smith and col-
leagues (1995), TEE was attempted in 101
blunt trauma patients but only completed in
93. TEE diagnosis of BTAI was corroborated

with aortography and surgery and/or autopsy.
Overall, TEE sensitivity was 100% and speci-
ficity was 98% with one false-positive result.
In these and other authors' hands, TEE is both
sensitive and specific in the diagnosis of
BTAI. Also, TEE provides precise anatomic
localization of the site of injury and does not
require patient transport, making it better
suited for the unstable patient (Fig. 14-5) . On
the negative side, TEE cannot be used in all
trauma patients (7% in this study) because
of patient combativeness, cervical spinal or
maxillofacial injury, and airway difficulty. In
addition, results are operator dependent, and
other authors have not been able to reliably
reproduce such excellent results, with sensi-
tivity for BTAI only 57% in one series. In ana-
lyzing 10 series totaling 407 patients
undergoing TEE to diagnose BTAI, Ben-
Menachem (1997) found this test's sensitiv-

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IV • SPECIFIC VASCULAR INJURIES

ity for BTAI to be 86% and inferior to that of
aortography. To summarize, the diagnostic
accuracy of TEE is open to question, it pos-
sesses "blind spots" to include the ascending
aorta, the aortic arch, and its branches, and
certain patients cannot tolerate the procedure.
However, it possesses a few advantages over
other techniques, including portability, rapid-
ity, and its safety profile. Until incontrovert-
ible documentation of superior accuracy,
TEE might best be reserved for the following
circumstances:

• Evaluation of unstable patients who are poor
risks for transport to the CT scanner or the
angiography suit

• Evaluation of patients in the operating room
during emergent laparotomy for intra-
abdominal hemorrhage

• Evaluation of the morbidly obese patient
whose weight may exceed table limits of the
CT scanner or angiography suite

PREOPERATIVE MANAGEMENT

Multisystem injuries are common in patients
with BTAI; thus, keeping the entire clinical
scenario in perspective is important when dis-
cussing management. It has been noted that
hypotension in patients with BTAI is generally
not due to the aortic injury because bleeding
from the aorta is rapidly fatal. Therefore, as
in all trauma patients, it is imperative to dis-
cover and address the etiology of hypotension.
Primary and secondary surveys will reveal sites
of external hemorrhage and sites of possible
occult blood loss such as pelvic and long bone
fractures. Chest x-ray and/or tube thoracos-
tomy will expose significant intrapleural hem-
orrhage. Intra-abdominal hemorrhage is best
evaluated in this situation by diagnostic peri-
toneal lavage (DPL) , CT, or abdominal ultra-
sonography. The advantages of DPL and
ultrasonography reside in their ability to be
performed quickly, in both unstable and stable
patients. The use of abdominal CT takes longer
and requires a stable patient but gives more
information and can be performed coincident
to CT of the chest, if already planned. In cases
of combined thoracic and abdominal injury,
laparotomy should follow thoracotomy when

signs of imminent BTAI rupture exist such as
left hemothorax, pseudocoarctation, or supr-
aclavicular hematoma. Otherwise, laparotomy
should generally precede aortography and/or
thoracotomy.

A subset of patients with BTAI and severe
associated injuries are poor candidates for
immediate aortic repair. Initial nonoperative
management can allow sufficient physiologic
recovery for delayed aortic repair. Akins and
colleagues (1981) suggest the following cri-
teria for delayed repair:

• Major intracranial injury

• Extensive burns

• Severe respiratory failure

• Extensively contaminated wound

• Sepsis

Similarly, some authors have advocated non-
operative therapy for patients with minimal
aortic injury (e.g., aortic intimal irregularity
without extravasation of contrast). These
patients should be followed with serial angio-
graphy or TEE to document resolution of their
aortic injury. Afterload reduction and (3-
blockade are useful medical adjuncts, tem-
porizing patients with delayed operative and
primary nonoperative management by mini-
mizing aortic wall stress.

Increasing experience with delayed opera-
tive management of BTAI is resulting in an
overall paradigm shift and change in man-
agement strategy for this injury. There is now
substantial evidence supporting that except-
ing BTAI patients presenting in extremis, in-
hospital rupture can be effectively prevented
by keeping the systolic blood pressure below
140 mm Hg. Most of these data have been
accrued through retrospective analysis of
prospective medical protocols using a com-
bination of esmolol, labetalol, and sodium
nitroprusside, and although outcomes were
simply compared to historical controls, virtu-
ally no deaths resulting from in-hospital
rupture of BTAI have occurred in these series
when adequate medical control of blood pres-
sure is ensured. This allows for a planned, con-
sidered, and prepared approach to the repair
of this problematic injury, ensuring optimal
patient physiologic condition and optimal hos-
pital resource support, rather than the sense

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14 • BLUNT THORACIC VASCULAR INJURY

277

of hurry and panic that can be engendered
from the perceived need to thwart a poten-
tial intrathoracic "time bomb."

It is further recommended that adequate
sedation be used at the time of endotracheal
intubation, should this be required, and that
fluid resuscitation be particularly judicious,
to minimize wall stress on the attenuated aorta.
Pneumatic antishock garments (PASGs), a
once common appliance of patients with mul-
tiple trauma brought to trauma centers, are
more clearly detrimental. No benefit to these
devices has been demonstrated clinically in
the management of BTAI and in a porcine
model of aortic injury, 100% of pigs with and
0% of pigs without PASG died of their injury.

Approximately one half of patients with BTAI
will also have a closed head injury (see Table
14-1). Optimally, a head CT scan should be
obtained before BTAI repair so craniotomy can
be planned if needed. Head CT findings will
also bear on surgical technique; for example,
systemic heparinization is contraindicated in
the presence of intracranial hemorrhage.

SURGICAL TECHNIQUE

Most patients with blunt thoracic vascular
injury are best served by repair via a left
posterolateral thoracotomy, because this
approach gives the best exposure to the aortic
isthmus where most injuries occur. There are
two main technical variables in the surgical
repair of a classic (aortic isthmus) BTAI (Fig.
14-6) , as follows:

• "Clamp-and-sew" technique versusshunt and

• Interposition graft versus primary repair

The clamp-and-sew technique is less
complex and more expedient than shunting.
Proponents of this technique argue that it is
superior to shunting in all cases of BTAI
because it does not require systemic hepar-
inization, does not have adjunct-associated
complications (e.g., insertion site hemor-
rhage or aortic dissection), and does not
require special equipment. Arguably, mor-
bidity and mortality rates are similar between
clamp-and-sew and shunt techniques. In short,
the key technical points in the clamp-and-sew
technique are as follows:

SURGICAL MODALITIES

AWlf

Primary Repair/ >.

Partial Left
Heart Bypass

Centrifugal
Pump Head

■ FIGURE 14-6

Options in operative repair techniques for rupture
of the descending thoracic aorta. A, Primary
or direct repair. B, Graft interposition without a
mechanical adjunct (clamp and sew). Use of a
mechanical adjunct in aortic repair: A, Aortoaortic
(Gott's) shunt. B, Left atrial femoral artery bypass
with a Bio-Medicus centrifugal flow pump. ■

1. Position the patient in the right lateral
decubitus position and create a standard
left posterolateral thoracotomy.

2. Identify left vagus and phrenic nerves;
retract left vagus.

3. Circumferentially dissect left subclavian
artery and secure with an umbilical tape.

4. Perform sharp and blunt dissection
between the left subclavian and left
common carotid arteries and place umbil-
ical tape around the proximal aorta.

5. Circumferentially dissect descending
aorta below hematoma and secure with
an umbilical tape.

6. Ligate and/or control intervening inter-
costal arteries.

7. Administer intravenous mannitol

8. First cross-clamp aortic arch, followed by
descending aorta and subclavian artery.

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IV • SPECIFIC VASCULAR INJURIES

9. Open hematoma and control back-
bleeding.

10. Debride devitalized aortic wall.

11. Anastomose aorta with or without inter-
vening prosthetic graft.

12. Back-bleed and vent aorta before secur-
ing suture line.

13. Notify anesthesiologist, then release
subclavian and descending aorta clamps,
followed by aortic arch clamp.

Shunt techniques of BTAI repair are similar
to "clamp and sew" with the exception that a
conduit is inserted proximal and distal to the
aortic injury. Benefits of this arrangement
include afterload reduction of the left ven-
tricle and preserved systemic perfusion during
aortic cross-clamp. The least complicated of
these techniques involve passive conduits
such as the heparin-bonded Gott shunt. This
is typically inserted into the left ventricle or
ascending aorta proximally and the femoral
artery distally. Passive conduits such as the Gott
shunt rely on cardiac output and therefore
may not provide adequate distal perfusion
if cardiac performance is impaired. Active
shunts employing centrifugal or roller pumps
are cardiac output independent but are at the
risk of stealing perfusion from the cerebral
and coronary circulation. In a trauma setting,
centrifugal pumps have the advantage over
roller pumps of not requiring systemic
heparinization. Like passive conduits, the
distal insertion of these shunts is usually in
the femoral artery and the proximal insertion
is in the left atrial appendage. Shunts may
decrease the incidence of ischemic spinal cord
injury, systemic acidosis, and renal injury, and
although the evidence in the trauma litera-
ture on this subject has in the past been
divided, more recent series support that the
incidence of postoperative paraplegia is lower
at centers that use partial left heart bypass with
a centrifugal flow pump. A recent prospec-
tive nationwide survey of trauma centers per-
forming BTAI repair found that although
mortality was no different between the two
groups, the incidence of postoperative para-
plegia was 16.4% among the 73 patients
treated with the clamp-and-sew technique,
versus 2.9% among the 69 patients treated

using centrifugal pump bypass (P<.004).
Citing similar results, another recent study
showed by multivariate regression analysis that
the factors independently predicting postop-
erative paraplegia included older age, oper-
ative technique (clamp and sew), clamp time
greater than 30 minutes, and the occurrence
of intraoperative hypotension.

Choice of primary repair versus use of pros-
thetic graft is largely dictated by the physical
characteristics of the native aorta and the
extent of aortic disruption. The advantages
of primary repair include shorter cross-clamp
times, decreased risk of infection, and less
intercostal artery sacrifice (possibly con-
tributing to ischemic spinal cord injury). In
the pediatric population, primary repair
abates the need for reoperation to upsize an
outgrown aortic prosthesis. Generally, pros-
thetic grafts are better suited for instances
when the edges of the torn aorta are widely
distracted making a tension-free anastomosis
impossible. One prominent series, however,
reports 32 consecutive aortic injuries repaired
primarily despite up to 5-cm separation of
the torn aortic edges. Another recent series
wherein primary repair was the preferential
mode of therapy for BTAI reports mortality
and paraplegia rates comparable to that those
reported with use of the centrifugal pump
bypass. Use of both Dacron and polytetraflu-
oroethylene (PTFE) have been described in
the literature, and both provide similarly good
results.

Still in its infancy, endovascular repair of
BTAI appears to be a promising area for study.
One published series of nine patients sus-
taining BTAI reports TEE-guided endolumi-
nal stent repair from 1 to 8 months after injury
with excellent results: no mortality, no rupture,
no occlusions, and no need for revision after
the initial procedure.

BLUNT INJURY TO OTHER
THORACIC VESSELS

Innominate Artery

Innominate and proximal carotid artery
injury is rare, comprising less than 5% of all

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14 • BLUNT THORACIC VASCULAR INJURY

279

blunt thoracic vascular trauma, although the
innominate artery is probably the most
common thoracic vessel injured by blunt
trauma after the thoracic aorta. Focal neuro-
logic deficits may be present with this injury,
but most injuries are picked up through
screening chest radiography, CT, and
aortography.

Optimal exposure is via median sternotomy,
plus or minus right neck extension, and repair
is advocated over ligation because of the
concern for cerebral ischemia and resultant
neurologic injury. Because most blunt innom-
inate injuries occur at its aortic insertion and
native tissue at that location may be compro-
mised, anastomosis at this location should
be avoided. Rather, the preferred approach
involves the construction of a Dacron or PTFE
bypass graft proximal to the injury by anas-
tomosis to the aorta using a partial-occlusion
clamp. No heparin, shunt, or cardiopul-
monary bypass is generally employed. The
bypass graft is sutured distally to uninjured
vessel or vessels, and the aorta at the site of
the innominate insertion is oversewn with
pledgeted sutures. Outcome is generally excel-
lent, and mortality should be 0% to 10%, based
on hemodynamic condition on admission and
concomitant injuries (which are common) .
Of note, endoluminal stent repair has also
been performed successfully for blunt innom-
inate artery injury.

Subclavian Artery

Approximately 1 % to 5% of blunt thoracic vas-
cular trauma involves the subclavian artery.
In contrast to BTAI, shoulder harness seat belts
have been implicated in the pathogenesis of
this injury. Signs concerning for subclavian
injury include supraclavicular hematoma,
pulse deficit, brachial plexus injury, clavicu-
lar fracture, and bruit (although none are par-
ticularly sensitive or specific) . Pulse deficit is
most characteristic but may be absent because
of extensive collateral flow often present
about the shoulder. Diagnosis of subclavian
artery injury, as in BTAI, is best made with
aortography. Optimal surgical exposure is
debated (see Table 14-2), although most
favor median sternotomy for right subclavian
and proximal left subclavian lesions, and left
supraclavicular incision for mid-subclavian to
distal subclavian injuries of the left side. Recon-
struction is generally done with prosthetic
graft. Concomitant subclavian vein injury
occurs in up to 20% of patients and can often
be treated with simple ligation. If collateral
venous return is compromised, reconstruction
of the subclavian vein is recommended and
can be performed with a saphenous vein inter-
position graft or an end-to-end subclavian
jugular vein bypass.

One variant of blunt subclavian vessel injury
occurs in the syndrome of scapulothoracic

TABLE 14-2

OPTIMAL AND ALTERNATIVE EXPOSURE FOR THORACIC VASCULAR INJURIES

Injured Vessel

Optimal Exposure

Alternate Exposure

Ascending aorta

Right subclavian

Innominate

Proximal common carotid

Left subclavian

Aortic arch

Aortic isthmus

Descending aorta

SVC

Suprahepatic IVC

P: MS with supraclavicular ext.

D: L. supraclavicular

L. posterolateral thoracotomy

Thoracoabdominal

D: R. supraclavicular

P: L. anterolateral thoracotomy

D, distal; IVC, inferior vena cava; L, left; MS, median sternotomy; P, proximal; R, right; SVC, superior vena cava.

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IV • SPECIFIC VASCULAR INJURIES

dissociation. In this devastating injury, a
strong torsion or rotational force is applied
to the shoulder joint, shearing the scapula and
shoulder girdle from the chest wall, resulting
in extensive complex fractures of the upper
extremity and avulsion of the brachial plexus
and subclavian vessels as they emerge from
the thoracic cavity. Patients present in shock
with massive swelling of the ipsilateral chest
and neurovascular deficiency of the arm. For
survival, treatment requires early recognition,
control of bleeding, reversal of shock, and
usually, substantial amputation of the involved
extremity.

Vena Cava

Blunt injury to the thoracic vena cava,
though less common than BTAI, has similar
mortality. This difference in incidence
between arterial and venous injuries is most
likely due to differences in vessel wall plas-
ticity. Surgical approach to the vena cava, and
in particular the suprahepatic vena cava, is
problematic and may require heroic measures
such as total hepatic vascular occlusion and
atriocaval shunting. When feasible, primary
repair with lateral venorrhaphy is preferred
even though this may result in vessel
narrowing;.

Pulmonary Artery and Vein

will ensure that few of these injuries are missed.
Chest helical CT is increasingly becoming both
the screening and the diagnostic test of choice
in centers that serve significant numbers of
blunt trauma patients; however, chest radi-
ography and aortography remain gold stan-
dards in the diagnostic algorithm.

Attentive medical management, based
around the use of intravenous (3-blockers to
keep systolic blood pressure below 140 mm Hg,
should be employed early in patients with
probable BTAI and may prevent in-hospital
rupture. Technique of operative repair is con-
troversial, and no single nationwide standard
of care has emerged for definitive operative
strategy. However, the preponderance of
medical evidence increasingly points to
decreased incidence of paraplegia after BTAI
repair when heparin-less centrifugal pump
bypass is employed.

Because of the common occurrence of
BTAI, the proclivity of its presence and repair
to result in mortality or morbidity, and the
wide diversity of management options that
have been used for care, it is strongly recom-
mended that each trauma center that deals
with this injury consider the use of a clinical
practice guideline for BTAI thatwould encour-
age a single safe standard for the diagnosis
and management of this injury. An excellent
example of such a practice guideline has been
developed and published by the Eastern Asso-
ciation for the Surgery of Trauma.

Blunt trauma to the pulmonary artery and vein
is rare. Patients with these injuries present in
shock from hemorrhage and/or cardiac tam-
ponade. The treatment of choice for these
injuries is lateral repair, but if the tear in the
vessel wall is not amenable to this, pneu-
monectomy is an option.

SUMMARY

BTAI is a common and often lethal injury. For
those who survive the initial insult, patients
with this injury are best served by expeditious
evaluation and prompt repair. A high index
of suspicion, based on mechanism of injury,

REFERENCES

Albrink MH, Rodriguez E, England GJ, et al: Impor-
tance of designated thoracic trauma surgeons
in the management of traumatic aortic transec-
tion. Southern Med J 1994;87:497-501.

Akins CW, Buckley MJ, Daggett W, et al: Acute trau-
matic disruption of the thoracic aorta: A 10-year
experience. Ann Thorac Surg 1981;31:305-309.

AliJ,VanderbyB,PurcellC:The effect of the pneu-
matic antishock garment (PASG) on hemody-
namics, hemorrhage, and survival in penetrating
thoracic aortic injury. J Trauma 1991 ;31 :846-851 .

Attar S, Cardarelli MG, Downing SW, et al: Trau-
matic aortic rupture: Recent outcome with
regard to neurologic deficit. Ann Thorac Surg
1999;67:959-965.

chl4.qxd 4/16/04 3:39PM Page 281

14 • BLUNT THORACIC VASCULAR INJURY

281

Axisa BM, Loftus IM, Fishwick G, et al: Endovas-
cular repair of an innominate artery false
aneurysm following blunt trauma. J Endovasc
Ther 2000;7:245-250.

Baker SP, O'Neill B, Haddon W, et al: The Injury
Severity Score: A method for describing patients
with multiple injuriesandevaluatingemergency
care. J Trauma 1974;14:187-196.

Ben-Menachem Y: Rupture of the thoracic aorta
by broadside impacts in road traffic and other
collisions: Further angiographic observations
and preliminary autopsy findings. J Trauma
1993;35:363-367.

Ben-Menachem Y: Assessment of blunt aortic-
brachiocephalic trauma: Should angiography be
supplanted by transesophageal echocardiogra-
phy? J Trauma 1997;42:969-972.

BormanKR,Aurbakken CM, Weige It JA: Treatment
priorities in combined blunt abdominal and
aortic trauma. Am J Surg 1982;144:728-732.

Brundage SI, Haruff R, Jurkovich GJ, et al: The
epidemiology of thoracic aortic injuries in pedes-
trians. J Trauma 1998;45:1010-1014.

Buckmaster MJ, Kearney PA, Johnson SB, et al:
Further experience with transesophageal
echocardiography in the evaluation of thoracic
aortic injury. J Trauma 1994;37:989-995.

Buscaglia LC, Walsh JC, Wilson JD, et al: Surgical
management of subclavian artery injury. Am J
Surg 1987;154:88-90.

Clark DE,Zieger MA, Wallace KL,etal: Bluntaortic
trauma: Signs of high risk.J Trauma 1990;30:701-
705.

Cohn SM, Burns GA, Jaffe C, et al: Exclusion of
aortic tear in the unstable trauma patient: The
utility of transesophageal echocardiography.
J Trauma 1995;39:1087-1090.

Cooper C, Rodriguez A, Omert L: Blunt vascular
trauma. Curr Probl Surg 1992;29:291-357.

Cox CS, Allen GS, Fischer RP, et al: Blunt versus
penetrating subclavian artery injury: Presenta-
tion, injury pattern, and outcome. J Trauma
1999;46:445-449.

Demetriades D, Gomez H, Velmahos GC, et al:
Routine helical computed tomographic evalua-
tion of the mediastinum in high-risk blunt
trauma patients. Arch Surg 1998;133:1084-1 088.

Duhaylongsod FG, Glower DD, Wolfe WG: Acute
traumatic aortic aneurysm: The Duke experience
from 1970 to 1990.J Vase Surg 1992;15:331-343.

Dyer AD, Moore EE, like DN, et al: Thoracic aortic
injury: How predictive is mechanism and is chest
computed tomography a reliable screening tool?

A prospective study of 1561 patients. J Trauma
2000;48:673-682.

Ebraheim NA, An HS, Jackson WT, et al: Scapu-
lothoracic dissociation. J Bone Joint Surg 1988;
70:428-432.

Fabian TC, Davis KA, Gavant ML, et al: Prospec-
tive study of blunt aortic injury: Helical CT is
diagnostic and antihypertensive therapy reduces
rupture. Ann Surg 1998;227:666-676.

Fabian TC, Richardson JD, Croce MA, et al:
Prospective study of blunt aortic injury: Multi-
center trial of the American Association for the
Surgery of Trauma. J Trauma 1997;42:374-380.

Feczko JD, Lynch L, PlessJE, et al: An autopsy case
review of 142 nonpenetrating (blunt) injuriesof
the aorta. J Trauma 1992;33:846-849.

Fenner MN, Fisher KS, Sergei NL, et al: Evalua-
tion of possible traumatic aortic injury using
aortography and CT, Am Surg 1990;56:497-
499.

Finkelmeier BA, Mentzer RM, Kaiser DL, et al:
Chronic traumatic thoracic aneurysm. Influence
of operative treatment on natural history: An
analysis of reported cases, 1950-1980. J Thorac
Cardiovasc Surg 1982;84:257-266.

Fisher RG, Oria RA, Mattox KL, et al: Conserva-
tive management of aortic lacerations due to
blunt trauma. J Trauma 1990;30:1562-1566.

Forbes AD, Asbaugh DG: Mechanical circulatory
support during repair of thoracic aortic injuries
improves morbidity and prevents spinal cord
injury. Arch Surg 1994;129:494-497.

GavantJL, Flick P, Menke P, et al: CT aortography
of thoracic aortic rupture. AJR Am J Roentgenol
1996;166:955-961.

Gavant ML, Menke PG, Fabian T, et al: Blunt trau-
matic aortic rupture: Detection with helical CT
of the chest. Radiology 1995;197:125-133.

Hajarizadeh H, Rohrer MJ, Cutler BS: Surgical
exposure of the left subclavian artery by median
sternotomy and left supraclavicular extension.
J Trauma 1996;41:136-139.

Hilgenberg AD, Logan DL, Akins CW, et al: Blunt
injuries of the thoracic aorta. Ann Thorac Surg
1992;53:233-239.

Hoff SJ, Reilly MK, Merrill WH, et al: Analysis of
blunt and penetrating injury of the innominate
and subclavian arteries. Am Surg 1994;60:151-
154.

Hunick MGM, Bos JJ: Triage of patients to angi-
ography for detection of aortic rupture after blunt
chest trauma: Cost-effectiveness analysis of using
CT. AJR Am J Roentgenol 1995;165:27-36.

chl4.qxd 4/16/04 3:39PM Page 282

282

IV • SPECIFIC VASCULAR INJURIES

HuntJP, Baker CC, Lentz CW, et al: Thoracic aorta
injuries: Management and outcome of 144
patients. J Trauma 1996;40:547-556.

Johansen K, Sangeorzan B, Copass MK: Traumatic
scapulo thoracic dissociation: Case report. J
Trauma 1991;31:147-149.

Johnston RH, Wall MJ, Mattox KL: Innominate
artery trauma: A thirty-year experience. J Vase
Surg 1993;17:134-140.

Katyal D, McLellan BA, Brenneman FD, et al:
Lateral impact motor vehicle collisions: Signifi-
cant cause of blunt traumatic rupture of the tho-
racic aorta. J Trauma 1997;42:769-772.

Kearney PA, Smith DW, Johnson SB, et al: Use of
transesophageal echocardiography in the eval-
uation of traumatic aortic injury. J Trauma 1993;
34:696-701.

Kieny R, Charpentier A: Traumatic lesions of the
thoracic aorta: A report of 73 cases. J Cardiovasc
Surg 1991;32:613-619.

Kram HB, Wohlmuth DA, Appel PL, et al: Clinical
and radiographic indications for aortography in
blunt chest trauma. J Vase Surg 1987;6:168-176.

Kudsk KA, Bongard F, Lim RC: Determinants of
survival after vena caval injury: Analysis of a 14-
year experience. Arch Surg 1984;1 1 9: 1009-1 01 2.

Madayag MA, Kirshenbaum KJ, Nadimpalli SR, et
al: Thoracic aortic trauma: Role of dynamic CT
Radiology 1991;179:853-855.

Mattox KL: Symposium: New approach in vascu-
lar trauma. J Vase Surg 1988;7:725-729.

Mattox KL, Feliciano DV, Burch J, et al: Five thou-
sand seven hundred sixty cardiovascular injuries
in 4459 patients: Epidemiologic evolution 1958
to 1987. Ann Surg 1989;209:698-707.

Mattox KL, Holzman M, Pickard LR, et al:
Clamp/repair: A safe technique for treatment
of blunt injury to the descending thoracic aorta.
Ann Thorac Surg 1985;40:456-463.

McCroskey BL, Moore EE, Moore FA, etal: Aunified
approach to the torn thoracic aorta. Am J Surg
1991;162:473-476.

Minard G, Schurr MJ, Croce MA, et al: A prospec-
tive analysis of transesophageal echocardiogra-
phy in the diagnosis of traumatic disruption of
the aorta. J Trauma 1996;40:225-230.

Mirvis SE, Pais So, Gens DR: Thoracic aortic rup-
ture: Advantages of intraarterial digital subtrac-
tion angiography. AJR Am J Roentgenol 1986;
146:987-991.

Mirvis SE, Shanmuganathan K, Buell J, et al: Use
of spiral computed tomography for the assess-

ment of blunt trauma patients with potential
aortic injury. J Trauma 1998;45:922-930.

Mirvis SE, Shanmuganathan K, Miller BH, et al:
Traumatic aortic injury: Diagnosis with contrast-
enhanced thoracic CT. Five-year experience at
a major trauma center. Radiology 1996;200:413-
422.

Morgan PW, Goodman LR, Aprahamian C, et al:
Evaluation of traumatic aortic injury: Does
dynamic contrast-enhanced CT play a role? Radi-
ology 1992;182:661-666.

Myers SI, Harward TRS, Cagle L: Isolated subcla-
vian artery disse c tion af te r blun t trauma . Surge ry
1991;109:336-338.

Nagy K, Fabian T, Rodman G, et al: Guidelines for
the Diagnosis and Management of Blunt Aortic
Injury. Eastern Association for the Surgery of
Trauma: Available at http://www.east.org. 2000.

Omert L, Rodriguez A, Simon B, et al: Blunt vas-
cular torso trauma: A review of 310 cases. Panam
J Trauma 1991;2:102-111.

Parmley LF, Mattingly TW, Manion WC, et al: Non-
penetrating traumatic injury of the aorta. Cir-
culation 1958;17:1086-1101.

Pate JW, Fabian TC, Walker W: Traumatic rupture
of the aortic isthmus: An emergency? World J
Surg 1995;19:119-126.

Pate JW, Gavant ML, Weiman DS, et al: Traumatic
rupture of the aortic isthmus: Program of selec-
tive management. WorldJ Surg 1999;23:59-63.

Pre'tre R, Chilcott M, Murith N, et al: Blunt injury
to the supra-aortic vessels. BrJSurgl997;84:603-
609.

Ramadan F, Rutledge R, Oiler D, et al: Carotid
artery trauma: A review of contemporary trauma
center experiences. J Vase Surg 1995;21:46-56.

Raptopoulos V: Chest CT for aortic injury: Maybe
not for everyone. AJR Am J Roentgenol 1994;
162:1053-1055.

Razzouk AJ, Gundry SR, Wang N, et al: Repair of
traumatic aortic rupture: A 25-year experience.
Arch Surg 2000;135:913-918.

Read RA, Moore EE, Moore FA, et al: Partial left
heart bypass for thoracic aorta repair: Survival
without paraplegia. Arch Surg 1993;128:746-752.

Richardson P, Mirvis SE, Scorpio R, et al: Value of
CT in determining the need for angiography
when findings of mediastinal hemorrhage on
chest radiographs are equivocal. AJR Am J
Roentgenol 1991;156:273-279.

Richardson JD, Smith JM III, Grover FL: Manage-
ment of subclavian and innominate artery

chl4.qxd 4/16/04 3:39PM Page 283

14 • BLUNT THORACIC VASCULAR INJURY

283

disruption due to blunt trauma. Am J Surg
1977;134:780.

Richardson JD, Wilson ME, MillerFB: The widened
mediastinum: Diagnostic and therapeutic pri-
orities. Ann Surg 1990;211:731-737.

Rodriguez A, Elliott D: Blunt traumatic rupture of
the thoracic aorta. In Maull et al. (eds) : Advances
in Trauma and Critical Care. St. Louis, Mosby,
1993;8:145-181.

Rousseau H, Soula P, Perreault P, et al: Delayed
treatment of traumatic rupture of the thoracic
aorta with endoluminal covered stent. Circula-
tion 1999;99:498-504.

Saletta S, Lederman E, Fein S, et al: Trans-
esophageal echocardiography for the initial
evaluation of the widened mediastinum in
trauma patients. J Trauma 1995;39:137-142.

Schmidt CA, Smith DC: Traumatic avulsion of arch
vessels in a child: Primary repair using hypother-
mic circulatory arrest (case report) . J Trauma
1989;29:248-250.

Schmidt CA, Wood MN, Razzouk AJ, et al: Primary
repair of traumatic aortic rupture: A preferred
approach. J Trauma 1992;32:588-592.

Sharma S, Reddy V, Ott G, et al: Surgical manage-
ment of traumatic aortic disruption. Am J Surg
1997;173:416-418.

Smith MD, Cassidy JM, Souther S, et al: Trans-
esophageal echocardiography in the diagnosis
of traumatic rupture of the aorta. New Engl J
Med 1995;332(6):356-362.

Sweeney MS, Young DJ, Frazier OH, et al: Trau-
matic aortic transections: Eight-year experience
with the "Clamp-Sew" technique. Ann Thorac
Surg 1997;64:384-389.

Szwerc MG, Benckart DH, Lin JC, et al: Recent clin-
ical experience with left heart bypass using a
centrifugal pump for repair of traumatic aortic
transection. Ann Surg 1999;230:484-492.

Townsend RN, ColellaJJ, Diamond DL: Traumatic
rupture of the aorta critical decisions for trauma
surgeons. J Trauma 1990;30:1 1 69-1 1 74.

Turney SZ, Rodriguez A: Injuries to the great tho-
racic vessels. In Turney SZ, Rodriguez A, Cowley
RA (eds): Management of Cardiothoracic
Trauma. Baltimore, Williams & Wilkins, 1990:
229-260.

Vignon P, Gueret P, Vedrinne JM, et al: Role of trans-
esophageal echocardiography in the diagnosis
and management of traumatic aortic disruption.
Circulation 1995;92:2959-2968.

Von Oppell UO, Dunne TT, De Groot KM, et al:
Spinal cord protection in the absence of collat-
eral circulation: Metaanalysis of mortality and
paraplegia. J Card Surg 1994;9:685-691.

Wahl WL, Michaels AJ, Wang SC, et al: Blunt tho-
racic aortic injury: Delayed or early repair?
J Trauma 1999;47:254-259.

Walls JT, Boley TM, Curtis JJ et al: Experience with
four surgical techniques to repair traumatic
aortic pseudoaneurysm. J Thorac Cardiovasc
Surg 1993;106:283-287.

Weiman DS, McCoy DW, Haan CK, et al: Blunt
injuries of the brachiocephalic artery. Am Surg
1998;64:383-387.

Williams JS, Graff JA, Uku JM, et al: Aortic injury
in vehicular trauma. Ann Thorac Surg 1994;
57:726-730.

WoodringJH, Dillon ML: Radiographic manifes-
tations of mediastinal hemorrhage from blunt
chest trauma. Ann Thorac Surg 1984;37:l7l-

178.

Zeiger MA, Clark DE, Morton JR: Reappraisal of
surgical treatment of traumatic transection of
the thoracic aorta.J Cardiovasc Surg 1990;31 :607-
610.

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Wounds of the Heart

MATTHEW J. WALL, JR
DAVID RICE
ERNESTO SOLTERO

O HISTORY

O INCIDENCE

O CLINICAL PATHOLOGY

O PATHOPHYSIOLOGY

O PREHOSPITAL MANAGEMENT

O EMERGENCY CENTER

O EMERGENCY CENTER PROCEDURES

O OPERATIVE MANAGEMENT OF CARDIAC INJURIES

Incisions

Aortic Occlusion

Cardiac Manipulation

Hemorrhage Control

Complex Injuries

Cardiac Septal Injuries

Cardiac Valvular Injury

Intrapericardial Inferior Vena Cava Injury
O SUMMARY

HISTORY

The heart has always been regarded as
the sustainer of life, and its wounds have

been approached through the ages with
awe and apprehension. Homer provided
antique literature with many references
to heart wounds. Their fatality was
clear.

285

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IV • SPECIFIC VASCULAR INJURIES

The insulting victor with disdain bestrode
The prostrate prince and on his bosom trod;
Then drew the weapon from his panting heart,
The reeking fibers clinging to the dart;
From the wide wound gushed out a stream of

blood
And the soul issues in the purple flood.

Beall, Gasior, and Brickeret (1971)

While originally recommending pericardio-
centesis, Beall, in 1961, advocated aggressive
use of thoracotomy and direct repair even in
the emergency center (EC) . Currently, this is
the most common approach, with pericar-
diocentesis being used only rarely for tem-
porary decompression of cardiac tamponade,
if indicated, before direct cardiac repair.

Attempts to treat wounds of the heart have
been recorded as early as the first century ad,
when Galen described therapy based on
anatomic and experimental study through
surgery of the pericardium. Ambroise Pare
tried to dispel the general belief that cardiac
injuries were usually fatal in his sixteenth
century reports. Yet even in 1709, Boerhaave
wrote that all heart wounds resulted in death.

Larrey is often credited with the first suc-
cessful decompression of the pericardium in
1810 during the Napoleon wars, but it is only
in the last 100 years that treatment of heart
wounds has been repeatedly beneficial to the
patient. Until 1896, pericardiocentesis, either
alone or combined with phlebotomy, was the
only method of surgical treatment for heart
wounds. Those treated were usually small pen-
etrating wounds of the pericardium. In 1896,
however, Cappelen attempted to repair a heart
by suturing a myocardial laceration. Although
this operation failed, in the same year Rehn,
in Frankfurt, was successful in relieving a
cardiac tamponade and in suturing a knife
wound of the heart. Rehn's accomplishment
is generally regarded as the first actual repair
of a heart wound, although in 1908, Matas
reported that Farina had performed a similar
operation, also in 1896. On September 14,
1902, Dr. Hill of Montgomery, Alabama,
became the first American physician to suc-
cessfully repair a cardiac injury.

Thus it is interesting that H.M. Sherman in
1902 noted, "The road to the heart is only 2
to 3 cm in a direct line, but it has taken surgery
nearly 2400 years to travel it," Considerable
controversy continued regarding the best
approach in managing penetrating cardiac
trauma. In 1943, Blalock and Ravitch still
advocated pericardiocentesis as a form of
definitive treatment for cardiac tamponade
secondary to penetrating wounds of the heart.

INCIDENCE

In 1908, Matas noted that there had been
160 reported cases of heart wounds after the
operations of 1896. Recent reports show an
increasing incidence of recognized cardiac
trauma. The greater number of gunshot
wounds in many urban centers is associated
with the rise in cases of penetrating heart
wounds, and true blunt cardiac trauma is
associated with high-speed transportation.

Parmley, Mattingly, andManion (1958) eval-
uated 456 postmortem cases of penetrating
wounds of the heart and aorta but stressed
that the true incidence of cardiac trauma had
not been established. Assessing numbers is
complicated by the high early mortality rate
of patients with these injuries. Isaacs (1959)
reported, for instance, that from 1937 to 1959,
more than 50% of the 133 patients were dead
on arrival at Johns Hopkins Hospital. Only 86
of the 459 patients analyzed by Sugg (1968)
arrived alive in the EC of Parkland Hospital
in Dallas.

Other reports of note were those of
Griswold and Drye (1954), who found 108
cardiac wounds at Louisville General Hospi-
tal in 20 years (1933 to 1953); Naclerio
(1964) , who recorded 249 penetrating wounds
in 13years (1950 to 1963); Wilson and Bassett
(1966), who saw 200 patients and 205 wounds
in 16.5 years (1949 to 1965); and Beall and
colleagues (1972) who had 269 patients with
penetrating cardiac injuries in Houston within
20 years (1951 to 1971). Similarly, in Atlanta,
Symbas, Harlaftis, and Waldo (1976) treated
102 patients with penetrating cardiac heart
wounds, between 1964 and 1974. In 1997, Wall
and Mattox reported 711 heart injuries over
a 30-year period in Houston, of which 60 were
complex.

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15 • WOUNDS OF THE HEART

287

The true incidence of cardiac trauma in the
military experience is difficult to ascertain.
On the battlefield, many cardiac wounds are
immediately fatal. This is emphasized by one
of the typical case reports from World War I.
Dixon and McEwan (1916) reported one
wounded heart in a series of 123 wounds of
the thorax. These authors proclaimed, "prob-
ably nearly all cardiac wounds produced
death from hemorrhage too quickly to allow
the patients being removed alive even to a
short distance from the battlefield." Interest
in wounds of the heart increased greatly
during World War II. Harken (1946) reported
a unique experience in removing foreign
bodies from the heart and adjacent major
vessels in 134 patients.

There was one major report of injuries to
the heart during the Korean conflict. Valle
(1955) reported an incidence of 4.2% of
injuries to the heart and mediastinum: 117
injuries in a group of 2811 chest casualties
treated at Tokyo Army Hospital from August
1950 to March 1953. In this group, however,
there were only 19 cases of foreign bodies in
the heart and 42 pericardial effusions. The
remainder of the injuries were to the medi-
astinum and structures adjacent to the heart.

Cardiac trauma during the Vietnam War
has not been completely documented.
Gielchinsky and McNamara (1970) reported
10 heart injuries at the 24th Evacuation Hos-
pital, an incidence of 2.8%. The records of
nearly 120 patients with cardiac wounds in
Vietnam are included in the long-term follow-
up effort in the Vietnam Vascular Registry.
Specifically, details of 96 cardiac injuries were
evaluated by Geer and Rich (1972). Most of
these injuries occurred between 1968 and
1970. At least 21 different surgical facilities
participated in the care of patients with
cardiac injuries (Table 15-1).

CLINICAL PATHOLOGY

Penetrating wounds of the pericardium and/
or the myocardium caused by sharp instru-
ments or low-velocity missiles are the most
frequent types of injuries reported. Recent re-
ports emphasize the vulnerability of the right

TABLE 15-1

ETIOLOGY OF CARDIAC TRAUMA
IN VIETNAM

Wounding
Agent

No. of Patients

Deaths

Fragment

74.0

Gunshot

11.5

Flechette

3.1

Stab

3.1

Unknown

8.3

Total

100

From T.M. Geer and N.M. Rich, Vietnam Vascular Registry,
unpublished data, 1972.

ventricle because of its anterior location. Our
service found that the site of injury among
patients with penetrating wounds of the peri-
cardium was the right ventricle in 40% of
patients, the left ventricle in 40% of patients,
the right atrium in 24%, and the left atrium
in3% (multiple injuries included) (Fig. 15-1).

The World War II combat experience as
described by Samson (1948) varies somewhat
in that the left ventricle was involved more
often than the right ventricle. This is the excep-
tion, however, because the location of cardiac
wounds in the Vietnam experience again
emphasizes the predominance of wounds of
the right ventricle (Table 15-2). As alluded
to earlier, most of these wounds are pene-
trating wounds.

True blunt cardiac trauma usually results
in diffuse contusion of the myocardium.
However, the extent of cardiac injuries sec-
ondary to blunt trauma to the chest may range

TABLE 15-2

CARDIAC TRAUMA IN VIETNAM:
LOCATION OF WOUNDS

Site

No.

Right ventricle

44.9

Left ventricle

24.7

Right atrium

7.9

Left atrium

5.6

Unknown

16.9

Total

100

From T.M. Geer and N.M. Rich, Vietnam Vascular Registry,
unpublished data, 1972.

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IV • SPECIFIC VASCULAR INJURIES

©Baylor College of Medicine 1997

■ FIGURE 1 5-1

Distribution of injuries to the four chambers of
the heart (multiple injuries included). The
posterior nature of the relatively protected left
atrium probably accounts for its low incidence
of injury. ■

from minor subepicardial or subendocardial
hemorrhage to actual rupture of the
myocardium. When there is sufficient force
involved in a nonpenetrating injury to cause
actual cardiac laceration, a fatal outcome fre-
quently occurs. Patients who have had blunt
trauma to the chest with cardiac trauma of
varying degrees may have electrocardio-
graphic changes, dysrhythmias, cardiac failure,
cardiac tamponade, or hemothorax. Cardiac
injuries from blunt trauma to the chest wall
may or may not be associated with rib frac-
tures or obvious chest wall deformity. When
Parmley and colleagues (1958) reviewed 546
autopsies in patients who had nonpenetrat-
ing traumatic cardiac injuries, they found that
353 of the 546 patients died of rupture of the

heart. Of these 353 patients, 106 had multi-
ple chamber ruptures.

In addition to the injuries of the myocar-
dial surface, other more unusual types of
injuries can be seen to the valves, the inter-
ventricular or interatrial septum, the coronary
vessels, and the conduction system of the
heart. Representative case reports of these
unusual injuries include the removal of a wire
lodged in the interventricular septum by
Kleinsasser (1961); two patients with pene-
trating wounds of cardiac valves, one with
mitral insufficiency and the other with tri-
cuspid insufficiency (Pate and Richardson,
1969); three patients with intracardiac lesions
including an aortic right ventricular fistula
(Hardy and Timmis, 1969) ; and coronary arte-
rial injuries (Tector and colleagues, 1973).
Patients have developed left ventricular
aneurysms after penetrating wounds, as
reported in the civilian experience by Kakos
and colleagues (1971) and in the military
experience by Aronstam and colleagues
(1970). There have been, in addition, more
recent series by Demetriades (1990),
Thandroyen (1981), and Wall (1997). In the
later, 60 patients had complex heart wounds
out of a total of 711 into the hemothorax.

Associated pathology frequently accompa-
nies cardiac wounds. This is emphasized by
the report of Ricks and colleagues, who found
that concomitant organ injury was associated
with a striking rise in the mortality from 12%
when there was injury of one associated organ
to 69% with two or more associated organ
injuries in their 31 patients with gunshot
wounds of the heart. All but 1 of the 31 patients
had one or both lungs injured together with
the associated cardiac wound. Sugg and col-
leagues found that 30 survivors of penetrat-
ing heart wounds had no associated injuries.
However, 33 patients who survived penetrat-
ing wounds of the heart had a total of 84 asso-
ciated injuries.

PATHOPHYSIOLOGY

Injuries to the heart can be divided into
simple and complex. Simple injuries to the
myocardium that result in bleeding from

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289

an injured chamber can present two ways. If
the injury through the pericardium is so small
that the bleeding is contained, tamponade
physiology results. The pericardium does not
distend acutely and can prevent the passive
filling of the heart. Thus the patient essen-
tially has an empty beating heart. If the injury
through the pericardium is large, the patient
may exsanguinate either externally or into the
hemithorax. How much blood is in the left
pleural cavity is often helpful to note during
an empiric exploration for cardiac injury
because the approach may be altered based
on whether exsanguination or tamponade
physiology is present. Most cardiac injuries are
simple lacerations and can be managed with
direct repair. However, complex cardiac
injuries that involve the coronary arteries,
cardiac valves, subvalvular apparatus, or the
cardiac septum, though rare, present a dif-
ferent challenge. Injuries to the coronary
arteries can result in an area of ischemic
myocardium. Treatment options are based on
the distribution and amount of ischemic
myocardium at risk. Injuries to the atrioven-
tricular valves often result in regurgitation,
which is commonly diagnosed postopera-
tively when a new murmur is noticed. Signif-
icant injury to the aortic valve is not well
tolerated in the acutely hypotensive patient,
and most of these patients die before arrival
at the hospital, so they are rarely seen. Cardiac
septal injuries from penetrating trauma often
initially are small and diagnosed postopera-
tively as a new murmur. Thus the common
scenario is that many of the valvular and septal
injuries are detected postoperatively after
the acutely bleeding cardiac injury is con-
trolled and are repaired subacutely at a later
operation.

PREHOSPITAL MANAGEMENT

These patients most commonly present with
a pattern of injury of penetrating trauma with
proximity to the heart with either hypovolemia
or tamponade physiology. Early consideration
of the possibility of a cardiac injury with appro-
priate transport to a center that can manage
it may be lifesaving. If the patient has a sys-

tolic blood pressure more than 80 mm Hg and
is awake, ancillary measures to artificially
elevate the blood pressure may not be helpful.
Thus time should not be wasted on large-
volume crystalloid resuscitation or the place-
ment of pneumatic antishock trousers. In a
patient in extremis, endotracheal intubation
to control ventilation and maximally oxy-
genate the remaining circulating blood may
be one of the few efficacious prehospital
maneuvers.

EMERGENCY CENTER

The diagnosis of a cardiac injury in the EC
is based on a high index of suspicion. A pen-
etrating injury in the area of the middle third
of the chest between the nipples laterally and
from the xiphoid to the sternal notch verti-
cally is a common presentation. The patients
often present in extremis and the cardiac
injury is diagnosed on empiric exploration
during EC thoracotomy. Low-energy mecha-
nisms such as stab wounds can be problem-
atic because tamponade physiology may not
immediately develop. Awake patients usually
have a profound anxiety. There are also
reports of tamponade manifesting 2 to 3 days
after the injury. Muffled heart sounds, dis-
tended neck veins, and hypotension are clas-
sically described. However, distended neck
veins and an elevated central venous pressure
are common in the anxious patient, and
muffled heart sounds are difficult to detect
in the noisy EC. Few diagnostic studies are
usually needed and only delay transfer to the
operating room for definitive therapy. The
problematic patients are the ones who present
hemodynamically stable with no signs of tam-
ponade that are being investigated for prox-
imity. These patients most benefit from
monitoring and further investigation.

Chest radiographs are commonly obtained.
This is often unhelpful for the diagnosis of
cardiac injury because these patients usually
have a normal mediastinum. Their primary
efficacy is to detect a pneumothorax or hemo-
thorax. Wound clips marking entrance and
exitwounds can be helpful, although missiles
often do not follow straight lines between these

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IV • SPECIFIC VASCULAR INJURIES

clips. Unexplained missile trajectories can be
problematic and may represent either a
missile bouncing off bony structures or an
intravascular missile that has embolized.

One diagnostic procedure that has had a
significant impact on the diagnosis of cardiac
injury has been ultrasound in the EC by the
surgical team. Blood around the heart may
be readily seen and diagnosed before the
hemodynamic affects of tamponade. In skilled
hands and the appropriate body habitus, the
use of ultrasound has probably superseded
other diagnostic entities such as central venous
pressure monitoring and subxiphoid peri-
cardial window. Formal echocardiography
(either transthoracic or transesophageal) has
little use in the hypotensive patient and only
delays therapy. Their primary use may be as
a second study or as a follow-up study after
operative repair of a cardiac injury to docu-
ment wall motion, septal integrity, and valvu-
lar function.

EMERGENCY CENTER
PROCEDURES

A patient with a penetrating wound to the
chest often requires a tube thoracostomy for
a concomitant hemothorax or pneumo-
thorax. In the hypotensive patient with a
suspected cardiacwound, an empiric tube tho-
racostomy may be used to rule out a tension
pneumothorax, which can present in a similar
manner. Chest tubes should be placed no
lower than the nipple level (to avoid the
diaphragm) in the midaxillary line directing
the tube posteriorly. After developing a tunnel
and dividing intercostal muscles, the pleural
space should be entered bluntly with the
finger to avoid injuring the lung or the
heart. During tube thoracostomy, the lung,
diaphragm, and pericardium should be pal-
pated. This is often referred to as a digital
thoracotomy. Before the wide use of ultra-
sound, balloting the pericardium could be
used to detect a tamponade and provide an
indication for operation. In a patient with
suspected stab wounds to the heart, the tube
thoracostomy incision is often placed slightly
more anterior so the apex of the heart can

be more readily palpated. Balloting the heart
to detect tamponade is a subtle maneuver
and should be done during each tube
thoracostomy.

Pericardiocentesis is often recommended
in some resuscitation courses to temporize
tamponade. Unfortunately, it is an unreliable
procedure that often results in significant
iatrogenic injuries. Even when a catheter is
successfully placed, the clotted blood is unre-
liably removed and may result in a false sense
of security. Thus with the availability of ultra-
sound, the use of pericardiocentesis as a diag-
nostic maneuver has practically disappeared.
At best, it may be a temporizing maneuver en
route to the operating room.

EC thoracotomy is one of the original
damage control procedures in surgery. Many
patients with cardiac injuries are often pre-
morbid on arrival and will not survive the trip
to the operating room. Using EC thoracotomy
to bring techniques of definitive care to the
EC has resulted in survivors. The primary
thrust of EC thoracotomy for cardiac injuries
is accessing the heart, relieving the tampon-
ade, and controlling bleeding. Once this is
accomplished, the patient can be moved to
the operating room for completion of the
procedure.

The EC thoracotomy is performed with the
patient supine after abducting the left arm.
The incision is made immediately below the
nipple in the male patient or beneath the
breast tracking up to the fourth intercostal
space in the female patient. The incision is
made from the sternum to the posterior axil-
lary line following the rib. Intercostal muscles
are divided entering the chest in one area and
the intercostal incision extended with the scis-
sors. The rib retractor is placed with the rack
toward the table and the retractor widely
opened. The pleural cavity is inspected for the
amount of blood to determine exsanguina-
tion versus tamponade and the pericardium
inspected. If tamponade is present and the
heart is still beating, the pericardium is
grasped between clamps anterior to the
phrenic nerve and the pericardium is opened
with the scissors. This is extended superiorly
and inferiorly evacuating the clot and may
result in a return of cardiac output. The heart
is brought into the left side of the chest and

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15 • WOUNDS OF THE HEART

291

inspected for injuries. For injuries to the right
side of the heart, the incision may need to be
extended across the chest with a Gigli saw,
Lebsche knife, or sternal saw. If relief of tam-
ponade does not result in return of perfusion,
the aorta is cross clamped with an aortic clamp
just distal to the left subclavian artery, being
careful to avoid the esophagus.

Immediate control of the injury is obtained
with the surgeon'sfinger. A4-0 polypropylene
suture on a large needle is then used to rapidly
close the laceration in a gentle running
fashion. The suture may be tied by an assis-
tant while the surgeon continues to hold the
heart. Because the incidence of needle stick
during EC cardiorrhaphy approaches more
than 30% , the skin stapler has often been used
to achieve rapid vascular control and mini-
mize the incidence of injury to the surgical
team (Fig. 15-2) . After repair, warm saline is
poured on the heart and the patient is rapidly
transferred to the operating room for defin-
itive repair. Pitfalls during the EC thoracotomy
involve taking too long to perform it, not
making a large enough incision initially, injur-
ing the heart and lung while opening the

chest, and injuring segmental vessels or the
esophagus during aortic cross clamping. The
outcomes of EC thoracotomy hinge on patient
selection. A significant number of patients who
have signs of life after an isolated stab wound
to the heart can be salvaged. Recent data by
Moore suggest that if a sustainable blood pres-
sure is not obtained in the EC, further efforts
in the operating room may be futile.

OPERATIVE MANAGEMENT OF
CARDIAC INJURIES

Incisions

For abdominal trauma, the midline laparo-
tomy offers almost universal exposure.
However, there are multiple incisions that can
be made to manage chest trauma. The two
most common incisions employed to manage
cardiac injuries are left anterolateral thora-
cotomy with possible extension across the
sternum or median sternotomy. Each incision
has advantages and disadvantages. The

■ FIGURE 1 5-2

Acute management of cardiac
injuries. A, Laceration of the left
ventricle. B, Continuous fine
polypropylene suture placed
for both repair and hemostasis.
C, A Foley balloon catheter can
be useful to achieve
hemostasis in the beating heart
before placement of sutures. D,
Because of the high incidence
of needle stick during
cardiorrhaphy, the skin stapler
may be useful acutely in the
emergency center for initial
control. ■

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IV • SPECIFIC VASCULAR INJURIES

median sternotomy, the standard elective
cardiac incision, is a midline incision that is
relatively bloodless. Though easy to perform,
it has the disadvantage of being difficult to
clamp the aorta for resuscitation. In addition,
efforts to retract the heart to repair a poste-
rior injury may result in intractable ventricu-
lar fibrillation in the cold, irritable injured
heart. In many centers the left anterolateral
thoracotomy is the incision of choice for
cardiac trauma. It is easily made with a
minimal number of instruments and offers
excellent exposure of the heart and descend-
ing thoracic aorta. In most cases the patient
is positioned supine with the arms out so they
are available to the anesthesia service. For
right-sided injuries, a transsternal extension
into the opposite chest is helpful. Left antero-
lateral thoracotomy has the additional advan-
tage in that injuries to the posterior heart can
be more readily visualized from this viewpoint
with less retraction and manipulation.

Aortic Occlusion

Occlusion of the descending thoracic aorta
may be helpful as a resuscitative maneuver.
The aorta is cross clamped just distal to the
left subclavian origin, being careful to avoid
injury to the esophagus. It is useful to dissect
anterior and posterior to the aorta and actu-
ally encircle it with a finger before applying
the clamp to ensure accurate positioning. This
ensures that blood is preferentially diverted
to the brain and heart. As the patient is resus-
citated, the aortic cross clamp can be gradu-
ally weaned and removed. It is extremely
common after hemorrhage is controlled for
patients to be over-resuscitated and the heart
may become distended. One technique to
decompress the heart is to remove the aortic
cross clamp and vent the heart into the sys-
temic circulation momentarily.

Cardiac Manipulation

The cold, empty injured heart can be
extremely irritable. Even minor manipulation
can cause significant dysrhythmias. Unfortu-
nately, in the cold patient, ventricular

fibrillation is often refractory. Thus all mani-
pulations of the heart should be gentle and
retraction minimized.

It has been learned from elective cardiac
surgery that significant retraction of the heart
can be performed if done slowly and in such
a manner that the heart can fill. Because the
filling of the heart is passive, it is important
not to compress the cardiac chambers as it is
retracted. Gentle manipulation with a drag-
ging motion can often allow one to completely
invert the heart out of the chest and still main-
tain cardiac output while allowing access to
the posterior aspect of the left atrium. If the
heart is not beating in an organized rhythm,
manual cardiac compression may be required.
This is best performed with a two-handed tech-
nique gently alternating between allowing the
heart to fill and compressing it from apex to
base. Cardiac compressions often are per-
formed with one hand by some doctors. Unfor-
tunately, the distended right ventricle can be
extremely thin walled and may be injured by
the thumb or fingers. In the bradycardic heart,
manual compression may serve to prevent it
from becoming distended by manually emp-
tying the chambers. Sutured temporary epi-
cardial leads can be helpful also.

Hemorrhage Control

Some injuries may be extremely difficult to
manage because of massive hemorrhage.
These may often be managed by cardiac inflow
occlusion to empty the heart before repair.
The superior and inferior vena cava can be
pinched between the fingers or clamped with
vascular clamps and the heart allowed to
empty. The injury can then be visualized and
the repair performed. If after a left-sided injury
is repaired there is concern about intracar-
diac air, the patient should be placed in a head-
down position and the ascending aorta vented
while a cardiac rhythm is restored. Inflow
occlusion allows a short interval of an empty
beating heart and the repair must be accom-
plished before its arrest.

Inflow occlusion can also be extremely
useful in repairing the distending heart or
repairing a thin soft aorta. To avoid placing
undo tension as the stitches are tied down,

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15 • WOUNDS OF THE HEART

293

inflow occlusion can be accomplished to tem-
porarily decrease the blood pressure while
tying down the repair.

The right atrium is a commonly injured
cardiac structure. Upon diagnosis of a right
atrial injury, it is helpful to extend the inci-
sion across the sternum for better visualiza-
tion. Initially, the injury is controlled with the
finger. Other adjuncts that may be useful are
a partial occluding clamp or a Foley catheter
placed through the injury for temporary
control (Fig. 15-2) . A 4-0 polypropylene or 5-
polypropylene suture is then used in a simple
continuous manner to close the injury and
effect repair. The repair of atrial injuries
close to the superior vena cava-right atrial
appendage junction may involve the sinoatrial
node and result in dysrhythmias.

Injuries to the left atrium can be difficult
to manage. The heart is gently and slowly
retracted while avoiding compression and per-
mitting passive filling of the heart. All instru-
ments and sutures should be prepared before
retracting the heart, and sutures can often be
placed in a back-hand manner. It may be
helpful for the surgeon to retract with one
hand and sew with the other so the cardiac
performance can be monitored and the heart
returned to the chest before arrest. It may take
multiple episodes of suturing to close these
injuries. As described earlier, inflow occlusion
can decrease bleeding through a posterior
injury so it can be more readily visualized.
Repairs in the empty heart should raise the
surgeon's suspicion of intracardiac air, and
the patient can be placed head down and the
aorta vented before restitution of inflow.

Whereas the left ventricle is a thick mus-
cular structure, the anterior wall of the right
ventricle is only approximately 5 mm thick.
Repair of the right ventricle can be initially
managed with digital pressure, followed by
repair with a fine suture. Pledgeted sutures
are not routinely needed though may be used
if the repair fails or the heart distends. Avoid-
ing over-resuscitation and inflow occlusion
may be helpful adjuncts in these repairs.
Injuries to the left ventricle are performed in
a similar manner, although these are often on
the posterior surface and require some
measure of retraction. If possible, the ventri-
cle should be carefully inspected to identify

injury to adjacent coronary arteries. It should
be remembered that the heart is a relatively
soft muscle and a gentle technique with a fine
suture often gets better results. Again, initial
control with a finger or a Foley balloon
catheter to arrest hemorrhage is often helpful.
With no intravenous access available, the Foley
catheter can be connected to an intravenous
catheter for direct infusion. It is our prefer-
ence not to aggressively resuscitate the heart
before repair because the empty bradycardic
heart is ideal for the placement of sutures.
Overzealous crystalloid resuscitation results
in an overdistended heart that not only fails
to hold stitches but also fails to beat well after
repair. Administration of pressor drugs before
repair results in a rapidly beating empty heart
that is extremely difficult to sew. Multiple
injuries and complex lacerations portend a
poorer prognosis.

Complex Injuries

Anterior stab wounds often occur immedi-
ately adjacent to the left anterior descending
coronary artery. If the coronary artery is unin-
jured, it is important to repair the laceration
without compromising the coronary artery.
Deep mattress sutures beneath the coronary
artery will permit repair while avoiding the
coronary artery. When a coronary artery is
injured, decision making is guided by its loca-
tion and the amount of myocardium at risk.
Small secondary branches of the coronary
arteries can usually be ligated. The patient can
then be observed for dysrhythmias or the
development of an akinetic area of the heart.
If there is any concern, many will place a hor-
izontal mattress suture and use a snare tourni-
quet and observe the heart before tying the
suture down. If a significant area of the heart
becomes akinetic and fails, then coronary
artery bypass may be indicated. If a small area
of the heart becomes akinetic and cardiac
function is borderline after ligation, the place-
ment of an intra-aortic balloon pump may tem-
porize the injury and the patient may be
treated similar to those having had a small
myocardial infarction. Though uncommon,
most coronary artery injuries that require
emergent bypass are proximal injuries of the

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294

IV • SPECIFIC VASCULAR INJURIES

■ FIGURE 1 5-3

Coronary artery bypass grafting
for injury involving the left
anterior descending coronary
artery. A, Anterior stab wound
to the chest. B, Injury involves
the proximal left anterior
descending coronary artery,
resulting in a large area of
ischemic myocardium. C,
Hemostasis is initially obtained
with continuous suture of the
laceration. D, Coronary artery
bypass from the ascending
aorta to the distal left anterior
ascending coronary artery
using cardiopulmonary bypass.
Fortunately, this is seldom
needed in most patients. ■

©Baylor College ol Medicine 1997

primary branches such as the left anterior
descending or the right coronary artery (Fig.
15-3). Although off-pump methods would
seem attractive, these patients often require
cardiopulmonary bypass to support the failing
heart. Because this is an emergent lifesaving
activity, the saphenous vein is most commonly
used as the conduit.

Cardiac Septal Injuries

The most common presentation for cardiac
septal injuries is when a new murmur is noted
postoperatively in the intensive care unit. Most
patients who survive cardiac repair who have
a septal injury often have small injuries that
may not be hemodynamically significant. The
diagnosis is confirmed with echocardiography.
A saturation run during catheterization of the

right side of the heart may be diagnostic and
can be used to calculate shunt fraction. If indi-
cated, most of these patients undergo car-
diopulmonary bypass in a subacute fashion
often weeks after the initial injury. A shunt
fraction of more than 2 : 1 is often used as an
indication for surgery. Smaller injuries with
smaller shunt fractions may be observed. The
patient however should be counseled about
the risk of endocarditis if they undergo other
invasive procedures.

These injuries are repaired using car-
diopulmonary bypass usually via a median ster-
notomy. For anterior stab wounds resulting
in ventricular septal defects, the injury may
be repaired through the previous myocardial
repair. Although ventriculotomy is avoided in
elective cardiac surgery, this area is often
scarred from the initial injury and offers excel-
lent exposure of the septal injury (Fig. 15-4) .

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15 • WOUNDS OF THE HEART

295

©Baylor College ol Medicine 1997

■ FIGURE 1 5-4

Repair of traumatic ventricular
septal defect. A, The acute
management of the injury to the
surface of the heart is with
either continuous or pledgeted
sutures controlling the
hemorrhage. Later in the
intensive care unit, a murmur is
detected and the ventricular
septal defect is diagnosed. B,
These injuries are most
commonly repaired subacutely
often weeks after the initial
injury. Because of the scarring
from the initial injury,
ventriculotomy can be
performed through the original
scar. C, This results in good
visualization of the septal
wound. These can be repaired
with either (D) interrupted
pledgeted sutures or (E) larger
defects closed with a Dacron
patch. ■

Knowledge of the conduction system of the
heart and counseling the patient preopera-
tively about the risk of conduction defects is
helpful. Smaller defects can be closed pri-
marily, but often the use of a prosthetic mate-
rial such as Dacron may be required. Small
ventricular septal defects located near the apex
of the heart can be extremely difficult to local-
ize and repair. Atrial septal defects can be
approached via the standard incision in the
right atrium. Again, knowledge of the path of
the conduction system can help avoid iatro-
genic injuries.

Cardiac Valvular Injury

esophageal echocardiography may be helpful
to adequately visualize the subvalvular appa-
ratus of the mitral valve. The injuries may
involve the leaflets of the valve or the sub-
valvular apparatus. Although it is often hoped
that a simple repair can be performed, upon
exploration, the valve often is found to be
totally destroyed and in need of being
replaced. Replacement is performed via
median sternotomy and the standard
approach using cardiopulmonary bypass.
Injury to the right-sided heart valves is not
common. The indications for operation are
the same as those for elective cases. Choice of
technique and prosthesis depends on the
pathology encountered at exploration.

Similar in presentation to septal injuries,
most cardiac valvular injuries in survivors are
detected as a new murmur postoperatively in
the intensive care unit. They are usually
injuries of the mitral or tricuspid valve and
are evaluated with echocardiography. Trans-

Intrapericardial Inferior Vena
Cava Injury

One injury that requires acute cardiopul-
monary bypass is a posterior injury to the

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296

IV • SPECIFIC VASCULAR INJURIES

■ FIGURE 1 5-5

Unusual injury of posterior
intrapericardial inferior vena
cava. A, These are often from
transaxial gunshot wounds. 6,
The injury is extremely difficult
to visualize and access. C,
Cardiopulmonary bypass is
instituted with cannulation of
the superior vena cava directly
and the inferior vena cava via
the groin for venous drainage.
D, Total cardiopulmonary
bypass allows the right atrium
to be opened and the injury
repaired from within. E, Larger
injuries may require the use
of a Dacron or pericardial
patch. ■

©Baylor College of M

intrapericardial inferior vena cava. This area
is extremely difficult to access, is a short vessel,
and difficult to visualize posteriorly. One tech-
nique available to address it is to cannulate
the groin for cardiopulmonary bypass and
place a superior vena caval cannula for total
cardiopulmonary bypass. The superior vena
cava is snared around the cannula and the
inferior vena cava is clamped immediately
above the liver. The injury is accessed by
opening the right atrium and repairing it from
inside. Though extremely uncommon, this is
one of the few areas in which cardiopulmonary
bypass may assist in managing cardiac injuries
acutely (Fig. 15-5).

SUMMARY

Injuries to the heart have fascinated trauma
surgeons for ages. As with many other injuries,

a repair that was originally thought to be futile,
with advances in technique, has resulted in
significant salvage. Cardiac injuries can
present as either tamponade or exsanguina-
tion and can be classified as either simple or
complex. Simple injuries primarily involve the
myocardium, and complex injuries involve the
coronary arteries, cardiac septa, and cardiac
valves. The EC thoracotomy is one of the
original damage-control procedures and
has resulted in a significant salvage rate for
patients with low-energy penetrating injuries
to the heart. Ultrasound has significantly aided
in the diagnostic accuracy of patients who
present hemodynamically stable. Cardiac
injuries are managed in the operating room
via left anterolateral thoracotomy with exten-
sion across the sternum. Cross clamping of
the descending thoracic aorta could be a sig-
nificant adjunct and various maneuvers such
as digital compression, Foley catheter occlu-
sion, stapling, and a partial occluding clamp

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15 • WOUNDS OF THE HEART

297

may provide initial hemostasis. The avoidance
of resuscitation until repair is complete, the
avoidance of cyclic hyper-resuscitation and the
avoidance of overdistention of the heart can
result in improved outcomes. It is important
to evaluate the patient postoperatively with
physical examination and echocardiography
to document wall motion and assess the
patient for occult septal and valvular injuries.
Most cardiac injuries can be managed by the
trauma surgeon without any specialized
cardiac technique. The need for cardiopul-
monary bypass is extremely rare and is seen
in fewer than 1 % of these patients.

REFERENCES

Surgical approach and initial management of
patients with cardiac injuries

Asensio JA, Stewart BM, Murray J, et al: Penetrat-
ing cardiac injuries. Surg Clin North Am
1996;76:685.

Beall AC Jr, Ochsner JL, Morris GC, et al: Pene-
trating wounds of the heart. J Trauma 1961 ;1:195.

Ivatury RR, Shah PM, Ito K, et al: Emergency room
thoracotomy for the resuscitation of patients with
"fatal" penetrating injuries of the heart. Ann
Thorac Surg 1981;32:377.

Mattox KL, Beall AC, Jordan GL, et al: Car-
diorrhaphy in the emergency center. J Thorac
Cardiovasc Surg 1974;68:886.

Diagnosis and management of complex cardiac
injuries to the coronary arteries, septa, and
valves

Demetriades D, Charalambides C, Sareli P,
Pantanowitz D: Late sequelae of penetrating
cardiac injuries. Br J Surg 1990;77:813-814.

Fallahnejad M, Kutty ACK, Wallace HW: Sec-
ondary lesions of penetrating cardiac injuries:
A frequent complication. Ann Surg 1980;
191:228-233.

Symbas PN, DiOrio DA, Tyras DH, et al: Penetrat-
ing cardiac wounds: Significant residual and
delayed sequelae. J Thorac Cardiovasc Surg
1973;66:526-532.

Wall MJ, Mattox KL, Chen C-D, Baldwin JC: Acute
management of complex cardiac injuries.
J Trauma 1997;42(5):905-912.

Management of intracardiac injuries

Asfaw I, Thorns NW, Arbulu A: Interventricular
septal defects from penetrating injuries of the
heart: A report of 12 cases and review of the lit-
erature. J Thorac Cardiovasc Surg 1975;69:450-

457.

Espada R, Whisennand HH, Mattox KL, Beall AC
Jr: Surgical management of penetrating injuries
to the coronary arteries. Surgery 1975;78:755-
760.

Thandroyen FT, Matisonn RE: Penetrating thoracic
trauma producing cardiac shunts. J Thorac Car-
diovasc Surg 1981;81:569-573.

Whisennand HH, Van Pelt SA, Beall AC Jr, et al:
Surgical management of traumatic intracardiac
injuries. Ann Thorac Surg 1979;28:530-536.

Ventricular aneurysms after cardiac injury

Aronstam EM, Strader LD, Geiger JP, Gomez AC:
Traumatic left ventricular aneurysms. J Thorac
Cardiovasc Surg 1970;59:239-242.

Morales RA, Garcia F, Grover FL, Trinkle JK:
Aneurysm of the left ventricle after repair of a
penetrating injury. J Thorac Cardiovasc Surg
1973;66:632-635.

chl6.qxd 4/16/04 3:40 PM Page 299

Injury to Abdominal Aorta and
Visceral Arteries

DAVID V. FELICIANO

O GENERAL
Incidence
Pathophysiology
Clinical Presentation
Areas of Abdominal Vascular Injuries
O OPERATION

Supramesocolic Area of Zone 1

Suprarenal Abdominal Aorta

Celiac Trunk

Superior Mesenteric Artery

Renal Artery
Inframesocolic Area of Zone 1

Infrarenal Abdominal Aorta
Zone 2 or Upper Lateral Retroperitoneum

Renal Artery
Complications

299

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300

IV • SPECIFIC VASCULAR INJURIES

GENERAL

Incidence

The incidence of injuries to the abdominal
aorta, celiac trunk or major branches, supe-
rior mesenteric artery, and renal artery is sur-
prisingly high in urban trauma centers in the
United States. This is a reflection of rapid trans-
port by prehospital emergency medical ser-
vices and the large number of patients who
are treated for penetrating wounds, parti-
cularly those caused by low-velocity civilian
handguns.

In one recently published review from the
Grady Memorial Hospital in Atlanta, Georgia,
300 patients with 205 abdominal arterial and
284 abdominal venous injuries were treated
at laparotomy during a 10-year period. Of
interest, the mechanism of injury was a pen-
etrating wound in 86.7% of patients, with
abdominal gunshot wounds (78%) account-
ing for the majority. The group of patients
with abdominal arterial injuries included 77
(37.5%) with injuries to the abdominal aorta,
18 (8.8%) with injuries to the renal artery, 16
(7.8%) with injuries to the superior mesen-
teric artery, and 16 with injuries to the celiac
trunk or major branches. This group there-
fore accounted for 62% of all abdominal
arterial injuries treated.

Another recently published review from the
Los Angeles County Hospital described 302
patients with 238 abdominal arterial and 266
abdominal venous injuries that were treated
at laparotomy during a 6-year period. Of inter-
est, the mechanism of injury was a penetrat-
ing wound in 88% of patients, with abdominal
gunshot wounds (81%) accounting for the
majority. Patients with injuries to the aorta,
celiac trunk or major branches, superior
mesenteric artery, and renal artery accounted
for 57% of all abdominal arterial injuries
treated.

In contrast to the aforementioned reports,
injuries to all abdominal vessels have been
uncommon in reviews of military conflicts.
This low incidence reflects the greater wound-
ing power of high-velocity military weapons
and the longer delays to definitive operation
that occur in all war zones. In the report by

DeBakey and Simeone of 2471 arterial injuries
during World War II, only 49 (2%) occurred
in the abdomen. In similar fashion, the report
by Hughes of 304 arterial injuries from the
Korean War included only 7 (2.3%) that
occurred in the abdomen. Finally, the report
by Rich and colleagues of 1000 arterial injuries
treated in the Vietnam conflict described only
29 (2.9%) involving abdominal vessels.

Pathophysiology

Penetrating injuries to the abdominal aorta
or visceral branches most commonly cause
lateral wall defects with intraperitoneal bleed-
ing or expanding pulsatile retroperitoneal or
mesenteric hematomas. Aless common injury
is complete transection of a visceral artery with
secondary bleeding, an expanding hematoma,
or complete thrombosis of both ends of the
vessel. On occasion, the track of a missile may
be in proximity to a visceral vessel and cause
a thrombosis because of disruption of the
intima from a blast effect. The rarest injury
related to a penetrating wound is the creation
of an upper abdominal arteriovenous fistula
involving the hepatic artery and portal vein,
the superior mesenteric vessels, or the renal
vessels.

Bluntinjuries to the abdominal aorta orvis-
ceral branches are most commonly caused by
deceleration, a direct anterior crushing mech-
anism (lap-type seatbelt), or a posterior blow
to the spine. Deceleration or direct anterior
blows have most commonly caused either
thrombosis of the infrarenal abdominal aorta,
superior mesenteric artery, or renal artery or
lateral wall defects in the superior mesenteric
artery at the base of the mesentery. Posterior
blows to the spine have most commonly
caused an intimal flap and secondary throm-
bosis of the infrarenal abdominal aorta.

Clinical Presentation

In patients with either a penetrating or a
blunt mechanism of injury, the clinical pre-
sentation will depend on several factors. The
first of these is the type of aortic or visceral
arterial injury. In patients with defects in the

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301

lateral wall, hemorrhage will occur and lead
to hypotension with or without peritonitis.
With complete transection of a visceral vessel
and hemorrhage, the presentations will be the
same. Should transection lead to thrombosis
of both ends of the visceral vessel, a rare event
in my experience, only abdominal pain (supe-
rior mesenteric artery) or hematuria (renal
artery) may be present. The same presenta-
tions along with ischemia of both lower
extremities (abdominal aorta) would occur if
blunt trauma, an intimal flap, and secondary
arterial thrombosis were present.

Clinical presentation is affected by the pres-
ence or absence of retroperitoneal or mesen-
teric tamponade, as well. In patients with
defects in the lateral wall of the abdominal
aorta or visceral arteries, retroperitoneal or
mesenteric tamponade is the most common
finding at a subsequent laparotomy. All
patients who have arterial injuries and tam-
ponade are still hypotensive at some point in
the preoperative period — in the field, in the
emergency center, or in the operating room
as general anesthesia is initiated. In contrast
to patients with abdominal venous injuries and
tamponade, any improvement in blood pres-
sure secondary to the infusion of crystalloid
solutions and blood is transient. If retroperi-
toneal or mesenteric tamponade does not
occur and there is active hemorrhage into the
peritoneal cavity, a confused or moribund
patient with profound hypotension, clear-
cut peritonitis, and a tight abdomen is the
presentation.

Areas of Abdominal
Vascular Injuries

As has been discussed in numerous other texts,
it is often helpful to describe the approaches
to abdominal vascular injuries in a "geographic
zone" fashion. Zone 1 includes the midline
retroperitoneum and base of the mesentery,
zone 2 is the upper lateral retroperitoneum
(renal vessels), and zone 3 is the pelvic
retroperitoneum (iliac vessels). Because they
are uncommon, injuries to the vessels in the
porta hepatis or retrohepatic area are usually
described separately, as well.

Zone 1, the topic of discussion in this
chapter, is best divided into suprameso colic and
inframeso colic areas, because the operative
approach is different for each, as is described.
A midline supramesocolic area of hematoma
or hemorrhage is likely to contain an injury
to the suprarenal abdominal aorta, celiac
trunk, proximal superior mesenteric artery,
proximal renal artery, superior mesenteric
vein, or obviously the pancreas. A midline
inframesocolic area of hematoma or
hemorrhage is likely to contain an injury to
the infrarenal abdominal aorta, left renal vein,
or inferior vena cava.

As a general rule, all hematomas in zone 1
(either supramesocolic or inframesocolic)
from either penetrating or blunt trauma are
opened by the surgeon using techniques to
be described. Hematomas from penetrating
wounds in zones 2, 3, and in the porta hepatis
are opened, as well. In contrast, hematomas
from blunt trauma that are located in zones
2 and 3 or in the retrohepatic area are opened
only if they are pulsatile, expanding rapidly,
or have already ruptured.

OPERATION

Supramesocolic Area of Zone 1

SUPRARENAL ABDOMINAL AORTA

The presence of a hematoma in the midline
supramesocolic area will usually give the
surgeon time to obtain proximal control of
the supraceliac abdominal aorta. Such a
hematoma is more likely to be present when
the injury to the abdominal aorta is in the
diaphragviatic aorta (in the aortic hiatus, itself)
rather than in the visceral aorta (origins of
visceral arteries) (Fig. 16-1).

The left-sided medial mobilization maneu-
ver is the preferred operative approach. This
maneuver includes division of the retroperi-
toneal attachments and reflection of the left
colon, left kidney, spleen, tail of the pancreas,
and fundus of the stomach to the midline (Fig.
16-2) . The advantage of this technique is that
it allows visualization of the entire abdominal
aorta from the aortic hiatus of the diaphragm

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302 IV • SPECIFIC VASCULAR INJURIES

Divisions of Suprarenal Aorta

Diaphragmatic
aorta

Visceral
aorta

■ FIGURE 16-1

Penetrating wounds of the diaphragmatic
abdominal aorta may be tamponaded by
muscle fibers of the aortic hiatus, and wounds
of the visceral abdominal aorta are obviously
more complex. (From Baylor College of
Medicine, 1987.) ■

to the aortic bifurcation (Fig. 16-3). Dis-
advantages include the time required to
complete the maneuver (4 to 5 minutes in
inexperienced hands); risk of damage to the
spleen, left kidney, or posterior left renal artery

Plane of Dissection

■ FIGURE 16-2

Left medial mobilization maneuver is initiated
by dividing lateral retroperitoneal attachments
of left colon, left kidney, spleen, tail of
pancreas, and fundus of stomach. (From
Feliciano DV: Truncal vascular trauma. In
Callow AD, Ernst CB [eds]: Vascular Surgery.
Theory and Practice. Stamford, Conn, Appleton
& Lange, 1995, pp 1059-1085.) ■

■ FIGURE 16-3

Completion of left medial mobilization
maneuver with all left-sided intra-abdominal
viscera elevated to the midline. ■

during the maneuver; and anatomic distor-
tion that results when the left kidney is rotated
anteriorly. One alternative is to leave the left
kidney in its fossa, thereby eliminating poten-
tial damage to or distortion resulting from
rotation of this structure.

There are three significant obstacles to com-
pleting the maneuver once the viscera are
mobilized. These include the length of the
hiatal muscle fibers surrounding the diaphrag-
matic aorta, the dense nature of the celiac
plexus of nerves connecting the right and left
celiac ganglia, and the thickened lymphatic
tissue around the aorta at this level. Although
it is possible to peel the hiatal muscle fibers
away and dissect through the celiac plexus of
nerves and lymphatics, these maneuvers may
be too time consuming in profoundly hypoten-
sive patients (Fig. 16-4). It is much easier to
transect the left crus of the aortic hiatus of
the diaphragm at the 2-o 'clock position to
allow for exposure of the distal descending
thoracic aorta above the hiatus. With the distal
descending thoracic aorta or abdominal aorta
in the hiatus exposed, the supraceliac aortic
clamp can be applied without difficulty.

An alternative approach in the patient with
a supramesocolic hematoma is to perform an
extensive Kocher maneuver, elevate the Cloop
of the duodenum and the head of the pan-
creas to the left, and incise the retroperitoneal
tissue to the left of the inferior vena cava. This

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303

Superior mesenteric a

Left renal a

» Baylor College of Med I

■ FIGURE 1 6-4

View of suprarenal abdominal aorta and major
branches after left-sided medial mobilization
maneuver and removal of all neural and
lymphatic tissue. Note the fold in the visceral
abdominal aorta created by mobilization of the
left kidney and renal artery. (From Baylor
College of Medicine, 1986.) ■

will expose the suprarenal abdominal aorta
between the celiac axis and the superior
mesenteric artery. The disadvantage of this
approach is that the exposure obtained is
below the level of any wounds to the
supraceliac aorta in the hiatus.

If active hemorrhage is coming from the
supramesocolic area of the abdominal aorta,
the surgeon may obtain temporary control
manually or with one of the aortic compres-
sion devices (Fig. 16-5). If this compression
prevents exposure and repair of the aortic
injury, the next maneuver is to divide the lesser
omentum manually, retract the stomach and
esophagus to the left, and digitally separate
the muscle fibers of the crura from the
supraceliac aorta to obtain the same exposure
as described for the left-sided medial mobi-
lization maneuver, but anteriorly and more
quickly. Distal control of the aorta in this loca-
tion is awkward because of the presence of
the visceral vessels. In young patients with
injury confined to the supraceliac aorta, the
celiac axis should be ligated and divided to
allow for more space for the distal aortic clamp
and subsequent vascular repair.

With small perforating wounds to the aorta
at this level, lateral aortorrhaphy with 3-0 or
4-0 polypropylene suture is preferred. If two
small perforations are adjacent to one another,

■ FIGURE 16-5

Aortic compression device applied to
supraceliac abdominal aorta for temporary
proximal control superior to wound in visceral
abdominal aorta. (From Baylor College of
Medicine, 1987.) ■

they should be connected and the defect
closed in a transverse fashion with the
polypropylene suture. When closure of the
perforation (s) results in significant narrow-
ing or if a portion of the aortic wall is missing,
patch aortoplasty with polytetrafluoroethylene
(PTFE) is indicated in the patient who is
hemodynamically stable without hypothermia,
significant acidosis, or an intraoperative
coagulopathy. The other option is to resect a
short segment of the injured aorta and
perform an end-to-end anastomosis. This is
difficult because of the limited mobility of both
ends of the aorta at this level.

On rare occasions, patients with extensive
injuries to the diaphragmatic or supraceliac
aorta will require insertion of a synthetic vas-
cular conduit or spiral graft after resection of
the area of injury. Many of these patients have
associated gastric, enteric, or colonic injuries.
Therefore, much concern has been expressed
about placing a synthetic conduit, such as a

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304

IV • SPECIFIC VASCULAR INJURIES

12-, 14-, or 16-mm woven Dacron, albumin-
coated Dacron, or PTFE prosthesis, in the
aorta. The data in the American literature
describing young patients with injuries to
nondiseased abdominal aortas do not support
the concern about infection occurring in
Dacron interposition grafts, and there are few
data relating to the use of PTFE grafts in pen-
etrating trauma to the abdominal aorta.
Despite the available data, some authors con-
tinue to recommend an extra-anatomic bypass
when injury to the abdominal aorta would
require replacement with a conduit in the
presence of gastrointestinal contamination.
To lower the risk of infection in a prosthetic
patch or graft inserted into the abdominal
aorta at any level, one should not perform
repairs of the intestine and the aorta simul-
taneously. Once the perforated bowel with
occlusion clamps applied has been packed
away and the surgeon has changed gloves, the
aortic prosthesis is sewn in place with 3-0 or
4-0 polypropylene suture. After appropriate
flushing of both ends of the aorta and removal
of the distal aortic clamp to flush air out from
the graft, the proximal aortic clamp should
be removed very slowly as the anesthesiolo-
gist rapidly infuses fluids. If a long aortic clamp
time has been necessary, the prophylactic
administration of intravenous bicarbonate is
indicated to reverse the "washout" acidosis

from the previously ischemic lower extremi-
ties. The retroperitoneum is then copiously
irrigated with an antibiotic solution and
closed in a watertight fashion with an
absorbable suture. At this point, the injuries
to the gastrointestinal tract are repaired.

The survival rate of patients with injuries
to the suprarenal abdominal aorta is approx-
imately 30% (Table 16-1). Combined injuries
to the suprarenal aorta and inferior vena cava
had a 100% mortality rate in the large series
from the Ben Taub General Hospital in 1987.

CELIAC TRUNK

When branches of the celiac trunk are
injured, they are often difficult to repair
because of the surrounding dense neural and
lymphatic tissue and the small size of the vessels
in a patient in shock with secondary vaso-
constriction. Therefore major injuries to
either the left gastric or the proximal splenic
artery should be ligated. The common hepatic
artery may have a larger diameter than the
other two vessels, and an injury to this vessel
may occasionally be amenable to lateral arte-
riorrhaphy, end-to-end anastomosis, or the
insertion of a saphenous vein or prosthetic
graft. In general, one should not worry about
ligating the common hepatic artery proximal

TABLE 16-1

SURVIVAL WITH INJURIES TO THE SUPRARENAL ABDOMINAL AORTA

Reference

Arch Surg 109:706, 1974

Am J Surg 128:823, 1974

Ann Surg 42:1, 1976

J Trauma 22:481, 1982

J Trauma 22:672,1982

Surg Gynecol Obstet 160:313, 1985

Am J Surg 154:613, 1987

Am Surg 58:622, 1992

J Trauma 50:1020, 2001

Diaphragmatic

Visceral

Suprarenal

Pararenal
Overall

No. Patients

No. Survivors

% Survival

29.4

35.7

80.0

100.0

44.4

46.6

28.4

0.0

11.1

0.0

20.0

191

29.8

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16 • INJURY TO ABDOMINAL AORTA AND VISCERAL ARTERIES

305

to the origin of the gastroduodenal artery,
because the extensive collateral flow from the
inferior pancreaticoduodenal artery in the
midgut will maintain the viability of the liver.
If the entire celiac trunk is injured, it is best
to ligate all three vessels and make no attempt
at repair. Ligation of the celiac trunk has never
caused any short-term morbidity or mortality
in properly resuscitated patients.

SUPERIOR MESENTERIC ARTERY

Injuries to the superior mesenteric artery may
occur at several levels. In 1972 Fullen and col-
leagues described an anatomic classification
of injuries to the superior mesenteric artery
that has been used only infrequently by sub-
sequent authors in the trauma literature. If
the injury to the superior mesenteric artery
is beneath the pancreas (Fullen zone I), the
pancreas may on rare occasions have to be
transected between Glassman or Dennis
intestinal clamps to control the bleeding point.
Because the superior mesenteric artery has
few branches at this level, proximal and distal
vascular control is relatively easy to obtain once
the overlying pancreas has been divided.
Another option is to perform medial rotation
of the left-sided intra-abdominal viscera, as pre-
viously described, and apply a clamp from the
left side of the aorta directly to the proximal
superior mesenteric artery at its origin. In this
instance the left kidney may be left in the
retroperitoneum as the medial rotation is
performed.

Injuries to the superior mesenteric artery
also occur beyond the pancreas at the base of
the transverse mesocolon (Fullen zone II,
between the pancreaticoduodenal and middle
colic branches of the artery) . Although there
is certainly more space in which to work in
this area, the proximity of the pancreas and
the potential for pancreatic leaks near the
arterial repair make injuries in this location
almost as difficult to handle as the more prox-
imal injuries. If the superior mesenteric artery
has to be ligated at its origin from the aorta
or beyond the pancreas (Fullen zone I or II) ,
collateral flow from both the foregut and the
hindgut should theoretically maintain the via-
bility of the midgut in the distribution of this

vessel. Exsanguinating hemorrhage from
injuries in this area, however, often leads to
profound shock with intense vasoconstriction
of the distal superior mesenteric artery. For
this reason, collateral flow is often inadequate
to maintain viability of the distal midgut,
especially the cecum and ascending colon. In
the hemodynamically unstable patient with
hypothermia, acidosis and a coagulopathy, the
insertion of a temporary intraluminal shunt
into the debrided ends of the superior mesen-
teric artery is a better choice than ligation and
fits the definition of damage control. If replace-
ment of the proximal superior mesenteric
artery is to be performed at a first operation
or at a reoperation after damage control, it is
safest to place a saphenous vein or prosthetic
graft on the distal infrarenal aorta, away from
the injury to the pancreas and other upper
abdominal organs (Fig. 16-6) . A graft in this
location should be tailored so that it will pass
through the posterior aspect of the mesen-
tery of the small bowel and then be sutured
to the mid or distal superior mesenteric
artery in an end-to-side or end-to-end fashion
without significant tension. It is mandatory to
cover the proximal suture line on the
infrarenal aorta with retroperitoneal fat or a
viable omental pedicle to avoid an aortoen-
teric fistula at a later time. Injuries to the more
distal superior mesenteric artery beyond the
transverse mesocolon (Fullen zone III, beyond
the middle colic branch) should be repaired
if at all possible to avoid ischemia of the distal
midgut. Injuries to the segmental branches
(Fullen zone IV) are usually ligated and fol-
lowed by resection of portions of the midgut
as needed.

The survival rate among patients with pen-
etrating injuries to the superior mesenteric
artery during the 1970s and 1980swas approx-
imately 58%, and this is still true (Table 16-
1). This decreases to 20% to 25% when any
form of repair more complex than lateral arte-
riorrhaphy is necessary. In three more recent
series in which 84 patients with injuries to the
superior mesenteric artery were described
(Asensio and colleagues, 2000; Davis and col-
leagues, 2001; Tyburski and colleagues, 2001 ) ,
survival was approximately 49% (Table 16-2).

A large multi-institutional review of such
injuries was reported in 2001 by Asensio and

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306

IV • SPECIFIC VASCULAR INJURIES

■ FIGURE 16-6

It may be dangerous to place
the proximal suture line of a
graft in Fullen zone I or II of the
superior mesenteric artery near
an associated pancreatic
injury. The proximal suture line
should be on the lower aorta,
away from the upper
abdominal injuries, and
covered with retroperitoneal
tissue. (From Baylor College of
Medicine, 1985.) ■

colleagues. There were 250 patients with
injuries to the superior mesenteric artery
(52% penetrating; 48% blunt) treated in 34
trauma centers over a 10-year period. Data
were available on operative management in
244 patients including 175 (72%) with liga-
tion's (22%) with suture repair, and 16 (6%)

with insertion of an autogenous (no. 10) or
PTFE (no. 6) graft. Overall survival was 61%
and ranged from 23.5% for patients with
Fullen zone I injuries to 76.9% for those with
Fullen zone IV injuries. Finally, logistic regres-
sion analysis was used to identify independent
risk factors for mortality. These risk factors

TABLE 16-2

SURVIVAL WITH INJURIES TO THE SUPERIOR MESENTERIC ARTERY

Reference

J Trauma 12:656, 1972
Surgery 84:835, 1978
Ann Surg 193:30, 1981
J Trauma 22:672,1982
J Trauma 23:372, 1983
J Trauma 26:313, 1986
Am J Surg 180:528, 2000
Am Surg 67:565, 2001*
J Trauma 50:1020, 2001
J Am Coll Surg 193:354, 2001

(multi-institutional)

Overall

No. Patients

No. Survivors

% Survival

62.5

60.6

66.7

70.0

31.8

46.4

53.3

48.8

250

153

61.2

450

261

58.0

'Excludes patients with exsanguination before repair or ligation.

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16 • INJURY TO ABDOMINAL AORTA AND VISCERAL ARTERIES

307

©Baylor College of Medicine 1980

■ FIGURE 16-7

Vessel loops or umbilical tapes
are placed around the proximal
renal vessels before perirenal
hematomas are entered. (From
Baylor College of Medicine,
1980.) ■

included the following: transfusion of more
than 10 units of packed red blood cells; intra-
operative acidosis; dysrhythmias; injury in
Fullen zone I or II; or the development of
multisystem organ failure.

RENAL ARTERY

Injuries to the proximal renal arteries may also
present with a supramesocolic hematoma or
with hemorrhage in this area. With an injury
to the proximal renal artery, supraceliac
control of the abdominal aorta by either of
the methods previously described will be nec-
essary. A tamponaded injury closer to the renal
hilum allows for proximal control of the renal
artery in the midline retroperitoneum (Fig.
16-7) . The transverse mesocolon is retracted
superiorly, and the small bowel is eviscerated
to the right. The ligament of Treitz is then
divided as the inferior mesenteric vein is
retracted to the left. With extensive mobi-
lization of the duodenojejunal junction, the
left renal vein crossing over the juxtarenal
abdominal aorta is exposed and mobilized,
as needed, by ligation and division of the left
adrenal, gonadal, and renal lumbar veins.
Such extensive mobilization will allow this vein

to be retracted 6 to 7cm in a superior direc-
tion. The origin of the left renal artery at the
4-o'clock position on the juxtarenal abdomi-
nal aorta is readily identified by dissection of
the surrounding retroperitoneal tissue of
modest density. A vessel loop is then passed
around the proximal left renal artery. To
expose the origin of the right renal artery at
the 7-o'clock position on the juxtarenal
abdominal aorta, the surgeon may need to
retract the adjacent infrarenal inferior vena
cava to the rightwith a vein retractor. The right
renal vein cannot be looped until an exten-
sive Kocher maneuver is performed to expose
the juxtarenal inferior vena cava. Options for
repair of either the proximal or the distal renal
artery are described later in this chapter.

Inframesocolic Area of Zone 1

INFRARENAL ABDOMINAL AORTA

The second major area of hematoma or
hemorrhage in the midline retroperitoneum
is the inframesocolic area. Patients with
injuries to the infrarenal (or suprarenal) abdom-
inal aorta and signs of life upon arrival in the
operating room always have a massive midline

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308

IV • SPECIFIC VASCULAR INJURIES

hematoma in the retroperitoneum. The size
of this hematoma is often intimidating to the
inexperienced trauma surgeon, but one
simple rule should be kept in mind: The hole
in the aorta is under the highest point of the
hematoma. Therefore, an injury just below
the base of the mesocolon is likely to involve
thejuxtarenal abdominal aorta and demands
proximal aortic control in the upper abdomen
by using the previously described techniques.
A midline hematoma over the lower lumbar
area is likely to be over an injury to the
infrarenal abdominal aorta, and exposure and
control will be easier. With either a true
inframesocolic hematoma or an area of hem-
orrhage, proximal aortic control is obtained
as described previously for exposure of the
proximal renal arteries. The transverse meso-
colon is elevated superiorly, the small bowel
is eviscerated to the right, and the ligament
of Treitz is divided to allow for application of
an aortic cross clamp in the infrarenal posi-
tion (Fig. 16-8). Exposure to allow for appli-
cation of the distal vascular clamp is obtained

■ FIGURE 16-8

Gunshot wound of infrarenal abdominal aorta
viewed through standard inframesocolic
exposure (head of patient is toward the
proximal clamp). (From Feliciano DV, Burch JM,
Graham JM: Abdominal vascular injury. In
Mattox KL, Moore EE, Feliciano DV [eds]:
Trauma, 1st ed. Stamford, Conn, Appleton &
Lange, 1988, pp 519-536.) ■

by dividing the midline retroperitoneum
down to the aortic bifurcation, carefully avoid-
ing the left-sided origin of the inferior mesen-
teric artery; however, this vessel may be
sacrificed whenever necessary for exposure
in young trauma patients.

As with injuries to the suprarenal aorta,
injuries in the infrarenal abdominal aorta are
repaired in a transverse fashion with 3-0 or 4-
polypropylene suture or by patch aortoplasty,
end-to-end anastomosis, or insertion of a
woven Dacron graft, an albumin-coated
Dacron graft, or a PTFE graft, none of which
requires preclotting. Because of the small size
of the aorta in young trauma patients, it is
unusual to be able to place a tube graft larger
than 12, 14, or 16 mm in diameter if one is
required, as previously noted. The principles
of completing the suture lines and flushing
are exactly the same as those for aortic repairs
in the suprarenal area. Because the retroperi-
toneal tissue is often thin in young patients,
it may be worthwhile to cover an extensive
aortic repair or the suture lines of a prosthe-
sis with mobilized omentum before closure
of the retroperitoneum. One option is to
divide the gastrocolic omentum, flip the
omentum superiorly into the lesser sac, and
make a window in the left side of the trans-
verse mesocolon. The mobilized pedicle is
passed through the window and placed over
the aortic repair or graft. The other option is
to mobilize the gastrocolic omentum away
from the right side of the transverse colon.
This mobilized pedicle is then placed lateral
to the ligament of Treitz and over the aortic
repair or graft. With either technique, 2-0 or
3-0 absorbable sutures are used to attach the
omental pedicle to the opened retroperitoneal
edges around the area of repair in the
infrarenal abdominal aorta.

The survival rate among patients with pen-
etrating injuries to the infrarenal abdominal
aorta during the 1970s, 1980s, and early 1990s
was approximately 46% (Table 16-3). In a
more recent series with 35 patients, the sur-
vival rate was 34.3% (Tyburski and colleagues,
2001). In three other recent series (Coimbra
and colleagues, 1996; Asensio and colleagues,
2000; Davis and colleagues, 2001) in which
140 patients with injuries to the abdominal
"aorta" (not specified as to whether the loca-

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16 • INJURY TO ABDOMINAL AORTA AND VISCERAL ARTERIES

309

TABLE 16-3

SURVIVAL WITH INJURIES TO THE INFRARENAL ABDOMINAL AORTA

Reference

Arch Surg 109:706, 1974

Am Surg 41:755, 1975*
J Trauma 22:672, 1982
J Trauma 22:481, 1982
Surg Gynecol Obstet 160:313, 1985
Am Surg 58:622, 1992
J Trauma 50:1020, 2001
Overall

No. Patients

No. Survivors

% Survival

46.7

40 (aortoiliac)

42.5

44.4

58.3

40.0

57.1

34.3

43.2

*Not included in overall figures.

tion was suprarenal or infrarenal) were
treated, the survival was 42.8% (12/28),
20.6% (13/63), and 39.1% (25/64, exclud-
ing 13 patients who exsanguinated before
repair) (Table 16-4). The overall survival of
approximately 32% for all aortic injuries in
these recent reviews, a decrease of approxi-
mately 6% of all the aortic injuries before 1993
(Tables 16-1 and 16-3) are included, is quite
interesting. The recent survival figures may
reflect shorter scene times in urban environ-
ments, which would bring more exsan-
guinated patients to the trauma center, or
this change may be a manifestation of
more patients with multiple penetrating
wounds and/or injuries.

There is one interesting report by Soldano
and colleagues (1988) of the long-term follow-
up of 11 survivors of penetrating wounds to
the abdominal aorta (9 infrarenal injuries and
5 suprarenal injuries in the 11 patients) from

the Vietnam War. Ankle-to-brachial pressure
ratios were decreased in five (one only with
exercise) , and all had calcification of the area
of repair on abdominal computed tomogra-
phy(CT).

Zone 2 or Upper
Lateral Retroperitoneum

RENAL ARTERY

If a hematoma or hemorrhage is present in
the lateral perirenal area, injury to either the
distal renal artery, the renal vein, or both or the
kidney should be suspected. In hemodynami-
cally stable patients who have suffered blunt
abdominal trauma and have normal preop-
erative IVP, renal arteriogram, or CT of the
kidneys, there is no justification for explor-
ing the kidney through its perirenal

TABLE 16-4

RECENT SURVIVAL WITH INJURIES TO THE ABDOMINAL AORTA (NOT
OTHERWISE SPECIFIED)

Reference

No.

Patients

No.

Survivors

% Survival

Am J Surg 172:541, 1996

42.8

Am J Surg 180:528, 2000

Isolated injury

21.7

With other arterial injury

17.6

Am Surg 67:565, 2001*

39.1

Overall

155

32.3

'Excludes patients with exsanguination before repair.

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310

IV • SPECIFIC VASCULAR INJURIES

hematoma at a laparotomy performed for
other injuries. As previously noted, the perire-
nal hematoma should be opened if it is pul-
satile, expanding rapidly, or has already
ruptured partially.

In highly selected and hemodynamically
stable patients withpenetratingwounds to the
flank, CT has been used to document an iso-
lated minor renal injury and operation has
been avoided. All other patients found to have
a perirenal hematoma at the time of explo-
ration for a penetrating abdominal wound
should have unroofing of the hematoma and
exploration of the underlying kidney ("Huey
Long rule").

If the hematoma is not rapidly expanding
and there is no free intra-abdominal bleed-
ing, most surgeons will loop the ipsilateral
renal artery with avascular tape in the midline
at the base of the mesocolon as previously
described. It should be noted that there is little
consensus on the value of preliminary arter-
ial control at the midline in stable patients.

If there is active bleeding from the kidney
through Gerota's fascia or from the retroperi-
toneum overlying the renal vessels, no central
renovascular control is necessary. The surgeon
should simply open the retroperitoneum
lateral to the injured kidney, divide Gerota's
fascia, and manually elevate the kidney directly
into the wound. A large vascular clamp can
be applied proximal to the hilum orjust lateral
to the inferior vena cava on the right to control
any further bleeding.

Renovascular injuries from penetrating
trauma are difficult to manage, especially
when the renal artery is involved. It is an ex-
traordinarily small vessel that is deeply em-
bedded in the retroperitoneum. Occasionally,
small perforations of the artery from pene-
trating wounds can be repaired by lateral arte-
riorrhaphy or resection with an end-to-end
anastomosis. Interposition grafting using
either a saphenous vein or a PTFE graft or
use of borrowed arteries, such as the splenic
artery to replace the left renal artery and the
hepatic artery to replace the right renal
artery, is indicated only when the renal artery
to the patient's only kidney is injured. In other
patients with multiple intra-abdominal injuries
or a long preoperative period of ischemia,
nephrectomy is a better choice, as long as

intraoperative palpation has confirmed a
normal contralateral kidney. The survival rate
for patients with injuries to the renal arteries
from penetrating trauma in two older series
(1980; 1990) was approximately 87%, with
renal salvage in only 30% to 40%.

Controversy continues to surround the
role of renal revascularization after the delayed
diagnosis of thrombosis of the renal artery
from blunt trauma. Intimal tears in the renal
arteries may result from deceleration in motor
vehicle crashes, automobile-pedestrian
crashes, and falls from heights. These usually
lead to secondary thrombosis of the vessel and
complaints of upper abdominal and flank
pain. One literature review in 1980 noted that
only 30% of patients with intimal tears in the
renal arteries had gross hematuria, 43% had
microscopic hematuria, and 27% had no
blood in the urine. A more recent report in
1998 documented that seven of eight patients
in whom a urinalysis was performed had hema-
turia. Therefore, the diagnosis may be missed,
because an IVP or CT may not be performed
in stable patients with normal abdominal
examinations and no hematuria or microhe-
maturia, only, after blunt trauma.

Lack of enhancement of a kidney with intra-
venous contrast on an abdominal CT is
pathognomonic of blunt thrombosis of the
ipsilateral renal artery. As the intimal tear is
always 2 to 4 cm from the abdominal aorta,
the value of a follow-up renal arteriogram
to confirm the diagnosis is questionable
(Fig. 16-9).

The operative technique when renal revas-
cularization is attempted is straightforward.
Resection of the area of the intimal tear and
an end-to-end anastomosis, insertion of an
aortorenal artery bypass graft, or ex vivo per-
fusion of the ischemic kidney followed by
autotransplantation into the pelvis can all be
performed by an experienced vascular or
transplantation surgery team. The value of
external cooling of the ischemic kidney or
infusing a cold renal perfusion solution
before a revascularization procedure after
the artery is opened is unclear. The same
can be said for the value of decapsulation of
the previously ischemic kidney to prevent a
post-revascularization "kidney compartment
syndrome."

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16 • INJURY TO ABDOMINAL AORTA AND VISCERAL ARTERIES

311

■ FIGURE 1 6-9

Blunt occlusion of the right
renal artery on an abdominal
aortogram. ■

The controversy regarding revascularization
is related to the poor results that have been
reported. The time from injury to revascu-
larization appears to be critical, as would be
expected when dealing with one kidney that
receives 12.5% of the cardiac output each
minute. In one review in 1978, some renal
function was restored in 80% of patients
undergoing renal revascularization within 12
hours of occlusion. This figure decreased to
57% if revascularization did not occur for 18
hours. A more recent report of 12 patients
with blunt thrombosis of the renal artery (one
bilateral) by Haas and colleagues in 1998 is
even more discouraging. In the group of five
patients who underwent attempted revascu-
larization of the renal artery at a median warm
ischemia time of 5 hours (4.5 to 36 hours),
four were felt to be "technically successful."
Immediate nephrectomy was performed in
another, with an unsuccessful attempt at
revascularization. The outcomes for the four
patients with successful revascularization were
as follows: nephrectomy at 1 day (no function
on postoperative renal scan) in one; death on
hemodialysis at 2 months in another; nephrec-
tomy at 6 months because of delayed hyper-
tension in a third; and minimal function (9%
differential) at 1 month on a renal scan in the
fourth. In the same series, seven patients with
blunt thrombosis of the renal artery did not
undergo revascularization. A delayed nephrec-
tomy was required at a mean time of 5 months
in three patients (43% ) who developed hyper-
tension, and four were normotensive at a mean

time of 11 months from injury. Based on the
historical and recent data, it is difficult to rec-
ommend revascularization of one renal artery
in a patient with a functioning contralateral
kidney after sustaining blunt trauma. This is
especially true if the patient has other serious
injuries and time to revascularization would
exceed 6 hours from injury. This conclusion,
of course, would not be acceptable to the
authors of case reports or reviews document-
ing successful late renal revascularization
(one or both kidneys) after bilateral throm-
bosis of the renal arteries. Such successful
repairs have been performed at 12, 15, 18,
and 19 hours, as reported by Greenholz and
colleagues (1986). Patients not undergoing
revascularization of one thrombosed renal
artery need to be monitored for 6 to 12 months
after injury to allow for early detection of
delayed hypertension.

There are isolated case reports in
which patients with failure of bilateral renal
revascularization and no revascularization
because of biopsy-proven renal necrosis had
return of renal function starting at 4 to 8
weeks after injury. This phenomenon is pre-
sumably related to maintenance of some
renal viability via collateral flow to renal
capsular vessels and to recanalization of
the thromboses in the renal arteries. If
patients with bilateral thrombosis with or
without attempts at renal revascularization
remain dependent on hemodialysis, they
should be put on a waiting list for renal
transplantation.

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312

IV • SPECIFIC VASCULAR INJURIES

■ FIGURE 16-10

Blunt intimal tear in the left
renal artery demonstrated on a
"pullout" abdominal aortogram.
(From Feliciano DV, Burch JM,
Graham JM: Vascular injuries of
the chest and abdomen. In
Rutherford RB, et al [eds]:
Vascular Surgery, 3rd ed.
Philadelphia, WB Saunders,
1989, pp 588-603.) ■

There are patients with blunt trauma who
undergo "pullout" abdominal aortograms
after evaluation of the thoracic aorta or pre-
liminary abdominal aortography before pelvic
arteriography who are found to have intimal
tears in the renal artery without thrombosis
(Fig. 16-10). When there is no extravasation
of contrast at the site of injury, observation
and follow-up arteriography within the first
week after injury are appropriate. The role of
anticoagulation is problematic because so
many of these patients have associated injuries.
In the absence of serious associated injuries,
anticoagulation would seem appropriate,
recognizing the absence of meaningful data.
An intimal or wall defect that was the pre-
sumed source of embolic infarctions in the
ipsilateral kidney has been treated successfully
by insertion of an endovascular stent in one
recent report by Villas and colleagues (1999).

Complications

The complications of repairs of the abdom-
inal aorta or visceral arteries include distal
embolization, thrombosis, dehiscence of a
suture line, and infection. Occlusion is not

uncommon when small vasoconstricted
vessels, such as the superior mesenteric artery
or renal artery, undergo lateral arteriorrha-
phy. In such patients, it may be valuable to
perform a second-look operation within 12
to 24 hours after the patient's blood pressure,
temperature, and coagulation abnormalities
have returned to normal. When this is done,
correction of a vascular thrombosis may be
successful.

As previously noted, dehiscence of vascu-
lar suture lines in the superior mesenteric
artery near a pancreatic injury may occur if
a small pancreatic leak occurs in the post-
operative period. For this reason the proxi-
mal anastomosis of such a graft should be on
the infrarenal aorta far away from the pan-
creas as described.

In addition, the postoperative develop-
ment of vascular enteric fistulas occurs most
commonly in patients who have anterior
aortic repairs, aortic grafts, or grafts to the
superior mesenteric artery from the aorta.
Again, this problem can be avoided by proper
coverage of suture lines on the aorta with
retroperitoneal tissue or a viable omental
pedicle and on the recipient vessel with
mesentery.

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313

REFERENCES

Asensio JA, Britt LD, Borzotta A, et al: Multiinsti-
tutional experience with the management of
superior mesenteric artery injuries. J Am Coll
Surg 2001;193:354-366.

Asensio JA, Chahwan S, Hanpeter D, et al:
Operative management and outcome of 302
abdominal vascular injuries. Am J Surg
2000;180:528-534.

Asensio JA, Forno W, Roldan G, et al: Abdominal
vascular injuries: Injuries to the aorta. Surg Clin
North Am 2001 Dec;81(6):1395-1416, xiii-xiv.
Review.

Coimbra R, Hoyt D, Winchell R, et al: The ongoing
challenge of retroperitoneal vascular injuries. Am
J Surg 1996;172:541-545.

Davis TP, Feliciano DV, Rozycki GS, et al: Results
with abdominal vascular trauma in the modern
era. Am Surg 2001;67:565-571.

Feliciano DV: Management of traumatic retroperi-
toneal hematoma. Ann Surg 1990;211:109-123.

Feliciano DV, Burch JM, Graham JM: Abdominal
vascular injury. In Mattox KL, Feliciano DV,
Moore EE (eds) : Trauma, 4th ed. New York,
McGraw-Hill, 2000, pp 783305.

Fry WR, Fry RE, Fry WJ: Operative exposure of the
abdominal arteries for trauma. Arch Surg
1991;126:289-291.

Haas CA, Dinchman KH, Nasrallah PF, SpirnakJP:
Traumatic renal artery occlusion: A 15-year
review. J Trauma 1998;45:557-561.

Meghoo CA, Gonzalez EA, Tyroch AH, Wohltmann
CD: Complete occlusion after blunt injury to the
abdominal aorta. J Trauma 2003 Oct;55(4) :795-
799.

Roth SM, Wheeler JR, Gregory RT, etal: Bluntinjury
of the abdominal aorta: A review. J Trauma
1997;42:748-755.

TyburskiJG, Wilson RF, Dente C, et al: Factors affect-
ing mortality rates in patients with abdominal
vascular injuries. J Trauma 2001;50:1020-1026.

chl7.qxd 4/16/04 3:38PM Page 315

Injuries of the Inferior
Vena Cava and Portal
Venous System

ROBERT F. BUCKMAN, JR.
ABHIJIT S. PATHAK
KEVIN M. BRADLEY

INJURIES OF THE INFERIOR VENA CAVA

Surgical Anatomy

Patterns of Injury

Initial Assessment and Management

Exposure and Control

Control of hemorrhage: intrahepatic inferior vena cava

Control of hemorrhage: retrohepatic inferior vena cava
Inferior Vena Cava Repair
Postoperative Management
Summary

PORTAL VEIN INJURIES
Surgical Anatomy

Portal vein

Superior mesenteric and splenic vein

Collaterals in portal obstruction
Patterns of Injury

Associated injuries
Initial Assessment and Management

315

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316

IV • SPECIFIC VASCULAR INJURIES

Exposure and Initial Vascular Control

Stable hematoma

Suprapancreatic exposure

Retropancreatic exposure

Pancreatic division

Control of multiple vascular injuries
Definitive Repair

Suprapancreatic wounds

Retropancreatic wounds

Portal vein ligation
Postoperative Management
Summary

Venous injury in the upper abdomen
most often involve the inferior vena
cava (IVC) and the portal venous
system. Often such injuries occur simultane-
ously. The literature on these injuries is
usually presented separately; therefore, these
injuries are presented in two sections of this
chapter.

INJURIES OF THE INFERIOR
VENA CAVA

The IVC, though deeply protected against the
accidents of nature, is by no means immune
to wounding. It has been estimated that 10%
to 15% of cases of abdominal penetration
result in an injury to a major vein and that 1
of every 50 gunshot wounds to the abdomen
strikes the IVC (Starzl and colleagues, 1962;
Wiencek and Wilson, 1986). Although pene-
trating mechanisms cause most caval injuries
and can involve any portion of the IVC, the
retrohepatic and intrapericardial sections are
the only portions of the vessel that are injured
by blunt trauma.

Whether caused by blunt or penetrating
mechanisms, caval wounds are highly lethal.
As many as 50% of patients with such injuries

die before reaching the hospital and the
mortality among patients who arrive at a
trauma center with signs of life has ranged
between 20% and 57% (Duke, Jones, and
Shires, 1965; Quast and colleagues, 1965;
Weichert and Hewitt, 1970; Burns and
Sherman, 1972; Graham and colleagues,
1978; Kudsk, Sheldon, and Lim, 1982;
Feliciano and colleagues, 1984; Wiencek and
Wilson, 1986; Klein, Baumgartner, and
Bongard, 1994; Burch and colleagues, 1998;
Asensio and colleagues, 2001). The three
factors that are most important in the prog-
nosis for survival are the hemodynamic con-
dition of the patient on arrival, the occurrence
of spontaneous tamponade of the caval injury,
and to a lesser degree, the location of the caval
laceration (Weichert and Hewitt, 1970;
Graham and colleagues, 1978; Kashuk and
colleagues, 1982; Kudsk, Sheldon, and Lim,
1982; Wiencek and Wilson, 1986; Klein,
Baumgartner, and Bongard, 1994; Burch and
colleagues, 1998). Patients who arrive in
shock and fail to respond to initial resuscita-
tive measures, those who are still actively bleed-
ing at the time of laparotomy, and those with
wounds of the retrohepatic vena cava have a
low probability of survival. Death is most com-
monly due to intraoperative exsanguination
(Nakamura and Tzuzuki, 1981; Wiencek and
Wilson, 1986; Burch and colleagues, 1998).

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317

Surgical Anatomy

The IVC originates by the confluence of the
common iliac veins just anterior to the body
of the fifth lumbar vertebra and posterior to
the right common iliac artery. As it ascends
along the right side of the lumbar vertebral
bodies, the cava receives numerous tributa-
ries including four or five pairs of lumbar
(sometimes called "segmental") veins, the
right gonadal vein, the renal veins, the right
adrenal vein, and finally the hepatic and
phrenic veins. It then traverses the mid-
diaphragm to reach the right atrium. The IVC
is a relatively delicate and thin-walled vessel,
1.5 inches in diameter, valveless throughout
its length, with a high flow at an intraluminal
pressure of about 5 cm H 2 0.

The intra-abdominal vena cava may be
divided into five sections, each of which has
anatomic peculiarities that affect the exposure
and control of injuries that section (Weichert
and Hewitt, 1970). The lowest section is the
bifurcation. Above this are the infrarenal, the
perirenal, the suprarenal/subhepatic, and
the retrohepatic sections. The management
of injuries in each of these segments is dis-
cussed separately.

An important anatomic feature of both the
bifurcation and the infrarenal sections of the
IVC is an abundant collateral circulation, of
which the lumbar veins constitute the prin-
cipal elements. These paired veins are con-
nected with one another, with the common
iliac, hypogastric, iliolumbar, and renal veins
and with the azygos and hemiazygos system
through bilateral ascending lumbar veins. This
extensive network is capable of bypassing
any obstruction of the bifurcation or of the
infrarenal segment of the vena cava, but the
very richness of the collateral circulation also
confounds efforts to achieve proximal and
distal control of injuries in these zones
(Fig. 17-1).

The perirenal area extends about 1 inch
above and below the renal veins and lies pos-
terior to the pancreas and duodenum. The
high flow from the renal veins requires that
these vessels and the IVC itself be occluded
to control bleeding from wounds in this
section of the cava (Wiencek and Wilson, 1986;
Burch and colleagues, 1998).

■ FIGURE 1 7-1

The abundant collaterals of the infrarenal vena
cava. Lumbar veins communicate with
ascending veins that drain into the azygos and
hemiazygos systems. (From Buckman RF Jr,
Pathak AS, Badellino MM, Bradley KM: Injuries
of the inferior vena cava. Surg Clin North Am
2001;81[6]:1433.) ■

Between the perirenal segment and the
beginning of the retrohepatic segment is a
short, suprarenal-subhepatic region of the
IVC. Injuries in this segment are difficult to
control because of the renal vessels below
and the proximity of the liver above, with the
passage of the cava underneath the liver into
the retrohepatic zone. The portal vein lies
immediately anterior to this short segment of
the IVC.

The segment of the IVC that has the most
unique anatomic features is the retrohepatic
section, lying above the right adrenal vein and
below the phrenic veins. This portion of the
cava, 7 to 10 cm in length, lies in a groove or
tunnel on the posterior aspect of the liver
within its "bare" area (Nakamura and Tzuzuki,
1981). This area, completely circumscribed
by the hepatic suspensory ligaments with the

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318

IV • SPECIFIC VASCULAR INJURIES

diaphragm behind and the liver in front, has
the ability to confine or contain bleeding asso-
ciated with retrohepatic caval injuries, pro-
vided that the diaphragm, the posterocentral
liver, or hepatic ligaments are not themselves
severely disrupted by the traumatic event
or by surgical intervention (Buckman,
Miraliakbari, and Badellino, 2000) . The retro-
hepatic vena cava is joined by two or three
major hepatic veins shortly before it traverses
the diaphragm and below this by seven or more
accessory hepaticveins of varying sizes. These
numerous tributaries bind the cava to the liver,
making its circumferential mobilization dan-
gerous. The exposure of caval injuries in the
retrohepatic zone is exceptionally difficult and
is usually unnecessary if spontaneous con-
tainment of hemorrhage has been achieved
by the suspensory ligaments, the liver, and the
diaphragm.

Patterns of Injury

With the exception of the retrohepatic and
intrapericardial vena cava, which may be
injured by blunt or penetrating trauma, vir-
tually all other IVC injuries are caused by pen-
etrating mechanisms. Gunshot wounds are
much more likely than stab wounds to lacer-
ate the IVC and generate far more destruc-
tive wounding patterns. Although stab wounds
cause linear lacerations of the vena cava, which
often spontaneously tamponade, gunshot
wounds, especially the high-energy wounds
of the current era, produce large tangential
avulsions involving varying amounts of the
circumference or actual transection of the
vessel.

Almost every patient with a penetrating
wound of the vena cava has injuries to other
viscera, other major vessels, or both (Bricker
and Wukasch, 1970; Bricker and colleagues,
1971; Mattox and colleagues, 1974, 1975).
Injuries of the liver, duodenum, pancreas,
bowel, and colon are common. Approxi-
mately 10% of the patients wounded in the
IVC have a second major vascular injury, most
commonly involving the aorta or portal vein
(Mattox and colleagues, 1975; Linker and
colleagues, 1982). In rare instances, the

combined penetration of the vena cava with
the aorta leads to the development of an aor-
tocaval fistula. Acute traumatic fistulas may
also occur between the cava and the renal
arteries or the cava and the duodenum.

Blunt injuries to the IVC are generally
caused by shearing forces in violent deceler-
ation accidents and may take the form of avul-
sion of the atriocaval junction or tearing of
hepaticveins from the retrohepatic vena cava.
Intraparenchymal lacerations of the hepatic
veins or the anterior surface of the retrohep-
atic cava may occur in severe blunt fractures
of the posterocentral liver caused by crush-
ing injuries.

For a caval or other venous injury to bleed
freely, there must exist, in addition to the
venous wound itself, a major breach of sur-
rounding tissues normally capable of confin-
ing or containing low-pressure hemorrhage.
The capacity for self-tamponade is charac-
teristic of caval injuries because it is of all
venous injuries and has important clinical
implications. Among patients with IVC
injuries, more than half will spontaneously
contain the site of injury with cessation of
bleeding (Ochsner, Crawford, and DeBakey,
1961; Starzl and colleagues, 1962; Duke,
Jones, and Shires, 1965; Weichert and Hewitt,
1970; Burch and colleagues, 1998) . This phe-
nomenon is more likely to occur with oblique,
crossing, low-velocity gunshot wounds and
with stab wounds than with straight, front-
to-back, high-powered gunshot wounds or
massive hepatic fractures. A beveled or slit-
like retroperitoneal track favors containment
and tamponade. Spontaneous tamponade is
also likely to occur in wounds of the cava that
are behind the pancreas, duodenum, or liver,
provided that the overlying viscera are not
extensively disrupted. In such instances
of a tamponaded injury, profuse iatrogenic
rebleeding occurs at the time of surgical
exposure.

Numerous authors have observed that the
retroperitoneal hematoma associated with a
caval injury may not be large, and that there
may be minimal free intraperitoneal blood if
the tamponade occurs early. Although survival
is far more likely in patients with spontaneous
cessation of bleeding (Starzl and colleagues,

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319

1962; Duke,Jones, and Shires, 1965; Weichert
and Hewitt, 1970; Mattox and colleagues,
1974), not all patients who have tamponaded
will survive. Up to 40% of them may die of
exsanguination after the tamponade is surgi-
cally decompressed unless the hemorrhage
from the cava and associated vascular injuries
can be completely and quickly controlled
(Duke, Jones, and Shires, 1965).

Initial Assessment
and Management

Approximately half of patients with wounds
of the IVC will present with some degree of
hypotension, often with profound hemody-
namic compromise (Ochsner, Crawford, and
DeBakey, 1961; Wiencek and Wilson, 1986;
Beal, 1990; Klein, Baumrartner, and Bongard,
1994). Of these, most will show temporary
improvement with the institution of ap-
propriate intravenous fluid resuscitation
(Feliciano and colleagues, 1984). The failure
of the hypotensive patient to respond to initial
volume repletion correlates with the presence
of continued active bleeding, that is, a failure
of spontaneous tamponade, and portends a
poor prognosis. At the other extreme, patients
with IVC injuries who have achieved early
spontaneous containment of their bleeding
are often normotensive on arrival. Rare pre-
sentations of caval injury include acute caval-
duodenal fistula with hypotension and copious
emesis of dark blood or acute aortocaval fistula
characterized by a wide pulse pressure, ab-
dominal bruit, and hematuria (Linker and
colleagues, 1982).

Patientswhose wound trajectories or clinical
presentations suggest the possibility of major
intraabdominal vascular wounding should
have supradiaphragmatic intravenous access
and be taken directly the operating room.
Those with the most extreme degrees of car-
diovascular collapse, who fail to respond to
initial appropriate resuscitative measures,
may require resuscitative thoracotomy, per-
formed in the emergency department. Most
patients, however, will show a dramatic hemo-
dynamic improvement with volume repletion
and can be transported for operation.

Exposure and Control

Injuries of the IVC most often present at
operation as stable hematomas of the central
retroperitoneum (Ochsner, Crawford, and
DeBakey, 1961; Starzl and colleagues, 1962;
Duke, Jones, and Shires, 1965; Burch and
colleagues, 1998) . Varying amounts of free
intraperitoneal blood may be present,
although active hemorrhage from the cava
often has ceased. When active bleeding is
occurring, the initial operative maneuver
should be the manual tamponade of the bleed-
ing point with a tightly rolled gauze pack.
Aortic compression may be indicated in
severely compromised patients until the hemo-
dynamic condition improves.

In most patients, tamponade having been
achieved either spontaneously or by the
assistance of the surgeon, some circumspec-
tion is possible before exploration of the
hematoma. It is often feasible, on the basis of
the location of the points of retroperitoneal
penetration to deduce the path of the wound-
ing agent relative to major retroperitoneal
structures.

Recalling that the vast majority of pa-
tients who die from IVC injuries succumb to
intraoperative exsanguination (Ochsner,
Crawford, and DeBakey, 1961; Duke, Jones,
and Shires, 1965; Weichert and Hewitt, 1970)
and that many of these patients have sponta-
neously tamponaded the wound before explo-
ration, the first question that the surgeon must
askis whether the hematoma surrounding the
suspected caval injury truly requires explo-
ration. Early writers on the subject of caval
injury and many experienced surgeons sub-
sequently have urged restraint in the explo-
ration of stable, nonpulsating retroperitoneal
hematomas, especially those behind the liver,
unless an injury to the pancreas, duodenum,
colon, kidney, or ureter or an associated
arterial injury is strongly suspected and
demands exposure (Ochsner, Crawford, and
DeBakey, 1961; Starzl and colleagues, 1962;
Duke, Jones, and Shires, 1965; Graham and
colleagues, 1978; Burch and colleagues, 1998;
Buckman, Miraliakbari, and Badellino, 2000) .

Nonpulsatile hematomas accompanying
presumed injuries to the retrohepatic (or the

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IV • SPECIFIC VASCULAR INJURIES

immediately subhepatic) vena cava that have
spontaneously tamponaded or that can be
induced to tamponade by manual compres-
sion or gauze packing are not often associ-
ated with other retroperitoneal injuries and
are probably better left unexplored. Decom-
pression of such hematomas by radical hepatic
mobilization is often associated with massive,
sometimes lethal, hemorrhage that cannot
any longer be controlled by packing after the
natural containment structures have been sur-
gically destroyed. Although rebleeding fol-
lowing spontaneous or assisted tamponade of
presumed caval injuries is rare, an estimated
10% to 40% of patients with originally stable
hematomas bleed to death following op-
erative exposure of a caval wound (Ochsner,
Crawford, and DeBakey, 1961; Duke, Jones,
and Shires, 1965; Weichert and Hewitt, 1970;
Burch and colleagues, 1998).Mosthematomas
below the level of the immediate subhepatic
segment of vena cava require exploration not
just to fix a possible caval wound, but because
of the risk of injuries to other retroperitoneal
visceral or vascular structures (Duke, Jones,
and Shires, 1965).

Having reached whatever conclusions are
possible regarding the probable location
and nature of the vascular injury in a central
hematoma, and having determined that either
active hemorrhage or the risk of associated
injuries outweighs the dangers of caval explo-
ration, preparations to enter the hematoma
should include an adequate supply of blood,
an autotransfuser, vascular instruments, skilled
assistance, large-bore venous access above the
diaphragm, rolled packs, stick sponges, ade-
quate suction, intravascular balloon occlusion
catheters, and 4-0 vascular suture on large
needles. Preliminary aortic control is obtained
if a major arterial injury is suspected and the
patient should be placed in a slight, reverse
Trendelenburg position to obviate venous air
embolism (Bricker and colleagues, 1971). As
the hematoma is opened, massive hemorrhage
should be expected. When encountered, it
must be immediately tamponaded with a
tightly rolled pack held by an assistant, until
more definitive control is established with
clamps or occlusion catheters. In most wounds
of the IVC, attempts to obtain remote proxi-
mal and distal control, before entering the

area of caval wounding, are not valuable
because of the abundant collateral circulation.

Wide exposure of the caval wound and any
associated injury is of the utmost importance.
Wounds of the vena cava from the immediate
subhepatic segment to the bifurcation are best
exposed by a mobilization of the duodenum,
the head of the pancreas, the right colon, and
the base of the mesentery from the cecum to
the duodenojejunal flexure (Fig. 17-2) . This
combined rotational maneuver provides expo-
sure, not only of the entire vena cava below
the liver but also of any associated aortic or
renovascular injury below the origin of the
superior mesenteric artery (Cattell and
Braasch, 1960; Hunt and colleagues, 1971;
Mattox and colleagues, 1975; Feliciano, 1988) .
In the course of this wide exposure, if a major
bleeding source is encountered, the mobi-
lization maneuvers are interrupted while a
tamponading pack is placed and held by an
assistant over the source of hemorrhage. Full
mobilization is then completed. It has been
observed that in most cases of caval injury,
shock is not maximal at the onset of the oper-
ation but during that portion of the proce-
dure when the hematoma is opened and caval
hemorrhage and caval compression occur.
The anesthesiologist should be forewarned of
this possibility (Weichert and Hewitt, 1970;
Burch and colleagues, 1998) .

Three sections of the intra-abdominal IVC,
the perirenal, the bifurcation, and the retro-
hepatic areas, may require special exposure
maneuvers beyond those listed earlier. The
posterior elements of wounds of the perire-
nal area may require medial rotation of one
kidney or division of the renal vein between
clamps to visualize the back of the cava at its
junction with a renal vein.

Full exposure of the caval bifurcation zone
is best achieved by division of the right
common iliac artery between clamps with
subsequent arterial reanastomosis (Salam
and Stewart, 1985) . This maneuver is more
likely to be necessary if repair of the IVC is
desired rather than simple caval ligation.

Active hemorrhage from the retrohepatic
cava, which cannot be controlled by any form of
tamponade, may rarely require caval expo-
sure to attempt hemostasis. Exposure of the
retrohepatic or immediate subhepatic cava

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321

Duodenum

Portal
vein

Cecum

■ FIGURE 1 7-2

Exposure of the inferior vena cava from
the liver to the bifurcation is best achieved
by a medial rotation of the duodenum and
pancreas together with the right colon
and mesenteric base. (From Buckman RF
Jr, Pathak AS, Badellino MM, Bradley KM:
Injuries of the inferior vena cava. Surg Clin
North Am 2001;81[6]:1438.) ■

necessitates extensive mobilization of the
right triangular ligament, including its caval
crossing point at the level of the right adrenal
vein (Mattox and colleagues, 1974). For left-
sided injuries, full incision of the left trian-
gular ligament is necessary. Because the
anterior surface of the retrohepatic cava is
bound to the liver by numerous tributaries, it
cannot be exposed except by dividing the liver
along the interlobar plane. Although some
have used resection of the left lateral segment
of liver to gain access to the left anterior as-
pect of the retrohepatic vena cava (Klein,
Baumgartner, and Bongard, 1994) and
Schrock, Blaisdell, and Mathewson (1968)
have actually suggested division of the liver
along the interlobar plane to expose the entire
retrohepatic cava, such maneuvers cannot be
recommended unless they constitute mere
completions of massive traumatic fractures
along these planes. A right thoracoabdomi-
nal incision or preferably a median sternotomy
often is required, in addition to the extensive
division of hepatic suspensory ligaments
to expose the retrohepatic cava (Klein,
Baumgartner, and Bongard, 1994). It cannot
be too strongly emphasized that radical hepatic

mobilization and exposure of retrohepatic vena
cava injuries is associated with an extremely
high mortality and is not advisable unless
active bleeding is present and cannot be
contained by perihepatic packing (Beal and
Ward, 1989; Beal, 1990; Cue and colleagues,
1990; Buckman, Miraliakbari, and Badellino,
2000).

CONTROL OF HEMORRHAGE:
INFRAHEPATIC INFERIOR VENA CAVA

Mostwounds of the infrahepatic vena cava can
be controlled by manual or pack pressure until
proximal and distal dissection is carried out
or a partial occlusion clamp applied. Care must
be taken to avoid avulsion of lumbar veins
during these attempts to gain clamp control
of the caval wound (Graham and colleagues,
1978).

The abundant lumbar collateral circulation
makes satisfactory proximal and distal control
of the infrarenal cava or confluence difficult.
In areas where there is a problem achieving
control with clamps, intraluminal balloon

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IV • SPECIFIC VASCULAR INJURIES

catheters may permit bleeding control with
minimal dissection (Ravikumar and Stahl,
1985; Buckman, Miraliakbari, and Badellino,
2000). Both urinary catheters and Fogarty
vascular catheters have been used for this
purpose. The widely recommended proximal
and distal compression of the IVC with stick
sponges is rapid but cumbersome and diffi-
cult to maintain during repair of the vein
(Graham and colleagues, 1978; Feliciano,
1988).

The method for control of caval wounds
used by the authors of this chapter consists of

the immediate tamponade of the wound with
a tightly rolled pack, followed by the slow
rolling of the pack down the wound from one
end, exposing small portions of the injury
while the remainder of the injury is still com-
pressed. As the opalescent venous intima is
visualized, revealing the location of the wound
edges, Babcock clamps are applied sequen-
tially to each exposed portion until the entire
wound has been coapted (Fig. 17-3). The
clamps are applied vertically in most wounds
but can be applied transversely to produce less
caval narrowing in suitable injuries.

■ FIGURE 1 7-3

Method of control of the inferior vena cava wound using tightly-rolled pack and Babcock clamps.
(From Buckman RF Jr, Pathak AS, Badellino MM, Bradley KM: Injuries of the inferior vena cava.
Surg Clin North Am 2001;81[6]:1440.) ■

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323

Once the hemorrhage has been controlled
by this method, the injury can be secondar-
ily underclamped with a partial occlusion
clamp or with Crafoord or "bulldog" clamps
from each end, to permit exact suturing or
patching of the defect (Fig. 17-4). Alterna-
tively, the Babcock clamps themselves can be
simply under-run with suture from end to end,
with this suture line constituting the final
repair.

Once the anterior and lateral aspects of the
wound have been controlled, lumbar veins can
be divided between ligatures and, if necessary,
the cava can be rotated to repair the poste-
rior parts of the wounds. The best "control"
for caval hemorrhage is with a rapid repair,
which can then be revised if improvement of
the initial closure is deemed necessary.

CONTROL OF HEMORRHAGE:
RETROHEPATIC INFERIOR VENA CAVA

The extreme dangers associated with expo-
sure of the retrohepatic vena cava have been
previously described. The most dire problems
with the initial control of caval hemorrhage
are those that occur following wide hepatic
mobilization and decompression of retro-
hepatic caval wounds (Carmona, Peck, and
Lim, 1984; Beal and Ward, 1989; Buechter
and colleagues, 1989; Beal, 1990; Cue and
colleagues, 1990; Burch and colleagues, 1998) .

This disaster is best avoided by reinforcing the
structures capable of tamponading a retro-
hepatic bleeding site rather than destroying
them by mobilizing the liver (Weichert and
Hewitt, 1970; Sharp and Locicero, 1992).

In cases of transparenchymal hepatic
venous or caval hemorrhage, containment
may be restored by omental packing, deep liver
sutures, and perihepatic gauze packing
(Weichert and Hewitt, 1970; Stone and Lamb,
1975; Carmona, Peck, and Lim, 1984; Beal,
1990; Cue and colleagues, 1990; Fabian and
colleagues, 1991 ) . Intracaval shunts generally
do not constitute a method of initial he-
morrhage control (Shrock, Blaisdell, and
Mathewson, 1968; Beal and Ward, 1989; Burch
and colleagues, 1998). In order to place the
shunt, if its use is deemed indispensable, bleed-
ing control should be achieved by tampon-
ade before the insertion of the shunt (Bricker
and colleagues, 1971; Wiencek and Wilson,
1986; Rovito, 1987; Beal and Ward, 1989;
Burch and colleagues, 1998) . However, if
bleeding can be stopped by packing, the use
of the atriocaval shunt is required only to
attempt a direct suture repair of the suspected
caval or hepatic vein injury (Shrock, Blaisdell,
and Mathewson, 1968) . There is no evidence
supporting the need for venous repair in this
area of the cava, and strategies that seek such
repairs are associated with mortality rates of
70% to 90%. (Kudsk, Sheldon, and Lim, 1982;
Moore, Moore, and Seagraves, 1985; Beal and

■ FIGURE 1 7-4

Technique of controlling caval wound by partially underclamping the wound from each end to
control lumbar inflow. (From Buckman RF Jr, Pathak AS, Badellino MM, Bradley KM: Injuries of the
inferior vena cava. Surg Clin North Am 2001 ;81[6]:1441.) ■

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IV • SPECIFIC VASCULAR INJURIES

Ward, 1989; Burch and colleagues, 1998;
Cogbill and colleagues, 1998) .

Direct clamping of the suprahepatic and
infrahepaticvena cava, together with the appli-
cation of portal inflow occlusion by a Pringle
maneuver, has also been advocated by some
as a method to limit retrohepatic bleeding in
pursuit of the strategy of direct repair of
the retrohepatic vena cava (Yellin, Chaffee,
and Donovan, 1971; Klein, Baumgartner,
and Bongard, 1994) . Vascular isolation by this
technique carries the danger of triggering a
cardiac arrest in a severely hypovolemic
patient (Weichert and Hewitt, 1970; Klein,
Baumgartner, and Bongard, 1994). Like all
methods used to approach and suture retro-
hepatic vena caval injuries, its use is associ-
ated with an extremely high likelihood of
death and cannot be recommended in any
case in which retrohepatic hemorrhage has
ceased spontaneously or can be contained by
perihepatic packing.

Venovenous bypass (Baumgartner and col-
leagues, 1995) and hypothermic circulatory
arrest (Shrock, Blaisdell, and Mathewson,
1968; Carmona, Peck, and Lim, 1984) have
also been reported to permit vascular isola-
tion and repair of the retrohepatic vena cava
in rare cases. These are not hemorrhage
control tactics but are practicable only when
prior control of the caval injury by manual
or pack tamponade has gained sufficient
time to institute the bypass procedure. As is
true for the techniques of atriocaval shunting
and clamp vascular isolation of the liver, their
sole value is in pursuing the highly dubious
goal of direct suture repair of the retrohepatic
cava.

Nearly all successful repairs of retrohepatic
vena caval injuries, in case reports describing
actual clinical events, have occurred in patients
who had stable hematomas at the time of oper-
ation (Bricker and Wukash, 1970; Burns and
Sherman, 1972; Fullen and colleagues, 1974;
DePinto, Mucha, and Powers, 1976; Mullin,
Lucas, and Ledgerwood, 1980; Misra, Wagner,
and Boneval, 1983; Rovito, 1987; Hartman
and colleagues, 1991; Baumgartner and
colleagues, 1995; Feldman, 1996). These
hematomas, having been disrupted by hepatic
mobilization, released a massive hemorrhage
that was then, in thefortunatepa.tients, stopped

by manual tamponade. Control by tampon-
ade allowed time for the insertion of an intra-
caval shunt or for the institution of venovenous
bypass in pursuit of direct suture repair of the
caval injury. This sequence permitted, in a few
lucky patients, successful repair of the injuries.
Aside from case reports such as those
described earlier, it is doubtful whether there
are any successful applications of these tech-
niques. Despite the occasional technical fea-
sibility of carrying it out, there is no evidence
that injuries of the retrohepatic or immedi-
ate subhepatic vena cava, associated with
spontaneously contained hematomas, require
repair to prevent recurrent hemorrhage or
thromboembolic complications. All strategies
and techniques designed to effect such repairs,
at the cost of disrupting a stable hematoma,
are ill founded and are less likely to produce
survival than methods that produce tampon-
ade or reinforce the spontaneously occurring
containment of retrohepatic hemorrhage
(Buckman, Miraliakbari, and Badellino,
2000).

Inferior Vena Cava Repair

At the outset of the discussion of definitive
caval repair, it is necessary to emphasize three
important facts: First, patients who do not die
of uncontrolled intraoperative hemorrhage
or the consequences of prolonged shock
tend to be long-term survivors regardless of
the method of managing the caval injury
(Weichert and Hewitt, 1970; Bricker and col-
leagues, 1971; Graham and colleagues,
1978; Wiencek and Wilson, 1986; Burch and
colleagues, 1998). Second, complications of
caval repairs or of the expectant management
of spontaneously tamponaded caval injuries
are very uncommon (Beal, 1990). Third,
the long-term outcome for ligation of the
infrarenal IVC is about the same as that for
repair (Duck, Jones, and Shires, 1965; Quast
and colleagues, 1965; Weichert and Hewitt,
1970; Graham and colleagues, 1978; Burch
and colleagues, 1998). It follows that mini-
mization of the shock period and rapid
control of active caval hemorrhage are the
principal goals to be pursued in the defini-
tive operative management of wounds of the

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325

intra-abdominal IVC. Sometimes, as indi-
cated earlier in this chapter, these goals can
be met without exposing or suturing the caval
wound.

Caval wounds that have demanded expo-
sure can be rapidly repaired, in most cases,
using a lateral suture technique with 4-0
cardiovascular suture material (Fullen and
colleagues, 1974; Burch and colleagues, 1998) .
The posterior portion of a wound may be
accessed by extension of the anterior wound
or by rotation of the cava. This type of repair,
in a patient with severe or multiple injuries
and shock, is preferable to struggling with fine
suture material on a tiny needle or attempt-
ing elegant caval reconstruction in locations,
such as the bifurcation or the infrarenal vena
cava, where precise repair has no provable
impact on outcome. After lateral repair, if the
narrowing of the cava is deemed unaccept-
able and the patient is stable, revision by patch
angioplasty or graft replacement to restore
luminal diameter can be considered. However,
the need for revision is not common.

Because retrohepatic caval injuries are best
managed expectantly or by tamponade, and
because there is no credible evidence that caval
narrowing or even ligation (Mullins, Lucas,
and Ledgerwood, 1980; Burch and colleagues,
1998) below the renal veins affects long-term
outcome, the issue regarding complex recon-
struction of the vena cava really devolves down
to injuries of the suprarenal and perirenal seg-
ments. In these sections, it is not known how
much narrowing of the vena cava can be tol-
erated, although caval ligation above the renal
veins is claimed to be incompatible with sur-
vival. A reduction of up to 75% of the luminal
cross section probably would be tolerated, but
this cannot be stated with certainty (Burch
and colleagues, 1998). In the absence of cer-
tainty, it is advisable that unless the patient
is exsanguinating, a lumen of at least 25% or
more should be preserved during repair of
the suprarenal or perirenal IVC. After the
initial repair, if the lumen is believed to be
less than this and the hemodynamic condi-
tion of the patient permits, patch angioplasty,
using vein or polytetrafluoroethylene (PTFE)
can be done (Klein, Baumgartner, and
Bongard, 1994) . Very rarely the replacement
of a damaged segment of the perirenal or

suprarenal IVC with panel grafts of vein or
externally supported PTFE may be justified
(Fig. 17-5).

Revision of narrowed repairs of the
infrarenal vena cava cannot be easily justified
because there is no evidence that the long-
term outcome is better with patent than with
thrombosed repairs or with any repair rather
than ligation. In severe caval wounds, espe-
cially with profound shock and multiple vas-
cular injuries, ligation of the infrarenal vena
cava or bifurcation, with separate ligation or
clipping of any lumbar veins entering the
wounded segment, is an acceptable method
of management (Duke, Jones, and Shires,
1965; Agarwal and colleagues, 1982; Moore,
Moore, and Seagraves, 1985; Burch and
colleagues, 1998) . All evidence suggests that
rapid enlargement of existing abundant
lumbar collaterals and the ascending lumbar
veins will allow the continuation of caval flow
around the area of ligation. It has been
reported that even suprarenal caval ligation
can be safely carried out, if the pressure in
the vena cava below the ligature does not rise
above 30 cm of saline and if indigo carmine
excretion by the kidney, following intravenous
administration, is demonstrated (Caplan,
Halasz, and Bloomer, 1964). The same
network of collaterals to the azygous and hemi-
azygous systems that permits infrarenal liga-
tion may also prove adequate in the case of
suprarenal ligation. The evidence on this
subject is not sufficient for a definite conclu-
sion to be drawn.

For an exposed but irreparable injury of
the suprarenal IVC in a patient unable to
withstand complex reconstruction, an alter-
native to ligation might be placement of a
temporary heparin-bonded shunt. In an
experimental model, caval shunts have
maintained their patency for up to 24 hours
(Aldridge, Buckman, and Badellino, 1997).
Clinical experience with this desperate
expedient is limited (Burch and colleagues,
1998).

Postoperative Management

Regardless of whether the IVC is repaired or
ligated or managed by tamponade, stagnation

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326 IV • SPECIFIC VASCULAR INJURIES

IVC

Saphenous
vein segment

Completed
graft

IVC with graft
in place

■ FIGURE 1 7-5

A-D, Reconstruction of a destroyed suprarenal segment of the inferior vena cava using a panel
graft of saphenous vein. (From Buckman RF Jr, Pathak AS, Badellino MM, Bradley KM: Injuries of
the inferior vena cava. Surg Clin North Am 2001;81[6]:1444.) ■

of blood in the lower extremities is undesir-
able. Leg elevation, elastic bandage wrapping,
and sequential compression devices promote
venous flow and may reduce thromboembolic
complications at and below the caval repair.
Whether the use of anticoagulants improves
the outcome of narrowed IVC repairs is not
known, but a postoperative infusion of dextran
for 24 hours is empirically used by many sur-
geons. Edema of the lower extremities may
occur in the early postoperative period
following caval repair or ligation, but it is
almost never a long-lasting or severe problem

(Mullins, Lucas, and Ledgerwood, 1980;
Burch and colleagues, 1998) .

Sudden death due to pulmonary embolism
has been reported to occasionally occur fol-
lowing IVC repair, especially in patients older
than 50 years (Burch and colleagues, 1998) .
Use of vena cava filters, placed above the
repair, may be considered in this subgroup.
The actual incidence of subclinical thrombotic
complications following caval repair or liga-
tion has not been determined by systematic

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327

Summary

Injuries of the IVC, whether caused by blunt
or penetrating mechanisms, are highly lethal.
Patients who arrive in shock and fail to
respond to initial resuscitative measures, those
who are still actively bleeding at the time of
laparotomy, and those with wounds of the
retrohepatic vena cava have a low probability
of survival. Death is most commonly due to
intraoperative exsanguination. Knowledge
of the anatomy and exposure techniques
for the five segments of the intraabdominal
vena cava is very important to the trauma
surgeon. Although some wounds of the vena
cava are best left unexplored, especially
those of the retrohepatic vena cava, most
injuries below this level can be exposed and
repaired by lateral suture technique. Preser-
vation of a lumen of at least 25% of normal
is probably important in the suprarenal
vena cava but is of no provable value below
the renal veins. There is no evidence sup-
porting the need to expose and repair wounds
of the vena cava that have spontaneously
stopped bleeding. Such wounds, especially in
the retrohepatic area, maybe managed expec-
tantly provided there is no strong suspicion
of an associated injury to a major artery or
hollow viscus.

1975) . Portal vein injuries are caused in 90%
of cases by penetrating trauma (Mattox,
Espada, and Beall, 1974; Bostwick and
Stone, 1975; Graham, Mattox, and Beall, 1978;
Peterson, Sheldon, and Lim, 1979; Busuttil
and colleagues, 1980), with gunshot wounds
more commonly the cause of the injury and
far more lethal than stab wounds. Not only
has there been no decrease in mortality from
this form of trauma over the last 20 years, but
the case-fatality rate may actually be increas-
ing, despite all the advances in prehospital and
hospital care, because of the increased fre-
quency of gunshot as the wounding mecha-
nism and the greater destructive power of
wounding weapons.

Surgical Anatomy

The portal system drains the splanchnic
territories supplied by the celiac and mesen-
teric arteries. Collecting effluent from the
unpaired abdominal viscera, the portal vein
delivers this blood, rich in oxygen and nutri-
ents, to the liver, accounting for nearly 80%
of total hepatic blood flow. Despite its high
flow, portal pressure is normally less than
6mm Hg.

PORTAL VEIN INJURIES

Wounds of the portal vein, though un-
common, represent one of the most highly
lethal of all vascular injuries. The reported
case-fatality rate among patients with such
wounds who reach the hospital alive has been
39% to 71% in most series (Chisholm and
Lenio, 1972; Mattox, Espada, and Beall, 1974;
Bostwick and Stone, 1975; Graham, Mattox,
and Beall, 1978; Peterson, Sheldon, and Lim,
1979; Busuttil and colleagues, 1980; Stone,
Fabian, and Turkelson, 1982; Sheldon and
colleagues, 1985; Dawson, Johansen, and
Jurkovich, 1991; Jurkovich and colleagues,
1995). This high death rate is due mainly
to intraoperative exsanguination during
attempts to control the injured vessel (Mattox,
Espada, and Beall, 1974; Bostwick and Stone,

PORTAL VEIN

The portal vein forms by the confluence of
the superior mesenteric vein and the slightly
smaller splenic vein behind the upper third
of the neck of the pancreas (Fig. 17-6). This
confluence is located just to the right of the
body of the second lumbar vertebra and imme-
diately anterior to the left border of the vena
cava. The inferior mesenteric vein, the third
major tributary contributing its flow to the
portal veinjoins either the splenic or the supe-
rior mesenteric vein in the immediate vicin-
ity of the major confluence. In as many as 30%
of patients, the inferior mesenteric vein enters
at the angle of the major confluence itself
(Ivatory and colleagues, 1987) . The retropan-
creatic confluence zone is not intimately
related to the superior mesenteric artery, the
bile duct, or the hepatic artery. A sound knowl-
edge of the anatomy of the portal confluence

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328

IV • SPECIFIC VASCULAR INJURIES

Anterior and posterior superior %^
pancreaticoduodenal veins

Superior

mesenteric

vein

■ FIGURE 1 7-6

Anterior (A) and posterior (B) views of the portal vein and its major tributaries in relation to the
pancreas. Wounds of the retropancreatic confluence zone are the most difficult portal injuries to
control and repair. (From Buckman RF Jr, Pathak AS, Badellino MM, Bradley KM: Portal vein injuries.
Surg Clin North Am 2001;81[6]:1450.) ■

(and potential anomalies) is of utmost impor-
tance to the trauma surgeon attempting to
manage injuries in this dangerous and unfa-
miliar area.

From its origin, the valveless portal vein
passes cephalad, inclining slightly rightward
over its course of 3 to 4 inches, to reach the
hilum of the liver, where it divides extrahep-
atically into right and left branches. During
its course, it passes, in succession, behind the
upper pancreatic neck, and the first portion
of the duodenum. Then, upon entering the
hepatoduodenal ligament, it comes into rela-
tionship with the hepatic artery and bile duct,
lying behind these structures and forming the
anterior border of the foramen of Winslow.
Throughout its length, the portal vein lies

immediately anterior to the suprarenal
segment of the IVC.

In addition to its main tributaries, the portal
vein receives the pyloric vein from the pan-
creas and duodenum, the coronary (left
gastric) vein, and the superior pancreatico-
duodenal vein (see Fig. 17-6). A cystic vein,
if present, also drains into the portal vein.
These veins represent major potential collat-
erals in cases of portal vein obstruction.

SUPERIOR MESENTERIC AND
SPLENIC VEIN

In addition to the anatomy of the portal vein
itself, certain features of its major tributaries

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329

are important to the trauma surgeon. The
superior mesenteric vein, representing the
confluence of all the tributaries that corre-
spond to the branches of the superior mesen-
teric artery, is formed in the mesentery as
numerous intestinal veins. The ileocolic,
right colic, and middle colic veins join the
main venous trunk. The mesenteric vein
also receives the right gastroepiploic vein, the
inferior pancreaticoduodenal vein, and in
some cases, the inferior mesenteric vein. In
addition, a number of small unnamed veins
drain into the right lateral aspect of the
superior mesenteric vein from the head of
the pancreas.

The main trunk of the superior mesenteric
vein passes anterior to the third portion of
the duodenum and in front of the uncinate
process. Then, it courses behind the neck of
the pancreas to enter confluence zone where
it converges with the splenic vein to form
the main portal vein. The proximal portion
of the superior mesenteric vein is located in
a groove of the pancreas behind the neck and
may be completely encircled by the pancre-
atic tissue. The numerous tributaries enter-
ing the superior mesenteric vein all along its
course provide abundant collateral pathways
in the event of obstruction of this vein. Of par-
ticular importance are the gastroepiploic
vein and the inferior pancreaticoduodenal
vein, which join the superior mesentericjust
before its confluence with the splenic vein,
and communicate with the portal vein above
the confluence.

The most important distinctions regarding
the superior mesenteric vein, from the trauma
surgical standpoint, are first that a part of the
superior mesenteric vein is retropancreatic
and difficult to expose, while most of it is infra-
pancreatic and easily accessible; and second,
that it has abundant collaterals.

The splenic vein, as it courses along the
dorsum of the pancreas, receives many small
pancreatic branches and often receives the
inferior mesenteric vein just prior to the con-
fluence of the splenic vein with the superior
mesentericvein. In addition to the splenic and
pancreaticoduodenal veins, a large accessory
pancreatic vein may be present and may enter
the portal vein directly.

COLLATERALS IN PORTAL
OBSTRUCTION

It is obvious from the regional vascular
anatomy that in the event of portal obstruc-
tion in the hepatic hilum, there would be vir-
tually no way for antegrade portal flow to be
reconstituted. In such a case, the portosystemic
collaterals would expand to drain the efflu-
ent of the portal circulation. However, it is
equally evident that the closer any of the major
veins (i.e., portal, mesenteric, or splenic) is
obstructed to the confluence of these veins,
the more abundant are the potential major
collateral veins that could reconstitute portal
flow. The regional vascular anatomy makes it
apparent that any retropancreatic injury of the
portal vein and its main tributaries could be ligated,
with probable preservation, not only of adequate
splanchnic drainage, but also, with the expectation
of collateral antegrade portal flow.

Patterns of Injury

ASSOCIATED INJURIES

Because of the dense crowding of major vessels
and viscera in the upper midabdomen, pen-
etrating portal venous injuries are almost
always associated with injury to the liver, biliary
tract, pancreas, duodenum, or bowel. Of far
greater concern, however, than these visceral
injuries, are major vascular wounds of the JVC,
aorta, superior mesenteric artery, or renal
vessels, which accompany portal vein wounds
in 70% to 90% of patients (Mattox, Espada,
and Beall, 1974; Bostwick and Stone, 1975;
Graham, Mattox, and Beall, 1978; Perterson,
Sheldon, and Lim, 1979; Stone, Fabian, and
Turkelson, 1982; Jurkovich and colleagues,
1995). The suprarenal vena cava, which lies
just behind the entire course of the portal vein,
is the most common vessel to be injured in
association with the portal vein, as might be
expected. In rare cases, the simultaneous
wounding of a major artery and the portal
vein may lead to an arteriovenous fistula
(Smith and Northrop, 1976; Dingledin,
Proctor, and Jaques, 1977; Robb and
Costa, 1984; Epstein and colleagues, 1987;

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330

IV • SPECIFIC VASCULAR INJURIES

Deitrick and colleagues, 1990; Lumsden and
colleagues, 1993).

Associated major vascular injuries are nearly
always posterior to the plane of the portal vein
itself and may be multiple, involving both
arteries and veins and tending, together with
the portal venous wound, to produce massive
and chaotic retropancreatic hemorrhage,
which is extremely difficult to control.

Portal venous wounds have been reported
to involve the supraduodenal and retropan-
creatic zones of the vein with similar frequency
(Peterson, Sheldon, and Lim, 1979; Sheldon
and colleagues, 1985; Dawson,Johansen, and
Jurkovich, 1991; Jurkovich and colleagues,
1995) . Hilar wounds are more rare. Whereas
stab wounds tend to produce limited portal
lacerations or clean transections, high-energy
gunshot wounds striking the portal vein
produce extensive avulsions or transection of
the impacted vessel and may disrupt impor-
tant potential collateral pathways, as well as
the main trunk of the portal vein. Damage to
other viscera and vessels is also more severe
with gunshot wounds. Wounds of this type,
involving the retropancreatic portal conflu-
ence zone, are almost uniformly fatal due to
rapid transpancreatic exsanguination (Stone,
Fabian, and Turkelson, 1982).

Initial Assessment
and Management

Most patients with portal venous injuries
arrive at the hospital in hemorrhagic shock,
with many in advanced circulatory collapse
(Mattox, Espada, and Beall, 1974; Bostwick
and Stone, 1975). Approximately one half
of such patients will respond to initial fluid
resuscitation, and these will usually be found
at operation to have achieved some degree of
spontaneous tamponade of their vascular
wounds. The remaining patients have active
hemorrhage and require immediate opera-
tion as an indispensable element of their
resuscitation. In patients with the most dire
degrees of hemodynamic collapse, resuscita-
tive thoracotomy and aortic cross clamping
may be required in the emergency depart-
ment. Few such patients will survive. More
commonly, immediate transport to the

operating room for emergency laparotomy is
required.

Exposure and Initial
Vascular Control

Even when accompanied by other vascular
wounds, especially to the IVC, portal injuries
may present at operation as stable hematomas
of the upper central retroperitoneum, hepa-
toduodenal ligament, or mesenteric root. In
perhaps one half of patients, active intraperi-
toneal bleeding is continuing at the time of
laparotomy. This bleeding may have its origin
from the portal vein injury itself or from an
associated vascular wound.

STABLE HEMATOMA

If there is a stable hematoma, determination
of the location of the points of retroperitoneal
penetration and consideration of the proba-
ble wound tract may allow a deduction to be
reached concerning the vessels most likely to
be wounded. Before opening the hematoma,
it is prudent to prepare the equipment that
may be necessary to control multiple vascu-
lar injuries. Vascular instruments, balloon
occlusion catheters, stick sponges, tightly
rolled laparotomy pads, and an adequate
supply of blood for transfusion must be at
hand. If an autotransfusion apparatus is avail-
able, it should be prepared for use. When a
major arterial injury is suspected, preliminary
control of the aorta is desirable. It is also wise
to place the patient in a mild reverse Tren-
delenburg position to obviate the possibility
of venous air embolism if a caval injury is
disclosed.

In penetration of the region of the portal
vein, multiplevasculdj: injuries are the rule, and
an apparently minor hematoma with modest
free hemoperitoneum may harbor major
wounds of both the portal vein and the vena
cava, which will bleed most impressively once
unroofed. The vast majority of patients who
die from portal vein injuries exsanguinate
intraoperatively, after exposure of their vas-
cular wounds. This misfortune may befall even
those who were stable preoperatively. Because

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331

the prevention of this type of death is the major
problem in the management of injuries of
the portal vein, the issue of vascular control
assumes the highest importance.

The initial procedure upon entry into the
abdomen of a severely shocked patient with
active transpancreatic hemorrhage is to man-
ually compress the aorta at its hiatus and then
to locate and manually compress the site of
bleeding. As these things are done, volume
repletion and the transfusion of blood may
be performed, to remove the patient from the
immediate danger of cardiac arrest.

Some reduction in flow in the portal vein
and other vessels in the region may be
obtained by double clamping the aorta, both
above the celiac axis and below the renal

vessels. This maneuver will reduce, but not
abolish, flow through the celiac and superior
mesenteric arteries, aorta, vena cava, and renal
vessels and will indirectly decrease portal vein
flow.

SUPRAPANCREATIC EXPOSURE

In patients with suspected injury to the portal
vein or its major tributaries, wide exposure to
locate and immediately control the sources
of hemorrhage is crucial. Wounds of the supra-
pancreatic portal vein can be exposed by a
wide Kocher maneuver with rotation of the
hepatic flexure of the colon as needed (Fig.
17-7). If a major source of hemorrhage is

Bile duct

Hepatic artery

Portal vein

■ FIGURE 1 7-7

Exposure of the retropancreatic portal vein and vena cava by a combined medial rotation of the
pancreas, duodenum, and hepatic flexure. (From Buckman RF Jr, Pathak AS, Badellino MM,
Bradley KM: Portal vein injuries. Surg Clin North Am 2001;81[6]:1455.) ■

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332 IV • SPECIFIC VASCULAR INJURIES

■ FIGURE 1 7-8

Control of a suprapancreatic portal vein injury
using intraluminal catheters for control of the
bifurcation and a clamp proximally. A wound of
this type may require an interposition vein graft.
(From Buckman RF Jr, PathakAS, Badellino
MM, Bradley KM: Portal vein injuries. Surg Clin
North Am 2001 ;81[6]:1456.) ■

encountered, it must be immediately con-
trolled with a pack held by an assistant. Fol-
lowing preliminary hepatic inflow occlusion
and the division of the cystic duct to facilitate
exposure, the suprapancreatic portal vein may
be dissected to obtain distal control with avas-
cular clamp or occlusion catheter (Peterson,
Sheldon, and Lim, 1979) (Fig. 17-8).

RETROPANCREATIC EXPOSURE

Retropancreatic wounds involving the portal
confluence or its major tributaries and supra-
pancreatic wounds with suspected additional
injury of the IVC or other vessels are exposed
by a combination of the Kocher maneuver and
mobilization of the entire right colon and
mesenteric base, from the cecum to the duo-
denojejunal flexure (Cattell and Braasch,
1960; Peterson, Sheldon, and Lim, 1979).
When combined with leftward mobilization
of the hepatic flexure, this maneuver provides
access to the entire portal vein and the prox-
imal portions of its major tributaries. It also
exposes the entire infrahepatic vena cava and
the aorta up to the origin of the superior

mesenteric artery. Rarely, left medial rotation
of the spleen and the tail of the pancreas may
be necessary to expose the left lateral aspect
of the portal vein confluence (Fish, 1966).

PANCREATIC DIVISION

Surgical transection of the neck of the pan-
creas has been occasionally used as a method
of exposing portal injuries (Stone, Fabian, and
Turkelson, 1982) . This maneuver takes time
and (in the opinion of the authors) is rarely
of value in controlling retropancreatic hem-
orrhage. Visualization of the anterior aspect
of a portal or superior mesenteric vein injury
is the only advantage gained by dividing the
pancreas, and the maneuver has generally
been performed in pursuit of precise lateral
repair of a portal or superior mesenteric
vein injury. It is not clear that this maneuver
is justified unless it represents the mere com-
pletion of a traumatic pancreatic fracture,
which would itself have necessitated proximal
or distal pancreatectomy. It is not a good
emergency maneuver for hemorrhage
control.

CONTROL OF MULTIPLE
VASCULAR INJURIES

Once the retroperitoneal hematoma has been
entered, the surgeon must be prepared to
immediately control two or more major vascu-
lar injuries. Clamp control of the portal injury
is often of secondary concern. Great vessel
lacerations deep to the plane of the portal vein
must usually be managed first while the
fingers of an assistant compress the portal
venous injury, behind or above the mobilized
pancreas. Rotation of the duodenum and
pancreatic head during a Kocher maneuver
provides an opportunity for broad manual
compression of the retropancreatic portal vein
and its major tributaries in a plane anterior
to the great vessels of the retroperitoneum.
This must provide immediate portal hemor-
rhage control while deeper and more des-
perate associated vascular injuries are
addressed.

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17 • INJURIES OF THE INFERIOR VENA CAVA AND PORTAL VENOUS SYSTEM

333

Definitive Repair

SUPRAPANCREATIC WOUNDS

In the suprapancreatic or hilar portions of
the portal vein, precise lateral repair, with or
without vein patching, or even vein graft inter-
position, may be used after proximal and distal
control has been obtained. In cases of com-
bined hepatic artery and portal vein wound-
ing, repair of the portal vein, following ligation
of the hepatic artery, is generally recom-
mended (Fuller and Anderson, 1978). Recon-
struction of a divided bile duct may also be
necessary in this location (Sheldon and col-
leagues, 1985) . End-to-end anastomosis of the
portal vein in the suprapancreatic zone is
generally not feasible because, as has been
described by Stone, Fabian, and Turkelson
(1982), there is a loss of exposure as the two
ends of the vein are brought together. For this
reason, interposition saphenous vein grafting
may be a wiser choice for the management
of a divided suprapancreatic portal in which
reconstruction is necessary. Ligation of the
portal vein in this location is compatible with
survival, provided that the hepatic artery is
intact (Fish, 1966; Pachter and colleagues,
1979).

RETROPANCREATIC WOUNDS

Wounds of the retropancreatic confluence
zone of the portal vein offer fewer and more
difficult options for repair. Although the
suprapancreatic portal vein can be fully mobi-
lized and exposed for precise repair, except
perhaps in the hilum itself, the situation in
the retropancreatic zone is far more chal-
lenging. Because of the relatively medial
location of the vein, and its fixation to the
pancreas by its numerous tributaries, only the
posterior aspect of the vein can be visualized
by the standard rotation maneuvers. Visual-
ization of the anterior portion of the vein
requires transection of the pancreas or full
mobilization of the confluence from the
numerous, laterally inserting tributaries.
Because of these hardships, as well as the near
inevitability of major hemorrhage, and the

difficulties of obtaining proximal and distal
control in a vessel with so many tributaries,
the opportunities for repair are severely
limited in wounds of the retropancreatic zone
(Stone, Fabian, and Turkelson, 1982) . Many
authors who have reported lateral "repairs"
in this zone have likely often oversewn the
vein in a way that amounted to complete or
near-complete obliteration of the lumen,
not only of the portal vein itself but also of its
major tributaries. No major complications
have been reported from the use of this
approach.

PORTAL VEIN LIGATION

A second approach to devastating wounds in
the retropancreatic zone, and an approach
that has been found to be life saving by expe-
rienced surgeons, is the deliberate and
immediate ligation of any portal injury that
cannot be easily repaired by lateral suture.
Despite the reports from some experienced
surgeons that ligation has, in their hands, been
associated with a higher mortality than lateral
repair (Mattox, Espada, and Beall, 1974;
Graham, Mattox, and Beall, 1978; Peterson,
Sheldon, and Lim, 1979; Busuttil and col-
leagues, 1980; Sheldon and colleagues, 1985;
Jurkovich and colleagues, 1995), the reported
experience does not permit a conclusion that
all or any of their purported repairs remained
patent, or that any form of repair offered a
survival advantage compared to ligation. The
best evidence on this subject comes from a
large series reported by Stone, Fabian, and
Turkelson (1982), in which survival was
achieved in 1 7 of 20 patients in whom imme-
diate portal ligation was carried out "when-
ever lateral repair was impossible or
impractical."

Because the cause of most deaths in por-
tal injury is uncontrolled hemorrhage, the
method that provides the quickest definitive
control should be preferred. Portal vein
repair is desirable, but prolonged efforts to
carry out complex venous repair, in the face
of continuing blood loss and shock, to avoid
ligation, cannot be justified by the existing
evidence. In fact, prolonged reconstructive

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334

IV • SPECIFIC VASCULAR INJURIES

efforts, followed by ligation as a desperation
maneuver, may explain why ligation has had
a high mortality in some series in which it
was rarely employed (Mattox, Espada, and
Beall, 1974; Graham, Mattox, and Beall, 1978;
Busuttil and colleagues, 1980; Sheldon and
colleagues, 1985; Jurkovich and colleagues,
1995), but not in other series in which liga-
tion was done quickly (Stone, Fabian, and
Turkelson, 1982).

Although a preponderance of evidence
casts doubt on the wisdom of undertaking
technically difficult and time-consuming
reconstruction of most portal venous injuries,
special circumstances make repair of the
portal vein necessary. The first is the destruc-
tion of the hepatic artery, as alluded to earlier
in this chapter. When both of the hepatic
inflow vessels are divided, one of them must
be repaired to permit survival (Fuller and
Anderson, 1978; Sheldon and colleagues,
1985; Jurkovich and colleagues, 1995). Most
authors have recommended that the portal
vein be reconstructed in this situation. The
second circumstance in which portal vein
reconstruction might be unavoidable would
be an extensive destruction of the potential
collateral pathways, in association with tran-
section of the portal vein itself. Under these
rare conditions, regardless of difficulty, the
portal vein may require reconstruction.
Interposition grafting using saphenous
vein (Symbas, Foster, and Scott, 1961; Stone,
Fabian, and Turkelson, 1982), a segment
of transposed splenic vein (Busuttil and
colleagues, 1980), or externally supported
PTFE to bridge a gap in the portal vein may
be technically feasible. Alternatively, the distal
end of the splenic vein may be anastomosed
to the proximal stump of the superior mesen-
teric vein (Busuttil and colleagues, 1980) (Fig.
17-9).

Portocaval or mesocaval shunting has
been used to provide effluent flow from the
intestines following portal vein ligation.
Experience with this method has been uni-
formly unfavorable, with nearly all patients
becoming encephalopathic. It should not be
considered an acceptable approach to the
management of portal or mesenteric vein
injuries (Fish, 1966; Stone, Fabian, and
Turkelson, 1982).

Postoperative Management

The postoperative care of patients who have
undergone portal vein reconstruction or lig-
ation is similar to that of any patient who has
suffered abdominal wounding with majorvas-
cular injury and hemorrhagic shock. However,
certain additional considerations apply to
patients who have undergone either portal lig-
ation or a repair of the portal vein in which
venous narrowing has led to the threat of
repair site thrombosis.

Acute occlusion of the portal vein causes
certain predictable effects, which were
described by Child and colleagues (1952) in
a classic series of experiments carried out a
half-century ago and by Milnes and Child
( 1 949) . There is a maj or but transient decrease
in systemic blood pressure caused by pooling
of blood in the splanchnic viscera, accompa-
nied by a marked elevation of the portal
pressure below the ligature or thrombo-
sis. Massive bowel edema is common. The
hypotensive effect of portal occlusion can be
ameliorated by intravenous volume repletion
in an amount sufficient to compensate for
blood trapped in the splanchnic veins. The
effects of splanchnic venous hypertension
resolve as collateral pathways enlarge over
a period of days to weeks. Chronic portal
hypertension appears to be rare (Pachter and
colleagues, 1979).

Any patient who has undergone portal vein
ligation or a venous repair that has markedly
constricted the portal vein may be expected
to have extraordinary fluid requirements in
the immediate postoperative period. Replace-
ment of this volume may be best guided with
a pulmonary artery catheter. Most will also
develop marked bowel edema with some small
risk of venous intestinal infarction (Bostwick
and Stone, 1975; Pachter and colleagues, 1979;
Peterson, Sheldon, and Lim, 1979; Sheldon
and colleagues, 1985). In the anticipation of
these consequences of portal vein ligation or
the acute thrombosis of a repair, considera-
tion may given to skin-only suture of the
abdominal wall at the conclusion of the pro-
cedure or even the placement of a temporary
abdominal wall prosthesis to avoid abdomi-
nal compartment syndrome when the bowel
edema becomes maximal over the first 24 to

chl7.qxd 4/16/04 3:38PM Page 335

17 • INJURIES OF THE INFERIOR VENA CAVA AND PORTAL VENOUS SYSTEM 335

■ FIGURE 1 7-9

Four methods of managing portal vein injuries. Of these, only lateral repair (A) and ligation (B) have
been commonly used. End-to-end anastomosis (C)and graft (D). (From Buckman RF Jr, Pathak AS,
Badellino MM, Bradley KM: Portal vein injuries. Surg Clin North Am 2001;81[6]:1460.) ■

48 hours. The use of a "second-look" proce-
dure to inspect the bowels for viability has
been recommended by some (Pachter and
colleagues, 1979; Peterson, Sheldon, and
Lim, 1979).

Administration of anticoagulants to prevent
mesenteric thrombosis is no trustified by exist-
ing evidence. Follow-up of the portal vein
repair using abdominal ultrasound has been
recommended (Milnes and Child, 1949).

Summary

Wounds of the portal vein are caused most
commonly by penetrating trauma and have
a very high mortality. Most deaths are due to
exsanguination, occurring intraoperatively
as the surgeon struggles to control the hem-
orrhage from the portal vein and associated
vascular injuries. A thorough knowledge of
the anatomy of the area and the likely pat-

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336

IV • SPECIFIC VASCULAR INJURIES

terns of wounding is important. At operation,
the surgeon must be prepared to deal with
multiple vessel wounding. Although most
authors have advocated lateral repair of the
portal vein when it can be accomplished,
portal ligation appears to be a safe alterna-
tive. Complex repairs are justified only when
a contraindication to ligation exists. Postop-
erative care must recognize the need for extra-
ordinary fluid replacement and the small risk
of postoperative bowel infarction following
repair or ligation of the portal vein.

REFERENCES

Agarwal N, Shah PM, Clauss RH, et al: Experience
with 115 civilian venous injuries. J Trauma
1982;22:827-832.

Aldridge SA, Buckman RF, Badellino MM:
Extended patency of intravascular shunts in an
experimental model of vascular injury. J
Cardiovasc Surg 1997;38:183-186.

AsensioJA, Chahwan S, HanpeterD, etal: Operative
management and outcome of 302 abdominal vas-
cular injuries. Am J Surg 2001;180:528-534.

Baumgartner F, Scudamore C, Nair C, et al: Veno-
venous bypass for major hepatic and caval
trauma. J Trauma 1995;39:671-673.

Beal SL: Fatal hepatic hemorrhage: an unresolved
problem in the management of complex liver
injuries. J Trauma 1990;30:163-169.

Beal SL, Ward RE: Successful atrial caval shunting
in the management of retro-hepatic venous
injuries. Am J Surg 1989;158:409-413.

Bostwick J, Stone HH: Trauma to the portal venous
system. South Med J 1975;68(11):1369-1372.

Bricker DL, Morton JR, Okies JE, et al: Surgical
management of injuries to the vena cava: Chang-
ing patterns of injury and newer techniques of
repair. J Trauma 1971 ;1 1 :725-735.

Bricker DL, Wukasch DC: Successful management
of an injury to the supra-renal inferior vena cava
using an internal vena caval shunt. Surg Clin
North Am 1970;50:999-1002.

Buckman RF, Miraliakbari R, Badellino MM:
Juxtahepatic venous injuries: A critical review of
reported management strategies. J Trauma
2000;48:978-983.

Buckman RF, Pathak AS, Badellino MM, Bradley
KM: Injuries of the inferior vena cava. Surg Clin
North Am 2001;81(6) :1431-1447.

Buechter KJ, Sereda D, Gomez G, Zeppa R: Retro-
hepatic vein injuries: Experience with 20 cases.
J Trauma 1989;29:1698-1704.

Burch JM, Feliciano DV, Mattox KL, Edelman M:
Injuries of the inferior vena cava. Am J Surg
1998;156:548-552.

Burns GR, Sherman RT: Trauma of the abdomi-
nal aorta and inferior vena cava. Am Surg 1972;
38:303-306.

Busuttil RW, Kitahama A, Cerise E, et al: Manage-
ment of blunt and penetrating injuries to the
porta hepatis. Ann Surg 1980;191 (3):641-
648.

Caplan BB, Halasz NA, Bloomer WE: Resection and
ligation of the supra renal inferior vena cava.
J Urol 1964;92:25-29.

Carmona RH, Peck DZ, Lim RC Jr: The role of
packing and planned re-operation in severe
hepatic trauma. J Trauma 1984;24:779-784.

Cattell RB, Braasch JW: A technique for exposure
of the third and fourth portions of the duode-
num. Surg Gynecol Obstet 1960;113:379-380.

Child CG III, Holswade GR, McClure RD Jr, et al:
Pancreaticoduodenectomy with resection of the
portal vein in the Macaca mulatta monkey and
in man. Surg Gynecol Obstet 1952;94:31-45.

Chisholm TP, Lenio PT: Traumatic injuries of the
portal vein. Am J Surg 1972;124:770-773.

Cogbill TH, Moore EE, Jurkovich GL, et al: Severe
hepatic trauma: A multicenter experience with
1335 liver injuries.J Trauma 1998;28:1433-1438.

Cue JL, Cryer HG, Miller FB, et al: Packing and
Planned re-exploration for hepatic and retroperi-
toneal hemorrhage: Critical refinements of a
useful technique. J Trauma 1990;30:1007-1013.

Dawson DL, Johansen KH, Jurkovich GJ. Injuries
to the portal triad. Am J Surg 1 991 ;1 61:545-
551.

Deitrick J, McNeill P, Posner MP, et al: Traumatic
superior mesenteric artery — portal vein fistula.
Ann Vase Surg 1990;4:72-76.

DePinto DJ, Mucha SJ, Powers PC: Major hepatic
vein ligation necessitated by blunt abdominal
trauma. Ann Surg 1976;183:243-246.

Dingledin GP, Proctor HJ, Jaques PF: Trau-
matic aorto-caval— portal-duodenal fistula: Case
Report. J Trauma 1977;17:474-476.

Douglas BE, Baggenstoss AH, HollinsheadWH:The
anatomy of the portal vein and its tributaries.
Surg Gynecol Obstet 1950;91:562-576.

Duke JH Jr, Jones RC, Shires GT: Management
of injuries to the inferior vena cava. Am J Surg
1965;110:759-763.

Epstein BM, Bocchiola FC, Andrews JC, Bester L:
Case report: Traumatic arterio-venous fistula

chl7.qxd 4/16/04 3:38PM Page 337

17 • INJURIES OF THE INFERIOR VENA CAVA AND PORTAL VENOUS SYSTEM

337

involving the portal venous system. Clin Radiol
1987;38:91-93.

Fabian TC, Croce MA, Stanford GG, et al: Factors
affecting morbidity following hepatic trauma: A
prospective analysis of 482 injuries. Ann Surg
1991;21:540-548.

Feldman EA: Injury to the hepatic vein. Am J Surg
1996;111:244-246.

Feliciano DV: Approach to major abdominal vas-
cular injury. J Vase Surg 1988;7:730-735.

Feliciano DV, Bitondo CG, Mattox KL, et al: Civil-
ian trauma in the 1980s. A one-year experience
with 456 vascular and cardiac injuries. Ann Surg
1984;199:717-724.

Fish JC: Reconstruction of the portal vein: Case
reports and literature review. Am Surgeon
1966;32(7):472-478.

Fullen WD, McDonough JJ, Popp MJ, Altemeier
WA: Sternal splitting approach for major hepatic
or retrohepatic vena cava injury. J Trauma
1974;14:903-911.

Fuller JW, Anderson PH: Operative management
of combined injuries to the portal vein and
hepatic artery. South Med J 1978;71:423-424.

Graham JM, Mattox KL, Beall AC: Portal venous
system injuries. J Trauma 1978;18:419-422.

Graham JM, Mattox KL, Beall AC Jr, Debakey MD:
Traumatic injuries of the inferior vena cava. Arch
Surg 1978;113:413-418.

Hartman AR, Yunis J, Frei L, et al: Profound
hypothermic circulatory arrest for the manage-
ment of penetrating retrohepatic venous injury:
Case report. J Trauma 1991;31:1310-1311.

Hunt TX, Leeds FH, Wanebo HJ, Blaisdell FW:
Arteriovenous fistulas of major vessels in the
abdomen. J Trauma 1971;11:483-493.

Ivatury RR, Nallathambi M, Lankin DH, et al: Portal
vein injuries. Ann Surg 1987;206(6):733-737.

Jurkovich GJ, Hoyt DB, Moore FA, et al: Portal triad
injuries. J Trauma 1995;39(3) :426-433.

Kashuk JL, Moore EE, Millikan JS, Moore JB:
Major abdominal vascular trauma — A unified
approach. J Trauma 1982;22:672-679.

Klein SR, Baumgartner FJ, Bongard FA: Contem-
porary management strategy for major inferior
vena caval injuries. J Trauma 1994;37:35-42.

Kudsk KA, Sheldon GF, Lim RC Jr: Arterial-caval
shunting (ACS) after trauma. J Trauma 1982;
22:81-85.

Linker RW, Crawford FAJr, Rittenbury MS, Barton
M: Traumatic aorto-cava fistula. J Trauma 1982;
22:81-85.

Lumsden AB, Allen RC, Sreeram S, et al: Hepatic
arterioportal fistula. Am Surg 1993;59:722-726.

Mattox KL, Espada R, Beall AC: Traumatic injury
to the portal vein. Ann Surg 1974;181(5):519-
522.

Mattox KL, McCollum WM, Jordon GL, et al: Man-
agement of upper abdominal vascular trauma.
Am J Surg 1974;128:823-828.

Mattox KL, Whisennand HH, Espada R, Beall AC
Jr: Management of acute combined injuries to
the aorta and inferior vena cava. Am J Surg
1975;130:720-725.

Milnes RF, Child CG III: Acute occlusion by liga-
ture of the portal vein in the macacus rhesus
monkey. Proc Soc Exp Biol Med 1947;70:332-
333.

Misra B, Wagner R, Boneval H: Injuries of hepatic
veins and retrohepatic vena cava. Am Surg
1983;49:55-60.

Moore FA, Moore EE, Seagraves A: Non-resectional
managementofmajor hepatic trauma: An evolv-
ing concept. Am J Surg 1985;150:725-729.

Mullins RJ, Lucas CE, Ledgerwood AM: The
natural history following venous ligation for
civilian injuries. J Trauma 1980;20:737-743.

Nakamura S, Tzuzuki T: Surgical anatomy of
the hepatic veins and inferior vena cava. Surg
Gynecol Obstet 1981;152:43-50.

Ochsner JL, Crawford ES, Debakey ME: Injuries of
the vena cava caused by external trauma. Surgery
1961;49:397-405.

Pachter HL, Drager S, Godfrey N, et al: Traumatic
injuries of the portal vein: The role of acute lig-
ation. Ann Surg 1979;189(4):383-385.

Pachter HL, Spencer FC, Hofstetter SR, et al: The
management of juxtahepatic venous injuries
without an atriocaval shunt: Preliminary clinical
observation. Surgery 1986;99:569-575.

Peterson SR, Sheldon GF, Lim RC: Management
of portal vein injuries. J Trauma 1979;19(8) :616-
620.

Quast DC, Shirkey AL, Fitzgerald JB, et al: Surgi-
cal correction of injuries of the vena cava: An
analysis of sixty-one cases. JTrauma 1965;5:1-10.

Ravikumar S, Stahl WM: Intra-luminal balloon
catheter occlusion for major vena cava injuries.
J Trauma 1985;25:458-460.

Robb JV, Costa M: Injuries to the great veins of
the abdomen. South Afr J Surg 1984;22(4) :223-
228.

Rovito PF: Atrial caval shunting in blunt hepatic
vascular injury. Ann Surg 1987;205:318-321.

chl7.qxd 4/16/04 3:38PM Page 338

338

IV • SPECIFIC VASCULAR INJURIES

Salam A, Stewart MT: New approach to wounds of
the aortic bifurcation and inferior vena cava.
Surgery 1985;98:105-108.

Sharp KW, Locicero RJ: Abdominal packing for
surgically uncontrollable hemorrhage. Arm Surg
1992;215:467-474.

Sheldon GF, Lim RC, Yee ES, et al: Management
of injuries to the porta hepatis. Ann Surg
1985;202(5):539-545.

Shrock T, Blaisdell W, Mathewson CJr: Manage-
ment of blunt trauma to the liver and hepatic
veins. Arch Surg 1968;96:698-704.

Smith CR, Northrop CH: Stab wound causing
mesenteric-portal arteriovenous fistula: An
unusual case with a spontaneous closure. J
Trauma 1976;16:408-410.

Starzl TH, Kaupp HA, Beheler EM, et al: The treat-
ment of penetrating wounds of the inferior vena
cava. Surgery 1962;51:195-204.

Stone HH, Fabian TC, Turkelson ML: Wounds
of the portal venous system. World J Surg
1982;6:335-341.

Stone HH, LambJM: Use of pedicled omentum as
an autogenous pack for control hemorrhage in
major injuries to the liver. Surg Gynecol Obstet
1975;141:92-94.

SymbasPN, Foster JH, Scott HW: Experimental vein
grafting in the portal venous system. Surgery
1961;50:97-106.

WeichertRF, Hewitt RL: Injuries to the inferiorvena
cava: report of 35 cases. J Trauma 1970;10:649-
657.

Wiencek RG, Wilson RF: Abdominal venous
injuries. J Trauma 1986;26:771-778.

Yellin AE, Chaffee CB, Donovan AJ: Vascular iso-
lation in the treatment of juxtahepatic venous
injuries. Arch Surg 1971;102:566-573.

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Iliac Vessel Injuries

DEMETRIOS DEMETRIADES

JAM

ES A. MUf

3RAY

JUA

N A. ASEN

SIO

INTRODUCTION

ANATOMY

INCIDENCE AND EPIDEMIOLOGY

CLINICAL PRESENTATION

DIAGNOSTIC INVESTIGATIONS

Radiographic Studies
Computed Tomography
Angiography

OPERATIVE MANAGEMENT

Arterial Injuries

Venous Injuries

Adjunct Measures for Bleeding Control

Fasciotomy

PERIOPERATIVE MANAGEMENT

Role of Interventional Radiology

Complications

Mortality

INTRODUCTION

Iliac vessel injuries are among some of the
most lethal injuries sustained by trauma

patients. Their complex anatomy and the
often associated injuries, particularly to the
gastrointestinal and genitourinary structures,
may challenge the skills of even the most expe-
rienced trauma surgeons. Rapid transport to

339

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IV • SPECIFIC VASCULAR INJURIES

a trauma center, prompt recognition of the
injury, good knowledge of the local anatomy,
and sound surgical judgment remain the
cornerstone for survival.

ANATOMY

The abdominal aorta bifurcates at approx-
imately the level of the fourth and fifth
lumbar vertebra into two common iliac arter-
ies. The level of the bifurcation corresponds
roughly to the level of the umbilicus. The
common iliac arteries course inferiorly and
laterally through the pelvis and divide at the
level of the sacroiliac joint into the internal
and external iliac arteries. The ureter crosses
over the bifurcation of the common iliac
artery. The external iliac artery courses along
the pelvis, exiting anteriorly beneath the
inguinal ligament to become the common

femoral artery. The internal iliac artery
provides blood supply to the pelvic viscera. It
divides at the level of the sciatic notch into
anterior and posterior divisions. The anterior
division includes the vesicular, obturator,
pudendal, and inferior gluteal branches. The
main posterior division includes the iliolum-
bar, superior gluteal, and lateral sacral
branches.

The common iliac veinsjoin at the level of
the fifth lumbar vertebra to form the inferior
vena cava. The confluence of the two veins
occurs below the level of the aortic bifurca-
tion and behind the right common iliac artery
(Fig. 1 8-1 ) . Theleft common iliac vein courses
behind and medial to the left common iliac
artery. The right common iliac vein passes infe-
riorly behind the junction of the right exter-
nal iliac and the right internal iliac artery. This
anatomic arrangement makes combined arte-
rial venous injuries common and complicates
the exposure of the right common iliac vein.

Phrenic artery

Celiac artery

SMA

■ FIGURE 18-1

Anatomy of the iliac vessels.
Note the confluence of the two
common iliac veins behind the
right iliac artery and the
relationship of the ureter with
the bifurcation of the common
iliac artery. ■

Left
Renal vein

Testicular
(Ovarian) vein

Testicular (Ovarian) artery

IMA

Ureter

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18 • ILIAC VESSEL INJURIES

341

TABLE 18-1

INCIDENCE OF ILIAC VESSEL INJURIES IN PATIENTS UNDERGOING LAPAROTOMY
FOR TRAUMA

Mech-
anism of
Injury

No. of
Laparotomies

Patients with
Iliac Vessel
Injuries (%)

Patients with
Iliac Artery
Injuries (%)

Patients with

Iliac Vein

Injuries (%)

Combined
Artery-Vein
Injuries (%)

Gunshot wound
Stab wound
Blunt trauma

1310
638
633

131 (10)

12(2)

33 (5.5)

64(5)

6(1)

30(5)

67(5)

6(1)

3 (0.5)

35(2.7)
2 (0.3)
1 (0.2)

From USC Trauma Center, 1993-2000. Unpublished trauma registry data.

Each common iliac vein is formed by thejunc-
tion of an internal and external iliac vein. The
external iliac vein accompanies the external
iliac artery, and the internal iliac vein is formed
by numerous small and delicate tributaries.

INCIDENCE AND
EPIDEMIOLOGY

Though uncommon, iliac vessel injuries are
not necessarily rare in busy urban trauma
centers. The incidence of iliac artery injury
varies depending on the setting. During
World War II DeBakey and Simeone (1946)
reported 43 iliac arterial injuries in 2471
patients for an incidence of 1.7%. Both
Hughes (1958) during the Korean conflict and
Rich, Baugh, and Hughes (1970) during the
Vietnam conflict reported incidences of 2. 3%
and 2.6%, respectively.

Iliac vessel injuries are reported with greater
frequency from the civilian arena. The inci-
dence of iliac vascular injuries in patients
undergoing laparotomy for trauma at the Uni-
versity of Southern California trauma center
is shown in Table 18—1. Overall, the incidence
of iliac vessel injuries is 10% for gunshot
wounds, 2% for stab wounds, and 5.5% in
blunt trauma. In a recent survey at an urban
level I trauma center, Bongard (1990) reported
that iliac arterial injuries represented only 10%
of abdominal vascular injuries and less than
2% of all vascular trauma. Mattox and col-

leagues (1989), in a series of 5760 cardiovas-
cular injuries in 4459 patients, reported 232
iliac artery and 289 iliac venous injuries, for
an overall incidence of 12% of patients or 9%
of cardiovascular injuries. In a series of 504
abdominal vascular injuries from the Los
Angeles County and University of Southern
California trauma center, there were 112 iliac
vessel injuries (22% of all abdominal vascu-
lar injuries) .

Burch and colleagues (1990) in a series of
233 patients sustaining iliac vessel injuries
reported that the common iliac artery was the
most frequently injured vessel, with an inci-
dence of 40%, and both external and inter-
nal iliac arteries accounted for 30% of these
injuries. In the venous system, the common
iliac vein was the most frequently injured vessel
(48%), the external iliac vein was injured in
32% of the patients, and the internal iliac vein
accounted for 20% of the venous injuries. In
this series, Burch and colleagues (1990)
reported a 70% incidence of combined arte-
riovenous injuries.

In contrast to penetrating injuries, blunt
trauma usually involves the internal iliac
vessels and their branches. Injury to the
common or external iliac artery following
blunt trauma is not common, although there
are several case reports. The usual mecha-
nism is stretching of the vessel over the pelvic
wall, resulting in intimal tear and possibly
thrombosis (Fig. 18-2). In addition, direct
laceration of a vessel may occur from a bone
fragment.

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IV • SPECIFIC VASCULAR INJURIES

■ FIGURE 18-2

Blunt trauma with pelvic
fracture. The patient had an
absent femoral pulse.
Angiography shows occlusion
of the right common iliac
artery. ■

CLINICAL PRESENTATION

Penetrating injuries to the lower abdomen,
hips, or buttock, especially in the presence of
shock, should prompt suspicion of an associ-
ated iliac vessel injury. Some of the signs and
symptoms associated with these injuries
include hemorrhagic shock, abdominal dis-
tention, and absent or diminished femoral
pulse. Additional evidence of injury to the
pelvic viscera such as gross hematuria or evi-
dence of rectal injuries should heighten con-
cerns for the presence of iliac vascular injury.
In most cases the diagnosis of vascular injury
is made intraoperatively.

Blunt injuries to the iliac arteries are typi-
cally but not always associated with pelvic frac-
tures. Absent or diminished femoral pulse is
highly suggestive of injury to the common or
external iliac arteries. Hemorrhage is typically
due to injury to the branches of the internal
iliac vessels. These patients may demonstrate
signs and symptoms of severe hemorrhagic
shock upon initial presentation requiring
aggressive resuscitation. Other patients may
present with gradual and persistent bleeding.
Both these scenarios require exclusion of
intraperitoneal hemorrhage. In the absence
of intraperitoneal hemorrhage or peritonitis,
these patients should undergo immediate
angiographic evaluation and possibly
embolization. In rare occasions with blunt

trauma, an arterial intimal tear may remain
undetected during the initial hospitalization,
only to manifest at a later stage with signs of
leg ischemia due to secondary thrombosis.

In patients with suspected pelvic fractures,
a thorough physical examination can deter-
mine the stability of the pelvis by examining
the anterior, lateral, and posterior compo-
nents of the pelvic ring. Injudicious and
repeated examinations can exacerbate bleed-
ing and lead to life-threatening hemorrhage.
Therefore once a patient has been noted to
have an unstable pelvis by one examiner,
further examinations by other physicians are
contraindicated. Radiographic examination
of the pelvis to confirm the clinical diagnosis
should follow expeditiously and measures to
stabilize the pelvis should be promptly insti-
tuted. Early application of a pelvic binder or
external pelvic fixation may contain the
expansion of the pelvic hematoma and reduce
bleeding (Fig. 18-3).

DIAGNOSTIC INVESTIGATIONS
Radiographic Studies

Radiographic evaluation of penetrating
injuries to the abdomen should be performed
only if the patient is hemodynamically fairly
stable. These investigations may include a

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18 • ILIAC VESSEL INJURIES

343

■ FIGURE 18-3

Pelvic binder may contain
the expansion of a pelvic
hematoma and reduce
bleeding from a pelvic
fracture. ■

plain radiograph of the abdomen and pelvis.
The presence of missiles or fragments in the
pelvis, especially in the presence of hypoten-
sion, should prompt the physician to suspect
injury to the iliac vessels (Fig. 18-4). In blunt
trauma, radiographic findings from the pelvis
known to be associated with increased risk of
bleeding from the internal iliac vessels include
the presence of symphysis pubis diastasis of
greater than 2.5 cm, sacroiliacjoint disruption,
and the presence of superior and inferior rami
fractures bilaterally ("butterfly fracture"). In
our center these patients undergo early angio-
graphic embolization before hemodynamic

decompensation and massive transfusions
are required.

COMPUTED TOMOGRAPHY

Computed tomography continues to play a
major role in the evaluation of hemodynam-
ically stable blunt trauma patients. The pres-
ence of a significant pelvic hematoma is
suggestive of an injury to the internal iliac
vessels or their branches. Extravasation of
intravenous contrast is diagnostic of arterial
bleeding or false aneurysm and requires

■ FIGURE 18-4

Missiles in the pelvis on
radiographs, especially in the
presence of shock, are
suggestive of iliac vessel
injury. ■

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IV • SPECIFIC VASCULAR INJURIES

prompt angiographic evaluation and possibly
embolization. Lack of contrast opacifying the
lumen of the major iliac vessels is consistent
with thrombosis and should be investigated
further with angiography to confirm the diag-
nosis, provided the extremity does not appear
threatened by ischemia. If the extremity
appears compromised, prompt surgical explo-
ration should be performed.

ANGIOGRAPHY

Angiography has dramatically improved the
management of patients with hemorrhage
from pelvic fractures secondary to blunt
trauma. It should be considered early in
patients with clinical evidence of severe bleed-
ing from the pelvis (low hematocrit or
hypotension) as soon as intraperitoneal
bleeding or peritonitis has been ruled out.
Similarly, the presence of extravasation of
intravenous contrast on computed tomo-
graphic scan or certain radiographic findings
on plain pelvic films (pubis diastasis >2.5 cm,
major sacroiliac joint disruption, and "but-
terfly" fracture) should prompt the surgeon
to seek an early angiogram. It is critical that
during angiography the patient is closely mon-
itored and resuscitated continuously under
the supervision of a senior member of the
trauma team.

Angiography is able to identify the site and
severity of bleeding and control bleeding with

embolization. Additionally, it may identify
occlusions or major intimal tears of the
common or external iliac arteries that require
operative intervention. If massive hemor-
rhage from a major artery is identified at the
time of angiographic evaluation, temporary
control of the bleeding may be achieved with
an intraluminal balloon while the patient is
transported to the operating room (Fig.
18-5).

OPERATIVE MANAGEMENT

The operative findings depend on the
mechanism of injury, associated injuries, and
the nature of vascular injury. In blunt trauma
the usual finding is a zone 3 retroperitoneal
hematoma, which may or may not be pulsatile
or expanding. However, in some cases with
intimal tear and thrombosis, often there is a
small or even no local hematoma and the
injury may be missed. Azone 3 retroperitoneal
hematoma resulting from blunt trauma
should not be explored routinely. Exploration
is indicated only if there is a suspicion of iliac
artery injury — that is, absent or diminished
femoral pulse.

In penetrating iliac vessel injuries upon
entering the abdominal cavity, the surgeon
may encounter free intraperitoneal bleeding,
azone 3 hematoma, or a combination of both.
It is an important surgical principle that all

■ FIGURE 18-5

Motor vehicle accident with
severe pelvic fracture.
Angiography showed massive
bleeding from the left common
iliac artery. Balloon occlusion of
the injured artery achieved
temporary control of the
bleeding and the patient was
taken to the operating room. ■

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18 • ILIAC VESSEL INJURIES

345

zone 3 hematomas caused by penetrating
trauma be explored.

Arterial Injuries

Any active bleeding is controlled initially by
direct compression and subsequently by prox-
imal and distal vascular control. The iliac
vessels may be exposed by direct dissection of
the peritoneum over the vessels or by dissec-
tion of the paracolic peritoneum and medial
rotation of the right or left colon. Care should
be taken to avoid injury to the ureter, which
crosses over the bifurcation of the common
iliac artery.

The anatomic level of proximal control
depends on the site of bleeding and the site
and size of the hematoma. For suspected
iliac artery injuries near the bifurcation of
the aorta, proximal arterial control may be
achieved with aortic cross clamping above
the bifurcation. In more distal external iliac
artery injuries, proximal control can be
achieved by applying a vessel tape around
the common iliac artery. During the dissec-
tion, care should be taken to avoid acciden-
tal injury to the underlying vein, especially
the right common iliac vein. Isolation and
control of the internal iliac artery is essential
because the bleeding may continue despite
proximal and distal control. The identifica-
tion and isolation of the internal iliac artery
can be facilitated by retracting the vascular
tapes proximally and distally and dissecting
toward the middle until the vessel is identi-
fied. A similar technique of gradual dissec-
tion of the vessel and progressive movement
of the vascular clamps toward the injury
can be used in cases with active bleeding or
large hematoma, in which a direct approach
to the injured site may be difficult. If
the exposure of the distal iliac vessels is
difficult, especially in men with a narrow
pelvis, extending the midline incision by
adding a transverse lower abdominal inci-
sion may be necessary. In some cases with
bleeding from the vessels near the groin or
in the presence of a large hematoma, distal
control can be facilitated by a longitudinal
incision over the groin and division of the

inguinal ligament.

Small common or external iliac artery
injuries can be managed by primary repair,
using a 4-0 or 5-0 vascular suture and taking
care to avoid significant stenosis. In the appro-
priate cases a venous or PTFE patch may be
necessary to avoid stenosis at the repair site.
This patch should not be excessive in size in
order to avoid aneurysmal dilation. In more
extensive injuries, especially in gunshot
wounds or blunt trauma in which debridement
is always necessary, an end-to-end anastomo-
sis with or without a prosthetic graft (size 6 or
8 PTFE) may be required. It is strongly
recommended that all vascular repairs are
performed under loupe magnification. Local
heparin (20 to 30 mL of solution of 100 units
of heparin per 100 mL) should be adminis-
tered to prevent thrombosis during the vas-
cular repair. A balloon-tipped catheter should
always be passed in the distal arterial tree to
remove any clots.

More complex procedures, such as extra-
anatomic femorofemoral bypass or mobiliza-
tion and use of the internal iliac artery to
replace the external iliac artery, are time
consuming and often technically difficult.
Extra-anatomic bypasses may be necessary in
patients with severe purulent peritonitis.
Burch performed six extra-anatomic bypasses
with poor results, including three deaths, three
amputations, three compartment syndrome,
and two graft thrombosis. The existing evi-
dence suggests that the presence of enteric
contamination is not a contraindication for
an end-to-end repair or a PTFE interposition
graft. In a study of 358 penetrating iliac vas-
cular injuries, Burch reported that in general
associated gastrointestinal or urologic injuries
did not influence the management of vascu-
lar injuries. However, many surgeons still
suggest that in the presence of significant
enteric contamination, an extra-anatomic
bypass should be performed. Any enteric
spillage should be controlled first and the peri-
toneum cleaned meticulously before any
vascular repair is performed. The peritoneum
should be closed over the graft whenever
possible.

Ligation of the common or external iliac
artery should never be considered, even in
the most critically injured patients. Ligation
is poorly tolerated and in most cases results

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IV • SPECIFIC VASCULAR INJURIES

■ FIGURE 18-6

Injuries to the right iliac artery
and vein. Because of the
critical condition of the patient,
the vein was ligated (white and
black arrows) and the artery
was shunted with a catheter
(white arrow). Definitive arterial
reconstruction was performed
24 hours later. ■

in ischemia of the leg and in about 50% of
patients limb loss. The ischemia may aggra-
vate the general condition of the patient by
release of toxic metabolites into the systemic
circulation. Subsequent attempts to re-
establish blood flow may be even more dan-
gerous because of reperfusion injury. In the
critically ill, hypothermic, and coagulopathy
patient, a temporary intraluminal shunt with
semielective reconstruction of the artery at a
later stage should be considered (Fig. 18-6).
The fastest and cheapest way to construct a
shunt is from a sterile intravenous or naso-
gastric tube. The shunt is secured in place with
proximal and distal ligatures. The incidence
of thrombosis of the shunt is high, and the
peripheral pulses and perfusion should be
monitored closely. Systemic anticoagulation
prophylaxis is usually contraindicated because
of associated coagulopathy.

Venous Injuries

Iliac venous injuries may be technically
more challenging than arterial injuries
because of the more difficult surgical expo-
sure and the risk of air embolism. The
anatomic location of the right common iliac
vein and the confluence of the two common
iliac veins behind the right common iliac

artery may make exposure a challenging task,
especially in elderly patients with atheroscle-
rosis and adhesions between the artery and
vein. These difficulties have led some authors
to recommend transection of the overlying
iliac artery. We believe that such a drastic
approach is excessive and should rarely be con-
sidered. As a rule, satisfactory surgical expo-
sure of the vein can be achieved by meticulous
and adequate mobilization and retraction
of the artery with vessel tapes. Ligation and
division of the internal iliac artery may also
facilitate exposure.

Repair of iliac venous injuries should always
be considered in cases in which it can be per-
formed by lateral venorrhaphy without pro-
ducing major stenosis. This is usually possible
in more than 50% of cases. The management
of complex venous injuries, which cannot be
repaired by lateral venorrhaphy, is a contro-
versial issue. Burch, in a study that included
192 iliac venous injuries, performed only one
PTFE reconstruction on a patient with exter-
nal iliac vein injury. Repair associated with
severe stenosis may result in thrombosis and
possibly pulmonary embolism. In these cases,
ligation of the vein maybe preferable to repair.
Burch reported two cases with fatal embolism
in a group of 82 patients with common or
external iliac vein injuries treated with repair
but none in 43 patients treated with ligation.

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347

Although theoretically a caval filter may
prevent pulmonary embolism, there is no pub-
lished clinical experience. The proponents of
ligation argue that complex repair with spiral
graft or other methods is time consuming and
increases blood loss, and that there is no evi-
dence of any improved outcome. Ligation is
usually tolerated very well by almost all
patients. Most patients develop transient leg
edema, which responds well to elevation and
elastic bandage wrapping. However, in some
cases ligation results in massive edema and
extremity compartment syndrome. In some
extreme cases with massive leg and scrotal
edema, we had to re-operate and re-establish
the continuity of the vein with a prosthetic
graft.

The management of complex iliac vein
injuries becomes even more controversial in
patients with associated iliac artery injuries.
Some surgeons have suggested that venous
repair may protect the arterial repair by
avoiding venous hypertension. However,
many others challenge this concept and
advocate ligation. These major injuries are
usually associated with severe blood loss, and
any complex procedures prolonging the
operation may increase mortality. We believe
that the decision to repair or ligate the vein
should be individualized according to the
condition of the patient and the nature of
the venous injury.

Adjunct Measures for
Bleeding Control

In some cases bleeding may persist even
after repair or ligation of the iliac vessels. The
source of bleeding is usually from deep vas-
cular branches to the pelvic wall or the
sacrum. Opening of the presacral fascia is ill-
advised and often aggravates the bleeding.
Damage control by packing, followed by post-
operative angiographic embolization, should
be considered at an early stage. Carillo and
colleagues (1998) reported significantly
reduced mortality in patients with iliac vas-
cular injuries undergoing abbreviated
laparotomy and damage control.

Bleeding from a gunshot wound involving
the bony pelvis can be troublesome and
difficult to control. In these cases we have
successfully used Foley catheter balloon
tamponade. The balloon is inflated in the
bone defect and the distal end of the catheter
is brought outside the abdominal cavity
through a small skin incision (Fig. 18-7). A
gentle traction on the catheter is maintained
by a clamp applied to the catheter just
above the skin. The clamp is removed and
the balloon is deflated 2 or 3 days postoper-
atively, and if no bleeding occurs through
the catheter, the Foley catheter is pulled
out.

■ FIGURE 18-7

Foley catheter balloon
tamponade of persistent
bleeding from the posterior
wall of the pelvis following a
gunshot wound. The catheter
is exiting through the left
buttock. The balloon was
removed 4 days later without
any recurrent bleeding. ■

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Fasciotomy

Therapeutic leg fasciotomy in patients with
extremity compartment syndrome should be
performed without any delay, even before
reconstruction or shunting of any arterial
injury. However, the role of liberal prophy-
lactic fasciotomy is controversial. Although
some authors advocate prophylactic fas-
ciotomies in all patients with delayed arterial
reconstruction or venous ligation, especially
in combined arteriovenous injuries, many
others practice a policy of "fasciotomy on
demand." These authors suggest that fas-
ciotomy is a procedure associated with sig-
nificant complications and inferior cosmetic
results and should be performed only for ther-
apeutic purposes. In a study of 94 patients with
fasciotomies for trauma, Velmahos and col-
leagues (1997) reported local complications
in 42% of patients with prophylactic fas-
ciotomies. In 57% of these patients, primary
closure of the wounds was not possible and
there was a need of skin grafting. If an expec-
tant policy is selected, the patient should be
monitored very closely with frequent clinical
examinations and measurements of com-
partment pressures in the appropriate cases.
Fasciotomy should be performed with the first
signs of compartment syndrome.

PERIOPERATIVE
MANAGEMENT

To avoid reperfusion injury following revas-
cularization of the extremity, the surgeon must
maintain good hydration and diuresis during
the operation and the first few hours postop-
eratively. In hemodynamically stable patients,
administration of mannitol (0.5g/kg of body
weight over 20 minutes) has many beneficial
effects because of its oxygen free radical scav-
enger, rheologic, and osmotic properties.
There is evidence that early administration of
mannitol blunts the effects of reperfusion
injury, reduces the risk of extremity com-
partment syndrome and the need for fas-
ciotomy, and improves the microcirculation
of tissues. It is our practice to administer a
second dose 4 to 6 hours after injury.

Mannitol is contraindicated in hypotensive
patients because its diuretic effect may aggra-
vate the hypotension. There is also concern
that the vasodilating and rheologic properties
of mannitol may increase bleeding in patients
with active uncontrolled hemorrhage.

The role of postoperative anticoagulation
in uncomplicated vascular repairs or in venous
ligations is not clear. Some authors use low-
molecular-weight heparin prophylaxis for the
first few days, followed by aspirin for the next
few weeks. In patients with venous thrombo-
sis after repair, oral anticoagulation should be
given for at least 3 months.

In venous injuries treated by ligation, it is
important to elevate the leg, apply early com-
pression elastic bandages, and monitor closely
for extremity compartment syndrome.

Role of Interventional
Radiology

Diagnostic angiography has a limited role in
the preoperative evaluation of penetrating
abdominal trauma. However, it may play a
useful therapeutic role postoperatively in
patients with incomplete hemostasis from
deep iliac artery branches. In blunt trauma
angiography may play a major diagnostic and
therapeutic role. It remains the most useful
investigation for the diagnosis of iliac artery
thrombosis or bleeding following blunt
trauma to the abdomen or pelvis. Bleeding
from peripheral branches may be effectively
controlled by embolization in most patients
(Fig. 1 8-8) . In cases with major bleeding from
the iliac artery, the interventional radiologist
may be able to achieve temporary control by
inflating an intraluminal balloon at the site
of injury until surgical control is achieved in
the operating room (Fig. 18-5).

Angiographically placed stents have an
important role in selected cases with iliac
artery injuries. Patients with false aneurysms,
arteriovenous fistulas, or significant intimal
tears may benefit from this procedure. Stent-
ing should not be attempted during the acute
stage in patients with a thrombosed iliac artery,
because of the risk of clot dislodgement and
major hemorrhage in cases with a transected
vessel. However, angiographic stenting may

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349

■ FIGURE 18-8

Patient with severe pelvic
fracture and major blood
loss. Angiography shows two
areas of significant bleeding
(arrows), which were
successfully controlled by
embolization (right frame), m

be a good option in patients with late iliac
artery thrombosis. In most cases a skillful
interventional radiologist may be able to pass
a guidewire through the clot and deploy a stent
(Fig. 18-9).

Complications

Complications directly related to the vascular
injuries may appear early during the initial
hospitalization or late. The overall incidence
of early vascular complications in patients sur-
viving for more than 24 hours is about 15%
for arterial injuries and 12% for venous
injuries.

Thrombosis of the repaired artery remains
the most common early arterial complication.
The most important factors for early throm-
bosis are the technique and the use of pros-
thetic grafts. Burch reported no thrombosis
in 25 patients with lateral suturing of the iliac
artery. On the other hand, 25% of 16 PTFE
grafts and 33% of 6 extra-anatomic bypasses
thrombosed. Good surgical techniques,
Fogarty balloon exploration and extraction
of any clots from the peripheral arteries, intra-
operative local heparinization, and liberal use
of on-table angiography may reduce the inci-
dence of early failure of the arterial repair.
Postoperatively, the peripheral pulses and per-
fusion should always be monitored closely and

■ FIGURE 1 8-9

An 18-year-old patient presenting with intermittent claudication many months after a major car
accident for which he required a splenectomy and small bowel resection. Angiography revealed
occlusion of the right common iliac artery (left frame). The occlusion was successfully stented by
interventional radiology (right frame), m

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IV • SPECIFIC VASCULAR INJURIES

emergency reoperation should be considered
in patients with evidence of arterial thrombosis.

Early postoperative bleeding is another
fairly common problem. Bleeding during the
first few hours after the operation may be due
to a technical problem with the suture line,
missed bleeding from a small vessel, or medical
bleeding resulting from coagulopathy.
Depending on the rate of bleeding and the
coagulation status of the patient, reoperation
may be necessary. Delayed bleeding a few days
after the initial procedure, especially in the
presence of other signs of infection, such as
fever or leucocytosis, may be due to local sepsis
and is an ominous sign. Infection of the
repaired vessel, especially in the presence of
a prosthetic graft, is a life-threatening com-
plication. The controversies regarding the role
of prosthetic grafts in a grossly contaminated
field have already been discussed. Early recog-
nition of the infection and aggressive anti-
biotic treatment may salvage the graft.
However, in advanced sepsis, especially in the
presence of bleeding, reoperation with
removal of the graft and ligation of the vessel
combined with an extra-anatomic bypass
remain the only option.

The overall incidence and nature of early
venous complications following iliac vein
injury depend on the extent of venous injury
and method of management. Generally,
lateral repairs are associated with a lower inci-
dence of venous complications than venous
ligations (5% vs. 25% in the series by Burch) .
Transient leg edema following ligation of the
common or external iliac vein is by far the
most common complication. The edema can
be avoided or minimized by elevation and
elastic wraps of the leg. Occasionally, the
swelling is so severe that it results in extremity
compartment syndrome, requiring fasciotomy.

Deep venous thrombosis may occur in
patients treated by ligation of the iliac vein or
in cases with thrombosis of the repaired vein.
The real incidence of early deep venous
thrombosis is not known because no study has
ever evaluated systematically all patients with
iliacvenousinjuries. Ithasbeen suggested that
anticoagulation prophylaxis and elastic wrap
on the leg should be used in all patients with
venous injuries.

The most dangerous complication follow-
ing iliac venous injury is pulmonary embolism .
Patients with repair producing major venous
stenosis are at risk of pulmonary embolism.
Earlier military experience suggested that
venous repairs may be associated with a high
incidence of pulmonary embolism, especially
if the lumen is narrowed more than 50 % . More
recent civilian experience reported an inci-
dence of about 2% of fatal pulmonary
embolism in patients treated with venous
repair. The role of prophylactic inferior vena
cava filters and long-term anticoagulation has
not been studied. It might be appropriate to
use these modalities in cases with major steno-
sis of the vein.

The incidence of late complications fol-
lowing iliac vascular trauma is not known. All
existing studies are retrospective and lack
systematic late follow-up. Late iliac artery
complications include false aneurysm and
arterial stenosis associated with intermittent
claudication or a threatened limb. The
method of treatment of these complications,
such as open surgery or angiographically
placed stents, should be individualized
according to the age of the victim, the nature
of the arterial pathology, and the experience
of the trauma center.

Late venous complications may include
chronic venous insufficiency with leg edema
and skin ulcers. The incidence of this com-
plication is not known, and the reported
figures from existing retrospective studies
may be misleading, because those patients
returning for late follow-up are usually the
symptomatic ones. There is evidence that
late venous complications are more likely to
occur in patients treated with iliac vein
ligation than in patients with lateral repair.
Mullins suggested that iliac vein ligation
does not often result in chronic venous com-
plications, especially if elevation of the leg is
instituted immediately after surgery. The
rationale for this practice is that elevation
may interrupt the cascade of events, which
lead the vascular damage during the critical
postinjury period. It certainly makes sense to
elevate the leg and apply elastic wraps in
these cases, but there is no proven evidence
of any benefit.

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Mortality

The mortality of iliac vascular injuries is high
and depends on the type of vascular trauma
(contained or free bleeding) , the presence of
other associated injuries, the clinical condi-
tion of the patient on admission, and the expe-
rience of the trauma team.

The mortality of patients undergoing emer-
gency department thoracotomy is almost
100%, with only very few survivors reported.
The reported overall mortality varies from
30% to 50% in arterial injuries and 25% to
40% in venous injuries. In isolated vascular
injuries, the mortality is about 20% for arter-
ial injuries and about 10% for venous injuries.

REFERENCES

Asensio JA, Chahwan S, Hanpeter D, et al: Oper-
ative management and outcome of 302 abdom-
inal vascular injuries. Am J Surg 2000;180:
528-534.

Asensio JA, Lejarraga M: Abdominal vascular
injuries. In Demetriades D, Asensio JA (eds):
Trauma Management. Georgetown, Tex, Landes
BioScience, 2000, pp 356-362.

Asensio JA, Petrone P, Roldan G, et al: Analysis
of 185 iliac vessel injuries: Risk factors and pre-
dictors of outcome. Arch Surg 2003;138(11):
1187-1193.

Bongard FS, Dubrow T, Klein SR: Vascular injuries
in the urban battleground: Experience at a
metropolitan trauma center. Ann Vase Surg
1990;4:415-418.

Burch JM, Richardson RJ, Martin RR, Mattox KL:
Penetrating iliac vascular injuries: Recent
experience with 233 consenting patients. J
Trauma 1990;30:1450.

Carillo EH, WohPtmann CD, Spain DA, et al:
Common and external iliac artery injuries asso-
ciated with pelvic fractures. J Orthop Trauma
1999;13:351-355.

Carillo EH, Spain DA, Wilson MA, et al: Alterna-
tives in the management of penetrating injuries
to the iliac vessels. J Trauma 1998;44:1024-1030.

DeBakey ME, Simeone FA: Battle injuries of the
arteries in World War II: An analysis of 2,471 cases.
Ann Surg 1946;123:534-579.

Degiannis E, Velmahos G, Levy R, et al: Penetrat-
ing injuries of the iliac arteries: A South Africa
experience. Surgery 1996;119:146-150.

Feliciano DV, Mattox KL, Graham JM, Bitondo
CA: Five-year experience with PTFE grafts in
vascular wounds. J Trauma 1985;25:75.

Haan J, Rodriguez A, Chiu W: Operative manage-
ment and outcome of iliac vessel injury: A ten-
year experience. Am Surg 2003;69(7):581-586.

Hughes CW: Arterial repair during the Korean War.
Ann Surg 1958;147:555-561.

Rich NM, Baugh JH, Hughes CW. Acute arterial
injuries in Vietnam: 1,000 cases. J Trauma,
1970:359-369.

Mattox KL: Penetrating injuries to the iliac
arteries. Am J Surg 1978;135:663.

Mattox KL, Feliciano DV, Burch J, et al: Five
thousand seven hundred and sixty cardio-
vascular injuries in 4,459 patients. Epidemiologic
evolution. Ann Surg 1989;209(6):698-707.

Rogers FB, Cipolle MD, Velmahos G, et al: Prac-
tice management guidelines for the prevention
of venous thromboembolism in trauma patients:
The EAST practice management guidelines
work group. J Trauma 2002;53(1):142-164.

Velmahos GC, Theodorou D, Demetriades D,
et al: Complications and nonclosure rates of
fasciotomy for trauma and related risk factors.
World J Surg 1997;21:247-253.

chl9.qxd 4/16/04 3:33PM Page 353

Extremity Vascular Trauma

MICHAEL J. SISE
STEVEN R. SHACKFORD

OVERVIEW OF EXTREMITY VASCULAR TRAUMA

Clinical Presentation

Diagnosis

Nonoperative Management

Operative Management

SUBCLAVIAN ARTERY INJURIES

Surgical Anatomy

Epidemiology and Etiology

Clinical Features and Diagnosis

Surgical Treatment

Results

Management of Scapulothoracic Dissociation

AXILLARY ARTERY INJURIES

Surgical Anatomy

Epidemiology and Etiology

Clinical Features and Diagnosis

Surgical Treatment

Results

BRACHIAL ARTERY INJURIES

Surgical Anatomy

Epidemiology and Etiology

Clinical Features and Diagnosis

353

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354 IV • SPECIFIC VASCULAR INJURIES

Surgical Treatment
Results
O RADIAL AND ULNAR ARTERY INJURY
Surgical Anatomy
Epidemiology and Etiology
Clinical Features and Diagnosis
Surgical Treatment
Results
O VENOUS INJURIES OF THE UPPER EXTREMITY
O COMPARTMENT SYNDROME OF THE UPPER EXTREMITY
O POST-TRAUMATIC CAUSALGIA
O LOWER EXTREMITY VASCULAR INJURIES

Common Femoral and Profunda Femoral Arteries

Surgical anatomy

Epidemiology and etiology

Clinical features and diagnosis

Surgical treatment

Results
Superficial Femoral Artery

Surgical anatomy

Epidemiology and etiology

Clinical features and diagnosis

Surgical treatment

Results
Popliteal and Tibial Arteries

Surgical anatomy

Epidemiology and etiology

Clinical features and diagnosis

Surgical treatment

Results
Lower Extremity Compartment Syndrome
Mangled Lower Extremity
Venous Injuries of the Lower Extremity

Surgical anatomy

Epidemiology and etiology

Clinical features and diagnosis

Surgical treatment

Results

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19 • EXTREMITY VASCULAR TRAUMA

355

OVERVIEW OF EXTREMITY
VASCULAR TRAUMA

Vascular trauma of the extremities is a highly
morbid injury that is becoming more
common. Improved prehospital management
and regionalization of trauma care with rapid
transport have increased the number of these
injuries seen at trauma centers in the last 3
decades. Patients who previously died in the
field or in transit because of severe isolated
peripheral vascular injuries or multiple
injuries with associated vascular trauma are
now presenting alive.

Successful management of extremity
vascular trauma is based on early diagnosis
and prompt treatment. The severity of
injury and the length of time until restora-
tion of perfusion are the major determi-
nants of outcome. The management strategy
must focus on minimizing the duration of
ischemia to maximize the chance of success-
ful recovery and rehabilitation. The often
insidious nature of extremity vascular trauma
significantly increases the opportunity for
errors in management. Clinically relevant
and practical protocols for both diagnosis
and treatment are the best tools for avoiding
these errors and ensuring the best possible
outcome.

Clinical Presentation

Extremity vascular trauma may be immediately
apparent on presentation because of exter-
nal hemorrhage, hematoma, or obvious limb
ischemia. A history of penetrating trauma asso-
ciated with hypotension, pulsatile bleeding,
or a large quantity of blood at the scene sug-
gests potential vascular injury. Blunt trauma
is also capable of causing significant vascular
injury that can be overlooked when serious
head, chest, or abdominal injuries are present
(Fig. 19-1).

Peripheral neurologic deficit should alert
the examining physician to a possible vascu-
lar injury. The deficit may be due to direct
injury of a nerve in close anatomic proximity
to an artery, or it may be the result of advanced
ischemia.

■ FIGURE 19-1

Brachial artery occlusion secondary to distal
shaft of humerus fracture in patient with
multiple injuries. Shown are (arrows,) collateral
flow filling distal brachial artery. Absent pulse
and low forearm systolic pressure prompted
arteriography. A saphenous vein interposition
graft was required to repair this lacerated and
contused artery. ■

Diagnosis

A thorough history and careful physical exam-
ination of the extremities for signs of vascu-
lar injury are the first and most important steps
in making the diagnosis of extremity vascular
trauma. Careful inspection of the injured sites,
examination of wounds, sensory and motor
assessment, and pulse examination must be
part of the extremity physical examination.
The presence of a hematoma, bruit, or thrill
must be noted. If distal pulses are diminished
or absent, ankle or wrist systolic blood pres-
sure should be determined with a continu-
ous-wave Doppler device and compared with
the normal side. A significant difference in
systolic blood pressure (>10mmHg) between
extremities may be an indication of vascular
injury. Duplex scanning of the extremities has
no role in the acute evaluation of extremity
vascular trauma.

Patients with "hard signs" of vascular injury
(Table 19-1) should be taken directly to the
operating room . In less straightforward cases,
arteriography may be indicated to rule out
the need for operation. Arteriography is
limited to suspected extremity vascular trauma
when no clear indication for immediate
operative therapy is present or when evidence
of peripheral ischemia and multiple sites of

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356

IV • SPECIFIC VASCULAR INJURIES

TABLE 19-1

"HARD" AND "SOFT"
VASCULAR INJURY

SIGNS OF

Hard Indicate need for operative intervention

Pulsatile bleeding
Expanding hematoma
Palpable thrill
Audible bruit
Evidence of regional ischemia

Pallor

Paresthesia

Paralysis

Pain

Pulselessness

Poikilothermia

Soft Suggest need for further evaluation

History of moderate hemorrhage
Injury (fracture, dislocation, or

penetrating wound)
Diminished but palpable pulse
Peripheral nerve deficit

injury in an extremity exist (e.g., a shotgun
injury with multiple pellet wounds) (Fig.
19-2) .Arteriography is both sensitive and spe-
cific in the diagnosis of extremity vascular
injuries. However, arteriography is time con-
suming, and successful management of these
injuries requires prompt control of hemor-
rhage and a timely restoration of adequate
blood flow.

Spiral computed tomographic angiography
with the latest generation scanners might
prove an acceptable alternative to formal

arteriography. Although this imaging tech-
nique requires contrast infusion, it does not
require arterial catheterization, is easily per-
formed, and is extremely rapid. Its use in the
diagnosis of peripheral vascular injury has not
yet been systematically evaluated.

Nonoperative Management

The widespread application of arteriography
in the evaluation of injured extremities results
in the detection of clinically insignificant
lesions. Intimal irregularity, focal spasm with
minimal narrowing, and small pseudo-
aneurysms are often asymptomatic and do not
progress. Considerable evidence suggests that
nonoperative therapy of many asymptomatic
lesions is safe and effective. However, suc-
cessful nonoperative therapy requires con-
tinuous surveillance for subsequent occlusion
or hemorrhage. Operative therapy is required
for thrombosis, symptoms of chronic ischemia,
and failure of small pseudoaneurysms to
resolve.

A limited role exists for interventional
radiologic techniques in the management of
extremity vascular injuries. This modality
requires special training, expertise, and an
established interventional radiology program .
Only an experienced interventionalist can suc-
cessfully manage an extremity vascular injury.
Amultidisciplinary approach in anticipation
of injuries amenable to endovascular therapy
is best led by a trauma surgeon skilled in the

■ FIGURE 19-2

Close-range shotgun injury to right medial knee. Pedal pulses were palpable but diminished.
Formal arteriograpy demonstrated patent popliteal artery and peroneal and posterior tibial arteries.
This patient was successfully treated nonoperatively. ■

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19 • EXTREMITY VASCULAR TRAUMA

357

management of extremity vascular trauma.
The indications for endovascular techniques
in the extremities are limited to hemorrhage
from branch vessels that may be occluded
without producing ischemia, acute pseudo-
aneurysms with a small lateral wall arterial
injury, intimal flap without significant under-
lying thrombosis, and acute arteriovenous
fistulas. Endovascular techniques are not
effective in acute arterial occlusion from
trauma. Endovascular placement of stents and
stent grafts for noniatrogenic vascular trauma
remains experimental and should be per-
formed only in the most carefully selected
cases (Fig. 19-3). Long-term results are not
yet available and their application remains
limited to specialized centers.

Operative Management

The operative management of extremity vas-
cular injuries must be carefully orchestrated

with the overall care of the patient. Intra-
venous broad-spectrum antibiotics should be
administered preoperatively. Systemic heparin
may be given preoperatively to patients with
isolated extremity injury (e.g., in whom
cavitary hemorrhage has been excluded) to
prevent propagation of thrombus. However,
heparin should be avoided in multi-injured
patients, especially those with central nervous
system trauma.

A generous sterile field should be prepared
to allow for adequate exposure of vessels,
to obtain proximal and distal control. This
includes the chest and abdomen in proximal
injuries of the upper and lower extremities.
An uninjured leg should be prepared for har-
vesting of autologous venous conduit.

An orthopedic surgeon has an essential role
in the surgical management of extremity vas-
cular trauma associated with skeletal injury
and should be involved before the surgical pro-
cedure begins. Restoration of blood flow is
imperative and can be achieved by an initial

■ FIGURE 19-3

A, Axillary artery laceration with
pseudoaneurysm (arrow) in a 36-year-old
man stabbed in the left upper chest.

B, Endovascular treatment was
accomplished with a covered stent seen in
place with exclusion of pseudoaneurysm
(arrows). C, Stent position in the axillary
artery (arrows). At 9 months follow-up, the
stent graft was patent and the patient had
resumed normal work activity. ■

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IV • SPECIFIC VASCULAR INJURIES

vascular repair or insertion of a vascular shunt.
The vascular surgeon's role does not end after
perfusion is restored. Careful surveillance
must be maintained to ensure that orthope-
dic appliances do not obstruct the shunt or
disrupt the arterial repair. The early involve-
ment of a plastic and reconstructive surgeon
is essential for the successful management
of vascular injuries associated with large soft
tissue defects.

The appropriate treatment of extremity
arterial and venous injuries consists of debride-
ment of the damaged vessel, a tension-free
repair, use of saphenous interposition graft-
ing when primary repair is not possible, and
adequate coverage with healthy vascularized
tissue.

Alimited role for primary amputation exists
in the management of complex extremity vas-
cular injuries. Patients with extensive soft tissue
loss, neurologic deficit, extensive fractures,
and vascular injuries should be evaluated
collaboratively with orthopedic and plastic
surgery colleagues to determine whether
primary amputation is the best initial man-
agement. These mangled extremities can be
objectively evaluated using a rating system that
accounts for the age of the patient, the type

of injury and the severity of the injury (Fig.
19-4; see also Table 19-1). However, the use
of this scoring system is for general assessment
and should never be a substitute for thought-
ful clinical judgment using the skills of ortho-
pedic and plastic surgery consultants.

Fasciotomy, particularly in the setting of
prolonged ischemia, remains an important
adjunct in the management of extremity vas-
cular injury. Elevated compartment pressure
is a sufficient indication to proceed with fas-
ciotomy, even before arterial repair. If normal
pressures are obtained, eventual reperfusion
edema and subsequent swelling may occur
with delayed compartment syndrome. Thus,
continuous or intermittent compartment
pressure monitoring may be necessary in the
postoperative period. Lack of a timely fas-
ciotomy remains the most common error
leading to preventable limb loss following
vascular trauma.

Frequent postoperative physical examina-
tions of the extremity with vascular repair
are essential. Any deterioration in the exam-
ination must be investigated. Loss of a pal-
pable pulse is an absolute indication for
re-exploration. Early and prompt return to
the operating room when thrombosis is

■ FIGURE 19-4

Extensive tissue destruction of the lower extremity in a man struck and rolled over by a bus. A, Right
leg neurovascular disruption was complete and there were fractures at multiple levels. B, The left
leg was similarly fractured but neurovascular function was normal. The right leg was amputated
right below the knee and external fixation device was placed immediately. Recovery was rapid and
functional outcome was acceptable. ■

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19 • EXTREMITY VASCULAR TRAUMA

359

suspected is the best way to ensure successful

limb salvage.

SUBCLAVIAN ARTERY INJURIES

The initial evaluation and management of
peripheral vascular trauma is summarized in
Table 19-2.

TABLE 19-2

SUMMARY OF THE MANAGEMENT OF
PERIPHERAL VASCULAR TRAUMA

1. Perform thorough clinical evaluation; formal
arteriography (uncommon).

2. Administer preoperative broad-spectrum
antibiotics.

3. Consider systemic heparinization for an isolated
vascular injury without any possibility of cavitary
hemorrhage.

4. Prepare and drape to allow harvesting of
autologous conduit.

5. Achieve proximal and distal control before direct
investigation of the injury.

6. Perform proximal and distal catheter
thrombectomy; proximal and distal infusion of
heparin.

7. Achieve complete debridement of damaged
vessel.

8. Cover vascular anastomoses with viable tissue.

9. Consider fasciotomy for elevated compartment
pressures or prolonged ischemia.

10. Monitor frequently during the postoperative
period.

Surgical Anatomy

The right subclavian artery originates from the
innominate artery and passes through the base
of the neck behind the sternoclavicular joint.
The left arises from the aortic arch and follows
a similar course (Fig. 19-5). Anomalies of
the subclavian arteries are rare. The most
common anomaly is a right subclavian origi-
nating from the descending aorta as the
most distal branch of the aortic arch and
passing posterior to the esophagus. This is
thought to occur in approximately 1% of the
population.

The subclavian artery has three parts based
on its relationship to the anterior scalene
muscle (Fig. 19-6); first or proximal (proxi-
mal to the muscle), second or middle (pos-
terior to the muscle) , and third or distal (from
the lateral border of the muscle to the lateral
border of the first rib) .

The first or proximal part gives off three
branches (vertebral, internal mammary, and
thyrocervical trunk) close to its termination
near the anterior scalene muscle. The proxi-
mal part of the first portion is free of branches
for 1 to 3 cm. Several important structures are

Inf. thyroid a
Trans, cervical a
Suprascapular a.

Dorsal
scapular a

Thyrocervic
Int. thorac
Vertebral
Right common carot

Brachiocephalii
(innominate a.

Scalenus medius m.
Scalenus anticus m.

Costocervical trunk
Left subclavian a.

Left common carotid a.

■ FIGURE 19-5

Anterior view of subclavian artery with branches of the subclavian artery arising from the right
side. ■

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360

IV • SPECIFIC VASCULAR INJURIES

■ FIGURE 19-6

The right lateral view of the
subclavian artery illustrating the
branches of the subclavian
artery with potential collateral
anastomoses. ■

Scalenus
anticus m

Scalenus
medius m

Costocervical
trunk

Dorsal
scapular a

Vertebral a.

Thyrocervical
trunk

Int. thoracic a.

related to the first portion: The phrenic and
vagus nerves cross anteriorly, the internal
jugular-subclavian vein confluence passes
anteriorly, and the cervical dome of the
pleura is located inferiorly. On both sides, the
venous confluence will contain the termina-
tion of lymphatic channels, which are often
multiple. On the left, the thoracic duct is easily
injured during retraction.

The second portion usually contains one
or two branches (costocervical trunk and
dorsal scapular) and is related closely to the
brachial plexus. The third portion contains
no branches and is closely related to the
plexus.

The branches of the subclavian artery
provide such a rich collateral network that
interruption of flow at any of the three parts
rarely produces limb-threatening ischemia
(Fig. 19-7). However, adjacent soft tissue
destruction can disrupt these collaterals and
threaten limb viability in the presence of sub-
clavian artery thrombosis.

Epidemiology and Etiology

Subclavian artery injuries are uncommon
and represent fewer than 5% of all arterial
injuries noted in most civilian and military
series (Rich and Spencer, 1978). This is

because the subclavian artery is relatively short,
is well protected by the sternum, clavicle, and
first rib, and when partially lacerated, can
produce rapid exsanguination and death in
the field before patients receive medical
attention.

A blunt mechanism of injury can produce
several types of subclavian artery injury:
avulsion of branches (producing significant
hemorrhage); contusion with intimal dis-
ruption and prolapse (producing thrombo-
sis); puncture or laceration from shards of
bone from either the clavicle or first rib (pro-
ducing hemorrhage); or severe stretching
producing complete separation of intima
and media with adventitia intact or disrupted
(producing hemorrhage, thrombosis, or
pseudoaneurysm). Recent civilian series
document a blunt mechanism of injury as high
as 45%.

Clinical Features and Diagnosis

Approximately 50% of patients with subcla-
vian artery injuries present to the hospital in
shock. The classic signs of advanced ischemia
(pulselessness, pallor, paresthesias, poikilo-
thermia, and paralysis) may be present but
are not common because of the substantial
collateral circulation available. Associated

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19 • EXTREMITY VASCULAR TRAUMA 361

Transverse cervical

Descending branch
of transverse cervical

Transverse scapular

Thoracoacromial

■4 Subclavian

Scapular
circumflex

Lateral thoracic

Subscapular

L Ascending branch of
profunda brachii
"-Brachial

mammary

■ FIGURE 19-7

Collateral circulation in the shoulder
region. Important collateral vessels
are the thoracoacromial, lateral
thoracic, subscapular, and anterior
and posterior humeral circumflex
arteries. (From Levin PM, Rich NM,
Hutton JE Jr: Collateral circulation in
arterial injuries. Arch Surg
1971;102:392-399.) ■

injuries to the chest wall, lung, and brachial
plexus are common.

The diagnosis may be obvious when a
patient presents with a penetrating wound at
the base of the neck or in the supraclavicular
fossa combined with loss of the ipsilateral
pulse. If these patients are in shock that is unre-
sponsive to volume resuscitation, they must
be taken to the operating room for control of
hemorrhage. However, if patients are stable
or stabilize with resuscitation, arteriography
is extremely useful to plan the operative
approach. The arteriogram can elucidate the
portion of the artery that has been injured
and allow the surgeon to determine the safest
exposure for obtaining proximal control. A
chest roentgenogram is also useful. In pene-
trating injuries, the entrance and exit wounds
should be marked with radiopaque material
before obtaining an x-ray film. In blunt
injuries, the chestx-ray film can provide infor-
mation about the mediastinum and unsus-
pected fractures of the ribs or clavicle.

Surgical Treatment

Surgical exposure of a subclavian artery injury
can be quite difficult because the clavicle and

sternum obstruct a direct route to the artery.
In addition, the area of the subclavian con-
tains many important anatomic structures
that can be injured in the haste to obtain
control. Surgical management of the injury
is difficult because the subclavian is not a
muscular or thick-walled artery and is intol-
erant of heavy-handed traction or imprecise
suturing.

The second and third portions of the
subclavian artery can be exposed through a
supraclavicular incision. On the right, the first
portion is best exposed through a median ster-
notomy. On the left, the first portion can be
exposed through either a median sternotomy
or a left anterolateral thoracotomy. For the
first portion on the left, we recommend the
thoracotomy approach because it is much
easier.

The location of the injury, the condition of
the wound, and the condition of the patient
determine the best approach. For patients in
shock or those with a massive hematoma of
the neck or chest wall, proximal control of
the first portion of the subclavian is the safest
approach (even if the injury is in the third
portion) . Thoracotomy or sternotomy in an
uninjured field allows rapid proximal control
and can be lifesaving. For patients with an

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362

IV • SPECIFIC VASCULAR INJURIES

injury to the third portion who are stable, the
artery can be approached through a supra-
clavicular incision. If uncontrollable bleeding
is encountered, the wound should be packed
and control should be obtained as discussed
earlier. If it appears that the bleeding or the
wound is directly behind the clavicle, the clav-
icle can be resected (completely or in part)
without significant long-term morbidity. For
all of these reasons, we recommend prepar-
ing and draping a wide field to include the
neck to the mastoid process superiorly, along
the trapezius to the deltoid, the entire ipsi-
lateral arm (extended on a board) , and the
entire chest. The arm should be supported
on a board but be mobile. The draping should
allow space for one operator to be positioned
cephalad to the arm support and one opera-
tor to be positioned caudad to the arm
support.

The operation follows general guidelines
specified previously and elsewhere (Shackford
and Rich, 2001). Following debridement,
catheter thrombectomy, and regional
heparinization, the subclavian should be
carefully inspected. Mobilization of the ends
to attempt an end-to-end anastomosis is rea-
sonable if no major branches are divided to
achieve the mobilization. We recommend
interposition grafting rather than attempting
an end-to-end anastomosis with any tension.
If tension exists, the anastomosis may tear

because the artery, by nature, is thin and
nonmuscular. Although experience with pros-
thetic material for interposition grafting of the
subclavian is extensive, the first choice for a
conduit should be autologous proximal saphe-
nous vein. We have found the size match
of the proximal to be reasonable for short
segment bypasses in both males and females.
Prosthetic material is certainly acceptable
when either no available suitable vein exists
or the patient's condition is such that pro-
longation of the operation to harvest a conduit
may jeopardize outcome.

Recent series have documented that most
injuries are treated with primary repair (42% ) ,
followed by interposition grafting with autol-
ogousvein (Table 19-3) .Another alternative,
when the patient is unstable, is ligation. As
previously described, the collateral circulation
around the shoulder and neck is extensive and
ligation of the subclavian artery is rarely asso-
ciated with limb loss.

Results

Many reports document experience with sub-
clavian artery injuries, but only a precious
few document immediate, short-term, or
long-term outcome. When outcome is
reported, it is usually immediate or short term
and focuses either on survival, on the patency

TABLE 19-3

SURGICAL TECHNIQUES USED FOR MANAGEMENT OF UPPER EXTREMITY
VASCULAR INJURY: SELECTED REVIEW OF THE RECENT LITERATURE*

Artery

Series*

Years*

None

(%)"

Primary
(%)'

ASV

(%r

Prosthetic

Ligate

(%)**

Subclavian

1988-2000

378

32 (8.5)

160(42.3)

128(33.8)

47 (12.4)

11(3)

Axillary

1982-1998

126

59 (46.8)

42 (33.3)

20(15.8)

5(4.1)

Brachial

1984-1994

223

5(2.2)

121 (54.3)

87 (39)

3(4.5)

Radial/ulnar

1984-1994

251

3(1.1)

161 (64.2)

30(11.9)

57(22.8)

'References available on request.

+ Number of published articles reviewed.

*Years covered by the aggregated publications.

§ l\lumber of patients.

"No repair or exploration undertaken.

"Either vein patch, end to end anastomosis or arteriography.

"Saphenous vein interposition.

^Prosthetic graft interposition.

**Ligation, no repair.

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19 • EXTREMITY VASCULAR TRAUMA

363

of the repair, or on limb salvage. Unfortu-
nately, these outcome measures lack relevance
because survival is rarely dependent solely on
repair of the subclavian artery injury and
thrombosis of the arterial repair rarely results
in amputation of the upper extremity because
of its abundant collateral circulation. Rather,
long-term outcome is determined primarily
by the neurologic function and secondarily
by the orthopedic outcome (Hardin and col-
leagues, 1985).

Mortality rates are highly variable after
subclavian artery injury because when death
occurs, it is usually because of associated
injuries. However, rare cases of death result-
ing from uncontrolled hemorrhage from
subclavian arterial lacerations that either go
unnoticed or undergo attempted repair
without proximal control have been reported.

Amputation is rare following subclavian
injuries and is usually a result of devastating
soft tissue loss, multiple arterial injuries, infec-
tion (primarily intractable osteomyelitis), or
severe neurologic injury with "flail arm" (see
"Scapulothoracic Dissociation," later in this
chapter) . Graft infection (either of prosthetic
material or vein) is uncommon and can be
treated by ligation and extra-anatomic bypass
(either carotid-subclavian or axilloaxillary)
if either claudication or limb-threatening
ischemia develops.

Complete resolution of infection, swelling,
pain, and neurologic deficit and complete
healing of all wounds define a good outcome

following upper extremity vascular injury
(Hardin and colleagues, 1985). When pa-
tients with scapulothoracic dissociation are
included, the long-term outcome following
subclavian artery injury is dismal, and only
30% of patients have a good outcome (Table
19-4) . Excluding those with scapulothoracic
dissociation improves the good outcome
to about 40%, with the balance of patients
having persistent disability due to nerve
injury, osteomyelitis, or causalgia.

Management of
Scapulothoracic Dissociation

Scapulothoracic dissociation is a devastating
injury of the upper extremity and shoulder
girdle caused by blunt injury. The mechanism
is stretch and avulsion of the vascular and neu-
rologic elements of the arm from their more
proximal origins in the shoulder and neck
regions. Substantial separation and/or frac-
ture of the musculoskeletal attachments of the
shoulder girdle can occur. Scapulothoracic dis-
sociation is a rare injury, with only 52 patients
reported in the literature (Sampson and
colleagues, 1993). On physical examination,
there is absence of the radial pulse associated
with a significant shoulder or chest wall
hematoma and absence of sensory or motor
function below the shoulder. Chest radiogra-
phy will demonstrate a laterally displaced
scapula (with acromioclavicular disruption

TABLE 19-4

OUTCOME FOLLOWING REPAIR OF UPPER EXTREMITY VASCULAR INJURY:
SELECTED REVIEW OF THE RECENT LITERATURE*

Artery

Series 1

Years*

N §

Die (%)"

AMP (%)' ABNML (%)*

NML (%)*

Subclavian

1984-1993

103

17 (16.5)

6 (5.8)

45 (43.6)

35(34.1)

Axillary

1982-1990

2(2.2)

1(1.1)

66(71.7)

23 (25)

Braohia

1984-1994

146

1 (0.6)

5(3.4)

42 (28.7)

98 (67.3)

Radial/ulnar

1984-1994

211

1 (0.5)

7 (3.5)

74 (35)

129(61)

'References available on request.

+ Number of published articles reviewed.

*Years covered by the aggregated publications.

§ Number of patients.

"Death.

"Amputation.

"Abnormal function (see text) does not include amputations.

^Normal function (see text).

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364

IV • SPECIFIC VASCULAR INJURIES

and increased distance between the distal
end of the clavicle and the acromion). An
associated displaced clavicle fracture or a
sternoclavicular disruption is often present
(Sampson and colleagues, 1993). Unfortu-
nately, the outcome is uniformly poor because
of the neurologic disruption, not the arterial
injury. Our experience and that of Sampson
and colleagues (1993) suggest that delayed
hemorrhage or limb-threatening ischemia
is very rare and there are no benefits to
revascularization. In the rare patient who is
actively bleeding, we recommend ligation. In
the infrequent patient with limb-threatening
ischemia, primary amputation should be
considered.

AXILLARY ARTERY INJURIES

Surgical Anatomy

The axillary artery begins at the lateral margin
of the first rib and ends at the lateral margin

of the teres major muscle. Three parts are
dependent on their relationship to the pec-
toralis minor muscle (Fig. 19-8) : proximal to
the muscle (first) and beneath (second) and
distal to the muscle (third) . The first part has
one branch (superior thoracic), the second
has two (thoracoacromial, lateral thoracic),
and the third has three (anterior and poste-
rior circumflex, subscapular) . These branches
provide a rich collateral circulation to this
region.

The axillary vein lies anterior and slightly
inferior to the axillary artery. Close proxim-
ity to the artery provides the anatomic basis
for the development of an arteriovenous
fistula following relatively minor trauma (e.g.,
arterial cannulation) . A similar close rela-
tionship exists to branches of the brachial
plexus (Fig. 19-9). Proximally, the plexus is
posterior/lateral to the artery. Distally, the
three cords of the plexus surround the second
and third parts of the artery. This intimate
relationship explains the high incidence of
concomitant nerve injuries in axillary arter-
ial trauma.

Superior thoracic a.

Ant. circumflex
humeral a

Post, circumflex
humeral a.

Subscapular a

Thoracoacromial a.

Lat. thoracic a.

■ FIGURE 19-8

Surgical anatomy of the axillary artery with the usual configuration of six branches coming from the
three parts of the artery. ■

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19 • EXTREMITY VASCULAR TRAUMA

365

AXILLARY ARTERIAL INJURIES

Upper trunk
Middle trun
Lower trunk
Medial cord
Post, cord

Musculocutaneous n

Circumflex n

Radial n

"Median n.
^Ulnar n.
"Axillary v.

■ FIGURE 19-9

The close proximity of the brachial plexus to the cord adjacent to the second part of the axillary
artery and the branches surrounding the third part demonstrate why there is a high incidence of
concomitant nerve injuries with axillary arterial trauma, as shown above. ■

Epidemiology and Etiology

Axillary artery injuries are only slightly more
common than subclavian artery injuries and
represent 5% to 10% of all arterial injuries in
most military and civilian injuries (Rich and
Spencer, 1978). More than 95% of axillary
artery injuries are from penetrating trauma.
Included in this group are patients with iatro-
genic injury following cannulation of the
artery for arterial pressure monitoring or con-
trast studies. Although blunt injuries are rare,
two types merit consideration. The first is
rupture, contusion, or stretching of the artery
following fracture of the proximal humerus
or anterior dislocation of the shoulder.
Approximately 1 % of shoulder dislocations
are associated with axillary artery injury
(Sparks and colleagues, 2000) . The second is
thrombosis following chronic repetitive
impingement by crutch use.

Clinical Features and Diagnosis

Patients with axillary artery injury commonly
present with regional signs and symptoms,

such as a pulse deficit, advanced ischemia, pul-
satile bleeding, or an expanding hematoma.
Shock solely due to an axillary artery injury
is rare. The most common associated injury
is vascular (axillary vein) followed very closely
by nerve (cords or branches of the brachial
plexus) .

The diagnosis of an axillary artery injury
should be suspected in a patient with a
penetrating wound of the axilla, a palpable
subclavian pulse (detected by palpation in the
supraclavicular fossa) , but no distal pulses. If
evidence of advanced ischemia is present, the
patient should be taken immediately to the
operating room.

Occasionally, a patient with a penetrating
injury near the axilla will present with a pal-
pable radial pulse and a thrill or bruit in the
region of the injury. An arteriovenous fistula
should be the primary consideration and
formal arteriography should be performed.
Formal arteriography can provide needed
diagnostic information and, if performed
by qualified and experienced angiographers,
can afford a potential opportunity for
endoluminal treatment (see Chapters 9
and 10).

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IV • SPECIFIC VASCULAR INJURIES

Surgical Treatment

Anticipate proximal control before entering
the site of the injury by preparing the site to
include all of the shoulder, ipsilateral neck
and supraclavicular fossa (to allow for expo-
sure of the subclavian artery) , the arm and
hand to the fingertips (to allow intraopera-
tive palpation of the radial pulse) , and the
contralateral leg (to allow a separate team to
harvest) for a conduit (Fig. 19-10). The arm
should be supported on a board but be mobile.
The draping should allow space for one oper-
ator to be positioned cephalad to the arm

■ FIGURE 19-10

Preparing for surgery. Note that the entire arm
is being prepared as well as the ipsilateral neck
and chest. We prefer to drape the contralateral
proximal thigh for a conduit as this allows a
second team to harvest the proximal
saphenous vein, while the primary team obtains
proximal control. The drapes should be placed
in such a way as to allow an assistant to stand
in the area cephalad to the shoulder and the
arm. ■

support and one operator to be positioned
caudad to the arm support.

Exposure of the proximal axillary artery is
best obtained by an infraclavicular incision,
made approximately one fingerbreadth below
and parallel to the clavicle. This proximal
exposure is recommended for all cases of axil-
lary artery trauma (Graham and colleagues,
1982) because injuries that are more distal are
often associated with significant hematoma
(Fig. 19-11). Obtaining control of an axillary

■ FIGURE 19-11

A, Close range shotgun wound to the anterior
axilla. Notice the large hematoma causing
significant swelling of the anterior chest
wall, axilla, and deltoid region of the arm.

B, Intraoperative photo from same perspective
(patient's head is located toward the right side
of this picture) demonstrating the infraclavicular
incision and exposure of the injury through a
second incision. After proximal control was first
obtained through the infraclavicular incision
(note the vascular clamp in the wound), the
hematoma was opened and evacuated,
allowing better visualization of the injury and
avoidance of iatrogenic trauma to the brachial
plexus. ■

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19 • EXTREMITY VASCULAR TRAUMA

367

arterial injury in the midst of a large
hematoma is fraught with problems that
inevitably lead to increased blood loss and pos-
sibly to an iatrogenic brachial plexus injury.
The infraclavicular incision can be extended
into the axilla and both the pectoralis minor
and the major tendons can be divided, if nec-
essary, to obtain distal control.

Conduct of the operation follows general
guidelines specified previously and elsewhere
(Shackford and Rich, 2001). Clamps should
never be blindly placed near the axillary artery
because its intimate relationship to the axil-
lary vein and to the brachial plexus mandate
precise clamp placement. In the event that
uncontrolled bleeding exists, tamponade can
be obtained by gentle finger compression or,
if the lumen can be visualized, insertion of a
balloon tipped catheter followed by careful
balloon expansion.

Following debridement, catheter thrombec-
tomy, and regional heparinization, the axil-
lary artery should be carefully inspected.
Mobilization of the ends to attempt an end-
to-end anastomosis is reasonable if no major
branches are divided to achieve the mobi-
lization. Recent series have documented that
most injuries are treated with primary repair
(47%) followed by interposition grafting with
autologous conduit (33%, see Table 19-3).
We recommend interposition grafting with
autologous proximal saphenous vein rather
than attempting an end-to-end anastomosis
with any tension. Ligation of the axillary artery
is acceptable (there is a rich collateral circu-
lation) in patients who are moribund and phys-
iologically unstable, but this is not encouraged.
Rather, if both ends of the artery can be
visualized, a temporary intravascular shunt
can be placed and the wound packed, towel
clipped or stapled until the patient has stabi-
lized. These shunts can be left in place several
days without systemic anticoagulation
(Granchi and colleagues, 2000).

Results

Similar to the literature describing treatment
results of subclavian artery injuries, only a few
reports document the outcome of axillary
artery repair. When outcome is reported, it is

usually immediate or short-term and focused
on survival, the patency of the repair or limb
salvage. Unfortunately, these outcome mea-
sures lack relevance because survival is rarely
dependent solely on repair of the axillary
artery injury and thrombosis of the arterial
repair rarely results in amputation of the upper
extremity because of the abundant collateral
circulation in the shoulder and arm. Rather,
long-term outcome is determined primarily
by the neurologic function and secondarily
by the orthopedic outcome (Hardin and
colleagues, 1985).

Mortality and amputation are rare fol-
lowing axillary artery injury (see Table 19-4) .
A good outcome following axillary repair
(as determined by complete resolution of
swelling, pain and neurologic deficit) is rare
because axillary artery injury is often accom-
panied by nerve injury, which ultimately
leads to long-term neuralgia or causalgia. In
four recently published series of axillary
artery injuries in which follow-up was docu-
mented for 92 patients, only 23 (25%) had
a good outcome (see Table 19-4) . The other
66 patients had neurologic dysfunction,
post-traumatic neuralgia producing dis-
ability, or diminished use because of chronic
pain associated with osseus or soft tissue
injury.

BRACHIAL ARTERY INJURIES

Surgical Anatomy

The brachial artery is a continuation of the
axillary artery and begins at the lower border
of the teres major muscle. Exiting the axilla,
the brachial artery is a relatively superficial
structure covered only by skin, subcutaneous
tissue, and deep fascia. Proximally, it lies
medial to the humerus and is accompanied
by the median nerve (superiorly and laterally)
and the ulnar and radial nerves (medially) .
Distally, it lies anterior to the elbow and is
crossed by the median nerve, which then lies
medial to the artery. Just proximal to the
elbow, the ulnar nerve is posterior to the artery
as it goes behind the medial epicondyle of the
ulna. The brachial artery terminates 1 inch

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368

IV • SPECIFIC VASCULAR INJURIES

below the elbow skin crease where it divides
into the radial and ulnar arteries.

The brachial artery has three main branches
(Fig. 19-12). The first (most proximal) is the
profunda brachii, which accompanied by
the radial nerve passes posteriorly between
the medial and long head of the triceps
muscle. The profunda brachii provides an
important collateral anastomosis with the axil-
lary artery through its posterior circumflex
humeral branch. The profunda also has a col-
lateral anastomosis with the radial recurrent
artery. The second main branch of the brachial
artery is the superior ulnar collateral, which
accompanied by the ulnar nerve passes behind
the medial epicondyle to provide a collateral
anastomosis with the posterior ulnar

recurrent. The third (most distal) main
branch is the inferior ulnar collateral, which
provides a rich anastomotic collateral network
around the elbow with the ulnar artery
through its anterior recurrent branch.

Epidemiology and Etiology

Brachial artery injury is the most commonly
reported arterial injury of the upper extrem-
ity. In large military and civilian series, brachial
artery injury constitutes 15% to 30% of all
peripheral arterial injuries. The reason for this
relatively high frequency is that the brachial
artery is relatively long, superficial, and
exposed as compared to other peripheral

Radial n

Median n

Ulnar n.

■ FIGURE 19-12

The brachial artery is a continuation of the axillary artery at the lower border of the teres major
muscle. It terminates approximately 1 inch below the transverse skin crease in the antecubital
fossa, where it divides into two branches. Important anatomic relationships include three associated
nerves, three associated veins, and three main branches with the brachial artery lying successively
on three muscles. ■

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19 • EXTREMITY VASCULAR TRAUMA

369

arteries. Furthermore, the upper extremity is
often used as a lever, hammer, and weapon,
as well as a protective or restraining device for
the torso, all of which put the brachial artery
in harm's way.

Penetrating trauma is the most common
cause of brachial artery injury. Recently, the
increase in the number of diagnostic cardiac
catheterizations has resulted in an increase
in the number of brachial artery injuries
seen at most tertiary medical centers. Blunt
injury of the brachial artery is much less
common but deserves emphasis because it can
easily be overlooked unless there is a high
index of suspicion. Supracondylar fracture
of the humerus, particularly with anterior
displacement or elbow dislocation (Endean
and colleagues, 1992), should alert the
clinician to the possibility of a brachial artery
injury.

Clinical Features and Diagnosis

Patients with brachial artery injuries classically
present with a cool, painful hand, no radial
pulse, and diminished sensory and motor
function of the forearm and hand. The classic
findings, however, are not always present.
Patients may have a complete thrombosis of
the brachial artery and loss of a palpable radial
pulse but have a warm hand without neuro-
logic dysfunction. Conversely, the patient
may have a laceration of the brachial artery
and have a palpable radial pulse. If symptoms
of ischemia associated with "hard" signs
are present, the diagnosis is not certain. In
patients with a supracondylar fracture or an
elbow dislocation where doubt about the diag-
nosis exists (diminished or absent pulse, but
a warm, pink hand) , arteriography is indi-
cated. In patients with closed blunt trauma
and primarily neurologic signs and symptoms
who have a warm pink hand and a palpable
radial pulse, plethysmography and segmen-
tal pressure determination can avoid a need-
less arteriogram.

Careful physical examination and com-
prehensive documentation of the pulses and
neurologic findings are essential, particularly
in patients who are to undergo operative
exploration. This point cannot be overem-

phasized in patients with brachial artery
injuries who have peripheral neurologic
deficits before operation. Lack of documen-
tation of the preoperative neurologic status
leads to the assumption that the deficits arose
out of some operative misadventure.

Surgical Treatment

Bleeding can be controlled by proximal com-
pression against the humerus or by direct pres-
sure over an open wound. Blindly attempting
to clamp a bleeding vessel in the arm is never
necessary and is fraught with the hazard of
significant injury to the median, radial, or
ulnar nerve.

For suspected proximal injury, prepare and
drape the patient similar to that used to
manage an axillary artery injury (see previ-
ous discussion). For injuries that are more
distal, prepare the arm and hand to the fin-
gertips (to allow intraoperative palpation of
the radial pulse) and a leg (to allow a sepa-
rate team to harvest) for a conduit. The arm
should be supported on a board but be mobile.
The draping should allow space for one oper-
ator to be positioned cephalad to the arm
support and one operator to be positioned
caudad to the arm support.

Exposure of the brachial artery is best
obtained by a longitudinal incision in the pal-
pable groove between the triceps and biceps
muscle along the medial aspect of the arm.
This incision can be extended distally across
the antecubital fossa or proximally across
the axilla with an 5-shaped curve (Fig. 19-13) .
No matter where the exposure is obtained
(proximally or distally), precise dissection
and careful handing of all structures are
mandatory. Careless dissection or heavy-
handed retraction may result in injury to the
associated nerve (particularly the median
nerve) .

Conduct of the operation follows general
guidelines specified previously and elsewhere
(Shackford and Rich, 2001). Following
debridement, catheter thrombectomy, and
regional heparinization, the brachial artery
should be carefully inspected. Small lateral
injuries, particularly those associated with
iatrogenic injuries, may be reapproximated

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IV • SPECIFIC VASCULAR INJURIES

Retracted biceps m

Cut bicipital
aponeuros

Cephalic v.-
Radial a

Cut median
cubital v.

F /

I Li — Ulnar

Median n.

Retracted pronator
teres m.

■ FIGURE 19-13

Surgical exposure of the brachial artery is rapidly obtained by a longitudinal incision along the
course of the artery with an extension as an S curve either across the axilla proximally or across the
antecubital fossa distally as needed. The median nerve and basilic veins are in close proximity to
the artery. ■

with simple interrupted sutures placed in the
same axis as the direction of the artery so no
luminal compromise occurs. If more than two
or three sutures are required, a vein patch is
a better alternative because the artery is easily
narrowed. Our preference for most injuries
is excision of the area of injury and either an
end-to-end anastomosis (performed with
interrupted sutures and with the ends of the
vessel distracted for placement of all sutures)
or an interposition autologous saphenous vein
graft. Recent civilian series support this

approach, with the majority of the repairs
being either primary end-to-end or interpo-
sition vein grafting (see Table 19-3). If asso-
ciated orthopedic injuries are present, our
preference is to place an indwelling tempo-
rary shunt in the artery and let the orthope-
dic surgeons achieve length and stability of
the arm before attempting definitive vascular
repair. Ligation should never be a considera-
tion because it carries a significant risk of
amputation. If the patient is in extremis from
other associated injuries, an indwelling

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19 • EXTREMITY VASCULAR TRAUMA

371

temporary shunt can be placed quickly and
left in place for several days without systemic
heparinization.

Results

Amputation or death is rare following brachial
artery repair. Long-term outcome following
brachial artery repair is decidedly better than
either subclavian or axillary artery injuries
because the incidence of associated nerve
injury is much less. In recent civilian series
(see Table 19-4), a good outcome (as deter-
mined by complete resolution of swelling,
pain, and neurologic deficit) was achieved in
almost 70% of patients. If patients develop
symptoms of arm claudication on follow-up,
they should undergo noninvasive vascular
testing to include plethysmography, segmen-
tal pressure determination, and duplex of the
area of injury. If stenosis or occlusion is
evident, the patients should have diagnostic
arteriography for possible endoluminal or
open revision.

RADIAL AND ULNAR
ARTERY INJURY

Surgical Anatomy

After the brachial artery crosses through the
cubital fossa, it bifurcates into the radial and
ulnar artery. The ulnar artery is the larger of
the two, but this size discrepancy exists only
in the proximal portion of the artery. Two
branches immediately arise from the proxi-
mal ulnar artery: the anterior and posterior
ulnar recurrent arteries that form collateral
anastomoses with the brachial artery around
the anterior and posterior aspects of the elbow,
respectively. The common interosseus also
arises from the proximal ulnar artery (Fig.
19-14) and passes laterally and posteriorly
toward the interosseus membrane where, at
the superior edge of the membrane, it divides
into the volar (anterior) and dorsal (poste-
rior) interosseus arteries. The dorsal
interosseus gives rise in its proximal portion
to the interosseus recurrent, which forms a

collateral anastomosis with branches of the
brachial artery. The ulnar artery terminates
in the superficial or volar palmar arch. In its
oblique proximal portion, it is crossed by the
pronator teres and by the median nerve. The
ulnar nerve joins the artery in its distal third
(Fig. 19-15).

The radial artery is unique in that no muscle
or nerve crosses it in its relatively direct course
to the wrist. The only major branch of the
radial artery is the radial recurrent, which
passes under the brachioradialis muscle to pass
proximally and form a collateral anastomosis
with branches of the profunda brachii. The
radial artery gives a small branch to the super-
ficial arch but terminates in the deep palmar
arch.

Epidemiology and Etiology

Arterial injuries of the forearm are often
reported in recent series describing vascular
injuries and now make up between 5% and
30% of the total peripheral vascular injuries.
Approximately 95% are due to penetrating
trauma. A relatively rare form of ulnar artery
injury occurs in individuals with a history of
repeatedly using their hypothenar eminence
as a hammer. It is thought that the repeated
trauma can produce aneurysmal dilatation,
distal embolization, or thrombosis.

Clinical Features and Diagnosis

Complete interruption of either the radial or
the ulnar artery will often have no adverse
effect on the circulation of the forearm or
hand because of the rich collateral circula-
tion. Signs of advanced ischemia warrant
surgical exploration or operating room
arteriography. If doubt exists about the
integrity of the circulation and the condition
of the patient and the condition of the arm
permit, formal arteriography with magnifi-
cation views of the hand are helpful for
diagnosis and the planning of operative
management.

Puncture wounds of the forearm can be
quite insidious because the small skin wound
will not allow sufficient egress of venous or

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IV • SPECIFIC VASCULAR INJURIES

Brachial a.
Radial collateral a.

Mid. collateral a.— V

Trans, branch inf.
ulnar collateral a.

Radial recurrent a

Interosseous
recurrent a.

Radial a.

Volar interosseous a

Superf. volar
branch radial a.

Superior ulnar
collateral a.

Inf. ulnar collateral a.

Ant. branch inf.
ulnar collateral a.

Post, ulnar recurrent a.
Ant. ulnar recurrent a.

Interosseous a.

Ulnar a.

Dorsal interosseous a.

Superf. & deep
branches ulnar a.

■ FIGURE 19-14

As the brachial artery divides into the radial artery (its more direct continuation) and the ulnar artery
(the larger of the two branches) in the forearm, there are important collateral branches, which help
form the rich anastomosis around the elbow. The common interosseus is also an important branch
of the ulnar artery. ■

arterial blood, which can accumulate in
significant quantity in the subcutaneous and
subfascial planes to produce a forearm com-
partment syndrome. Physical signs that should
alert the examiner to the possibility of an
expanding hematoma include marked tension
in the dorsal or volar forearm, superficial
venous engorgement, paresthesias in the
hand, or diminished sensation to light touch
in the fingers. Without fasciotomy, these
patients are at risk of developing a Volkmann
contracture.

Surgical Treatment

Control of hemorrhage from either the radial
or the ulnar artery is easily achievable by direct

pressure. Tourniquets or blind clamping in
an open wound is not warranted. Prepare the
arm and hand to the fingertips (to allow intra-
operative palpation of the radial pulse) and
a leg (to allow a separate team to harvest) for
a conduit. The arm should be supported on
a board but be mobile. The draping should
allow space for one operator to be positioned
cephalad to the arm support and one opera-
tor to be positioned caudad to the arm
support.

Exposure of the proximal portions of both
arteries can be accomplished through an
5-shaped incision in the cubital fossa (Fig.
19-16). The distal arteries can be exposed
through longitudinal incisions over the course
of the artery just proximal to the hand.
Conduct of the operation follows general

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19 • EXTREMITY VASCULAR TRAUMA

373

Brachioradialis m
Radial n
Brachial a
Bicipital aponeurosis

Boon radial n. fl|«lL ^ ^ ' '

Brachioradialis m.-HW ' !,' v/pi'Km

Pronator teres m

Superf. radia

Radial a. 41

Flexor pollicis Ml
longus m

ceps m. (medial
termuscular septum)
Median n.
Brachialis m.

Pronator teres m.

Flexor carpi radialis m.
Common interosseous a.

Flexor digitorum
sublimis m.
Inar a.

Abductor pollicis
longus m.

Median i

IS* : •

is , M> 'ii\l ' \-Flexor carpi ulnaris m

"'Wltlli. \Z -P^UInarn.

M '■ W

' V lit

■ I n It

Flexor carpi radialis t

r lexor digitorum
Drofundus m.

Dorsal cutaneous
branch ulnar n.
#-Flexor digitorum
f superficialis tt.

Palmaris longus t.
Ulnar a. & n.
Palmar carpal lig.

■ FIGURE 19-15

The relationship of the radial and ulnar arteries to the important nerves, major muscle groups, and
tendons. Particularly note the crossing of the proximal ulnar artery by the median nerve and the
close approximation of the ulnar nerve to the distal two thirds of the ulnar artery. The cross section
through the upper third of the forearm emphasizes the relatively deep location of the ulnar artery
compared with the more superficial radial artery. ■

guidelines specified previously and elsewhere
(Shackford and Rich, 2001). Following
debridement, catheter thrombectomy, and
regional heparinization, the area of injury
should be carefully inspected. If both arter-
ies are injured, repair of the ulnar is less tech-
nically taxing because of its relatively larger
size. If only one artery is injured and no sign
of ischemia is seen in the hand (as docu-
mented by a comprehensive physical exami-
nation and confirmed by Doppler signals in
the palmar arch and digits), ligation is rea-
sonable (Johnson, Ford andjohansen, 1993) .
For small "clean" lacerations or puncture
wounds, lateral suture repair may suffice. More
severe lacerations will require resection and
end-to-end anastomosis, which is the most

common technique used in recent series (see
Table 19-3) . Reversed autologous saphenous
vein from the distal leg can be used if signif-
icant arterial debridement is required or when
an end-to-end anastomosis will create tension
on the suture line.

Results

Amputation is rare following radial or ulnar
artery injury. When amputation does occur,
it is often the result of massive soft tissue
destruction (with interruption of both the
radial and the ulnar arteries) associated with
sepsis or chronic osteomyelitis. Few studies
document adequate long-term follow-up.

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IV • SPECIFIC VASCULAR INJURIES

Ulnar a.

Ulnar n.

Flexor carpi ulnaris m.

■ FIGURE 19-16

Elective incisions that can be used for approach to the radial and ulnar arteries. A, An S-type
incision starting along the course of the distal brachial artery, carried through the antecubital fossa
and continued down on the forearm will give excellent exposure of the proximal ulnar and radial
arteries, as well as the origin of the common interosseous artery (A). An extension off this incision
(B) along the course of the radial artery can be used for exposure to the wrist level. A separate
incision can be used over the course of the ulnar artery (C). B, This drawing demonstrates
exposure of the ulnar neurovascular bundle within the deep muscle layers, which have been split
proximally. ■

Recent series with adequate documentation
of follow-up demonstrate good results (as
determined by complete resolution of
swelling, pain, and neurologic deficit) fol-
lowing radial or ulnar repair in 65% of
patients (see Table 19-4) . Poor results are not
related to the vascular repair, but to the asso-
ciated nerve or tendon injuries. In fact, in one
study, patency of the vascular repair when
only one artery (either radial or ulnar) was
injured was 50% (Johnson, Ford, and
Johansen, 1993) . Despite the high failure rate
of radial or ulnar repairs, no patients had
claudication.

VENOUS INJURIES OF THE
UPPER EXTREMITY

Injuries to the subclavian or axillary vein
should be repaired if the patient's condition
permits. In most cases, repair will consist of
lateral venorrhaphy or end-to-end anasto-
mosis. After appropriate debridement, when
a direct repair cannot be performed because
it will result in tension on the suture line or
will significantly narrow the vein, repair can
be accomplished with autologous vein patch,
interposition vein grafting, or a panel or

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19 • EXTREMITY VASCULAR TRAUMA

375

spiral graft made from autologous vein. Early
patency of these venous repairs is 50% to 90%
(Meyer and colleagues, 1987; Pappas and
colleagues, 1997), but long-term patency
approaches 100% because it appears that the
thrombus recanalizes and provides adequate
function (Nypaver and colleagues, 1992;
Pappas and colleagues, 1997). If the patient
is in extremis, ligation of the subclavian or
axillary vein is acceptable with minimal
long-term sequelae (Timberlake and Kerstein,
1995). If symptoms of venous claudication or
severe swelling develop during rehabilitation
or with the return of vigorous arm function,
a subclavian venous bypass using autologous
vein or ajugular venous "turn down"with tem-
porary distal arteriovenous fistula provides
satisfactory relief of symptoms.

COMPARTMENT SYNDROME
OF THE UPPER EXTREMITY

A compartment syndrome can develop in
either the upper arm (triceps, deltoid, or
along the axillary sheath) or the forearm. The
forearm compartment syndrome is more
common. Increased tissue pressure can follow
either blunt or penetrating trauma because
of hematoma, post-traumatic transudation of
serum into the interstitial space, venous
thrombosis, or reperfusion following ischemia
(Shackford and Rich, 2001). The possibility
of a compartment syndrome must always be
a consideration in a patient who has been
injured, particularly one with prolonged
ischemia before reperfusion.

The diagnosis of compartment syndrome
should be suspected in any patient com-
plaining of increasing pain following injury.
The physical findings include a tense com-
partment, pain on passive range of motion,
progressive loss of sensation, and weakness.
The loss of arterial pulses is a late finding,
which usually indicates a poor prognosis. Neu-
rologic signs and symptoms, while helpful, are
neither sensitive nor specific in the upper
extremity following arterial injury because
associated peripheral nerve injury often exists.
Early diagnosis must be predicated on mea-
surement of compartment pressures. The

normal tissue compartment pressure ranges
from to 9 mm Hg. Much controversy exists
about what constitutes a pathologic elevation.
Our approach has been to perform fas-
ciotomy when compartment pressure exceeds
30mmHg.

Treatment consists of complete fasciotomy
of the involved compartment. For the volar
compartment, the skin incision begins 1 cm
proximal and 2 cm lateral to the medial epi-
condyle. It is carried obliquely across the skin
crease at the antecubital fossa and continued
obliquely for the proximal part of the forearm.
It is then curved medially, reaching the
midline at thejunction of the middle and distal
third of the forearm, and is continued in a
straight line to the wrist crease at a point on
the medial side of the palmaris longus tendon.
The incision is then curved obliquely across
the wrist crease and terminated in the mid
palm. This allows routine decompression of
the carpal tunnel. A superficial fasciotomy
adequately decompresses the volar com-
partment in most cases. If any doubt exists
about adequate decompression, intraopera-
tive measurement of compartment pressures
should be performed. For the dorsal com-
partment, the incision begins 2 cm distal to
the lateral epicondyle. It is carried straight
distally in the midline for approximately 7 to
10 cm. The skin edges are undermined and
the dorsal fascia incised directly in line with
the skin incision.

POST-TRAUMATIC CAUSALGIA

Persistent pain following upper extremity vas-
cular injury is common due to associated
peripheral nerve injury and resultant trau-
matic neuralgia. Some patients may have pain
that appears to be sympathetically mediated,
but not all will have causalgia. Causalgia
(complex regional pain syndrome type 2)
occurs in about 3% of patients suffering
peripheral nerve injuries (Costa and Robbs,
1988) and is often confused with reflex sym-
pathetic dystrophy (complex regional pain
syndrome type 1). Several characteristics dis-
tinguish causalgia: a burning pain noted
within 24 hours of injury of a large mixed

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IV • SPECIFIC VASCULAR INJURIES

nerve with a pain distribution similar to that
of the nerve. Onset of reflex sympathetic
dystrophy usually occurs weeks to months
following the injury, is not always burning in
character, and has a distribution that does not
follow a specific anatomic distribution of a
mixed nerve in the extremity. Causalgia typ-
ically presents early and is associated with
hypalgesia in the area of the partial denerva-
tion followed by constant burning pain that
can be increased by nonpainful stimuli (allo-
dynia). Abnormal sympathetic function is
evident in the region (e.g., vasomotion or
hyperhidrosis) and the pain can be exagger-
ated by emotional upset.

The diagnosis should be suspected
when the aforementioned characteristics are
present. It can be confirmed by the relief
of symptoms with a sympathetic block (Costa
and Robbs, 1988). Some patients may
have resolution of the syndrome with a single
sympathetic block. For symptom recurrence,
surgical sympathectomy is the treatment of
choice.

LOWER EXTREMITY
VASCULAR INJURIES

Common Femoral and
Profunda Femoral Arteries

SURGICAL ANATOMY

The common femoral artery emerges from
under the inguinal ligament as a continua-
tion of the external iliac artery at the mid-
point between the anterosuperior iliac spine
and the pubic tubercle. It is relatively exposed
with only subcutaneous fat and lymphatic
tissue overlying. Along its course are three to
five branches of varying size and location. The
most prominent are the superficial circum-
flex iliac and the superficial epigastric, which
arise within 1 cm of the inguinal ligament.
Approximately 5 cm below the inguinal liga-
ment, the common femoral artery bifurcates
into the superficial femoral and profunda
femoral arteries.

The profunda femoral artery usually
originates as a single posterolateral branch.
However, more than one profunda branch
may be present. The lateral femoral circum-
flex vein crosses the profunda anteriorly and
transversely within 3 cm of its origin from
the common femoral artery. At this level,
the artery usually bifurcates into two large
branches, the medial and lateral circumflex
arteries. The proximity of the crossing vein
demands careful attention when exposing the
distal profunda.

Numerous collaterals come from the
branches of the hypogastric artery to the pro-
funda femoral artery but are usually not suf-
ficient to sustain adequate blood flow in the
presence of an acute occlusion of the common
femoral artery. The distal branches of the pro-
funda femoral artery provide collateral flow
to the popliteal artery through the lateral supe-
rior genicular artery and the descending
genicular artery. Following acute occlusion of
the superficial femoral artery, these collater-
als are not sufficient to sustain adequate blood
flow to the lower leg (Fig. 19-17).

The femoral nerve, composed predomi-
nantly of the motor fibers of the quadriceps,
traverses the femoral region along the lateral
aspect of the femoral sheath and can be
injured during exposure of the femoral vessels
if an inadvertently lateral incision is used or
excessive lateral retraction is present.

EPIDEMIOLOGY AND ETIOLOGY

Trauma to the femoral vessels accounts for
one third of all vascular injuries in military
series and 7% to 35% in civilian series (Rich,
Baugh, and Hughes, 1970; Mattox and col-
leagues, 1989; Humphrey, Nichols, and Silver,
1994; Hafez, Woolgar, and Robbs, 2001 ) . Pen-
etrating injuries are more common than
blunt. Low-caliber gunshot wounds are the
most common cause of penetrating injuries;
knife wounds are less common (Hafez,
Woolgar, and Robbs, 2001). Anterior dislo-
cation of the femoral head is a rare cause of
blunt injury. Laceration of the common
femoral artery can cause severe hemorrhage
that can be fatal if not tamponaded or
controlled. In survivable injuries, the femoral

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19 • EXTREMITY VASCULAR TRAUMA

377

Ext. iliac a
Deep iliac

Superf. iliac
circumflex a
Superf
epigastric a

Ascend, branch lat. 7
circumflex a. | [
Transverse branch lat
circumflex femoral a
Lat. circumflex
femoral a.

Descend, branch lat
circumflex femoral a

Perforating branches

deep femoral a

Right
common iliac a.

Int. iliac a.
uj — Superior
'*' gluteal a.
Inf. gluteal a.

Common
femoral a.

Obturator a.

Medial circumflex
femoral a.

Superf.
femoral a.

Deep femoral a.

Descend,
genicular a.

Lat. sup. genicular a

■ FIGURE 19-17

This anatomic drawing traces the course of the superficial femoral artery, the main conduit between
the common femoral and popliteal arteries. In addition to numerous muscular branches, the
supreme genicular (descending genicular) is an important collateral to the rich anastomosis around
the knee. ■

sheath contains the hemorrhage and the
vessel thromboses or forms an acute
pseudoaneurysm.

CLINICAL FEATURES AND DIAGNOSIS

Hemorrhage is the most common presenting
sign. Less commonly, the lacerated or tran-
sected common femoral artery thromboses
and distal ischemia results. Associated injury

to the femoral vein is very common in pene-
trating trauma.

The superficial location of the femoral
bifurcation allows for accurate clinical assess-
ment by inspection and palpation. In patients
with active hemorrhage from the femoral
area, no diagnostic workup is needed; expedi-
tious control of hemorrhage is required.
Arteriography is reserved for patients with
multiple associated injuries and an equivocal
examination. Emergency department arteri-

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IV • SPECIFIC VASCULAR INJURIES

ogram is usually not helpful in this area
because of the difficulty of adequately visual-
izing the common femoral artery and the
femoral bifurcation. If arteriography is
required, it should be performed formally in
the angiography suite.

SURGICAL TREATMENT

Both groins, the lower abdomen (beginning
at the umbilicus) , and both lower extremities
should be completely prepared and draped.
Preparing the lower abdomen allows for prox-
imal extension of the incision and more prox-
imal control if necessary. Having the uninjured
groin prepared allows access to an alternative
source of inflow. Preparing the uninjured leg
provides access to autogenous conduit.

The common femoral artery is best exposed
through a longitudinal incision overlying its
course from the inguinal ligament inferiorly
for 8 to 12 cm (Fig. 19-18) . Occasionally, prox-
imal control may require exposure of the
external iliac artery. This is best accomplished
through an oblique muscle splitting lower
quadrant abdominal incision carried down to
the retroperitoneum where the artery and vein
can be controlled with medial retraction of
the peritoneal structures.

The profunda femoral artery is exposed
through the same incision used for the
common femoral artery. Dissection is carried
distal and anterior along the proximal portion
of the superficial femoral artery and poste-
rior laterally to identify the origin of the
profunda femoral. The proximal 2 cm of the
artery is easily exposed. Beyond this point,
ligating and dividing the lateral circumflex
femoral vein exposes the artery. This vein is
broad and short and should be carefully
ligated to avoid significant hemorrhage.

Severe hemorrhage usually dictates the
initial steps of the surgical procedure. Proxi-
mal and distal control prior to exposure of
the injury site prevents secondary injury to
the vessels. The use of vascular clamps, Silas-
tic vessel loops, optical magnification, and
fine monofilament sutures are essential to
successful management. There is no role for
blind clamp placement. Direct repair, when
possible, is preferred. Longitudinal laceration

■ FIGURE 19-18

Exposure of the common femoral artery and its
branches is best obtained through a
longitudinal incision directly over the artery.
Silastic loops double passed around the
arteries provide control without causing
secondary arterial trauma. The profunda
femoral artery is exposed by carrying this
dissection distally and by ligating the lateral
femoral circumflex vein. (From Rutherford RB:
Atlas of vascular surgery: Basic techniques
and exposures. Philadelphia: WB Saunders,
1993.) ■

or defects may be repaired with a vein patch
angioplasty. However, if injury is extensive and
debridement results in a significant loss of
artery such that there would be tension on
the repair, an interposition graft should be
placed.

Saphenous vein is the first choice for inter-
position grafting. However, vein diameter may
not be adequate. Although spiral vein graft
construction is an alternative, it is time con-
suming and technically demanding. Dacron
or polytetrafluoroethylene (PTFE) interposi-
tion grafts are acceptable alternatives. In
general, PTFE is preferred because of its
relative resistance to infection compared to
Dacron. Short-segment synthetic grafts in this
area of high flow are durable and have accept-
able long-term patency rates (Feliciano and
colleagues, 1985, 1988).

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19 • EXTREMITY VASCULAR TRAUMA

379

Profunda femoral artery injuries should
be repaired whenever possible. However, if
serious associated injuries are present or the
patient is unstable, the vessel should be
ligated. Long-term sequelae are uncommon
as long as the superficial femoral artery is
patent. Proximal injuries to the profunda
femoral artery may be managed by placing a
short interposition graft or by proximal liga-
tion and reimplantation of the vessel to the
proximal superficial femoral artery. The pro-
funda femoral artery should be repaired only
if the patient is stable and the repair is rela-
tively easy to accomplish.

RESULTS

Successful repair of the common femoral and
profunda femoral arteries is dependent
on restoration of adequate arterial lumen
diameter and avoiding infection. Once groin
wound infection occurs in patients who had
an arterial repair, the first priority is to deter-
mine whether the graft or suture line is
exposed or involved in the infection. If the
suture line is involved, immediate graft
removal, ligation of the proximal and distal
arteries, and extra-anatomic bypass are
the only acceptable option to prevent life-
threatening hemorrhage and eventual limb
loss. If the graft is exposed, but the suture line
is not and the graft is patent, the graft may be
salvaged by coverage with a proximally based
sartorius flap.

Long-term patency rates of successful
primary repair and short segment interposi-
tion grafts are very good. Acute thrombosis,
though uncommon, usually causes limb-
threatening ischemia and requires immediate
treatment. Early stenosis of vein interposition
grafts is uncommon. These patients should
have regular follow-up to assess graft patency
and the adequacy of limb blood flow. Calf
claudication is the first clinical indication of
stenosis at the repair site.

Lower extremity function following vascu-
lar repair is predominantly determined by the
severity of associated musculoskeletal and
nerve trauma. The most disabling associated
injury is femoral nerve transection. Loss of
quadriceps function results in significant gait

problems. Extensive venous injury with venous
outflow obstruction at the femoral level causes
venous insufficiency with long-term sequelae
of venous stasis dermatitis and ulceration.

Amputation rates following femoral artery
injury vary from 15% to 35% and are deter-
mined by the severity of musculoskeletal and
neurologic injury (Mattox and colleagues,
1989; Hafez, Woolgar, and Robbs, 2001 ) . Pen-
etrating injuries are much less likely to result
in amputation. In contrast, blunt injuries that
cause vascular disruption usually involve force
loading sufficient to cause significant neuro-
logic and musculoskeletal injuries with limb-
threatening sequelae. The most discouraging
outcome is successful revascularization of a
limb, which ultimately requires amputation
for chronic recurring pressure ulceration and
infection because of denervation.

Superficial Femoral Artery

SURGICAL ANATOMY

The superficial femoral artery originates in
the femoral triangle and travels from an ante-
rior location to the medial aspect of the thigh
at the adductor canal where it transitions to
the popliteal artery. It is superficially located
in the groin and moves deeper as it traverses
the medial thigh beneath the sartorius muscle
approaching the adductor magnus muscle.
The only significant branch is the descend-
ing genicular artery, which forms a collateral
anastomosis with the genicular branches of
the popliteal artery. The superficial femoral
vein travels in close posteromedial proximity
to the artery and is frequently duplicated.
The saphenous nerve, a cutaneous sensory
nerve to the medial calf and foot, lies ante-
rior to the superficial femoral artery for most
of its course. The nerve leaves the artery to
join the saphenous vein near the adductor
hiatus.

EPIDEMIOLOGY AND ETIOLOGY

Penetrating

injury of superficial femoral
artery is more common than blunt. The pres-
ence of a femoral shaft fracture should alert

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IV • SPECIFIC VASCULAR INJURIES

the examining physician of the possibility of
a superficial femoral artery injury, but fewer
than 5% of fractures will have vascular trauma
(Rosental and colleagues, 1975; Romanoff and
Goldberg, 1979).

CLINICAL FEATURES AND DIAGNOSIS

Hemorrhage is the predominant feature of
penetrating vascular injuries in the thigh,
whereas thrombosis is the usual presentation
following a blunt mechanism.

High-velocity gunshot wounds of the thigh,
though common in the military setting,
remain rare in the civilian environment. Con-
tusion and thrombosis of the superficial
femoral artery produced by the temporary cav-
itational effects of high-energy rounds may
present as either initial or delayed lower
extremity ischemia. The severity of tissue
destruction, neurologic deficit, and vascular
spasm may make peripheral vascular exami-
nation difficult in this setting.

Inspection and palpation with attention to
distal pulses is usually accurate in assessing
the superficial femoral artery. Frequent re-
examination, particularly in patients with
midshaft femur fracture, must be performed
to avoid missing a delayed arterial thrombo-
sis. Patients with active hemorrhage from
penetrating wounds require immediate
operation for hemorrhage control and diag-
nosis. Arteriography is reserved for patients
with equivocal signs of arterial injury, palpa-
ble but diminished pulses, or the suspicion
of pseudoaneurysm or arteriovenous fistula.
Emergency department or operating room
arteriography is accurate for detecting
superficial femoral artery injuries and is time
saving in patients with multiple injuries and
the need for immediate thoracotomy or
celiotomy.

SURGICAL TREATMENT

Both groins and both legs should be prepared
and draped. Preparing the contralateral groin
provides an alternative source of inflow and
the contralateral leg provides a source for
autologous conduit. Proximal superficial

femoral artery injuries are best exposed
through a longitudinal groin incision similar
to that used for femoral bifurcation exposure.
The middle and distal artery can be
approached through an oblique incision in
the thigh over the course of the sartorius
muscle. The muscle is retracted medially and
the artery found immediately below in the
adductor (Hunter) canal. Exposure of the
distal artery at the superficial femoropopliteal
arteryjunction may require transection of the
adductor magnus tendon.

Primary repair is possible for those few
wounds that produce a small, clean laceration.
Saphenous vein interposition grafting is the
best procedure for more severe injuries of the
superficial femoral artery. Careful vascular
technique, avoiding undue tension in the
repair, preserving lumen diameter, and com-
pletion angiogram are essential to the suc-
cessful repair of the superficial femoral artery.
A synthetic graft is an acceptable conduit if
no vein is available or the patient is too unsta-
ble to prolong the procedure to harvest a vein.
Long-term patency rates of PTFE and Dacron
grafts are significantly lower than that of autol-
ogous vein graft.

Primary amputation is rarely indicated in
the management of superficial femoral artery
injuries. Extensive crush injury with avulsion
of the thigh muscles from the femur is one of
the few indications for lifesaving above-
knee amputation. Refractory hemorrhage
into the thigh is striking in these patients and
attempts at direct surgical control of hemor-
rhage are usually futile. High above-knee
amputation may be the only way to control
life-threatening hemorrhage in this setting.

RESULTS

Superficial femoral artery repair, if done prop-
erly, has long-term patency that approaches
100% . Associated neurologic injury is uncom-
mon and femur fractures are usually amenable
to successful orthopedic management. Fre-
quent postoperative assessment for graft
failure or calf compartment syndrome is nec-
essary to facilitate early reoperation or fas-
ciotomy should these complications occurs.
Amputation rates vary from 10% to 30% and

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19 • EXTREMITY VASCULAR TRAUMA

381

depend on the timeliness and success of the
vascular repair and the severity of associated
injuries (Mattox and colleagues, 1989; Hafez,
Woolgar, and Robbs, 2001).

Patients with superficial femoral artery
injuries require long-term follow-up. Yearly
assessment of distal pulses and, if indicated,
segmental lower extremity arterial pressures
should be performed. Five percent to twenty
percent of patients will require some form
of secondary reconstruction for lower
extremity arterial insufficiency because of a
late failure (stenosis or thrombosis) of the
repair.

Popliteal and Tibial Arteries

SURGICAL ANATOMY

The popliteal artery originates at the adduc-
tor magnus hiatus as the continuation of the
superficial femoral artery. Throughout its
course, the popliteal artery is located deep in
the popliteal fossa along the posterior aspect
of the femur, in proximity to the joint line,
and the tibial plateau. The artery is covered

proximally by the semimembranous muscle
and in its midportion by subcutaneous tissue.
The artery continues distally to the upper calf
where it terminates at the origin of the ante-
rior tibial artery at the triceps surae formed
by the two heads of the gastrocnemius muscle
and the soleus muscle. Along its course, the
popliteal artery has six to eight small genicu-
late branches, which are usually paired. These
form an anastomotic network around the knee
(Fig. 19-19). However, in acute occlusion of
the popliteal artery, these branches are not
sufficient to provide adequate distal blood
flow.

The relationship of the popliteal artery to
the muscles of the thigh and calf places it at
risk for severe injury in the dislocation of the
knee. In full extension of the knee, the
popliteal artery is on tension across the back
of the knee joint. Knee dislocation stretches
the popliteal artery over the posterior edge
of the tibial plateau resulting in severe intimal
injury or transection.

The three tibial vessels have a variable
origin. In 85% to 90% of patients, the popliteal
bifurcates into the anterior tibial and tibial
peroneal trunk arteries. The posterior tibial

Descend, branch
tat. circumflex
femoral a.

Popliteal a.

Superior lat
genicular a

Inf. lat. genicular a

Ant. tibial
recurrent a.

Ant. tibial a

Femoral a.

Descend,
genicular a.

Articular branches
descend, genicular a.

Superior medial
genicular a.

Inf. medial
genicular a.

Post, tibial a.

■ FIGURE 19-19

Anterior view of the knee with the popliteal artery and its branches. These collaterals are usually not
sufficient to provide adequate distal perfusion in patients with acute traumatic occlusion. ■

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IV • SPECIFIC VASCULAR INJURIES

and peroneal artery arise 3 to 6 cm distally.
In 10% to 15%, variations are seen in the
tibial vessel origins from the popliteal artery
including an origin of the anterior or poste-
rior tibial arteries at or above the knee joint
line. The popliteal and tibial arteries are
accompanied in their course by single or
paired veins.

The anterior tibial artery traverses the
superior edge of the interosseus membrane
to enter the anterior compartment of the calf.
It courses along the membrane accompanied
by the deep peroneal nerve and the anterior
tibial vein. This neurovascular bundle lies deep
to the extensor muscles. The artery contin-
ues across the ankle joint beneath the exten-
sor retinaculum to emerge on the top of the
foot at the dorsalis pedis artery. Along its
course, the anterior tibial artery gives off
numerous muscular branches. The dorsalis
pedis terminates in the superficial plantar
arch.

The posterior tibial and peroneal arteries
originate at the bifurcation of the tibial-
peroneal trunk in the upper calf deep to the
soleus muscle. The posterior tibial artery con-
tinues along the fascia of the deep posterior
muscle compartment accompanied by the
tibial and paired posterior tibial veins. It tra-
verses the ankle joint posterior to the medial
malleolus and terminates in the medial and
lateral plantar arteries, which contribute to
the deep and superficial plantar arches. Anas-
tomotic connections between the anterior
tibial artery and posterior tibial artery allow
for adequate foot perfusion as long as one of
the vessels remains patent.

The peroneal artery parallels the posterior
tibial artery in a lateral course deep to the
flexor hallucis longus muscle. It is accompa-
nied by paired veins. Distally it terminates in
lateral calcanean branches that anastomose
with distal branches of the anterior tibial and
posterior tibial arteries. These connections are
small and may not be sufficient to supply the
foot in acute occlusion of the other tibial
vessels. The distal anterior or posterior tibial
arteries may be supplied by a large terminal
branch of the peroneal artery either as a
congenital anomaly or because of collateral-
ization after chronic occlusion of those vessels.

EPIDEMIOLOGY AND ETIOLOGY

Blunt trauma causes most civilian popliteal
and tibial arterial injuries. Fracture or dislo-
cation in the area of the knee is the predom-
inate mechanism. In the military experience,
penetrating injuries are more common. Occlu-
sion of a single tibial vessel is well tolerated as
long as no preexisting occlusion of the other
vessels is present.

CLINICAL FEATURES AND DIAGNOSIS

Thrombosis with distal ischemia is the most
common presentation of popliteal artery
injury. Concomitant venous and neurologic
trauma makes these injuries extremely
morbid. Most patients with occlusion of the
popliteal or more than one tibial artery occlu-
sion have calf and foot ischemia. On the other
hand, knee dislocation with spontaneous
reduction may be overlooked unless a thor-
ough peripheral vascular examination is per-
formed. In these cases, the dislocation causes
a shear effect producing intimal injury and
delayed thrombosis.

A thorough peripheral vascular examina-
tion in all injured patients is the key to prompt
recognition of popliteal and tibial artery
injuries. Delays in diagnosis are invariably due
to the lack of a physical examination of the
pulses augmented with Doppler pressure
determination when indicated. Ankle Doppler
pressure determination allows rapid assess-
ment of the patient with diminished distal
pulses. Absence of Doppler flow sounds, an
ankle brachial index of less than 0.8 or a
20mmHg decrease compared to the unin-
jured leg all indicate the need for further
evaluation.

Duplex scanning has no role in the assess-
ment of acute arterial trauma, adds nothing
to physical examination augmented by
Doppler pressure measurement, and is not
accurate enough to assist in planning surgi-
cal treatment. Even when used by experienced
surgeons or technicians, this technology does
not obviate the need for arteriography or accu-
rately predict the success of nonoperative
therapy.

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19 • EXTREMITY VASCULAR TRAUMA

383

Arteriography is accurate in the evaluation
of patients with suspected popliteal or tibial
arterial injury but is time consuming and
should be reserved for patients with equivo-
cal physical findings. Emergency department
or intraoperative angiography is also accurate
and should be considered when formal
angiography is not readily available.

SURGICAL TREATMENT

Both groins and both lower extremities should
be prepared and draped. Contralateral saphe-
nous vein is the conduit of choice for bypass
and should be readily accessible. Popliteal
injuries are best approached through a
generous medial incision (Fig. 19-20). The
simplest landmarks for the incision are the
posterior margin of the femur proximally and
the posterior margin of the tibia below the

knee. During the medial exposure, care
should be taken to avoid lacerating the saphe-
nous vein. Post-traumatic deep venous insuf-
ficiency is common and this superficial vein
may become an important collateral route of
venous drainage. The proximal popliteal
artery is exposed as it emerges from adduc-
tor canal. Exposure of the artery in the area
of the kneejoint requires division of the medial
head of the gastrocnemius, semimembra-
nosus, and semitendinosus muscles. The distal
popliteal artery is exposed with an incision
along the posterior margin of the tibia
(Fig. 19-21).

Tibial vessel exposure requires careful dis-
section in the upper medial aspect of the calf.
The origin of these vessels is exposed by con-
tinuing dissection from the distal popliteal
artery through the area of the triceps surae.
The exposure is facilitated by incising the
soleus muscle longitudinally 2 cm posterior to

Sciatii

Posterior Approach

Popliteal vv.

■ FIGURE 1 9-20

The posterior and medial
approaches to the popliteal artery.
A, A modified S-shaped incision is
used in the posterior approach to
avoid contracture across the knee
joint. B, The medial approach
requires a more extensive dissection
but provides better access to
proximal and distal vessels. C, Both
approaches can be successfully
used in the exposure and repair of
the popliteal vessels. ■

chl9.qxd 4/16/04 3:33PM Page 384

384

IV • SPECIFIC VASCULAR INJURIES

■ FIGURE 19-21

A, Distal popliteal exposure is obtained through an incision posterior to the tibia. 6 and C, The
soleus muscle is divided longitudinally to expose the neurovascular bundle. D, The distal popliteal
artery and anterior tibial artery origin is exposed ligating the anterior tibial vein and retracting the
popliteal vein posteriorly. E, The tibioperoneal trunk and origins of the peroneal and posterior tibial
arteries are exposed by retracting the popliteal vein anteriorly. (From Rutherford RB: Atlas of
vascular surgery: Basic techniques and exposures. Philadelphia: WB Saunders, 1993.) ■

chl9.qxd 4/16/04 3:33PM Page 385

the tibia, taking care to avoid the soleal plexus
of veins adjacent to the tibia. The anterior
tibial artery origin is exposed by retracting the
popliteal vein posteriorly. The anterior tibial
vein should be carefully ligated. This short
broad vein is difficult to control if lacerated.
Once divided, it allows for exposure of the
origin of the anterior tibial artery and the tibial
peroneal trunk. The vessels distal to the ante-
rior tibial origin are best exposed by retract-
ing the veins anteriorly. Paired veins with
crossing branches envelop the proximal pos-
terior tibial and peroneal arteries. Distal
exposure of these vessels is obtained through
a medial incision along the posterior margin
of the tibia down to the space posterior to the
medial malleolus. The anterior tibial artery
is exposed through an incision along the
middle of the anterior compartment. Dissec-
tion is carried deep between the extensor hal-
lucis and extensor digitorum muscles to the
level of the interosseus membrane and the
artery (Fig. 19-22).

Popliteal and tibial arterial injuries are
rarely simple lacerations. Repair usually
requires saphenous vein interposition.
Primary repair of the popliteal artery is appro-
priate in lacerations from knife wounds,
which result in little arterial disruption. Blunt
injuries and gunshot wounds should be treated
by careful debridement of all injured vessel
wall and tension-free repair with vein inter-
position grafting (Shah and colleagues, 1985) .

Arterial repair at the popliteal and tibial
level should always be evaluated with inter-
operative completion angiography. Any defect
in the repair should be immediately addressed
with either a catheter thrombectomy or a revi-
sion of the anastomosis. Early occlusion with
platelet thrombus should be carefully inves-
tigated to rule out a technical defect in the
repair. If platelet deposition in the area of
repair occurs, a continuous infusion of low-
molecular-weight dextran should be started.
This is a treacherous clinical problem and
must be aggressively treated.

Soft tissue coverage of arterial repairs in the
region of the knee and calf is essential to suc-
cessful limb salvage. Infection or exposure of
vein interposition grafts always leads to throm-
bosis or hemorrhage and a high rate of limb
loss.

19 • EXTREMITY VASCULAR TRAUMA 385

RESULTS

Injury of the popliteal and tibial vessel level
is associated with significant long-term dis-
ability. The initial outcome is dependent on
successful arterial repair and the extent of
soft tissue damage and ischemia. Infections
of arterial repairs at this level are usually asso-
ciated with inadequate soft tissue coverage.
Long-term results are dependent on the
extent of musculoskeletal and neurologic
injury. Tibial nerve transection is associated
with poor long-term results. Early physical
therapy is essential to maximize the recovery
of function in all lower extremity vascular
injuries.

Lower Extremity
Compartment Syndrome

Compartment syndrome may present 12 to
24 hours after reperfusion. If not promptly
diagnosed and treated, the risk of limb loss
or severe dysfunction is high. Calf compart-
ment syndrome most commonly results from
prolonged ischemia or a crush injury. Fre-
quent physical examinations augmented
with compartment pressure measurements are
necessary to detect this complication in its
early stage. The first complaint may be sensory
loss in the foot. Thigh compartment syndrome
is rare. Thigh muscle swelling and pain out
of proportion to the severity of injury are the
most common findings.

Mangled Lower Extremity

Every effort must be made to balance the sur-
gical reconstruction of the mangled extrem-
ity with the overall status of the patient both
immediately following injury and during the
rehabilitation phases of care. Primary ampu-
tation should be considered in patients with
severe soft tissue injury and a dysvascular
extremity. Objective rating scales or scoring
systems are an adjunct to clinical judgment
but not a substitute for careful consideration
of what is reasonable and appropriate for the
patient's short-term and long-term recovery
(Gregory and colleagues, 1985; Johansen

chl9.qxd 4/16/04 3:33PM Page 386

386

IV • SPECIFIC VASCULAR INJURIES

■ FIGURE 19-22

A, Proximal exposure of the anterior tibial artery is obtained through an incision along the
anterolateral aspect of the calf. B, The extensor muscles are retracted anteriorly and posteriorly to
expose the anterior tibial neurovascular bundle on the interosseous membrane. C, Distal exposure
is obtained through an incision along the extensor digitorum tendon. D, The anterior tibial artery lies
adjacent to the tibia beneath the flexor tendons and the extensor retinaculum. (From Rutherford RB:
Atlas of vascular surgery: Basic techniques and exposures. Philadelphia: WB Saunders, 1993.) ■

chl9.qxd 4/16/04 3:33PM Page 387

19 • EXTREMITY VASCULAR TRAUMA

387

■ FIGURE 19-23

Mangled extremity with severe degloving injury
associated with an open femur fracture. This
limb was initially thought to be unsalvageable,
but with appropriate revascularization and
debridement, the extremity was saved and was
functional. ■

and colleagues, 1990; Bonanni, Rhodes, and
Lucke, 1993). Delayed amputation following
initially successful vascular repair remains an
unfortunate possibility in patients with exten-
sive musculoskeletal and neurologic injury.
Most trauma centers pursue an aggressive
approach to young patients with these
complex injuries. Mangled extremities are
often salvaged with a multidisciplinary
approach; however, amputation is eventually
the best choice for a pain-free return to func-
tional status in some patients (Fig. 19-23) . This
decision is never easily made and is based on
a strong physician-patient partnership.
Setting reasonable expectations immediately
after injury is the best starting point in
this process. Early involvement of a multi-
disciplinary approach also allows for a timely
decision about amputation. This remains one
of the most challenging problems for trauma
surgeons.

chronic disability. A balanced approach that
includes ligation for injuries of minor veins
or for life-threatening injuries in unstable
patients, and repair or reconstruction
whenever possible may be the best strategy
(Nypaver and colleagues, 1992; Timberlake
and Kerstein, 1995; Zamir and colleagues,
1998).

SURGICAL ANATOMY

Paired veins form from muscle branches in
the calf and course parallel to the tibial vessels
and coalesce into the popliteal vein, which may
also be paired. The calf is also drained by
numerous subcutaneous veins that flow to
either the greater or the lesser saphenous vein.
The greater saphenous veinjoins the common
femoral vein in the groin and the lesser saphe-
nous vein travels proximally along the back
of the calf to join the popliteal vein. Numer-
ous perforating veins connect the greater
saphenous to the deep system. Flow is directed
deep and proximally by valves in both the
superficial and the deep system.

The popliteal vein transitions the adductor
canal to become the superficial femoral vein.
Numerous muscular branches join this vein.
The profunda femoral vein drains the quadri-
ceps and deep muscles and joins the superfi-
cial femoral vein to form a single large
common femoral vein. All of the lower extrem-
ity veins collateralize to form an extensive
network of alternative venous drainage routes.
In the absence of disruption of these collat-
erals, a single-level venous occlusion does not
prevent adequate venous drainage.

EPIDEMIOLOGY AND ETIOLOGY

Venous Injuries of the
Lower Extremity

The aggressive approach to arterial injuries
in the extremities has not been matched with
equal enthusiasm for venous repair. Instead,
ligation is frequently performed. However, lig-
ation may result in thrombosis and venous
insufficiency, ultimately leading to significant

Venous injury is usually associated with arte-
rial injury and is most commonly due to pen-
etrating trauma. Veins are much more elastic
than arteries and are less frequently injured
in blunt force trauma. Fractures, however, can
lead to lacerations and thrombosis. The low-
pressure venous system allows for tamponade,
and significant external hemorrhage is
uncommon except in large lacerations of the
femoral and popliteal veins.

chl9.qxd 4/16/04 3:33PM Page 388

388 IV • SPECIFIC VASCULAR INJURIES

CLINICAL FEATURES AND DIAGNOSIS

Most clinically significant venous injuries
present as persistent hemorrhage of dark red
blood from a penetrating wound. In the
absence of external hemorrhage or the need
for surgical exploration for concomitant arte-
rial trauma, the diagnosis of venous injury is
usually delayed. Venous hypertension fol-
lowing major vein injury and thrombosis is
usually well tolerated despite causing distal
extremity edema. Lower extremity ischemia
is rare following venous injury and is the result
of extensive soft tissue damage and loss of col-
lateral venous flow. Compartment syndrome
is also uncommon and is usually delayed in
onset when it occurs.

Duplex scanning is an effective and accu-
rate diagnostic modality to assess venous
patency in blunt-force injuries. Most trauma
centers periodically perform surveillance
duplex scanning of the lower extremities of
trauma patients following major injuries.
Dynamic computed tomographic scanning
and arteriography are rarely used to diagnose
venous injuries. Most venous injuries of clin-
ical significance are diagnosed at the time of
surgical exploration for arterial trauma due
to the high rate of coincidental injuries.

SURGICAL TREATMENT

The veins of the lower extremity are exposed
by the same incisions used to expose the asso-
ciated arteries. Direct pressure and proximal
and distal dissection in adjacent tissue allows
hemostatic control. Clamp application should
be carefully performed or control obtained
with Silastic vessel loops to avoid secondary
venous trauma.

The choice of technique for venous repair
depends on the patient's overall status, the
extent of venous and soft tissue injury, and
the duration of ischemia from associated arte-
rial injury. Life-threatening associated injuries
or hemodynamic instability mandate ligation
of venous injuries. Extensive soft tissue injury
and loss of collateral venous flow mandate
venous reconstruction. Prolonged ischemia
from arterial occlusion leads to a dilemma
when venous injury is associated. If possible,

the vein should be repaired first. Simple lac-
erations may be repaired by lateral suture,
taking care to avoid stenosis. Occasionally, end-
to-end repair is possible.

If extensive venous reconstruction is
required and associated arterial injury is
present, it is best to restore arterial perfusion
with a shunt. Venous interposition grafts or
venous panel grafts should be used to restore
adequate lumen diameter. Panel grafts are
constructed by harvesting a sufficient length
of contralateral saphenous vein, opening the
vein longitudinally, wrapping it in a spiral
fashion around an appropriately sized chest
tube, and sewing the vein into a conduit for
interposition in the injured vein. This tedious
and time-consuming procedure requires
loupe magnification and precise technique.
The use of synthetic grafts for the repair of
lower extremity venous injuries is to be
avoided because of the certainty of early
thrombosis.

The use of small arteriovenous fistula
upstream from the venous repair to maintain
high flow has been suggested. This technique
is time consuming and unproven in its effi-
cacy in the management of venous injuries.
A low-molecular-weight dextran infusion to
limit platelet adhesion carries a low risk of
bleeding complications and may help main-
tain early patency of the repaired vein. Dextran
40 is infused at 40 mL per hour for 24 hours.
Full anticoagulation with intravenous hepa-
rin is associated with a significant risk of bleed-
ing and is best reserved for proven deep
venous thrombosis.

RESULTS

A traditional skepticism exists among surgeons
about the likelihood of venous patency after
reconstruction for trauma. Well-performed
repairs remain patent at an encouraging rate.
Early patency depends on the avoidance of
stenosis and prevention of thrombosis. If early
thrombosis occurs, recanalization occurs in a
significant number of patients. If ligation is
required, early postinjury edema can be
minimized by placing the lower extremity in
a continuous passive mobilization device.
Pulmonary emboli are uncommon following

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19 • EXTREMITY VASCULAR TRAUMA

389

venous repair (Nypaver and colleagues, 1992;
Timberlake and Kerstein, 1995; Zamir and col-
leagues, 1998), but chronic venous insuffi-
ciency is common.

REFERENCES

Bonamii F, Rhodes M, Lucke JF: The futility of pre-
dictive scoring of mangled lower extremities.
J Trauma 1993;34:99-105.

Costa MC, Robbs JV: Nonpenetrating subclavian
artery trauma. J Vase Surg 1988;8:71-75.

Endean ED, Veldenz HC, Schwarcz TH, Hyde GL.
Recognition of arterial injury in elbow disloca-
tion. J Vase Surg 1992;16:402-406.

Feliciano DV, Herskowitz K, O'Gorman RB, et al:
Management of vascular injuries in the lower
extremity. J Trauma 1988;28:319-328.

Feliciano DV, Mattox KL, Graham JM, Bitondo CG:
Five-year experience with PTFE grafts in vascu-
lar wounds. J Trauma 1985;25:71-82.

Graham JM, Mattox KL, Feliciano DV, DeBakey
ME: Vascular injuries of the axilla. Ann Surg
1982;195:232-238.

Granchi T, Schmittling Z, VasquezJ, et al: Prolonged
use of intraluminal arterial shunts without sys-
temic anticoagulation. Am J Surg 2000;180:493-
497.

Gregory RT, GouldRJ,PecletM,etal: The mangled
extremity syndrome (MES): a severity grading
system for multi-system injury of the extremity.
J Trauma 1985;25:1147-1150.

Hafez HM, Woolgar J, Robbs JV: Lower extremity
arterial injury: results of 550 cases and review of
risk factors associated with limb loss. J Vase Surg
2001;33:1212-1219.

Hardin WD, O'Connell RC, Adinolfi MF, Kerstein

MD: Traumatic injuries of the upper extremity:
determinants of disability. Am J Surg 1985;150:
266-270.

Humphrey PW, Nichols WK, Silver D: Rural vas-
cular trauma: a twenty year review. Ann Vase Surg
1994;8:179-185.

Johansen K, Dames M, Howey T, et al: Objective
criteria accurately predict amputation following
lower extremity trauma. J Trauma 1990;30:568-
573.

Johnson M, Ford M, Johansen K: Radial or ulnar
artery laceration. Repair or ligate? Arch Surg
1993;128:971-975.

Mattox KL, Feliciano DV, Burch J, et al: Five thou-
sand seven hundred sixty cardiovascular injuries
in 4459 patients. Epidemiologic evolution 1958
to 1987. Ann Surg 1989;209:698-674.

Meyer J, Walsh J, Schuler J, et al: The early fate of
venous repair after civilian vascular trauma. A
clinical, hemodynamic, and venographic assess-
ment. Ann Surg 1987;206:458-464.

Nypaver TJ, Schuler JJ, McDonnell P, et al: Long-
term results of venous reconstruction after
vascular trauma in civilian practice. J Vase Surg
1992;16:762-768.

Pappas PJ, Haser PB, Teehan EP, et al: Outcome
of complex venous reconstructions in patients
with trauma. J Vase Surg 1997;25:398-404.

Rich NM, Baugh JH, Hughes CW: Acute arterial
injuries in Vietnam: 1 ,000 cases. J Trauma 1970;
10:359-369.

Rich NM, Spencer FC: Subclavian artery injuries.
In: Vascular Trauma. Philadelphia: WB Saunders,
1978:307-329.

Romanoff H, Goldberger S: Combined severe vas-
cular and skeletal trauma: management and
results. J Cardiovasc Surg 1979;20:493-498.

RosentalJJ, Caspar MR, Gjerdrum TC, Newman J:
Vascular injuries associated with fractured femur.
Arch Surg 1975;110:494-499.

Rozycki GS, Tremblay LN, Feliciano DV,
McClelland WB: Blunt vascular trauma in the
extremity: Diagnosis, management, and outcome.
J Trauma 2003;55(5) :814-824.

Sampson LN, Britton JC, Eldrup-Jorgensen J, et al:
The neurovascular outcome of scapulothoracic
dissociation. J Vase Surg 1993;17:1083-1089.

Shackford SR, Rich NM: Peripheral vascular injury.
In: Mattox KL, Moore EE, Feliciano DV, eds.
Trauma. Philadelphia: WB Saunders, 2001 :101 1-
1046.

Shah DM, Naraynsingh V, Leather RP, et al:
Advances in the management of popliteal vas-
cular blunt injuries. J Trauma 1985;25:793-799.

Sparks SR, DeLaRosa J, Bergan JJ, et al: Arterial
injury in uncomplicated upper extremity dislo-
cations. Ann Vase Surg 2000;14:110-113.

Timberlake GA, Kerstein MD: Venous injury: to
repair or ligate, the dilemma revisited. Am Surg
1995;61:139-145.

Zamir G, Berlatzky Y, Rivkind A, et al: Results of
reconstruction in major pelvic and extremity
venous injuries. J Vase Surg 1998;28:901-908.

ch20.qxd 4/16/04 3:31PM Page 393

Special Problems

ERIC R. FRYKBERG

POPLITEAL ARTERY INJURIES
History and Epidemiology
Diagnostic Issues

General principles and modalities
Posterior Knee Dislocation
Treatment

General principles and techniques

Surgical adjuncts

Nonoperative observation
MANAGEMENT OF VENOUS INJURIES
History and Epidemiology
Diagnosis
Treatment

General principles

Venous repair considerations

Venous ligation considerations

Roles of ligation and repair
COMBINED VASCULAR AND SKELETAL EXTREMITY TRAUMA
Epidemiology and Prognostic Factors
Diagnosis
Treatment

Indications for Amputation
VASCULAR GRAFTS: ROLE AND COMPLICATIONS
FAILED RECONSTRUCTION OF ARTERIAL TRAUMA

393

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394

V • SPECIAL PROBLEMS AND COMPLICATIONS

There are a number of distinct clinical
presentations, problems, and issues
in vascular trauma that pose special
challenges in diagnosis and management for
the surgeon who is confronted with these
injuries. Each of these special problems is
plagued by relatively poor outcomes, even in
the most experienced trauma centers. They
tend to be uncommon and complex and
require rapid detection and treatment, mul-
tidisciplinary prioritization, and innovative
management techniques. The purpose of this
chapter is to provide a thorough knowledge
of the history, epidemiology, current litera-
ture, and suggested approaches for some of
the most difficult of these problems to opti-
mize outcome.

POPLITEAL ARTERY INJURIES

The special challenge of injury to the
popliteal artery lies primarily in the anatomy
of this vessel, which begins as the continua-
tion of the superficial femoral artery as it
courses through the hiatus of the adductor
magnus muscle. Covered proximally by the
semimembranosus muscle, it lies only in sub-
cutaneous tissue in the popliteal fossa behind
the knee joint, situated between the two heads
of the gastrocnemius muscle. It is in this fossa
that the popliteal artery is especially vulnera-
ble to stretch and direct injury from extrin-
sic forces and skeletal distortions, such as
fractures and knee dislocations, being teth-
ered proximally and distally to the femur and
tibia by tendons of the adductor and soleus
muscles. It most often bifurcates twice. As
the anterior tibial artery branches laterally
through the interosseous septum, the main
artery continues for another 2 to 3 cm as the
tibioperoneal trunk. This vessel then termi-
nally bifurcates into the peroneal and poste-
rior tibial arteries. Several geniculate, sural,
and muscular collateral vessels branch from
the popliteal artery behind the knee, which
anastomose in a rich network with branches
of the profunda femoris artery proximally and
tibial arteries distally. However, this collateral
supply is frail and subject to obliteration and

thrombosis by injury to the main artery and
surrounding tissues. These collaterals cannot
maintain viability of the leg and foot on their
own.

The fact that the popliteal artery is a true
end artery with a tenuous collateral support
explains why injury to it is so dangerous, and
why such injury has long been recognized as
the most limb threatening of all peripheral
vascular trauma. Nonetheless, several recent
advances in diagnosis and treatment of
popliteal artery injury have led to dramatic
reductions in limb loss and limb morbidity.

History and Epidemiology

General Albert Sidney Johnston died in the
American Civil War during the Battle of
Shiloh in April 1862 of exsanguination from
a gunshot wound to the popliteal artery, an
injury that currently would be considered
quite treatable and not life threatening. In
1906, the first use of autogenous vein to repair
an arterial injury was reported by Goyanes for
a traumatic aneurysm of the popliteal artery.
Injuries of this artery represented 12% of all
arterial injuries in British troops in World
War I, 20% of arterial injuries in American
troops in World War II, 26% of those in
the Korean War, and 217 (21.7%) of 1000
arterial injuries in the Vietnam War. These
were virtually all due to penetrating trauma,
from bomb and land-mine fragments and
high-velocity gunshots. Over the past 25 years,
popliteal artery injuries in the civilian sector
account for approximately 20% of all extrem-
ity arterial injuries reported in the published
literature, and as many as 20% to 75% of cases
in this setting are caused by blunt mechanisms.
The standard treatment of all extremity
arterial trauma before the Korean War was
ligation. DeBakey and Simeone (1946) doc-
umented this approach to result in limb loss
in 72.5% of all popliteal artery injuries in
World War II, the highest of any extremity
artery. Additionally, many salvaged limbs had
severe functional disability. During the Korean
and Vietnam Wars, when acute surgical repair
replaced ligation for arterial trauma, the inci-
dence of amputation following popliteal

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20 • SPECIAL PROBLEMS

395

artery injury improved substantially to only
29.5%, with fewer problems of morbidity and
disability in salvaged limbs. As repair tech-
niques and the use of surgical adjuncts have
improved, there has been further substantial
improvement in outcome since Vietnam fol-
lowing repair of highly destructive combat
injuries of this artery, with limb salvage now
approaching 90% (Table 20-1).

As this military experience with arterial
repair was adopted in the civilian sector, the
same improvements in limb salvage have been
realized since the 1950s, despite the higher
incidence of more destructive blunt trauma
in this setting. Fabian and colleagues (1982)
reported 165 civilian popliteal artery injuries
treated over 30 years, showing an improve-
ment in amputation rates from 74% to 6%
during this period. Daugherty and colleagues
(1978) documented a reduction of amputa-
tion rates from 54% to 9% among 24 civilian
popliteal artery injuries over a 1 0-year period.
Thomas and colleagues (1989) similarly
showed a reduction in limb loss from 30%
before 1980 to 15% after 1980 in their review
of 610 cases of civilian popliteal artery injuries
in 25 published series. During the 1980s, four
published civilian series reported 78 cases of
both penetrating and blunt popliteal artery
injury without a single amputation. Although
there has been a tendency toward improve-
ment in limb salvage as time has progressed,
continued reports of high rates of limb loss
even in recent years emphasize how danger-
ous these injuries remain (Table 20-2) .

Diagnostic Issues

GENERAL PRINCIPLES AND
MODALITIES

The time interval from popliteal artery injury
to repair is the most important factor in limb
salvage. Virtually all reports document that
the most common reason for limb loss in
this setting is a delay in recognition and revas-
cularization. This is because of the time-
dependent nature of the major consequences
of vascular injury, tissue ischemia, and hem-
orrhage, to which the popliteal circulation is
especially vulnerable. Therefore, a prompt
and accurate diagnosis of popliteal artery
trauma, within 6 hours of injury, is an extremely
important factor influencing outcome.

Diagnosis can be made in most cases by phys-
ical examination, as long as the significance
of the clinical manifestations of popliteal
artery injury is understood. Obvious physical
findings of arterial injury, also known as hard
signs, are present in 70% to 90% of these cases,
including active hemorrhage, large, expand-
ing, or pulsatile hematoma, bruit or thrill,
absent distal pulses, and distal ischemia (pain,
pallor, paralysis, paresthesias, and coolness) .
These findings must never be ignored. In the
setting of uncomplicated penetrating trauma
to the lower extremity, any of these signs
mandate immediate surgery, because the
probability of a major arterial injury requir-
ing repair approaches 100%, and the
penetrating wounds clearly show where that

TABLE 20-1

MILITARY EXPERIENCE WITH POPLITEAL ARTERY INJURIES*

Author

Year

Conflict

No. Cases

No. Amputations (%)

Makins

1922

WWI

144

62 (43)

DeBakey, Simeone

1946

WWII

502

364 (72.5)

Hughes

1958

Korea

22 (32.4)

Rich

1970

Vietnam

217

64 (29.5)

D'Sa

1980

Ireland

4(12.5)

Sfeir

1992

Lebanon

118

14(12)

Total

1081

530 (49)

*AII injuries were ligated in WWI and WWII and were repaired in all remaining series. WWI, World War I; WWII, World War II.

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396

V • SPECIAL PROBLEMS AND COMPLICATIONS

TABLE 20-2

MANAGEMENT RESULTS OF CIVILIAN POPLITEAL ARTERY INJURIES

Author

Year

No. Cases

No. Penetrating

No. Blunt

No.

Amputations (%)

Conkle

1975

12 (44)

Daugherty

1978

8(33)

O'Reilly

1978

6(12)

Lim

1980

Holleman

1981

4(12.5)

Fabian

1982

165

125

44 (27)

Jaggers

1982

9(15)

Snyder

1982

110

14(13)

McCabe

1983

4(17)

Orcutt

1983

6(16)

Yeager

1984

Shah

1985

Downs

1986

18(29)

Krige

1987

3(11)

Weimann

1987

1 (3.6)

Armstrong

1988

9(12)

Peck

1990

108

13(12)

Reed

1990

Martin

1994

6(15)

DeGiannis

1995

5(14)

Fainzilber

1995

13(16)

Pretre

1996

6(19)

Harrell

1997

14(37)

Melton

1997

102

25 (25)

Razuk

1998

6(24)

Total

1270

728 (57%)

543 (43%)

226(18)

injury is located. Any further diagnostic tests
would be superfluous, unnecessarily costly,
and potentially dangerous in view of the
adverse impact of the inevitable delay on
outcome. Exceptions to this include any cir-
cumstance in which the physical examination
does not clearly reflect the presence or loca-
tion of arterial injury (e.g., blunt trauma,
elderly patient with chronic vascular insuffi-
ciency, associated skeletal trauma, shotgun
wounds, thoracic outlet wounds, and estab-
lished complications of delay), in which case
arteriographic imaging is warranted.

Arteriography is now known to be unnec-
essary in injured extremities that do not
manifest any hard signs of popliteal artery
injury, regardless of mechanism or wound
complexity. In the past, all asymptomatic
wounds (i.e., those with no hard signs) placing
the popliteal artery at risk either were surgi-
cally explored or underwent routine arteri-

ography. These included penetrating injuries
in proximity to the artery and all high-risk blunt
trauma, such as lower extremity crush, distal
femur or proximal tibia fractures, and poste-
rior knee dislocations. It has long been known
that in this setting, occult vascular injury may
still be present in 10% to 15% of cases.
However, recent studies have shown that such
asymptomatic vascular injuries are consis-
tently nonocclusive and have a benign and self-
limited natural history with a high rate of
spontaneous resolution. They, therefore,
require neither surgical repair, nor the con-
siderable expense and resources necessary
for routine detection. Virtually all limb-
threatening complications of delayed diagnosis
of popliteal artery injury are due to overlooked
hard signs, rather than an absence of relevant
physical findings, on initial presentation.

Noninvasive testing with Doppler pressure
measurements and duplex ultrasonography

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20 • SPECIAL PROBLEMS

397

has been applied to the evaluation of injured
extremities for popliteal artery trauma, with
the potential of being less invasive and less
costly than, while equally accurate, as arteri-
ography and surgery. However, these modal-
ities have not realized their theoretical
potential for a number of reasons, including
equipment expense, lack of round-the-clock
availability of the necessary skill and exper-
tise in most hospitals, and a failure to show
any advantage over physical examination
alone. Several authors have documented
these modalities to have no benefit in this
setting (Bergstein et al, 1992; Tominaga et al,
1996).

Posterior Knee Dislocation

Posterior knee dislocation has been associated
with a substantial incidence of popliteal artery
trauma, for which reason mandatory arteri-
ography or popliteal exploration has been
advocated to avoid the high risk of limb loss
from delayed diagnosis of popliteal artery
injury. At least six published studies from the
past decade, which report 264 cases of poste-
rior knee dislocation, have related the initial
clinical findings to outcome (Table 20-3) . The

results demonstrate that only 23% (range,
13% to 25%) of all cases present with hard
signs of popliteal artery injury, and 70% of
this group (range, 18% to 100%) had arter-
ial injury requiring surgical repair (i.e., 30%
false-positive rate of physical examination for
the detection of surgically significant arterial
injury) . Among the 77% of all cases of pos-
terior knee dislocation presenting without
hard signs, there was not a single popliteal
artery injury that required surgical repair, a
result confirmed by follow-up studies of up to
1 year. These findings are consistent with those
of all other forms of extremity injury in con-
firming the reliability of physical examination
to exclude arterial injury. This has enormous
economic implications when considering the
expense and morbidity of routine diagnostic
workup that can be avoided in such a large
majority of patients, especially considering
how tight resources are in so many trauma
centers and other hospitals. Surgical explo-
ration of the popliteal artery is warranted in
the minority of patients presenting with hard
signs, especially when obviously due to arter-
ial disruption (e.g., pulsatile hemorrhage and
cool ischemic limb without pulses) . However,
preoperative arteriography in less obvious
cases of hard signs (e.g., transient pulse loss

TABLE 20-3

PUBLISHED CASES OF KNEE DISLOCATION RELATING PHYSICAL FINDINGS OF
VASCULAR INJURY TO OUTCOME

Hard Signs

Present

Hard Signs

Absent

Author

Year

No. KD

No.

(%)*

No. AIRS O^

No.

(%)*

No. AIRS

Treiman

1992

115

(25)

22 (75)

(75)

Kendall

1993

(16)

6(100)

(84)

Kaufman

1992

(21)

4(100)

(79)

0«

Dennis

1993

(13)

2(100)

(87)

Miranda

2000

(25)

6(75)

(75)

Martinez

2001

(48)

2(18)

(52)

Total

264

(23)

42 (70)

204

(77)

'Percentage of total knee dislocations.

♦Percentage of all patients with hard signs.

♦includes nine minimal arterial injuries with 6 months of average follow-up.

includes two minimal arterial injuries with 3 and 23 months of follow-up.

"Includes seven minimal arterial injuries with 1 1 .5 months of average follow-up.

includes five minimal arterial injuries with 3 months of average follow-up.

AIRS, arterial injuries requiring surgery; KD, knee dislocations.

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V • SPECIAL PROBLEMS AND COMPLICATIONS

and hematoma) may allow avoidance of
unnecessary vascular exploration in about
20% of cases by demonstrating an intact artery.

Treatment

GENERAL PRINCIPLES AND
TECHNIQUES

Prompt transport to the operating room and
induction of general anesthesia are necessary
once popliteal artery injury has been docu-
mented. The patient should be supine and
the injured leg should be prepared and
draped into the operative field, as should
one uninjured extremity in the event that
autogenous vein must be harvested. The leg
should be abducted and externally rotated
with a support under the knee, to facilitate
the standard longitudinal medial incision
above the knee for optimal popliteal artery
exposure. Retraction of the sartorius and semi-
membranosus muscles posteriorly opens the
popliteal space where the artery lies, with the
vein and nerve medial and posterior to it. Divi-
sion of the medial head of the gastrocnemius
muscle and tendons of the semimembranosus,
semitendinosus, and gracilis muscles allows
exposure of the more distal tibioperoneal
trunk. Although these structures may be
repaired, this is not necessary for an excel-
lent functional result. Arterial repair is per-
formed by the standard techniques ofvascular
surgery.

Hemorrhage from the injured artery should
be controlled by digital pressure until proxi-
mal and distal control can be obtained with
clamps or vessel loops. Obviously damaged
portions of the artery should be debrided back
to grossly normal vessel. Balloon catheter
thrombectomy should be performed proxi-
mally and distally, followed by distal injection
of heparinized saline to retard any further
thrombus formation. Systemic heparinization
may be used if associated injuries permit.

Lateral arteriorrhaphy may be performed
with clean lacerations involving less than 30%
of the arterial circumference, although
only 10% 15% of popliteal artery injuries are
amenable to this. Care must be taken to avoid

stenosis and thrombosis, and vein patch angio-
plasty may facilitate this. End-to-end anasto-
mosis is preferred if it can be done without
undue tension but is generally not possible if
more than 2 cm of artery is lost. Geniculate
collaterals should not be divided to achieve
mobility because of the detrimental effect this
may have on limb perfusion. In this setting,
interposition grafting should be performed,
preferably using reversed autogenous saphe-
nous vein. Prosthetic grafts across the knee
joint tend to have lower patency rates. Arter-
ial anastomosis and repair are performed with
a running monofilament nonabsorbable
suture, achieving intimal coaptation. Surgical
repair should not be considered complete
until distal perfusion is clearly documented
with palpable pulses in the feet.

SURGICAL ADJUNCTS

A number of measures are available in addi-
tion to standard surgical repair of popliteal
artery trauma, which should further improve
outcome from these dangerous injuries. The
liberal use of preoperative and intraoperative
systemic and regional anticoagulation with
intravenous heparin has been mentioned.
Postoperative anticoagulation should almost
never be necessary, because it cannot substi-
tute for the meticulous and appropriate tech-
nique, which is the most important factor in
a successful surgical repair. Any failure of arte-
rial repair should mandate exploration and
revision. Completion arteriography is impor-
tant to ensure patency and distal runoff, espe-
cially if there is any doubt about the adequacy
of revascularization. This can be done on the
operating table by direct needle puncture of
the vessel proximal to the injury and injec-
tion of water-soluble contrast.

Extra-anatomic bypass should be consid-
ered when the native vessel bed is unsuitable
for vascular repair, because of contamination,
devitalized tissue, or lack of soft tissue cover-
age. A prosthetic or autogenous vein inter-
position is tunneled laterally through clean
tissue planes from uninvolved proximal and
distal portions of the artery, allowing open
management of the wound without worry
about the vessel.

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20 • SPECIAL PROBLEMS

399

Fasciotomy to release excessive pressure
within the major tissue compartments of the
lower leg is a critical adjunct to popliteal artery
repair, because injury to this artery poses
a high risk of compartmental hypertension
and tissue loss (see Chapter 27) . Early or pro-
phylactic fasciotomy in this setting has been
associated with improved limb salvage and
function.

Intraluminal shunting of injured popliteal
arteries can be a useful adjunct in those cir-
cumstances in which a delay is necessary for
skeletal stabilization, soft tissue debridement
or vein repair. This immediately restores per-
fusion, allowing these other problems to
be addressed deliberately without ongoing
ischemia, before definitive arterial repair is
performed.

NONOPERATIVE OBSERVATION

A select group of arterial injuries are nonoc-
clusive and manifest no hard signs, and these
have been shown to have a high rate of spon-
taneous resolution or nonprogression when
left untreated. These include intimal flaps,
vessel narrowing, and small false aneurysms
and arteriovenous fistulas, in which the artery
and its runoff remain intact. When found
on arteriography, the safety of nonoperative
observation of these asymptomatic arterial
injuries has been established by long-term
follow-up averaging 10 years. This category of
arterial injuries exclusively includes the 10%
to 15% of arterial injuries known to occur in
the setting of asymptomatic lower extremity
trauma that places the popliteal artery at risk,
such as penetrating proximity wounds and
high-risk fractures and posterior knee dislo-
cation. This is what justifies the simple obser-
vation of asymptomatic lower extremity
trauma without the need for routine surgery
or diagnostic imaging for popliteal artery
injury (see Table 20-3). The safe avoidance
of this routine diagnostic workup on the basis
of only a negative physical examination has
clear advantages in terms of substantial savings
of cost and resource use, as well as reduced
limb morbidity.

MANAGEMENT OF VENOUS
INJURIES

History and Epidemiology

The evolution of the management principles
and techniques for venous injuries has
followed the same path as that for arterial
injuries, although an appreciation for the dis-
tinct differences in venous response to injury
and repair did not occur until relatively
recently. The first successful surgical repair of
a venous injury is credited to the German
surgeon Schede in 1882, who reported the
lateral suture of a femoral vein. Kummel per-
formed the first successful end-to-end venous
anastomosis in 1899, and Goodman reported
four cases of lateral venorrhaphy in World War
I. Ligation of all injured and uninjured veins
adjacent to an arterial injury was advocated
by Makins in World War I, to theoretically
increase the "dwell time" of blood within the
injured extremity after arterial ligation.
Venous ligation remained standard practice
through World War II and the Korea War,
although 20 venous injuries underwent
surgical repair in the latter conflict. In the
Vietnam War, an aggressive approach toward
routine repair of all venous injuries was advo-
cated after reviewing the major complications
resulting from venous ligation in the Vietnam
Vascular Registry. The overall rate of venous
repair rose to 33% in this conflict, and the
clear benefits of repair were demonstrated.
The fears of previous years that repair would
lead to increased levels of thrombophlebitis
and embolism were proven groundless and
were shown to occur more often when veins
were ligated. This military experience rapidly
spread into the civilian sector. In 1960, Caspar
and Treiman published the first large series
of civilian venous injuries, which confirmed
the problems with ligation and the safety
and feasibility of routine repair of venous
injuries.

The actual incidence of peripheral venous
injuries is unknown, because many are known
to be asymptomatic, heal spontaneously, and
are never discovered. Venous injuries made
up 39% of all vascular injuries in the Korean
War and 27% of all vascular injuries in the

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V • SPECIAL PROBLEMS AND COMPLICATIONS

Vietnam War. They were most often (86%)
associated with an adjacent arterial injury in
both conflicts. These were largely peripheral
in location, because abdominal and cervical
venous injuries are highly lethal in military
settings, and virtually all were due to destruc-
tive and high-velocity penetrating mecha-
nisms. In the civilian sector, venous injuries
similarly comprise between 13% and 51% of
all vascular injuries, and 35% to 63% of all
extremity vascular trauma. In this setting, they
also are most commonly due to penetrating,
though low-velocity, mechanisms and most
commonly occur in association with an adja-
cent arterial injury. Blunt mechanisms cause
5% to 15% of all civilian venous injuries (Table
20-4) . Isolated venous injuries are most likely
to result from stab wounds than from other
blunt or penetrating agents. Abdominal
venous injuries comprise as much as 15% of
all civilian vascular trauma. The superficial
femoral vein and the popliteal vein are the
most commonly injured veins overall in
military and civilian series, respectively,
consistent with the most common sites of
arterial injury. The inferior vena cava is the
most common site of abdominal venous
injury.

Diagnosis

Peripheral venous injuries are most commonly
found incidentally during exploration for an

arterial injury. Although they may manifest
hard signs, these signs are not specific for
venous trauma. Bleeding from the low-
pressure venous system is generally easily tam-
ponaded by surrounding structures, which is
why venous injuries often are not detected in
the absence of arterial injuries. When isolated,
venous injuries most commonly present
as hemorrhage or large hematoma, which
prompts the surgical exploration leading to
their detection. Venous trauma is most likely
to present with severe bleeding, shock, or
hypotension when combined with an arterial
injury or when involving one of the major
abdominal veins.

Routine venography following extremity
trauma has been advocated. Gerlock and col-
leagues (1976) performed this imaging in 30
consecutive pati en ts with penetrating extrem-
ity trauma, detecting five venous injuries
(17%). However, four of these five injuries had
associated arterial injuries that would have led
to their detection without venography. Gagne
and colleagues (1995) found venography of
injured extremities to be suboptimal and to
be difficult to perform, with more than 50%
of attempts technically unsuccessful and only
43% of all venous injuries detected. The only
benefit of routine venography would be in
its detection of previously unsuspected and
asymptomatic venous injuries, but there is no
evidence to support that such occult venous
trauma results in any adverse sequelae when
left untreated. In fact, occult venous trauma,

TABLE 20-

-4

EXTREMITY VENOUS INJURIES:

MECHANISM AND MANAGEMENT

Author

Year

Total No.

No. Penetrating

No. Isolated

No. Repaired

Rich*

1970

377

124

Sullivan*

1971

Agarwal

1982

Phifer

1984

Ross

1985

Pasoh

1986

Borman

1987

Meyer

1987

Ye Ion

1992

Timberlake

1995

322

292

Total

1108

956 (95%) f

220 (20%)

502 (45%)

'Military series.

+ Based on 1004 injuries that could be evaluated.

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20 • SPECIAL PROBLEMS

401

even in the inferior vena cava, has been shown
to have no long-term complications, suggest-
ing that routine diagnostic imaging for this
purpose is unnecessary and not cost effective.
On the other hand, Gagne and colleagues
(1995) found major thromboembolic com-
plications to occur in 50% of patients with
documented asymptomatic venous injuries
following penetrating extremity trauma,
although whether this was specifically related
to the venous trauma is not clear.

Duplex ultrasonography has been applied
to the detection of arterial injuries following
extremity trauma by several authors. Gagne
and colleagues (1995) reported the detection
of occult venous injuries in 22% of patients
with asymptomatic penetrating extremity
trauma, although the benefits of this detec-
tion were not clear.

Currently most trauma centers do not
perform venous imaging of any sort follow-
ing torso or extremity trauma. In cases pre-
senting with hard signs, imaging is generally
contraindicated, because immediate surgery
is warranted. In the absence of hard signs,
imaging is unnecessary because there is no
clear benefit to intervention for occult venous
injury. Only if subsequent symptoms develop,
such as venous insufficiency or thromboem-
bolic events, would venous imaging be
justified.

Unlike arterial trauma, minimal debride-
ment of injured veins is generally necessary.
Proximal and distal thrombectomy should
be done by gentle milking and the judicious
use of balloon catheters, to avoid valvular
damage. In combined venoarterial extremity
trauma, especially with obvious ischemic
changes, intraluminal shunting of the artery
restores distal perfusion immediately, allow-
ing deliberate venous repair, as well as any
necessary soft tissue or skeletal repairs,
without the danger of ongoing ischemia and
tissue loss. Another consideration in such
combined vascular injuries is to shunt the
vein while first repairing the artery, to provide
adequate outflow for the artery during its
repair and optimizing its success. The shunted
vessel in either case then can be definitively
repaired.

A variety of techniques that correspond to
the same techniques used for arterial injuries
have been described for repair of venous
injuries. Lateral venorrhaphy, for partial cir-
cumferential lacerations, and end-to-end
anastomosis, for transections with little loss of
vessel length, are the most common methods,
as well as the quickest and easiest to perform.
Uncommonly used and more difficult and
time consuming are interposition grafting with
either reversed autogenous vein or prosthetic
graft and the construction of spiral grafts or
panel grafts from segments of autogenous
vein.

Treatment

GENERAL PRINCIPLES

Management of the patient with venous injury
is essentially identical to that for any vascular
injury. Prompt digital or manual control of
any active external bleeding is followed by
volume resuscitation through large-bore in-
travenous catheters placed in uninjured
areas. Longitudinal incisions directly over the
injured vessels should be made. Digital control
of the injury, sponge-stick compression, in-
traluminal balloon catheters, or occluding
clamps are methods that control venous
bleedingfrom the area of injury while thevein
is dissected free and formal proximal and distal
control can be achieved using clamps or elastic
vessel loops.

VENOUS REPAIR CONSIDERATIONS

The motivation for repair rather than ligation
of venous injuries began with the observation
of the sequelae of venous hypertension and
venous insufficiency following ligation in the
Korean War. Rich and colleagues (1976) con-
firmed these observations during the Vietnam
War, noting a substantially greater incidence
of extremity edema, stasis dermatitis, ulcera-
tion, and chronic venous insufficiency in limbs
that underwent major venous ligation com-
pared with those undergoing venous repair.
This difference was especially true for the
popliteal vein, which provides the major
channel for venous drainage from the lower
extremity. Several cases of limb amputation
were attributed directly to ligation or failed

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V • SPECIAL PROBLEMS AND COMPLICATIONS

repair of popliteal vein injuries. An aggressive
approach toward routine repair of all venous
trauma, especially in the popliteal system, led
to dramatic improvements in limb salvage and
function and dispelled the fears of earlier
years that repair would lead to problems with
thrombophlebitis and venous thromboem-
bolism. A long-term follow-up of 1 10 popliteal
vein injuries from this conflict (Rich, 1982)
demonstrated a reduction of significant limb
edema from 51% in cases of vein ligation to
only 1 3% in those undergoing vein repair. The
safety and feasibility of venous injury repair
had also been shown in the civilian sector by
Caspar and Treiman (1960) and by experi-
mental studies. Repair of the inferiorvena cava
not only prevents lower limb edema but also
restores venous return to the heart to offset
hemorrhagic and cardiogenic shock. Pul-
monary embolism has been reported in only
2% of these cases.

The natural history of surgically repaired
venous injuries is characterized by a substan-
tial rate of thrombosis in the postoperative
period that far exceeds that seen following
arterial repair. This was documented by Rich
(1970) in the Vietnam War in isolated cases.
In the civilian sector, Meyer and colleagues
(1987) found that 39% of their peripheral
venous repairs thrombosed within 1 week by
venography, and that this thrombosis rate
was higher in complex repairs (59%) than in
simple repairs (21 % ) . Hobson and colleagues
(1983) reported postoperative thrombosis in
26% of femoral vein repairs, but a significantly
higher rate of limb edema (75%) in these
occluded repairs than in those remaining
patent (23.5%). Agarwal and colleagues
(1982) found postoperative thrombosis in
80% of vein repairs followed by venography,
and Nypaver and colleagues (1992) found this
to occur in 28% of their venous repairs.

Despite these findings, restoration ofvenous
continuity appears to offer major advantages
over ligation. Most series have reported few
if any adverse sequelae in the limbs of patients
with thrombosed venous repairs, indicating
that venous repair allows the development of
venous collaterals. Also, a number of long-
term follow-up studies have shown a high
rate of recanalization of thrombosed venous
repairs, which cannot occur following ligation.

Nypaver and colleagues (1992) documented
that 88% of previously thrombosed vein
repairs were subsequently patent by color-flow
duplex sonography over a 49-month average
follow-up, providing a 90% long-term patency
rate. Phifer and colleagues (1985) showed
100% patency of five femoral vein repairs over
follow-ups ranging from 6 to 20 years.

These results indicate that veins are
extremely sensitive to injury and surgical
manipulation, and that meticulous technique
is essential to minimize postoperative throm-
bosis. Gentle handling of venous endothe-
lium, rigorous attention to intimal apposition,
and precise suture techniques that restore the
vein lumen to its normal diameter without
stricture have all been recommended to opti-
mize patency. The use of vein patch or inter-
position grafting is suggested if simple repair
narrows the venous lumen. Completion
venography has been recommended to ensure
widely patent surgical repairs, but few prac-
tice this. Although prosthetic grafts for venous
injury repair result in especially high rates
of thrombosis, they have the advantage of
allowing rapid restoration of continuity and
reducing operative bleeding in large open
wounds with extensive soft tissue disruption
and at fasciotomy sites, by providing imme-
diate venous drainage and avoiding venous
hypertension.

A number of adjuncts to venous injury
repair have been reported to improve post-
operative results. Temporary arteriovenous
shunts or arteriovenous fistulas created distal
to extremity venous repairs have improved
patency rates but have the disadvantages
of increased limb edema from the higher
venous flow, reduction in arterial flow, and
the need for a second operative procedure to
take these down. Systemic anticoagulation and
antiplatelet therapy has been applied to
reduce postoperative thrombosis, but Hobson
and colleagues (1973) showed no effect of
these measures on improving postoperative
patency rates. Intermittent pneumatic com-
pression devices offer theoretical promise but
have not been studied for any benefit in this
setting.

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20 • SPECIAL PROBLEMS

403

VENOUS LIGATION CONSIDERATIONS

Clinical experience with the morbid seque-
lae of the standard practice of ligation of
venous injuries during the Vietnam War
called this practice into question. Several pub-
lished experimental studies by Stallworth and
colleagues (1967), Barcia and colleagues
(1972), Hobson and colleagues (1973), and
Wright and colleagues (1973, 1974) docu-
mented that acute femoral venous occlusion
in uninjured canine limbs resulted in signif-
icant reductions in arterial inflow. This
reduced flow returned to baseline within 72
hours, suggesting venous collateral develop-
ment, but the jeopardy this poses to an
injured limb, especially in the presence of a
fresh arterial repair, is obvious. Clinical inves-
tigations from military and civilian settings
confirmed these findings in showing increased
limb morbidity and limb loss following venous
ligation, especially in the popliteal system.

Since the Vietnam War, the enthusiasm for
routine repair of venous injuries that these
studies fostered has been tempered by several
civilian studies showing remarkably uncom-
plicated outcomes following ligation of major
veins in injured extremities. Muffins, Lucas,
and Ledgerwood (1980) showed the absence
of any clinically significant short- or long-term
impairment of limb function in 46 patients
undergoing ligation of injured major veins,
70% of which were in the lower extremity.
Eight of these patients had moderate edema
requiring support stockings, but no limitation
of activity. Several other authors have since
documented acceptable levels of limb mor-
bidity following lower extremity vein ligation,
including inferior vena cava and iliac veins,
though with varying levels of postoperative
edema in up to 50% of patients. There have
been no instances of limb loss attributable to
venous ligation in these reports. Studies by
Meyer and colleagues (1987), Pasch and col-
leagues (1986), Yelon and Scalea (1992), and
Timberlake and Kerstein (1995) report a total
of 440 patients with major peripheral venous
injury, including the popliteal and femoral
veins, with no limb loss and no significant long-
term edema following vein ligation, as well as
no difference in outcome between patients
undergoing vein ligation and those under-

going vein repair. Ligation of major venous
injury is consistently tolerated without prob-
lems in the upper extremities and neck, attrib-
utable to the greater collateral drainage than
that found in the lower extremities.

Recent studies of inferior vena cava and iliac
vein injuries show similar results for repair and
ligation, although these tend to be more
severely compromised patients because of
the shock and blood loss accompanying
these injuries. Burch and colleagues (1990)
reported 161 iliac vein injuries, with a higher
rate of venous morbidity (26%) among cases
that were ligated (consisting only of limb
edema and deep vein thrombosis) than in
those repaired (4.9%, two cases edema and
two of pulmonary embolism) , but without any
limb loss.

Successful outcome of limb salvage and
function following venous ligation demands
an aggressive use of several adjunctive mea-
sures to promote venous drainage. These
patients should be placed on bed rest, with
avoidance of dependent positioning of their
limbs. Lower extremities should be wrapped
in elastic bandages and elevated for several
days before carefully beginning ambulation.
Four-compartment lower leg fasciotomy
should be applied liberally and prophylacti-
cally, to offset the very high probability of
development of compartment syndrome. If
fasciotomy is not performed, careful serial
measurement of compartment pressures is
necessary. Routine anticoagulation has no
proven benefit.

ROLES OF LIGATION AND REPAIR

Although the published evidence appears con-
tradictory in many ways regarding the rela-
tive merits of ligation or repair of venous
injuries, each can clearly be successful under
certain conditions (see Table 20-4) . Which
approach is best in any setting requires that
the reported differences in outcome be under-
stood and reconciled. Venous ligation results
in the worst outcome in military series and
experimental models, which can be explained
by the greater collateral damage of bone and
soft tissue, as well as the total venous outflow
occlusion, which occurs in these settings. In

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V • SPECIAL PROBLEMS AND COMPLICATIONS

actual clinical venous injury in the civilian
setting, the better results of ligation can be
explained by the simpler, less destructive
wounds without major associated trauma and
by the fact that ligation of any single vein does
not totally occlude limb outflow.

Most authorities agree that all injuries to
major veins should undergo surgical repair,
unless there are more pressing priorities, such
as life-threatening problems, which preclude
it. Hemodynamic instability, ongoing hem-
orrhage, and life-threatening associated
injuries to other body systems that require
immediate attention are the most common
indications to revert to ligation of venous
injuries. This is a basic tenet of the damage
control approach to severely injured patients,
because venous repair always requires more
time to accomplish than ligation, and complex
repairs take more time than simple repairs.
Some authors recommend that ligation be
performed if repair requires anything more
complex than lateral suture or end-to-end
anastomosis, in view of the added time and
worse outcome of complex repairs. Deaths
have been attributed to ill-considered attempts
at complex venous repairs. Ligation of all
upper extremity veins and unilateral internal
jugular veins can be performed without a
problem. Patients generally tolerate ligation
of any vein in the body as long as adjunctive
measures are properly applied. Also, ligated
veins can be reversed by elective definitive
repair if necessary in those uncommon
instances that severe complications develop
in the future.

It is important to recognize those circum-
stances in which venous repair should be
attempted even under suboptimal conditions
of patient instability or complex trauma. In
patients with injuries involving massive tissue
destruction, from blunt or high-velocity pen-
etrating trauma, repair of a major vein may
be critical in providing limb outflow, even
if that repair must be complex or requires a
prosthetic graft. In combined arteriovenous
trauma in the same extremity, venous repair
should be undertaken to provide outflow for
the arterial repair and optimize its success.
Any popliteal vein injury merits all possible
effort to repair rather than ligate due to the
known severe and limb-threatening morbid-

ity that is associated with ligation. Bilateral
internal jugular vein injuries in the neck
warrant repair of one side to provide critical
intracranial venous outflow. In critical cir-
cumstances, temporary intraluminal shunts
may be used as a damage-control measure to
quickly restore venous outflow, allowing defin-
itive repair to be done later when conditions
stabilize.

Some authors advocate routine follow-up
imaging of repaired venous injuries with
venography or duplex scanning, to detect
thrombosis early. However, an understanding
of the natural history of venous repairs makes
clear why this practice is unnecessary and is
not used by most centers. The known high
incidence of postoperative thrombosis is
typically followed by spontaneous recanaliza-
tion to provide a very high long-term patency.
Also, even thrombosed repairs manifest very
few clinical problems. Imaging should be
applied only to those few patients in whom
symptoms of disabling edema and chronic
venous insufficiency develop, in which case
anticoagulation or surgical revision may be
considered.

COMBINED VASCULAR
AND SKELETAL
EXTREMITY TRAUMA

Extremity trauma that involves both skeletal
and vascular injuries poses one of the
most difficult management problems. These
complex injuries often involve extensive soft
tissue and nerve damage as well and are some-
times termed mangled extremities. It is impor-
tant to understand the unique considerations
of epidemiology, pathophysiology, prognosis,
diagnosis, and multidisciplinary priorities in
this setting, to reduce the substantial risks of
limb loss that currently prevail.

Epidemiology and
Prognostic Factors

Combined vascular and skeletal extremity
injuries are relatively uncommon, making up
only 0.2% of all military or civilian trauma.

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20 • SPECIAL PROBLEMS

405

Vascular and trauma surgeons are more likely
to see this combined trauma than orthopedic
surgeons, because only 1.5% to 6.5% of all
extremity skeletal traumas are associated with
an arterial injury of the same extremity,
whereas 10% to 73% of all extremity arterial
injuries may be associated with skeletal frac-
tures and dislocations.

Combined vascular and skeletal extremity
injuries pose a substantially increased risk of
amputation and limb morbidity than isolated
arterial or skeletal injuries. This was docu-
mented in several military series dating back
to World War II. These reports showed that
combined injuries were associated with ampu-
tation rates ranging up to ten times those from
isolated arterial extremity injuries, even as the
outcomes for both simple arterial and com-

bined combat extremity injuries improved
over the past 50years (Table 20-5) .McNamara
and colleagues (1973) also showed a signifi-
cantly higher incidence of failed vascular
repair among combined extremity injuries
(33%) than among isolated arterial injuries
of the extremity in the Vietnam War (5%).
Similar striking differences have been re-
ported in the civilian sector even in recent
years. At a time when isolated arterial or skele-
tal extremity trauma can be expected to result
in limb loss in far less than 5 % of civilian cases,
the combination of these injuries in the same
extremity still are associated with amputation
rates up to 68% in the most experienced
trauma centers (Table 20-6). Even many sal-
vaged extremities are significantly disabled.
These results are largely due to delayed recog-

TABLE 20-5

AMPUTATION RATES (%) FOLLOWING COMBAT EXTREMITY ARTERIAL INJURIES
WITH AND WITHOUT ASSOCIATED SKELETAL TRAUMA

Author

Year

Conflict

DeBakey

1946

World War

Spencer

1955

Korea

McNamara

1973

Vietnam

Romanoff

1979

srae

Lovric

1994

Croatia

Isolated Arterial Injury

42
15
2.5
11

Combined Injury

60
55
23

36
10

TABLE 20-6

MECHANISM AND OUTCOME OF COMBINED CIVILIAN VASCULAR/SKELETAL
EXTREMITY TRAUMA

Author

Schlickwei

Van Wijngarden

Alexander

Johansen

Odland

Lange

Palazzo

Howe

Bongard

Drost

Bishara

Attebery

Year

1992
1993
1991
1990
1990
1985
1986
1987
1989
1989
1986
1996

% Penetrating

9
<10
10
13
18
24
30
36
57
71

% Amputation

41.5

7(0)

3(0)

7(0)

'Numbers in parentheses refer to amputations among penetrating injuries only.

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406

V • SPECIAL PROBLEMS AND COMPLICATIONS

nition of vascular injury, major nerve damage,
and increased failure of vascular of repair due
to disruption of collaterals from soft tissue
injury, soft tissue infection from inadequate
debridement, failure to provide adequate
tissue coverage over sutured vessels, and
delayed recognition and treatment of com-
partmental hypertension.

Mechanism of injury is another important
determinant of outcome in this setting. Vir-
tually all combined extremity injuries in mil-
itary series are due to destructive high-velocity
penetrating mechanisms. These approximate
the level of tissue damage found in most blunt
trauma, which has been the predominant
mechanism for this distinct category of
extremity trauma in most civilian series.
However, an increasing incidence of simple
penetrating trauma has been reported as a
cause of these injuries in the civilian sector
over the past decade, ranging from 18% to
71 % of cases. Some correlation is also evident
between the extent of penetrating trauma and
an improved outcome in these series (see
Table 20-6). Among 119 patients with com-
bined vascular and skeletal extremity injuries
reported in three of these series (Bishara and
colleagues, 1986; Palazzo, 1986; Attebery
and colleagues, 1996), 63 cases (53%) were
due to penetrating trauma, and the total
amputation rate was the lowest ever reported
(well below 10%), with no amputations among
any of the cases due to penetrating injury.

It is generally accepted that penetrating
trauma has a better outcome than blunt

trauma, because of less severe and extensive
associated tissue damage. Therefore, it should
be no surprise that the increasing trend in
low-velocity penetration as an etiology for com-
bined vascular and skeletal extremity trauma
in the civilian sector appears responsible for
the most substantial contribution yet to reduc-
ing limb loss from these devastating injuries.
Five civilian series of combined extremity
trauma have been published since 1986 in
which more than 50% of cases were due to
penetrating mechanisms (Table 20-7). The
overall rate of penetration among all 228
reported cases was 64.5%. The overall ampu-
tation rate was 17%, but among penetrating
injuries, itwas only 6%. Only 23% of all ampu-
tations were in patients with penetrating
trauma. Among 88 patients with penetrating
combined injuries reported in three of these
series, remarkably there were no amputations.
Although some published series of combined
extremity trauma report no difference in
outcome between blunt and penetrating
mechanisms, and some report a higher ampu-
tation rate among penetrating injuries, these
series involve small numbers and particularly
severe injuries. Nonetheless, they demonstrate
that a number of variables other than mech-
anism affect outcome.

Diagnosis

Prompt and accurate diagnosis of vascular
injury is critically important in the setting of

TABLE 20-7

OUTCOME OF PREDOMINANTLY PENETRATING COMBINED CIVILIAN
VASCULAR/SKELETAL EXTREMITY TRAUMA

No.

Amputations (%)

Author

Year

No. Patients

No. Penetrating (%)

Total

Penetrating

Norman

1995

30(100)

Attebery

1996

29(71)

3(7)

Swetnam

1986

24 (67)

16(44)

8(33)

Bishara

1986

29 (57)

1(2)

Russell

1991

35 (50)

19(27)

1(3)

Total

228

147(64.5)

39(17)

9(6)

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20 • SPECIAL PROBLEMS

407

an extremity fracture or dislocation, because
prolonged ischemia and delay in restoration
of blood flow are cited in most studies as major
contributors to limb loss and limb morbidity.
The clinical presentation of the patient and
the physical examination are the key elements,
and in many cases the only elements, neces-
sary for diagnosis or exclusion of vascular
injury in this setting. Contrast-enhanced arte-
riography is the standard imaging modality
used to make this diagnosis, although its exact
role is debated.

The presence of hard signs (hemorrhage,
hematoma, bruit or thrill, absent pulse, distal
ischemia) in uncomplicated extremity trauma
has been shown to predict major vascular
injury with an accuracy approaching 100%
and therefore generally mandates immediate
operation without any imaging. However,
combined skeletal and soft tissue disruption
substantially reduces the positive predictive
value (i.e., hard signs present) of physical
examination for surgically significant vascu-
lar injury. Applebaum and colleagues (1990)
reported 53 cases of complex blunt extrem-
ity trauma, documenting vascular injuries in
39% of all cases manifesting hard signs, but
in only 13% of cases did these injuries require
surgical repair. This represented an 87% false-
positive rate of physical examination for the
detection of surgically significant vascular
injury, the only ones to require detection and
treatment, similar to that reported in other
series. This can be explained by the fact that
fractures, soft tissue disruption, traction, and
distortion of arteries by bony fragments,
nerve injuries, and compartment syndrome,
all common features of complex limb trauma,
can cause hard signs in the absence of injury
to a major artery. Arteriography is recom-
mended in complex extremity trauma that
manifests hard signs, to exclude an arterial
injury to avoid as much as an 87% rate of
unnecessary vascular exploration in these
already compromised limbs (Figs. 20-1 and
20-2).

On the other hand, arterial imaging does
not appear necessary in complex extremity
trauma without hard signs. Current evidence
indicates that a negative physical examination
result (i.e., no hard signs) excludes surgically
significant arterial injury as reliably as both

■ FIGURE 20-1

Arteriogram performed for displaced
supracondylar femur fracture manifesting
hematoma and uncertain distal pulses,
confirming intact popliteal artery and runoff and
sparing unnecessary vascular exploration. ■

arteriography and surgical exploration.
Nonocclusive vascular injuries may still occur
but are known to have a benign natural history
and therefore do not require detection. The
economic advantages of avoiding routine
arteriography in this group of patients are
obvious, as discussed in previous sections of
this chapter (see "Popliteal Artery Injuries"
and "Posterior Knee Dislocation," earlier in
this chapter) .

When indicated for complex extremity
trauma, arteriography is best performed as a
percutaneous hand-injected study right in the
trauma center or on the operating table with
the extremity already prepared and draped
(see Fig. 20-2) . This technique is easily per-
formed by any surgeon, using a simple intra-
venous catheter slipped over a needle directly
into the femoral artery at the groin or brachial
artery above an occluding blood pressure cuff,
with a radiographic plate placed under the
injured extremity, and injecting 30 mL of
water-soluble contrast while the x-ray film is
exposed by a portable unit. Substantial time
is saved by this procedure, as formal arteri-
ography in the radiology suite takes at least 1
to 3 hours even in major trauma centers. This

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408

V • SPECIAL PROBLEMS AND COMPLICATIONS

■ FIGURE 20-2

Percutaneous one-shot hand-injected
arteriogram on operating table following
comminuted tibial plateau fracture with
hematoma and poorly palpable distal pulses,
showing occluded anterior tibial artery,
narrowed tibioperoneal trunk, and intact
posterior tibial artery with nonocclusive intimal
defect (arrow). No vascular repair was
necessary, skeletal repair was immediately
performed, and distal perfusion remained intact
without subsequent problems. ■

is critical to optimize limb salvage. On-table
arteriography is also highly accurate, provides
excellent resolution, and allows immediate
treatment to begin on either the vascular or
the skeletal injury, depending on the arteri-
ogram results.

Although noninvasive vascular studies with
Doppler pressure monitoring and duplex
ultrasonography have been applied to the eval-
uation of complex extremity trauma for
vascular injury, there is as yet no clear role for
these modalities. In fact, the expertise
required for interpretation of these tests, their
lack of round-the-clock availability in most

hospitals, and the significant swelling, skele-
tal disruption, and bulky splints and dressings,
which characterize these extremities, cast
doubt on the utility and accuracy of nonin-
vasive tests in this setting. Any use of these
tests for diagnosis or exclusion of vascular
trauma should be within the context of a con-
trolled study, and their results should be inter-
preted with caution. Arteriography remains
the standard modality of choice for evalua-
tion of high-risk complex extremity trauma
for vascular injury.

Treatment

Combined vascular and skeletal trauma
requires a multidisciplinary approach to treat-
ment, which can succeed only with the smooth
and coordinated interaction between the
various specialties involved in caring for the
skeletal, soft tissue, and vascular injuries,
as well as for the patient as a whole. All life-
threatening injuries must be treated as a first
priority. Once the extremity is addressed,
orthopedic surgeons and plastic surgeons
should be involved integrally in the treatment
decisions, along with the trauma or vascular
surgeon, as soon as a diagnosis of combined
extremity trauma is established.

Prompt restoration of blood flow within 6
hours of any extremity vascular injury is the
most critical of the many factors that deter-
mine limb salvage and function. Clinical and
experimental studies consistently demon-
strate a direct linear relationship between the
time interval to extremity reperfusion and the
amputation rate. Associated skeletal and soft
tissue injury makes this time factor even more
important. A small number of retrospective
studies fail to show a correlation between time
delay and outcome, but this again emphasizes
that multiple variables are at play in these dev-
astating extremity injuries. The weight of evi-
dence mandates that rapid diagnosis, based
on the clinical manifestations and selective
application of one-shot on-table arteriography,
be followed as expeditiously as possible by
restoration of blood flow.

Prioritization of management of the vas-
cular and skeletal extremity injuries has been
subject to debate and uncertainty, leading to

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20 • SPECIAL PROBLEMS

409

wide variations in practice. Early studies rec-
ommended that skeletal repair take priority
in combined extremity trauma, to avoid the
potential disruption of an initial fresh vascu-
lar anastomosis by subsequent manipulation
of bone fragments or length discrepancies in
any initial vascular repair caused by subse-
quent stabilization of comminuted, unstable
skeletal injuries. It was believed that some delay
in reperfusion is acceptable in the absence of
overt ischemia. However, these conjectures
have been refuted by much published evi-
dence. Substantial tissue damage can occur
in the absence of signs of ischemia, as has been
made clear by our understanding of com-
partment syndrome. Disruption of an initial
vascular repair by subsequent skeletal manip-
ulation occurs only rarely. Snyder and col-
leagues (1982) reported this to occur in only
7% of cases, and Downs and colleagues (1986)
reported this in only 2% of all cases of com-
bined extremity trauma undergoing initial vas-
cular repair, and in each case, the repair was
immediately revised with no effect on limb
salvage. Howe and colleagues (1987) reported
no vascular disruption in 21 such cases.
Jahnke and Seeley (1953) generally per-
formed initial vascular repairs in combined
extremity injuries in the Korean War without
adverse sequelae. Also, the resistance of
repaired vessels to disruption has been under-
estimated. Connolly and colleagues (1969)
demonstrated that the strength of fresh
anastomoses of transected canine femoral
arteries with associated femur fractures
approximated that of native vessels, resisting
disruption by either 30 pounds of traction or
by bone fragment impalement. These data
are further supported by clinical studies
(Romanoff, 1979; McCabe, 1983), which
demonstrate a substantially higher rate of limb
salvage among combined extremity injuries
in which vascular repair is undertaken first,
compared with those in which revasculariza-
tion is delayed until skeletal stabilization/
repair is completed. Most importantly, no dis-
advantage has ever been documented for
initial revascularization, whereas the dangers
of delay are well established. Any delay in revas-
cularization must be considered a gamble. Of
course, this makes eminent sense, because
perfusion, rather than immediate skeletal

continuity, is the sine qua wow of limb survival.
Furthermore, as mentioned earlier, published
studies consistently report that the most
common reason for limb loss in this setting is
delay or failure of revascularization, not of
skeletal repair.

It must be emphasized that restoration of
extremity perfusion does not always require
definitive vascular repair. Temporary plastic
or Silastic intraluminal shunts placed in
the severed ends of vessels following distal
thrombectomy can restore distal perfusion
within minutes. In fact, a formal vascular repair
should be avoided in the setting of unstable
and severely comminuted fractures and dis-
locations, segmental bone loss, or severe soft
tissue disruption and contamination. Shunt-
ing in these cases allows deliberate attention
to wide debridement and skeletal stabilization
and fixation without ongoing ischemia, after
which definitive vascular repair can be per-
formed (Fig. 20-3). This avoids major stress
on a vascular suture line from bone manipu-
lation or undue tension or slack on the
repaired vessel when the limb is fixed at its
proper length. Alternatively, initial revascu-
larization can and should be accomplished by
immediate definitive arterial repair in the
setting of stable skeletal injuries in which
minimal subsequent manipulation and length
discrepancy is anticipated (Fig. 20-4) .The con-
sensus in the literature now strongly favors
limb revascularization as the immediate man-
agement priority in all combined extremity
trauma, as the aforementioned considerations
render moot any possible disadvantages. How
the revascularization is accomplished is a
matter of judgment, which depends primar-
ily on the nature of the skeletal and soft tissue
injuries.

Current evidence suggests that asympto-
matic nonocclusive arterial injuries found on
extremity arteriography are safe to observe
nonoperatively in the setting of combined
extremity trauma, where they have been
shown to have the same benign natural history
as in uncomplicated penetrating extremity
and neck trauma. Three published series
(Applebaum, 1990; Norman, 1995; Attebery
and colleagues, 1996) report a total of 98
asymptomatic arterial injuries in extremities
with associated skeletal trauma from both

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410 V • SPECIAL PROBLEMS AND COMPLICATIONS

* ■ . .

« 9

BUn

■ FIGURE 20-3

/A, Unstable elbow dislocation with brachial artery avulsion and loss of overlying skin. Distal
perfusion immediately restored by intraluminal brachial artery shunt, allowing cross-joint external
fixation and soft tissue debridement. 6, Artery was then repaired with autogenous vein graft, and a
pedicle flap provided immediate coverage. ■

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20 • SPECIAL PROBLEMS

411

■ FIGURE 20-4

A, Midshaft femur fracture with superficial femoral
artery thrombosis manifesting distal pulse deficit and
ischemia. B, Completion arteriogram showing vascular
injury repair by resection and autogenous saphenous
vein graft interposition (arrow) before the skeletal
injury was addressed. C, Intramedullary rod fixation of
femur fracture was then performed without vascular
complication. ■

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412

V • SPECIAL PROBLEMS AND COMPLICATIONS

blunt and penetrating mechanisms, of which
only one (1%) underwent surgical repair, and
that was a nonocclusive intimal flap of the
distal radial artery, which was probably unnec-
essary. There was no limb loss, limb morbid-
ity, or subsequent vascular problems. Attebery
and colleagues (1996) followed 15 asympto-
matic nonocclusive arterial injuries (35% of
all 41 vascular injuries associated with extrem-
ity skeletal trauma) for a mean interval of 6.5
months, and none ever required intervention
or became symptomatic. This series reported
one of the lowest rates of limb loss in this
setting (7.3%), and this was attributed in part
to the avoidance of unnecessary vascular
exploration in so many of these severely
injured limbs. These data add support to the
avoidance of diagnostic arteriography in
complex extremity trauma that does not man-
ifest hard signs of vascular injury.

The optimal method of fracture manage-
ment in combined vascular and skeletal
extremity trauma has evolved over the past
few decades. The military experience from the
Vietnam War demonstrated substantially
higher risks of limb loss following internal
skeletal fixation than was found after exter-
nal fixation (Rich, 1971; McNamara and col-
leagues, 1973). At least 50% of amputations
following internal fixation were due to infec-
tion. The civilian experience demonstrates
acceptable results with both internal and exter-
nal fixation, most likely because of the less
extensive bone damage in this setting. This
evidence suggests that combined extremity
injuries with a high risk of infection (e.g., open,
contaminated, extensive soft tissue injury) ,
comminuted or unstable skeletal trauma, or
those in unstable patients who require rapid
treatment undergo external skeletal fixation,
either as a definitive or as a temporizing
measure. Otherwise internal fixation is appro-
priate, either immediately or as a later defin-
itive measure.

Liberal use of a variety of surgical adjuncts
has shown some correlation with improved
limb salvage following combined extremity
trauma, just as it has in isolated extremity vas-
cular injuries. Completion intraoperative arte-
riography should be performed routinely
before completing vascular repairs to docu-

ment arterial patency and runoff, because any
technical errors in this tenuous limb could
easily lead to limb loss. Four-compartment fas-
ciotomy should be applied liberally and very
early or prophylactically in this setting because
of the especially high risk of compartment syn-
drome following reperfusion. Extra-anatomic
bypass or pedicle or free tissue flap coverage
may be necessary to protect vascular repairs
in the setting of severe contamination and soft
tissue injury or loss (see Fig. 20-3).

Indications for Amputation

Extensive and prolonged attempts to salvage
extremities with severe and complex injuries
may actually harm patients in a variety of ways,
especially if these efforts ultimately end in
amputation anyway. Financial costs, hospital
and intensive care unit days, infectious com-
plications, number of operative procedures,
time lost from work, permanent disability, and
even death have all been shown to be signif-
icantly greater when limb salvage becomes
unnecessarily prolonged compared with early
amputation. Those combined extremity
injuries that ultimately result in limb loss or
limb dysfunction can largely be predicted
within a few days of injury by a number
of prognostic factors that closely relate to
outcome. Transected major nerves and
Gustilo III-C injuries (open comminuted
tibiofibular fractures with arterial injury) are
the most common indications for considera-
tion of immediate amputation (Box 20-1).
Primary amputation at the time of presenta-
tion or early amputation within a few days
should be considered strongly whenever these
prognostic factors are present. The sophisti-
cation of limb prostheses, the early return to
work, short hospitalization, and lower costs
and complications following early amputation
are usually preferable to salvage attempts,
which may take months or years and still have
uncertain success.

Primary amputation without any attempt
at limb salvage is reported in 10% to 22% of
cases of complex extremity trauma, and such
immediate amputations account for more
than 50% of all amputations following these

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20 • SPECIAL PROBLEMS

413

COMBINED VASCULAR/SKELETAL EXTREMITY TRAUMA:
PREDICTIVE FACTORS FOR ULTIMATE LIMB LOSS OR
DYSFUNCTION

Transected tibial or sciatic nerve

Transection of two of three upper extremity nerves

Gustilo lll-C skeletal injuries

Prolonged ischemia (>6-12hr)

Below-knee arterial injury

Multiple fractures

Extensive soft tissue loss

Crush injury

Severe contamination

Elderly with medical comorbidity

Shock and life-threatening associated injuries

injuries. The decision to perform early ampu-
tation is one of the most difficult for trauma
surgeons. Although a number of predictive
scoring indices have been developed, using
factors known to correlate with limb salvage
(see Box 20-1) , none are sufficiently reliable
as prospective tools to make the decision for
us. In the end, it must be a matter of judg-
ment based on each individual case. This deci-
sion should always involve and require the
assent of the entire team involved in the care
of the patient, including the trauma, vascu-
lar, orthopedic, and plastic surgeons, reha-
bilitation specialist, psychologist, nursing,
and especially the patient and family.

A major consideration in the decision for
amputation is whether the injury is in the
upper or lower extremity. The upper extrem-
ity is more tolerant than the lower of deficits
in protective sensation, nerve function, and
length discrepancy, and prostheses are less sat-
isfactory. Therefore, amputation is generally
less necessary in the upper extremity for any
given level of tissue damage.

There are extremity injuries of such sever-
ity that a decision for primary amputation is
not difficult at all (Fig. 20-5). Any obvious
impossibility or futility of revascularization,

■ FIGURE 20-5

Gustilo lll-C complex extremity crush injury in a
64-year-old diabetic man with absent pulses
and severe ischemia and no arterial filling on
arteriogram. Primary above-knee amputation
was performed immediately without attempting
limb salvage. ■

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414

V • SPECIAL PROBLEMS AND COMPLICATIONS

transected major nerves, or associated life-
threatening injuries that prevent any atten-
tion to the limbs are clear indications for
immediate amputation. Nerve transection
must be confirmed by direct visualization,
because vascular insufficiency by itself may
cause profound nerve deficits.

However, most complex extremity injuries
are not that clear-cut. In these cases, revascu-
larization should be performed immediately
to prevent further tissue damage (including
aggressive use of surgical adjuncts such as fas-
ciotomy), the skeleton should be quickly sta-
bilized by either traction or external fixation,
and the limb then should be observed over
the next 48 hours for the level of function that
returns. If either revascularization fails, tissue
loss is profound or worsens, systemic sepsis or
crush syndrome develops, or profound neu-
rologic dysfunction persists, then amputation
should be performed. If improvement is
noted, each successive stage of limb salvage
should be assessed just as critically to mini-
mize unnecessarily prolonged, costly, and
futile efforts. The ultimate goal is to return
the patient to a comfortable and productive
life as quickly as possible.

VASCULAR GRAFTS:

ROLE AND COMPLICATIONS

Simple repairs of vascular injuries are always
preferred if at all possible, including lateral
suture and resection with end-to-end anasto-
mosis. Interposition or patch grafting is used
when simple repair is not possible or not
preferable, but restoration of the circulation
is attainable. Any segmental loss of vessel of
more than 2 cm, as is seen in complex injuries
with extensive tissue damage, is generally an
indication for vascular interposition. In true
end arteries, such as the popliteal artery, lig-
ation of tenuous collaterals to achieve ade-
quate mobilization for primary anastomosis
is best avoided, and interposition grafting is
preferred. Patch grafting of a partially lacer-
ated vessel is occasionally useful to avoid steno-
sis in smaller vessels such as the brachial or
popliteal arteries and allows avoidance of
resection.

In the Vietnam War, Rich and colleagues
(1970) reported interposition grafting as the
most common method of surgical repair of
arterial injuries, with autogenous vein being
used in 46% of cases and prosthetic grafts
in only 0.4%. Several civilian series since
then have corroborated these findings. Most
authors agree that autogenous reversed
saphenous vein is the conduit of choice for
arterial interposition grafting because of its
high patency rates and low incidence of infec-
tion with antibiotic control. Rich and Hughes
(1972) reported an 18% amputation rate in
Vietnam among arterial repairs undergoing
autogenous vein interposition, compared
with 12% in Korea. McCready and colleagues
(1987) reported an 89.5% long-term patency
rate for autogenous vein grafts in 86 cases of
extremity arterial injuries, with five graft fail-
ures leading to amputation and infection the
cause of three graft failures. Keen and col-
leagues (1991) reported 134 patients with
autogenous vein grafts of extremity arterial
injuries. In follow-ups ranging up to 24
months, they found a 98% cumulative primary
patency rate and 99% cumulative secondary
patency rate, with one amputation resulting
from graft failure and no perioperative graft
infections. Autogenous vein is also the inter-
position graft of choice for the repair of venous
injuries, though having a somewhat higher
rate of thrombosis. McCready and colleagues
(1987) reported that 17 (77%) of 22 autoge-
nous vein interpositions for extremity vein
injuries remained patent.

Prosthetic grafts have been applied increas-
ingly to the repair of vascular injuries over the
past 3 decades, following their widespread and
successful use in elective vascular surgery.
However, the contaminated nature of trau-
matic wounds led to doubts about the suit-
ability of prosthetic grafting, because of the
assumption that these materials are highly
prone to infection. Rich and Hughes (1972)
reported dismal results using prosthetic grafts
in contaminated combat vascular injuries in
Vietnam, with a 77% graft failure rate (most
commonly from infection and thrombosis)
and a 31% amputation rate, significantly
worse than autogenous vein in this setting. The
lack of an endothelial surface is the most likely
explanation for the higher rate of thrombo-

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20 • SPECIAL PROBLEMS

415

sis of prosthetic grafts. This was supported by
some experimental studies in animals in the
1970s.

However, a number of subsequent clinical
studies of civilian vascular trauma have demon-
strated consistently good results with the use
of both polytetrafluoroethylene (PTFE) and
Dacron prosthetic grafts placed in contami-
nated wounds. Shah and colleagues (1984)
reported only one arterial and one venous
graft thrombosis in 25 vascular reconstructions
with PTFE in grossly contaminated wounds
with no graft infections. In a report of 236
PTFE grafts placed in contaminated wounds,
Feliciano and colleagues (1985) showed a
higher graft thrombosis rate than autogenous
vein, but no instances of peripheral graft infec-
tion in the absence of exposure of the graft
or osteomyelitis. The liberal use of antibiotics
and adequate full-thickness tissue coverage of
these grafts is necessary to achieve these
results. Failure to cover any graft and vascu-
lar anastomosis inevitably leads to infection,
thrombosis, and suture line breakdown.

One advantage of prosthetic grafts over
autogenous vein lies in the differential
response of these materials to infection. Auto-
genous vein and arterial homografts both
develop transmural necrosis when subject to
exposure and/or infection, which leads to
sudden blowout of the anastomosis as sutures
pull through, with massive life-threatening
hemorrhage. Infected prosthetic grafts do not
break down in this disastrous way but gradu-
ally develop suture pull-through at the anas-
tomosis with native vessel, leading to contained
false aneurysm. This allows time for them to
be removed electively and new revasculariza-
tion to be performed. For this reason, pros-
thetic grafts are considered the material of
choice to be used if revascularization must be
done in a contaminated field . If they fail, their
temporary placement may still allow time to
debride devitalized tissue and clean the field
of contamination so that vein maybe used sub-
sequently.

Other advantages that prosthetic grafts
have over autogenous vein for repair of vas-
cular injuries tend to outweigh their higher
rate of thrombosis in specific circumstances.
They are more suitable for interposition graft-
ing of larger vessels without size discrepancy.

Their ready availability, without the need for
harvesting and preparation that autogenous
veins require, is preferable when time is an
important factor, as in unstable patients.
Keen and colleagues (1991) dispute this
latter point, reporting an average harvesting
time of less than 8 minutes for autogenous
veins, which had no adverse impact on limb
salvage.

There are circumstances in which prosthetic
grafts are best avoided. Injury to small-caliber
vessels, such as the brachial or tibial arteries,
are more amenable to autogenous vein inter-
position, because prosthetic grafts smaller
than 6 mm in diameter have a prohibitive rate
of thrombosis. Grafts that must cross the knee
or elbow joint should be autogenous vein,
because prosthetic grafts tend to kink and
thrombose more readily. Most prosthetic
grafts used to repair venous injuries appear
to thrombose early, although Feliciano and
colleagues (1985) have reported that even
their temporary use for this purpose may dra-
matically diminish hemorrhage from major
soft tissue wounds and fasciotomy sites that
venous ligation produces, by relieving venous
outflow pressure. If used as a venous substi-
tute, prosthetic grafts with external ring
support should be applied to enhance their
patency.

The proper management of infected pros-
thetic grafts should begin with measures to
prevent infection altogether. Routine cover-
age of vascular repairs with intravenous broad-
spectrum antibiotics, and full-thickness tissue
coverage of repairs using primary closure, or
pedicled or free flap tissue transfers are essen-
tial elements to avoid infection in this setting.
If immediate closure of wounds is not possi-
ble because of extensive contamination, devi-
talized tissue, or extensive soft tissue loss,
porcine xenografts have been used success-
fully to temporarily cover vascular repairs until
the wound is clean, and primary closure or
flap transfers can be done. Extra-anatomic
bypass through clean and uninjured tissues is
another option for immediate revasculariza-
tion, which permits adequate coverage despite
a hostile wound and allows for appropriately
aggressive wound management and an op-
timal functional and cosmetic result. Auto-
genous vein is preferred for extra-anatomic

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V • SPECIAL PROBLEMS AND COMPLICATIONS

bypass, but externally supported prosthetic
grafts may also be used.

Graft infection must be assumed whenever
obvious purulence is found in its vicinity, espe-
cially if it becomes exposed and has failed to
incorporate with surrounding tissue. Arterial
graft blowout is another manifestation of infec-
tion. Immediate excision of the graft is nec-
essary in this setting, and the native vessel
should be debrided back to uninvolved tissue
and ligated there to prevent secondary hem-
orrhage. This should be followed by extra-
anatomic bypass to restore distal perfusion,
leaving the infected bed open for debridement
and dressing to ultimately granulate and heal
secondarily. Simply placing a new graft in the
same infected bed is a futile gesture destined
for failure. Although there are isolated reports
of successful conservative management of
exposed and infected prosthetic grafts, this
approach is not recommended.

FAILED RECONSTRUCTION OF
ARTERIAL TRAUMA

There are two primary measures of success of
peripheral arterial injury management: limb
salvage and limb function. Certainly the
salvage of a viable extremity is the first goal
of arterial injury management, but that does
not necessarily mean that a patient is fully
restored to their normal lifestyle. The neu-
rologic and skeletal function of the salvaged
limb, as well as cosmetic appearance, can have
a major impact on the patient's life and may
actually be detrimental enough that amputa-
tion would be better. Therefore, the ultimate
goal of peripheral arterial injury management
must be the salvage of aviable, functional, and
cosmetically acceptable extremity. The deci-
sions made and the approaches taken in the
immediate postinjury period actually have the
greatest impact on ultimate outcome.

The first problem that could lead to a failed
repair of an arterial injury is delay in its diag-
nosis and treatment. The direct correlation
between delay in revascularization and limb
loss is related to irreversible tissue damage
that develops with more than 4 to 6 hours of

ischemia. Even if the limb remains viable after
a treatment delay, permanent disability from
nerve and muscle damage ispossible even with
successful revascularization. Prompt assess-
ment of all injured extremities for hard signs
of vascular injury, appropriate and selective
use of hand-injected, on-table arteriography,
and immediate arterial repair are essential to
minimizing delay. Nonvascular tissue damage
also adversely affects the salvage of a viable
and functional limb in the setting of a con-
comitant arterial injury. The increased rate
of limb loss that occurs in combined vascular
and skeletal extremity trauma has been dis-
cussed in a previous section of this chapter
(Combined Vascular and Skeletal Extremity
Trauma). Extensive soft tissue damage dis-
rupts collaterals and increases the sensitivity
of an injured extremity to interruption of
blood flow. Nerve damage affects the ultimate
function of an injured extremity independent
of how well it is revascularized. Injury to a
major vein in an extremity with arterial injury
increases the chance of failure of the arterial
repair byjeopardizingvenous outflow. In these
circumstances, early diagnosis and revascu-
larization and optimal use of surgical adjuncts
to improve the success of vascular repair are
critically important factors.

Technical errors may lead to failure of arte-
rial repair and to limb loss or limb dysfunc-
tion, and therefore must be stringently
avoided. Strict attention is necessary to a
number of technical factors, including gentle
dissection, thorough debridement, appro-
priate prioritization of multiple injuries,
meticulous technique in suturing arteries and
veins, proximal and distal thrombectomy,
regional and systemic heparinization to pre-
vent further thrombosis, proper choice of
repair technique to avoid stenosis, undue
tension and collateral damage, full-thickness
tissue coverage of the repair, and confirma-
tion of restoration of blood flow by palpation
of pulses and clinical signs of normal perfu-
sion. Completion arteriography should be
done routinely to detect those unsuspected
problems with the vascular repair or distal
runoff that even the most experienced centers
find in up to 16% of cases, which can be im-
mediately fixed and will avert a subsequent

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20 • SPECIAL PROBLEMS

417

failure of the arterial reconstruction. Certainly,
any doubts about the arterial repair must be
assessed by an intraoperative arteriogram.
Anticoagulation should not be necessary fol-
lowing arterial repairs and cannot substitute
for technical perfection.

Postoperative surveillance of the arterial
reconstruction with frequent checks of pulses,
clinical signs of perfusion, bleeding, and
Doppler pressure monitoring is necessary to
detect any thrombosis or anastomotic dis-
ruption early and permit immediate revisions.
Any sign of perfusion deficit or active bleed-
ing must be investigated promptly by arteri-
ography or operative exploration. The cause
of a failed reconstruction should be deter-
mined, to allow appropriate repair. Any throm-
bosis must be assumed to be due to technical
problems, and the anastomosis or suture lines
should be redone following distal thrombec-
tomy. An intraoperative arteriogram must
confirm an adequate repair before comple-
tion of the surgery. If infection is found as the
cause of failed reconstruction, consideration
must be given to extra-anatomic bypass fol-
lowing excision of the infected portion of
vessel and ligation in a clean field.

Compartment hypertension can be insidi-
ous in its presentation and devastating in how
much tissue and limb function it can destroy
following repair of arterial injuries, even with
successful revascularization and in the pres-
ence of normal pulses. Any suspicion of this
problem mandates immediate and complete
fasciotomy of the injured extremity. It is best
to perform fasciotomy early, and even pro-
phylactically, in extremities known to be at risk
for compartment syndrome, to avert its onset
altogether. Those factors posing a high risk
for compartment syndrome are well estab-
lished (see Chapter 27).

Each instance of failure of arterial recon-
struction following extremity vascular injury
substantially reduces the chance of ultimate
limb salvage. Prevention of these failures
through optimal diagnosis and initial man-
agement is the best way to minimize limb loss.
If a failure occurs, limb salvage and good limb
function is still possible if recognized and
treated promptly.

REFERENCES

Agarwal N, Shah PM, Clauss RH, et al: Experience
with 115 civilian venous injuries. J Trauma
1982;22:827.

Alexander JJ, Piotrowski JJ, Graham D, et al:
Outcome of complex orrthopedic and vascular
injuries of the lower extremity. Am J Surg
1991;162:111.

Applebaum R, \fellin AE, Weaver FA, et al: Role of
routine arteriography in blunt lower extremity
trauma. Am J Surg 1990;1 60:221.

Armstrong K, Sfeir R, Rice J, et al: Popliteal vas-
cular and war: Are Beirut and New Orleans
similar? J Trauma 1988;28:836.

AtteberyLR, DennisJW, Russo-Alesi Fetal: Chang-
ing patterns of arterial injuries associated with
fractures and dislocations. J Am Coll Surg
1996;183:377.

Barcia PJ, Nelson TG, Whelan TJ: Importance of
venous occlusion in arterial repair failure: An
experimental study. Ann Surg 1972;1 75:223.

BarrosD'Sa AA, HassardTH, Livingston RH, etal:
Missile-induced vascular trauma. Injury
1980;12:13.

Bergstein JM, Blair JF, Edwards J, et al: Pitfalls in
the use of color-flow duplex ultrasound for
screening of suspected arterial injuries in pen-
etrated extremities. J Trauma 1992;33:395.

Bongard FS, White GH, Klein SR: Management
strategy of complex extremity injuries. Am J Surg
1989;158:151.

Bishara RA, Pasch AR, Lim LT, et al: Improved
results in the treatment of civilian vascular
injuries associated with fractures and disloca-
tions. J Vase Surg 1986;3:707.

Bishara RA, Pasch AR, Lim LT, et al: Improved
results in the treatment of civilian vascular
injuries associated with fractures and disloca-
tions. J Vase Surg 1976;3:707.

Borman KR, Jones GH, Snyder WH: A decade of
lower extremity venous trauma. Am J Surg
1987;154:608.

Burch JM, Richardson RJ, Martin RR, et al: Pene-
trating iliac vascular injuries: Recent experience
with 233 consecutive patients. J Trauma
1990;34:1450.

Conkle DM, Richie RE, Sawyers JL, et al: Surgical
treatment of popliteal artery injuries. Arch Surg
1975:110:1351.

ch20.qxd 4/16/04 3:31PM Page 418

418

V • SPECIAL PROBLEMS AND COMPLICATIONS

Connolly JE, Williams E, Whittaker D: The influ-
ence of fracture stabilization on the outcome of
arterial repair in combined fracture -arterial
injuries. Surg Forum 1969;20:450.

Daugherty ME, Sachatello CR, Ernst CB: Improved
treatment of popliteal arterial injuries. Arch Surg
1978;113:1317.

DeBakey ME, Simeone FA: Battle injuries of the
arteries in World War II: An analysis of 2,471 cases.
Ann Surg 1946;1 23:534.

DeGiannis E, Levy RD, Sofianos C, et al: Arterial
gunshot injuries of the extremities: A South
African experience. J Trauma 1995;39:570.

Dennis JW, Frykberg ER, Veldenz HC, et al:
Reassessing the role of arteriograms in the man-
agement of posterior knee dislocations. J Trauma
1993;35:692.

Downs AR, MacDonald P: Popliteal artery injuries:
Civilian experience with sixty-three patients
during a 24 year period (1960 through 1984).
JVascSurgl986;4:55.

DrostTF,RosemurgyAS,ProctorD,etal: Outcome
of treatment of combined orthopedic and arte-
rial trauma to the lower extremity. J Trauma
1989;29:1331.

Fabian TC, Turkleson ML, Connelly TL, etal: Injury
to the popliteal artery. Am J Surg 1982;143:225.

Fainzilber G, Roy-Shapir A, Wall MJ, et al: Predic-
tors of amputation for popliteal artery injuries.
Am J Surg 1995;170:568.

Feliciano DV, Accola KD, Burch JM, et al:
Extraanatomic bypass for peripheral arterial
injuries. Am J Surg 1989;158:506.

Feliciano DV, Cruse PA, Spjut-Patrinely V, et al: Fas-
ciotomy after trauma to the extremities. Am J
Surg 1988;156:533.

Feliciano DV, Mattox KL, Graham JM, et al: Five-
year experience with PTFE grafts in vascular
wounds. J Trauma 1985;25:7l.

Frykberg ER: Popliteal vascular injuries. Surg Clin
North Am 2002;82(l):67-89.

Frykberg ER, Crump JM, Dennis JW, et al: Non-
operative observation of clinically occult arter-
ial injuries: A prospective evaluation. Surgery
1991;109:85.

Gagne PJ, Cone JB, McFarland D, et al: Proximity
penetrating extremity trauma: The role of duplex
ultrasound in the detection of occult venous
injuries. J Trauma 1995;39:1157.

Caspar MR, Treiman RL: The management of
injuries to major veins. Am J Surg 1960;100:
171.

Gerlock AJ, Thai ER, Snyder WH: Venography in
penetrating injuries of the extremities. AJR
1976;126:1023.

Harrell DJ, Spain DA, Bergamini TM, et al: Blunt
popliteal artery trauma: A challenging injury.
Am Surg 1997;63:228.

Hobson RW, Croom RD, Rich NM: Influence of
heparin and low molecular weight dextran on
the patency of autogenous vein grafts in the
venous system. Ann Surg 1973;178:773.

Hobson RW, Howard EW, Wright CB, et al: Hemo-
dynamics of canine femoral venous ligation:
Significance in combined arterial and venous
injuries. Surgery 1973;74:824.

Hobson RW, \feager RA, Lynch TG, et al: Femoral
venous trauma: Techniques for surgical man-
agement and early results. Am J Surg
1983;146:220.

HollemanJH, KillebrewLH: Injury to the popliteal
artery. Surg Gynecol Obstet 1981;153:392.

Howe HR, Poole GV, Hansen KJ, et al: Salvage of
lower extremities following combined orthope-
dic and vascular trauma: A predictive salvage
index. Am Surg 1987;53:205.

Hughes CW: Arterial repair during the Korean War.
Ann Surg 1958;147:555.

Jaggers RC, Feliciano DV, Mattox KL, et al: Injury
to popliteal vessels. Arch Surg 1982;1 17:657.

Jahnke EJ, Seeley SF: Acute vascular injuries in the
Korean War: An analysis of 77 consecutive cases.
Ann Surg 1953;138:158.

Johansen K, Daines M, Howey T, et al: Objective
criteria accurately predict amputation following
lower extremity trauma. J Trauma 1990;30:
568.

Kaufman SL, Martin LG: Arterial injuries associ-
ated with complete dislocation of the knee. Radi-
ology 1992;184:153.

Keen RR, Meyer JP, Durham JR, et al: Autogenous
vein graft repair of injured extremity arteries:
Early and late results with 134 consecutive
patients. J Vase Surg 1991;13:664.

Kendall RW, Taylor DC, Salvian AJ, et al: The role
of arteriography in assessing vascular injuries
associated with dislocations fo the knee .J Trauma
1993;35:875.

Krige JEJ, Spence RAJ: Popliteal artery trauma:
A high risk injury. Br J Surg 1987;74:91.

Lange RH, Bach AW, Hansen ST, et al: Open
tibial fractures with associated vascular injuries:

ch20.qxd 4/16/04 3:31PM Page 419

20 • SPECIAL PROBLEMS

419

Prognosis for limb salvage. J Trauma 1985;25:
203.

Lim LT, Michuda MS, Flanigan DP, et al: Popliteal
artery trauma: 31 consecutive cases without
amputation. Arch Surg 1980;115:1307.

Lin C-H, Weif-C, Levin LS, et al: The functional
outcome of lower extremity fractures with vas-
cular injury. J Trauma 1997;43:480.

Lovric Z, Wertheimer B, Candrlic K, et al: War
injuries of major extremity vessels. J Trauma
1994;36:248.

Makins GH: Injuries to the bloodvessels. In: Offi-
cial History of the Great War Medical Services:
Surgery of the War. London: His Majesty's
Stationery Office, 1922;170-296.

Martin LC, McKenny MG, Sosa JL, et al: Manage-
ment of lower extremity arterial trauma. J
Trauma 1994;37:591.

Martinez D, Sweatman K, Thompson EC: Popliteal
artery injury associated with knee dislocations.
AmSurg2001;67:165.

McCabe CJ, Ferguson CM, Ottinger LW: Improved
limb salvage in popliteal artery injuries. J Trauma
1983;23:982.

McCready RA, Logan NM, Dangherty ME, et al:
Long-term results with antogenous tissue repair
of traumatic extremity vascular injuries. Ann Surg
1987;206:804.

Melton SM, Croce MA, Patton JH, et al: Popliteal
artery trauma: Systemic anticoagulation and
intraoperative thrombolysis improves limb
salvage. Ann Surg 1997;225:518.

McNamara JJ, Brief DK, Stremple JF, et al: Man-
agement of fractures with associated arterial
injury in combat casualties. J Trauma 1973;13:17.

Meyer J, Walsh J, Schuler J, et al: The early fate of
venous repair after civilian vascular trauma: a
clinical, hemodynamic, and venographic assess-
ment. Ann Surg 1987;206:458.

Miranda FE, Dennis JW, Veldenz HC, et al: Con-
firmation of the safety and accuracy of physical
examination in the evaluation of knee disloca-
tion for popliteal artery injury: A prospective
study. J Trauma 2000;49:375.

Miranda FE, Dennis JW, Veldenz HC, et al: Con-
firmation of the safety and accuracy of physical
examination in the evaluation of knee disloca-
tion for injury of the popliteal artery: A prospec-
tive study. J Trauma 2002;52(2):247-251.

Mullins RJ, Lucas CE, Ledgerwood AM: The
natural history followingvenous ligation for civil-
ian injuries. J Trauma 1980;20:737.

Norman J, Gahtan V, Franz M, et al: Occult vascu-
lar injuries following gunshot wounds resulting

in long bone fractures of the extremities. Am
Surgl995;61:146.

Nypaver TJ, Schuler JJ, McDonnel P, et al:
Long-term results ofvenous reconstruction after
vascular trauma. J Vase Surg 1992;16:762.

Odland MD, Gisbert VL, Gustilo RB, et al: Com-
bined orthopedic and vascular injury in the lower
extremities: Indicationsforamputation. Surgery
1990;108:660.

O'Reilly MJG, HoodJM, Livingston RH, etal: Pen-
etrating injuries of the popliteal artery. BrJ Surg
1978;65:789.

Orcutt MB, Levine BA, Root HD, et al: The con-
tinuing challenge of popliteal vascular injuries.
AmJ Surg 1983;146:758.

Palazzo JC, Ristow AB, CuryJM, et al: Traumatic
vascular lesions associated with fractures and dis-
locations. J Cardiovasc Surg 1986;27:688.

Pasch AR, Bishara RA, Schuler JJ, et al: Results of
venous reconstruction after civilian vascular
trauma. Arch Surg 1986;1 21:607.

PeckJJ, Eastman AB, Bergan JJ, et al: Popliteal vas-
cular trauma: A community experience. Arch
Surgl990;125:1339.

Phifer TJ, Gerlock AJ, Rich NM, et al: Long term
patency of venous repairs demonstrated by
venography. J Trauma 1985;25:342.

Pretre R, Bruschweiler I, RossierJ, etal: Lower limb
trauma with injury to the popliteal vessels.
J Trauma 1996;40:595.

Razuk AF, Nunes H, Coimbra R, et al: Popliteal
artery injuries: Risk factors for limb loss. Panam
J Trauma 1998;7:93.

Reed MK, Lowry PA, Myers SI: Successful repair of
pediatric popliteal artery trauma. Am J Surg
1990;160:287.

Rich NM: Principles and indications for primary
venous repair. Surgery 1982;91:492.

Rich NM, Baugh JH, Hughes CW: Acute arterial
injuries in Vietnam: 1,000 cases. J Trauma
1970;10:359.

Rich NM, Hobson RW, Collins GJ, et al: The effect
of acute popliteal venous interruption. Ann Surg
1976;183:365.

Rich NM, Hughes CW: The fate of prosthetic mate-
rial used to repair vascular injuries in contami-
nated wounds. J Trauma 1972;21:459.

Rich NM, Hughes CW, Baugh JH: Management of
venous injuries. Ann Surg 1970;171:724.

Rich NM, Metz CW, HuttonJE, etal: Internal versus
external fixation of fractures with concomitant
vascular injuries in Vietnam. J Trauma 1971;
11:463.

ch20.qxd 4/16/04 3:31PM Page 420

420

V • SPECIAL PROBLEMS AND COMPLICATIONS

Romanoff H, Goldberger S: Combined severe
vascular and skeletal trauma: management and
results. J Cardiovasc Surg 1979;20:493.

Ross SE, Ransom KJ, Shatney CH: The manage-
ment of venous injuries in blunt extremity
trauma. J Trauma 1985;25:150.

Schlickewei W, Kuner EH, Mullaji AB, et al:
Upper and lower limb fractures with concomi-
tant arterial injury. J Bone Joint Surg 1992;74:
181.

Sfeir RE, Khoury GS, Haddad FF, et al: Injury to
the popliteal vessels: The Lebanese War experi-
ence. WorldJ Surg 1992;16:1156.

Shah DM, Leather RP, Corson JD, et al: Polytetra-
fluoroethylene grafts in the rapid reconstruction
of acute contaminated peripheral vascular
injuries. Am J Surg 1984;148:229.

Shah DM, Naraynsingh V, Leather RP, et al:
Advances in the management of acute popliteal
vascular blunt injuries. J Trauma 1985;25:793.

Spencer FC, Grewe RF: The management of arte-
rial injuries in battle casualties. Ann Surg
1955;141:304.

Snyder WH: Vascular injuries near the knee: An
updated series and overview of the problem.
Surgery 1982;91:502.

Swetnam JA, Hardin WD, Kerstein MD: Successful
management of trifurcation injuries. Am Surg
1986;52:585.

Thomas DD, Wilson RF, Wiencek RG: Vascular
injury about the knee: Improved outcome. Am
Surg 1989;55:370.

Timberlake GA, Kerstein MD: Venous injury: To
repair or ligate-the dilemma revisited. Am Surg
1995;61:139.

Treiman GS, Yellin AE, Weaver FA, et al: Exami-
nation of the patientwith a knee dislocation: The
case for selective arteriography. Arch Surg
1992;127:1056.

Van Wijngaarden M, Omert L, Rodriguez A, et al:
Management of blunt vascular trauma to the
extremities. Surg Gynecol Obstet 1993;177:41.

Weimann S, San Nicolo M, Sandblicher P, et al:
Civilian popliteal artery trauma. J Cardiovasc
Surg 1987;28:145.

Wright CB, Hobson RW: Hemodynamic effects of
femoral venous occlusion in the subhuman
primate. Surgery 1974;75:453.

Yeager RA, Hobson RW, Lynch TG, et al: Popliteal
and infrapopliteal arterial injuries: Differential
management and amputation rates. Am Surg
1984;50:155.

Yelon JA, Scalea TM: Venous injuries of the lower
extremities and pelvis: repair versus ligation.
J Trauma 1992;33:532.

ch21.qxd 4/16/04 3:30 PM Page 421

Illicit Street Drugs and
Vascular Injury

CHARLES E. LUCAS
ANNA M. LEDGERWOOD

O INTRODUCTION

O PERIVASCULAR HEMATOMA AND ABSCESS

O DIRECT ARTERIAL INJECTION

O MYCOTIC ANEURYSMS

O VASCULAR RECONSTRUCTION

O MYCOTIC ANEURYSMS OF CAROTID VESSELS

O VENOUS ANEURYSMS

O VASCULAR INJURY FROM COCAINE

INTRODUCTION

The use of illicit street drugs is very common
in our society, especially amongyoungpeople
who are most susceptible to trauma. The
method of administration and the pharma-
cologic responses of these drugs produce a
unique pattern of vascular injury. This chapter
is dedicated to the specific type of vascular
problems associated with illicit drug usage.

PERIVASCULAR HEMATOMA
AND ABSCESS

A common phenomenon in illicit drug
users using intravenous access is a missed
venous puncture that results in the needle
entering an adjacent artery. This is often
recognized by the withdrawal of bright red
blood, known as "a pinky" among the users.
When recognized, the needle is removed and

421

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V • SPECIAL PROBLEMS AND COMPLICATIONS

direct pressure is placed over the puncture
site; despite this precaution, a hematoma often
results. Treatment consists of observation and
oral antibiotics, which are readily available on
the street. Formal medical care is avoided
unless complications ensue.

Because of the high incidence of contami-
nation associated with the drug preparation
including the multiple dilutions, which are
performed to maximize profits, the hematoma
has a high risk of becoming seeded from the
contaminated injectable. This typically leads
to infection of the perivascular clot and sub-
sequent abscess formation. Sometimes a frag-
ment of needle will be found within the abscess
cavity. Physical examination identifies an area
of cellulitis overlying the neurovascular
bundle, which commonly is at the wrist or the
groin. Transmitted pulsations may lead to the
suspicion that this is a false aneurysm. When
confusion exists about the nature of the
pulsatile inflammatory mass, preoperative
arteriography is warranted. During operative
evacuation of these abscesses, the surgeon
should avoid breaking all the adhesions
because one end of the abscess cavity will abut
the arterial wall. Overaggressive drainage of
abscesses in this setting will lead to bleeding
from the adjacent artery, where the puncture
site had been sealed by an established platelet
and fibrin plug.

Concomitant antibiotic therapy using
broad-spectrum coverage is needed. During
a 12-month interval at the Detroit Receiving
Hospital, 651 patients had abscesses drained
by the surgical services; 421 of these patients
had abscesses that resulted from illicit street
drug use. Most patients who have a single
organism cultured will have a Staphylococcus
aureus infection, which often is resistant to
methicillin (methicillin-resistant S. aureus) .
(3-streptococcus is also commonly found as
an isolated organism. Approximately 25% of
patients will have a mixed infection with gram-
negative coliform organisms being part of this
mixture. Many of the users were using their
larger veins (mainlining) so the heroin mix
would be injected into the subcutaneous
plane (skin-popping) . This compromises the
surgeon's ability to determine whether the
underlying cellulitis is related to the skin-
popping or to an arterial injury.

DIRECT ARTERIAL INJECTION

Often patients who hit a "pinky" are already
under the influence of alcohol or drugs and
do not recognize that the needle has been
inserted into an artery. The heroin mix is then
injected intra-arterially followed by an imme-
diate burning pain in the distribution area of
that artery. This results from the emboliza-
tion of particulate matter that has been used
to dilute the heroin mix, the so-called "mixed
jive, "which plugs the distal microvascular tree.
When small vessel occlusion occurs after a
radial artery or ulnar artery injection, the
ischemic necrosis typically involves the skin
and subcutaneous tissues along the distribu-
tion of the thumb or the first and second
fingers after a radial artery injection or along
the distribution of the third and fourth fingers
after an ulnar artery injection. This soft tissue
insult is extremely painful. When patients
present to an emergency department, the
underlying etiology often is not recognized
and the patients are treated with oral anal-
gesics and sometimes antimicrobials. When
first seen by a surgeon, there is usually evi-
dence of full-thickness skin and sometimes
subcutaneous necrosis. The prime therapeu-
tic objectives are prevention of superimposed
infection and amelioration of the constant
pain. The role of intra-arterial crystalloid irri-
gation, heparin infusion, or other intra-
arterial modalities of treatment have not
been successful in this group of patients.
Systemic analgesics provide minimal relief.
Significant amelioration can be achieved by
sympathetic blockade. Transient upper
extremity pain relief may be obtained by a stel-
late block. Patients who experience significant
relief on two separate stellate blocks likely will
benefit from a dorsal sympathectomy per-
formed through a small transaxillary incision.
Patients undergoing sympathectomy in this
setting will have increased warmth of the
involved hand and a striking but not complete
reduction in pain.

Sometimes the ischemic changes are asso-
ciated with rapidly spreading infection that
involves the adjacent muscles and leads to
myonecrosis. Such patients will need ampu-
tation, which following lower limb or groin

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423

injection is a below-knee amputation; seldom
is an above-knee amputation needed. When
myonecrosis occurs in the hand, individual
digits may need amputation. Unfortunately,
we have performed several hands and even
forearm amputations following wrist injections
or brachial artery injections, respectively.
Lack of an aggressive approach to myone-
crosis after injections with contaminated
street narcotics will lead to severe systemic
septicemia, rhabdomyolysis, and renal
shutdown.

MYCOTIC ANEURYSMS

In 1851 Koch described the first mycotic
aneurysm. This occurred in a 22-year-old
woman with a history of rheumatic fever with
consequent endocarditis. Bacteria embolized
from the heart valves into the superior
mesenteric artery, which became aneurysmal,
ruptured, and caused death. Autopsy demon-
strated that the aneurysm was in one of the
secondary arcades of the superior mesenteric
artery. In 1885 Osier coined the term "mycotic
aneurysm" when he described a 30-year-old
patient who had a history of rheumatic fever
with endocarditis and then developed four
thoracic aortic aneurysms. One of these
aneurysms ruptured causing death. At
postmortem examination, Osier was
impressed by the appearance of "fresh fungus
vegetations" around the aneurysm. These
were not fungus mounds, but inflammatory
masses around bacteria-induced infection.
The cause for mycotic aneurysm formation
was endocarditis, resulting in embolization of
bacteria into the vasa vasorum resulting in arte-
rial wall infection and consequent aneurys-
mal dilation.

Mycotic aneurysms (infected pseudoa-
neurysms) in drug addicts are due to direct
arterial trauma from an errant needle stick
resulting in a perivascular hematoma that
becomes infected. Huebl and Reid in 1966
described this sequence of events and referred
to this entity as "aneurysmal abscess." During
a 20-month interval at the Detroit Receiving
Hospital, the surgeons excised 52 mycotic
aneurysms or aneurysmal abscesses in 50

patients following intra-arterial injection with
heroin mix, or "mixedjive." Often, the patient
gave a history of a pinky but more often the
intra-arterial injection was not recognized.
The patient typically presented with pain,
swelling, fever, and leukocytosis around
the area of injection. About half of the
patients had obvious pulsation of the inflam-
matory mass at the time of the original
examination. The duration of symptoms
usually was about 1 week. About 25% of
patients had a decreased or absent peripheral
pulse distal to the inflammatory mass. Few
patients (10%) had symptoms of limb
ischemia. An associated neural deficit is
usually caused by a direct injection into or
around the adjacent nerve rather than
ischemia. The most common missed diagno-
sis was cellulitis, especially when not seen
promptly by a surgeon. The resultant admin-
istration of intravenous antibiotics was
followed by a lack of rapid response, which
signaled the presence of the mycotic
aneurysm.

When mycotic aneurysm is considered, arte-
riography is recommended. This confirms the
diagnosis and serves as a road map defining
both the site of leakage and the extent of
collateralization. The operative approach
should entail careful proximal and distal
control of all involved vessels. This often is
difficult because of the intense inflammation
in the tissues around the abscess. This is due
to the multiple prior injections in this area.
Extensive fibrosis from repeated soft tissue
exposure to mixed jive mistakenly injected
around the vein impedesrapid safe dissection.
Consequently, one must dissect very slowly
after obtaining vascular control, to have as
much anatomy displayed as possible before
actually getting into the aneurysmal abscess.
Very slow and careful dissection helps avoid
injury to nearby structures, particularly the
adjacent vein, which is often encased in this
inflammatory mass.

Once fully exposed, the mycotic aneurysm
with the adjacent artery should be excised,
followed by proximal and distal ligation of
uninvolved arterial wall. Suture ligation of the
aneurysm artery without excision likely will
lead to rebleeding. Aneurysmectomy will be
tolerated without tissue loss in most patients

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V • SPECIAL PROBLEMS AND COMPLICATIONS

with upper extremity aneurysmal abscesses
and in mostpatientswith aneurysmal abscesses
involving the superficial femoral artery or the
profunda femoral artery. Even the involved
popliteal artery has been excised without tissue
loss, although this artery is not commonly
involved with a mycotic aneurysm. The
need to perform aneurysmectomy of the
common femoral artery with triple ligation
of the common femoral artery, superficial
femoral artery, and profunda femoral artery
leads to a high incidence of ischemia
and necrosis requiring amputation. Attempts
to predict, from preoperative arteriographic
findings, the level of resultant ischemia
after aneurysmectomy are fraught with
failure.

VASCULAR RECONSTRUCTION

Ideally, major artery aneurysmectomy is
followed by vascular reconstruction. This aim
however is hindered after mycotic aneurys-
mectomy in narcotic addicts by the sur-
rounding inflammation and cellulitis. Efforts
at reconstruction therefore must be directed
toward extra-anatomic routes. External iliac
artery mycotic aneurysms are rare; when such
aneurysms are excised, reconstruction is best
achieved by a femoral-to-femoral artery bypass
if neither groin is involved with drug-related
cellulitis. The timing of extra-anatomic recon-
struction depends on the patient's presenta-
tion. When preoperative ischemic pain exists
and there is an available extra-anatomic route,
the bypass may be established before aneurys-
mectomy. When preoperative ischemic pain
is absent, aneurysmectomy without bypass is
indicated.

When common femoral artery aneurys-
mectomy with triple ligation leads to ischemia,
the patient will wake up complaining of
severe, unrelenting pain in the foot. When
neither the lower abdominal wall nor the distal
thigh has cellulitis, the patient should be taken
back to the operating room for placement
of an extra-anatomic bypass between the
external iliac artery and the distal femoral
artery or proximal popliteal artery. The

extra-anatomic bypass is best performed
through the obturator foramen. The exter-
nal iliac artery is most easily exposed through
an oblique suprainguinal incision in Langer's
lines followed by retroperitoneal dissection,
which also allows access to the obturator
foramen. The thigh incision must stay distal
to the inflammatory changes abutting the
groin cellulitis. This procedure is technically
challenging and therefore dangerous because
of the extensive collateral circulation associ-
ated with the groin cellulitis. The surgeon
should detach the obturator membrane from
its anterior and medial osseous insertion,
thereby minimizing the threats of venous
hemorrhage and neural contusion. The
danger of rerouting through the obturator
foramen has resulted in the recommendation
that the lateral femoral triangle be used for
this bypass. This approach, whereby, the graft
goesjust medial to the anterior superior spine,
is really not extra-anatomic and is prone to
failure in patients who have cellulitis involv-
ing the femoral triangle. Avein is almost never
available in these patients because they have
already destroyed their veins with prior injec-
tions. Consequently, one must use a synthetic
graft. We prefer to use the Dacron graft,
although the long-term patency rates between
Dacron and PTFE grafts are not different.

The long-term success of extra-anatomic
bypass grafts in these patients is directly
related to recidivism of the drug usage. When-
ever a patient goes back to using heroin mix
and resorts to intravascular injection, the like-
lihood for thrombosis of the obturator
foramen bypass graft approaches 100%. When
thrombosis does occur, some patients have
ischemia that is tolerable and other patients
require amputation, which is usually at the
below-knee level.

While treating patients with aneurysmal
abscesses, antibiotic therapy is necessary. Most
patients will have positive culture results for
methicillin-resistant S. aureus, whereas a sig-
nificant number of patients will have positive
culture results for Pseudomonas aeruginosa.
About 20% of the patients will have a mixed
flora within the aneurysmal abscess, so
broad-spectrum antibiotics are necessary.
Likewise, the skin over the aneurysmal

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21 • ILLICIT STREET DRUGS AND VASCULAR INJURY

425

excision site should be left open to heal by
second intent.

VENOUS ANEURYSMS

MYCOTIC ANEURYSMS OF
CAROTID VESSELS

The potential for an infected pseu-
doaneurysm extends to any artery being
injected. Some mainliners have avoided
using the groin as a site of injection for fear
of losing their legs. Somehow the thought
that the blood supply to the brain could be
compromised by carotid artery injection is
not considered. The differential diagnostic
challenge for a mycotic aneurysm involving
the common or innominate arteries is the
same as in the extremities. The lack of reso-
lution of an inflammatory mass to antibiotic
therapy should highlight the fact that this
may be an aneurysmal abscess. The princi-
ples of treatment are the same. The surgeon
must obtain proximal and distal control.
Unfortunately, after excision of the infected
pseudoaneurysm of the carotid or innomi-
nates arteries, there is never a plane that is
not involved with cellulitis, so there is no
potential for placing a bypass graft. Fortu-
nately, these patients usually have good col-
lateralization and do not develop evidence of
cerebral ischemia after mycotic aneurysmec-
tomy of aneurysms of the innominate artery,
external carotid artery, common carotid
artery, or internal carotid artery. The post-
operative care requires the same con-
siderations regarding antibiotics with
broad-spectrum coverage and leaving the
skin open to heal by second intent.

Occasionally, patients with mycotic
aneurysms will have a fistula between the
artery and the vein. The principles of care in
such patients are the same as those for either
a mycotic arterial aneurysm or a venous
aneurysm. Proximal and distal control is nec-
essary to get the arterial component isolated.
The venous component should then be con-
trolled proximally and distally before enter-
ing the artery and doing the aneurysmectomy.
The care in dissection is especially important
in patients with an arteriovenous fistula.

Septic phlebitis is a common coexistent con-
dition in patients with drug injection-related
cellulitis caused by mainlining or skin-
popping. By the time the patient goes to the
emergency department with complications
from missed hits, several misses have occurred
over the many previous weeks and months.
The suspicion that a patient has something
more than simple cellulitis is enhanced by the
appearance of systemic sepsis that exceeds the
severity typical of localized cellulitis. The pres-
ence of bilateral lung abscesses typifies the
patient who has a venous aneurysm that is
embolizing bacteria to the lungs. These
changes in the lung are not caused by blood
clots but are caused by embolization of bac-
teria. Anticoagulation should be avoided in
this setting because the patient may also have
endocarditis and small intracerebral infarcts
from bacterial embolization. Anticoagulation
may cause one of these intracerebral infarcts
to hemorrhage. The surgical approach for
mycotic venous aneurysm is excision plus
proximal and distal venous ligation. Again, the
dissection should be done very carefully to
avoid injury to adjacent arteries and nerves.
Fogarty catheterization may be helpful in
retracting infected clot after venous control
is obtained. After excision of a venous pseudo-
aneurysm, the patient is maintained on antibi-
otics and the limb is elevated. The skin is
allowed to heal by second intent. Long-term
care involves support wraps until the wounds
have healed, after which time lifelongwearing
of a customized venous support hose is nec-
essary. These patients are not candidates for
long-term anticoagulation, and they are not
candidates for later vein graft inner position
for their venous insufficiency.

VASCULAR INJURY FROM
COCAINE

Cocaine in various forms has become a very
popular substance abuse agent in all walks of
life. The vasospastic effects of cocaine produce

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V • SPECIAL PROBLEMS AND COMPLICATIONS

a multitude of clinical problems that involve
the vascular surgeon. The intense vasocon-
strictive effects causes multiple-organ dys-
function in young patients. These include
myocardial infarction, cardiac arrhythmia,
acute renal failure, cerebral vascular ischemia,
and rhabdomyolysis. Thrombosis of small
vessels is typically associated with ischemia of
the distal part and is treated symptomatically
with plasma volume expansion and observa-
tion. Occasionally, the ischemia will lead
to severe myonecrosis, necessitating
amputation.

Cocaine may also cause thrombosis of
larger vessels including the abdominal aorta.
This occlusion is thought to result from
spasm of the vasa vasorum, resulting in an
intimal injury followed by platelet deposition
and clot formation. We treated one patient
who had cocaine-induced thrombosis of the
abdominal aorta, both renal arteries, the
right iliac artery, the profunda femoris
artery, and the popliteal artery, in addition
to having distal small vessel occlusion with
rhabdomyolysis and renal failure. Aggressive
surgical therapy was needed to preserve life
and threatened tissues. When the cocaine-
induced thrombosis threatens the distal
part, emergency operation with thrombec-
tomy is indicated. Alternatively, when the
occlusion is not associated with distal
ischemia, nonoperative therapy with a full
course of heparinization will result in com-
plete resolution of the cocaine-induced
thrombus. One must be certain that such
patients do not have other intracerebral
embolic infarcts from prior heroin use
before anticoagulation unless the hepari-
nization lead to intracerebral hemorrhage.
Fortunately, most patients do not combine

cocaine and heroin or use them in temporal
proximity.

ACKNOWLEDGMENTS

This work was supported by the Interstitial
Fluid Fund (account 4-44966) .

REFERENCES

Fromm SH, Lucas CE: Obtura tor bypass for mycotic
aneurysm in the drug addict. Arch Surg
1970;100:82-83.

Huebel H, Read C: Aneurysmal abscess. Minn Med
1966;46:11-16.

Johnson JR, Ledgerwood AM, Lucas CE: Mycotic
aneurysm: New concepts in therapy. Arch Surg
1983;118:577-582.

Johnson JE, Lucas CE, Ledgerwood AM,Jacobs LA:
Infected venous pseudoaneurysm: A complica-
tion of drug addiction. Arch Surg 1984;1 19:1097-
1098.

Koch L: German "Ueber Aneurysma Dir Arteriae
Mesenterichae Superioris, Inaug Dural-Abhand-
lung." Erlangen J Barfus' Schen Universitates-
Buchdruckerei 1851:5-23.

Ledgerwood AM, Lucas CE: Mycotic aneurysm of
the carotid artery. Arch Surg 1974;109:496-498.

Osier W: The gulstonian lectures on malignant
endocarditis. Br Med J 1885;1:467.

Shanti CM, Lucas CE: Cocaine and the injured
patient. Crit Care Med 2003;31:

Wallace JR, Lucas CE, Ledgerwood AM: Social, eco-
nomic and surgical anatomy of a drug-related
abscess. Am Surg 1986;52(7):398-401.

Webber J, Kline RA, Lucas CE: Aortic thrombosis
associated with cocaine use: Reportof two cases.
Ann Vase Surg 1999;13:302-304.

ch22.qxd 4/16/04 3:28 PM Page 427

Iatrogenic Vascular Trauma

SAMUEL R. MONEY
MICHAEL R. LEPORE, JR

O INTRODUCTION

O PERCUTANEOUS VASCULAR ACCESS

Pseudoaneurysms

Hemorrhage

Arterial Closure Devices

Central Venous Access

Intra-Aortic Balloon Pump
O INTRAOPERATIVE VASCULAR INJURIES

Colorectal Procedures

Pancreatobiliary Procedures

Laparoscopic Procedures

Vascular/Endovascular Surgery

Orthopedic Surgery

Neurosurgery
O SUMMARY

INTRODUCTION

Patterns of injury for civilian arterial and
venous trauma have long been recognized and
discussed in both the vascular and the trauma
literature. Most of the discussions are centered

around arterial injuries resulting from either
blunt or penetrating forces. These mecha-
nisms are usually relatively easy to identify
given the circumstances behind a motor
vehicle accident or a fall, as is the case in blunt
traumatic injury. Identification of the level
of injury in the arterial tree, secondary to

427

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428

V • SPECIAL PROBLEMS AND COMPLICATIONS

penetrating trauma, necessitates thorough
knowledge of arterial anatomy and recogni-
tion of the possible pathway of injury. Iatro-
genic patterns of injury are not generally
considered in conjunction with vascular
trauma. It should, however, be considered as
a subheading both trauma and vascular surgery.

These are the injuries that no clinician likes
to collect or report in a personal series, but
of which the vascular surgeon is well aware.
Complications related to arterial access (e.g.,
pseudoaneurysms, hemorrhage, hematoma,
and ischemia) or intra-aortic balloon pump
(IABP) placement and venous access (e.g.,
venous injuries, arterial injuries, and arteri-
ovenous fistula) are not uncommon. In addi-
tion, there are patterns of arterial injury that
are specific to different surgical procedures
and subspecialties such as colorectal, pan-
creatobiliary, laparoscopic, orthopedic, and
neurosurgery. As enthusiasm for new proce-
dures grows, such as endovascular aortic stent
grafting for abdominal aortic aneurysms, a
new pattern of iatrogenic arterial injuries
evolves.

We discuss and illustrate some of the more
commonly encountered iatrogenic vascular
injuries. Prevention and management of these
injuries necessitates an understanding of the
mechanism of injury, as it does with all forms
of trauma.

PERCUTANEOUS VASCULAR
ACCESS

Complications related to percutaneous vas-
cular access are not a new phenomenon.
Translumbar aortography was first introduced
in the late 1920s and early 1930s by dos Santos.
The next generation in the evolution of per-
cutaneous access was fostered by Seldinger
who introduced the concept of catheter
exchange over a guidewire in 1953. Since that
time, technology has continued to advance
the field. Percutaneous arterial or venous
access has become an almost routine part of
clinical patient management.

During the 1990s, there have been major
technological advances in the treatment of
peripheral vascular and coronary arterial

disease. As a result of these new "endovascu-
lar" techniques, various types of sheaths (i.e.,
crossover sheaths and shuttle sheaths) with
increasing diameters have been developed
to deliver newer and more complex intra-
luminal devices for advanced endovascular
procedures. Add the increasing use of anti-
coagulants and the powerful antiplatelet
agents (e.g., group Ilb/IIIa platelet receptor
inhibitors and adenosine diphosphate [ADP]
receptor inhibitors) and it is no surprise that
the incidence of iatrogenic arterial and venous
injuries has mirrored the enthusiasm and
growth of percutaneous interventional/
endovascular techniques.

The more complex interventions that
require larger delivery systems (8- and 9-
French sheaths) are mainly performed by
femoral arterial approach. Fortunately, for the
increasing number of patients undergoing
these procedures, vascular occlusion and
uncontrolled hemorrhage are the least
common complications. Vascular occlusion
secondary to thrombosis or dissection does
occur but may be treated percutaneously, if
recognized, as demonstrated in Figure 22-1.
Most surgeons would agree that vascular
occlusion or thrombosis that is not amenable
to percutaneous therapy requires surgical
exploration with treatment dictated by the
respective etiology.

Techniques for radial artery access are being
used more frequently by interventional car-
diologists, mainly for diagnostic coronary
studies. As the emphasis toward endovascu-
lar intervention continues, peripheral diag-
nostic angiography and balloon angioplasty
via radial arterial access are becoming more
prevalent with lower profile percutaneous
systems. These procedures are performed
through a 6- or 7-French introducer sheath.
As a result, such complications as infection,
pseudoaneurysm, and thrombosis are not
uncommon. Infection may occur and require
some local drainage and antibiotics. Pseudo-
aneurysm of the radial artery can be treated
with similar techniques for femoral pseudo-
aneurysm, discussed later discussion. Throm-
bosis is typically well tolerated because the
ulnar artery is usually the dominant artery of
the hand. Thrombosis that leads to sympto-
matic hand ischemia and/or major vascular

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22 • IATROGENIC VASCULAR TRAUMA 429

■ FIGURE 22-1

Left common iliac dissection secondary to a crossover sheath on right. Left common iliac post-
stent placement on right. ■

■ FIGURE 22-2

A, Wire in radial artery. B, Sheath and wire removed. C, Wire with piece of radial artery attached.

injury (Fig. 22-2) requires immediate surgi-
cal intervention using standard techniques of
thrombectomy and or arterial reconstruction.

Pseudoaneurysms

Ever since Seldinger's technique for femoral
arterial access became more commonplace,

pseudoaneurysm has been recognized as one
of the most frequently encountered compli-
cations. Classic vascular surgical treatmenthas
required open arterial repair, evacuation of
the hematoma, and drain placement as
needed. In turn, this necessitates further hos-
pitalization for the patient and the accompa-
nying discomfort inherent to recovery from
surgery. Open repair still remains the

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V • SPECIAL PROBLEMS AND COMPLICATIONS

standard of care for more complicated femoral
arterial injuries; however, newer and less inva-
sive techniques have been developed.

The technique of ultrasound-guided
pseudoaneurysm compression was introduced
in the early 1990s. An experienced sonogra-
pher is required to apply between 10 and 120
minutes of compression to the "neck" of the
pseudoaneurysm. Initial success rates for this
procedure have been reported between 60%
and 90%, with no further surgical interven-
tion required. Unfortunately, recurrence rates
have been reported at 25% to 30%. Many
times, the pseudoaneurysm is tender and the
patients require significant amounts of seda-
tion before undergoing compression. In addi-
tion, ultrasound-guided compression has even
lower success rates for patients who are taking
anticoagulation or antiplatelet agents. This
represents a significant number of patients
who undergo percutaneous procedures with
concomitant cardiac and peripheral arterial
disease.

A combined modality using ultrasound
guidance and thrombin injection has been
proven more effective in the treatment of
pseudoaneurysms. Success rates as high as
96% have been reported even when nearly
25% of the patients were anticoagulated. An
experienced sonographer is still required to
help identify the respective pseudoaneurysm
in the appropriate axis for orientation. The
needle is introduced under real-time ultra-
sonography and the pseudoaneurysm is punc-
tured directly with the needle. Appropriate
orientation is crucial because the supplying
artery should not be crossed (Fig. 22-3) . The
thrombin (1000 IU) is then slowly injected
into the pseudoaneurysm only, and throm-
bosis can be seen immediately by ultrasound
(Fig. 22-4) . Observing the ultrasound during
injection ensures instillation of a minimal
amount of thrombin. As thrombosis begins
to occur, injection can be performed incre-
mentally while the rest of the pseudoaneurysm
thromboses. The greatest risk is from direct
thrombin injection into the supplying artery,
which occurs infrequently given adequate
sonographic imaging. Many of the patients
simply require some local anesthetic. This is
performed as an outpatient procedure and
the patients can walk 1 hour after injection.

Common
Femoral A.

■ FIGURE 22-3

Injection of common femoral artery from lateral
approach to avoid intraluminal thrombin
injection. ■

Newer echogenic needles can reportedly
improve visualization of the needle, avoid-
ing thrombin injection into the supplying
artery. We simply use a 22-gauge spinal
needle, moving the obturator in and out to
improve ultrasonographic visualization before
injection.

Enthusiasts of endovascular therapy have
reported on the use of covered stents to
exclude a pseudoaneurysm or arteriovenous
fistula. The early success rates were reason-
able, with an 88% immediate result. On initial
follow-up, however, there was nearly a 20%
failure rate. The use of any stent, covered or
uncovered, in the femoropopliteal region has
been shown to have relatively poor results
when compared to surgery; this is why covered
stents should remain investigational in this
anatomic region.

Hemorrhage

As discussed earlier, uncontrolled hemor-
rhage from percutaneous access is not a

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22 • IATROGENIC VASCULAR TRAUMA

431

■ FIGURE 22-4

Common femoral pseudoaneurysm on left with flow. Thrombosed pseudoaneurysm on right post-
thrombin injection. ■

common phenomenon. The patientwho has
obvious pulsatile bleeding from the puncture
site or a growing hematoma should immedi-
ately have the hemorrhage controlled with
direct pressure on the artery proximal to the
puncture, usually over the femoral head. Occa-
sionally the puncture is too cephalad (exter-
nal iliac) or the femoral artery is damaged
too severely for simple compression. This may
be the case in the presence of severe arterial
laceration or avulsion. Operative repair using
the standard vascular principles of adequate
exposure and proximal/distal vascular control
should be performed immediately.

The more dangerous scenario is that of
insidious and unrecognized hemorrhage.
Patients who have uncontrolled bleeding
without the obvious stigmas (e.g., pulsatile
bleeding and expanding hematoma) initially
exhibit very subtle clinical signs of hemor-
rhage. Relative hypotension and mild tachy-
cardia that transiently improves with
administration of fluids should alert the astute
clinician and necessitate further investigation.
Once suspected, a decreasing hemoglobin
level verifies the likelihood of a retroperitoneal
hematoma. Once again, the location of the
puncture may provide some clues (i.e., above
the inguinal ligament) to ongoing bleeding.
An abdominal computed tomographic (CT)
scan will verify the presence, location, and size

of the retroperitoneal hematoma (Fig. 22-5) .
Surgical exploration should rarely be
required, as the retroperitoneum serves to
tamponade the bleeding. Adequate resusci-
tation, reversal of any underlying coagulopa-
thy, and identification and correction of
medications that may exacerbate the bleed-
ing (e.g., Ilb/IIIa antiplatelet agents) should
be first and foremost before any surgical explo-
ration is performed.

Arterial Closure Devices

Given the growing field of endovascular tech-
niques, combined with the accompanying
increase in percutaneous access complica-
tions, industry has answered with newer prod-
ucts in an attempt to decrease access
complications and reduce personnel time
holding pressure on groins. The goal is to
achieve immediate hemostasis following per-
cutaneous arterial access. Different devices
have been designed, each with its own tech-
nique toward achieving hemostasis. One
approach is to "plug" the hole using collagen-
based materials. Another technique involves
closing the site with a suture. Still, one other
involves using chemicals (procoagulant) to
initiate early hemostasis. The development
of these devices has created a new set of

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V • SPECIAL PROBLEMS AND COMPLICATIONS

■ FIGURE 22-5

Computed tomographic scan of retroperitoneal hematoma (H).

■ FIGURE 22-6

Angio-Seal device in vessel and post-deployment with intraluminal anchor in position.

complications. Treating any of the respective
complications requires some understanding
of how each device functions.

Angio-Seal (Sherwood Davis and Geek, St.
Louis, Missouri) makes use of the collagen
plug philosophy. The plug is sutured to a small,
flat, rectangular anchor that is deployed intra-
luminally (Fig. 22-6). The plug is "tamped"
down and secured extraluminally for near-
immediate hemostasis. Initial success rates
have been reported in the range of 88% to
92 %. Success rates are claimed to improve with
experience, as the manufacturers report an
inherent learning curve. Given the typical
nature of femoral vessels in this patient pop-
ulation, leaving anything intraluminally is
disturbing. Rates of infection, stenosis, and

vascular occlusion or acute ischemia have been
reported to be 2% to 3%. The risk of infec-
tion seems high when compared to simple
manual compression. However, it continues
to be used by many interventionalists in con-
junction with prophylactic antibiotics (not a
recommendation of the manufacturer).

The collagen plug technology is shared by
VasoSeal (Datascope, New Jersey) but in a
different manner. This device requires pre-
dilation with measurements of the length of
the subcutaneous tract. The plug is then
deployed extraluminally (Fig. 22-7) and pres-
sure is applied for 2 to 3 minutes. Immediate
success, defined as hemostasis, was achieved
in 87% to 95% of the patients. The hematoma
rate was alarmingly high, at 21% with

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22 • IATROGENIC VASCULAR TRAUMA

433

A B

■ FIGURE 22-7

VasoSeal device with extraluminal placement of collagen plug.

■ FIGURE 22-8

Duett device illustrating intraluminal balloon inflated and procoagulant injected after compression
on right. ■

1% requiring surgery. If the plug is not ade-
quately placed, then the vessel continues to
bleed into the surrounding tissue. This would
explain the decreased success rate (58.8%)
in obese (>90-kg) patients. The device did not
perform as well for patients on anticoagulants
or antiplatelet therapy, as success rates were
79%. In addition, embolization of the colla-
gen plug, late bleeding, and infection have
required surgical intervention in as many as
5% of patients.

The Duett device (Vascular Solutions, Inc.,
Minneapolis, Minnesota) makes use of a pro-
coagulant to seal the arterial puncture site. A
small balloon is inflated on the luminal side

of the puncture site, to avoid introduction of
material into the respective vessel, and pro-
coagulant is injected (Fig. 22-8). Once the
balloon is deflated, the device is removed and
2 minutes of manual compression is required.
A European multicenter registry reported a
96% deployment rate with successful hemo-
stasis in 2 to 5 minutes in 95% of the patients
with the Duett device. The overall complica-
tion rate was 2.6%, including pseudo-
aneurysms and complete arterial occlusions.
Surgical intervention was required in fewer
than 1% of patients. The use of anticoagu-
lants or antiplatelet agents was not an exclu-
sion criterion for the study.

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434 V • SPECIAL PROBLEMS AND COMPLICATIONS

■ FIGURE 22-9

A, Perclose device in lumen of the vessel. B, Post-deployment with suture in place.

■ FIGURE 22-10

A, Angiogram of introducer sheath entering the left common femoral artery just proximal to the
profunda femoris artery. 6, Angiogram exhibiting high-grade stenosis of common femoral and
profunda femoris arteries. ■

The last, and probably most frequently used,
device uses suture to close the puncture site.
Perclose (Perclose Inc., Menlo Park, Califor-
nia) uses two needles and a preloaded suture
to puncture the vessel in a cephalad to caudad
orientation and close the puncture site (Fig.
22-9) . The ends of the suture come out
through the device and are tied extracorpo-
really. A knot pusher then slides the knot down
to the vessel. Early success rates are reported
at 85% to 90%. Complications are reported
at 1.8% and relate to inadequate deployment
or pseudoaneurysm formation. Device failures

are usually recognized immediately for lack
of hemostasis. Given the size of the needles,
the device does not function on thick calci-
fied vessels. We have seen delayed injuries, with
development of severe claudication (Fig.
22-10), which ultimately leads to common
femoral endarterectomy and profundoplasty.
The aforementioned devices are more fre-
quently being used and this trend will con-
tinue. Aside from the acute need for surgical
intervention, some delayed complications
exist that may mandate surgical intervention.
Although none of the studies discuss any of

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22 • IATROGENIC VASCULAR TRAUMA 435

the local tissue changes, we have experiences
with all of them at our institution. The sur-
rounding scarring and inflammation encoun-
tered when one of these devices has been used
is similar to that seen in a "reoperative groin."

Central Venous Access

Venous access by either the internal jugular
or the subclavian vein approach has become
a frequently performed procedure, with more
than 3 million central venous catheters
inserted annually. The obvious risk of pneu-
mothorax and/or tension pneumothorax is
a well-known complication of this procedure.
Prevention of complications requires strict
adherence to anatomic landmarks. Most
venous injuries will respond to manual digital
compression for hemostasis because it is a low-
pressure system. The most common compli-
cations, however, are from injuries to adjacent
structures.

The internal jugular vein can be
approached from either side of the neck. It
is one of the easiest veins on which to obtain
digital compression. The more common sig-
nificant injury in this location involves the
carotid artery, given its proximity (Fig. 22-11).
Although it is a higher pressure vessel, again,
digital control is relatively easy here. The
serious injuries occur with laceration of the
vessel or when unrecognized cannulation of
the artery occurs with subsequent large-bore
dilation for placement of a resuscitation
catheter (12 French) or a cordis (8 to 10
French). Additionally, unrecognized cannu-
lation of the internal jugular vein through a
portion of the artery may lead to an arteri-
ovenous fistula (Fig. 22-12).

Subclavian venous access has the greater risk
of morbidity and mortality. It is more difficult
to apply digital pressure to the subclavian vein
or the subclavian artery, given their relative
anatomic location posterior to the clavicle
(Fig. 22-13). Cannulation of the right sub-
clavian vein is felt to be potentially more
hazardous secondary to its abrupt angulation
into the superior vena cava. Passage of the
dilator can lacerate or perforate the vein or
the superior vena cava, with an incidence
reported as high as 1% of the time, leading

■ FIGURE 22-11

Illustration depicting carotid artery and internal
jugular vein relationships. ■

to exsanguination and possible death. Passage
through the artery into the vein can lead to
arteriovenous fistula (Fig. 22-14) formation
as well. Aortic perforation and subclavian
artery aneurysm, though not common, have
been reported as a consequence of central
venous access as well.

Intra-Aortic Balloon Pump

The IABPwas first instituted, clinically, 30years
ago, and it has become the most widely applied
mechanical circulatory assist device, inserted
in 2% to 12% of all patients, as an adjunct to
heart surgery. However, it has its own set of
accompanying vascular complications. Com-
plications have been reported to occur
between 12% and 30% of the time.

The most commonly encountered compli-
cation is that of ipsilateral lower extremity
ischemia. Although most patients will improve
with simple removal of the balloon, some
patients still require surgical intervention even

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436

V • SPECIAL PROBLEMS AND COMPLICATIONS

■ FIGURE 22-12

A, Duplex ultrasound of carotid/internal jugular vein fistula from access injury. 6, Corresponding
angiogram of fistula filling vein. ■

Subclavian A
Subclavian V.

■ FIGURE 22-13

Illustration depicts location of subclavian vein
and artery behind the clavicle. ■

*■•- *

■ *' !

mwm

<►„■ ^^__

Subclavian AV Fistula

■ FIGURE 22-14

Duplex ultrasound of subclavian vein/artery
fistula secondary to access. AVF, arteriovenous
fistula; SCA, subclavian artery; SCV, subclavian
vein. ■

after it is removed. Other patients are just not
stable enough to have the balloon removed
and may need contralateral placement. Ipsi-
lateral iliac dissection, thrombosis of
iliac /femoral arteries, and distal embolization
are the most frequently encountered arterial
pathology. A dissection may be treated by

endovascular techniques and stenting. Throm-
bosis requires immediate surgical attention
and intraoperative decisions dictated by the
anatomic location of occlusion. Distal
embolization may occur and the severity of
distal embolization will dictate treatment. A

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22 • IATROGENIC VASCULAR TRAUMA

437

patient who experiences acute popliteal occlu-
sion leading to a nonviable leg should undergo
immediate exploration, thrombectomy, and
potentially bypass. In contrast, patients with
"blue toes" and intact pulses are best observed
for further tissue demarcation and improve-
ment. Luckily, aortic perforation does not
occur frequently (<1%) as it carries a near-
100% mortality rate in this population.

INTRAOPERATIVE VASCULAR
INJURIES

Vascular injuries that occur as a consequence
of another operative intervention are more
prevalent than is reported. Not many surgeons
are willing to report on their series of intra-
operative vascular injuries. However, it is well
known that certain operations and different
procedures have inherent risks of vascular
injuries. The injuries that require intraoper-
ative, urgent vascular consultation are usually
severe and life threatening, as most surgeons
will deal with the less severe injuries
themselves.

Colorectal Procedures

Many colorectal operations require dissection
into the pelvis. The low anterior resection,
total proctocolectomy, abdominoperineal
resection, and especially complicated diver-
ticulitis place iliac vascular structures at risk.
The arterial injuries are usually fairly simple
to recognize and repair following standard vas-
cular surgical principles. However, venous
injuries to the iliac veins or inferior vena cava
may be more challenging and can lead to sig-
nificant blood loss. Simple ligation or over-
sewing of the bleeding may slow the bleeding
enough that compression or packing of the
pelvis may stop the hemorrhage. By the time
a vascular surgeon is called, the patient has
usually bled significantly. Initial packing of the
pelvis, while resuscitation and correction of
an underlying coagulopathy can begin, is the
most prudent first step in this situation. Once
corrected, the packing can be removed in a
systematic fashion to identify the source of

bleeding for subsequent repair. All venous
repairs should use pledgeted sutures of fine
Prolene.

Pancreatobiliary Procedures

Pancreatobiliary operations can be difficult
without a thorough understanding of the
anatomy of the region. The pancreatobiliary
structures lie in a peritoneal and retroperi-
toneal location (Fig. 22-15) that places them
in proximity to the superior mesenteric,
splenic, renal, and portal veins, as well as the
superior mesenteric, celiac, splenic, and
hepatic arteries, in addition to the vena cava
and aorta. Even though these vascular injuries
are not often reported, it has been estimated
that they may approach 4%.

Injuries of aforementioned vessels occur
most frequently to the portal vein, followed
by superior mesenteric vein, right hepatic
artery, splenic vein, superior mesenteric artery
(SMA), and common hepatic artery. Injury
patterns will be dictated by the types and fre-
quency of the pancreatobiliary operation
(e.g., Whipple versus laparoscopic cholecys-
tectomy) performed. Sometimes these vas-
cular injuries are recognized only after the
retractors have been pulled back and the
bowel is ischemic (SMA injury) .

In the trauma setting of a severely injured
patient, many injuries may be ligated or over-
sewn. However, elective pancreatobiliary
surgery often destroys the collateral connec-
tions that are required to maintain viability
after simple ligation. For this reason, it is advis-
able to repair these injuries when recognized
and feasible. Venous injuries may require
simple venorrhaphy or mobilization and
primary anastomosis. In the case of arterial
injuries, primary repair is the goal, but not
always possible given the type of resection and
length of remaining artery. Autogenous recon-
struction with saphenousvein is our preferred
method of repair in this setting.

Laparoscopic Procedures

Laparoscopic surgery has become routine
in surgical practice. Some of the early

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438

V • SPECIAL PROBLEMS AND COMPLICATIONS

■ FIGURE 22-15

Pancreatobiliary anatomic relationships and in cross section. Ao, aorta; IVC, inferior vena cava;
SMA, superior mesenteric artery; SMV, superior mesenteric vein. ■

complications from this "minimally invasive"
technique have completely disappeared.
However, some of the vascular complications
have persisted over theyears. The mechanism
of injury has not changed, even today.

The overall vascular complication rate is
quite low (0.08% to 0.1%) when compared
with that of many other operations. Most com-
monly, vascular injuries reported in the largest
series continue to be to the distal abdominal
aorta, iliac arteries, inferior vena cava, and iliac
veins. These structures are susceptible to
injury from introduction of the Veress needle,
for blind abdominal insufflation, or trocars
into the lower abdomen. The distance, after
compression of the periumbilical region with
a Veress needle or trocar, between the abdom-
inal wall and the vessels during insertion
is generally not appreciated by the inex-
perienced laparoscopist (Fig. 22-16). The
result is major vascular injury. It is usually

immediately recognized though, requiring
conversion to open laparotomy with repair of
the respective vascular injury.

Vascular/Endovascular Surgery

Iatrogenic vascular injuries during vascular
procedures are again an area that is likely un-
reported for two reasons. The first is that the
vascular surgeon is going to repair the injury
at the time it occurs and the second involves
the lack of willingness to report vascular com-
plications. Nonetheless, some well-established
injuries are known to be associated with dif-
ferent operations and have been discussed for
many years. For example, iliac vein injury
during aortobiliary bypass for aneurysmal
disease. Endovascular surgery has borne out
a whole new set of complications relative
to aortic-stent grafts that are still in the

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22 • IATROGENIC VASCULAR TRAUMA

439

■ FIGURE 22-16

Iliac artery injury from Veress needle
placement. ■

discovery phase. The complications associated
with percutaneous access have been discussed
at length.

Thoracoabdominal aortic operations are
generally recognized, by most, as one of the
highest risk operations a vascular surgeon

performs. The large experience of E. Stanley
Crawford and colleagues at Baylor /Methodist
set the standard for this procedure. Respira-
tory failure, renal failure, cardiac complica-
tions, and stroke have all been well established
and are beyond the scope of this chapter. Thor-
ough familiarity with retroperitoneal anatomy
is imperative if one is to perform these oper-
ations safely. Some of the most dangerous
bleeding involves the network of veins that
should be avoided while approaching the
aorta. Examples include the lumbar and
gonadal veins behind the left kidney (Fig.
22-17) and the azygous system. As in trans-
abdominal aortic operations, the vena cava
and iliac veins can lead to massive exsan-
guination and even intraoperative death if
injured. These vessels are difficult to control
and should be packed/compressed initially.
If the injury is too large, then adequate expo-
sure with ligation and/or oversewing still
remains the standard treatment for these
dreaded injuries.

Endovascular aortic aneurysm repair is
still in its infancy in the United States. The
Europeans, however, have been using multi-
ple devices since the early 1990s. Certain com-
plications such as iliac limb occlusion, distal
migration, and device malfunction are

Aortic
Aneurysm

Gondal V. — ' > — Lumbar '

■ FIGURE 22-17

Gonadal and lumbar veins to be avoided during thoracoabdominal exposure of the aorta.

ch22.qxd 4/16/04 3:28 PM Page 440

440

V • SPECIAL PROBLEMS AND COMPLICATIONS

specific to different devices, the subject of
another chapter. Identification of common
vascular complications to the procedure itself
is more important. The Eurostar Collabora-
tors, 56 European centers, identified a 3% vas-
cular complication rate in more than 1500
patients. These complications were identified
as (1) arterial rupture, perforation, or dis-
section; (2) thrombus, obstruction, or steno-
sis; (3) embolization; (4) occlusion of renal
artery; and (5) other injuries. This does not
include the need for open conversion, which
was required in 2.5% of the patients, or late
ruptures as a result of endoleaks.

The Fogarty balloon catheter was first
introduced in 1963. Although it is an instru-
mental part of the vascular surgical arma-
mentarium, some potential complications
are associated with its use. The most common
injuries that have been documented include
(1) perforation of the artery by the catheter
tip, (2) rupture of the artery resulting from
overinflation of the balloon, (3) disruption
or injury to the arterial intima, (4) emboliza-
tion of fragments of the ruptured balloon or
catheter tip, (5) arteriovenous fistula, and (6)
pseudoaneurysm formation.

Many of these injuries are the result of
overzealous inflation and thrombectomy by
the operator, which can be avoided as follows:

(1) Before using the balloon in the vessel,
place a 3-way stopcock on the end of the
catheter to inflate the balloon to the proper
volume (size) under direct visualization, then
turn the stopcock to expel the excess saline;

(2) tactile feel of catheter resistance to with-
drawal in conjunction with careful control of
the syringe to avoid overinflation; (3) if sig-
nificant resistance is encountered and the
anatomy unclear, then dilute the syringe with
some contrast and monitor balloon passage
fluoroscopically. Another method would be
to simply proceed with an intraoperative
angiogram and use an "over-the-wire" balloon
thrombectomy catheter.

Orthopedic Surgery

Common vascular injuries that occur sec-
ondary to orthopedic injuries such as frac-
tures and dislocations have been well
recognized and reported. Given the nature

of a subspecialty that requires placement of
rods and screws for fixation of fractures, it is
amazing that iatrogenic vascular injuries are
not more common. Aside from complete mis-
placement of a rod, the most common injuries
are reported with arthroplasty.

Total knee arthroplasty has been performed
for more than 30 years now. The incidence of
vascular injury is reported to be as low as
0.03%. This operation is typically performed
under tourniquet control, so the injury may
not be recognized initially. The mechanism
of injury, when direct trauma is not involved,
has been theorized to be secondary to arter-
ial stretching or disruption of arterial plaques
from the tourniquet placement. A thorough
preoperative vascular assessment for reference
is not always available when one is consulted
on these patients acutely. In this case, the best
approach is to determine the viability of the
affected leg and compare it to the uninvolved
extremity as a baseline. The most common
complication is that of acute occlusion of the
popliteal artery, requiring immediate explo-
ration with thrombectomy or potential bypass.

One of the other well-established vascular
injuries occurs secondary to screw placement
for total hip arthroplasty. The vascular injuries
that have been reported are related to
intrapelvic extrusion of cement or damage to
the common iliac vein during reaming for
prosthesis placement. Orthopedic surgeons
are well acquainted with the structures that
are anterior, superior, and posterior to the
acetabulum but are relatively unaware of those
that lie medial to it. During the developmental
period of total hip arthroplasty, after some cat-
astrophic complications, it became widely rec-
ognized that the screws for the acetabular
component placed medial structures at risk.
Medial to the acetabulum lie the external iliac
vein, obturator artery, and obturator vein. The
anterior part of the acetabulum became rec-
ognized as the danger zone with the highest
risk for vascular injury during screw place-
ment. Through education, this complication
has been reduced dramatically.

Neurosurgery

Neurosurgical vascular emergencies are not
common. Intracranial vascular complications

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22 • IATROGENIC VASCULAR TRAUMA

441

will be primarily handled by the neurosurgeon
and obviously not the vascular surgeon. Back
operations, such as disk surgery or corrective
scoliosis surgery, have the highest potential
for iatrogenic vascular complications in neu-
rosurgery. Typically, large multilevel spine
operations require adequate exposure. It is
not uncommon for a general surgeon or a vas-
cular surgeon to provide anatomic exposure
for the neurosurgeon.

In the case of scoliosis surgery, prevention
of major vessel injury during anterior expo-
sures to the spine is of major concern. Given
their anatomic proximity to the spine, the
aorta and vena cava are at greatest risk. Typ-
ically, laceration or avulsion type of injuries
occur secondary to rigorous retraction.
Penetrating injuries may occur during
removal of the rim of the disk annulus by the
neurosurgeon. The recommended preven-
tive technique is for placement of an elevator
between the vessels and the spinal column
during disk removal. Appropriate-length
screws will avoid further vascular injury as
well. However, late hemorrhage resulting
from erosion, leakage, or false aneurysm
of adjacent vessels has been reported.
Retroperitoneal exposure to the spine is
fraught with the same hazards as those dis-
cussed earlier with relation to thoraco-
abdominal exposure. The lumbar veins and
arteries are the most commonly injured
vessels because of avulsion or laceration.
Digital pressure should be attempted ini-
tially, followed by suture ligation if unsuc-
cessful. These can be troublesome injuries
that result in a significant amount of blood
loss.

Vascular injuries in lumbar disk surgery
are rare (0.05%) but serious complications.
They may be delayed in presentation or dif-
ficult to recognize given the anatomic
approach. The most commonly seen vascular
injuries are lacerations of the iliac veins,
lumbar veins, abdominal aorta, median
sacral artery, and arteriovenous fistulas.
Because of the relative rarity of these
injuries, no large series has been published
that discusses the surgical approach to any of
these injuries. It is important to keep the pos-
sibility in the back of one's mind, when
recent back surgery has been performed,
that the potential for vascular injury exists.

Early recognition of these injuries will help
avoid unrecognized and ongoing hemor-

rhage.

SUMMARY

Any busy vascular surgeon is fully aware that
a number of iatrogenic vascular injuries occur
with varying frequencies based on anatomic
location. However, reliable data about to the
true incidence of these complications are not
easily obtained. As previously discussed, this
is not a series that any surgeon in any sub-
specialty would like to collect and report. The
incidence and prevalence of iatrogenic vas-
cular injuries are likely even higher than has
been reported.

Our population continues to age and the
greater percentage of the population will be
older than 55 years within 10 years. That trans-
lates into more general, vascular, and cardio-
vascular disease. In turn, a greater number of
operations are likely to be performed in all
of the surgical subspecialties. As technologic
advances continue to develop more devices
for performance of endovascular techniques,
there will continue to be a concomitant
increase in the iatrogenic vascular injuries that
accompany these techniques. The vascular
surgeon will need to be well trained to handle
different types of injuries that will continue
to evolve with advancing technology. This will
require a current knowledge base regarding
to this ever-changing and rapidly developing
technology.

REFERENCES

Arafa OE, Pedersen TH, Svennevig JL, et al: Vas-
cular complications of the Intraaortic balloon
pump in patients undergoing open heart oper-
ations: 15-year experience. Ann Thorac Surg
1999;67:645-651.

Bridwell KH, DeWald RL: The Textbook of Spinal
Surgery, 2nd ed. Philadelphia, Lippincott —
Raven Publishers, 1997.

Buth J, Laheij RJF, et al: Early complications and
endoleaks after endovascular abdominal aortic
aneurysm repair: Report of a multicenter study.
J Vase Surg 2000;31:134-146.

ch22.qxd 4/16/04 3:28 PM Page 442

442

V • SPECIAL PROBLEMS AND COMPLICATIONS

Cikrit DF, Dalsing MC, Sawchuk AP, et al: Vascular
injuries during pancreatobiliary surgery. Am
Surg 1993;59:692-697.

Fruhwith J, Koch G, Mischinger HJ, et al: Vascular
complications in minimally invasive surgery. Surg
Laparosc Enclose 1997;7(3):251-254.

Gonze MD, Sternbergh WC II, Salartash K, et al:
Complications associated with percutaneous
closure devices. Am J Surg 1999;178:209-211.

Goyen M, Manz S, Kroger K et al: Interventional
therapy of vascular complication caused by the
hemostatic puncture closure device Angio-Seal.
Cathet Cardiovasc Intervent 2000;49:142-147.

Kang SS, Labropoulos N, Mansour MA, et al:
Expanded indications of ultrasound-guided
thrombin injection of pseudoaneurysms. J Vase
Surg 2000;31:289-298.

Keating ME, Ritter MA, Faris PM: Structures at risk
from medially placed acetabular screws. J Bone
Joint Surg 1990;72-A(4):509-511.

Lazarides MK, Tsoupanos SS, Georgopoulos SE, et
al: Incidence and patterns of iatrogenic arterial

injuries. Adecade's experience. J Cardiovasc Surg
1998;39:281-285.

Menlhorn U, Kroner A, de Vivie ER: 30 years clin-
ical intra-aortic balloon pumping: Facts and
figures. Thorac Cardiovasc Surg 1999;47
(Suppl):298-303.

Robinson JF, Robinson WA, Cohn A, et al: Perfo-
ration of the great vessels during central venous
line placement. Arch Intern Med 1995;155:1225-
1228.

Silber S, Tofte AJ, Kjellevand TO, et al: Final report
of the European multi-center registry using the
Duett vascular sealing device. Herz 1999;24(8):
620-623.

Sorell KA, Feinberg RL, Wheeler JR, et al: Color-
flow duplex-directed manual occlusion of
femoral false aneurysms. J Vase Surg 1993;1 7:571-

577.

Svensson LG, Crawford ES, Hess KR, et al: Expe-
rience with 1509 patients undergoing thora-
coabdominal operations. J Vase Surg 1993;
17:357-370.

ch23.qxd 4/16/04 3:27 PM Page 443

Compartment Syndromes

THOMAS S. GRANCHI
PRISCILLA GARCIA
KENNETH L. MATTOX
MICHAEL E. DEBAKEY

PRESENTATION

ANATOMY

Calf

Thigh

Arm/Hand

Abdomen

Spinal Cord

Pericardium

DIAGNOSIS

Extremity Compartment Measurements

Noninvasive Assessment of Compartment Compromise

Laboratory Evaluation

Pathophysiology

TREATMENT OF EXTREMITY COMPARTMENT SYNDROME

Technique of Decompression

SUMMARY

443

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444

V • SPECIAL PROBLEMS AND COMPLICATIONS

Compartment syndrome occurs when
pressure in a rigid compartment
exceeds perfusion pressure. It can
occur in any limb, the anterior chamber of
the eye, the spinal canal, the pericardium, or
in the abdomen and is seen in many clinical
settings, threatening life, limb, sight, and/or
neurologic function. Despite technology
advances in noninvasive measurements
and a better understanding of the anatomy,
biology, and chemistry of reperfusion injury,
diagnosis of this complication may still be
missed or delayed. Operative decompression
of the compartment is the mainstay of treat-
ment. Fasciotomy treats compartment syn-
drome in limbs, laparotomy is the treatment
for abdominal compartment syndrome, peri-
cardiotomy treats cardiac tamponade, and
spinal canal decompression has been used to
treat reperfusion-related spinal compartment
syndrome. For these reasons, compartment
syndrome poses many potential pitfalls for
trauma, vascular, and orthopedic surgeons.
Medical treatments to reduce swelling and
protect against cellular injury may have
adjunct roles but do not replace the timely
operative decompression.

Common clinical presentations include
reperfusion injury after blunt trauma, vascu-
lar injury and repair, closed fractures, and elec-
trical injuries. Additionally, compartment
syndromes have been reported following use
of compressive devices, such as the military
antishock trousers. In these clinical settings,
the astute clinician suspects compartment syn-
drome on initial physical examination and
must then develop diagnostic and therapeu-
tic actions, to include serial examinations
of the involved region or extremity, serial
pressure measurements, and/or use of new
machines that evaluate tissue perfusion.

Excessive pain and loss of motor and
sensory function in a limb are late clinical
findings. In patients with a high risk for com-
partment syndrome, but in who repeated
examination is not feasible, immediate com-
partment pressure measurement or immedi-
ate prophylactic fasciotomies should be
considered. Pressure measurements can
be graded, but a direct pressure of 25 cm H 2
or a pressure differential between mean arte-
rial pressure and compartment pressure of

more than 50mmHg indicates the need for
immediate decompression.

Pericardial compartment syndrome is asso-
ciated with increasing pressures in the peri-
cardial sac and can be secondary to venous,
arterial, or cardiac injury. Beck's triad of ele-
vated central venous pressure, hypotension,
and muffled heart sounds is a late manifes-
tation of the pericardial compartment
syndrome. Early detection of post-traumatic
hemopericardium should lead to immediate
thoracic decompression before the late man-
ifestations develop. Narrowed pulse pressure
and cardiac arrest from pericardial tampon-
ade are very late manifestations and usually
occur in patients with multisystem injury
where the attention of the examining physi-
cian has been diverted, causing delayed
or missed diagnosis of the compartment
syndrome.

Spinal compartment syndrome has been
evaluated most often in patients undergoing
operation for extensive thoracoabdominal
aortic surgery, where drainage of cere-
brospinal fluid and reducing the spinal canal
pressure are performed to reduce the inci-
dence of paraplegia. Post-traumatic paraple-
gia, even associated with treatments of blunt
injury of the descending thoracic aorta, has
not been treated with spinal canal decom-
pression. However, because paraplegia is
associated with increased pressures in a
closed compartment, decreasing pressure dif-
ferentials, spinal cord swelling, and ischemia/
reperfusion conditions undoubtedly con-
forms to the definition of a compartment syn-
drome. Further research in patients with
thoracic aortic injury, post-traumatic para-
plegia, and direct spinal column injury is
required to define the post-traumatic spinal
cord compartment syndrome. One might raise
the argument that any potential value of use
of corticosteroids in paraplegia following
blunt injury to the spinal cord is actually
an attempt to treat a spinal compartment
syndrome.

Abdominal compartment syndrome can
occur in patients with intra-abdominal injuries
and hemorrhagic shock but is not directly
related to these conditions. Abdominal com-
partment syndrome also occurs in some
patients with no abdominal injury but who

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23 • COMPARTMENT SYNDROMES

445

have treatment for remote conditions, such
as cardiopulmonary bypass and excessive
fluid resuscitation. In the abdomen, elevated
compartment pressure is manifested by the
following triad:

• Oliguria

• Reduced cardiac output that does not
improve with intravascular fluid
replacement

• Increased airway pressures

Organ impairment and increased airway
pressure can be detected at intra-abdominal
pressures as low as 1 5 mm Hg. At 25 to 30 mm
Hg, organ failure is evident and immediate
laparotomy should be performed (Burch and
colleagues, 1996) . Measuring intra-abdominal
pressures will confirm an already suspected
clinical diagnosis.

PRESENTATION

Surgeons caring for trauma patients most com-
monly diagnose and treat compartment syn-
dromes, because this condition is often seen
in association with injury. Pediatric, ortho-
pedic, plastic, replantation, microvascular,
vascular, and thoracic surgeons also often
encounter compartment syndromes. Arterial
or venous occlusion followed by reperfusion
injury is a common presentation, whether
occlusion is secondary to injury or vascular
control during attempted reconstruction.
Long bone fractures often precipitate com-
partment syndrome because of hematoma and
tissue swelling at the site. Traditionally, calf
compartment syndromes have been the most
commonly diagnosed, treated, and reported.
Gulli and Templeton (1994) report that com-
partment syndrome occurs in 3% to 17% of
closed tibia fractures. Compartment syn-
drome associated with femur injuries is rare
if the fracture occurs at the shaft and absent
associated vascular injuries (Schwartz and
colleagues, 1989; Russel and colleagues, 2002) .
Compartment syndrome occurring in the
thigh is often overlooked because of other life-
threatening injuries that distract the surgeon.

Pericardial compartment syndromes are often
detected during the surgeon performed
ultrasound examination in the emergency
center. Rarely, a patient with unexplained
continuing hypotension in the operating
room following laparotomy will be found to
have an occult pericardial compartment
syndrome.

Although most cases of compartment
syndrome from vascular etiologies occur with
arterial injuries, it can also occur with venous
pathology. There are many reports of com-
partment syndrome occurring with phleg-
masia cerulea dolens (Dennis, 1945; Cywes
andLouw, 1962; Wood and colleagues, 2000).
Venous bleeding in the calf, thigh, abdomen,
arm, and neck has also produced compart-
ment syndromes. The individual fascial and
muscle compartments in each of these areas
deserve careful attention.

In the upper arm and forearm, compart-
ment syndrome may occur with supracondy-
lar humerus fractures, intravenous drug
abuse, electrical injuries, intravenous line
insertion site complications, prolonged
tourniquetuse, and even weight lifting (Moore
and Friedman, 1989) . Historically, when home
washing machines had mechanical wringers
attached to the machine, children getting
arms caught in the wringer was an extremely
common cause of both humeral fracture and
compartment syndrome, known then as
Volkmann 's ischemic contracture. Many of these
patients will present in ambulatory settings,
where the index of suspicion may be low. Deep
pain and tense swelling of the limb should
prompt further investigation.

Abdominal compartment syndrome often
develops in trauma patients who have under-
gone recent laparotomy and been excessively
resuscitated for hemorrhagic shock using
large volumes of crystalloid solution. The
abdominal cavity will stretch anteriorly and
superiorly (along the diaphragm) to accom-
modate visceral edema or accumulating blood
until it reaches the limits of its compliance.
At this point, the abdomen becomes a rigid
compartment and pressure rises sharply,
impairing organ function. Increased vascular
resistance and reduced venous return impair
cardiac output. Reduced renal perfusion
pressure causes oliguria. Much of the post-

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446

V • SPECIAL PROBLEMS AND COMPLICATIONS

traumatic renal failure reported in the liter-
ature during the 1960s and 1970s appears now
to have been secondary to an abdominal com-
partment syndrome, which at that time had
not yet been described. Transference of the
abdominal pressure to chest and tension on
the diaphragm increase ventilator and airway
pressures. Loss of functional residual capac-
ity and ventilation-perfusion mismatch causes
hypoxia (Ivatory, Sugerman, and Peiztman,
2001).

Several systemic diseases are associated
with compartment syndromes. Rutgers, van
derHarst, andKoumans (1991) reported four
cases on nontraumatic rhabdomyolysis and
compartment syndrome in young male alco-
holics receiving treatment with benzodi-
azepines. Ergotamine use and cocaine
intoxication have also been implicated in the
development of compartment syndrome
(Gilman, Goodman, and Murad, 1989).
Patients with type I diabetes mellitus can suf-
fer spontaneous compartment syndrome
(Lafforgue and colleagues, 1999; Smith and
Laing, 1999; Silberstein and colleagues, 2001) .
Systemic diseases or drugs that cause vaso-
constriction can induce muscle ischemia and
subsequent compartment syndrome. Local
factors including hematoma, fluid injection,
infection, and metastatic melanoma that
increase mass within the inelastic fascial com-
partments can also raise intracompartment
pressure sufficiently to cause the feared
syndrome (Simmons, 2000).

ANATOMY
Calf

The four muscle compartments of the calf are
the anterior, lateral, superficial posterior, and
deep posterior. The anterior compartment is
bounded by the tibia medially, the interosseous
membrane posteriorly anterior crural inter-
muscular septum laterally, and the crural fascia
anteriorly. It contains the tibialis anterior, the
extensor digitorum longus, and the extensor
hallucis longus muscles. It also contains the

anterior tibial artery and vein, as well as the
deep peroneal nerve. The lateral compart-
ment contains the peroneus longus and brevis
muscles and the superficial peroneal nerve.
The superficial posterior compartment con-
tains the bulky soleus muscle. The deep pos-
terior compartment encloses the tibialis
posterior, flexor digitorum longus, and flexor
hallucis longus muscles. The posterior tibial
vessels and the tibial nerve run within this com-
partment. Note that the saphenous vein
courses in the subcutaneous tissue along the
medial border of the superficial compartment.
It can be damaged during fasciotomy if
care is not taken to protect it. Also, the sural
nerve runs along the posterior lateral border
of the superficial posterior compartment
(Clemente, 1981). Lateral and medial inci-
sions are made throughout the extent of the
calf, with retraction of the more superficial
muscles to expose the deep compartment so
that all compartments are decompressed. His-
torically, small skin incisions with incisions in
the superficial fascia only and use of a lateral
fibulectomy fasciotomy did not adequately
decompress all calf fascial compartments.
These procedures have little utility in today's
trauma armamentarium.

Thigh

The thigh has three muscle compartments:
anterior, medial, and posterior. The anterior
compartment contains the quadriceps, sar-
torius, iliacus, and psoas muscles, as well as
the femoral vessels and nerve and the lateral
cutaneous nerve. The medial compartment
encloses the adductor muscles, and the pos-
terior compartment encircles the biceps
femoris muscle and the sciatic nerve. Com-
partment syndrome of the thigh usually
involves the anterior and lateral compart-
ments (McGee and Dalsey, 1992) . The gluteal
muscle group also constitutes a compartment
that is enclosed by the fascia lata. Gluteal com-
partment syndrome occurs but is often diag-
nosed late (Hill and Bianchi, 1997) . A liberal
lateral fasciotomy will usually decompress a
thigh compartment syndrome.

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23 • COMPARTMENT SYNDROMES

447

Arm/Hand

The muscles of the arm, forearm, and hand
are also grouped into compartments but are
no t as defined by tight investing fascia as those
of the calf (Doyle, 1998). The arm has ante-
rior and posterior compartments. The ante-
rior compartment contains the biceps muscle,
the brachial vessels, and the median, ulnar,
and musculocutaneous nerves. The posterior
compartment contains the triceps muscle and
the radial nerve. The forearm has three com-
partments the volar, dorsal, and the "mobile
wad." The volar compartment contains the
flexor and pronator muscles, the radial and

ulnar arteries, and the median and ulnar
nerves. The dorsal compartment contains the
extensor muscles. The "mobile wad" is closely
associated with the dorsal compartment and
contains the radial nerve. The hand has
four compartments: the central, thenar,
hypothenar, and interossei. The thick reti-
naculum cutis and the carpal tunnel serve as
a venous obstruction at the wrist for com-
partment syndromes of the forearm and
hand. Fasciotomies of the forearm, usually
carried out with "zig-zag" and "straight" inci-
sions, are carried across the carpal tunnel onto
the hand to achieve a complete decompres-
sion (Fig. 23-1).

Ulnar a.

Ulnar n.

Flexor carpi ulnaris m.

■ FIGURE 23-1

Elective incisions that can be used for approach to the radial and ulnar arteries. A, An S-type
incision starting along the course of the distal brachial artery, carried throughout the antecubital
fossa and continued down on the forearm will give excellent exposure of the proximal ulnar and
radial arteries as well as the origin of the common interosseous artery (A). An extension of this
incision (B) along the course of the radial artery can be used for exposure to the wrist level. A
separate incision can be used over the course of the ulnar artery (C). B, This drawing demonstrates
exposure of the ulnar neurovascular bundle within the deep muscle layers, which have been split
proximally. ■

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V • SPECIAL PROBLEMS AND COMPLICATIONS

Abdomen

The abdominal viscera are encircled with peri-
toneum and the intra-abdominal contents are
contained within the endoabdominal fascia,
named in various locations as the transversalis
fascia or Gerota's fascia. This investing fascia
is contiguous with the esophageal hiatus and
abdominal outlets at the groins. Numerous
layers of muscles exist outside the endoab-
dominal fascia. Both the retroperitoneal and
intraperitoneal organs are within this fascia.
Swelling, gaseous distention, tissue edema,
and hemorrhage are contained within this
fascia. Although having great capacity to
contain large quantities of fluid, tissue edema
combined with large volumes of fluid increases
abdominal pressure.

Spinal Cord

The spinal cord is surrounded by thick dura
and is contained within a bony encasement.
It is supplied by radicular arteries from the
thoracic and abdominal aorta. A single radic-
ular artery from the segmental arteries divides
into anterior and posterior radicular arteries.
The anterior radicular artery feeds a single
anterior spinal artery, and the posterior radic-
ular artery feeds paired posterior spinal
arteries. The anterior spinal artery is more
rudimentary and may even be interrupted,
thus explaining the more common anterior
spinal artery syndrome. Nine paired segment
arteries arise in the chest, although the
number may ranges from three to twelve. On
occasion, one of the segmental arteries off of
the aorta is much larger than the others and
has been called the artery of Adamkiewicz.
This variation is not consistent. Any condition
from swelling of the spinal cord to pericord
hematomas can contribute to a spinal column
compartment syndrome.

Pericardium

Contained within the pericardial sac are the
heart, ascending aorta, intrathoracic inferior
vena cava, superior vena cava, pulmonary
artery, right and left main pulmonary arter-

ies, azygous vein, lymphatic channels, and peri-
cardial vessels. Any condition that results in
increasing fluid within the pericardial sac may
contribute to hemopericardium and the devel-
opment of pericardial compartment syn-
drome. Concomitant injury to the anterior
pericardium and internal mammary arteries
can also produce hemopericardium. Iatro-
genic causes of hemopericardium, such as
puncture of the heart or vessels during peri-
cardiocentesis or trocar chest tube insertion,
have been described.

DIAGNOSIS

The symptoms of deep muscle pain, pain on
passive motion, muscle weakness or paralysis,
hyperesthesia, and tense muscle compart-
ments have been well described and repeated
to generations of surgery residents (Matsen,
Windquist, and Krugmire, 1980; Perry, 1988;
Velmahos and Toutouzas, 2002) . Recognition
of the symptom constellation should prompt
immediate measurement of compartment
pressure, using any of the several accurate
devices available. If accurate measurements
cannot be performed, or if the results are con-
flicting, a clinical diagnosis of compartment
syndrome should lead to strong consideration
for compartment decompression. Once diag-
nosis is made, immediate release of pressure
is indicated.

Abdominal compartment syndrome should
be suspected in the patient with a tense,
distended abdomen within a few hours of
laparotomy for trauma or massive bleeding.
Visceral swelling or continued bleeding
push abdominal compliance beyond its
limits. Oliguria that does not respond to fluid
boluses or frequent ventilator alarms should
prompt immediate measurement of the
intra-abdominal pressure. This can be accom-
plished easily at the bedside by measuring the
bladder pressure through a Foley catheter
(Burch and colleagues, 1996; Ivatury,
Sugerman, and Peiztman, 2001).

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23 • COMPARTMENT SYNDROMES

449

Extremity Compartment
Measurements

There are several techniques for measuring
extremity compartment pressures (Matsen
and colleagues, 1976; Perron, Brady, and
Keats, 2001; Hargens and colleagues, 1977).
There are two variations of the catheter tech-
nique, the wick and the slit catheters. The
catheters are inserted into the muscle through
large-bore needles and then connected to a
pressure transducer or manometer via saline-
filled tubing. Because insertion and connec-
tion of the catheters are cumbersome,
measuring several compartment pressures is
difficult. The new electronic transducer-
tipped catheter is promising but shares many
of the shortcomings with the other catheter
techniques, such as need for tubes, catheter
kinking, and poor placement beneath the
fascia (Willy, Gerngross, and Sterk, 1999) .
Commercial devices for measuring compart-
ment pressures are readily available at the
bedside and are easier to use.

Manufactured pressure monitors such as
the Stryker (Stryker Instruments, Kalamazoo,
Michigan) and Ace (Ace Medical Company,
Los Angeles, California) instruments employ
modifications of the needle technique and
measure pressure directly through a needle
inserted into the muscle compartment. These
self-contained units require no assembly,
making multiple measurements at different
sites and times easier.

Regardless of the device used, multiple mea-
surements should be taken at various sites in
the muscle and in different compartments.
Pressure is not uniformly distributed through-
out each compartment, and measurements
can be highly variable. In the calf, the ante-
rior and deep posterior compartments, at
least, should be measured. The highest mea-
surement in each compartment should be
used for clinical decisions.

Noninvasive Assessment of
Compartment Compromise

The persistent trend in medicine toward non-
invasive diagnosis and treatment extends to

compartment syndrome. Several techniques
that have clinical utility in other settings have
been tried here, including near-infrared spec-
troscopy (NIRS) , have been studied (Garr and
colleagues, 1999; Giannotti and colleagues,
2000; Gentilello and colleagues, 2001). NIRS
measures muscle perfusion, not pressure,
and can reliably diagnose ischemic tissue.
Oxyhemoglobin saturation of less than 60%
correlates with muscle compromise of
compartment syndrome. Champions for its
use argue that it directly identifies ischemic
tissue rather than compartment pressure,
which is a proxy for tissue compromise. If clin-
icians monitor for tissue ischemia rather than
a rise in pressure, unnecessary fasciotomies
might be prevented. Conversely, skeptics
argue that waiting until ischemia is manifest
may delay surgery. Also, the probe's range is
limited to 2 cm or less below the skin surface.
Therefore, it may miss deep muscle ischemia.
Of the noninvasive tests discussed, NIRS
holds the most promise. It reliably identifies
ischemic tissue and can provide continuous
measurements. The latter makes it particularly
attractive for use in the operating room and
intensive care unit, where serial physical
examinations are difficult on unconscious
and or multi-injured patients. Continuous
monitoring may identify development of
compartment syndrome while surgeons are
occupied with other injuries. Reliable
measurements and safe thresholds for oper-
ation may reduce the unnecessary prophy-
lactic fasciotomies. Studies of these questions
continue.

Continuous compartment pressure or NIRS
monitoring may influence the decision to
refrain from fasciotomy. If the surgeon has
continuous reliable monitoring, an operation
should not be performed unless pressure
or tissue perfusion reaches the threshold.
However, the risk of compartment syndrome
must be recognized and frequent or contin-
uous measurements must be undertaken,
always keeping in focus the clear indications
for fasciotomy and the consequences of failing
to act expeditiously.

Although it has been suggested, digital pulse
oximetry is not sensitive in diagnosing com-
partment syndrome and muscle ischemia. It
relies on pulsatile arterial flow to the distal

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450

V • SPECIAL PROBLEMS AND COMPLICATIONS

digit to accurately measure the hemoglobin
oxygen saturation. Because the arterial blood
measured in the toe or finger bypasses the
muscle compartments, measuring the former
gives little useful information of the latter
(Mars and Hadley, 1994).

Scintigraphy using technetium-99 methoxy-
isobutyl isonitrile ( 99m Tc-MIBI) has been used
to diagnose chronic exertional compartment
syndrome (Edwards and colleagues, 1999;
Owens and colleagues, 1999). The study
requires a stable, ambulating patient, a trip
to the nuclear medicine department, and a
subsequent study the next day with the patient
at rest. With these limitations, this study
cannot diagnose acute compartment syn-
drome in time to save the limb. We found no
reports that it has been studied in acute com-
partment syndromes.

Laboratory Evaluation

There are no laboratory tests that will predict
or diagnose early compartment syndrome.
Serum creatinine phosphokinase, a marker
for muscle cell injury, is a finding in late or
missed compartment syndrome (Robbs and
Baker, 1979; Moore and Friedman, 1989).
Postoperative levels may be useful in moni-
toring response to treatment.

Similarly, myoglobinuria is a marker for
muscle injury. It often occurs with crush or
electrical injuries, which often lead to com-
partment syndrome. The presence of myo-
globinuria in such patients does not per se
diagnose compartment syndrome. The muscle
injury may follow from direct trauma rather
than ischemia secondary to elevated com-
partment pressures. Therefore, myoglobin-
uria has little value in diagnosing acute early
compartment syndrome.

Pathophysiology

Restoration of oxygenated blood flow to an
ischemic limb often worsens the initial cellu-
lar damage. The reperfused tissue suffers from
the initial ischemia and from free radical tox-
icity. If microvascular flow slows or stops, then
ischemia recurs and free radicals accumulate,

compounding the injury. This sequence of
events produces reperfusion injury, which
is a common etiology of compartment
syndrome.

The cellular damage and capillary leak
result from oxygen free radical and neutrophil
activity. Hypoxanthine accumulates as a
product of dephosphorylated adenosine and
is converted to urate in the presence of xan-
thine oxidase and oxygen. The enzyme xan-
thine oxidase also catalyzes the reduction of
molecular oxygen to superoxide and hydro-
gen peroxide. These radicals contribute to
increased microvascular permeability. Super-
oxide can also generate the hydroxyl radical
in the presence of Fe 3+ , which is reduced to
Fe 2+ . The hydroxyl radical is highly cytotoxic
through lipid peroxidation of the cell
membrane. Neutrophils adhere to damaged
microvascular endothelium and release
superoxide radicals and proteases, con-
tributing further to reperfusion injury
(Granger, 1988) .

TREATMENT OF EXTREMITY
COMPARTMENT SYNDROME

Surgery has and continues to be the mainstay
of treatment of compartment syndromes.
Releasing the pressure through generous
fascial incisions restores microvascular flow
and rescues the threatened tissue. Nonoper-
ative therapies received minimal theoretical
initial enthusiasm and support; however, to
date, none have demonstrated adequate
efficacy. Choices in operative treatment are
choices of incision and wound closure. The
necessity of fasciotomy for diagnosed
compartment syndrome remains unassail-
able. Indications for prophylactic fasciotomies,
however, have been questioned (Field and
colleagues, 1994; Velmahos and colleagues,
1997; Velmahos and Toutouzas, 2002).

Prophylactic fasciotomies in the calves have
been advocated for combined popliteal artery
and vein injuries and for ischemic times of
more than 6 hours. Advocates argue that while
waiting for compartment pressures to reach
threshold for precise diagnosis may lead to

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23 • COMPARTMENT SYNDROMES

451

severe dysfunction or need for an amputation;
therefore, Hofmeister and Shin (1998) rec-
ommend liberal fasciotomies, especially in the
anesthetized or comatose patient.

Hofmeister and Shin (1998) recommend
prophylactic fasciotomy of all muscle com-
partments of the arm after replantation,
because replantation requires 5 to 10 hours
to accomplish, and the already compromised
muscle relies on tenuous arterial and
venous anastomosis. Fasciotomy, therefore,
should be performed before compartment
syndrome develops (Hofmeister and Shin,
1998) . Under these circumstances, fasciotomy
is prudent.

Technique of Decompression

The four compartments of the lower leg can
be decompressed through a single lateral

incision (Fig. 23-2) or through lateral and
medial incisions (Fig. 23-3) . The two-incision
technique is more common because it is
technically easier to reach the posterior com-
partments through the medial incision.
Fibulectomy has been described but aban-
doned because easier and less morbid oper-
ations accomplish adequate decompression
(Mubarak and Owen, 1977; Gulli and Tem-
pleton, 1994) . Care must be taken at the upper
end of a lateral calf fasciotomy incision to avoid
injury to the peroneal nerve. Likewise, care
must be taken to not incise or damage the
long saphenous vein while making a medial
calf fasciotomy incision.

Less invasive methods have been attempted.
Surgical textbooks of the 1960s showed draw-
ings of small skin incisions, and using long
scissors, a continuous medial and lateral
fascial incisions would be made. As the fascial
compartments then had increased swelling,

l-unsecltd p'C? : '■■• . : rtt ■■■■ I

Tibia

poster to*
■ : .-" .• •■ partn enl '■ ■ ' " " d 1 1 i I

■ i •

m FIGURE 23-2

In selected patients, a fasciotomy by means of the subperiosteal fibulectomy technique may have
merit in obtaining adequate decompression of all four major compartments of the leg. The
completed fibulectomy/fasciotomy is shown. A, A cross section at the midcalf level, showing
(arrows)tbe direction to be followed for four-compartment decompression. 6, The area
decompressed. (From Ernst CB, Kauder HJ: Fibulectomy-fasciotomy. An important adjunct in the
management of lower extremity arterial trauma. J Trauma 1971 ;1 1[3]:365-380.) ■

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452

V • SPECIAL PROBLEMS AND COMPLICATIONS

Saphenous
vein

Anterior
compartment

Lateral
compartment

Deep posterior
compartment

Superficial posterior
compartment

Lateral

■ FIGURE 23-3

Drawing depicting medial and lateral calf incisions to decompress four of the fascial compartments
of the lower leg. Specifically, note the proximity of the superficial peroneal nerve and saphenous
vein, which must be protected. (Redrawn from Baylor College of Medicine, 1987.) ■

the skin became an investing constriction.
Ota and colleagues (1999) described endo-
scopic release of the anterior leg compartment
using an arthroscope and a transparent
outer tube for chronic compartment syn-
drome in an athlete. The patient enjoyed relief
of symptoms postoperatively, and the com-
partment pressures diminished (Ota and col-
leagues, 1999) . Other authors have been less
enthusiastic about endoscopic fasciotomies.
Havig, Leversedge, and Seiler (1999) com-
pared endoscopic and open forearm
fasciotomies in cadavers. They found the
endoscopic procedure reduced compartment
pressures, but not as dramatically as the open
procedure, and cautioned against using the
endoscopic forearm fasciotomy in the clini-
cal setting.

After diagnosing compartment syndrome
and performing fasciotomy, the surgeon faces
a large problematic wound. Primary closure

is usually impossible because of exuberant
muscle swelling. Delayed primary closure or
later skin grafting is the most common method
of wound closure.

Advocates of liberal fasciotomies tend to dis-
count the morbidity of the scars. Conversely,
other experts hold that complications from
fasciotomies, including prophylactic ones, can
be significant (Field and colleagues, 1994;
Velmahos and colleagues, 1997; Fitzgerald
and colleagues, 2000) . Wound complications
include ulcers, skin tethering to the muscle,
paresthesias, pruritus, muscle herniation, and
disfigurement. Fitzgerald and colleagues
(2000) report that unsightly scars resulted in
life changes for many patients and recom-
mend primary closure of the wounds when-
ever possible.

Delayed primary closure of extremity
wounds offers the benefit of a smaller scar but
is usually labor intensive. This method involves

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23 • COMPARTMENT SYNDROMES

453

some daily manipulation of sutures, wires, or
elastic bands. Steri-Strips (3M Surgical Prod-
ucts, St. Paul, Minnesota) have been used for
gradual approximation of skin edges, closing
the wound in 5 to 8 days (Harrah and col-
leagues, 2000) . Chiverton and Redden (2000)
used subcuticular polypropylene sutures to
achieve skin closure. Harris (1993) described
using rubber vessel loops stretched between
skin staples in shoelace fashion. One historic
technique involved using interrupted wires
stretched between skin staples, but this tech-
nique has been abandoned because of the
difficulty endured by physician, patient, and
nurses. The technique required adding
tension daily by twisting of 20 to 30 interrupted
wires spanning the incisions. The theory was
attractive, but the practice was arduous.

Wound closure with split-thickness skin
grafts is accomplished in 5 to 7 days after the
fasciotomy. This method requires little bedside
wound manipulation and achieves closure of
large wound. It requires an additional general
anesthetic for the patient and produces a sig-
nificant scar. Skin grafting, however, is a main-
stay in this setting because of its simplicity and
coverage of large wound areas.

Because of the morbidity of fasciotomy,
medical treatments have been researched in
animals. The results are equivocal. Most are
used to ameliorate the damage from oxygen
free radicals (Hofmeister and Shin, 1998) .
They include deferoxamine to chelate iron,
xanthine oxidase inhibitors, such as allop-
urinol, to block production of hypoxan thine,
and superoxide dismutase, an enzyme to cat-
alyze the superoxide radical to hydrogen per-
oxide. These antioxidants have been studied
in many animal models, but not in humans.
Currently, such nonprocedural therapies are
not recommended.

In the abdomen, primary closure of the
fascia is usually impossible, and sometimes, a
skin-only closure can be accomplished. The
most common forms of closure after laparo-
tomy for abdominal compartment syndrome
involve some form of temporary prosthesis
such as a "Bogota bag" or vacuum pack
(Burch and colleagues, 1996; Ivatury, Suger-
man, and Peiztman, 2001). These prostheses
maintain protection of the visceral while

allowing loss of domain and effectively increas-
ing the volume of the abdominal cavity.
Removal of the prosthesis may be accom-
plished when swelling recedes. If delayed
primary closure cannot be performed, skin
grafting or component separation can cover
the viscera. For the most severe forms of
abdominal compartment syndrome in
patients with multisystem trauma and pro-
longed intensive care unit stays, secondary
reconstruction of the abdominal wall, using
prosthetic material sewn to the fascia, may
be accomplished several months later, often
longer than 12 months.

SUMMARY

Compartment syndrome, if not detected early,
can result in loss of limb, organ function, and
even life. Effective treatment relies on early
diagnosis through clinical examination and
bedside measurements of compartment pres-
sures. Measurements are accomplished using
one of several commercially available devices.
NIRS may have benefit as a noninvasive
harbinger of muscle compromise. Although
research has mapped the complex reactions
in reperfusion injury, it has not produced a
means for prevention or effective medical
treatment.

Once diagnosis is made, the surgeon must
perform expeditious decompression. Avariety
of incisions have been described. In the lower
leg, median and lateral longitudinal incisions
are m ost comm only used . In the forearm , volar
and radial incisions are preferred. For the
abdomen, a midline laparotomy accomplishes
decompression. Pericardiotomy relieves
compartment syndrome of the pericardium.

Prophylactic fasciotomy for high-risk
patients is common. With newer, more reliable
methods of tissue perfusion and compartment
pressure measurements, prophylactic fas-
ciotomy may be performed less commonly.
Obviously, unnecessary fasciotomy should be
avoided if possible. However, if muscle, organ,
or limb loss is the alternative, decompression
of the compartment is always indicated.

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REFERENCES

Burch JM, Moore EE, Moore FA, Franciose R: The
abdominal compartment syndrome in complex
and challenging problems in trauma surgery.
Surg Clin North Am 1996;76(4):883-843.

Chiverton N, Redden JF: A new technique for
delayed primary closure of fasciotomy wounds.
Injury 2000;31 (l):21-24.

Clemente C: Anatomy, a Regional Atlas of the
Human Body, 2nd ed. Baltimore: Urban &
Schwarzenberg, 1981.

Cywes S, LouwJH: Phlegmasia cerulea dolens: suc-
cessful treatmentby relieving fasciotomy. Surgery
1962;51:169-172.

Dennis C: Disaster following femoral vein ligation
for thrombophlebitis; relief by fasciotomy; clin-
ical case of renal impairment following crush
injury. Surgery 1945;17:264-269.

Doyle J: Anatomy of the upper extremity muscle
compartments. Hand Clin 1998;14:343-364.

Edwards PD, Miles KA, Owens SJ, et al: A new non-
invasive test for detection of compartment syn-
dromes. Nuclear Med Commun 1999;20(3):
215-218.

Field CK, SenkowskyJ, Hollier LH, et al: Fasciotomy
in vascular trauma: is it too much, too often? Am
Surg 1994;60(6):409-411.

Fitzgerald AM, Gaston P, Quaba A, McQueen MM:
Long term sequelae of fasciotomy wounds. Br J
Plast Surg 2000;53:690-693.

GarrJL, Gentilello LM, Cole PA, etal: Monitoring
for compartmental syndrome using near-infrared
spectroscopy: a noninvasive, continuous, trans-
cutaneous monitoring technique. J Trauma
Injury Infect Crit Care 1999;46(4):613-618.

Gentilello LM, Sanzone A, Wang L, et al: Near-
infrared spectroscopy versus compartment pres-
sure for the diagnosis of lower extremity
compartmental syndrome using electromyog-
raphy-determined measurements of neuromus-
cular function. J Trauma Injury Infect Crit Care
2001;51(l):l-9.

Giannotti G, Cohn SM, Brown M, et al: Utility of
near-infrared spectroscopy in the diagnosis
of lower extremity compartment syndrome. J
Trauma Injury Infect Crit Care 2000;48(3) :396-
401.

Gilman AG, Goodman LS , Murad F: Goodman and
Gilman's The Pharmacological Basis of Thera-
peutics, 8th ed. New York: Macmillan, 1989.

Granger DN: Role of xanthine oxidase and gran-
ulocytes in ischemia-reperfusion injury. Am J
Physiol 1988;246:H1269-H1275.

Gulli B, Templeton D: Compartment syndrome of
the lower extremity. Orthoped Clin North Am
1994;25(4):677-684.

Hargens AR, Mubarak SJ, Owen CA, et al: Inter-
stitial fluid pressure in muscle and compartment
syndromes in man. Microvasc Res 1977;14:1-10.

Harrah J, Gates R, Carl J, Harrah JD: A simpler,
less expensive technique for delayed primary
closure of fasciotomies. AmJ Surg 2000;180(1) :
55-57.

Harris I: Gradual closure of fasciotomy wounds
vising a vessel loop shoelace. Injury 1993;24(8) :
565-567.

Havig MT, Leversedge FJ, Seller JG 3rd: Forearm
compartment pressure: an in vitro analysis of
open and endoscopic assisted fasciotomy. J Hand
Surg Am 1999;24(6):1289-1297.

Hill SL, BianchiJ: The gluteal compartment syn-
drome. Am Surg 1997;9:823-826.

Hofmeister EP, Shin AY: The role of prophylactic
fasciotomy and medical treatment in limb
ischemia and revascularization, in compartment
syndrome and Volkmann's ischemic contracture.
Hand Clin 1998;14(3):457-465.

Ivatury RR, Sugerman HJ, Peiztman AB: Abdomi-
nal compartment syndrome: recognition and
management. In: Advances in surgery, vol. 35.
St. Louis, MO: Mosby, 2001:251-269.

Lafforgue P, Janand-Delenne B, Lassman-Vague V,
et al: Painful swelling of the thigh in a diabetic
patient: Diabetic muscle infarction. Diabetes
Metab 1999;25(3):255-260.

Mars M, Hadley GP: Failure of pulse oximetry in
the assessment of raised limb intracompart-
mental pressure. Injury 1994;25(6):379-381.

Matsen FA, Mayo KA, Sheridan GW, Krugmire RB:
Monitoring of intramuscular pressure. Surgery
1976;79(6):702-709.

Matsen FA, Windquist RA, Krugmire RB: Diagno-
sis and management of compartmental syn-
dromes. J Bone Joint Surg Am 1980;62:286.

McGee DL, Dalsey WC: The mangled extremity;
compartment syndrome and amputations, in soft
tissue emergencies. Emerg Med Clin North Am
1992;10(4):783-800.

Moore RE III, Friedman RJ: Current concepts in
pathophysiology and diagnosis of compartment
syndromes. J Emerg Med 1989;7:657-662.

Mubarak SJ, Owen CA: Double-incision fasciotomy
of the leg for decompression in compartment
syndromes. J Bone Joint Surg 1977;59A:184-
187.

ch23.qxd 4/16/04 3:27 PM Page 455

23 • COMPARTMENT SYNDROMES

455

Ota Y, Senda M, Hashizume H, Inoue H: Chronic
compartment syndrome of the lower leg: a new
diagnostic method using near-infrared spec-
troscopy and a new endoscopic fasciotomy.
Arthroscopy 1999;15(4) :439-443.

Owens S, Edwards P, Miles K, et al: Chronic com-
partment syndrome affecting the lower limb:
MIBI perfusion imaging as an alternative to pres-
sure monitoring: two case reports. Br J Sport
Medl999;33(l):49-51.

Perron AD, Brady WJ, Keats TE: Orthopedic pit-
falls in the ED: acute compartment syndrome.
Am J Emerg Med 2001;19(5):413-416.

Perry MO: Compartment syndromes and re per-
fusion injury. Vase Trauma Surg Clin North Am
1988;68(4):853-864.

Robbs JV, Baker LW: Late revascularization of the
lower limb following acute arterial occlusion. Br
J Surg 1979;78:490-493.

Russel GV, Kregor PJ, Jarre t CA, Zlowodowski M:
Complicated femoral shaft fractures, in treat-
ment of complex fractures. Orthop Clin North
Am2002;33(l):l-17.

Rutgers PH, van der Harst E, Koumans RKJ: Sur-
gical implications of drug induced rhabdomy-
olysis. Br J Surg 1991;78:490-492.

Schwartz JTJr, Brumback RJ, Lakatos R, et al: Acute
compartment syndrome of the thigh, a spectrum
of injury.JBone Joint Surg Am 1989;71:392-400.

Silberstein L, Britton KE, Marsh FP, et al: An unex-
pected cause of muscle pain in diabetes. Ann
Rheum Dis 2001;60(4):310-312.

Simmons DJ: Compartment syndrome complicat-
ing metastatic malignant melanoma. Br J Plast
Surg 2000;53(3):255-257.

Singhal P, Horowitz B, Quinones QC, et al: Acute
renal failure following cocaine abuse. Nephron
1989;52:76-78.

Smith AL, Laing PW: Spontaneous tibial com-
partment syndrome in type I diabetes mellitus.
Diabetes Med 1999;16(2):168-169.

Velmahos GC, Theodorou D, Demetriades D, et
al: Complications and nonclosure rates of fas-
ciotomy for trauma and related risk factors. World
J Surg 1997;21:247-253.

Velmahos GC, Toutouzas KG: Vascular trauma and
compartment syndromes, in vascular trauma:
complex and challenging injuries, part II. Surg
Clin North Am 2002;82(1):1 25-141.

Willy C, Gerngross H, SterkJ: Measurement of in tra-
compartmental pressure with use of a new elec-
tronic transducer-tipped catheter system.J Bone
Joint Surg Am 1999;81 (2) : 158-1 68.

Wood KE, Reedy JS, Pozniak MA, Coursin DB:
Phlegmasia cerulean dolens with compartment
syndrome: a complication of femoral vein cau-
terization. Crit Care Med 2000;28 (5) :1 626-1 630.

ch24.qxd 4/16/04 3:25 PM Page 457

Historic Review of
Arteriovenous Fistulas and
Traumatic False Aneurysms

NORMAN M. RICH

ARTERIOVENOUS FISTULA

History

Incidence

Etiology

Pathophysiology

Clinical Pathology

Clinical Features

Diagnostic Considerations

Surgical Treatment

Spontaneous Cure

Results

Follow-up

TRAUMATIC FALSE ANEURYSMS

History

Incidence

Etiology

Clinical Pathology

Clinical Features

Diagnostic Considerations

Surgical Treatment

Spontaneous Cure

Follow-up

457

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V • SPECIAL PROBLEMS AND COMPLICATIONS

ARTERIOVENOUS FISTULA

If it should be found by experience, that a
large artery, when wounded, may be healed
up by this kind of suture, without becoming
impervious, it would be an important
discovery in surgery. It would make the
operation for the Aneurysm still more
successful in the arm, when the main trunk
is wounded; and by this method, perhaps,
we might be able to cure the wounds of
some arteries that would otherwise require
amputation, or be altogether incurable.
Lambert, 1762; quoted in Hallowell, 1762

It is generally accepted that the first successful
arterial repair was performed by Hallowell in
1759. His comments emphasize his realization
that repair of false aneurysms and arteriove-
nous fistulas (AVFs) could be valuable. The
diagnosis, pathophysiology, and surgical man-
agement of AVFs and false aneurysms have
stimulated the intellectual curiosity and chal-
lenged the technical abilities of surgeons for
more than 200 years. These lesions are often
found in association, and they are often dis-
cussed together, despite the variable aspects
that exist. Appropriate emphasis is given
where indicated.

Because of the outstanding contributions
of Matas, Halsted, Reid, Holman, Elkin,
Shumacker, Hughes, and others and a
plethora of reports from three major armed
conflicts in this century, considerable docu-
mentation exists regarding principles of diag-
nosis and management of AVFs and false
aneurysms. During the Korean Conflict,
Hughes, Jahnke, and Spencer documented
that arterial repair could be successful, even
in a combat zone. Consequently, more vascular
repairs were done at the time of initial wound-
ing, with a resultant decrease in the number
of AVFs and false aneurysms that required later
repair. With the rapid progress that was made
in vascular surgery in the 10 years preceding
the increased American military involvement
in Southeast Asia in 1965, hundreds of well-
trained young surgeons from both military
and civilian training programs were available

and eager to perform vascular repairs
during the fighting in the Republic of South
Vietnam.

With the establishment of the Vietnam Vas-
cular Registry at Walter Reed Army Medical
Center in 1966, an effort was made to docu-
ment as accurately as possible all vascular
injuries that occurred among American casu-
alties in Southeast Asia and to provide long-
term follow-up of these casualties. The initial
analysis was important in providing guide-
lines for determining the ultimate success
or failure following various types of repairs.
It was believed that there would be relatively
few AVFs and false aneurysms, compared with
other recent wars. Nevertheless, it was re-
cognized that a number of factors, such as
multiple wounds and other more serious
problems, might lead to delayed recognition
of both AVFs and false aneurysms. In later
follow-up from the registry, it was shown that
there were more AVFs and false aneurysms
than initially anticipated. The registry report
provided an analysis of information gathered
over 9 years for nearly 7500 records of
American casualties, showing that there were
558 AVFs and false aneurysms among 509
combat casualties (Rich, Hobson, and Collins,
1975) (Fig. 24-1).

History

Hunter (1757, 1762) provided documentation
more than 200 years ago that the heart
enlarged in a patient with an AVF and that
the arterial dilation occurred proximal to an
arteriovenous communication (Table 24-1).
Norris (1843) noted the recurrence of phys-
ical findings associated with an arteriovenous
aneurysm 10 days after ligation of the artery
above and below the fistula. Nicoladoni (1875)
andBranham (1890) described slowing of the
heart with pressure occlusion of an arteri-
ovenous communication, and their names are
often associated with this physical finding (the
Nicoladoni-Branham sign) . Annandale (1875)
described the successful management of a
popliteal AVF by the ligature of the popliteal
artery and vein. Eisenbrey (1913) described
pathologic changes associated with arteri-
ovenous aneurysms of the superficial femoral

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

459

■ FIGURE 24-1

Multiple fragments from various exploding
devices were responsible for the majority
(87.3%) of arteriovenous fistulas and false
aneurysms in this study. The subtraction study of
an arch angiogram helped confirm the clinical
impression of an arteriovenous communication in
the patient's right neck at the level of the
common carotid bifurcation. Excision of the
fistula with ligation of the external jugular vein
was performed at Walter Reed Army Medical
Center in 1971 . (From Rich NM, Hobson RW II,
Collins GJ Jr: Traumatic arteriovenous fistulas
and false aneurysms: A review of 558 lesions.
Surgery 1975;78:817-828.) ■

TABLE 24-1

ACHIEVEMENTS AND UNDERSTANDING IN TREATING ARTERIOVENOUS FISTULAS:
REPRESENTATIVE HISTORICAL NOTES

Author (Yr)

Hunter (1757)

Norris(1843)
Breshet(1833)

Nicoladoni (1875)

Branham (1890)

Stewart (1913)

Gunderman (1915)

Reid (1920)

Nanu and colleagues (1922)

Franz

Holman (1937)

Contribution

Recognized an abnormal communication between an artery and vein.

Described the associated thrill and bruit.

Eliminated the thrill and bruit by pressure over the proximal artery or site

of communication.
Noted tortuosity and dilation of the artery proximal to the fistula.
Cured an arteriovenous fistula by double arterial ligation.
Described two patients in whom ligation of the artery proximal to the

arteriovenous communication was followed by gangrene.
The first to demonstrate the remarkable slowing of the pulse rate by

compression of the artery proximal to the arteriovenous fistula.
Emphasized the slowing of the pulse rate by obliterating a large

acquired arteriovenous fistula (Branham-Nicoladoni sign).
Noted that the heart diminished in size within 10 days after elimination

of the arteriovenous fistula.
The first to mention an increase in blood pressure on obliteration of an

acquired arteriovenous fistula.
Presented experimental evidence of cardiac enlargement in the

presence of an arteriovenous fistula.
Accurately described the effect on the blood pressure of closure of

the arteriovenous fistula.
Observed an increase in skin temperature and an increase in extremity

growth in the presence of a femoral fistula of 18 months' duration in a

12-year-old boy.
Clarified many of the anatomic and hemodynamic variations seen with

arteriovenous fistulas.

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460

V • SPECIAL PROBLEMS AND COMPLICATIONS

vessels (Fig. 24-2). Holman (1937), in his
classic monograph, described the patho-
physiology associated with abnormal com-
munications between arterial and venous
circulations. Holman (1940, 1962) has also
provided reviews of the pathophysiology of
AVFs. Osier (1893, 1905) made a number of
early observations on AVFs. His respect for
these lesions is exemplified by a quotation
from an article written in 1905, "The great
danger of operating is in the gangrene which
is apt to follow."

Halsted made numerous contributions in
the field of vascular surgery, including the

management of AVFs. He referred to case pre-
sentation by Bernheim in 1916, when the latter
used an interposition autogenous saphenous
vein graft as a replacement for a popliteal
repair (Halsted, 1916). He noted the impor-
tant contributions of Carrel and specifically
stated that the operation of Lexer, which Bern-
heim also was advocating, was the "the ideal
operation." Reid, in two important contribu-
tions (1920, 1925), described abnormal arte-
riovenous communications. Using the vast
World War II experience, Elkin ( 1945) , Elkin
and DeBakey (1955), and Shumacker (1946,
1950) documented a number of important

■ FIGURE 24-2

An arteriovenous communication with
extensive vascular alterations. (From
EisenbreyAB. JAMA 1913;61:2155-
2157.) ■

Sat ov\U*

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

461

findings. Shumacker (1946) outlined the sur-
gical approach to various AVFs and false
aneurysms. He recognized the important
work by Matas (1901, 1908), who made sig-
nificant contributions to the present man-
agement of both AVFs and false aneurysms.
The management of 215 AVFs and false
aneurysms during the Korean Conflict was
reported by Hughes andjahnke (1958).

Incidence

The lessons learned in Korea, the advances
made in the techniques of vascular surgery,
the increased numbers of surgeons trained
in vascular techniques, plus rapid
evacuation, new instruments and antibiotics
have resulted in practically all arterial
injuries occurring in Vietnam being repaired
primarily with a high degree of success, so
that only rarely do patients develop an
arteriovenous fistula or false aneurysm.

It is difficult to determine the true incidence
of AVFs. Some series combine congenital with
traumatic lesions. False aneurysms may or may
not be included. Some reports of arterial
lesions include AVFs and others do not. Often
the diagnosis is not made until years later. As
an example, AVFs are still diagnosed at this
time amongWorld War II veterans, more than
30 years after their original injury.

Encouraged by Halsted, Callander (1920)
made a literature review of 447 AVFs to 1914,
including some from World War I. In the
earliest reports of management of combat-
incurred AVFs, Soubbotitch (1913) reported
a insignificant percentage of vascular injuries:
77 injuries to large blood vessels among
20,000 wounded. The numerous separate
reports by Elkin, Shumacker, Freeman, and
others from their vast experience during
World War II are included in a final bound
report (Elkin and DeBakey, 1955). A total of
593AVFswere treated; however, no incidence
was given for these lesions among World War
II combat casualties. In the Korean Conflict,
202 patients were treated for 215 AVFs and
false aneurysms, with notation made for inci-
dence among all combat casualties (Hughes
andjahnke, 1958).

The only statistic from the Vietnam
experience of any value was an incidence
of approximately 7% of AVFs and false
aneurysms among nearly 7500 American casu-
al tiesin Southeast Asia who suffered some type
of vascular trauma. When Heaton and col-
leagues (1966) evaluated the initial military
surgical practices of the U.S. Army in Vietnam,
they recorded the following:

The factors mentioned certainly played a
significant role in limiting the number of
AVFs and false aneurysms. With time, however,
an increasing number of AVFs and false
aneurysms were recorded. In many cases,
these occurred in patients sustaining multi-
ple small fragment wounds over a large
portion of the body, which made it impracti-
cal to explore every artery in which a vascu-
lar injury might be present.

Hewitt and Collins (1969) reported a 10%
incidence of AVFs among 60 patients with arte-
rial injuries treated between December 1966
and October 1967, at the Eighteenth Surgi-
cal Hospital and during November 1967 at
the Seventy-first Evacuation Hospital in
Vietnam. Five of the six lesions were acute
AVFs, which were noted on admission of the
patients to the hospital within 1 to 6 hours
after injury.

Civilian reports of vascular trauma have
increased in the past 40 years, and some
include reviews of experience in managing
AVFs. Patman, Poulos, and Shires (1964)
included six patients with AVFs among their
256 patients with civilian arterial injuries, an
incidence of 2.3%. Drapanas and colleagues
(1970) stated that because the immediate
repair of all acute arterial injuries is advocated,
the development of serious delayed compli-
cations, including AVFs and false aneurysms,
should largely be prevented. They found that
chronic AVFs and false aneurysms declined
noticeably during the last period of their study,
between 1958 and 1969 at Charity Hospital in
New Orleans (Fig. 24-3) . Hewitt, Smith, and
Drapanas (1973) reported a 6.8% incidence,
with 14 cases of acute AVFs among 206
patients with acute arterial injuries treated

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462

V • SPECIAL PROBLEMS AND COMPLICATIONS

[2 12-

5 iO-
1*-

v .

u. 61

2 2-
0-

1 1 1 | A i A X X

58 60 62 64 66 68 70
YEAR

■ FIGURE 24-3

The number of patients with chronic
arteriovenous fistulas and false aneurysms
admitted to Charity Hospital in New Orleans on
the Tulane Service between 1958 and 1969.
There has been a notable decline in the
incidence of these vascular injuries with
delayed recognition. (From Drapanas T, Hewitt
RL, Weichert RF, Smith AD: Civilian vascular
injuries: A critical appraisal of three decades of
management. Ann Surg 1970;172:351-360.) ■

on the Tulane University Surgical Service
(Fig. 24-4).

The incidence of AVFs compared to that of
false aneurysms has varied from one series
to another. Shumacker and Carter (1946)
studied 364 AVFs and false aneurysms in 351
individuals. There were 245 AVFs and 119
aneurysms, with 206 and 82, respectively,
operated upon at one of the three Vascular
Centers, Mayo General Hospital, established
by the Army Surgeon General during World
War II (Fig. 24-5; Table 24-2). In the 1964
series of Patman, Poulos, and Shires from
Dallas, there were 17 patients who developed
late complications, but only five AVFs were
reported, compared with 12 false aneurysms.
Thus, in their series, the false aneurysms out-
numbered the AVFs by 2 : 1, a ratio opposite
to that reported by Hughes andjahnke (1958)
from the Korean experience.

Seel ey and colleagues (1952) reported that
AVFs occurred in at least twice as often as false

CAROTID- JUGULAR/(2

I 1 SUBCLAVIAN

2) AXILLARY

EXTERNAL ILIAC ( I

2) COMMON FEMORAL

POPLITEAL

■ FIGURE 24-4

Distribution of acute arteriovenous fistulas in 14
of 206 patients with acute civilian arterial
injuries in New Orleans: an incidence of 6.8%.
(From Hewitt RL, Smith AD, Drapanas T: Acute
traumatic arteriovenous fistulas. J Trauma
1973;13:901-906.) ■

aneurysms in 106 cases seen at Walter Reed
General Hospital. Most of the patients sus-
tained their injury in the earlier part of the
Korean Conflict. The incidence was nearly
equal in the Vietnam experience (Rich, 1975) ,
although there were fewer AVFs than false
aneurysms (Table 24-3). AVFs and false
aneurysms are often found together in var-
ious anatomic configurations (Figs. 24-6 and
24-7). Shumacker and Wayson (1950) out-
lined the development of AVFs, showing that
pulsating hematomas may present initially,
with well-formed saccular aneurysms devel-
oping subsequently. Notes made at the time

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS 463

ARTERIOVENOUS FISTULAS

INNOMINATE,
CAROTID,
VERTEBRAL,
ft BRANCHES

SUBCLAVIAN,

AXILLARY,

BRACHIAL,

RADIAL,

ULNAR,

* BRANCHES

EXTERNAL ILIAC,
HYPOGASTRIC,
ft BRANCHES

27 (11%)

47 (19.255)

5 (250

ARTERIAL ANEURYSMS

9 (7.6J5)

COMMON FEMORAL,

FEMORAL,

PROFUNDA, 78 (51. 8#)

ft BRANCHES

POPLITEAL,
ft BRANCHES

46 (18.4J?)

ANTERIOR TIBIAL,
POSTERIOR TIBIAL,
PERONEAL, 4J (17.651)
ft BRANCHES

64 (46.470

2 (1.75!)

21 (17.6J5)

21 (17.655)

12 (10. 150

■ FIGURE 24-5

General distribution of arteriovenous fistulas and false aneurysms in a study from the Mayo General
Hospital during World War II. (From Shumacker HB Jr, Carter KL: Arteriovenous fistulas and false
aneurysms in military personnel. Surgery 1946;20:9-25.) ■

TABLE 24-2

COMPARISON OF INCIDENCE OF ARTERIAL ANEURYSMS AND ARTERIOVENOUS
FISTULAS IN THE MAIN PERIPHERAL ARTERIES: MAYO GENERAL HOSPITAL,
WORLD WAR II

Involved Artery

Arteriovenous Fistulas

No.

Subclavian

4.1

Axillary

4.9

Brachial

5.3

Common femoral and femoral

26.9

Popliteal

17.1

Arterial Aneurysm

No. %

5
15
28
17
21

4.2

12.6
23.5
14.3
17.6

From Shumacker HB Jr, Carter KL: Arteriovenous fistulas and false aneurysms in military personnel. Surgery 1946;20:9-25.

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464

V • SPECIAL PROBLEMS AND COMPLICATIONS

TABLE 24-3

ARTERIOVENOUS FISTULAS AND
FALSE ANEURYSMS: VIETNAM
VASCULAR REGISTRY

Lesions

No.

False aneurysms
Arteriovenous fistulas
Total

296
262
558

53.1

46.9

100.0

From Rich NM, Hobson RW II, Collins GJ Jr: Traumatic
arteriovenous fistulas and false aneurysms: A review of
558 lesions. Surgery 1975;78:817-828.

CD A

(fill

■ FIGURE 24-6

This diagrammatic representation of various types of arteriovenous fistulas and associated
aneurysms evolved from a study of 195 cases of arteriovenous fistulas. There was an associated
aneurysm in 60% of the arteriovenous fistulas. A, artery; S, sac; V, vein. (From Shumacker HB Jr,
Wayson EE: Spontaneous cure of aneurysms and arteriovenous fistulas, with some notes on
intravascular thrombosis. Am J Surg 1950;79:532-544.) ■

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

465

■ FIGURE 24-7

Femoral angiogram demonstrating an
arteriovenous fistula at the level of the right
common femoral arterial bifurcation. There is an
associated false aneurysm (arrow).
Arteriorrhaphy of the origin of the profunda
femoris artery and venorrhaphy of the common
femoral vein were successfully accomplished
at Walter Reed Army Medical Center in 1970.
(From Rich NM, Hobson RW II, Collins GJ Jr:
Traumatic arteriovenous fistulas and false
aneurysms: A review of 558 lesions. Surgery
1975;78:817-828.) ■

of operation and on examination of the
excised specimen permitted an analysis of the
presence or absence of an aneurysms in 195
cases of AVFs. There was no associated
aneurysms in 78 cases, or 40%. The 60%
majority had one or more aneurysm. Multi-
ple lesions may also exist in various anatomic
sites (Table 24-4).

A wide variation exists in the regional dis-
tribution of AVFs. This may include specific
arteries, as well as regional areas. During a
15-year period from 1947 through 1962, 50
patients with AVFs were admitted to the
Baylor University College of Medicine-
affiliated hospitals in Houston. The greatest

TABLE 24-4

ARTERIOVENOUS FISTULAS AND
FALSE ANEURYSMS; MULTIPLE
LESIONS AT VARIOUS ANATOMIC
SITES: VIETNAM VASCULAR REGISTRY

Patients

Lesions

Total

468

509

558

From Rich NM, Hobson RW II, Collins GJ Jr: Traumatic
arteriovenous fistulas and false aneurysms: a review of
558 lesions. Surgery 1975;78:817-828.

TABLE 24-5

LOCATION OF ARTERIOVENOUS
ANEURYSMS: BAYLOR UNIVERSITY
COLLEGE OF MEDICINE AFFILIATED
HOSPITALS

Location

Popliteal

Femoral

Brachial

Common carotid

Radial

Subclavian

External carotid

Internal carotid

Posterior tibial

Temporal

Aortic arch

Internal iliac

External iliac

Occipital

Internal maxillary

Thyrocervical

Uterine

Peroneal

Medial circumflex femoral

Total

From Beall AC Jr, Harrington BO, Crawford ES, DeBakey ME:
Surgical management of traumatic arteriovenous aneurysms.
Am J Surg 1963;106:610-618.

number of these lesions were found in the
extremities, with the lower extremities being
more commonly involved than the upper
(Table 24-5). Vollmar and Krumhaar (1968)
found that nearly 50% of the AVFs in their

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466

V • SPECIAL PROBLEMS AND COMPLICATIONS

series were localized in the lower extremities
(Fig. 24-8). Next in frequency were fistulas
of the upper extremities and shoulders (27%) ,
head and neck (22.5%), and trunk (2%).
Table 24-6 outlines representative World War
II statistics concerning predominantly lower
extremity injuries, specifically those involving
the femoral and popliteal vessels. Involve-
ment of major (Table 24-7) and minor (Table
24-8) vessels was outlined from the Korean
experience by Hughes and Jahnke (1958). The
Vietnam data centered around lower extrem-
ity involvement (Table 24-9) , with the super-
ficial femoral and popliteal arteries being most
commonly injured (Table 24-10).

There are hundreds of reports of specific
or unusual AVFs. Complete analysis is beyond
the scope of this review. Creech, Gantt, and
Wren (1965) presented a series of traumatic
AVFs at unusual sites, including the superior
gluteal, hepatic-portal, coronary, and vertebral
vessels. Conn and colleagues (1971) reported
challenging arterial injuries, including an aor-
tocaval fistula, an iliac AVF, and a mesenteric
AVF in eight patients.

Other representative reports include the fol-
lowing (additional information can be found
in specific chapters): Hunt and colleagues
(1971) reported their experience in manag-
ing five AVFs of major vessels in the abdomen.

LOCALIZATION OF 200 TRAUMATIC ARTERIOVENOUS FISTULAE
( Surg. Clin of the Univ. of Heidelberg, 1939 - 1967 ).

Carotis interna(8\^ f \ J^f) Carotis- Sin. cavern.

(9) Carotis externa

Thyreoideosup
Carotis commun

Transversa scapul.
Anonyma C~2\-

Axillans

Cubitahs(2_

Ulnans\3)

Popliteal)

\T) Vertebra lis

~\f) Thyreoidea inf.

J7)Subclavia
i)Pulmonalis

2T)Brachialis

T) Aorta
f)lliacacomm

MjFemoralis

(^Tibialis post.

m FIGURE 24-8

In the cases seen at Heidelberg University, nearly 50% of the arteriovenous fistulas were found in
the lower extremities. (From Vollmar J, Krumhaar D: In: Hiertonn T, Rybeck B, eds. Traumatic arterial
lesions. Stockholm, Sweden: Research Institute of National Defense, 1968.) ■

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

467

TABLE 24-6

DISTRIBUTION OF FALSE ANEURYSMS AND ARTERIOVENOUS FISTULAS: MAYO
GENERAL HOSPITAL

Arteriovenous Fistulas:

No. of Cases

Arterial

Aneurysms:

No. of Cases

Operation

Operation at

at Mayo

Mayo

Involved

General

Operation

"Spontaneous

General

Operation

"Spontaneous

Artery

Hospital

Elsewhere

Cure"

Hospital

Elsewhere

Cure"

Aorta

Innominate

Internal carotid

External carotid

Common

carotid

Vertebral

Lingual

Occipital

Cirsoid, nose,

ear

Superior

temporal

Transverse

cervical

Deep cervical

Internal

mammary

Subclavian

Axillary

Branch axillary

Brachial

Radial

Ulnar

External iliac

Hypogastric

Superior gluteal

Obturator

Common

femoral

Femoral

Profunda

femoris

Branch

profunda

Popliteal

Geniculate

Posterior tibial

Anterior tibial

Peroneal

Branches in

calf

Total

206

From Shumacker HB Jr, Carter KL: Arteriovenous fistulas and arterial aneurysms in military personnel. Surgery 1946;20:9-25.

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468

V • SPECIAL PROBLEMS AND COMPLICATIONS

TABLE 24-7

LOCATION OF TOTAL MAJOR VESSEL LESIONS: ARTERIOVENOUS FISTULAS;
KOREAN EXPERIENCE

Vessel

Common carotid

Internal carotid

Subclavian

Axillary

Brachial

Iliac

Common femoral

Superior femoral

Popliteal

Total

Arteriovenous Fistulas

9
10

7
24
_22
91

False Aneurysms

7
10
43

Total

134

From Hughes CW, Jahnke EJ Jr: The surgery of traumatic arteriovenous fistulas and aneurysms: A five-year followup study of
215 lesions. Ann Surg 1958;148:790-797.

TABLE 24-8

LOCATION OF ARTERIOVENOUS FISTULAS: TOTAL MINOR VESSEL LESIONS
TREATED; KOREAN EXPERIENCE

Vessel

Lesions

Treatment

Arteriovenous
Fistulas

False
Aneurysms

Ligation

Spontaneous

Closure Anastomosis

Total

Occipital

Supraorbital

—

Superior temporal

Vertebral

—

Superior thyroid

—

Inferior thyroid

—

Thoracoacromial

—

Thoracodorsal

Posterior humeral circumflex

Subscapular

—

Profunda brachii

—

Radial

Ulnar

Posterior interosseous

—

Anterior interosseous

—

Digital

—

Profunda femoris

—

Muscular branch femoral

—

Circumflex femoral, lateral

Inferior genu

Posterior tibial

Peroneal

Anterior tibial

Dorsalis pedis

—

Deep mantar

_1_

—

Total

2
1
3
3
1
2
2
3
2
1
1
6
4
1
2
1

10
1
2
3

13
9
6
1

From Hughes CW, Jahnke EJ Jr: The surgery of traumatic arteriovenous fistulas and aneurysms: A five-year followup study of
215 lesions. Ann Surg 1958;148:790-797.

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS 469

TABLE 24-9

ARTERIOVENOUS FISTULAS AND
FALSE ANEURYSMS: ANATOMIC
LOCATION; VIETNAM VASCULAR
REGISTRY

Location No.

Head/neck

7.5

Upper extremity

134

24.0

Thorax

3.1

Abdomen

3.9

Lower extremity

343

61.5

Total

558

100.0

From Rich NM, Hobson RW II, Collins GJ Jr: Traumatic
arteriovenous fistulas and false aneurysms: A review of
558 lesions. Surgery 1975;78:817-828.

TABLE 24-10

ARTERIOVENOUS FISTULAS AND FALSE ANEURYSMS: ARTERIAL INJURIES;
VIETNAM VASCULAR REGISTRY

Arteriovenous

False

Artery

Fistulas

Aneurysms

Total

Common carotid

2.0

Internal carotid

1.1

External carotid

0.7

Vertebral

1.4

Subclavian

1.4

Axillary

3.2

Brachial

9.9

Radial

4.8

Ulnar

4.1

Innominate

0.4

Thoracic aorta

0.4

Abdominal aorta

0.2

Common iliac

0.4

External iliac

1.1

Internal iliac

0.2

Common femoral

2.0

Superficial femoral

15.8

Deep femoral

6.6

Popliteal

12.4

Posterior tibial

11.3

Anterior tibial

6.8

Peroneal

4.3

Miscellaneous

9.5

Total

262

296

558

100.0

From Rich NM, Hobson RW II, Collins GJ Jr: Traumatic arteriovenous fistulas and false aneurysms: A review of 558 lesions.
Surgery 1975;78:817-828.

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470

V • SPECIAL PROBLEMS AND COMPLICATIONS

One of the cases was unique in that the authors
could find no previous report of successful
repair of a fistula between the aorta, the renal
vein and the portal vein (Fig. 24-9). They also
described immediate repair of a mesenteric
AVF and other fistulas involving the portal
and renal veins. Dillard, Nelson, and Norman
(1968) reported one case in which a 29-year-
old woman was stabbed in the right flank
and 3 years later was found to have severe
hypertension. After correction of the renal
AVF, the patient's blood pressure returned to
normal.

Etiology

Although AVFs may be either acquired or
congenital, we are essentially concerned with
those that are acquired by trauma. On the
other hand, one cannot be knowledgeable
about acquired AVFs without also under-
standing the anatomic and pathophysiologic
aspects of congenital AVFs (Table 24-11).
Long-standing acquired AVFs must be differ-
entiated from congenital AVFs, because there
is a considerable difference in their surgical
management, as well as the final results. An

■ FIGURE 24-9

Abdominal aorta injured by a small-caliber bullet. This angiogram reveals the tip of the catheter in
the area of injury; the portal vein fills selectively. The additional injury to the renal vein could not be
shown simultaneously in this unique lesion involving the aorta, the renal vein, and the portal vein.
(From Hunt TK, Leeds FH, Wanebo HJ, Blaisdell FW: Arteriovenous fistulas of major vessels in the
abdomen. J Trauma 1971 ;1 1 :483-493.) ■

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

471

TABLE 24-11

ARTERIOVENOUS FISTULAS: 10-YEAR
EXPERIENCE AT THE MAYO CLINIC

Congenital Acquired

AV fistulas of the

extremities
Aorta-inferior vena

cava fistulas
Pulmonary AV fistulas
Renal AV fistulas
AV fistulas of the

portal system
AV fistulas of the neck

and face
Pelvic AV fistulas
AV fistulas of the chest

wall
Total

139

6
1

5
2

AV, arteriovenous.

Modified from Gomes MMR : Gernatz PE: Arteriovenous
fistulas: A review and 10-year experience at the Mayo Clinic.
Mayo Clin Proc 1970;45:81-102.

acquired AVF can have one, or possibly two,
communications, whereas the communication
between the arteries and the veins in the con-
genital type of AVF may be myriad.

Usually an AVF results from a simultaneous
injury of an artery and adjacent vein, which
permits blood to flow directly from the injured
artery into the vein. Penetrating injuries are
usually responsible for these lesions. In mili-
tary injuries, penetrating missiles are the major
cause, and in civilian injuries, stab wounds, as
well as missile wounds, are associated with
these lesions. The largest series of AVFs have
been associated with recent combat wounds
that have occurred during wars in the past
century (Table 24-12). Both gunshot and
fragment wounds have created AVFs that have
been recognized either in the immediate or
in the acute state or after a delayed period of
several weeks or months. One of the ironies
of the combat situation in Vietnam, where
modern weapons have been employed, is that
the primitive punji stick has also caused AVFs.
I saw such an injury of the anterior tibial artery
and vein at the Second Surgical Hospital in
1966.

Vollmar and Krumhaar (1968), based on
their experience with 200 traumatic AVFs

TABLE 24-12

ARTERIOVENOUS FISTULAS AND
FALSE ANEURYSMS: ETIOLOGY OF
INJURY; VIETNAM VASCULAR
REGISTRY

Wounding Agent

Fragment
Bullet
Blunt

Punji stick
Total

No.

487

87.3

10.6

1.2

0.9

558

100.0

From Rich NM, Hobson RW II, Collins GJ Jr: Traumatic
arteriovenous fistulas and false aneurysms: a review of 558
lesions. Surgery 1975;78:817-828.

treated at the Surgical Clinic at the Univer-
sity of Heidelberg between 1939 and 1967
(Table 24-13), reported that two world wars
greatly increased the incidence of traumatic
AVFs.

In civilian experience, many AVFs result
from stab wounds, although they can also be
caused by bullets. However, these are usually
low-velocity gunshot wounds. Beall (1963)
reported that 36 of 50 of AVFs in their 15-year
study of vascular injuries resulted from
gunshot wounds (Table 24-14).

Sako and Varco (1970) reported their expe-
rience in managing 57 patients with congen-
ital and acquired AVFs of the extremities,
abdomen, and chest wall during a 20-year

TABLE 24-13

ETIOLOGY OF 200 TRAUMATIC
ARTERIOVENOUS FISTULAS;
SURGICAL CLINIC OF THE UNIVERSITY
OF HEIDELBERG: 1939-1967

Wounding Agent

No.

War projectiles

177

88.5

Fractures

5.0

Stab wounds

3.5

Iatrogenic trauma

2.0

Gunshot wounds (civil)

1.0

Total

200

100.0

From Vollmar J, Krumhaar D: In: Traumatic Arterial Lesions.
Hiertonn T, Rybeck B, eds. Stockholm, Sweden: Research
Institute of National Defense, 1968.

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V • SPECIAL PROBLEMS AND COMPLICATIONS

TABLE 24-14

TYPES OF INJURIES RESULTING IN
ARTERIOVENOUS ANEURYSMS:
BAYLOR UNIVERSITY COLLEGE OF
MEDICINE AFFILIATED HOSPITALS

Type of Injury

No.

Gunshot wounds 36

Stab wounds and lacerations 10

Shrapnel injuries 3

Blunt trauma 1

Total 50

From Beall AC Jr, Harrington OB, Crawford ES, DeBakey ME:
Surgical management of traumatic arteriovenous aneurysms.
Am J Surg 1963;106:610-618.

period (1949 to 1969). Fewer than 50%, or
25 patients, had acquired AVFs. The etiology
of these injuries included small-arms fire in
nine, penetration with a knife or glass in six,
a shell fragment or land mine explosion in
three, multiple puncture for cardiac catheter-
ization in two, blunt injury of the hand in one,
pelvic fracture in one, renal needle biopsy
in one, rupture of an aneurysm in one, and
following gastrectomy in one.

Though uncommon, traumatic AVFs have
been reported after both major and minor
surgical procedures (Fig. 24-10). The vessels
that have been involved include the superior
thyroid (Ranshoff, 1935), renal (Muller and
Goodwin, 1956), intercostal (Reid and
McGuire, 1938), uterine (Elkin and Banner,
1946), and aortocaval (DeBakey, 1958).
Pridgen and Jacobs (1962) reviewed three
postoperative AVFs treated in a 3-year period
at Vanderbilt University. They emphasized the
necessity for exercising extreme care to avoid
accidental injury to vessels during any surgi-
cal procedure. In one of their cases, they also
emphasized that en masse ligation must be care-
fully avoided. They felt that the suture liga-
ture had passed through the right superior
epigastric artery and vein in one of their
patients to result in an arteriovenous com-
munication. AVFs have occurred following
mass ligature of the renal vessels during
nephrectomy and of the blood supply to the
thyroid gland during lobectomy. One case
report from Walter Reed General Hospital

■ FIGURE 24-10

Arteriogram of the aortoiliac vessels
demonstrating an inferior epigastric artery false
aneurysm, which occurred as a complication of
abdominal retention sutures. (From Ello FV,
Nunn DB: False aneurysm of the inferior
epigastric artery as a complication of
abdominal retention sutures. Surgery
1973;74:460-461.) ■

documented the development of an AVF fol-
lowing subtotal gastric resection (Blackmore
and Whelan, 1965) (Fig. 24-11).

Beattie, Oldhan, and Ross (1961) pre-
sented the case of a 25-year-old man with an
AVF of the superior thyroid vessels. Approxi-
mately 18 months earlier, he had a partial thy-
roidectomy for primary thyrotoxicosis. The
superior thyroid pedicles were each ligatured
with one ligature of no. 40 linen thread.
Approximately 5 months after his partial thy-
roidectomy, the patient noted swelling in his
neck and was aware of a "humming" in the
region of the swelling. After angiographic
demonstration of the superior thyroid AVF
between the superior thyroid artery and vein,

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

473

■ FIGURE 24-11

A, Antegrade aortogram showing larger anomalous artery to the left of the aorta communicating
with veins in the lower part of the abdomen. B, The specimen in situ showing the artery ending in a
cul-de-sac communicating with dilated veins. The Kutner dissector has been placed beneath the
arteriovenous fistula. The transverse colon and mesocolon lie inferior to the fistula. (From Blackwell
TL, Whelan TJ: Arteriovenous fistulas as a complication of gastrectomy. Am J Surg 1965;109:197-
200.) ■

excision of the remnant of the left lobe of the
thyroid gland was accomplished.

There have been unusual forms of AVFs
reported following essentially every type of sur-
gical operation and every type diagnostic or
therapeutic procedure: For example, an
AVF was reported following removal of an
intervertebral disk with injury to the iliac
artery and vein. Another such fistula oc-
curred following a percutaneous transaxillary
angiogram performed at Walter Reed General
Hospital. Lester (1966) described AVFs as a
complication of selective vertebral angi-
ography. One of these lesions has also been
treated at Walter Reed General Hospital.

White, Talbert, and Haller (1968) stated
that there was an increasing awareness of
peripheral arterial injuries in infants and chil-
dren. One of their patients, a 3-month-old
female, had a right femoral vein right heart

catheterization to investigate a small ventric-
ular septal defect and mild pulmonic steno-
sis. Over the following 3 years, she developed
borderline heart failure, with a pulse rate of
120 and an increase in her heart size. At the
age of 4.5 years, a thrill was noted over the
left groin, and the left leg was 2 cm longer than
the right. The proximal fibula was present on
the left and not on the right. A large AVF (Fig.
24-12) was demonstrated between the pro-
funda femoris artery and profunda femoris
vein. Arterial blood gases had been measured
and samples obtained from arterial punctures
of the right femoral artery. The needle must
have been inserted in a lateral and downward
direction, penetrating the femoral vein before
puncturing the femoral artery for the blood
samples. A direct AVF was created by the
needle. After ligation of this fistula and
without sacrifice of either the artery or the

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474

V • SPECIAL PROBLEMS AND COMPLICATIONS

■ FIGURE 24-12

Angiogram demonstrating an arteriovenous
communication between the right profunda
femoris artery and the deep femoral vein
following arterial puncture for blood gas
analysis. Over the subsequent 3 years, the
patient was in borderline heart failure, with an
increased heart rate and increased growth in
her lower extremity. (From White JJ, Talbert JL,
Haller JA Jr. Peripheral arterial injuries in infants
and children. Ann Surg 1968;167:757-766.) ■

vein, over the next several months, her pulse
rate gradually returned to normal and her
cardiac failure decreased.

Lord, Ehrenfeld, and Wylie (1968) pre-
sented the case of a profunda femoris AVF
caused by passage of a Fogarty arterial catheter.
At the time of their report, they stated that
there were two other similar incidences in the
literature. Subsequent reports include those
of Rob and Battle (1971) and Gaspard and
Caspar (1972).

AVFs occasionally occur with fractures
(additional details are given in Chapter 5) .
Harris (1963) reported an AVF following
closed fracture of the tibia and fibula in a 35-
year-old man (Fig. 24-13). Vascular injuries
have occurred with orthopedic procedures
rather than those involved in the management
of fractures. Ferguson (1914) presented an
infant who developed an AVF following an
osteotomy of the femur genu valgum.

■ FIGURE 24-13

A, Closed fracture of the tibia and fibula; the arteriogram shows an arteriovenous fistula of the
peroneal artery and the arterial phase of filling. B, The arteriogram shows the venous phase of filling
of the peroneal arteriovenous fistula. C, A postoperative arteriogram following excision of the fistula.
Note the rapid advance and union of the fracture of the tibia and fibula following excision of the
fistula. (From Harris JD: A case of arteriovenous fistula following closed fracture of tibia and fibula.
Br J Surg 1963;50:774-776.) ■

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

475

Anthopoulos, Johnson, and Spellman
(1965) reported on the unusual case of 23-
year-old woman who at age 9 years had sus-
tained a human bite at the base of the finger.
The authors believed that the AVF of the fifth
finger developed as a complication of the
human bite. There was spontaneous, periodic
subungual spurting of the arterial blood, as
well as increased growth, venous distention,
increased local temperature, and more rapid
growth of the nail. Surgical excision of
the aneurysmal sacs and ligation of visible
communications on two separate occasions
resulted in relief of symptoms and enabled
the patient to resume her occupation as a
typist.

Pathophysiology

As a student at the Johns Hopkins Medical
School in 1917, my curiosity about
arteriovenous fistulas was aroused and
repeatedly whetted by Doctor Halsted's
recurrent expressions of great puzzlement
at the occasional massive enlargement of
the heart to the point of cardiac failure and
at the marked dilatation of the proximal
artery that could accompany an
arteriovenous fistula, usually one long
duration. Equally puzzling was the fact that
this heart enlargement and arterial dilatation
occurred with some but not all fistulas.
Holman, 1971

There is a sense of anatomic and pathologic
changes that evolve when an AVF is produced
(Fig. 24-14). An AVF is an abnormal com-
munication between the arterial and venous
systems that creates a shorter circuit in rela-
tion to the heart by allowing blood to pass from
the higher peripheral resistance of the arter-
ial system to the lower peripheral resistance
of the venous system (Fig. 24-15). The sec-
ondary circuit, which has a constant tendency
to divert the arterial blood into the lower
resistance venous system through the fistula,
causes a number of hemodynamic distur-
bances. The effective systemic blood flow is
reduced, and there is a decreased mean sys-

■ FIGURE 24-14

This schema shows the circulation in the
presence of a right femoral arteriovenous fistula
establishing a second circuit of blood. A
progressively increasing volume of blood is
sequestered in circuit B as long as resistance
in the fistula circuit is less than resistance in the
capillary bed in circuit A. (From Holman E:
Arteriovenous aneurysms: Abnormal
communication between the arterial and
venous circulations. New York: Macmillan,
1937.) ■

temic arterial pressure. However, there is an
increase in the blood volume, total cardiac
output, stroke volume, heart rate, left arter-
ial pressure and pulmonary arterial pressure,
as has been described by Holman (1937,
1968). Holman also emphasized that the size
of the AVF, the location of the communica-
tion in the vascular tree and the distensibility
of the vascular rim are the factors that deter-
mine the volume of the blood that is diverted
through the AVF's border permits progressive
increase of the blood shunted through the
secondary circuit of the fistula, with additional

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V • SPECIAL PROBLEMS AND COMPLICATIONS

Artery

■ FIGURE 24-15

A, Immediately following the development of an
arteriovenous fistula, there is shunting of blood
from the artery through the fistula into the vein,
from which it returns to the heart. This results in
a decrease in peripheral vascular resistance, a
decrease in diastolic blood pressure, and an
increase in heart rate. The venous pressure
rises in the involved vein. Peripheral blood flow
is decreased in the involved artery. B, After
several weeks, collateral circulation enlarges
around the fistula because of the decreased
vascular resistance at the site of the fistula. As
the collateral circulation develops, the involved
artery and vein also dilate, increasing the
amount of blood flowing through the fistula.
C, After several years, extensive dilation may
develop about a fistula with marked
enlargement of collateral circulation. In
addition, there is enlargement of the artery
immediately distal to the fistula, through which
blood flows in a retrograde fashion through the
fistula toward the heart. The vein may enlarge
to marked proportions, creating varicosities in
the extremity. Ultimately such progressive
dilation after some years may result in
congestive heart failure from the increased
cardiac output. (From Spencer FC, Schwartz
SI: Principles of surgery. New York: McGraw-
Hill, 1974.) ■

increase in the blood volume and dilatation
of the heart. Lewis (1940) demonstrated that
the entire circuit gradually dilates to accom-
modate the increased volume of blood flow;
this includes dilatation of the cardiac cham-
bers, the arterial tree proximal to the fistula,
the proximal vein and vena cava and even the
AVF itself. Nakano and DeSchryver (1964)
studied the effects of AVFs on systematic and
pulmonary circulation and stated that the
increase in cardiac output was essentially a
result of the increase in stroke volume, noting
that the heart rate may change very little.

Holman (1965) reviewed abnormal arteri-
ovenous communications with particular ref-
erence to the delayed development of cardiac
failure. He emphasized that low resistance in
the venous system to the shunt of blood at the
site of the fistula and the decrease in periph-
eral perfusion distal to the AVF were strong
stimuli for the development of collateral
circulation. Holman (1940) documented
significant structural changes in both the
arteries and the veins associated with the
hemodynamic disturbances of an AVF. With
a small communication, the vein gradually
assumes the appearance of an artery, and it
may not be easily distinguished from the artery
at the end of 6 to 9 months. In contrast, with
larger fistulas, the vein may become so dis-
tended that it appears to be a false aneurys-
mal sac. As has been known since the first
description by Hunter in 1 757, the artery prox-
imal to the AVF can be dilated; however,
Holman (1940) stated that the dilatation of
the artery can also occur distal to the fistula.
It is not the initial injury that creates the AVF;
the arterial walls at the fistula or proximal to
it may become rigid as a result of deposition
of fibrous tissue, or the lumen may even
become stenotic by contraction of surround-
ing fibrous tissues.

AVFs may be associated with decreased
resistance in the peripheral arterial tree. The
consequent enlargement of superficial ven-
ous collaterals can be mistaken for changes
associated with chronic venous insufficiency.
One Vietnam casualty seen subsequently at
Walter Reed General Hospital had been
treated for varicose veins of his left lower
extremity for 5 years, when in actuality the
increase in his left thigh and associated

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

477

superficial varicosities were associated with an
acquired femoral AVE

According to Petrovsky and Milinov (1967) ,
the structural changes that occur in the walls
of both the arteries and the veins associated
with an AVF are called "venization" of ar-
teries and "arterialization" of veins. The
alterations in the venous walls are easier to
understand because they can be caused by an
abrupt increase in the venous pressure and
can be a consequence of adaptions. There is
more difficulty in understanding the changes
in Petrovsky and Milinov ( 1967) — performed
experiments, which showed thickening of the
media of the venous wall due to an increase
in the amount of muscular and connective
tissue elements, marked elastosis of all layers
of the vessel wall, intimal thickening, and an
increase in the vasa vasorum, which made it
resemble the wall of an artery. They saw an
increase in muscular fibers and fibrosis in the
arterial wall, with a corresponding increase
of mucopolysaccharides and extracellular
fibers, elastosis and later dystrophy of the
elastic fibers, focal necrosis of connective tissue
elements in the adventitia, and diminution of
the vasa vasorum. It was felt that a decrease
in the oxidative process accounted for the
accumulation of mucopolysaccharides, the
extracellular fibrosis, and the elastolysis
(decrease in oxidative process and tissue
hypoxia, which results from a decreased blood
supply in the arterial wall) .

Holman (1940) stated that hemodynamic
changes caused by AVFs were reversible.
However, some structural changes may notbe
reversible, such as dilatation of the proximal
artery associated with a long-standing AVF,
which may not regress if aneurysmal deterio-
ration of the wall has occurred. Also, cardiac
enlargement associated with long-standing
AVFs and dilatation may not revert to normal.

Eisenbrey (1913) emphasized the extensive
alterations in both the artery and the vein up
to the bifurcation of the aorta and vena cava
in a patient with a superficial femoral AVF (see
Fig. 24-2). The patient complained of short-
ness of breath and presented symptoms of
cardiac insufficiency. Eighteen years earlier,
the patient had been shot in the thigh with
a small-caliber (probably .22-caliber) rifle
bullet. Terminal illness allowed necropsy

examination of the aneurysmal dilatation and
tortuosity of the artery and vein.

Subsequent studies have augmented the
original and monumental contributions of
Holman. Schenk and colleagues (1957) eval-
uated the regional hemodynamics of experi-
mental acute AVFs. Their objective was to use
the newer electronic methods for pressure and
flow measurements to investigate the pressure-
flow changes that occurred immediately
upon opening an experimental fistula. Figure
24-16 summarizes the pressure-flow data in
a representative model.

Johnson, Peters, and Dart (1967) studied
the cardiac vein negative pressure in AVFs with
a plastic model. They demonstrated creation
of negative pressure in the cardiac vein, the
result of transformation of energy, and
explained this by the use of the principles of
flow through a conduit (Fig. 24-17).

Johnson and Blythe (1970) evaluated eight
patients with AVFs created for hemodialysis
over a period of 3 years. Their study demon-
strated that peripheral AVFs created for
hemodialysis in patients with chronic renal
failure result in a slight increase in cardiac
output and pulse rate and a decrease in the
total peripheral resistance. Although these
alterations in hemodynamics did not lead
to perceptible cardiac strain, a warning was

PRESSURE -MM.U 3

FLOW - CC/MIN.

PROXIMAL PROXIMAL
ARTERY VEIN

305 ,

ms/isl

/OS)/

\90/£0\
UTS) \

/ /

\ IT0\

DISTAL

01STAL

ARTERY

VEIN

ARTERY

VEIN

■ FIGURE 24-16

Schematic summary of pressure-flow data in a
representative animal after a large femoral
arteriovenous fistula was opened. (From
Schenk WG Jr, Bahn RA, Cordell A, Stephens
JG: Surg Gynecol Obstet 1957;105:733.) ■

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478

V • SPECIAL PROBLEMS AND COMPLICATIONS

CARDIAD
ARTERY

CARDIAD
VEIN

PERIPHERAL PERIPHERAL
ARTERY VEIN

m FIGURE 24-17

Flow pattern through fistula. In model, pressure
at 1 was -10 mm Hg, at 2 it was -5 mm Hg, and
at 3 it was -4 mm Hg, emphasizing the
negative pressure in the cardiac vein and
arteriovenous fistula. (From Johnson G Jr,
Peters RM, Dart CH Jr: A study of cardiac vein
negative pressure in arteriovenous fistula. Surg
Gynecol Obstet 1967;124:82-86.) ■

■ FIGURE 24-18

This small fragment wound of the upper right
thigh created an arteriovenous fistula that was
not diagnosed initially. The surrounding
increased density on the roentgenogram was
caused by an associated pulsating hematoma.
(From Rich NM: Vascular trauma in Vietnam.
J Cardiovasc Surg 1970;11:368-377.) ■

made that physicians managing these patients
should be cognizant of this possibility, espe-
cially in patients on long-term hemodialysis.

Clinical Pathology

The capillary circulation is bypassed in an AVF
when there is a direct communication between
an artery and a vein. Although this type of
communication can be a normal function of
the microcirculation, the AVF becomes patho-
logic when its size or location causes signifi-
cant hemodynamic alterations. An AVF may
be established immediately after a penetrat-
ing injury in which blood flows directly from
the injured artery into the vein. On the other
hand, thrombus may surround the AVF, and
the communication may not be obvious until
days or weeks later when the surrounding clot
becomes liquefied (Fig. 24-18).

Once atraumatic AVF has been established,
there is usually little difficulty in its recogni-
tion. The previous history of trauma, the
finding of a prominent pulsation and palpa-
ble thrill, and the presence of an audible

machinery-like murmur, or any combination
of these findings should alert one to the pres-
ence of an AVF. A bruit often appears over
the sight of arteriovenous communications
within a matter of hours after the establish-
ment of the lesion. Other signs and symptoms
that can develop distal to an AVF include inter-
mittent claudication, edema (Fig. 24-19), and
prominent veins (Fig. 24-20) , which are often
accompanied by bluish discoloration of the
skin and venous stasis. The last two findings
result from shunting of the arterial blood into
the venous system.

More than 200 years ago, in 1757 William
Hunter recognized an abnormal communi-
cation between an artery and a vein and accu-
rately described the thrill and bruit associated
with the communication. He noted that he
can eliminate both the thrill and the bruit by
pressure over either the proximal artery or
the site of the communication. He also doc-
umented his observation of tortuosity and dila-
tion of the artery proximal to the fistula.

Nicoladoniin 1875 is generally given credit
for being the first to demonstrate the remark-
able fact that the pulse rate could be lowered

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

479

■ FIGURE 24-19

Edema can be associated with arteriovenous fistulas. The massive swelling of the left lower
extremity in this Vietnam casualty is obvious. He had a femoral arteriovenous fistula of 5 years'
duration; however, he had been treated as a patient with varicose veins. (NMR Vietnam Vascular
Registry #630 1972.) ■

■ FIGURE 24-20

The position of an arteriovenous fistula and pulsating venous lakes
(circled); note the difference in size of the two lakes. The site of the
fistula is indicated by a cross. (From Holman EF: Arch Surg
1923;7:64-82.) ■

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480

V • SPECIAL PROBLEMS AND COMPLICATIONS

by compression of the artery proximal to the
AVE Fifteen years later, in 1890 Branham again
called attention to the reduction of the pulse
rate by obliteration of a large acquired AVE
This phenomenon is frequently referred to
as the "Branham-Nicoladoni sign."

oftheheartin the presence of an AVE In 1913,
Stewart noted that the heart diminished in
size within 10 days after elimination of the
fistula.

Clinical Features

The most mysterious phenomenon connected
with the case, one which I have not been
able to explain myself, or to obtain a
satisfactory reason for from others, was
slowing of the heart's beat, when
compression of the common femoral was
employed. This began to be noticeable after
the wound had entirely healed. The patient
was apparently well, with exception of the
injured vessel, which necessitated his
confinement to bed. This symptom became
more marked until pressure of the artery
above the wound caused the heart's beat to
fall from 80 to 35 to 40 per minute, and so
remain until the pressure was relieved.
Harris H. Branham, 1890

While working as a student of Halsted, Reid
(1920) established that there was enlargement

If the patient has had a penetrating injury,
the possibility of an AVF must be recognized;
however, this may not be immediately obvious.
As previously noted, if the arteriovenous com-
munication has surrounding thrombus, the
classic findings of the thrill and bruit may not
exist until several days or weeks later. There
may be little evidence of vascular trauma in
the way of blood loss or loss of peripheral
pulses (Fig. 24-21). The patient may or may
not be aware of a buzzing sensation when his
fingers are placed over the area of the arteri-
ovenous communication. One patient in the
registry had originally been wounded in
Korea; however, it was nearly 15 years later,
when he was piloting a helicopter in Vietnam,
that he noticed a buzzing sensation in his
popliteal fossa. It may be more unusual for
the patient to present with one of the com-
plications of AVF, such as infection within the

■ FIGURE 24-21

A small wound may deceive the casual observer as to the extent of underlying vascular pathology.
(NMR Vietnam Vascular Registry #2513 1971 .) ■

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

481

vascular system, peripheral embolization, or
congestive heart failure.

Errors in diagnosis can exist. Patients with
AVFs have been treated for years for varicose
veins (see Fig. 24-19). Venous hypertension
with resultant varices, peripheral pigmenta-
tion, and ulceration from venous insuffi-
ciency can confuse the diagnosis; however, the
classic findings of a thrill and bruit should be
carefully sought.

There may or may not be a soft diffuse mass
on physical examination. Depending on the
period of time that the AVF has existed, dilated
veins may surround the area. A thrill, with its
maximal component during systole, is usually
felt very easily on palpation. A "machinery
murmur" is usually heard easily on ausculta-
tion, the loudest part of the continuous
murmur occurring during systole. Detection
of this classic finding differentiates an
AVF from an arterial false aneurysm. The
Nicoladoni-Branham sign, which has been
previously described, is another significant
finding if a slowing pulse can be demonstrated
when the fistula is obliterated by digital com-
pression. Ironically, this test was not positive
in many of the Vietnam casualties with AVFs.
The peripheral resistance increases when the
fistula is digitally occluded, causing the blood
pressure to rise, with reflex slowing of the heart
rate and consequent slowing of the pulse. The
temporary bradycardia results from a neuro-
genic reflex mediated through pressure-
sensitive receptors in the carotid sinuses and
great vessels.

With large AVFs and large shunting of
blood, cardiac enlargement and, more rarely,
cardiac failure may occur (Fig. 24-22) . Smith
(1963) found the most serious complication
of AVF, left ventricular myocardial failure, in
two of their patients. One of these was a 16-
year-old male who had been shot in the right
thigh with a .22-caliber rifle bullet. Nine days
after the accident, the patient developed a
gallop rhythm and severe dyspnea. A chest
roentgenogram revealed a marked enlarge-
ment of the cardiac shadow. An emergency
operation was performed to correct a
common femoral arteriovenous communica-
tion. The signs of congestive cardiac failure
regressed in 3 weeks. The authors pointed out
that there was a regrettable error of omission

in the immediate exploration of the wound.
They felt that the rapid development of
cardiac decompensation, which made surgi-
cal intervention most urgent, was an unusual
aspect of the case.

Diagnostic Considerations

The history of a penetrating injury and the
classic physical findings usually establish
the diagnosis of an AVF. Establishment of the
diagnosis may be more difficult if the lesion
is within the thoracic or abdominal cavity.
Angiography readily demonstrates the rapid
filling of an adjacent vein and increased col-
lateral circulation (Fig. 24-23) . Angiographic
demonstration of most arteriovenous lesions
is usually not necessary from the diagnostic
standpoint, but it may be helpful in planning
the surgical correction. This is particularly true
if multiple arteriovenous communications
exist, or if one or more false aneurysms are
associated with the arteriovenous communi-
cation (Fig. 24-24) . Bell and Cockshott (1965)
demonstrated the angiographic features
found in patients with both acute and chronic
AVFs.

Cardiac enlargement may be noted on
roentgenogram of the chest. Shumacker and
Stahl (1949) evaluated the cardiac frontal area
in patients with AVFs to determine the heart
size before and after operative obliteration of
the fistula in a large group of patients. They
studied 185 soldiers with traumatic peripheral
AVFs of relatively short duration. Cardiac
enlargement was noted in a large number
before operative excision of the fistula, and
the reduction in the heart size occurred in a
comparable number after operation. These
authors believe that the location of the fistula,
the size of the artery involved, the size and
age of the fistula, and the magnitude of
the pulse and blood pressure response to
temporary occlusion of the fistula could be
correlated with the tendency toward early
development of cardiac enlargement. These
studies showed conclusively that demon-
strable evidence of cardiac enlargement was
present in approximately 50% of young sub-
jects with peripheral AVFs of relatively short
duration; however, few had symptoms of

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482

V • SPECIAL PROBLEMS AND COMPLICATIONS

■ FIGURE 24-22

A, Cardiac enlargement may occur with large arteriovenous fistulas and occasionally progress to
cardiac fistulas and occasionally progress to cardiac failure. B, This patient had an arteriovenous
fistula 1 .0 x 1.5cm between the right common iliac artery and the left common iliac vein following
disk surgery. C, The heart returned to normal size limits after closure of the fistula by lateral suture of
the vein and resection of a small segment of artery followed by end-to-end anastomosis. (From
Jarstfer BS, Rich NM: The challenge of arteriovenous fistula formation following disk surgery: A
collective review. J Trauma 1976;16:726-733.) ■

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

483

■ FIGURE 24-23

A, Angiography is helpful in identifying the site of communication in an arteriovenous fistula. Left,
Contrast media descends in the artery to the fistula. Right, The dilated veins are then rapidly
visualized by passage of contrast media through the fistula. B, From left to right, the distal
superficial femoral artery is visualized angiographically with rapid filling of the adjacent vein.
(A, From NMR, Vietnam Vascular Registry #7182; B, from Vietnam Vascular Registry #2760, Walter
Reed General Hospital.) ■

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484

V • SPECIAL PROBLEMS AND COMPLICATIONS

■ FIGURE 24-24

Multiple false aneurysms and arteriovenous
fistulas were demonstrated angiographically in
this Vietnam casualty. The extent of pathologic
involvement of the posterior tibial and peroneal
vessels could not be determined clinically.
(From Vietnam Vascular Registry #2761, Walter
Reed General Hospital.) ■

cardiac strain, and there was essentially no
evidence of cardiac failure. This fact was
confirmed by a measurable reduction in car-
diac size after operation in a comparable per-
centage. Cardiac failure has been reported in
a series of 14 patients (Pate and colleagues,
1965).

Surgical Treatment

A literature review and a successful personal
repair of an AVFs prompted Stewart (1913)
to write, "With angiorrhaphy the aneurysm
can be dealt with radically and the vessels
conservatively, thus effecting cure without
interrupting the bloodstream and without pro-
ducing gangrene."

Despite his interest in repair of AVFs, he
noted that suture of vessels was not always pos-

sible. He cited that in a number of instances,
the surgeon had planned to repair the vessel
but was forced to abandon the idea because
of hemorrhage (Delanglade), friability of
the artery, (Thompson) , the large size of
the opening (Mignon), dense adhesions
(Cranwell), or obliteration of the sutured
vessel (Cestan).

Shumacker (1948) stated, "It has long been
recognized that the ideal method of treating
aneurysms and arteriovenous fistula involving
important arteries is the extirpation of the
lesion combined with some procedure which
permits maintenance or re-establishment of
the continuity of the affected artery."

The best time for surgical cure of a trau-
matic AVF is immediately after the establish-
ment of the communication.

There has been a period of profound
changes in the surgical management of AVFs.
Surgeons' energies were formally directed
toward the selection of a time when maximal
collateral circulation would have developed.
If the intervention was properly timed and
if the collateral circulation was adequate,
ligation of the four component vascular
trunks without excision of the fistula cured
the lesion, the extremity remaining viable
despite the fact that there might be some arte-
rial and venous insufficiency. The important
change, which was strongly influenced by the
experience at Walter Reed General Hospital
in managing Korean battle casualties, con-
centrated on dissection of the proximal and
distal communicating artery and vein with
repair of defects in both vessels (Seeley and
colleagues, 1952).

The initial treatment of AVFs included a
delay of 2 to 6 months to allow collateral cir-
culation to develop. It was anticipated that this
would improve extremity survival after liga-
tion of the involved artery. However, it should
be emphasized that some of the earliest
vascular repairs, including venorrhaphy and
arteriorrhaphy, of this century involved AVFs.
At present, division of the fistula with venous,
as well as arterial, repair is preferred. Exci-
sion with multiple ligations is accepted for
smaller vessels not essential to normal circu-
lation, such as one of the tibial arteries or veins.
There is currently an interest in treating AVFs
when they are initially diagnosed. If the lesion

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

485

■ FIGURE 24-25

Proximal and distal control of both the artery and the vein is important in the successful
management of arteriovenous fistulas. It was possible to repair the popliteal vein by lateral suture
and the popliteal artery by an end-to-end anastomosis to correct the arteriovenous fistula. (From
Rich NM: In: Beebe HG, ed. Complications in vascular surgery. Philadelphia: JB Lippincott,
1973.) ■

is discovered on the third or fourth day after
an injury, it is usually better to wait until 3
weeks have passed to allow soft tissue healing
to occur and edema to subside.

Elective incisions should be used, as was
emphasized for arterial repair and for venous
repair. Adequate exposure of the artery and
vein proximal and distal to the fistula should
be accomplished before the fistula is directly
approached (Fig. 24-25). When these vessels
are isolated and temporarily occluded, the
arteriovenous communication can be incised
and directly isolated (Fig. 24-26). There
usually is a small lesion between the artery
and the vein, and the size of the surrounding
false sac may vary greatly. Nevertheless, a small
segment of the artery is usually involved, the
remainder of the artery being freed from the
false sac during mobilization to perform the
arterial repair. Lateral venorrhaphy is usually
possible. Only in large arteries is arterior-
rhaphy by lateral suture possible. Frequently,
minimal excision of the damaged artery and

■ FIGURE 24-26

Proximal and distal control of both artery and
vein has been obtained with silk suture loops in
place. Multiple ligatures with excision of the
arteriovenous fistula and false aneurysm were
elected for this distal posterior tibial lesion.
(From NMR, Vietnam Vascular Registry #1806,
1969.) ■

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486

V • SPECIAL PROBLEMS AND COMPLICATIONS

end-to-end anastomosis are possible. Other-
wise, segmental replacement with autogenous
greater saphenous vein is preferred.

Intra-arterial balloon catheter control of
hemorrhage and many other useful tech-
niques used in arterial repair are covered in
more detail in Chapter 19 and in the discus-
sions of specific arteries. LeVeen and Cerruti
(1963) described a method for intra-arterial
balloon tamponade of blood vessels in the
surgical management of AVFs (Fig. 24-27).
Noon (1969) emphasized the use of balloon
catheters to provide temporary arterial occlu-
sions for control of hemorrhage. The use of

multiple balloon catheters to control intra-
arterial hemorrhage and venous bleeding
has been successful in the management of
Vietnam casualties with AVFs at Walter Reed
Army Medical Center (Fig. 24-28).

Spontaneous Cure

Shumacker and Wayson (1950) evaluated
spontaneous cure of aneurysms and AVFs.
They studied 122 aneurysms and 245 AVFs.
Thrombosis appeared to be responsible for
the obliteration of the lesions. Fibrosis can also

MEf tiger ft 4, TcrtHou*
JMt*rr>4.'

/*46&mtk/jfo&ktJtm

n j-f v t4

■ FIGURE 24-27

A Woodruff catheter was inserted through the open brachial artery and the balloon inflated at the
region of the arteriovenous fistula. A, Dilated vessels anterior to the fistula. This was a method for
intra-arterial balloon tamponade of blood vessels in the surgical management of arteriovenous
fistulas. (From LeVeen HH, Cerruti MM: Surgery of large inaccessible arteriovenous fistulas. Ann
Surg 1963;158:285-289.) ■

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

487

■ FIGURE 24-28

Intraoperative photograph
showing a Fogarty balloon
catheter in the distal internal
carotid artery for intraluminal
arterial control of hemorrhage
(small arrow) and a Foley
balloon catheter inserted into
the adjacent internal jugular
vein for temporary control of
venous hemorrhage during
repair of a distal
carotid-internal jugular
arteriovenous fistula. (From
NMR, Walter Reed General
Hospital, 1972.) ■

occur as a more gradual process. Because there
are only five spontaneous cures, only 2% of
the 245 AVFs (four of five arteriovenous lesions
that healed spontaneously did so suddenly and
within three months of the original injury),
the authors stated, "Satisfactory spontaneous
cures occurred in our series so infrequently
as to make consideration of this possibility of
little or no importance in reaching a decision
as to the necessity for or the proper time for
surgical treatment of the lesion."

Spontaneous closure of the AVFs has been
a relatively unusual event. Billings, Nasca, and
Griffin (1973) reported one such instance in

a 19-year-old Marine who had sustained
multiple fragment wounds from a land mine
explosion in August 19 70 while on duty in the
Republic of Vietnam. In September, a 3-cm
pulsating mass was noted in the right axilla,
and there was continuous bruit and thrill over
the mass. An axillary AVF was demonstrated
by angiography (Fig. 24-29). Treatment of
other multiple wounds was carried out,
and during the first week in November, the
axillary mass was no longer palpable. A second
arteriogram demonstrated that there had
been spontaneous closure of the AVF
(Fig. 24-30) . Two similar patients — Vietnam

■ FIGURE 24-29

Subtraction print demonstrating the early arterial phase of an arteriogram performed via subclavian
injection. The right axillary artery (-t+») communicates with the axillary vein (— >) through a large
arteriovenous fistula (+-»). (From Billings KJ, Nasca RJ, Griffin HA: Traumatic arteriovenous fistula
with spontaneous closure. J Trauma 1973;13:741-743.) ■

ch24.qxd 4/16/04 3:26 PH Page 488

488

V • SPECIAL PROBLEMS AND COMPLICATIONS

■ FIGURE 24-30

A second arteriogram performed 6 weeks later, demonstrating that the arteriovenous
communication in the axillary vessels (see Fig. 24-29) is no longer present. Elective operative
closure had not been performed because of a wound infection. The site of "thrombosis" is visible as
a small, contrast-filled saccule on the inferior surface of the axillary artery. (From Billings KJ, Nasca
RJ, Griffin HA: Traumatic arteriovenous fistula with spontaneous closure. J Trauma 1973;13:74-1-
743.) ■

casualties — were seen at Walter Reed General
Hospital.

Results

Annandale (1875) reported the successful lig-
ature of a popliteal artery and vein in the
treatment of a traumatic popliteal AVE Pick
(1883) reported the case of a 28-year-old man
who sustained a gunshot wound of the thigh
with a resultant AVF of the femoral vessels.
He stated that the only operative procedure
that appeared to hold any hope for success
was ligature of the artery above and below
the point of communication. According to
Murphy (1897), Von Zoege-Manteuffel suc-
cessfully repaired a femoral arteriovenous
aneurysm by lateral suture of the wall in 1895.
When the first end-to-end arterial anastomo-
sis in a human was reported by Murphy (1897) ,
he described his successful treatment in 1896
of a common femoral AVF. In addition to the
end-to-end arterial anastomosis following
resection of the damaged portion of the artery,
he closed the wound in the vein by lateral
venorrhaphy. Bickham (1904) suggested
that Matas endoaneurysmorrhaphy could be
employed for the intravascular repair of AVFs.
He also recommended transverse closure of
the defects in the vascular walls as a practical

method of preserving the continuity of both
the injured artery and the injured vein. Matas
emphasized the reason for failure when partial
ligation was used in the treatment of AVFs was
the remaining patency in other vessels not
ligated (Fig. 24-31).

Soubbotitch (1913) reported on the mili-
tary experience in the Serbo-Turkish and
Serbo-Bulgarian Wars. There were 16 differ-
ent surgeons who performed ligation of large
vessels on 41 arteries and 4 veins and partial
suture on 17 vessels — 8 arteries and 9 veins.
Circular suture was employed on 15 vessels —
11 arteries and 4 veins — to bring the total
number of vessels sutured to 32 (19 arterior-
rhaphies and 13 venorrhaphies). The 60
arteries and 17veinsmadeofatotal 77 injuries
to the larger blood vessels among 20,000
wounded. Osier (1915) stated that there was
agreement with a conclusion arrived at by
Soubbotitch, senior surgeon at the Belgrade
State Hospital, from his experience in the
Balkan War, "that arteriovenous aneurysms
should be operated upon, as they offer small
prospect of spontaneous cure, although they
often remain stationary for a long time and
cause relatively little trouble."

World War I contributed little significant
data compared to World War II. Because
competent vascular surgeons had chosen to
head three centers for vascular surgery during

ch24.qxd 4/16/04 3:26 PH Page 489

24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS 489
AKTERX

ART&RY

E-PF-BRWt
Y&IH

EPPfcMST ARTERY

A.WERBNT VEIN

V£IH

■ FIGURE 24-31

Schematic drawing showing the communications of an arteriovenous fistula and the necessity of not
only quadruple ligation but also complete excision including all branches. (From Matas R: Military
surgery of the vascular system. In: Keene's surgery, vol. 7. Philadelphia: WB Saunders, 1921.) ■

World War II, a large number of AVFs and
arterial aneurysms were managed. Elkin and
Shumacker (1955) outlined the techniques
of operative treatment of 585 AVFs (Table
24-15). Arterial repair was used in only 34
lesions.

The representative material that follows
covers a small portion of the World War II
experience. Freeman and Shumacker (1955)
outlined various approaches in the manage-
ment of AVFs. Figure 24-32 shows one of the
approaches, which involved the following:

5pltt ii»rnum'

Innominal^ v

ouoclavian vaii-i

■ FIGURE 24-32

Transvenous repair of an arteriovenous fistula involving the left subclavian artery and innominate
vein. Insert shows the surgical approach to the lesion that was used to manage a World War II
combat casualty at DeWitt General Hospital in 1945. (From Freeman NE, Shumacker HB Jr,
DeBakey ME: Vascular surgery. Washington, DC: US Government Printing Office, 1955.) ■

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490

V • SPECIAL PROBLEMS AND COMPLICATIONS

TABLE 24-15

TECHNIQUES OF OPERATIVE TREATMENT IN 585 ARTERIOVENOUS FISTULAS:
WORLD WAR II EXPERIENCE

Quadruple

Ligation Alone (Mass

Arterial

Ligation and

Proximal, Distal, or

Total

Location

Repair

Excision

Proximal and

Distal)

Cases

Upper extremity

Axillary

—

Brachial

—

29*

Cervical, transverse

—

Humeral, posterior

—

circumflex

Interosseous,

—

common

Radial

—

Scapular, transverse

—

Subclavian

18*

Ulnar

—

Lower extremity

—

Calf, to muscles of

—

Circumflex, lateral

—

Femoral

124

141 s

Geniculate

—

Gluteal, inferior

—

Gluteal, superior

—

Peroneal

—

Plantar

—

Popliteal

—

102

Profunda femoris

—

Profunda branch

—

Tibial

—

Head and neck

Carotid

48*

Cirsoid

—

Lingual

—

Occipital

—

Temporal,

—

superficial

Vertebral

—

Trunk

Aorta-vena cava

—

Hypogastric

—

Iliac

—

Innominate

—

Mammary, internal

—

Obturator-iliac vein

—

Subscapular

—

Thoracoacromial

—

Total

526

585

*This total does not include two fistulas: one in which the method of management was not stated and one in which spontaneous

cure occurred.

*This total does not include one fistula in which the method of management was not stated.

*This total does not include one fistula in which spontaneous cure occurred.

5 This total does not include three fistulas: one in which methods of management were not stated and two in which spontaneous

cure occurred.

From Elkin DC, Shumacker HB Jr: In: Vascular Surgery in World War II. Elkin DC, DeBakey ME, eds. Washington, DC:

Government Printing Office, 1955.

ch24.qxd 4/16/04 3:26 PH Page 491

24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

491

1. Mass ligation of the fistula

2. Quadruple ligation and division of the
main vessels with excision of the fistula

3. Transvenous closure of the arterial opening

4. Repair of the opening in both the artery
and vein

Shumacker (1948) stressed the importance
of maintaining arterial continuity in the
repair of aneurysms and AVFs. In his early
experience, he performed only four repara-
tive procedures, with 2.9% of 138 cases in-
volving the innominate, common carotid,
extracranial internal carotid, subclavian, axil-

lary, brachial, iliac, common femoral, femoral,
and popliteal arteries. In later experience, he
repaired 52.6% of the arteries: 30 of 57 cases.
This included lateral arteriorrhaphy, end-to-
end anastomosis, and vein graft repair (Table
24-16) . The types of autogenous interposition
venous grafts used range from the saphenous
to a branch of the femoral. Figures 24-33 and
24-34 reveal patency of the venous grafts and
no dilatation of the grafts in the early follow-
up period of 7 to 10 weeks.

Shumacker (1948) also used oscillometry
to evaluate the patency of arterial repair (Table
24-17). The results of oscillometry were
good in those cases in which arterial repairs

■ FIGURE 24-33

This arteriogram taken 10 weeks after repair of
a fistula between the femoral and profunda
femoral arteries and the femoral vein, with
resection and end-to-end anastomosis of the
profunda femoral artery proximally to the
superficial femoral artery distally, shows no
narrowing at the suture line after 70% Diodrast
was injected into the common femoral artery.
(From Shumacker HB Jr: Problems of
maintaining continuity of artery in surgery of
aneurysms and arteriovenous fistulae; notes on
development and clinical application of
methods of arterial suture. Ann Surg
1948;127:207-230.) ■

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492

V • SPECIAL PROBLEMS AND COMPLICATIONS

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

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ch24.qxd 4/16/04 3:26 PM Page 494

494

V • SPECIAL PROBLEMS AND COMPLICATIONS

■ FIGURE 24-34

Left, Arteriogram, taken 7 weeks after repair of
an arteriovenous fistula between the superficial
femoral artery and vein, with interposition of a
segment of a large branch of the femoral vein
2cm in length, reveals that the venous insert
and the artery have relative diameters about
equal to those observed at completion of the
operation (case 2). Right, Arteriogram showing
no dilatation of the venous segment of a 2-cm
piece of saphenous vein used to reconstruct
the superficial femoral vessels (case 1). There
was no dilatation at the completion of the
anastomosis, and no dilatation was seen on
this arteriogram performed 10 weeks later.
(From Shumacker HB Jr: Problems of
maintaining continuity of artery in surgery of
aneurysms and arteriovenous fistulae; notes
on development and clinical application of
methods of arterial suture. Ann Surg
1948;127:207-230.) ■

remained patent and poor in those in which
arterial repair failed due to thrombosis.

Hughes and Jahnke (1958) performed
end-to-end anastomosis in the majority of AVFs
(61/134) from the Korean Conflict (Table
24-18). As a result of the Korean Conflict,
more than 200 patients with false aneurysms
and AVFs, 133 of the injuries involving major
vessels, were seen atWalter Reed General Hos-
pital. The lesions were excised, with repara-
tive or reconstructive surgery of the major
vessel, without loss of a single limb. Treatment

of minor vessel lesions has previously been
outlined in Table 24-8. Repair of major veins
was performed whenever possible to prevent
venous insufficiency. This venous repair was
possible in about 30% of major veins involved
in fistula formation. Cardiac dilatation was
common with large fistulas; however, only two
patients showed cardiac failure.

Rich, Hobson, and Collins (1975) reported
the experience from Vietnam. Of 558 lesions
identified in 509 patients, there was almost
an equal number of AVFs (262 AVFs) and false
aneurysms (296 false aneurysms). As might
be anticipated by the number of American
troops committed to Southeast Asia in that
year, the largest number of lesions resulted
from wounds in 1968 (Table 24-19). There
was also a relatively large number of similar
wounds in 1967 and 1969. The time from
injury to recognition of the lesion was arbi-
trarily divided into four categories: immedi-
ate, early, delayed, and remote. The largest
number of lesions was recognized in the early
period of 1 to 30 days: 273, or 48.9% (Table
24-20). Nearly an equal number was diag-
nosed in the delayed period between 1 and 6
months. In the remote group, all but 7 of the
35 patients had recognition and treatment of
their lesions in less than 2 years. Only two had
recognition and treatment of their lesions
after more than 5 years following the initial
injury, and both were treated in less than 6
years. Nearly an equal number of lesions were
treated in the intermediate hospitals in Japan
and similar Far West locations as were treated
in the continental United States (Table
24-21). Several hundred surgeons were
involved in these repairs. Approximately one
fifth of these operations were performed at
Walter Reed Army Medical Center.

Table 24-22 outlines the method of treat-
ment used for the various arterial and venous
injuries. Arterial ligation was used in 290
lesions, or 52.0%. Compelling problems often
caused this method to be used over the favored
and desired arterial repair. Infection, associ-
ated injuries, poor general condition of the
patient, and involvement of smaller caliber
arteries were considered. The overall mortality
rate for the 509 patients was 1.8%, or 7 deaths
(Table 24-23) . Even considering this low mor-
tality rate, only two deaths could be directly

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

495

TABLE 24-18

TOTAL OPERATIONS FOR MAJOR VESSEL LESIONS: MILITARY SERIES FROM
KOREAN CONFLICT

Ligation

and

Vein

Artery

Lateral

Division of

Spontaneous

Vessel

Excision

Anastomosis

Graft

Repair

Fistula

Closure

Total

HHHH

Common

carotid

nternal

—

carotid

Subclavian

—

Axillary

—

Brachial

—

Iliac

—

Common

—

femoral

Superficial

—

femoral

Popliteal

—

Total

134

From Hughes CW, Jahnke EJ Jr: The surgery of traumatic arteriovenous fistulas and aneurysms: A five-year followup study of
215 lesions. Ann Surg 1958;148:790-797.

TABLE 24-19

ARTERIOVENOUS FISTULAS AND
FALSE ANEURYSMS BY YEAR:
VIETNAM VASCULAR REGISTRY

Year

1963
1964
1965
1966
1967
1968
1969
1970
1971
1972
Total

No.

116

249

124

558

0.2

0.0

2.0

7.9

20.8

44.6

22.2

0.9

1.2

0.2

100.0

From Rich NM, Hobson RW II, Collins GJ Jr: Traumatic
arteriovenous fistulas and false aneurysms: A review of
558 lesions. Surgery 1975;78:817-828.

attributed to the vascular problem. The mor-
bidity rate of 6.8% included 35 complications:
hemorrhage in 14, thrombosis in 12, stenosis
in 2, and persistent, immediately adjacent, or
recurrent AVFs requiring additional opera-
tions in 7.

TABLE 24-20

ARTERIOVENOUS FISTULAS AND
FALSE ANEURYSMS, BY TIME OF
DIAGNOSIS: VIETNAM VASCULAR
REGISTRY

Time

Immediate (24hr)
Early (1-30 days)
Delayed (1-6 mo)
Remote (>6mo)
Total

No.

22
273
228

558

3.9
48.9
40.9

6.3
100.0

From Rich NM, Hobson RW II, Collins GJ Jr: Traumatic
arteriovenous fistulas and false aneurysms: A review of
558 lesions. Surgery 1975;78:817-828.

Experience in the civilian hospitals is
increasing. Hershey (1961) encountered a
technical complication. The artery proximal
to the AVF had dilated and become fragile; it
was crushed by clamp, and a hematoma devel-
oped (Fig. 24-35).

Beall (1968) repaired 8 of 50 AVFs within
24 hours of injury; an additional 17 were
repaired within 24 hours to 3 months follow-
ing injury. However, there was a delayed repair

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496

V • SPECIAL PROBLEMS AND COMPLICATIONS

TABLE 24-21

ARTERIOVENOUS FISTULAS AND
FALSE ANEURYSMS, BY HOSPITAL
LOCATION FOR REPAIR: VIETNAM
VASCULAR REGISTRY

Location

No.

of Repairs

Vietnam

10.2

Japan, etc.

238

42.7

CONUS

251

45.0

No repair

2.1

Total

558

100.0

From Rich NM, Hobson RW II, Collins GJ Jr: Traumatic
arteriovenous fistulas and false aneurysms: a review of
558 lesions. Surgery 1975;78:817-828.

TABLE 24-23

ARTERIOVENOUS FISTULAS AND
ANEURYSMS, MORTALITY AND
MORBIDITY RATES: VIETNAM
VASCULAR REGISTRY

No.

Deaths

Morbidity
Amputations
Complications

1.8

1.7

6.3

From Rich NM, Hobson RW II, Collins GJ Jr: Traumatic
arteriovenous fistulas and false aneurysms: a review of
558 lesions. Surgery 1975;78:817-828.

TABLE 24-22

ARTERIOVENOUS FISTULAS AND
FALSE ANEURYSMS, BY METHOD OF
MANAGEMENT: VIETNAM VASCULAR
REGISTRY

Type

No.

Arterial

Ligation

290

52.0

End-to-end anastomosis

143

25.6

Vein graft

10.2

Lateral suture

7.2

Prosthesis

0.3

Miscellaneous

4.7

Total

558

100.0

Venous

Ligation

138

52.7

Suture

30.1

Miscellaneous

17.2

Total

262

100.0

From Rich NM, Hobson RW II, Collins GJ Jr: Traumatic
arteriovenous fistulas and false aneurysms: a review of
558 lesions. Surgery 1975;78:817-828.

of more than 3 months following injury for
23, or nearly 50%, of these lesions. No repair
was performed for two of the AVFs. Excision
and repair was used for 27 lesions and liga-
tion and excision for 17 lesions. No deaths
were reported. There were no amputations
required. Not counting two patients lost in
follow-up who had no treatment, 42 were

asymptomatic. Six patients were sympto-
matic after their original definitive surgical
procedure, and three required subsequent
operations.

In the civilian series of 61 arterial injuries
reported by Smith, Foran, and Caspar (1963),
approximately two thirds of the 33 chronic or
late lesions were AVFs. They mentioned
that the time interval from original injury to
treatment varied considerably from a few days
to 29 years, with most patients, 57%, being
treated after 1 year. Of the six patients with
AVFs reported by Patman, Poulos, and Shires
(1964), five did not have initial explorations
of the area. The remaining patient did have
initial exploration; however, the AVFs were
not diagnosed until 4 hours after injury. The
authors stressed that this development demon-
strated the rapidity with which an AVF can
develop. The common and superficial femoral
arteries were involved in AVFs. The remain-
ing four fistulas were equally divided among
the smaller radial and posterior tibial arter-
ies. There were no deaths, amputations, or
other significant complications in any of the
patients.

Dillard, Nelson, and Norman (1968)
reported a number of AVFs including (1) a
29-year-old female who was stabbed in the right
flank and 3 years later was found to have severe
hypertension; after correction of the renal
AVF, the patient's blood pressure returned to
normal; (2) a patient with severe leg ulcers
that healed only after correction of an AVF in

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

497

3cm

■ FIGURE 24-35

A, Artist's sketch of a superficial femoral arteriovenous fistula. B, End-to-end anastomosis after
excision of the fistula. An intraluminal hematoma developed at the site of a Blalock clamp. C, Sketch
of the vein graft after excision of the hematoma, showing size discrepancies. D, Postoperative
arteriogram showing (arrows,) the site of anastomosis. (From Hershey FB: Secondary repair of
arterial injuries. Am Surg 1961 ;27:33-41 .) ■

the same extremity between the common
femoral artery and vein; and (3) a patient with
an AVF between the popliteal artery and vein,
which resulted in amputation. Two of the
nine AVFs reported by Dillard, Nelson, and
Norman (1968) involved high-output failure.
One of these fistulas occurred between the
subcapsular artery and the axillary vein, and
the other between the right iliac artery and
the left common iliac vein.

Sako and Varco (1970) reported corrective
procedures in 25 patients with acquired AVFs.
Excisions of the fistula with arterial and
venous repair were performed in more than
50%, or 16 lesions. Quadruple ligation was
used in six and multiple ligation in two, and
included in the arterial repairs were 13
primary anastomoses, 3 autologous venous
grafts, and 1 homograft. All of the acquired
fistulas were cured by the surgical procedures
described without a death.

Gaspard and Caspar (1972) reported two
patients who developed AVF after Fogarty
catheter thrombectomy in the lower extrem-
ity. They emphasized that neither of their
patients required immediate operation for
limb salvage or had an operation performed
subsequently. They cited the report by Rob

and Battle (1971) in which correction of the
AVF 26 days after the use of the Fogarty
catheter was mandatory because the distal
extremity was in jeopardy.

Hewitt, Smith, and Drapanas (1973) advo-
cated immediate repair of acute AVFs. This
was possible in 13 of the 14 patients in their
series, and they reported satisfactory results
in all repairs, including resection with end-
to-end anastomosis in 6, saphenous vein graft
in 2, saphenous vein patch graft in 2, and
lateral suture repair in 3, with ligation being
required only for one distal internal carotid
artery.

In addition to the anticipated complications
of cardiac enlargement, cardiac failure, endo-
carditis, and proximal arterial aneurysm
formation, unusual complications have been
reported. Rhodes, Cox, and Silver (1973)
reported a case of a 53-year-old male with a
10-day history of bruising easily, hematoma,
and bleeding from his tongue. The patient
was involved in a shooting accident 17 years
previously and had acquired an AVF between
the left subclavian artery and vein as a result.
The authors attributed the local sustained
intravascular coagulation that caused a man's
symptoms to turbulence from the fistula and

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498

V • SPECIAL PROBLEMS AND COMPLICATIONS

■ FIGURE 24-36

A, Arteriography after excision and anastomosis of the superficial femoral artery shows an excellent
lumen. A vein graft inserted into the popliteal artery is demonstrated by angiography approximately
6 months after operation. B, Examination of this patient 5.5 years after operation showed the vein
graft to be functioning perfectly without clinical evidence of dilatation. C, Arteriography was used to
demonstrated an arterial homograft that replaced the common femoral artery. These angiograms
were part of the follow-up of Korean casualties who had repair of arteriovenous fistulas. (From
Hughes CW, Jahnke EJ Jr: The surgery of traumatic arteriovenous fistulas and aneurysms: A five-
year follow up study of 215 lesions. Ann Surg 1958;148:790-797.) ■

stasis from the aneurysm. The coagulopathy
and bleeding responded to surgical elimina-
tion of the fistula and aneurysm. The authors
felt that this was the first report of a con-
sumption coagulopathy resulting from an AVF
and false aneurysm.

Follow-up

Hughes and Jahnke (1958) included a 5-year
follow-up of 148 lesions treated during the
Korean Conflict, with satisfactory results
being obtained in most of the patients
(Fig. 24-36).

The Vietnam Vascular Registry continues
to follow patients included in the report by
Rich (1975). More than one fourth — 149
patients or 29.3% — have been evaluated in the
vascular clinic at Walter Reed Medical Center.
Many of these patients can be expected to live
50 years or more (Fig. 24-37).

SakoandVarco (1970) reported long-term
follow-up of 14 of 25 patients with acquired
AVFs who were cured of their lesions for 5 to
16 years. Seven additional patients were fol-
lowed for more than 2 years and were all cured.
One patient in this group had a portion of
the anterior tibial artery repaired after exci-
sion of the fistula, but the artery was occluded
within the first year. Two were lost to follow-
up after the first year, and one had quadru-
ple ligation of the subclavian AVF. When last
seen, he had symptoms indicating some
ischemia of the arm. The other patient lost
to follow-up had quadruple ligation of the
gluteal AVF. The remaining two patients
who had an aneurysmal dilatation in the prox-
imal artery excised and replaced with pros-
thetic graft were well 8 and 1 1 years after the
operation (Fig. 24-38) . The other two patients
with aneurysmal dilatation of the artery
proximal to the fistula had not yet had these
corrected.

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

499

■ FIGURE 24-37

This angiogram corroborated the clinical
impression of a left femoral arteriovenous fistula.
Additional assistance, however, was provided to
establish that the communication involved a
muscular branch of the superficial femoral artery
and the superficial femoral vein. Note the
development collaterals. Also note the proximal
arterial dilatation of the superficial femoral artery
in this former soldier who had been wounded 5
years before this study. (From Rich NM: In:
Beebe HG, ed. Complications in vascular
surgery. Philadelphia: JB Lippincott, 1973.) ■

■ FIGURE 24-38

In this operative photograph, aneurysmal dilatation of the superficial femoral artery (A), the
narrowed segment (B) where the artery traversed Hunter's canal, and a popliteal aneurysm (C) are
demonstrated. This patient had closure of an arteriovenous fistula of 21 years' duration, which
involved the anterior tibial vessels. Fourteen years after the fistula closure, multiple aneurysms of
femoropopliteal arteries developed. (From Sako Y, Varco RL: Arteriovenous fistula: Results of
management of congenital and acquired forms, blood flow measurements, and observations on
proximal arterial degeneration. Surgery 1970;67:40-61.) ■

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500

V • SPECIAL PROBLEMS AND COMPLICATIONS

TRAUMATIC FALSE
ANEURYSMS

He was bled at his own desire by a bleeder
who had performed the same operation for
him, and generally in the same arm, some
30 or 40 times. Bleeding from an orifice was
done by firm compression, and on the day
following finding the bandage tight, he
removed it, and found the orifice to be
completely closed. A short time after this, a
small pulsating swelling was observed by
him at this point which slowly increased till a
day or two previous to my seeing him when
after some exertion with his arm he
observed a very considerable augmentation
of its size.
Norris, 1843

History

Since antiquity, the management of false
aneurysms has been closely allied to vascular
surgery. It has been repeatedly recorded
that Antyllus in the second century treated
an arterial aneurysm by ligature above and
below the lesion, with incision of the an-
eurysm and extraction of the clot. Schwartz
(1958) reported that Antyllus treated small
peripheral traumatic aneurysms by ligating
both ends and puncturing the center; however,
he advised against this practice in large
aneurysms. Figure 24-39 shows some of the
early methods of treatment of aneurysms.
Hunter electively ligated the femoral artery
proximal to a popliteal aneurysm in 1786 to
reduce blood loss during subsequent attempts
at excision of the aneurysm. Pick (1873) pro-
vided an interesting and detailed account of
his management of a large femoral false
aneurysm by digital compression, which had

Arxtyllua

Ar\al

■ FIGURE 24-39

Various types of operations employed for the treatment of aneurysms before the introduction of
Matas' endoaneurysmorrhaphy in 1888. (From Elkin DC: Traumatic aneurysms; Matas operation-
57 years after. Surg Gynecol Obstet 1946;82:1-12.) ■

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

501

■ FIGURE 24-40

A, Matas used a contemporary compressor applied
to the femoral artery at Hunter's canal to test the
collateral circulation in lesion such as this popliteal
aneurysm. B, In World War II, Elkin found the Matas
compressor to be an inexpensive and easily
constructed instrument that could compress various
arteries to determine the development of collateral
circulation. (A, From Matas R: Keene's surgery, vol. 7.
Philadelphia: WB Saunders, 1921; B, from Elkin DC:
Vascular injuries of warfare. Ann Surg 1944;1 20:284-
310.) ■

disastrous final results. This digital compres-
sion directly over the pulsating mass was
applied fairly continuously initially and then
for a considerable period of the waking hours
until 4 days later when the area became so
tender that the compression had to be dis-
continued. Not only did this initiate throm-
bus formation in the false aneurysm, but it
also became evident in less than 1 week that
the distal pulses could not be felt over either
the anterior or the posterior tibial artery.
Gangrene developed approximately 3 weeks
after the initiation of the digital compression,
an amputation was performed at the hip
level. The patient had a stormy postoperative
course for approximately 3 hours before he
died.

Matas (1888) described an endoaneurys-
morrhaphy operation, a method of intrasac-
cular suture, for the treatment of a brachial
arterial aneurysm. Within a few years, Matas
(1903) also recommended restoration of cir-
culation through the damaged artery as the
ideal treatment for arterial aneurysms. He
developed a compressor (Fig. 24-40) to test

the development of collateral circulation
before performing his endoaneurysmor-
rhaphy. His approach to widely open the
aneurysm and to suture the communications
into the artery (Fig. 24-41) was the standard
treatment, with minimal modification, for
more than 50 years, a period that included
World War II.

Despite the acceptance of the Matas endo-
aneurysmorrhaphy during World War I and
World War II, interest in preserving arterial
continuity was maintained. Lexer (1907) was
the first to use a segment of saphenous vein
as an interposition graft in an arterial defect
caused by excision of a traumatic axillary
aneurysm. Some of the problems associated
with arterial repair have been detailed in
Chapter 1 . Individual series of successful arte-
rial repairs have been reported. Soubbotitch
(1913) used suture repair, as has previously
been described in Chapter 1. Elkin (1946)
emphasized that all of the previous approaches
outlined by Antyllus, Anel, Hunter, and
Brasdor and Wardrop were frequently fol-
lowed by infection, hemorrhage, gangrene,

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V • SPECIAL PROBLEMS AND COMPLICATIONS

or failure to cure the false aneurysm. Only
the Matas procedure avoided these compli-
cations during the World War II experience.
The following methods of managing arterial
aneurysms were outlined by Freeman and
Shum acker (1955):

1. Endoaneurysmorrhaphy of Matas

2. Measures designed to produce clot in the
aneurysmal sac or to induce formation of
fibrous tissue about it to prevent further
expansion and possible rupture

3. Obliteration of the sac by closure of the
offending vessel

4. Extirpation of the aneurysm-bearing is
portion of the artery

5. Extirpation of the lesion, combined with
some procedure to permit maintenance or
to reestablish continuity of the affected
artery.

The extensive World War II experience is
documented in detail by Elkin, by Shumacker,
and by DeBakey and Elkin (1955).

Since the Korean Conflict in which arter-
ial repair was emphasized, vascular recon-

struction has become the procedure of choice
in restoring arterial continuity in the repair
of false aneurysms, in both the military and
the civilian situation. Hughes and Jahnke
(1958) reviewed the Korean experience and
provided a 5-year follow-up. A similar exten-
sive review has been completed recently for
the Vietnam experience (Rich, 1975).

As might be anticipated, a smaller number
of false aneurysms have been documented in
civilian experience than in recent military
experience. Patman, Poulos, and Shires
(1964) reported 12 patients who developed
false aneurysms in their series of 256 patients
with civilian arterial injuries in Dallas, an inci-
dence of 4.7%. None of these patients had
an initial exploration. Among the major
vessels that developed false aneurysms were
the aorta (1), subclavian (1), axillary (2),
superficial femoral (1), and popliteal (1).
There were also three radial artery false
aneurysms and single false aneurysms of the
profunda femoris, anterior tibial, and poste-
rior tibial arteries. The ratio of false aneurysms
to AVFs was 2:1 in their series, which was the
opposite of the ratio reported by Hughes and
Jahnke (1958) from the Korean experience.

■ FIGURE 24-41

This diagram illustrates the obliterative
endoaneurysmorrhaphy of Matas. Although
Matas also believed in the reconstructive
endoaneurysmorrhaphy, he elected to use the
obliterative technique in this case in 1917
involving a gunshot wound of the superficial
femoral artery because collateral circulation had
been established and the obliterative suture
could be applied with safety to the limb. A
continuous intrasaccular silk suture obliterated
the orifices of the communication with the main
artery, both proximally and distally. (From Matas
R: Keene's surgery, vol. 7. Philadelphia: WB
Saunders, 1921.) ■

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

503

Incidence

With the increased interest in primary arter-
ial repair of injured arteries during the past
25 years, many anticipated that there would
be a resultant decrease in false aneurysms. This
was particularly true in Vietnam (Rich 1975) .
However, considering the various etiologic
factors, remaining diagnostic problems, and
priorities of managing a patient with multi-
ple life-threatening injuries, it should be
obvious that the treatment of false aneurysms
remains an important aspect of vascular
surgery.

Similar to the varying incidence of arterial
injuries in the injured patient in general and
of AVFs, there is considerable disparity in the
reported incidence of false aneurysms, in both
civilian and military experience. One expla-
nation for this is at times false aneurysms are
included in series of arterial trauma and at
other times they are not. Also, some series do
not distinguish AVFs from false aneurysms in
combined reports.

Shumacker and Carter (1946) compared
the incidence of arterial aneurysms and AVFs
in large caliber peripheral arteries in their
World War II experience (see Table 24-2) .
Brachial false aneurysms were more prevalent
than brachial AVFs, and the converse was true
with femoral AVFs and false aneurysms.
Hughes and Jahnke (1958) found that there
were approximately twice as many AVFs as false
aneurysms in the Korean experience. When
major vessel lesions were considered (see
Table 24-7), they also noted fewer femoral
false aneurysms than AVFs. Rich (1975)
reported a somewhat different experience in
Vietnam, where there were slightly more false
aneurysms than AVFs (see Table 24-3).

In the relatively small series of arterial
injuries reported by Dillard, Nelson, and
Norman (1968), false aneurysms (nine
injuries) were more common than AVFs
(seven injuries) in their civilian experience
in St. Louis.

Etiology

Penetrating injuries are usually responsible for
a false aneurysm, or traumatic aneurysm,

which is produced by a tangential laceration
through all three layers of the wall of an artery.
In the military experience, fragments from
various exploding devices and bullets account
for the penetrating missile wounds (Fig.
24-42). In Civilian experience, stab wounds,
in addition to low-velocity bullet wounds, are
often associated with false aneurysms.

The increased use of fragmenting missiles
in combat parallels the relatively high inci-
dence of the development of these aneurysms
in a number of wars, particularly before the
advent of vascular repair. Hughes (1954)
noted that 85% of the vascular wounds in
Korea resulted from fragmenting missiles,
with only 15% being from bullets. Rich
(1975) found that a similar percentage, about
87%, of fragment wounds were responsible
for 558 false aneurysms and AVFs (see Table
24-12).

Diagnostic and therapeutic procedures can
result in false aneurysms if the placement of

m 1

■ FIGURE 24-42

Representative of military wounds associated
with false aneurysms is this large fragment
wound of the popliteal fossa with a large false
aneurysm of the popliteal artery demonstrated
angiographically. (From Vietnam Vascular
Registry #2967, NMR, Walter Reed General
Hospital.) ■

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V • SPECIAL PROBLEMS AND COMPLICATIONS

needles and catheters injures the arteries. The
first lesions that were successfully treated by
Lambert (1759) and Norris (1843) resulted
from bloodletting. At Walter Reed General
Hospital, four false aneurysms developed
following catheterization for angiographic
procedures (Rich, 1975). Postoperative false
aneurysms, other than anastomotic false
aneurysms, have been associated with many
operations. Smith (1963) cited development
of a false aneurysm of the common femoral
artery following an inguinal herniorrhaphy.
There was sudden profuse arterial bleeding
in the course of the herniorrhaphy, and
hemostasis was eventually secured by multi-
ple silk sutures. Approximately 2 weeks after
the operation, a pulsatile, firm, and tender
mass measuring 8 by 6 by 4 cm was palpated
in the area of the left inguinal ligament.
Despite tile fact, there was a purulent exudate
surrounding the area of the 1-cm tear in the
common femoral artery where a number of
sutures had been placed in the defect. It was
elected to excise the traumatized area and
perform an end-to-end anastomosis. Five days
after this second procedure, severe hemor-
rhage occurred and it was necessary to ligate
the common femoral artery. Nevertheless, via-
bility of the extremity persisted.

The fact that a false aneurysm can develop
following the operative removal of a herni-
ated nucleus pulposus was documented by
Seeley (1954). Seeley mentioned treating a
20-year-old patient with a right common iliac
artery aneurysm who had been operated on
the L4-5 intervertebral space 1 month before
his admission at Walter Reed General Hospi-
tal. Six weeks following the initial disk oper-
ation, a second operation was performed and
an enormous false sac was found surround-
ing a right common iliac artery defect (Fig.
24-43). It was necessary to restore arterial
continuity by inserting a 2-cm homologous
arterial graft. Subsequent complications asso-
ciated with disruption of the graft necessitated
ligation of the right common iliac artery and
vein. Fortunately, viability of the extremity was
maintained.

Fractures can be associated with false
aneurysm formation. Cameron, Laird, and
Carroll (1972) presented an interesting review
of 10 cases of false aneurysms complicating

■ FIGURE 24-43

An enormous false aneurysm from a defect in
the right common iliac artery was operated on
at Walter Reed General Hospital 6 weeks after
the initial disk operation. The right ureter was
displaced laterally by the mass. The segment
of the artery with the posterior defect was
excised, and the hypogastric artery ligated. A
2-cm homologous arterial graft was used to
bridge the defect. (From Seeley SF, Hughes
CW, Jahnke EJ Jr: Major vessel damage in
lumbar disc operation. Surgery 1954;35:421-
429.) ■

closed fractures in a variety of anatomic loca-
tions (Table 24-24) . Singh and Gorman
(1972) emphasized that the formation of a
false aneurysm as a result of a closed trauma
to the lower extremity was unusual. They pre-
sented a case of a 51-year-old man who sus-
tained a closed fracture at the junction of the
middle and distal thirds of the tibia and fibula
when his leg was caught by an encircling boat
cable in a ship-building yard in 1966. Initially,
a closed reduction of the fracture was
performed, with immobilization of the limb
in a long leg cast. This was replaced by a
walking cast, which was kept on for 6 months
before it was determined that the fracture was
healed. At that time, the patient noted super-
ficial varicosities. The examining physician
stated that his extremity had the typical post-
phlebitic syndrome appearance, except that

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

505

TABLE 24-24

REPORTED CASES OF FALSE ANEURYSMS COMPLICATING CLOSED FRACTURES

Author

Robson

Year

1957

Crellin

1963

Meyer and Slager

1964

Dameron

1964

Staheli

1967

Smith

1963

Stein

1958

Bassett

and Houck

1964

Bassett

and Silver

1966

Harrow

1970

Artery Involved

Fourth lumbar artery

Anterior tibial artery
Profunda femoral artery
Profunda femoral artery
Popliteal artery
One false aneurysm with closed

fracture in 61 arterial injuries;

site not stated
Anterior tibial artery
Profunda femoral artery
Thoracic aorta
Right internal iliac artery

Fracture

Fractured spinous processes and

traumatic spondylolisthesis
Fracture upper third tibia
Subtrochanteric osteotomy
Screwn blade plate
Fracture distal femoral shaft

Fracture of tibial plateau

Blade plate for subtrochanteric osteotomy

Eleventh dorsal vertebra

Pelvis

Modified from Cameron HS, Laird JJ, Carroll SE: False aneurysms complicating closed fractures. J Trauma 1972;12:67-74.

there was a pulsatile mass with a bruit located
over the posteromedial aspect of the distal
tibia. A femoral arteriogram revealed a large
false aneurysm and an AVF of the distal part
of the posterior tibial artery and accompany-
ing veins (Fig. 24-44). It was possible to
perform a lateral repair of the posterior tibial
artery with interruption of the venous com-
ponent. Six months later, the patient was
asymptomatic with no extremity edema.

Blunt trauma without an associated fracture
can also result in a false aneurysm. Lai,
Hoffman, and Adamkiewicz (1966) presented
an unusual case of dissecting aneurysm of
the cervical carotid artery in a 21-year-old
male following a hyperextension neck injury
sustained in an automobile accident. The
patient presented at the Johns Hopkins Hos-
pital with a chief complaint of pain of the left
side of his head and neck 6 months after the
car he was driving collided with a truck. A firm,
tender, 4-by-4cm mass high in the left cervi-
cal area was obvious, and a bruit was heard
over the mass. A left carotid angiogram
revealed considerable lateral displacement
of the internal carotid artery, and the mass
promptly filled with contrast media. A 4-by-6
cm dissecting aneurysm of the internal carotid
artery was found at the time of exploration,
with the hypoglossal nerve, the vagus nerve,
and the spinal accessory nerve all being
displaced by the aneurysmal sac. Because

the superior portion of the aneurysmal sac
approached the base of the skull, it was
necessary to ligate the internal and external
carotid arteries. The patient had an unevent-
ful postoperative recovery with no abnormal
neurologic findings other than the cranial
nerve deficits present before surgery.

Clinical Pathology

A false aneurysm, or traumatic aneurysm, is
caused by trauma that lacerates or ruptures
all three layers of the wall of an artery. Arter-
ial flow through the artery is usually main-
tained, and the extravasated blood through
the laceration is contained by surrounding
tissues to become a pulsating hematoma and
subsequently an encapsulated false aneurysm.
The hematoma that is formed compresses and
seals the point of injury. Within days to weeks
later, the thrombus gradually liquefies. False
aneurysms are distinguished from true
aneurysms. Whether the true aneurysm is
congenital in origin, arteriosclerotic, mycotic,
syphilitic, or caused by unusual systemic dis-
eases such as polyarteritis nodosa, the true
aneurysm has a sac composed of one or more
layers of the artery rather than a rupture
through all of the walls of the artery, as occurs
in the traumatic false aneurysm. Indirect
or blunt trauma can actually cause a true

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506

V • SPECIAL PROBLEMS AND COMPLICATIONS

■ FIGURE 24-44

A, A large false aneurysm of the posterior tibial artery and a posterior tibial arteriovenous fistula
were demonstrated angiographically in a 51 -year-old man who sustained a closed fracture at the
junction of the middle and distal thirds of the tibia and fibula. B, The large posterior tibial false
aneurysm was demonstrated at the time of surgical exploration. (From Singh I, Gorman JF:
Vascular injuries in closed fractures near junction of middle and lower thirds of the tibia. J Trauma
1972;12:592-598.) ■

aneurysm. True traumatic aneurysms caused
by blunt, nonpenetrating trauma form a small
group compared to traumatic false aneurysms.
Blunt trauma causes a confusion of the arte-
rial wall, with the damaged arterial segment
progressively dilating and forming a true

aneurysm. Early recognition and treatment
are rarely possible because the injury will
usually not be apparent until a true aneurysm
develops to a significant size. Only pathologic
evaluation may differentiate a traumatic true
aneurysm from a traumatic false aneurysm.

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

507

An unrepaired laceration of an artery with
an inevitable periarterial hematoma usually
has partial liquefaction of the latter, and a com-
munication is established between the artery
and the hematoma. Apseudocapsule of con-
nective tissue forms gradually, and the pul-
sating hematoma becomes a false aneurysmal
sac. The lesion will usually continue to expand,
often causing pressure symptoms. One of the
most easily recognizable results of pressure is
a neuropathy, such as the easily recognizable
neurologic deficits that develop in the hand
from pressure on the median nerve by a false
aneurysm (Fig. 24-45). False aneurysms may
eventually rupture. The potential for exsan-
guinating hemorrhage endangers not only the
limb but also the patient's life. If there is an
associated infection, the threat of rupture is
even greater (Fig. 24-46) .

The size, configuration, and location of
false aneurysms can vary greatly. The false
aneurysm can be one single sac (Fig. 24-47)
or it can be bilobed (Fig. 24-48). The distri-
bution of 82 false aneurysms treated in World
War II shows that the brachial artery was
involved most often, followed by the popliteal

artery (see Table 24-6) . The anatomic region
most often involved with 558 false aneurysms
and AVFs in Vietnam casualties was the lower
extremity (see Table 24-9) . The most common
involved arteries were the posterior tibial and
brachial, followed closely by the superficial
femoral and popliteal arteries (see Table
24-10). Multiple lesions can exist. Table
24-4 shows that 41 out of the 509 Vietnam
casualties had two or more lesions, for a total
of 90 separate lesions (Fig. 24-49).

Expanding false aneurysms can cause
neurologic changes due to direct pressure on
major nerves (Fig. 24-50). Shumacker and
Carter (1946) emphasized the high frequency
of false aneurysms of upper extremity major
arteries with associated nerve lesions that
required operations (Table 24-25).

Usual pathologic changes can occur with
false aneurysms. Distal embolization of a
thrombus (Fig. 24-51) from a false aneurysm
(Fig. 24-52) is unusual, but the potential
threatwith possible disastrous sequelae always
exists. Sachtello, Ernst, and Griffen (1974)
described the case of one patient with a false
subclavian aneurysm who had distal embolism

■ FIGURE 24-45

Pressure from a false aneurysm can compress an adjacent nerve. Fairly rapid expansion of the
false aneurysm of the brachial artery caused external compression of both the median and the
ulnar nerves with resultant neurologic deficit. (From Rich NM: In: Beebe HG, ed. Complications
in vascular surgery. Philadelphia: JB Lippincott, 1973.) ■

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508

V • SPECIAL PROBLEMS AND COMPLICATIONS

■ FIGURE 24-46

A false aneurysm associated with surrounding infection has an increased potential for rupture and
exsanguinating hemorrhage. An infected false aneurysm of the superficial femoral artery resulted
in intermittent hemorrhage through the open wound of the thigh in a Vietnam casualty. (From NMR,
Vietnam Vascular Registry #837.) ■

■ FIGURE 24-47

A false aneurysm can exist in a large variety of
sizes and configurations. It may be a single
sac, as shown in this arteriogram. (From NMR,
Vietnam Vascular Registry #2590.) ■

■ FIGURE 24-48

Among the variety of configurations of false
aneurysms is a double or bilobed sac, as
shown in this arteriogram of the common
carotid artery. The offending fragment is seen
adjacent to the carotid artery. (From NMR,
Vietnam Vascular Registry #826.) ■

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

509

TABLE 24-25

PERIPHERAL NERVE LESIONS ASSOCIATED WITH ARTERIAL ANEURYSMS

Artery Involved

Nerve Lesion
Requiring
Operation

Nerve Lesion Not
Requiring
Operation

No Nerve
Lesion

Brachial

Axillary

Subclavian

Popliteal

Femoral

Others

Total

No.

85.7

3.6

10.7

73.3

6.7

20.0

60.0

20.0

9.5

28.6

61.9

6.2

18.8

75.0

13.0

24.0

63.0

40.3

21.0

38.7

Modified from Shumacker HB Jr, Carter KL: Arteriovenous fistulas and arterial aneurysms in military personnel. Surgery
1946;20:9-25.

■ FIGURE 24-50

There is a groove made by the median nerve
in the excised axillary false aneurysm. Direct
pressure on the median nerve had resulted in a
neuropathy. (From Elkin DC: Vascular injuries of
warfare. Ann Surg 1944;120:284-310.) ■

■ FIGURE 24-49

Multiple lesions can occur, as evidenced
by this Vietnam casualty who had a false
aneurysm of the anterior tibial artery, which was
obvious, and a false aneurysm of the distal
popliteal artery, which was diagnosed only by
angiography. (From NMR, Vietnam Vascular
Registry #51 89.) ■

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510

V • SPECIAL PROBLEMS AND COMPLICATIONS

■ FIGURE 24-51

Mural thrombus may embolize from either a
false aneurysm or an arteriovenous fistula. This
angiogram demonstrates an embolus from a
proximal popliteal artery false aneurysm to the
distal popliteal and proximal posterior tibial
arteries. (From Rich NM: In: Beebe HG, ed.
Complications in vascular surgery.
Philadelphia: JB Lippincott, 1973.) ■

from a thrombus within a false aneurysm. They
managed the problem by resection of the
clavicle, resection of the subclavian false
aneurysm with vein graft replacement and
brachial arterial embolectomy. Pulses were
restored. Rhodes, Cox, and Silver (1973)
reported the unusual complication of con-
sumption coagulopathy, which developed in
a patient with a false aneurysm and an AVE

Clinical Features

The most obvious clinical finding with a false
aneurysm is a mass that is usually pulsatile.
There is often evidence of a penetrating
wound (Fig. 24-53) . The mass may or may
not be painful. On examination, the borders
of the mass can be ill defined because the false
aneurysm is beneath the deep fascia. Depend-
ing on the amount of thrombus within the
false aneurysm, the mass may or may not be
pulsatile. There is often an associated systolic
bruit over the mass, and there can be con-
siderable radiation of the bruit into the
surrounding anatomy.

Gradual enlargement of the false aneurysm
may occur (Fig. 24-54), with the development

■ FIGURE 24-52

Except for 14% of the lesions that were
associated with external hemorrhage into open
wounds, there were rare preoperative
complications associated with arteriovenous
fistulas and false aneurysms in this series. One
of these was embolization of thrombus from
popliteal arterial false aneurysm, identified in
the arteriogram with its adjacent wounding
fragment. In 1968 at Walter Reed Army Medical
Center, the false aneurysm was resected, the
thrombus was removed with a Fogarty catheter,
and arterial continuity was reestablished by
end-to-end anastomosis. (From Rich NM,
Hobson RW II, Collins GJ Jr: Traumatic
arteriovenous fistulas and false aneurysms: A
review of 558 lesions. Surgery 1975;78:817-
828.) ■

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

511

■ FIGURE 24-53

The diagnosis of a false aneurysm may be obvious with the physical finding of a pulsating mass.
There is usually evidence of a penetrating wound. (From NMR, Vietnam Vascular Registry #3273.

■ FIGURE 24-

Enlargement of a false aneurysm may be gradual, or there may be rapid expansion of a mass. The
size of the mass may also be quite variable, as in this large false aneurysm of the profunda femoris
artery. The mass may be painful, and there may be warmth and tenderness on examination. (From
NMR, Vietnam Vascular Registry #3159.) ■

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512

V • SPECIAL PROBLEMS AND COMPLICATIONS

of a firm, warm, tender area. Confusion with
an abscess has occurred in the differential
diagnosis. A stable false aneurysm of longer
duration can also be confused with a cyst or
neoplasm.

If the false aneurysm is associated with an
AVF, a continuous bruit and thrill over the
sight of injury may also be present. As previ-
ously noted, pressure on adjacent nerves may
result in neurologic deficits, and the first
symptom or physical finding may result from
neuropathy. Distal pulses are usually intact and
considered to be normal on examination.

Diagnostic Considerations

Diagnosis is usually made by physical exami-
nation of a pulsatile mass. Roentgenograms
in the anteroposterior and lateral views might
identify an offending metallic foreign body
in the anatomical location of an artery.

Nevertheless, angiography may be necessary
to establish the diagnosis (Fig. 24-55). The
size of the false aneurysm may be misleadingly
small because of the amount of laminated clot
filling the sac (Fig. 24-56) . Angiography may
delineate a clinically unsuspected adjacent
AVF (Fig. 24-57) or multiple vascular lesions,
as demonstrated in Fig. 24-49.

Angiography may be necessary to make the
diagnosis of the false aneurysms in arteries
that are not easily acceptable to physical exam-
ination, such as those within the chest and
abdomen (Fig. 24-58).

Newer investigative techniques, such as
sonography, can also be valuable in deter-
mining the size and location of false
aneurysms. This was emphasized by Bole,
Purdy, and Munda (1976) (Fig. 24-59). The
diagnostic value of sonography for both true
aneurysms and false aneurysms has been
demonstrated with increasing utilization of
this modality at Walter Reed General Hospital.

■ FIGURE 24-55

Preoperative angiography is helpful in confirming clinical impressions, outlining the site of the
vascular defect, and ruling out additional adjacent vascular injuries. When not preoperatively
available or practical, angiograms can be obtained easily. This one demonstrates a popliteal arterial
false aneurysm seen at Walter Reed Army Medical Center in 1969 before resection and end-to-end
anastomosis. Similar angiograms in the operating room immediately after repair have helped
establish the status of vascular repair. (From Rich NM, Hobson RW II, Collins GJ Jr: Traumatic
arteriovenous fistulas and false aneurysms: A review of 558 lesions. Surgery 1975;78:817-828.) ■

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

513

■ FIGURE 24-56

This series of film in an angiogram of the right brachial artery demonstrates early filling of the false
aneurysm adjacent to the offending fragment (left); the obvious false aneurysm, which was
angiographically much smaller than the large palpable mass because of the laminated clot that
filled the false aneurysm sac (middle); and residual contrast in the false aneurysm sac (right). (From
NMR, Vietnam Vascular Registry #3159.) ■

■ FIGURE 24-57

A large false aneurysm, such as this one demonstrated
angiographically, can cause local arterial compression.
In this Vietnam casualty, the large false aneurysm of the
popliteal artery compressed the artery sufficiently to
nearly obliterated the associated arteriovenous fistula.
There was no associated classic "machinery-type" bruit,
and the arteriovenous fistula was diagnosed
angiographically. Also, the patient had weak pedal
pulses because of the compression of the popliteal
artery by the large false aneurysm, in contrast to what
has previously been described in most patients who
have intact distal pulses. (From NMR, Vietnam Vascular
Registry #2513159.) ■

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V • SPECIAL PROBLEMS AND COMPLICATIONS

■ FIGURE 24-58

Compression and lateral displacement of the
abdominal aorta toward the patient's left side are
demonstrated in this subtraction study of an
angiogram of the aorta. The offending fragment
from an M26 grenade caused a large false
aneurysm of the aorta, which was repaired by
lateral suture technique with interrupted sutures
at Walter Reed Army Medical Center in 1967.
(From Rich NM, Hobson RW II, Collins GJ Jr:
Traumatic arteriovenous fistulas and false
aneurysms: a review of 558 lesions. Surgery
1975;78:817-828.) ■

■ FIGURE 24-59

Ultrasonic tomography of the upper abdomen in a transverse plane showing the pseudoaneurysm
(open arrow) in a patient with nonpulsatile diffuse mass. Thrombus echoes and irregular contour of
the aneurysm are noted (solid arrows). Vertebral body (V) and the left kidney (K) are also visualized.
(From Bole PV, Purdy RT, Munda R, et al: Traumatic pseudoaneurysms: A review of 32 cases. J
Trauma 1976;16:63-70.) ■

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS 515

Left Brachial

SupProfyj

. Liqaiu re

Prof

//Radial
■Recur r.

R ec r/;A\Recurr.\\
Ulnar Radial

■ FIGURE 24-60

The original photograph and drawing shown in the report of Dr. Matas, Philadelphia Medical News,
October 27, 1988, when he proposed his endoaneurysmorrhaphy approach to the management of
false aneurysms. (From Elkin DC: Traumatic aneurysm; Matas operation — 57 years after. Surg
Gynecol Obstet 1946;82:1-12.) ■

Surgical Treatment

The report of the first operation performed
by Matas in 1 888 was presented again by Elkin
(1946) to emphasize that the Matas operation
has stood the test of time for 5 7 years and had
had a profound impact on the surgery of blood
vessels (Fig. 24-60) .

On April 6, 1988, I operated on a young
male Negro for a very large traumatic (mul-
tiple gunshot) aneurysm of the brachial
artery, extending from the armpit to the elbow,
which opened my eyes to the possibilities of
an entirely new method of conservative treat-
ment, which was to revolutionize my previous
notions of aneurysmal surgery. In this case,
successive ligation of the main artery on the
proximal and distal poles of the aneurysm had
been followed by relapse, and it seemed to
me that I had no other alternative but to
extirpate the sac. When I exposed the sac and
emptied its contents, the failure of the liga-
tions to control the circulation was easily
explained by the appearance in the bottom
of the sac of the large orifices corresponding
to the collateral branches, which opened into
the sac in the segment of the artery included

in between the ligatures (Fig. 24-61). It was
evident that it was these collateral orifices that
fed the sac despite the ligatures that had been
placed at each one of its poles. I, at first,
intended to secure these collaterals by excis-
ing the sac, but the branches of the brachial
plexus of nerves were so densely incorporated
in its walls that I could have not dissected them
and detached them, without serious damage,
thereby paralyzing the arm. It occurred to me
then that the easiest way out of this awkward
dilemma was to steal the orifices of all the
bleeding collaterals by suturing them as we
would an intestinal wound, leaving the sac
attached and undisturbed in the wound. This
procedure was at once put into effect and the
hemostasis was so perfect and satisfactory that
it seemed to me strange that no one should
have thought of so simple an expedient
before.

Matas used the intrasaccular suture (see
Figs. 24-41 and 24-61); however, he was also
interested in reconstructive endoaneury-
smorrhaphy (Fig. 24-62).

In the management of a false aneurysm,
repair of the arterial defect is usually the goal
that should be sought. An elective incision

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516

V • SPECIAL PROBLEMS AND COMPLICATIONS

■ FIGURE 24-6 1

The Matas obliterative aneurysmorrhaphy is
demonstrated in this intrasaccular suture
ligature of a ruptured popliteal aneurysm. The
dotted line shows the area of extravasation
filled with clot. Arterial reconstruction was
considered impractical in this specific case,
and the distal and proximal popliteal arteries
were obliterated with encircling sutures.
Collateral circulation was adequate to maintain
extremity viability. (From Matas R: Surgery, vol.
7. Philadelphia: WB Saunders, 1921.) ■

should be made thatwill allow adequate expo-
sure for proximal and distal control. Exam-
ples were afforded by the extensive World War
II experience. Shumacker (1946) described
in detail the incisions that could be success-
fully employed in the surgical approach to
aneurysms, especially those in antecubital
(Fig. 24-63) and popliteal (Fig. 24-64) fossae.
His report was based on his extensive
experience in managing false aneurysms in
hundreds of American combat casualties.
Specifically, these incisions were devised to
replace longitudinal incisions across the
popliteal and antecubital creases, which were
often associated with heavy scars or keloids,

contracture, or ulceration. Although resection
of the false aneurysm is often recommended,
an alternative plan that is presently employed
has several advantages. The laminated clot
within the false aneurysm should be evacuated
after temporary proximal and distal control
is obtained with vascular clamps, but the major-
ity of the sac can usually be left in place. This
will shorten the length of the operative pro-
cedure and decrease the possibility of damage
to associated structures, such as tearing of the
popliteal vein, which has become closely
adherent and attenuated to an adjacent
popliteal arterial false aneurysm. If the false
aneurysm is inadvertently entered before
obtaining proximal and distal control, digital
control will usually suffice as an expedient
measure. Unnecessary resection of normal
artery can also be avoided if careful dissec-
tion of both the proximal and the distal artery
toward the side of the defect is carried out.
In this manner, a more limited resection of
artery will be necessary.

Occasionally, lateral suture of a punctuate
wound of an artery is possible, without con-
striction of the arterial lumen. However,
limited arterial resection and end-to-end anas-
tomosis is usually the procedure of choice. If
it is necessary to use an arterial replacement,
an autogenous vein graft is usually preferred.
This graft should be placed in tissue as normal
as possible, which is often difficult because of
considerable inflammation and cicatrix. If
there is extensive scarring, it might be possi-
ble to place a graft in an extra-anatomic area
of adjacent tissues in a position away from the
usual course of the major vessel. In the case
of noncritical arteries, such as the radial artery
or distal posterior tibial artery, ligation is
usually satisfactory. This is particularly impor-
tant if there is an infected false aneurysm.
However, arterial repair is preferred even in
small caliber arteries.

Surgical correction of a false aneurysm
should be performed as soon as possible after
the diagnosis is made to prevent the compli-
cations of rupture or rapid expansion with
resultant pressure on adjacent nerves. Imme-
diate surgery should be advocated if neuro-
logic symptoms develop.

Additional information related to specific
arterial false aneurysms, such as those of the

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS 517

■ FIGURE 24-62

In addition to the obliterative aneurysmorrhaphy for the treatment of the false aneurysms, Matas
encouraged selective reconstructive endoaneurysmorrhaphy, as was used in this repair of a false
aneurysm of the brachial artery. (From Matas R: Surgery, vol. 7. Philadelphia: WB Saunders,
1921.) ■

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518

V • SPECIAL PROBLEMS AND COMPLICATIONS

■ FIGURE 24-63

Incisions used in exposure of vessels in the antecubital
fossa. A, The usual incision for exposure of brachial
vessels in antecubital space. B, Incision used when the
lesion is suspected in proximal portion of ulnar vessels.
C, Incision used when brachial vessels are involved just
proximal to antecubital creased. D, Incision used for
exploration of distal end of brachial or proximal end of
radial vessels. (From Shumacker HB Jr: Incisions in
surgery of aneurysms, with special reference to
exploration in antecubital and popliteal fossae. Ann Surg
1946;124:586-598.) ■

■ FIGURE 24-64

Skin incisions used in exploring the popliteal vessels in the surgical approach to false aneurysms in
World War II. A, Incision used when the lesion exists in the midpopliteal space. B, Incision used
when the lesion is higher in the popliteal fossa. C and D, Incisions used for exploring the distal
popliteal vessels. E, A modified incision useful when associated nerve lesion require exploration.
(From Shumacker HB Jr: Incisions in surgery of aneurysms, with special reference to exploration in
antecubital and popliteal fossae. Ann Surg 1946;124:586-598.) ■

subclavian artery, can be found in specific
chapters. Details of arterial repair and specific
techniques, such as intraluminal control of
hemorrhage with a balloon catheter, are to
be found in Chapter 19.

Elkin (1946) reported the results of oper-
ating on 106 false aneurysms at the Ashford
General Hospital Vascular Center in White

Sulfur Springs, West Virginia, in a 30-month
period. The Matas procedure was employed
in 61 of the operations, and some other type
of operation, usually complete excision of a
small sac, was employed in the remaining 45
cases. There were no deaths in his series, no
recurrence of the false aneurysm, and no
incidence of gangrene. Table 24-26 shows

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

519

TABLE 24-26

LOCATION OF INJURY AND NUMBER
OF PATIENTS TREATED BY MATAS
ENDOANEURYSMORRHAPHY:
ASHFORD GENERAL HOSPITAL
VASCULAR CENTER, WHITE SULFUR
SPRINGS, WORLD WAR II EXPERIENCE

Artery Involved

Axillary

Brachial

Femoral

Iliac

Peroneal

Popliteal

Profunda femoris

Radial

Superior gluteal

Tibial, anterior

Tibial, posterior

Ulnar

Total

Cases

14
11

8
_2
61

From Elkins DC: Traumatic aneurysm; Matas operation — 57
years after. Surg Gynecol Obstet 1946;82:1-12.

the location and number of injuries
treated by endoaneurysmorrhaphy. Elkin and
Shumacker (1955) outlined the operative
treatment of 209 arterial aneurysms (Table
24-27) . Nearly an equal number were treated
by endoaneurysmorrhaphy as by excision.
Shumacker (1948) reported successful results
with vein graft repair of arteries that had false
aneurysms (see Table 24-16).

De Takats and Pirani (1954) stated that
Herlyn, a pupil of Stich in Gottingen, reported
he performed 164 ligatures and 230 recon-
structive operations in World War II. This
emphasized that the trend in German was
surgery, and Herlyn felt that the artery should
never be ligated for traumatic aneurysm
unless it was small or the patient's life was in
danger.

Hughes and Jahnke (1958) reported on 215
false aneurysms and AVFs treated at Walter
Reed Army Medical Center in the early 1950s,
mainly in casualties from the Korean Conflict.
The various operations used in managing 43
false aneurysms and 91 AVFs in large vessels
are reviewed in Table 24-18. Similar data con-

cerning smaller caliber arteries are given in
Table 24-8.

Rich, Hobson, and Collins (1975) reported
the experience from the Vietnam War. There
were 296 false aneurysms among 558 AVFs and
false aneurysms identified in 509 patients.
As might be anticipated by the number of
American troops committed in Southeast
Asia, the largest number of lesions resulted
from wounds during 1968, with a relatively
large number of lesions in 1967 and 1969. The
time from injury to recognition of the AVFs
and false aneurysms was arbitrarily considered
to be immediate if recognized within the first
24 hours, early if recognized between the
second and thirtieth day, delayed if recognized
between the second through the sixth month,
and remote if recognized after 6 months. In
this study, the largest number of lesions (273
or 48.9%) was recognized in the early period
(see Table 24-20) . A nearly equal number of
lesions, 228, was recognized in the delayed
period. In the immediate group, there were
22 acute lesions operated on in Vietnam. In
the remote group, all but 7 of the 35 patients
had recognition and treatment of their lesions
in less than 2 years. Only two had recognition
and treatment of their lesions more than 5
years following the initial injury, and both were
less than 6 years. Nearly an equal number of
operations were performed in the inter-
mediate hospitals, mainly in Japan, and in
hospitals in the continental United States (see
Table 24-21). Several hundred surgeons were
involved in performing the repairs. Table
24-22 outlines the methods of treatment used
for the various repairs. Arterial ligation was
used in 290 lesions, 52%. The overall mor-
bidity rate for the 509 patients was 1.8% (seven
deaths) (see Table 24-23). Only two of these
deaths could be directly attributed to the vas-
cular problem. One patient died from a rup-
tured external iliac arterial false aneurysm.
The overall morbidity included five compli-
cations, for a morbidity rate of 6.3%. Hem-
orrhage occurred in 14, thrombosis in 12, and
stenosis in 2.

The numerous reports of the management
of false aneurysms from civilian experience
range from individual case reports to reports
of 20 to 30 lesions. However, the civilian expe-
rience has not been as extensive as the warfare

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520

V • SPECIAL PROBLEMS AND COMPLICATIONS

TABLE 24-27

TECHNIQUES OF OPERATIVE TREATMENT IN 209 ARTERIAL ANEURYSMS:
WORLD WAR II EXPERIENCE

Location

Upper extremity
Axillary
Brachial
Radial
Subclavian
Ulnar

Lower extremity:
Femoral
Gastrocnemius,

muscle branch
Peroneal
Popliteal

Profunda femoris
Profunda branch
Tibial, anterior
Tibial, posterior

Head and neck:
Carotid

Cervical, deep
Temporal, superficial

Trunk:

Gluteal, superior
Iliac

Innominate
Thoracic, lateral
Thoracoacromial

Total

Endoaneurysmorrhaphy

10
16

2
5
7

Proximal

End-to-End

Total No

Excision

Ligation

Anastomosis

Cases

—

47*

—

13+

—

4
1

—

18*

—

215

2
5

15'

—

13'
1
2

—

4
1

1
1

209

*This total does not include one aneurysm in which cure occurred spontaneously.

+ This total does not include two aneurysms in which methods of management were not stated.

*This total does not include two aneurysms in which cure occurred spontaneously.

§ This total does not include three aneurysms: two in which methods of management were not stated and one in which

spontaneous cure occurred.

'This total does not include two aneurysms in which cure occurred spontaneously.

From Elkin DC, Shumacker HB Jr: In: Vascular Surgery in World War II. Elkin DC, DeBakey ME, eds. Washington, DC: US

Government Printing Office, 1955.

experience in this century. Examples of the
civilian experience are the reports of Lloyd
(1957), Baird and Doran (1964), Engelman,
Clements, and Herrmann (1969), and Bole,
Purdy, and Munda (1976). Particularly note-
worthy is the report of the management of 23
traumatic false aneurysm in 23 patients treated
in New York City over a 5-year period starting
in 1968. Table 24-28 outlines the method of

management of these false aneurysms, with
lateral suture repair, resection and end-to-end
anastomosis, and ligation being used almost
equally. These authors reported no mortality,
no recurrence, and no distal edema or arte-
rial insufficiency. They did have two patients
who continued to have pain, and three wound
infections occurred.

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24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

521

TABLE 24-28

TYPE OF REPAIR: CIVILIAN
EXPERIENCE IN NEW YORK CITY

Resection and end-to-end anastomosis 8

Resection and graft replacement 1

Lateral repair 7

Ligation 5

Spontaneous closure 1

Refused treatment 1

Total 23

From Bole PV, Munda R, Purdy RT, et al: Traumatic
pseudoaneurysms: a review of 32 cases. J Trauma
1976;16:63-70.

Spontaneous Cure

Shumacker and Wayson (1950) evaluated
spontaneous cure of false aneurysms and
AVFs. They studied 122 aneurysms and 245
AVFs. They felt that thrombosis was respon-
sible for the obliteration of these lesions.
Because there were only eight satisfactory
spontaneous cures of false aneurysm — 6.6%
of 22 lesions — these authors though that there
was little merit in awaiting the possibility of
this occurrence. This was only slightly better
than the 2% spontaneous cure for AVFs.
Although some case reports have been
documented, recent experience has not
witnessed a change in the low incidence of
spontaneous cure of false aneurysms. This is
undoubtedly also affected by early surgical
intervention for the mass majority of false
aneurysms.

Follow-up

Hughes andjahnke (1958) provided a 5-year
follow-up study of 250 AVFs and false
aneurysms treated at Walter Reed Army
Medical Center. Most of the patients had been
injured during the Korean Conflict. This long-
term follow-up was one of the first and one of
the few extensive follow-up studies to be con-
ducted. This study emphasized the difficulty
in evaluating vascular trauma in combat casu-
alties because of the many associated injuries.
Neither of the two deaths in this follow-up

study were related to vascular problems
following repair of false aneurysms. Residual
pain, coldness, and claudication in the
involved extremity were noted; however, no
distinction was made between those patients
treated for AVFs and those treated for false
aneurysms. In the follow-up of the Vietnam
casualties through the Vietnam Vascular
Registry, more than one fourth — 29.3% — or
149 of the 509 patients with AVFs and false
aneurysms have been evaluated at Walter
Reed Army Medical Center. In the long-term
follow-up, which extends to 10 years for many
patients, additional problems and sympto-
matic residuals have been limited. Unfortu-
nately, some of these patients have been lost
to the long-term follow-up effort because of
untimely deaths. One patient was killed in
subsequent action during a second tour in
Vietnam, and another patient died in an
automobile accident. In the civilian reports,
there are very limited data regarding long-
term follow-up of patients who have false
aneurysms. While few wanted to be reminded
of the unfortunate Vietnam experience for
more than 25 years in the United States, as
we enter the twenty-first century, there is a
realization that data in the Vietnam Vascular
Registry are of value. A concerted effort is
being developed to expand the long-term
follow-up, which will be helpful to collective
experiences in the civilian community and in
responding to military interventions.

REFERENCES

Albuquerque FCJavedan SP, McDougall CG: Endo-
vascular management of penetrating vertebral
artery injuries. J Trauma 2002;53(3) :574-580.

Annandale T: Traumatic popliteal arteriovenous
aneurysm treated successfully by ligature of the
popliteal artery and vein. Lancet 1875;1:568.

Anthopoulos LP, Johnson JB, Spellman M:
Arteriovenous Fistula in multiple saccular
arterial aneurysms of a finger, following child-
hood human bite. Angiology 1965;16:89.

Baird RJ, Doran ML: The false aneurysm. Can Med
AssocJ 1964;91:281-284.

Basse ttFH, HouckWS: False aneurysm of profunda
femoris artery after subtrochanteric osteotomy
and nail-plate fixation. J Bone Joint Surg 1964;
46A:583-585.

ch24.qxd 4/16/04 3:26 PH Page 522

522

V • SPECIAL PROBLEMS AND COMPLICATIONS

Basse tt FH, Silver D: Arterial injury associated with
fractures. Arch Surg 1966;92:13-19.

Beattie EJJr, Oldham JB, RossJA: Superior thyroid
arteriovenous aneurysm. Br J Surg 1961 ;48:456-
457.

Bell D, Cockshott WP: Angiography of traumatic
arterio-venousfistulae. Clin Radiol 1965;16:241-

247.

Bickham WS: Arteriovenous aneurysm. Ann Surg
1904;39:767-775.

Billings KJ, Nasca RJ, Griffin HA: Traumatic arte-
riovenous fistula with spontaneous closure. J
Trauma 1973;13:741-743.

Blackmore TL, Whelan TJ: Arteriovenous fistula
as a complication of gastrectomy. AmJ Surg 1 965;
109:197.

Bole PV, Munda R, Purdy RT: Traumatic pseudo-
aneurysms: A review of 32 cases. J Trauma
1976;16:63-70.

Bole PV, Purdy RT, Munda RT, et al: Civilian arterial
injuries. Ann Surg 1976;183:13-23.

Branham HH: Aneurysmal varix of the femoral
artery and vein following a gunshot wound. Int
JSurgl890;3:250.

Callander CL: Study of arteriovenous fistula with
an analysis of 447 cases. Ann Surg 1920;19:428-
459.

Cameron HS, Laird Jj, Carroll SE: False aneurysms
complicating closed fractures. J Trauma 1972;
12:67-74.

Conn JH, Hardy JD, Chavez CM, Fain WR: Chal-
lenging arterial injuries. J Trauma 197l;ll:167-
177.

Creech O Jr, Gantt J, Wren H: Traumatic arteri-
ovenous fistula at unusual sites. Ann Surg
1965;161:908-920.

Dameron TB Jr: False aneurysm of femoral pro-
fundus artery resulting from internal-fixation
device (screw) J Bone Joint Surg 1964;46A:577-580.

De Takats G, Pirani C: Aneurysms: General con-
siderations. Angiology 1954;5:173-208.

Dillard BM, Nelson DL, Norman HG: Review of 85
major traumatic arterial injuries. Surgery 1968;
63:391-395.

DrapanasT, Hewitt RL, WeichertRF III, Smith AD:
Civilian vascular injuries: A critical appraisal of
three decades of management. Ann Surg 1970;
172:351-360.

Eisenbrey AB: Arteriovenous aneurysm of the sup-
erficial femoral vessels.JAMA 1913;61:2155-21 57.

Elkin DC: Arteriovenous aneurysm. Surg Gynecol
Obstet 1945;80:217-224.

Elkin DC: Traumatic aneurysm: the Matas

Operation 57 years after. Surg Gynecol Obstet

1946;82:1-12.
Elkin DC, Banner EA: Arteriovenous aneurysms

following surgical operations. JAMA 1946;131:

1117-1119.

Elkin DC, DeBakey ME: Vascular surgery in World
War II. Washington, DC, US Government
Printing Office, 1955.

Engleman RM, Clements JM, Herrmann JB: Stab
wounds and traumatic false aneurysms in the
extremities. J Trauma 1969;9:77-87.

Ferguson WM: Arteriovenous aneurysm following
osteotomy for genu valgum. Lancet 1914;1:532.

Freeman NE, Shumacker HB Jr: Vascular surgery.
In Elkin DC, DeBakey ME (eds): Washington,
DC, US Government Printing Office, 1955.

Gaspard DJ, Caspar MR: Arteriovenous fistula after
Fogarty catheter thrombectomy. Arch Surg
1972;105:90-92.

Hallowell. Extract of a letter from Mr. Lambert,
surgeon at Newcastle upon Tyne, to Dr. Hunter,
giving an account of new method of treating an
aneurysm. Med Obser Inq 1762;30:360.

Halsted W: Discussion in Bernheim, BM. Bull Johns
Hopkins Hosp 1916;27:93.

Harris JD: A case of arteriovenous fistula following
closed fracture of tibia and fibula. Br J Surg
1963;50:774-776.

Heaton LD, Hughes CW, Rosegay H, et al: Military
surgical practices of the United States Army in
Vietnam. In Current Problems in Surgery.
Chicago, Year Book Medical Publishers, 1966.

Hershey FB. Secondary repair of arterial injuries.
Am Surg 1961;27:33-41.

Hewitt RL, Collins DJ: Acute arteriovenous
fistulas in war injuries. Ann Surg 1969;169:447-
449.

Hewitt RL, Smith AD, Drapanas T: Acute traumatic
arteriovenous fistulas. J Trauma 1973;13:901-906.

Holman E: Arteriovenous Aneurysms: Abnormal
Communication between the Arterial and
Venous Circulations. New York, Macmillan, 1937.

Holman E: Clinical and experimental observations
on arteriovenous fistulae. Ann Surg 1940;112:
840-875.

Holman E: Contributions to cardiovascular physi-
ology gleaned from clinical and experimental
observations of abnormal arteriovenous com-
munications. J Cardiovasc Surg 1962;3:48-63.

Holman E: Abnormal arteriovenous communica-
tions. Great variability of effects with particular

ch24.qxd 4/16/04 3:26 PM Page 523

24 • ARTERIOVENOUS FISTULAS AND TRAUMATIC FALSE ANEURYSMS

523

reference to delayed development of cardiac
failure. Circulation 1965;32:1001-1009.

Holman E: Abnormal Arteriovenous Communi-
cations: Peripheral and Intracardiac, Acquired
and Congenital, 2nd ed. Springfield, 111, Charles
C Thomas, 1968.

Holman EF: Physiology of an arteriovenous fistula.
Arch Surg 1971;7:64-82.

Hughes CW: Acute vascular trauma in Korean War
casualties: An analysis of 180 cases. Surg Gynec
Obstet 1954;99:91-100.

Hughes CW,Jahnke EJJr: The surgery of traumatic
arteriovenous fistulas and aneurysms: A five-year
follow up study of 215 lesions. Surg Clin North
Am 1958;148:790-797.

Hunt TK, Leeds FH, Wanebo HJ, Blaisdell FW:
Arteriovenous fistulas of major vessels of the
abdomen. J Trauma 1971 ;1 1 :483-493.

Hunter W: The history of an aneurysm of the aorta,
with some remarks on aneurysms in general. Med
Obs Soc Phys Lond 1757;1:323.

Hunter W: Further observations upon a particu-
lar species of aneurysm. Med Obs Soc Phys Lond
1762;2:390.

Johnson G Jr, Blythe WB: Hemodynamic effects of
arteriovenous shunts used for hemodialysis.
Ann Surg 1970;171:715-723.

Johnson GJr, Peters RM, Dart CH Jr: A study of
cardiac vein negative pressure in arterio-
venous fistula. Surg Gynecol Obstet 1967;1 24:82-
86.

Lai MD, Hoffman HB, Adamkiewicz JJ: Dissecting
aneurysm of internal carotid artery after non-
penetrating neck injury. Acta Radiol Diag
1966;5:290-295.

Lester J: Arteriovenous fistula after percutaneous
vertebral angiography. Acta Radiol Diag
1966;5:337-340.

LeVeen H, Cerruti M: Surgery of large inaccessible
arteriovenous fistulas. Ann Surg 1963;158:285-
289.

Lewis T: The adjustment of blood flow to the
affected limb in arteriovenous fistula. Clin Sci
1940;4:277-285.

Lexer E: Die ideale operation des arteriellen und
des arteriell-venosen aneurysma. Arch Klin Chir
1907;83:459-477.

Lord R, Ehrenfeld W, Wylie EJ: Arterial injury from
the Fogarty catheter. Med J Aust 1968;2:70-71.

Matas R: Traumatic aneurysm of the left
brachial artery — Incision and partial excision of
sac: Recovery. Phil Med News 1888;53:462-466.

Matas R: Traumatic arteriovenous aneurysms of the
subclavian vessels, with an analytical study of
fifteen reported cases, including one operated.
Trans Am Surg Assoc 1901;19:237.

Matas R: An operation for radical cure of aneurysm
based on arteriography. Ann Surg 1903;37:161-
196.

Matas R: Recent advances in the technique of
thoracotomy and pericardiotomy for wounds of
the heart. South Med J 1908;1:75-81.

Meyer TJ, Slager R: False aneurysm following
subtrochanteric osteotomy. J Bone Joint Surg
1964;46:581-582.

Muller WJ, Goodwin W: Renal arteriovenous fistula
following nephrectomy. Ann Surg 1956;144:240-
244.

Murphy J: Resection of arteries and veins injured
in continuity end-to-end suture. Exp Clin Res
Med Rec 1897;51:73-104.

NakanoJ, DeSchryver C: Effects of arteriovenous
fistula on systemic and pulmonary circulations.
AmJ Physiol 1964;207:1319.

Nicoladoni C: Phlebarteriectasie der rechten
oberen extremitat. Arch Klin Chir 1875;18:252.

Norris G: Varicose aneurysm at the bend of the
arm: Ligature of the artery above and below the
sac; secondary hemorrhages with a return of the
aneurysm thrill on the tenth day; cure . AmJ Med

Sci 1843;5:17.

Osier W: Case of arterio-venous aneurysm of the
axillary artery and vein of 1 4 years duration . Ann
Surg 1893;17:37-40.

Osier W: Report of a case of arteriovenous
aneurysm of the thigh. Johns Hopkins Hosp Bull
1905;16:119.

Osier W: Remarks on arteriovenous aneurysm.
Lancet 1915;1:949.

Pate J, Sherman R, Jackson T, Wilson H: Cardiac
failure following traumatic arteriovenous fistula:
A report of 14 cases. J Trauma 1965;5:398-
403.

Patman R, Poulos E, Shires G: The management
of civilian arterial injuries. Surg Gynecol Obstet
1964;118:725-738.

Petrovsky B, Milinov O: "Arterialization" and
"venization" ofvessels involved in traumatic arte-
riovenous fistulae: Aetiology and pathogenesis
(an experimental study). J Cardiovasc Surg
1967;8:396-407.

Pick T: On partial rupture of arteries from exter-
nal violence. St George's Hosp Rep (Lond)
1873:6:161.

ch24.qxd 4/16/04 3:26 PM Page 524

524

V • SPECIAL PROBLEMS AND COMPLICATIONS

Pick T: A clinical lecture of a case of arteriovenous
aneurysm. Lond Med Times Gaz 1883;2:677.

Pridgen W, Jacobs J: Postoperative arteriovenous
fistula. Surgery 1962;51:205.

Ranshoff J: Arteriovenous aneurysm of the supe-
rior thyroid artery and vein. Surg Gynecol
Obstetl935;61:816.

Reid M: The effect of arteriovenous fistula upon
the heart and blood vessels: An experiment and
clinical study. Bull Johns Hopkins Hosp
1920;31:43-50.

Reid M: Abnormal arteriovenous communica-
tions. Acquired and congenital, II. The orgin and
nature of arteriovenous aneurysms, cirsoid
aneurysms and simple angiomas. Arch Surg
(Chicago) 1925;10:996-1009.

Reid M, McGuire J: Arteriovenous aneurysm. Ann
Surg 1938;108:643-693.

Rhodes G, Cox C, Silver D: Arteriovenous fistula
and false aneurysm as the cause of consumption
coagulopathy. Surgery 1973;73:535-540.

Rich NM, Hobson RW II, Collins GJ Jr: Traumatic
arteriovenous fistulas and false aneurysms:
A review of 558 lesions. Surgery 1975;78:817-
828.

Rob CG, Battle S: Arteriovenous fistula following
the use of the Fogarty balloon catheter. Arch Surg
1971;102:144-145.

Sachtello C, Ernst CB, Griffen WJ: The acute
ischemic upper extremity: Selected manage-
ment. Surgery 1974;76:1002.

Sako Y, Varco R: Arteriovenous fistula: Results of
management of congenital and acquired forms,
blood flow measurements and observations on
proximal arterial degeneration. Surgery 1970;67:
40-61.

Schenk WJ, Bahn RA, Cordell A, Stephens J: The
regional hemodynamics of acute experimental
arteriovenous fistulas. Surg Gynecol Obstet 1957;
105:733.

Schwartz A: The historical development of methods
of hemostasis. Surgery 1958;44:604.

Seeley S: Vascular surgery at Walter Reed Army
Hospital. US Armed Forces Med J 1954;8.

Seeley S, Hughes CW, Cooke F, Elkin DC: Traumatic
arteriovenous fistulas and aneurysms in war
wounded. Am J Surg 1952;83:471-479.

Shumacker HBJr: Incisions in surgery of aneurysm:
With special reference to explorations in the
antecubital and popliteal fossae. Ann Surg
1946;124:586-598.

Shumacker HB Jr: Problem of maintaining the
continuity of artery in surgery of aneurysms and
arteriovenous fistulae; notes on the development
and clinical application of methods of arterial
suture. Ann Surg 1948;127:207-230.

Shumacker HBJr, Carter KL: Arteriovenous fistu-
las and false aneurysms in military personnel.
Surgery 1946;20:9-25.

Shumacker HBJr, Stahl N: A study of the cardiac
frontal area in patients with arteriovenous
fistulas. Surgery 1949;26:928-944.

Shumacker HBJr, Wayson EE: Spontaneous cure
of aneurysms and arteriovenous fistulas, with
some notes on intravascular thrombosis. Am J
Surg 1950;79:532-544.

Singh I, Gorman JF: Vascular injuries in closed
fractures near junction of middle and lower
thirds of the tibia. J Trauma 1972;12:592-598.

Smith L, Foran R, Caspar MR: Acute arterial injuries
of the upper extremity. AmJ Surg 1963;106:144-
151.

Soubbotitch V: Military experiences of traumatic
aneurysms. Lancet 1913;2:720-721.

Stewart F: Arteriovenous aneurysm treated by
angiography (angiorrhaphy) . Abb Surg 1 91 3;57:
247-254.

Vollmar J, Krumhaar D: Surgical experience with
200 traumatic arteriovenous fistulae. In Hiertonn
T, Rybeck B (eds): Traumatic Arterial Lesions.
Stockholm, Forsvarets Forskningsanstalt, 1968.

White J, TalbertJ, HallerJAJr: Peripheral arterial
injury in infants and children. Ann Surg
1968;167:757-766.

ch25.qxd 4/16/04 3:22 PM Page 525

Thromboembolic
Complications in
Trauma Patients

M. MARGARET KNUDSON

HISTORICAL PERSPECTIVES

PATHOPHYSIOLOGY

CLINICAL EPIDEMIOLOGY AND RISK FACTOR ANALYSIS

PROPHYLACTIC MEASURES
Mechanical Prophylactic Devices
Unfractionated Heparin
Low-Molecular-Weight Heparin
Prophylactic Vena Cava Filters

DIAGNOSISANDTREATMENTOFPOST-TRAUMATICTHROMBOEMBOLIC
COMPLICATIONS

OUTCOMES RESEARCH IN PREVENTION OF THROMBOEMBOLISM IN

TRAUMA PATIENTS

CURRENT RECOMMENDATIONS AND FUTURE DIRECTIONS

HISTORICAL PERSPECTIVES

In the 1934 volume of the American Journal of
Pathology, McCartney initially suggested that
there was an association between trauma and

death from pulmonary embolism (PE), and
that this association was particularly strong in
patients with lower extremity fractures. This
observation was followed by a number of
autopsy studies that not only confirmed the
relationship between injury and throm-

525

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526

V • SPECIAL PROBLEMS AND COMPLICATIONS

boembolic complications but also further
suggested that these thromboembolic events
were rarely diagnosed premortem. These
preliminary studies stimulated the sentinel
work by Freeark, Boswick, and Fardin (1967) ,
who performed venograms on 124 trauma
patients, demonstrating venous thrombosis in
35% of fracture patients. Thrombus forma-
tion was observed within 24 hours of injury
and involved both the injured and the unin-
jured extremity. More than two thirds of the
patients with roentgenographic evidence of
deep venous thrombosis (DVT) had no symp-
toms or physical findings to suggest its occur-
rence. These authors were among the first to
advocate studies to examine the effectiveness
of prophylactic measures in reducing postin-
jury thromboembolism.

PATHOPHYSIOLOGY

The basic factors leading to the development
of venous thrombosis have long been defined
by the Virchow triad, which includes stasis,
endothelial damage, and a prothrombotic
state. In the microcirculation, a series of steps
linking thrombosis and inflammation has
been suggested. This inflammatory process
involves platelets, neutrophils, monocytes,
and substances released from the activated
platelets and neutrophils, such as adenosine
diphosphate, neutrophil-activating pep tide-2,
and cathepsin G. More recently, direct injury
to the venous endothelium, induced by the
venodilation that occurs under anesthesia, has
been implicated as the initiating step in this
inflammatory process. The exposed suben-
dothelial surface acts as a nidus for platelets
and leukocytes, thus setting the stage for clot
formation.

Trauma patients are at risk for throm-
boembolic complications for a number of
reasons. Trauma patients are normally in a
hypercoagulable state by the third day after
trauma and often have depressed levels of
an ti thrombin. Most trauma patients are immo-
bilized for at least some period, and many are
paralyzed to facilitate respiratory care or sec-
ondary to neurologic injuries. Additionally,
many trauma patients have direct venous

injuries either associated with fractures or fol-
lowing penetrating trauma. We have detected
lower extremity thrombi by duplex sono-
graphy within 12 hours of injury, and other
investigators have documented that 6% of
post-traumatic pulmonary emboli occur on
day 1 following injury. Many of these injured
patients are young and have no known pre-
existing risk factors for thromboembolism. It
is thus imperative that research in this field
be directed toward understanding both the
pathogenesis and the prevention of post-
traumatic thromboembolism.

CLINICAL EPIDEMIOLOGY AND
RISK FACTOR ANALYSIS

The overall incidence of post-traumatic DVT
is estimated to be between 10% and 20% in
patients who are not receiving any method of
prophylaxis. The actual incidence will vary
with such factors as the age of the patient, the
nature of the injuries, the geographic loca-
tion, and the method used to detect occult
DVT. In addition to its association with
potentially fatal PE, undetected (and thus
untreated) DVT can also result in permanent
postphlebitic changes. PE occurs in at least
1% to 2% of injured patients, with an associ-
ated mortality as high as 50%. The true inci-
dence of PE is probably much higher, as most
PEs in trauma patients are clinically silent.
Additionally, a practical method of screening
high-risk trauma patients for PE has not
been developed. Importantly, many of the
deaths attributable to PE occur in trauma
patients who would otherwise recover fully
from their injuries. This recognition has
inspired many clinical investigators to attempt
to describe the risk factors associated with the
development of post-traumatic thromboem-
bolic complications as the first step in pre-
venting them.

As mentioned, early autopsy studies docu-
mented the association between injured
patients with fractures and deaths from PE.
Burned patients were also found to be at high
risk for thromboembolism. More recently,
various investigators have identified increased
age, the presence of head injury, spinal cord

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25 • THROMBOEMBOLIC COMPLICATIONS

527

injury with paralysis, and prolonged immo-
bilization as important risk factors for post-
traumatic thromboembolism. Direct venous
injury, either resulting from the trauma itself
or induced by large-caliber venous access
devices, has also been implicated. Burch and
colleagues (1990) were among the first to
warn of the risk of DVT and/or fatal PE fol-
lowing ligation or repair of penetrating iliac
vascular injuries. A report from Sue, Davis,
and Parks (1995) supports the concept that
direct iliac venous injuries are associated
with a significant risk for thromboembolic
complications.

In a recent study that used venography
to identify distal (calf) and proximal (thigh/
pelvic) lower extremity DVT, the incidence of
DVT was found to be 54% in patients with
head injuries and 62% in those with spinal
injuries. Sixty-nine percent of injured patients
with lower extremity or pelvic fractures who
underwent venography had evidence of DVT
within 14 to 21 days after the injury. The overall
incidence of proximal DVT was 18%. Prophy-
laxis against thromboembolism was not used
in any of the patients in this study.

A group of investigators dedicated to the
field of thromboembolic research in injured
patients recently collaborated in compiling a
risk factor assessment scale. The risk factors
included underlying conditions, iatrogenic
factors, injury-related factors, and age (Table
25-1) . Each factor was given a weight, based
on the perceived association with the devel-
opment of DVT/PE (i.e., a weight of 2 was
relatively low risk and a score of 4 represented
the highest risk factors) . When adding up the
weighted scores for each patient, a trauma
patient with a score of 5 or greater was con-
sidered at high risk for thromboembolic com-
plications and a candidate for prophylaxis.
Further research by this group, using a
prospective study, confirmed that five of these
factors were significantly associated with the
development of post-traumatic DVT. Patients
with one or more of these five factors had an
overall rate of DVT at 10% despite aggressive
prophylaxis. It should be noted that although
the authors of this particular study did not
find spinal cord injury to be a significant risk
factor, this likely represents a type II statisti-
cal error due to a low number of patients

TABLE 25-1

RISK ASSESSMENT PROFILE

Risk Factors Points

Assigned

Underlying condition

Obesity*

Malignancy

Abnormal coagulation

History of thromboembolism

Iatrogenic factors

Femoral venous lines

Transfusion > 4 units*

Operation > 2 hours*

Major venous repair

Injury-related factors

ChestAIS>2

Abdomen AIS > 2

Head AIS>2*

Spinal fractures

Glasgow Coma Scale score < 8

Severe lower extremity fracture*

Pelvic fracture

Spinal cord injury

Age (yr)

40-59

60-74

>75

'Factors found to be significantly associated with deep
venous thrombosis/pulmonary embolism on subsequent
prospective analysis.
AIS, Abbreviated Injury Severity Score.
From Greenfield LJ, Proctor MC, Rodriquez JL, et al: Post-
traumatic thromboembolic prophylaxis. J Trauma
1997;42:100-103.

(seven total) enrolled with this injury. All other
studies have included patients with spinal cord
injuries as among the highest risk patients,
with rates of DVT approaching 80% and PE
rates at 5%. In fact, PE is one of the most
common causes of death following spinal cord
injury.

PROPHYLACTIC MEASURES

Definitive randomized controlled clinical
studies on prophylactic measures in trauma
patients with multiple injuries do not exist.
Unlike other surgical patients with isolated
disease (e.g., hip-replacement patients and

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V • SPECIAL PROBLEMS AND COMPLICATIONS

colectomy patients), the injured patients are
a heterogeneous group and difficult to "cat-
egorize." They can have isolated injuries or
any combination of injuries, making stratifi-
cation extremely difficult. Additionally, many
patients are excluded from one type of pro-
phylactic measure or another by the very
nature of their injuries. For example, bilat-
eral leg compression devices cannot be used
with external fixators, and some head-injured
patients cannot receive anticoagulants. Con-
sidering all of these factors, a large multicenter
trial with thousands of patients and defined
endpoints would be needed to definitively
answer the questions of which trauma patients
need prophylaxis and which prophylactic
measures are effective for a given combina-
tion of traumatic injuries. To date, no funding
source for this important study has been iden-
tified. However, several smaller prospective
studies on injured patients have been
attempted, and recommendations can be
made based on the best available data.

Prophylactic measures can generally be
divided into two categories: mechanical and
pharmacologic. Mechanical measures are
aimed at reducing stasis, whereas drug therapy
attempts to alter some part of the extrinsic
clotting system. An extreme example of a
mechanical measure is a "prophylactic" vena
cava filter (VCF) , placed before the develop-
ment of PE/DVT in a high-risk patient. Each
of these methods is described in the follow-
ing sections.

Mechanical Prophylactic
Devices

The mechanical devices, which vary from a
simple elastic stocking to a full-length sequen-
tial compression sleeve, are attractive because
of their safety. Few if any complications can
be attributed to the use of these devices if they
are properly fit according to the directions
supplied by the manufacturer for each patient
and used appropriately. The only real "com-
plication" is the lack of compliance in patients
who are awake enough to remove the devices.
Despite their widespread use, however, there
are no level I trials demonstrating protection

from DVT/PE in trauma patients using any
type of mechanical device. Knudson and col-
leagues (1991) demonstrated that the sequen-
tial pneumatic compression device (SCD) was
more effective than no prophylaxis in head-
injured patients, but not in trauma patients
with other injuries. In another study, which
included trauma patients without orthopedic
injuries, 62 were randomized to wear calf-thigh
sequential pneumatic compression and 62
wore plantar compression devices ("foot
pumps") only. DVT developed in 21% of the
patients wearing the plantar device and in
6.5% of those wearing the calf-thigh device
(P=.009). Studies by Ginzburg and col-
leagues (2001) and Knudson and colleagues
(1996) have demonstrated clearly that com-
pression devices are less effective than
low-molecular-weight heparin (LMWH) in
preventing thromboembolic complications
after trauma. No data exist on the use of
mechanical devices combined with anticoag-
ulant therapy in patients with multiple injuries,
and there is no documented benefit in com-
pressing only one leg or an arm, in hopes of
stimulating fibrinolytic activity. Based on the
current available data, trauma patients who
are considered at risk for DVT/PE and who
cannot safely be given an anticoagulant drug
should receive bilateral whole leg pneumatic
compression. Anything short of that should
be considered inadequate protection.

Unfractionated Heparin

Of all the methods of prophylaxis, low-dose
unfractionated heparin (LDUH, 5000 units
given subcutaneously 2 hours before surgery
and then every 12 hours for 7 days postoper-
atively) has been the most widely studied
and the most effective method of preventing
thromboembolic complications in surgical
patients. In 20 trials in which more than 8000
general surgery patients were enrolled, LDUH
reduced the incidence of leg DVT from 25%
to 8% and consistently reduced the incidence
of/atoZPE by 50%. Unfortunately, in patients
undergoing elective hip and knee surgery, in
which the risk of proximal DVT is more than
30% and fatal PE up to 6%, LDUH does not

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25 • THROMBOEMBOLIC COMPLICATIONS

529

offer sufficient protection. Similarly, in trauma
patients, LDUH does not appear to be any
more effective than no prophylaxis, and its
use in trauma patients as the sole method of
protection should be discouraged.

Low-Molecular -Weight Heparin

LMWHs are fragments of unfractionated
heparin, induced by a controlled enzymatic
or chemical depolymerization process that
yields chains of glycosaminoglycans with a
mean molecular weight of around 5000.
These shorted chains retain their anticoagu-
lant activity by their ability to interact with
antithrombin but have relatively less activity
against thrombin and platelets. LMWH has a
more predictable anticoagulant response than
LDUH because of increased bioavailability,
longer half-life, and dose-independent clear-
ance. Thus, LMWH results in improved anti-
coagulant activi ty while causing less bleeding.
In hip and knee replacement surgery, LMWH
has been demonstrated to be highly effec-
tive in preventing DVT/PE even when given
postoperatively.

To date, only the LMWH enoxaparin
(Lovenox) has been studied in trauma
patients. However, two large prospective
studies have documented the effectiveness of
the LMWH enoxaparin in preventing post-
traumatic thromboembolism. Geerts and col-
leagues (1994) compared LDUH with LMWH
(30 mg given subcutaneously every 1 2 hours) ,
both started within 36 hours after injury, in
344 major trauma patients without frank
intracranial bleeding. Bilateral contrast venog-
raphy was performed between postinjury days
10 and 14. The proximal DVT rate was 15%
with LDUH and 6% with LMWH (risk reduc-
tion with LMWH of 58%, P= .01) . The overall
rate of major bleeding was less than 2% with
no significant differences between the groups,
thus demonstrating both the efficacy and the
safety of LMWH in trauma patients. The study
by Knudson and colleagues (1996) included
372 patients with multiple trauma and com-
pared LMWH to mechanical compression.
Patients were followed with serial duplex ultra-
sound examinations. Of the 120 patients who

were randomized to receive LMWH, only 1
developed DVT by ultrasound (0.8%). In
the mechanical compression group (199
patients), the incidence of DVT was 2.5%.
Only one patient had a major bleeding com-
plication with LMWH. Although LMWH was
withheld in patients with injuries to the spleen
and/or liver who were being managed without
operation, recent data suggest that LMWH can
be given safely in these situations, without
inducing bleeding. In patients with major
head injury and evidence of bleeding on a
head computed tomographic (CT) scan,
LMWH is generally withheld until the injury
has been demonstrated to be stable. For now
then, LMWH is considered the most effective
form of prophylaxis against DVT/PE in
trauma patients and it should be initiated once
bleeding is under control and early postin-
jury coagulopathy has been corrected.

Prophylactic Vena Cava Filters

The effectiveness of a VCF in the prevention
of PE in patients with proximal DVT has been
well established. Traditionally, these filters
have been placed in patients with acute prox-
imal DVT or a recent PE who have a con-
traindication to anticoagulation. Filters can
be placed percutaneously with relative ease
and have long-term patency rates of more than
95%. Some trauma surgeons have advocated
the prophylactic placement of a VCF in high-
risk trauma patients, especially in those
patients who have relative contraindications
to anticoagulation. A recently described tech-
nique of placing Inferior Vena Cava (IVC)
filters at the bedside using ultrasound guid-
ance makes it even easier to advocate for an
aggressive approach in critically injured
patients.

The problems associated with the use of
IVC filters in trauma patients include the
following:

1. Recurrent PE: Despite the presence of a
filter, recurrent PE occurs in 3% of trauma
patients. This complication may result
from filter tilt or strut malposition and has
been fatal in a few reported injured
patients.

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V • SPECIAL PROBLEMS AND COMPLICATIONS

2. -DVT: An IVC filter does nothing to prevent
DVT and, in fact, may promote thrombo-
sis. In studies reported by Rodriquez and
colleagues (1996), 10% of injured patients
who had a prophylactic filter demon-
strated caval thrombosis and 50% of these
patients had long-term lower extremity
edema.

3. Permanence: Because all currently mar-
keted VCFs are designed to be permanently
implanted, patients are at risk for compli-
cations for their lifetime. In addition to
filter-associated thromboembolic events
and filter migration, complicationswith vas-
cular access procedures including trapping
of the guidewire in the filter have been
described.

4. Timing: We and others have documented
PE as early as 12 to 24 hours postinjury. In
the study by Owings and colleagues (1997) ,
4 (6%) of 63 patients had embolism within
1 day of their trauma. It would be highly
unlikely that a prophylactic filter would be
placed within such a narrow time frame in
patients with multiple trauma who are in
need of various other procedures to address
their injuries.

No data support the routine use of pro-
phylactic VCFs in high-risk trauma patients.
Their use should be restricted to the occa-
sional injured patients who are at prolonged
exceedingly high risk for PE, as described in
Table 25-1, and in whom no other prophy-
lactic measures can be used.

DIAGNOSIS AND TREATMENT
OF POST-TRAUMATIC
THROMBOEMBOLIC
COMPLICATIONS

Most venous thrombi are clinically silent, pre-
sumably because they do not totally obstruct
the vein and because of the existence of col-
lateral circulation. Even when symptoms do
develop, they are nonspecific and may include
pain, swelling, or fever. In trauma patients,
these symptoms may be totally overlooked or
attributed to bone or soft tissue injury. In most

trauma patients, DVT is clinically occult. The
symptoms associated with PE depend on the
quantity of the embolus involved and the car-
diopulmonary status of the patient. Signs and
symptoms may include chest pain, dyspnea,
tachypnea, anxiety, cyanosis, and fever. Arte-
rial blood gas analyses may reveal hypoxia and
an acute decrease in carbon dioxide. Unfor-
tunately, the first sign of PE in many injured
patients is sudden death.

For many years, the standard diagnostic test
for DVT was ascending phlebography (venog-
raphy) . Venography can reliably detect both
proximal (pelvic, thigh, popliteal) and distal
(calf) thrombosis. Side effects include aller-
gic reactions to the contrast, renal toxicity, and
a 2% to 3% incidence of contrast-induced
DVT. Additionally, venography cannot easily
be repeated and is thus impractical for sur-
veillance in high-risk patients. Thrombi have
also been visualized incidentally during com-
puterized scanning of the abdomen or pelvis
performed for other indications. Recently,
duplex ultrasound (color flow Doppler [CFD]
imaging) has become the method of choice
for detecting DVT in many centers. CFD
imaging allows information on flow to be over-
laid onto the real time two-dimensional image
of the vein. Venous sonography is 90% sensi-
tive (100% specific) in detecting proximal
DVT in symptomatic patients, but the sensi-
tivity drops significantly in asymptomatic
patients, most likely related to the small size
of the clot in this latter group of patients. The
most reliable sign of DVT is lack of com-
pressibility of the vein on ultrasound imaging
(Fig. 25-1). Other signs of acute DVT include
the loss of flow augmentation with the Val-
salva maneuver or with muscle contraction and
the presence of a homogenous thrombus with
low echogenicity. The involved vein is dis-
tended and noncompressible, with decreased
or absent flow and no collateral channels.
The limitations of color duplex sonography
include the difficulty in imaging pelvic veins
and the fact that the quality of the examina-
tion is highly dependent on the experience
and expertise of the sonographer.

We have performed venous ultrasound
examinations on hundreds of trauma patients
during our research studies investigating
thromboembolism prophylaxis. DVT detected

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25 • THROMBOEMBOLIC COMPLICATIONS

531

■ FIGURE 25-1

Appearance of a clot in the iliac vein by color
flow duplex sonography. ■

via ultrasound was the main outcome measure
in three prospective studies on trauma patients
at our center, and we have been impressed
with our ability to detect clinically silent DVT
with surveillance scanning. Our results have
been confirmed by other investigators, in
which color flow imaging surveillance in
high-risk trauma patients revealed an overall
DVT incidence of between 10% and 18%.
Interestingly, up to 30% of the cases of DVT
involved the upper extremity, an area not rou-
tinely studied with venography. Some authors
have argued that there is no need to detect
clinically occult DVT, and that the number of
cases detected does not justify the expense of
surveillance. Mostwould agree, however, that
given the incomplete protection offered by
available methods of prophylaxis, some type
of surveillance is warranted in extremely high-
risk trauma patients (see Fig. 24-3) . Treatment
of occult DVT is most likely the key factor
contributing to the low incidence in of PE
in our center and in other centers that
perform venous imaging liberally in trauma
patients.

Pulmonary angiography remains the gold
standard for the diagnosis of pulmonary
emboli. Ventilatory-perfusion scans have not
been useful in trauma patients, primarily
because few trauma patients at risk for PE have
anormal chestx-rayfilm. Additionally, the risks
associated with full-dose anticoagulation in
injured patients are significant, and the diag-
nosis must be secured by the most sensitive
and specific study. Pulmonary angiography

requires transportation to the radiology suite,
and there is the potential for allergic reactions,
contrast-induced nephropathy, or vascular
injuries during the procedure. Combining
noninvasive diagnostic tests has been advo-
cated for critically ill patients who cannot
be moved out of the intensive care unit.
For example, the combination of a positive
ultrasound of the lower extremities and a
transthoracic echocardiogram showing right
ventricular hypokinesis is pathognomonic for
PE. Whole-blood D-dimer levels are always ele-
vated in patients with thrombosis, but this test
is not very specific. Still, the combination of
a normal D-dimer level and a negative venous
ultrasound examination virtually rules out PE.
Recently, calculation of the late pulmonary
dead space fraction, calculated from the C0 2
expirogram, was found to be valuable as a
bedside screening technique for detection
ofPE.

Spiral CT of the chest with contrast is
another excellent screening tool for PE. This
study is most sensitive (90%) in detecting
emboli that are located in the proximal pul-
monary vascular tree. In the presence of a pos-
itive CT scan, anticoagulant therapy should
be initiated immediately (Fig. 25-2). If more
distal emboli are suspected and the initial CT
scan is negative, pulmonary angiography
should be performed. In a recent analysis of
15 combinations of diagnostic tests (spiral CT,
lower limb ultrasonography, ventilation-
perfusion scintigraphy, pulmonary arteri-
ography, and D-dimer plasma levels), the
combination of spiral CT and lower limb
ultrasonography was found to be the least
morbid and the most cost-effective combina-
tion of studies per life saved.

Heparin remains the first line of treatment
for both DVT and PE. In patients with DVT,
a bolus of heparin (5000 units) is given imme-
diately, followed by a continuous drip of
18U/kg per hour. The heparin dose is
adjusted to keep the partial thromboplastin
time twice normal or between 60 and 80
seconds. For PE, especially when accompanied
by hypoxia, a bolus of 10,000 units of heparin
is initiated, followed by a continuous drip.
Alternatively, a fully anticoagulating dose of
enoxaparin (lmg/kg given subcutaneously
twice daily) has been found to be effective

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V • SPECIAL PROBLEMS AND COMPLICATIONS

■ FIGURE 25-2

A, Spiral computed tomographic scan of the chest demonstrating pulmonary emboli in the right
pulmonary artery. B, Lung window on the same patient. Note the area of infarction in the right lower
lobe. ■

treatment for both DVT and PE. The advan-
tage of enoxaparin is the ability to treat DVT
as an outpatient with twice-daily injections
performed by the patient. We have used this
approach in patients with venous injuries who
are anticoagulated for a short period (1 to
2 months) . For documented cases of DVT/PE
however, we advocate anticoagulation for
6 months, and this is best accomplished by
converting the patient from heparin (either
unfractionated or LMWH) to Coumadin
before discharge from the hospital. In patients
with documented DVT and/or PE who cannot
receive full-dose anticoagulation because of
the nature of their injuries, a VCF should be
placed. On rare occasions, trauma patients
with life-threatening PE and persistent hypoxia
may be candidates for transvenous catheter
embolectomy.

OUTCOMES RESEARCH IN
PREVENTION OF
THROMBOEMBOLISM IN
TRAUMA PATIENTS

As mentioned, no large-scale, prospective, ran-
domized trials that definitively establish the
safety and effectiveness of any prophylactic

measures have been performed in trauma
patients. Several investigators have attempted
to review all of the data available to assist in
the development of outcome-driven guide-
lines for DVT/PE prophylaxis in injured
patients. Brasel, Borgstrom, and Weigelt
(1997) used decision-tree analysis to compare
three approaches for PE prevention in trauma
patients: no intervention, surveillance ultra-
sound, and VCF. The probabilities in each
subtree were taken from available published
data. Their findings support the use of sur-
veillance duplex ultrasound examinations,
with a cost/PE prevented of $46,300 compared
to $93,700 per PE prevented with the use of
a prophylactic VCF. However, these costs were
based on the assumption that the filter was
placed in the radiology suite and that the
patient was hospitalized for at least 2 weeks.
A VCF may be more cost-effective in patients
requiring prolonged hospitalization.

Three other groups have attempted to
develop cost-effective guidelines for DVT
prevention in trauma patients by employing
Cochrane-type principles in literature reviews.
These groups include the Eastern Association
for the Surgery of Trauma (EAST) , the Amer-
ican College of Chest Physicians (ACCP) , and
the Southern California Evidence-Based Prac-
tice Center (SCEPC). The recommendations
developed by each of these groups are

ch25.qxd 4/16/04 3:23PM Page 533

25 • THROMBOEMBOLIC COMPLICATIONS

533

TABLE 25-2

SUMMARY OF RECOMMENDATIONS FOR THROMBOEMBOLIC PROPHYLAXIS FOR
THREE INDEPENDENT REVIEWS

Group

LDUH

SCD

LMWH

Foot Pump

IVC Filter

Ultrasound

EAST
ACCP
SCEPC

N/R

Equal to LMWH

Level II
Level II
R

Level II
Level 1

Equal to LDUH

Level III

N/A

Level II
Level III
No data

Level II
Level III
N/A

ACCP, American College of Chest Physicians; EAST, Eastern Association for the Surgery of Trauma; IVC, Inferior Vena Cava;
LDUH, low-dose unfractionated heparin; LMWH, low-molecular-weight heparin; N/R, not recommended; R, recommend use;
SCD, sequential pneumatic compression device; SCEPC, Southern California Evidence-Based Practice Center.

summarized in Table 25-2. The EAST guide-
lines recommend LMWH for patients with one
ofthe following injury patterns: (1) pelvicfrac-
tures requiring operative fixation or pro-
longed bed rest (>5 days) ; (2) complex lower
extremity fractures (defined as open fractures
or multiple fractures in one extremity) requir-
ing operative fixation or prolonged bed rest
(>5 days) ; and (3) spinal cord injury with com-
plete or incomplete motor paralysis. SCDs
were recommended for high-risk patients with
head injuries, spinal cord injuries, or pelvis
or hip fractures. Foot pumps were given only
a level III recommendation, due to insufficient
data. Prophylactic VCFs in trauma patients
without established PE or DVT were recom-
mended only in patients who (1) could not
receive anticoagulation because of increased
bleeding risk and (2) who had one ofthe fol-
lowing injuries:

• Severe closed head injury (Glasgow Coma
Scale score <8)

• Incomplete spinal cord injury with para-
plegia or quadriplegia

• Complex pelvic fracture with associated
long bone fractures

• Multiple long bone fractures

These recommendations are based on class
II/III data. The ACCP recommendations are
similar to EAST. However, the SCEPC inves-
tigators concluded that there was no evidence
that any existing method of prophylaxis was
clearly superior to other methods or even to
no prophylaxis. They concluded that LMWH
was not superior to LDUH and they could

make no conclusions on the role of IVC filters,
based on their review of the literature.
Although I do not agree with the conclusions
drawn by the SCEPC investigators, I do agree
that a large, multicenter, prospective trial on
prophylactic methods in trauma patients is
long overdue.

CURRENT RECOMMENDATIONS
AND FUTURE DIRECTIONS

At the San Francisco General Hospital, we have
had a long-standing interest in the prevention
of thromboembolic complications in trauma
patients. Before implementing a standardized
protocol for DVT/PE prevention, our inci-
dence of DVT was 10% (established by sur-
veillance ultrasound scanning). Since 1992,
we have prospectively followed more than
12,000 patients for the clinical development
of DVT or PE and used a standardized man-
agement algorithm for DVT prophylaxis (Fig.
25-3) . Our overall incidence of DVT is 0.003%
and the PE rate is 0.002%. The death rate for
PE, however, was 17%. In a detailed audit of
our patients, we found that 20% ofthe time,
trauma clinical case managers had to inter-
vene to ensure that the house staff ordered
the proper prophylactic measure. All cases of
DVT/PE are thoroughly reviewed to assess
whether the protocol was implemented and
followed correctly. In our experience, in most
patients in whom thromboembolic compli-
cations occurred, prophylactic measures were
inappropriately withheld early in the patients'
postinjury course. Only one patient with PE

ch25.qxd 4/16/04 3:23PM Page 534

534

V • SPECIAL PROBLEMS AND COMPLICATIONS

■ FIGURE 25-3

Algorithm for deep venous
thrombosis prophylaxis in the
trauma patient from the San
Francisco General Hospital. ■

Trauma Patient Requiring Hospital Admission

Does patient have any risk factors for DVT?

Yes

> r

No indication for specific DVT
prophylaxis

Does the patient have
contraindication for Heparin?

Yes

Begin low-molecular-weight
Heparin within 36 hours

Does the patient have

contraindication for

(lower extremity) intermittent

pneumatic compression?

Yes

Begin intermittent pneumatic
compression (IPC)

Is the patient HIGH RISK

for DVT?

(multiple risk factors)

Yes

Apply bilateral foot pumps.
Consider serial monitoring
using color duplex scans.

Is the DVT risk permanent

or long term?

(e.g., spinal cord injury)

Yes

■

Apply bilateral foot pumps.

Monitor closely using serial

color duplex scans.

Consider placement of an

IVC filter and/or serial

color duplex scans.

fell outside of our established risk factors and
thus did not receive prophylaxis. We encour-
age other institutions to prospectively study
the guidelines in place at their institution, so
that high-quality, evidence-based outcome
data will be available for analysis.

Future investigations will include new and
potentially more effective drugs that target not
only the various steps in the coagulation
cascade, but perhaps even the venous wall
itself. One such agent, Aristra/Xantidar, a syn-
thetic pentasaccharide that acts as an indirect
inhibitor of factor Xa, has recently been shown
to be more effective than LMWH in the

prevention of DVT following orthopedic
surgery. In the area of mechanical prophylaxis,
a prototype removable IVC filter has been
developed. This Tulip filter can be used as
either a permanent or a temporary device and
has been removed from a small number of
patients as early as 5 days after insertion
without injuring the vena cava. A temporary
filter would obviously be more attractive in
young trauma patients in whom the risk of
developing thromboembolic complications is
also temporary. Armed with an appreciation
for and a better understanding of throm-
boembolism in trauma patients, and coupled

ch25.qxd 4/16/04 3:23PM Page 535

25 • THROMBOEMBOLIC COMPLICATIONS

535

with effective and safe prophylactic mea-
sures, we should be able to offer our future
trauma patients protection from both the mor-
bidity of DVT and the risk of a premature death
from PE.

REFERENCES

Anderson JT, OwingsJT, Goodnight JE: Bedside
noninvasive detection of acute pulmonary
embolism in critically ill surgical patients. Arch
Surg 1999;134:869-875.

Brasel KJ, Borgstrom DC, Weigelt JA: Cost-
effective prevention of pulmonary embolus in
high-risk trauma patients. J Trauma 1 997;42:456-
462.

Burch JN, Richardson RJ, Martin RR, Mattox KL:
Penetrating iliac vascular injuries: recent expe-
rience with 233 consecutive patients. J Trauma
1990;30:1450-1990.

Claget GP, Anderson FA, Geerts W, Heit JA,
Rnudson MM et al: Prevention of venous throm-
boembolism. Chest 1998;114:531S-560S.

Coon WW: Risk factors in pulmonary embolism.
Surg Gynecol Obstet 1976;143:385-390.

Elliott CG, Dudney TMN, Egger M, e t al: Calf-thigh
sequential pneumatic compression compared
with plantar venous pneumatic compression to
prevent deep-vein thrombosis after non-lower
extremity trauma. J Trauma 1999;47:25-32.

Freeark RJ, Boswick J, Fardin R: Posttraumatic
venous thrombosis. Arch Surg 1967;95:567-573.

Gearhart MM, Luchette FA, Proctor MA, et al: The
risk assessment profile score identified trauma
patients at risk for deep vein thrombosis. Surgery
2000;128:631-640.

Geerts WH, Code KI, Jay RM, et al: A prospective
study of venous thromboembolism after major
trauma. N EnglJ Med 1994;331:1601-1606.

Merli G, Geerts W, Ginzburg E, et al: for the Spinal
Cord Injury Thromboprophylaxis Investigators:
Prevention of venous thromboembolism in the
acute treatment phase after spinal cord injury:
A randomized multicenter trial comparing
low-dose heparin plus intermittent pneumatic
compression with Enoxaparin. J Trauma 2003;
54:1116-1126.

Knudson MM, Lewis FR, Clinton A et al: Preven-
tion of venous thromboembolism in trauma
patients. J Trauma 1994;37:480-487.

Knudson MM, Morabito D, Paiement GD, Shack-
leford S: Use of low-molecular-weight heparin

in preventing thromboembolism in trauma
patients. J Trauma 1996;41 :446-459.

McCartney JS: Pulmonary embolism following
trauma. Am J Pathol 1934;10:709-710.

Meredith JW, Young JS, O'Neil EA, et al: Femoral
catheters and deep venous thrombosis: a prospec-
tive evaluation with venous duplex sonography.
J Trauma 1993;35:187.

Millward SF, Bhargava A, Aquino J, et al: Gunther
Tulip filter: preliminary clinical experience with
retrieval. JVIR 2000;1 1 :75-82.

OwingsJT, Kraut E, Battistella F et al: Timing of
occurrence of pulmonary embolism in trauma
patients. Arch Surg 1997;132;862-867.

Roergs FB, Cipolli MD, Velmahos GC, et al: Prac-
tice guidelines for the prevention of venous
thromboembolism in trauma patients: The EAST
Practice Management Guidelines Work Group.
J Trauma 2002;53:142-164.

Rodriquez JL, Lopez JM, Proctor MC, et al: Early
placement of prophylactic vena caval filters in
injured patients at high risk for pulmonary
embolism. J Trauma 1996;40:797-804.

Rogers FB, Cipolle MD, Velmahos G, et al: Prac-
tice management guidelines for the preven-
tion of venous thromboembolism in trauma
patients: The EAST practice management
guidelines work group. J Trauma 2002;53(1):
142-164.

Rogers FB, Shackford ST, Ricci MA, et al: Routine
prophylactic vena cava filter insertion in severely
injured trauma patients decreases the incidence
of pulmonary embolism. J Am Coll Surg
1995;180:641-647.

Sevitt S, Gallagher N: Venous thrombosis and pul-
monary embolism: a clinico-pathological study
in injured and burned patients. Br J Surg
1960;48:475-488.

Sue LP, Davis JW, Parks SN: Iliofemoral venous
injuries: an indication for prophylactic caval filter
placement. J Trauma 1995;39:693-695.

Turpie AGG, Gallus AS, HoekJA: A synthetic pen-
tasaccharide for the prevention of deep vein
thrombosis after total hip replacement. N Engl
J Med 2001;344:619-625.

Van Erkel AR, van Rossum AB, Bloem JL, et al: Spiral
CT angiography for suspected pulmonary
embolism: a cost-effectiveness analysis. Radiol-
ogy 1996;201:29-36.

Velmahos GC, Kern JK, Chan LS et al: Prevention
of venous thromboembolism after injury: an
evidence-based report. J Trauma 2000:49:132-
144.

RE.qxd 4/16/04 3:19 PM Page 539

Rich's Historic Collection of
Vascular References

Aaland M, Bryan FC, Sherman R: Two dimensional echocardiogram in hemo-

dynamically stable victims of penetrating precordial trauma. Am Surg

1994;60:412-415.
Aarabi B, McQueen JD: Traumatic internal carotid occlusion at the base of the

skull. Surg Neurol 1978;10:233-236.
Abbe R: The surgery of the hand. N YMed J 1894.
Abbott JA, Cousineau M, Cheitlin M, et al: Late sequelae of penetrating cardiac

wounds. J Thorac Cardiovasc Surg 1978;75:510-518.
Abbott WM, Darling RC: Axillary artery aneurysms secondary to crutch trauma.

Am J Surg 1973;125:515-520.
Abdo F, Massad M, Slim M, et al: Wandering intravascular missiles: Report of

five cases from the Lebanon war. Surgery 1988;103:376-380.
Abdul-Razek MS, Mnaymneh W, Yacoubian HD: Acute injuries of peripheral

arteries with associated bone and soft tissue injury. J Trauma 1973;13:907-

910.
Abouljoud M: Arterial injuries of the thoracic outlet: A ten-year review. Am

Surgeon 1993;59:590-595.
Accola KD, Feliciano DV, Mattox KL, et al: Management of injuries to the supe-
rior mesenteric artery. J Trauma 1986;26:313-317.
Accola KD, Feliciano DV, Mattox KL, et al: Management of injuries to the

suprarenal aorta. Am J Surg 1987;154:613-618.
Adar R, Bass A, Walden R: Five years' experience in general and vascular surgery

in a university hospital. Ann Surg 1982;196:725-729.
Adar R, Nerubay J, Katznelson A: Management of acute vascular injuries. J

Cardiovasc Surg 1970;11:435-439.
Adar R, Schramek A, Khodadadi J, et al: Arterial combat injuries of the upper

extremity. J Trauma 1980;20:297-302.
Adebonojo SA: Management of chest trauma: A review. West Afr J Med 1993;

12:122-132.
Adinolfi MF, Hardin WD, O'Connell RC, Kerstein MD: Amputations after vas-
cular trauma in civilians. South Med J 1983;76:1241-1248.
Adkins RB Jr, Bitseff ELJr, Meacham PW: Abdominal vascular injuries. South

MedJ 1985;78:1152-1160.
Adkins RB, WhiteneckJM, Woltering EA: Penetrating chest wall and thoracic

injuries. Am Surg 1985;51:140-148.

539

RE.qxd 4/16/04 3:19 PM Page 540

540 VI • THE RICH REFERENCE COLLECTION

Agee CK, Metzler MH, Churchill RJ, Mitchell FL: Computed tomographic eval-
uation to exclude traumatic aortic disruption. J Trauma 1992;33:876-881.
Agnew D II: The Principles and Practice of Surgery. Philadelphia, JB Lippin-

cott Co, 1978.
Agrwal N, Shah PM, Clauss RH, et al: Experience with 115 civilian venous injuries.

J Trauma 1982;22:827-832.
Aitken RJ, Matley PJ, Immelman EJ: Lower limb vein trauma: A long-term

clinical and physiological assessment. Br J Surg 1989;76:585-588.
Akins CW, Buckley MJ, Daggett W, et al: Acute traumatic disruption of the

thoracic aorta: A ten-year experience. Ann Thorac Surg 1981;31:305-309.
Akins EW, Carmichael MJ, HillJA, Mancuso AA: Preoperative evaluation of he

thoracic aorta using MRI and angiography. Ann Thorac Surg 1987;44:499-

507.
Al Zharani HA: False aneurysm of the abdominal aorta after blunt trauma. Eur

J Vase Surg 1991;5:685-687.
Alberty RE, Goodfried G, Boyden AM: Popliteal artery injury with fracture dis-
location of the knee. Am J Surg 1981;142:36-40.
Albo D Jr, Christensen C, Rasmussen BL: Massive liver trauma involving the

suprarenal vena cava. Am J Surg 1969;118:960-963.
Albrik MH, Rodriguez E, England GJ, et al: Importance of designated thoracic

trauma surgeons in the management of traumatic aortic transection. South

MedJ 1994;87:497-501.
Alexander EL, Szentpetery S, Greenfield L: Posttraumatic thoracic aortic

aneurysm associated with a diaphragmatic hernia. Ann Thorac Surg

1985;40:195-198.
Alexander JJ, Imbembo AL: Aorta-vena cava fistula. Surgery 1989;105:1-12.
Ali IS, Fitzgerald PG, Gillis DA, Lau HYC: Bunt traumatic disruption of the

thoracic aorta: A rare injury in children 10-year-old .J Pediatr Surg 1992;27:

1281-1284.
Ali J, Vanderby B, Purcell C: The effect of the pneumatic antishock garment

(PASG) on hemodynamics, hemorrhage, and survival in penetrating tho-
racic aortic injury. J Trauma 1991;31:846-851.
Allen MJ, Stirling AJ, Crawshaw CW, Barnes MR: Intracompartmental pressure

monitor of leg injuries: An aid to management. J Bone Joint Surg 1985;67-

B:53-57.
Allen MJ, White GH, Harris JP, et al: Iatrogenic vascular trauma associated with

intra-aortic balloon pumping: Identification of risk factors. Am Surg

1993;59:813-817.
Allen RE, Blaisdell FW: Injuries to the inferior vena cava. Surg Clin North Am

1972;52:699-710.
Allen TR, FranklinJD, Withers EH, DavisJL: Extremity salvage utilizing microvas-
cular free tissue transfer. Surgery 1981;90:1047-1054.
Allen TW, Reul GJ, Morton JR, Beall AC Jr: Surgical management of aortic

trauma. J Trauma 1972;12:862-868.
AlpertJ, Bhaktan EK, Gielchinsky I: Vascular complications of intra-aortic balloon

counterpulsation. Arch Surg 1976;111:1190-1195.
AlpertJ, O'DonnellJA, Parsonnet V, et al: Clinically recognized limb ischemia

in the neonate after umbilical artery catheterization. AmJ Surg 1980;140:413-

418.
AlpertJ, Parsonnet V, Goldenkranz RJ, et al: Limb ischemia during intra-aortic

balloon pumping: Indication for femoro-femoral crossover graft. J Thorac

Cardiovasc Surg 1980;79:729-734.

RE.qxd 4/16/04 3:19 PM Page 541

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 541

Alsofrom DJ, Marcus NH, Seigel RS, et al: Shotgun pellet embolization from
the chest to the middle cerebral arteries. J Trauma 1982;22:155-157.

Althaus SJ, Keskey TS, Harker CP: Percutaneous placement of self expanding
stent for acute traumatic arterial injury. J Trauma 1996;41:145-148.

Amato JJ, Billy LJ, Gruber RP, et al: Vascular injuries: An experimental study
of high and low velocity missile wounds. Arch Surg 1970;101:167-174.

Amato JJ, Billy LJ, Gruber RP, Rich NML: Temporary cavitation in high veloc-
ity pulmonary missile injury. Ann Thor Surg 1974;18:565-570.

Amato JJ, Billy LJ, Lawson NS, Rich NM: High velocity missile injury. Am J Surg
1974;127:454-459.

Amato JJ, Rich NM: Temporary cavity effects in blood vessel injury by high
velocity missiles. J Cardiovasc Surg 1972;13:147-155.

Amato JJ, Rich NM, Billy LJ, et al: High velocity arterial injury: A study of the
mechanism of injury. J Trauma 1971;11:412-416.

Amato JJ, Syracuse D, Seaver PRJr, Rich NM: Bone as a secondary missile: An
experimental study in the fragmenting of bone by high missiles. J Trauma
1989;29:609-612.

Amato JJ, Vanecko RM, Yao JST, Weinberg M Jr: Emergency approach to
the subclavian and innominate vessels. Ann Thorac Surg 1969;8:537-541.

Amin A, Alexander JB, O'Malley KF, Doolin E. Blunt abdominal aortic trauma
in children: Case report. J Trauma 1993;34:293-297.

Amine ARC, Sugar O: Repair of severed brachial plexus: A plea to emergency
room physicians. JAMA 1976;235:1039.

Ammons MA, Moore EE, Moore FA, Hopeman AR: Intra-aortic balloon pump
for combined myocardial contusion and thoracic aortic rupture. J Trauma
1990;30:1606-1608.

Anamah NV, Konstam PG: Traumatic dissecting aneurysm of the abdominal
aorta. Br J Surg 1965;52:981-982.

Anastasia LF: Traumatic disruption of the thoracic aorta treated with external
shunt. Am J Surg 1970;120:810-812.

Anderson RJ, Hobson RW II, Lee BC, et al: Reduced dependency on arterio-
graphy for penetrating extremity trauma: Influence of wound location and
non-invasive vascular studies. J Trauma 1990;30:1059-1065.

Anderson RJ, Hobson RW II, Padberg FT Jr: Reduced dependency on arteri-
ography for penetrating extremity trauma (PET) : Influence of wound loca-
tion and noninvasive studies. J Trauma 1989;29:1024.

Anderson RJ, Hobson RW II, Padberg FT Jr, et al: Penetrating extremity trauma:
Identification of patients at high-risk requiring arteriography. J Vase Surg
1990;11:544-548.

Andrade-Alegre R, Mon L: Subxiphoid pericardial window in the diagnosis of
penetrating cardiac trauma. Ann Thorac Surg 1994;58:1139-1141.

Anfossi A, Bertoglio C, Iurilli L, et al: Delayed development and rupture of an
aortic aneurysm after closed abdominal trauma. J Cardiovasc Surg 1987;
28:35-37.

Annandale T: Traumatic popliteal arteriovenous aneurysm treated successfully
by ligature of the popliteal artery and vein. Lancet 1875;1:568.

Anthopoulos LP, Johnson JB, Spellman M: Arteriovenous fistula in multiple
saccular arterial aneurysms of a finger, following childhood human bite.
Angiology 1965;16:89.

Anton GE, Hertzer NR, Beven EG, et al: Surgical management of popliteal
aneurysms: Trends in presentation, treatment, and results from 1952 to
1984. J Vase Surg 1986;3:125-134.

RE.qxd 4/16/04 3:19 PM Page 542

542 VI • THE RICH REFERENCE COLLECTION

Antonovic R, RoschJ, Dotter CT: Complications of percutaneous transaxillary
catheterization for arteriography and selective chemotherapy. Am J
Roentgenol 1976;126:386-393.

An tunes MJ: Acute traumatic rupture of the aorta: Repair by simple aortic cross-
clamping. Ann Thorac Surg 1987;44:257-259.

An tunes MJ, Fernandes LE, Oliveira JM: Ventricular septal defects and arteri-
ovenous fistulas, with and without valvular lesions, resulting from pene-
trating injury of the heart and aorta. J Thorac Cardiovasc Surg 1988;
95:902-907.

Antyllus. Oribasius4:52 (Daemberg Edition). Cited by: Olser. Lancet 1915;1:949.

Appelbaum A, Karp RB, Kirklin JW: Surgical treatment for closed thoracic aortic
injuries. J Thorac Cardiovasc Surg 1976;71:458-460.

Applebaum R, Yellin AE, Weaver FA, et al: Role of routine arteriography in
blunt lower-extremity trauma. Am J Surg 1990;160:221.

Aprahamina C, Thompson BM, TowneJB, Darin JC: The effect of a paramedic
system on mortality open intra-abdominal vascular trauma. J Trauma
1983;23:687-690.

Arajarvi E, Santavirta S: Chest injuries sustained in severe traffic accidents by
seatbelt wearers. J Trauma 1989;29:37-41.

Arajarvi E, Santavirta S, TolonenJ: Aortic ruptures in seat belt wearers. J Thorac
Cardiovasc Surg 1989;98:355-361.

Archambault R, Archambault FLA, Mizeres NJ: Rupture of the thoracoacromial
artery and anterior dislocation of the shoulder. Am J Surg 1959;97:782-
783.

Armstrong K, Sfeir R, Rice J, Kerstein M: Popliteal vascular injuries and war:
Are Beirut and New Orleans similar? J Trauma 1988;28:836-839.

Arnon RG, Allen RG: Traumatic aortic aneurysm in a child. J Pediatr Surg
1981;16:72-74.

Arom KV, Richardson JD, Webb G, et al: Subxyphoid pericardial window in
patients with suspected traumatic pericardial tamponade. Ann Thorac Surg
1977;23:545-549.

Aronstam EM, Gomez AC, O'Connell TJ, Geiger JP: Recent surgical and phar-
macologic experience with acute dissecting and traumatic aneurysms.
J Thorac Cardiovasc Surg 1970;59:231-238.

Aronstam EM, Strader LD, Geiger JP, Gomez AC: Traumatic left ventricular
aneurysms. J Thorac Cardiovasc Surg 1970;59:239-242.

Artz T, Huffer JM: A major complication of the modified Bristow procedure
for recurrent dislocation of the shoulder. J Bonejoint Surg 1972;54-A: 1293-
1296.

Asensio J, Hanpeter D, Demetriades D: The Futility of Liberal Utilization of
Emergency Department Thoracotomy: Proceedings of the American
Association for the Surgery of Trauma, 58th Annual Meeting. 1998,
p210.

AsensioJ, Ierardi R: Exsanguination: Evolving issues in emergency trauma. Emerg
Care Q 1991;9:59-75.

AsensioJ, Murray J, Demetriades D: Penetrating cardiac injuries: A prospective
study of variables predicting outcomes. JACS 1998;186:24-34.

Asensio JA: Exsanguination from penetrating injuries. Trauma Q 1989;16:1-25.

Asensio JA, BerneJD, Chahwan S, et al: Traumatic injury to the superior mesen-
teric artery. Am J Surg 1999;178:235-239.

Asensio JA, BerneJD, Demetriades D: One hundred five penetrating cardiac
injuries. J Trauma 1998;44:1073-1082.

RE.qxd 4/16/04 3:19 PM Page 543

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 543

Asensio JA, Britt LD, Borzotta A: Multi-institutional experience with the man-
agement of superior mesenteric artery injuries. J Am Coll Surg 2001 ;193:354-

366.
Asensio JA, Chahwan S, Hanpeter D. Operative management and outcome of

302 abdominal vascular injuries: AAST-OIS Correlates well with mortality.

Am J Surg 2000;180:528-534.
Asensio JA, Forno W, Gambaro E, et al: Abdominal vascular injuries: The trauma

surgeon's challenge. Anales Chirurgiae Gynaecol 2000;89:71-78.
Asensio JA, Lejarraga M: Abdominal vascular injury. In Demetiades D, Asensio

JA (eds). Trauma Handbook. Austin, Tex, Landes Bioscience, 2000, pp

356-362.
Asensio JA, Stewart BM, MurrayJ: Penetrating cardiac injuries. Surg Clin North

Am 1996;76:685-724.
Asensio JA, VoystockJ, Khatri VJ, Kerstein MD: Toracotomia en el Centro de

Urgencias. Procedimientos en el Paciente Critico 1993;111:337-341.
Asensio JA, Wall M, Minel J: Practice management guidelines for emergency

department thoracotomy. J Am Coll Surg 2001;193:303-309.
Asfaw I, Arbulu A: Penetrating wounds of the pericardium and heart. Surg Clin

North Am 1977;57:37-48.
Asfaw I, Ramadan H, Talbert JG, Arbulu A: Double traumatic rupture of the

thoracic aorta. J Trauma 1985;25:1102-1104.
Ashbell TS, Kleinert HE, KutzJE: Vascular injuries about the elbow. Clin Orthop

1967;50:107-127.
Ash ton F, Slaney G: Arterial injuries in civilian surgical practice. Injury 1970;1 :303-

314.
Ashworth EM, Daising MC, Glover JL, Reilly MK: Lower extremity vascular trauma.

J Trauma 1988;28:329-336.
Assalia A, Schein M: Resuscitation of haemorrhagic shock. Br J Surg 1993;80:213.
Attar S, Ayella RJ, McLaughlin JS: The widened mediastinum in trauma. Ann

Thorac Surg 1972;13:435-449.
Aufranc OE, Jones WN, Stewart WGJr: Common fracture with unusual associ-
ated vascular injury. JAMA 1965;191:1073-1075.
Aust JC, Bredenberg CE, Murray DG: Mechanisms of arterial injuries associ-
ated with total hip replacement. Arch Surg 1981;116:345-349.
Austin JH, Carsen GM: Acute traumatic hematoma of aorta. J Thorac Cardio-

vascSurgl976;71:321.
Ayella RJ, Hankins JR, Turney SZ, Cowley RA: Ruptured thoracic aorta due to

blunt trauma. J Trauma 1977;17:199-205.
Ayres ML, Winspur I: Major injuries and bullet wounds. Injury 1976;7:221-224.
Ayuyao AM, Kaledzi YL, Parsa MH, Freeman HP: Penetrating neck wounds:

Mandatory versus selective exploration. Ann Surg 1985;202:563-567.
Baadsgaard SE, Bille S, Egeblad K: Major vascular injury during gynecologic

laparoscopy: Report of case and review of published cases. Acta Obstet

Gynecol Scand 1986;68:283-285.
Babu SC, Piccorelli GO, Shah PM, et al: Incidence and results of arterial com-
plications among 1 6,350 patients undergoing cardiac catheterization.J Vase

Surg 1989;10:113-116.
Bacharach JM, Garratt KN, Rooke TW: Chronic traumatic thoracic aneurysm:

Report of two cases with the question of timing for surgical intervention.

J Vase Surg 1993;17:780-783.
Baek SM, Brown RS, Shoemaker WC: Cardiac tamponade following wound tract

injection. J Trauma 1973;13:85-87.

RE.qxd 4/16/04 3:19 PM Page 544

544 VI • THE RICH REFERENCE COLLECTION

Baik S, Uku JM, Joo KG: Seat belt injuries to the left common carotid
artery and left internal carotid artery. Am J Forens Med Pathol 1988;9:38-
39.

Bailey H: Wounds of the neck. In Bailey H (ed): Surgery of Modern Warfare.
Edinburgh, E & S Livingston, 1944.

Baillot R, Dontigny L, Verdant A, et al: Penetrating chest trauma: A 20-year
experience. J Trauma 1987;27:994-997.

Baillot R, Dontigny L, Verdant A, et al: Intrapericardial trauma: Surgical expe-
rience. J Trauma 1989;29:736-740.

Baird RJ, Doran ML: The false aneurysm. Can Med Assoc J 1964;91:281-
284.

Baker CC, Thomas AN, Trunkey DD: The role of emergency room thoraco-
tomy on trauma. J Trauma 1980;20:848-855.

Baker MS: Recognition of vascular injury in the trauma patient. Milit Med
1990;155:225.

Baker SP, O'Neill B, Haddon WJr, Long WB: A method for describing patients
with multiple injuries and evaluating emergency care.J Trauma 1974; 14: 187-
196.

Bakker FC, Patka P, Haarman HJ: Combined repair of a traumatic rapture of
the aorta an anterior stabilization of a thoracic spine fracture: Case report.
J Trauma 1996;40:128-129.

Bakker KW, Cast LF: Retroperitoneal haemorrhage from the superior gluteal
artery: A late complication of total hip arthroplasty. Clin Rheumatol
1990;9:249.

Ballance C: The surgery of the heart (Bradshaw Lecture). Lancet 1920;1:1.

BaltschJ, Klose KJ, GonningerJ: Angiography in acute arterial trauma of periph-
eral vessels and the aorta. Vasa 1987;16:246-250.

Bandt RL, Foley WJ, FinkGH, Regan WJ: Mechanism of perforation of the heart
with production of hydropericardium by a venous catheter and its pre-
vention. Am J Surg 2001;33:311-316.

Banks E, Chun J, Weaver FA: Chronic innominate artery dissection after blunt
thoracic trauma: Case report. J Trauma 1995;38:975-978.

Barcia PJ, Nelson TG, Whelan TJ: Importance of venous occlusion in arterial
repair failure: An experimental study. Ann Surg 1972;175:223-227.

Barcia TC, Livoni JP: Indications for angiography in blunt thoracic trauma.
Radiology 1983;147:15-19.

Baret AC, DeLong RP, Tukanowicz SA, Blakemore WS: Transfixation of the
aorta accompanied by a Browne-Syndrome: A case report. J Trauma
1958;35:359-362.

Barker NW, Hines EAJr: Arterial occlusion in the hands and fingers associated
with repeated occupational trauma. Proc Staff Meet Mayo Clin 1944;19:345-
349.

Barker JE, Knight KR, Romeo R, et al: Targeted disruption of the nitric oxide
synthase 2 gene protects against ischaemia/reperfusion injury to skeletal
muscle. J Pathol 2001;194:109-115.

Barkun JS, Terazza O, Daignault P, et al: The fate of venous repair after shock
and trauma. J Trauma 1988;28:1322-1329.

Barner HB: Sutureless intraluminal aortic prosthesis in traumatic aortic rupture:
Is it appropriate? J Trauma 1988;28:1607-1608.

Barnes RW, Petersen JL, Krugmire RB, Strandness DEJr: Complications of per-
cutaneous femoral arterial catheterization: Prospective evaluation with the
Doppler ultrasonic velocity detector. Am J Cardiol 1974;33:259-263.

RE.qxd 4/16/04 3:19 PM Page 545

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 545

Barone GW, Kahn MB, Cook JM, et al: Traumatic left renal artery stenosis
managed with splenorenal bypass: Case report. J Trauma 1990;30:1594-
1596.

Barros D'Sa AAB: A decade of missile-induced vascular trauma. Ann Surg
1981;64:37-44.

Barros D'Sa AAB: Management of vascular injuries of civil strife. Injury 1982;14:51-
57.

Barros D'Sa AAB: The Rationale for Arterial and Venous Shunting in the Man-
agement. Belfast, Northern Ireland, Grune &Stratton, 1989.

Barros D'Sa AAB, Hassard TH, Livingston RH, Irwin JW: Missile-induced vas-
cular trauma. Injury 1980;12:13-30.

Bass A, Papa M, Morag B, Adar R: Aortic false aneurysm following blunt trauma
of the abdomen. J Trauma 1983;23:1072-1073.

Bass A, Allison EJ, Reines HD: Thigh compartment syndrome without lower
extremity trauma following application of pneumatic antishock trousers.
Ann Emerg Med 1983;12:382-384.

Bassett FH, Houck WS: False aneurysm of profunda femoris artery after sub-
trochanteric osteotomy and nail-plate fixation. J Bone Joint Surg
1964;46A:583-585.

Bassett FH, Silver D: Arterial injury associated with fractures. Arch Surg
1966;92:13-19.

BattM, Hassen-KhoudjaR, BayadaJM, etal: Traumatic fistula between the aorta
and the left renal vein: Case report and review of the literature. J Vase Surg
1989;9:812-816.

Batzdorf U, BentsonJR, Machleder HI: Blunt trauma to the high cervical carotid
artery. Neurosurgery 1979;5:192-201.

Baumgartner F, White GH, White RA, et al: Delayed, exsanguinating pelvic
hemorrhage after blunt trauma without bony fracture: Case report.J Trauma
1990;30:1603-1605.

Baxter BT, Moore EE, Synhorst DR et al: Graded experimental cardiac contu-
sion: Impact on cardiac rhythm, coronary artery flow, ventricular function,
and myocardial oxygen consumption. J Trauma 1988;28:1411-1417.

Beall ACJr: Penetrating wounds of the aorta. Am J Surg 1960;99:770-774.

Beall ACJr, Arbergast NR, Hallman GL: Complete transection of the thoracic
aorta due to rapid deceleration. Am J Surg 1967;114:769-773.

Beall ACJr, Arbergast NR, Ripepi AC, et al: Aortic laceration due to rapid dece-
leration. Arch Surg 1969;98:595-601.

Beall ACJr, Crosthwait RW, Crawford ES, DeBakey ME: Gunshot wounds of the
chest: A plea for individualization. J Trauma 1964;4:382.

Beall ACJr, Diethrich EB, Cooley DA, DeBakey ME: Surgical management of
penetrating cardiovascular trauma. South Med J 1967;60:698-704.

Beall ACJr, Diethrich EB, Crawford HW, et al: Surgical management of pene-
trating cardiac injuries. Am J Surg 1966;112:686-692.

Beall ACJr, Diethrich EB, Morris GC Jr, DeBakey ME: Surgical management of
vascular trauma. Surg Clin North Am 1966;46:1001-1011.

Beall ACJr, Gasior RM, Bricker DL: Gunshot wounds of the heart: Changing
patterns of surgical management. Ann Thorac Surg 1971;11:523-531.

Beall ACJr, Harrington OB, Crawford ES, DeBakey ME: Surgical management
of traumatic arteriovenous aneurysms. Am J Surg 1963;106:610-618.

Beall ACJr, Morris GC Jr, Cooley DA: Temporary cardiopulmonary bypass in
the management of penetrating wounds of the heart. Surgery 1962;52:330-
337.

RE.qxd 4/16/04 3:19 PM Page 546

546 VI • THE RICH REFERENCE COLLECTION

Beall AC Jr, Ochsner JL, Morris GC Jr, et al: Penetrating wounds to the heart.
J Trauma 1961;1:195-207.

Beall AC Jr, Patrick TA, Okies JE, et al: Penetrating wounds of the heart: Chang-
ing patterns of surgical management. J Trauma 1972;12:468-473.

Beall AC Jr, Roof WR, DeBakey ME: Successful surgical management of through
and through stab wound of the aortic arch. Ann Surg 1962;156:283-286.

Beall AC Jr, ShirkeyAL, DeBakey ME: Penetrating wounds of the carotid arter-
ies. J Trauma 1963;3:276-287.

Beattie EJJr, Greer D: Laceration of the aorta: Case report of successful repair
forty-eight hours after injury. J Thorac Surg 1952;23:293-298.

Beattie EJJr, Oldham JB, RossJA: Superior thyroid arteriovenous aneurysm.
Br J Surg 1961;48:456-457.

Beatty RA: Dissecting hematoma of the internal carotid artery following
chiropractic cervical manipulation. J Trauma 1977;17:248-249.

BeckCS: Wounds of the heart: The technique of suture. Arch Surg 1926;13:205-
227.

Beck CS: Further observations on stab wounds of the heart. Ann Surg
1942;115:698-704.

Beck DE, Robison JG, Hallett JE Jr: Popliteal artery pseudoaneurysm following
arthroscopy. J Trauma 1986;26:87-89.

Becker G, Palmaz J, Rees C: Angioplasty-induced dissections in human iliac
arteries: Management with Palmaz-balloon-expandable intraluminal
stents. Radiology 1990;176:31.

Becker HM, Ramirez J, Echave V, Heberer G: Traumatic aneurysms of the
descending thoracic aorta. Ann Vase Surg 1986;1:196-200.

Becker HM, WexlerJ, Frater RW: False aneurysm of aorta secondary to partial
occlusion clamp injury diagnosis by nuclear flow study. Chest 1981;80:331-
333.

BednarskiJJ, Nayduch DA: Thoracic aorta rupture as a cause of paraplegia: A
diagnostic dilemma (case report). J Trauma 1989;29:531-533.

Beebe GW, Bergan JJ, Bergqvist D, et al: Classification and grading of chronic
venous disease in the lower limbs. A consensus statement. Eur Vase Endovasc
Surg 1996;12:487-492.

Beebe HG: Complications in Vascular Surgery. Philadelphia, JB Lippincott Co,
1973.

Beel T, Harwood AL: Traumatic rupture of the thoracic aorta. Ann Emerg Med
1980;9:483-486.

BeggJW: Recanalization of autogenous vein graft. Southern MedJ 1988;81:1446-
1447.

Beggs CW, Helling TS, Evans LL, et al: Evaluation of cardiac injury by two-
dimensional echocardiography in patients suffering blunt chest trauma.
Ann Emerg Med 1987;16:542-545.

Belcaro G, Nicolaides AN: Pressure index in hypotensive of hypertensive patients.
J Cardiovasc Surg 1989;30:614-617.

Beless DJ, Muller DS, Perez H: Aortoiliac occlusion secondary to atheroscle-
rotic plaque rapture as the result of blunt trauma. Ann Emerg Med
1990;19:922-924.

Belkin M, Dunton R, Crombie HD Jr, Lowe R: Preoperative percutaneous intra-
luminal balloon catheter control of major arterial hemorrhage. J Trauma
1988;28:548-550.

Bell D, Cockshott WP: Angiography of traumatic arterio-venous fistulae. Clin
Radiol 1965;16:241-247.

RE.qxd 4/16/04 3:19 PM Page 547

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 547

Bell J: Principles of surgery. Discourse 1801;9:4.

Bell KA, Simon BK: Aneurysm of popliteal artery after medial meniscectomy:

An unusual complication. South MedJ 1979;72:1126-1134.
Bellamy RF: The causes of death in conventional land warfare: Implications for

combat casualty care research. Mil Med 1984;149:55-62.
Belley G, Gallix BP, Derossis AM, et al: Profound hypotension in blunt trauma

associated with superior gluteal artery rupture without pelvic fracture.

J Trauma 1997;43:703-705.
Ben-Menachem Y: Vascular injuries of the extremities: Hazards of unnecessary

delays in diagnosis. Orthopedics 1986;9:333-338.
Ben-Menachem Y: Avulsion of the innominate artery associated with fracture

of the sternum. Am J Cardiol 1988;150:621-622.
Ben-Menachem Y: Rupture of the thoracic aorta by broadside impacts in road

traffic and other collisions: Further angiographic observations. J Trauma

1993;36:363-367.
Ben Hur N, Gemer M, Milwidsky H: Perforating injury of the heart caused by

nail fired from a studgun. J Trauma 1964;84:850-853.
Benckart DH, Magovern GJ, Lievler GA, et al: Traumatic aortic transection:

Repair using left arterial to femoral bypass. J Cardiac Surg 1989;4:43-49.
Benitez PR, Newell MA: Vascular trauma in drug abuse: Patterns of injury. Ann

Vase Surg 1986;1:175-180.
Benito MC, Garcia F, Fernandez-Quero L, et al: Lesion of the internal carotid

artery caused by a car safety belt. J Trauma 1990;30:116-117.
Bennett DE, CherryJK: The natural history of traumatic aneurysms of the aorta.

Surgery 1967;61:516.
Bennett JE: Expanding forearm hematoma after apparent minor injury. Plastic

Reconstr Surg 1965;36:622-625.
BenvenutoR, Rodman FS, Glimour J, etal: Composite venous grafts for replace-
ment of the superior vena cava. Arch Surg 1962;84:570-573.
BerendesJN, BredeeJJ, SchipperheynJJ, Mashhour YAS: Mechanisms of spinal

cord injury after cross-clamping of the descending thoracic aorta. Circu-
lation 1982;66:112-116.
BerganF: Traumatic intimal rupture of the popliteal artery with acute ischemia

of the limb in cases with supracondylar fractures of the femur. J Cardiac

Surg 1963;4:300-302.
Bergan JJ, Conn J Jr, Trippel OH: Severe ischemia of the hand. Ann Surg

1971;173:301-307.
Bergan JJ, Dean RH, Yao JST: Vascular injuries in pelvic cancer surgery. Am J

Obstet Gynecol 1976;124:562-566.
Bergan JJ, Yao JST: Symposium on Venous Problems in Honor of Geza de Takats.

Chicago, Year Book Medical Publishers, 1978.
Bergan JJ, Yao JST: Surgery of the Veins. Orlando, Grune & Stratton, 1985.
Bergen tz SE, Bergqvist D: Iatrogenic Vascular Injuries. New York: Springer-Verlag,

1989.
Bergen tz SE, Hansson LO, Norback B: Surgical management of complications

to arterial puncture. Ann Surg 1966;164:1021-1026.
Bergin PJ: Aortic thrombosis and peripheral embolization after thoracic gunshot

wound by transesophageal echocardiography. Am Heart 1990;1 19:688-

690.
Berglund B, Swanbeck G, Hedin H: Low molecular weight dextran therapy for

digital ischemia due to collagen vascular disease. Dermatologica 1981;

163:353-357.

RE.qxd 4/16/04 3:19 PM Page 548

548 VI • THE RICH REFERENCE COLLECTION

Bergman K, Spence L, Wesson D, Dykes E: Thoracic vascular injuries: A post
mortem study. J Trauma 1990;30:604-606.

Bergquist D, Takolander R: Aortic occlusion following blunt trauma of the
abdomen. J Trauma 1981;21:319-322.

Bergquist D, Carlsson AS, Ericsson BF: Vascular complications after total hip
arthroplasty. Acta Orthop Scand 1983;54:157-163.

Berguer R, Feldman AJ, Wilner HI, Lazo A: Arteriovenous vertebral fistulae:
Cure by combination of operation and detachable intravascular balloon.
Ann Surg 1982;196:65-68.

Berkoff HA, Carpenter EW, Frey CF: Evaluation of balloon tamponade of the
abdominal aorta. J Surgery 1971;11:496-500.

Bernheim BM: Surgery of the vascular system. Philadelphia, JB Lippincott Co,
1913.

Bernheim BM: Bloodvessel surgery in the war. Surg Gynecol Obstet 1920;30:564-
567.

BertiniJEJr, Flechner SM, Miller P, et al: The natural history of traumatic branch
renal artery injury. J Urol 1986;135:228-230.

Bezreh AA: Injuries resulting from hostile action against army aircrew members
in flight over Vietnam. Aerospace Med 1970;41:763.

Bhatnagar MK, Smith GS: Trauma in the Afghan Guerilla War: Effects of lack
of access to care. Surgery 1989;105:699.

Bickell WH, Shaftan GW, Mattox KL: Intravenous fluid administration and uncon-
trolled hemorrhage. J Trauma 1989;29:409.

Bickell WH, Wall MJ Jr, Pepe PE, et al: Immediate versus delayed fluid resusci-
tation for hypotensive patients with penetrating thoracoabdominal trauma.
N EnglJ Med 1994;331:1105-1109.

Bickham WS: Arteriovenous aneurysm. Ann Surg 1904;39:767-775.

Bigger IA: Heart wounds: A report of seventeen patients operated upon in the
Medical College of Virginia Hospitals and discussion of the treatment and
prognosis. J Thorac Surg 1939;8:239-253.

Billings KJ, Nasca RJ, Griffin HA: Traumatic arteriovenous fistula with sponta-
neous closure. J Trauma 1973;13:741-743.

Billroth T: The surgery of the heart (Bradshaw Lecture). Lancet 1920;1-1:73-
134.

Billroth T: Wounds of the heart: The technique of suture. Arch Surg 1926; 13:205-
227.

Billroth T: Historical studies on the nature and treatment of gunshot wounds
from the 15th century to the present time. YaleJ Biol Med 1931;4:16-36.

Billy LJ, Amato JJ, Rich NM: Aortic injuries in Vietnam. Surgery 1971;70:385-
391.

BinetJP, LangloisJ, Cormier JM, Saint Florent GD: A case of recent traumatic
avulsion of the innominate artery at its origin from the aortic arch: Suc-
cessful surgical repair with deep hypothermia. J Thorac Cardiovasc Surg
1962;43:670-676.

Binkley FM, Wylie EJ: A new technique for obliteration of cerebrovascular arte-
riovenous fistulae. Arch Surg 1973;106:524-527.

Birchall D, Fields JM, Chalmers N, Walker MG: Case report: Delayed superfi-
cial femoral artery pseudoaneurysm rupture following successful com-
pression therapy. Clin Radial 1997;52:629-630.

BirchardJD, Pichara DR, Brown PM: External iliac artery and lumbosacral plexus
injury secondary to an open book fracture of the pelvis: Report of a case.
J Trauma 1990;30:906-908.

RE.qxd 4/16/04 3:19 PM Page 549

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 549

Birkeland IW, Taylor TK: Major vascular injuries in lumbar disc surgery. J Bone
Joint Surg 1969;51B:4-19.

Birnholz JC: Radionuclide angiography in the diagnosis of aortocaval fistula.
J Thorac Cardiovasc Surg 1973;65:292-295.

Bisenkov LN, Isamukhamedov T, Panin SM: Heart wound with migration of a
bullet into the abdominal aorta. Vestn Khir 1983;131:97-98.

Bishara RA, Pasch AR, Lim LT, et al: Improved results in the treatment of civil-
ian vascular injuries associated with fractures and dislocations. J Vase Surg
1986;3:707-711.

BizerL: Peripheral vascular injuries in the Vietnam War. Arch Surg 1969;98:165-
166.

Blackford JM, McLaughlin JS: Pseudoaneurysm of the carotid artery. Am Surg
1973;39:257-260.

Blacklay PF, Duggan E, Wood RFM: Vascular trauma. Br J Surg 1987;74:1077-
1083.

Blackmore TL, Whelan TJ: Arteriovenous fistula as a complication of gastrec-
tomy. Am J Surg 1965;109:197.

Bladergroen M, Brockman R, Luna G, et al: A twelve-year survey of cervicothoracic
vascular injuries. Am J Surg 1989;157:483-486.

Blaisdell FW: Discussion in Buscaglia: Penetrating abdominal vascular injuries.
Arch Surg 1969;109:197.

Blaisdell FW, Cooley DA: The mechanism of paraplegia after temporary tho-
racic aortic occlusion and its relationship to spinal fluid pressure. Surgery
1962;51:351-355.

Blaisdell FW, Hall AD, Lim RC: Aortoiliac arterial substitution utilizing subcu-
taneous grafts. Ann Surg 1970;172:775-780.

Blake HA, Inmon TW, Spencer FC: Emergency use of antegrade aortography
in diagnosis of acute aortic rupture. Ann Surg 1960;152:954-956.

Blakemore AH: Restorative endoaneurysmorrhaphy by vein graft inlay. Ann
Surg 1947;126:841-849.

Blakemore AH, Lord JE Jr: A non-suture method of blood vessel anastomosis:
Review of experimental study and report of clinical cases. Ann Surg 1945;121:
435-453.

Blakemore AH, Lord JW, Stefko PL: The severed primary artery in the war
wounded; a non suture method of bridging arterial defects. Surgery
1942;12:488-508.

Blalock A: A successful suture of a wound of the ascending aorta. JAMA
1934;103:1617-1618.

Blalock A, Ravitch MM: Consideration of the non-operative treatment of cardiac
tamponade resulting from wounds to the heart. Surgery 1943;14:157-
162.

Blanchard DG, Kimura BJ, Dittrich HC, DeMaria AN: Transesophageal echocar-
diography of the aorta. JAMA 1994;272:546-551.

Bland-Sutton J: A lecture on missiles as emboli. Lancet 1919;1:773-775.

Bland EF, Beebe GW: Missiles in the heart. A twenty-year follow-up report of
World War II cases. New Engl J Med 1966;274:1039-1046.

Blatchford JW III, Anderson RW: The evolution of the management of pene-
trating wounds of the heart. Ann Surg 1985;202:615-623.

Blegvad S, Lippert H, Lund O, et al: Acute delayed surgical treatment of trau-
matic rupture of the descending aorta. J Cardiovasc Surg 1989;30:559-564.

Blickenstaff KL, Weaver FA, Yellin AE, et al: Trends in management of trau-
matic vertebral artery injuries. Am J Surg 1989;158:101-106.

RE.qxd 4/16/04 3:19 PM Page 550

550 VI • THE RICH REFERENCE COLLECTION

Blohme I, Brynger H: Emergency ligation of the external iliac artery. Ann Surg

1985;201:505-510.
Bloom AI, Sasson T, Ravkind A, Pikarski B-ZJ: Diagnosis of traumatic rupture

of the thoracic aorta using dynamic rapid sequence axial computerized

tomography. Isr J Med Sci 1995;31:314-320.
Bloom JD, Mozersky DJ, Buckley CG, Hagood COJr: Defective limb growth as

a complication of catheterization of the femoral artery. Surg Gynecol Obstet

1974;138:524-526.
Blumoff RL, Powell T, Johnson GJr: Femoral venous trauma in a university

referral center. J Trauma 1982;22:703-705.
Blumoff RL, Proctor HJ, Johnson GJr: Recanalization of a saphenous vein inter-
position venous graft. J Trauma 1981;21:407-408.
Bodai BI, Smith P, Ward RE: Emergency thoracotomy in the management of

trauma: A review. JAMA 1983;249:1891.
Bodily K, Perry JF, Strate R, Fischer RP: The salvageability of patients with post-
traumatic rupture of the descending thoracic aorta in a primary trauma

center. J Trauma 1977;17:754-760.
Boerhaave H: Cited in Elkin 1941. Aphorismi de Cognoscendis et Curandis

Morbis (aphorism 170). 1709.
Bogaert AM, DeScheerder I, Calardyn F: Successful treatment of aortic rupture

presenting as a syncope: The role of echocardiography in diagnosis. IntJ

Cardiology 1987;16:212-214.
Bolanowki PJP, Swaminatham AP, Neville WE: Aggressive surgical management

of penetrating cardiac injuries. J Thorac Cardiovasc Surg 1973;66:52-57.
Bolasny BL, Killen DA: Surgical management of arterial injuries secondary to

angiography. Ann Surg 1971;174:962-964.
Bole P, Andronaco JT, Purdy R: Superior mesenteric arteriovenous fistula

secondary to a gunshot wound. J Cardiac Surg 1973;14:456.
Bole PV, Cortes LE, Munda RT, et al: Repair of false aneurysm of the abdomi-
nal aorta. J Trauma 1975;15:255-259.
Bole PV, Katz M, Cohen NH, Clauss RH: Carotid crossover bypass: Cerebral

revascularization after ligation of common carotid artery. Cardiovasc Surg

1977;18:533-538.
Bole PV, Munda R, Purdy RT: Traumatic pseudoaneurysms: A review of 32 cases.

J Trauma 1976;16:63-70.
Bole PV, Purdy RT, Munda RT, et al: Civilian arterial injuries. Ann Surg

1976;183:13-23.
Bollett AJ: Wounded presidents: 1981 almost repeats the events of 1881. Mil

Med 1981;109:19-23.
Bongard F, Dubrow T, Klein S: Vascular injuries in the urban battleground:

Experience at a metropolitan trauma center. Ann Vase Surg 1990;4:415.
Bongard F,Johs SM, Leighton TA, Klein SR: Peripheral arterial shotgun missile

emboli: Diagnostic and therapeutic management case reports. J Trauma

1991;31:1426-1431.
Bongard FS, White GH, Klein SR: Management strategy of complex extremity

injuries. Am J Surg 1989;158:151-155.
Bongard FS, Wilson SE, Perry MO: Vascular injuries in surgical practice. In

Bongard FS, Wilson SE, Perry MO (eds) : Norwalk, Conn, Appleton & Lange,

1991.
Boontje AH: Iatrogenic vascular trauma. J Cardiac Surg 1978;19:335-340.
Boontje AH: True aneurysm of the abdominal aorta due to blunt trauma.

J Cardiac Surg 1978;19:359-363.

RE.qxd 4/16/04 3:19 PM Page 551

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 551

BordeauxJ, GuysJM, Magnan PE: Multiple aneurysms in a seven-year-old child.

Ann Vase Surg 1990;4:26-28.
Borja AR, Lansing AM: Thrombosis of the abdominal aorta caused by blunt

trauma. J Trauma 1970;10:499-501.
Borja AR, Lansing AM: Traumatic rupture of the heart: A case successfully treated.

J Vase Surg 1970;171:438-440.
Borlase BC, Metcalf RK, Moora EE: Penetrating wounds to the anterior chest.

Analysis of thoracotomy and laparotomy. Am J Surg 1986;6:649.
Borlase BC, Moore EE, Moore FA: The abdominal trauma index: A critical

reassessment and validation. J Trauma 1990;30:1340-1344.
Borman KR, Aurbakken CM, WeigeltJA: Treatment priorities in combined blunt

abdominal and aortic trauma. Am J Surg 1982;144:728-732.
Borman KR, Jones GH, Snyder WH Jr: A decade of lower extremity venous

trauma: Patency and outcome. Am J Surg 1987;154:608-612.
Borman KR, Snyder WH III, WeigeltJA: Civilian arterial trauma of the upper

extremity: 1 1-year experience in 267 patients. Am J Surg 1984;148:796-799.
Boruchow IB, Iyengar R,JudeJR: Injury to ascending aorta root trauma.J Thorac

Cardiovasc Surg 1977;73:303-305.
Boruchow IB: Delayed death from aortic root trauma. Ann Thorac Surg

1991;51:317-319.
Bosher LH, Freed TA: The surgical treatment of traumatic rupture of avulsion

of the innominate artery. J Thorac Cardiovasc Surg 1967;54:732-739.
Bouchard JF, Lamontagne D: Protection afforded by preconditioning to the

diabetic heart against ischaemic injury. Cardiovasc Res 1998;37:82-90.
Bourland WA, Kispert JF, Hyde GL, Kazmers A: Trauma to the proximal supe-
rior mesenteric artery: A case report and review of the literature. J Vase

Surg 1992;15:669-674.
Bower TC, Murray MJ, Gloviczki P: Effects of thoracic aortic occlusion and cere-
brospinal fluid drainage on regional spinal cord blood flow in dogs: Cor-
relation with neurologic outcome. J Vase Surg 1989;9:135-144.
Boyd DP, Farha GJ: Arteriovenous fistula and isolated vascular injuries secondary

to intervertebral disk surgery: Report of four cases and review of the lit-
erature. Ann Surg 1965;161:524-531.
Boyd TF, Strieder JW: Immediate surgery for traumatic heart disease. J Thorac

Cardiovasc Surg 1965;50:305-315.
Boyden AM: Personal communication, 1970.
Boyle EM Jr, Canty T Jr, Morgan E, et al: Treating myocardial ischemia-

reperfusion injury by targeting endothelial cell transcription. Ann Thor

Surg 1999;68:1949-1953.
Bradham GB, Nunn D, Brailsford LE: Successful repair of a bullet wound of

the abdominal aorta. Ann Surg 1962;155:86-89.
Bradham RR, Buxton J, StallworthJ: Arterial injury of the lower extremity. Surg

Gynecol Obstet 1964;118:995-1000.
Bradham WG, Lewis J, Sewell D, Garrett A: Bullet embolus to the ascending

aorta following a gunshot wound to the chest. J Tenn Med Assoc

1991;84:592-593.
Bradley EL III: Management of penetrating carotid injuries: An alternative

approach. J Trauma 1973;13:248-255.
BrandayJM, Kumar E, Spencer H: Intrapericardial heart and great vessel injuries.

West Indian Med J 1984;33:176-119.
Branham HH: Aneurysmal varix of the femoral artery and vein following a

gunshot wound. IntJ Surg 1890;3:250.

RE.qxd 4/16/04 3:19 PM Page 552

552 VI • THE RICH REFERENCE COLLECTION

Brantigan CO: Delayed major vessel hemorrhage following tracheostomy.
J Trauma 1973;13:235-237.

Brathwaite CE, Rodriguez: Injuries of the abdominal aorta from blunt trauma.
Am Surg 1992;58:350-352.

Brathwaite CE, CilleyJ, O'Connor W, et al: The pivotal role of transesophageal
echocardiography in the management of traumatic thoracic aortic rupture
with associated intra-abdominal hemorrhage. Chest 1994;105:1899.

Brawley RK, Murray G, Crisler C, Cameron J: Management of wounds of the
innominate, subclavian and axillary blood vessels. Surg Gynecol Obstet
1970;131:1130-1140.

Breaux EP, Dupont J Jr, Alvert HM, et al: Cardiac tamponade following pene-
trating mediastinal injuries: Improved survival with early pericardiocen-
tesis. J Trauma 1979;19:461-466.

Brener BJ, Couch N: Peripheral arterial complications of left heart catheteri-
zation and their management. Am J Surg 1973;125:521-526.

Brengman ML, O'Donnell S, Mullenix P, et al: The fate of a patent carotid
artery contralateral to an occlusion. Ann Vase Surg 2000;14:77-81.

Brentlinger A, Hunter J: Perforation of the external iliac artery and ureter pre-
senting as acute hemorrhagic cystitis after total hip replacement. J Bone
Joint Surg 1987;69:620-622.

Brewer LA III: Wounds of the chest in war and peace, 1943-1968. Ann Thorac
Surg 1969;7:387-408.

Brewer LA III: The contributions of the Second Auxiliary Surgical Group to
military surgery during World War II with special reference to thoracic
surgery. Ann Surg 1983;197:318-326.

Brewer LA III, Carter R: Wounds of the great vessels of the thorax: Diagnosis
and surgical approach in twenty-four cases. Am J Surg 1967;1 14:340-
350.

Brewer LA III, Carter R: Elective cardiac arrest for the management of mas-
sively bleeding heart wounds. JAMA 1967;200:1023-1025.

Brewer LA III, Carter R: A rational treatment of small and large wounds of the
heart. Surg Gynecol Obstet 1968;126:977-985.

Brewer PL, Schramel R, Menendez C, Creech O Jr: Injuries of the popliteal
artery: A report of sixteen cases. Am J Surg 1969;118:36-42.

Brewster D, May A, Darling RC: Variable manifestations of vascular injury during
lumbar disk surgery. Arch Surg 1979;114:1026-1030.

Brewster SA, Thirlby R, Synder WH: Subxiphoid pericardial window and
penetrating cardiac trauma. 1988.

Bricker D, Hallman GL: Complete transection of the thoracic aorta: Manage-
ment of a case associated with massive total body injury. J Trauma
1970;10:420-426.

Bricker DL, Beall ACJr, DeBakey ME: The differential response to infection of
autogenous vein versus Dacron arterial prosthesis. Chest 1970;58:566-
570.

Bricker DL, Morton JR, Okies JE, Beall ACJr: Surgical management of injuries
the vena cava: Changing patterns of injury and newer techniques of repair.
J Trauma 1971;11:725-735.

Bricker DL, Noon G, Beall ACJr: Vascular injuries of the thoracic outlet.J Trauma
1970;10:1-15.

Bricker DL, Waltz T, Telford R, Beall ACJr: Major abdominal and thoracic
trauma associated with spinal cord injury: Problems in management.
J Trauma 1971;11:63-75.

RE.qxd 4/16/04 3:19 PM Page 553

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 553

Brigham RA, Eddleman W, Clagett GP, Rich NM: Isolated venous injury pro-
duced by penetrating trauma to the lower extremity. J Trauma 1983;23:255-
257.

Brigham RA, Salander J, Rich NM: Abdominal venous trauma. In Scribner RG,
Brown WH, Tawes RL (eds): Decision Making in Vascular Surgery.
Toronto, BC Decker, 1988.

Brigham RA, Salander JM, Rich NM: Extremity venous trauma. In Scribner RG,
Brown WH, Tawes RL (eds): Decision Making in Vascular Surgery.
Toronto, BC Decker, 1988.

Bright EF, Beck CS: Nonpenetrating wounds of the heart. Am Chest J 1935;
10:293-320.

Brink BE: Vascular trauma. Surg Clin North Am 1977;57:189-196.

Brinton M, Miller S, Lim RC Jr, Trunkey DD: Acute abdominal aortic injuries.
J Trauma 1982;22:481-486.

Brisbin RL, Geib PO, Eiseman B: Secondary disruption of vascular repair fol-
lowing war wounds. Arch Surg 1969;99:787-791.

Brittain RS, Marchioro TL, Hermann G, et al: Accidental hepatic artery liga-
tion in humans. Am J Surg 1964;107:822-832.

Bromley LL, HobbsJT, Robinson RE: Early repair of traumatic rupture of the
aorta. Br MedJ 1965;2:17-19.

Brooks AL, Fowler SB: Axillary artery thrombosis after prolonged use of crutches.
J Bone Joint Surg 1964;46-A:863-864.

Brooks AP, Olson LK, Shackford SR: Computed tomography in the diagnosis
of traumatic rupture of the thoracic aorta. Clinical Radiology 1989;40:133-
138.

Brooks SW, Cmolik BL, Young JC, et al: Transesophageal echocardiographic
examination of a patient with traumatic aortic transection from blunt chest
trauma: A case report. J Trauma 1991;31:841-845.

Brooks SW, Young JC, Cmolik BL, et al: The use of transesophageal echocar-
diography in the evaluation of chest trauma. J Trauma 1992;23:761-765.

Brophy DP, Sheiman RG, Amatulle P, Akbari CM: Iatrogenic femoral pseudoa-
neurysms: Thrombin injection after failed US-guided compression. Radi-
ology 2001;214:278-282.

Bross W: Injuries of the thoracic aorta. J Cardiac Surg 1971;12:95-103.

Brotman S, Browner B, Cox E: MAST trousers improperly applied causing com-
partmental syndrome in lower extremity trauma. J Trauma 1982;22:598-
599.

Brown AJ: Old masterpieces in Surgery: The surgery of HieronymusBrunschwig.
Surg Gynecol Obstet 1924;38:133.

Brown C: Inadvertent prolonged cannulation of the carotid artery. Anesth Analg
1982;61:150-152.

Brown JJ, Greene FL, McMillan RD: Vascular injuries associated with pelvic frac-
tures. Am J Surg 1984;140:802-806.

Brown MF, Graham JM, Feliciano DV, et al: Carotid artery injuries. Am J Surg
1982;144:748-753.

Brown OW, Kerstein MD: Injuries to the peripheral vasculature: In Manage-
ment of Vascular Trauma. Baltimore, University Park Press, 1985.

Brown PS Jr, Nath R, Votapka T, et al: Traumatic ventricular septal defect and
disruption of the descending thoracic aorta. Ann Thorac Surg 1991 ;52: 143-
144.

Brown RS, Boyd DR, Masuda T, Lowe R: Temporary internal vascular shunt for
retrohepatic vena cava injury. J Trauma 1971;11:736-737.

RE.qxd 4/16/04 3:19 PM Page 554

554 VI • THE RICH REFERENCE COLLECTION

Brunner JH, Stanley RJ: Superior mesenteric arteriovenous fistula. JAMA

1973;223:316.
Brunsting LA, Ouriel K: Traumatic fracture of the abdominal aorta: Rupture

of a calcified abdominal aorta with minimal trauma.J Vase Surg 1988;8:184-

186.
Bryant MF Jr, Lazenby WD, Howard JM: Experimental replacement of short

segment of veins. Arch Surg 1958;76:289-293.
Brzowski BK, Mills JL, Beckett M, Beckett WC: Iatrogenic subclavian artery

pseudoaneurysms: Case reports. J Trauma 1990;30:1-3.
Buchbinder D, Karmody A, Leather R, Shah D: Hypertonic mannitol: Its use

in prevention of revascularization syndrome after acute arterial ischemia.

Arch Surg 1981;116:414-421.
Buchman RJ, Thomas PAJ, Park B: Carotid artery injuries: Follow-up of fifteen

patients treated in Vietnam. Angiology 1972;23:97-102.
Buchmaster MJ, Kearney PA, Johnson SB, et al: Further experience with trans-
esophageal echocardiography in the evaluation of thoracic aortic injury.

J Trauma 1994;37:989-995.
Buchness MP, Lo Gerfo FW, Mason GR: Gunshot wounds of the suprarenal

abdominal aorta. Am Surg 1976;42:1-7.
Buckman RF, Badellino MM, Mauro LH, AsensioJA: Penetrating cardiac wounds:

Prospective study of factors influencing initial resuscitation. J Trauma

1993;34:717-727.
Buckner F, Lyons C, Perkins R: Management of lacerations of the great vessels

of the upper thorax and base of the neck. Surg Gynecol Obstet 1958;107:135-

142.
Buechter KH, Gomez GA, Zeppa R: A new technique for exposure of injuries

at the confluence of the retrohepatic veins and the retrohepatic vena cava.

J Trauma 1990;30:328-331.
Buechter KJ, Sereda D, Gomez G, Zeppa R: Retrohepatic vein injuries: Expe-
rience with twenty cases. J Trauma 1989;29:1698-1704.
BuntTJ: Iatrogenic vascular injury: A discourse on surgical technique. Mt. Kisco,

Futura Publishing, 1990.
Bunt TJ, MaloneJM, Moody M, et al: Frequency of vascular injury with blunt

trauma-induced extremity injury. Am J Surg 1190;160:226.
Bunt TJ, Manship L, Moore W: Iatrogenic vascular injury during peripheral

revascularization. J Vase Surg 1985;2:491-498.
Burch JM, Brock JC, Gevirtzman L, et al: The injured colon. Ann Surg

1986;203:701-711.
Burch JM, Feliciano DV, Mattox KL: The atriocaval shunt: Facts and fiction.

Ann Surg 1988;207:555-568.
Burch JM, Feliciano DV, Mattox KL: Colostomy and drainage for civilian rectal

injuries: Is that all? Ann Surg 1989;209:600-611.
Burch JM, Feliciano DV, Mattox KL, Edelman M: Injuries of the inferior vena

cava. Am J Surg 1988;156:548-552.
Burch JM, Richardson RJ, Martin RR, Mattox KL: Penetrating iliac vascular

injuries: Recent experience with 233 consecutive patients. J Trauma

1990;30:1450-1459.
Burihan I, Pepe EVA, Miranda R: Bullet embolism following gunshot wound

of the chest. J Cardiovasc Surg 1980;21:711-716.
Burnett HF, Parnell CL, Williams GD, Campbell GS: Peripheral arterial injuries:

A reassessment. Ann Surg 1976;183:701-709.

RE.qxd 4/16/04 3:19 PM Page 555

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 555

BurneyRE, Gundry SR, MacKenzieJR, etal: Comparison of mediastinal width,
mediastinal-thoracicandcardioratios, and "mediastinal widening" in detec-
tion of traumatic aortic rupture. Ann Emerg Med 1983;12:668-671.

Burney RE, Gundry SR, MacKenzie JR, et al: Chest roentgenograms in diag-
nosis of traumatic rupture of the aorta. Chest 1984;85:605-609.

Burns GR, Sherman RT: Trauma of the abdominal aorta and inferior vena cava.
Am Surg 1972;38:303-306.

Burnsed DW, Weiss JB, Campbell GS, William GD: The relative merits of the
heparin-bonded shunt vs. femoral bypass of aortic arch injury. Surgery
1975;78:176-180.

Burrell HL: Ligature of the innominate artery with a report of a case. Am Soc
A1895;13:291.

Burrows PE, Tubman DE: Multiple extracranial arterial lesions following closed
cranial facial trauma. J Trauma 1981;21:497-498.

Buscaglia LC, Blaisdell FW, Lim RCJr: Penetrating abdominal vascular injuries.
Arch Surg 1969;99:764-769.

Buscaglia LC, Matolo N, Macbeth A: Common iliac artery injury from blunt
trauma: Case reports. J Trauma 1989;29:697-699.

Busuttil RW, Kitahama A, Cerise E, et al: Management of blunt and penetrat-
ing injuries to the porta hepatis. Ann Surg 1980;191:641-648.

Byrne DE, Pass HI, Crawford FAJr: Traumatic vena caval injuries. Am J Surg
1980;140:600-602.

Cabrera A, Palomar S, Pastor E: Aortic rupture in a child diagnosed by cross
sectional echocardiography. IntJ Cardiol 1987;15:249-252.

Caes LF, Cham B, Sacre J, et al: A patient with two chronic posttraumatic
aneurysms of the thoracic aorta. Thorac Cardiovasc Surg 1989;37:105-106.

Caldeira CCB, Velmahos GC, Modrall JG: Acute suprarenal aortogastric fistu-
lae caused by gunshot wounds: The importance of early recognition in
directing surgical strategy. J Trauma 1996;40:838-839.

CalhoonJH, Hoffmann TH, TrinkleJK, et al: Management of blunt rupture of
the heart. J Trauma 1986;26:495-502.

Callander CL: Study of arteriovenous fistula with an analysis of 447 cases. Ann
Surg 1920;19:428-459.

Cameron HS, Laird JJ, Carroll SE: False aneurysms complicating closed frac-
tures. J Trauma 1972;12:67-74.

Cammack K, Rapport R, Paul J, Baird WC: Deceleration injuries of the thoracic
aorta. Arch Surg 1959;79:244-251.

Campbell DK, Austin RF: Seat belt injury: Injury of the abdominal aorta. Radi-
ology 1969;92:123-124.

Campt PC, Rogers FB, Shackford SR, et al: Blunt traumatic thoracic aortic
lacerations in the elderly: An analysis of outcome. J Trauma 1994;37:
418-425.

Capone AC, Safar P, Stezoski W, et al: Improved outcome with fluid restriction
in treatment of uncontrolled hemorrhagic shock. J Am Coll Surg
1995;180:49-56.

Cappelen A: Vulnus cordis, sutur of hjrtet. Nor Mag f Laegevidensk 1 896;1 1 :285-
288.

Carden DL, Granger DN: Pathophysiology of ischaemia-reperfusion injury.
J Pathol 2000;190:255-266.

Cargile JS III, Hunt JL, Purdue GF: Femoral vascular trauma: A review of 218
cases. J Trauma 1991;31:1025.

RE.qxd 4/16/04 3:19 PM Page 556

556 VI • THE RICH REFERENCE COLLECTION

Cargile JS III, Hunt JL, Purdue GF: Acute trauma of the femoral artery and

vein. J Trauma 1992;32:364-371.
Carlsson E, Silander T: Rupture of the subclavian and innominate artery due

to nonpenetrating trauma of the chest. Acta Chir Scand 1963;125:294-300.
Carrasquilla C, Weaver AW: Aneurysm of the saphenous graft to the common

carotid artery. Vase Surg 1972;6:66-68.
Carrasquilla C, Wilson RE Walt AJ, Arbulu A: Gunshot wounds of the heart.

Ann Thorac Surg 1972;13:208-213.
Carrel A: La technique operatories des anastomoses vasculaires et la trans-
plantation des visceres. Lyon Medical 1902;98:859.
Carrel A: The surgery of blood vessels. Bull Johns Hopkins Hosp 1907;18:18.
Carrel A: Results of transplantation of blood vessels, organs and limbs. JAMA

1908;51:1662-1667.
Carrel A, Guthrie CC: Uniterminal and biterminal venous transplantations.

Surg Gynecol Obstet 1906;2:266-286.
Carroll PR, McAninch JW, Klosterman P, Greenblatt M: Renovascular trauma:

Risk assessment, surgical management, and outcome.J Trauma 1990;30:547-

554.
Carter BN, DeBakey ME: Current observations on war wounds of the chest.

J Thorac Surg 1944;13:271-293.
Carter SL, McKenzie JG, Hess DR: Blunt trauma to the common femoral artery.

J Trauma 1981;21:178-179.
Cass AS, Luxemberg M: Management of renal artery injuries from external

trauma. J Urol 1987;138:266-268.
Cass AS, Luxemberg M: Traumatic thrombosis of a segmental branch of the

renal artery. J Urol 1987;137:1115-1116.
Catinella FP, De Laria GA, De Wald RL: False aneurysm of the superior gluteal

artery: A complication of iliac crest bone grafting. Spine 1990;15:1360.
Catoire P, Bonnet F, Delaunay L, et al: Traumatic laceration of the ascending

aorta detected by transesophageal echocardiography. Ann Emerg Med

1994;23:356-359.
Catoire P, Orliaguet G, Liu N, et al: Systematic transesophageal echocardio-
graphy for detection of mediastinal lesions in patients with multiple injuries.

J Trauma 1995;38:96-102.
Caudros CL, Hutchinson JE, Mogtader AH: Laceration of a mitral papillary

muscle and the aortic root as a result of blunt trauma to the chest. J Thorac

Cardiovasc Surg 1984;88:134-140.
Cerino M, McGrawJY, LukeJC: Autogenous vein graft replacement of throm-
bosed deep veins: Experimental approach to the treatment of the post

phlebitic syndrome. Surgery 1964;55:123-134.
Cernaianu AC, Cilley JH Jr, Baldino WA, et al: Determinants of outcome in

lesions of the thoracic aorta in patients with multiorgan system trauma.

Chest 1992;101:331-335.
Cernaianu AC, Olah A, Cilley JH Jr, et al: Effect of sodium nitroprusside on

paraplegia during cross-clamping of the thoracic aorta. Ann Thorac Surg

1993;56:1035-1037.
Chaikof EL, Shamberger RC, Brewster DC: Traumatic pseudoaneurysms of the

abdominal aorta. J Trauma 1985;25:169-173.
Champion HR, Sacco WJ, Carnazzo AJ, et al: Trauma score. Crit Care Med

1981;9:672-676.
Champion MC, Sullivan SN, Coles JC, et al: Aortoenteric fistula: Incidence,

presentation, recognition and management. Ann Surg 1982;195:314-317.

RE.qxd 4/16/04 3:19 PM Page 557

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 557

Chan EL, Bardin JA, Bernstein EF: Inferior vena cava bypass. J Vase Surg
1984;1:675-680.

Chandler JG, Knapp RW: Early definitive treatment of vascular injuries in the
Vietnam conflict. JAMA 1967;202:960-966.

Chang FC, Harrison PB, Beech RR, Helmer SD: PASG: Does it help in the man-
agement of traumatic shock? J Trauma 1995;39:453-456.

Chang H, Chu SH, Lee YT: Traumatic aorto-right arterial fistula blunt chest
injury. Ann Thorac Surg 1989;47:778-779.

Chapman AJ, McClain J: Wandering missiles: Autopsy study. J Trauma
1984;24:634-637.

Charles KP, Davidson KG, Miller H, Caves PK: Traumatic rupture of the ascend-
ing aorta and aortic valve following blunt chest trauma. J Thorac Cardio-
vasc Surg 1977;73:208-211.

Chase CW, Layman TS, Barker DE, Clements JB: Traumatic abdominal aortic
pseudoaneurysm causing biliary obstruction: A case report and review of
the literature. J Vase Surg 1997;25:936-940.

Chase MD, Schwartz SI: Suture anastomosis of small arteries. Surg Gynecol
Obstet 1963;117:44-46.

Chaudry IH: Cellular mechanisms in shock and ischemia and their correction.
Am J Physiol 1983;245:R117-R134.

Chaudry IH: ATP-MgC12 and liver blood flow following shock and ischemia.
Prog Clin Biol Res 1989;299:19-31.

Chaudry IH: The use of ATP following shock and ischemia. In Dubyak BR,
FedanJS (eds): Biological Actions of Extracellular ATP. Ann NY Acad Sci,
1990: 130-141.

Chaudry IH, Ohkawa M, Clemens MG: Improved mitochondrial function
following ischemia and reflow by ATP-MgCL. Am J Physiol
1984;246:R799-R804.

Chaudry IH, Ohkawa M, Clemens MG, Baue AE: Alterations in electron trans-
port and cellular metabolism with shock and trauma. Prog Clin Biol Res
1983;111:67-88.

Chedid MK, Deeb ZL, Rothfus WE, et al: Major cerebral vessel injury caused
by a seatbelt strap: Case report. J Trauma 1989;29:1601-1603.

Cheek RC, Pope JC, Smith HF, et al: Diagnosis and management of major
vascular injuries: A review of 200 operative cases. Am Surg 1975;41:755-
760.

Cherng WJ, Bullard MJ, Chang HJ, Lin FC: Diagnosis of coronary artery dis-
section following blunt chest trauma by transesophageal echocardiogra-
phy. J Trauma 1995;39:772-774.

CherryJK, Bennett DE: False aneurysm of the aorta following penetrating trauma:
Report of a case with secondary infection and delayed rupture. Arch Surg
1966;93:404-408.

Chervu A, Quinones-Baldrich WJ: Vascular complications in orthopaedic surgery.
Clin Orthop 1988;235:275-288.

Chew FS, Panicek DM, Heitzman ER: Late discovery of a posttraumatic right
aortic arch aneurysm. AJR Am J Roentgenol 1985;145:1001-1002.

Childs D, Wilkes RG: Puncture of the ascending aorta. A complication of sub-
clavian venous cannulation. Anesthesia 1986;41:331-332.

Chitwood W, Austin E: Cardiac trauma: Penetrating and blunt. In Trauma
Surgery. Philadelphia, JB Lippincott Co, 1988.

Chiu CL, Roelofs JD, Go RT: Coronary angiographic and scintigraphic find-
ings in experimental cardiac contusion. Radiology 1975;116:679-683.

RE.qxd 4/16/04 3:19 PM Page 558

558 VI • THE RICH REFERENCE COLLECTION

Choo MH, Chia BL, Chia FK: Penetrating cardiac injury evaluated by two-
dimensional echocardiography. Am HeartJ 1984;108:417-420.

Ciaravella JM, Ochsner JL, Mills NL: Traumatic avulsion of the innominate
artery: A case report and literature review. J Trauma 1976;16:751-754.

Cikrit DF, Dalsing MC, Bryant BJ, Lalka SG: An experience with upper-
extremity vascular trauma. Am J Surg 1990;160:229.

Cioffi WG Jr, Pruitt BA Jr: Vascular abnormalities associated with thermal
and electrical trauma. In Flanigan DP (ed): Civilian Vascular Trauma.
Philadelphia, Lea & Febiger, 1992, pp 255-264.

Clark DE, Georgia JW, Ray FS: Renal arterial injuries caused by blunt trauma.
Surgery 1981;90:87-96.

Clark DE, Zeiger MA, Wallace KL, et al: Blunt aortic trauma: Signs of high risk.
J Trauma 1990;30:701-705.

Clarke CP, Brandt PW, Cole DS, Barratt-Boyes BG: Traumatic rupture of the
thoracic aorta: Diagnosis and treatment. Br J Surg 1967;54:353-358.

Clarke P, Whittaker M: Traumatic aneurysm of the internal carotid artery and
rupture of the duodenum following seatbelt injury. Injury 1980;12:158-
160.

Clemens MG, McDonagh PF, Chaudry IH, Baue AE: Hepatic microcirculatory
failure afterischemia and reperfusion: improvement with ATP-MgCl 2 treat-
ment. Am J Physiol 1985;248:H804-H811.

Clermont G: Suture laterale et circulaire des veines. Presse Med 1901;1:
229.

Cleveland JC, Cleveland RJ: Successful repair of aortic root and aortic valve
injury caused by blunt chest trauma in a patient with prior aortic dissec-
tion. Chest 1974;66:447-450.

Cleveland JC, Ellis J, DagueJ: Complete disruption of axillary artery caused
by severe atherosclerosis and trivial non-penetrating trauma. J Trauma
1979;19:635-636.

Clyne CAC, Ashbrooke EA: Seat-belt aorta: Isolated abdominal aortic injury
following blunt injury. Br J Surg 1985;72:239.

Coelho JC, Siegel B, Flanigan DP, et al: Arteriographic and ultrasonic evalua-
tion of vascular clamp injury using an in vitro human experimental model.
Surg Gynecol Obstet 1982;155:506-512.

Cogbill TH, Moora EE, Jurkovich GJ, et al: Severe hepatic trauma: A multi-
center experience with 1,335 liver injuries. J Trauma 1988;28:1433-1438.

Cogbill TH, Moore EE, Milikan JS, Cleveland HC: Rationale for selective appli-
cation of emergency department thoracotomy in trauma. J Trauma
1983;23:453-460.

Cohen A, Baldwin JN, Grant RN: Problems in the management of battlefield
vascular injuries. Am J Surg 1969;118:526-530.

Cohen A, Brief D, Mathewson CJr: Carotid artery injuries: An analysis of 85
cases. Am J Surg 1970;120:210-214.

Cohen AM, Crass JR, Thomas HA, et al: CT evidence for the "osseous pinch"
mechanism for traumatic aortic injury. AJR Am J Roentgenol 1992; 159:271-
274.

Cohn SM, Burns GA,Jaffe C, Milner KA: Exclusion of aortic tear in the unsta-
ble trauma patient: The utility of transesophageal echocardiography.
J Trauma 1995;39:1087-1090.

Coimbra R, Pinto MC, Razuk A: Penetrating cardiac wounds: Predictive value
of trauma indices and the necessity of terminology of standardization. Am
Surg 1995;61:448-452.

RE.qxd 4/16/04 3:19 PM Page 559

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 559

Coin D, Crighton J, Schorn L: Successful management of hepatic vein injury

from blunt trauma in children. Am J Surg 1980;140:858.
Coley RW. Case of rupture of the carotid artery and wound of several of its

branches successfully treated by tying off the common trunk of the carotid

itself. Med ChirJ (Lond) 1817;3:2.
Collicott PE: Initial assessment of the trauma patient. In Mattox KL, Moore EE,

Feliciano DV (eds) : Trauma. EastNorwalk, Conn, Appleton & Lange, 1988,

pp 107-124.
Collins HA, Jacobs JK: Acute arterial injuries due to blunt trauma. J Bone Joint

Surg 1961;43-A:193-197.
Collins JA: Recent developments in the area of massive transfusion. World J

Surg 1987;11:75-81.
Collins PS, Golocvsky M, Salander JM, et al: Intra-abdominal vascular

injury secondary to penetrating trauma. J Trauma 1988;28:S165-

S168.
Collins RE, Douglass FM: Small vein anastomosis with and without operative

microscope: A comparative study. Arch Surg 1964;88:740-742.
Colon R, Frazier OH, Cooley DA, McAllistr HA: Hypothermic regional perfu-
sion for protection of the spinal cord during periods of ischemia. Ann

Thorac Surg 1987;43:639-643.
ConeJB: Vascular injury associated with fracture-dislocations of the lower extrem-
ity. Clin Orthop 1989:30.
Conkle DM, Richie RE: Surgical treatment of popliteal artery injuries. Arch

Surg 1975;110:1351-1353.
Conn J, Trippel OH, Bergan JJ: A new atraumatic aortic occluder. Surgery

1968;64:1158.
ConnJH, Hardy JD, Chavez CM, Fain WR: Challenging arterial injuries. J Trauma

1971;11:167-177.
Connelly JE, Brownell DA, Levine EF: Complications of renal dialysis access

procedures. Arch Surg 1984;119:1325-1328.
Connery C, Geller E, Dulchavsky S, Kreis DJ: Paraparesis following emergency

room thoracotomy: Case report. J Trauma 1990;30:362-363.
Connolly J, Williams E, Whittaker D: The influence of fracture stabilization on

the outcome of arterial repair in combined fracture-arterial injuries. Surg

Forum 1969;20:450-452.
ConnollyJ: Management of fractures associated with arterial injuries. Am J Surg

1970;120:331.
Connolly JE: Prevention of paraplegia secondary to operations on the aorta.

J Cardiovasc Surg 1986;27:410-417.
Connolly JE, KwaanJHM, McCart PM: Complications after percutaneous trans-
luminal angioplasty. Am J Surg 1981;142:60-66.
Connolly JF, Whittaker D, Williams E: Femoral and tibial fractures combined

with injuries to the femoral or popliteal artery. J Bone Joint Surg 1971;53-

A56-67.
Conti VR, Calverley J, Safley WL, et al: Arterial spinal artery syndrome with

chronic traumatic thoracic aortic aneurysm. Ann Thorac Surg 1982;33:81-

85.
Contino JP, Follette DM, Berkoff HA, et al: Use of Carmeda-coated femoral-
femoral bypass repair of traumatic aortic pseudoaneurysm. Arch Surg

1994;129:933-937.
Cook FW, Haller JAJr: Penetrating injuries of the subclavian vessels associated

with venous complications. Ann Surg 1962;155:370-372.

RE.qxd 4/16/04 3:19 PM Page 560

560 VI • THE RICH REFERENCE COLLECTION

Cook P, Erdoes L, Selzer P: Dissection of the external iliac artery in highly

trained athletes. J Vase Surg 1995;22:173.
Cook TA, Jones AJ, Webb AK, Baird RN: Traumatic abdominal aortic aneurysm.

Eur J Vase Surg 1994;8:364-365.
Cooley DA, Dunn JR, Brockman HL, DeBakey ME: Treatment of penetrating

wounds of the heart: Experimental and clinical observations. Surgery

1955;37:882.
Cooper B: Wounds in arteries and traumatic aneurysms. Guys Hosp Rep

1852;8:195.
Cope C, Zeit R: Coagulation of aneurysms by direct percutaneous thrombin

injection. AJR Am J Roentgenol 1986;147:383-387.
Copper ES: Aneurysm of the right carotid and subclavian arteries. Am J Med

Sci 1859;38:395.
Cornwell EE, Kennedy F, Berne TV, et al: Gunshot wounds to the thoracic aorta

in the '90s: Only prevention will make a difference. Am Surg 1995;61:721-

723.
Cosby RL, Miller PD, Schirir RW: Traumatic renal artery thrombosis. Am J Med

1986;81:890-894.
CoselliJS, Crawford ES: Surgical treatment of aneurysms of the intrathoracic

segment of the subclavian artery. Chest 1987;91:704-708.
Costa M, Robbs JV: Management of retroperitoneal haematoma following

penetrating trauma. Br J Surg 1985;72:662-664.
Costa MC, Robbs JV: Nonpenetrating subclavian artery trauma. J Vase Surg

1988;8:71-75.
Couch NP, Cerundolo D: A clip for the rapid control of the vascular injuries.

Surg Gynecol Obstet 1981;153:408-409.
Courcy PA, Brotman S, Oster-Granite ML, et al: Superior mesenteric artery and

vein injury from blunt abdominal trauma. J Trauma 1984;24:843-845.
Couves CM, Lumpkin MB, Howard JM: Arterial injuries due to blunt-

nonpenetrating trauma: Experiences with 15 patients. Can J Surg 1958;

1:197-200.
Cowgill LD, Campbell DN, Clarke DR, et al: Ventricular septal defect due to

non-penetrating chest trauma: Use of the intra-aortic balloon pump.

J Trauma 1987;27:1087-1090.
Cranley JJ, Krause RJ: Injury to the axillary artery following anterior disloca-
tion of the shoulder. Am J Surg 1958;95:524-526.
Crawford ES, FenstermacherJM, Richardson W, Frank S: Reappraisal of adjuncts

to avoid ischemia in the treatment thoracic aortic aneurysms. Surgery

1970;67:182-196.
Crawford ES, Mizrahi EM, Hess KR, et al: The impact of distal aortic perfusion

and somatosensory evoked potential monitoring on prevention of

paraplegia after aortic aneurysm operation. J Thorac Cardiovasc Surg

1988;95:357-367.
Crawford ES, Morris GCJr, Myhre HO, Roehm JO: Celiac axis, superior mesen-
teric artery and inferior mesenteric artery occlusion: considerations. Surgery

1977;82:856-866.
Crawford ES, Svensson LG, Hess KR, et al: A prospective randomized study of

cerebrospinal fluid drainage to prevent paraplegia after high-risk surgery

on the thoracoabdominal aorta. J Vase Surg 1991;13:36-46.
Creagh TA, Broe PJ, Grace PA, Bouchier-Hayes DJ: Blunt trauma induced upper

extremity vascular injuries. J R Coll Surg Edinb 1991;36:158.
Creech O Jr: Acute arterial injuries. Postgrad Med 1961;29:581.

RE.qxd 4/16/04 3:19 PM Page 561

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 561

Creech O Jr, Gantt J, Wren H: Traumatic arteriovenous fistula at unusual sites.

Ann Surg 1965;161:908-920.
CreppsJTJr, Rodriguez A: Combined abdominal aortic and visceral artery injury

secondary to blunt trauma. Injury 1989;20:176-177.
Crissey MM, Bernstein EF: Delayed presentation of carotid intimal tear following

blunt craniocervical trauma. Surgery 1974;75:543-549.
CronenwettJL, Walsh DB, Garrett HE: Tibial artery pseudoaneurysms: delayed

complication of balloon catheter embolectomy. J Vase Surg 1988;8:483-

488.
CronenwettJL, McDaniel M, Zwolak R, et al: Limb salvage despite extensive

tissue loss: Free tissue transfer combined with distal revascularization. Arch

Surg 1989;124:609-615.
Cryer HM, Miller FB, Evers M, et al: Pelvic fracture classification: Correlation

with hemorrhage. J Trauma 1988;28:973-980.
Cterctko G, Mok CK: Aorto-esophageal fistula induced by a foreign body: The

first recorded survival. J Thorac Cardiovasc Surg 1980;80:233-235.
Curley SA, Demarest G, Hauswald M: Pericardial tamponade and hemothorax

after penetrating injury to the internal mammary artery. J Trauma

1987;27:957-958.
Currarino G, Engle ME: The effects of ligation of the subclavian artery on the

bones and soft tissues of the arms. J Pediatr 1965;67:808-811.
Curtin JJ, Goodman LR, Thorsen MR: Aortic traumatic lesion: Has tomoden-

sitometry a role? J Radiol 1993;74:523-530.
CusickJF, Daniels D: Spontaneous reversal of internal carotid artery occlusion:

Case report. J Neurosurg 1981;54:811-813.
DainkoEA: Complications of the use of the Fogarty balloon catheter. Arch Surg

1972;105:79-82.
Dajani OM, Haddad FF, Hajj HA, et al: Injury to the femoral vessels: The Lebanese

War experience. Eur J Vase Surg 1988;2:293-296.
Dajee H, Richardson IW, Iype MO: Seatbelt aorta: Acute dissection and throm-
bosis of the abdominal aorta. Surgery 1979;85:263-267.
Dale WA: Chronic iliofemoral venous occlusion including seven cases of cross-
over vein grafting. Surgery 1966;59:117-132.
Dale WA: Management of arterial occlusive disease (national conference on

management of arterial occlusive disease, Naashville, 1970). In Dale WA

(ed): Chicago, Year Book Publisher Inc, 1971.
Dale WA: The beginnings of vascular surgery. Surgery 1974;76:849-866.
Dale WA, Harris J, Terry RB: Polytetrafluoroethylene reconstruction of the

inferior vena cava. Surgery 1984;95:625-630.
Dalton HC: Report of a case of stab wound of the pericardium, terminating in

recovery after resection of a rib and suture of the pericardium. Ann Surg

1895;21:147-152.
Dameron TB Jr: False aneurysm of femoral profundus artery resulting

from internal-fixation device (screw). J Bone Joint Surg 1964;46A:577-

580.
Damron T, McBeath A: Diagnosis and management of vascular injuries associ-
ated with skeletal trauma. Orthop Rev 1990;19:1063.
Dana A, Skarli M, Papakrivopoulou J, Yellon DM: Adenosine A(l) receptor

induced delayed preconditioning in rabbits: Induction of p38 mitogen-

activated protein kinase. Circ Res 2000;86:989-997.
Danielson GK, Wood R, Holloway JB: Traumatic avulsion of the innominate

artery from the aorta. Ann Thorac Surg 1968;5:451-458.

RE.qxd 4/16/04 3:19 PM Page 562

562 VI • THE RICH REFERENCE COLLECTION

Danto LA, Wolfman EFJr: Linear abdominal trauma. J Trauma 1976;16:179-

183.
Danza R, Mauro L, Arias J: Reconstruction of the femoro-popliteal vessels with

a double graft (arterial and venous) in severe injury of the limb. J Cardiac

Surg 1970;11:60-64.
Dart CH Jr, Braitman HE: Traumatic rupture of the thoracic aorta: diagnosis

and management. Arch Surg 1976;111:697-702.
Dart CH Jr, Braitman HE: Popliteal artery injury following fracture or disloca-
tion at the knee: Diagnosis and management. Arch Surg 1977;112:969-973.
David D, Blumenberg RM: Subintimal aortic dissection with occlusion after

blunt abdominal trauma. Arch Surg 1970;100:302-304.
Davie JC, Coxe W: Occlusive disease of the carotid artery in children. Arch

Neurol 1967;17:313-323.
Davies MG, Hagen PO: The vascular endothelium: A new horizon. Ann Surg

1993;218:593-609.
Davis. 1834. Cited in: Straus R. Pulmonary embolism caused by lead bullet fol-
lowing gunshot wound of abdomen. Arch Path 1942;33:63-68.
Davis JM, Zimmerman RA: Injury of the carotid and vertebral arteries. Neuro-
radiology 1983;25:55-69.
Davis TP, Feliciano DV, Rozycki GS: Results with abdominal vascular trauma in

the modern era. Am Surg 2001;67:565-571.
Dawson D, Johanse K, Jurkovich G: Injuries to the portal triad. Am J Surg

1991;161:545.
Daxini BV, Desai AG, Sharma S: Echo-Doppler diagnosis of aortocaval fistula

following blunt trauma to abdomen. Am HeartJ 1989;118:843-844.
de Guzman E, Shankar MN, Mattox KL: Limited volume resuscitation in

penetrating thoracoabdominal trauma. AACN Clin Issues 1999;10:61-68.
De Nayer P, Jaumin P, Linard D: Lesions osteo-articulaires des membres com-

pliquees de traumatismes vascularies. Acta Chir Belg 1973;72:427.
De Takats G: Vascular surgery in the war. War Med 1943;3:291-296.
De Takats G: Vascular Surgery. Philadelphia, WB Saunders, 1959.
De Takats G: Symptoms and signs of peripheral arterial disease. Med Clin North

Am 1962;46:647-657.
De Takats G: Trauma to the arteriosclerotic limb. J Trauma 1963;4:47.
De Takats G, Pirani C: Aneurysms: General considerations. Angiology 1954;5: 1 73-

208.
De Wet LubbeJJ, Janson PM: Penetrating wounds of the heart and great vessels:

Experience with cases including three with intracardiac defects. South Afr

MedJ 1975;29:512-516.
Dean RH: Management of renal artery trauma. J Vase Surg 1988;8:89-90.
DeBakey ME, Simeone FA: Battle injuries of the arteries in World War II: An

analysis of 2,471 cases. Ann Surg 1946;123:534-579.
DeBakey ME, Cooley DA, Morris GCJr, Collins H: Arteriovenous fistula involv-
ing the abdominal aorta: Report of four cases with successful repair. Ann

Surg 1958;147:646-658.
DeBakey ME, Beall ACJr, WukaschDC: Recent developments in vascular surgery

with particular reference to orthopaedics. Am J Surg 1 965; 109: 134-

142.
DeBakey ME: The development of vascular surgery. Am J Surg 1979;137:697-

738.
Defore WWJr, Mattox KL, Jordan GLJr: Management of 1590 consecutive cases

of liver trauma. Arch Surg 1976;111:493-497.

RE.qxd 4/16/04 3:19 PM Page 563

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 563

Degianni E, Levy RD, Sofianos C, et al: Arterial gunshot injuries of the extrem-
ities: A South African experience. J Trauma 1995;39:570-575.

DelRossi AJ, Cernaianu AC, Cilley JH Jr, et al: Multiple traumatic disruptions
of the thoracic aorta. Chest 1990;97:1307-1309.

DelRossi AJ, Cernaianu AC, Madden LD, et al: Traumatic disruptions of the
thoracic aorta: Treatment and outcome. Surgery 1990;108:864-870.

DeLucia A III, Fromm D: Retropancreatic control of the suprarenal aorta. Surg
Gynecol Obstet 1988;166:475-476.

Demetriades D: Cardiac wounds. Ann Surg 1986;203:315-317.

Demetriades D, Rabinowitz B, Pezikis A, et al: Subclavian vascular injuries. Br
J Surg 1987;74:1001-1003.

Demetriades D, SkalkidesJ, Safianos C: Carotid artery injuries: Experience with
124 cases. J Trauma 1989;29:91-94.

Corrected

Demetriades D, Charalam bides L, Sareli P: Later sequelae of penetrating cardiac
injuries. Br J Surg 1990;77:813-814.

Demetriades D, Theodorou D, Murray J, et al: Mortality and prognostic factors
in penetrating injuries of the aorta. J Trauma 1996;40:761-763.

Demetriades D, Chan L, Cornwell E, et al: Paramedic vs. private transportation
of trauma patients. Arch Surg 1996;131:133-138.

DeMeulesJE, Cramer G, Perry JFJr: Rupture of aorta and great vessels due to
blunt thoracic trauma. J Thorac Cardiovasc Surg 1971;61:438-442.

DeMuth WE: Bullet velocity makes the difference. J Trauma 1969;9:642-
643.

DeMuth WE Jr, Baue AE, Odom JA Jr: Contusions of the heart. J Trauma
1967;7:443-445.

DeMuth WE Jr, Roe H, Hobbie W: Immediate repair of traumatic rupture of
the aorta. Arch Surg 1965;91:602-603.

Dennis JW, Frykberg ER, Crump JM, et al: New perspectives on the manage-
ment of penetrating trauma in proximity to major limb arteries. J Vase Surg
1990;11:85-93.

Dent RI,Jena GP: Missile injuries of the abdomen in Zimbabwe-Rhodesia. Br
J Surg 1980;67:305-310.

DePriest W, Barish R, Almquist T, Groleau G: Echocardiographic diagnosis of
acute pericardial effusion in penetrating chest trauma. Am J Emerg Med
1988;6:21-23.

DeSa'Neto A, Padnick MB, Desser KB, Steinhoff NG: Right sinus of Valsalva-
right atrial fistula secondary to nonpenetrating chest trauma. Circulation
1979;60:205-209.

Desai SB, ModheJM, Aulakh BG: Percutaneous transcatheter steel-coil emboliza-
tion of a large proximal post-traumatic superior mesenteric arteriovenous
fistula. J Trauma 1987;27:1091.

DeSaussure RL: Vascular injury coincident to disc surgery. J Neurosurg
1959;16:222-228.

DesChamps GT, Morano JU: Intracranial bullet migration: A sign of brain abscess:
Case report. J Trauma 1991;31:293-295.

DesForges G, Ridder WP, Lenoci RJ: Successful suture of ruptured myocardium
after nonpenetrating injury. N Engl J Med 1955;252:567-569.

Detwiler K, GoderskyJC, Gentry L: Pseudoaneurysm of the extracranial verte-
bral artery. J Neurosurg 1987;67:935-939.

DeWeese JA, Mattox KL, Seltzer SE, BukleyJM: Symposium on traumatic tho-
racic aortic rupture. Contemp Surg 1984;24:109-131.

RE.qxd 4/16/04 3:19 PM Page 564

564 VI • THE RICH REFERENCE COLLECTION

Dharker SR, Dharker RS: Traumatic occlusion of internal carotid artery in an
infant. Surg Neurol 1978;9:77-78.

Dichtel WJ, Miller RH, Woodson GE, et al: Lateral mandibulotomy: A tech-
nique of exposure for penetrating injuries of the internal carotid artery at
the base of the skull. Laryngoscope 1984;94:1140-1144.

Dickerman RM, Gewertz BL, Foley DW, Fry WJ: Selective intra-arterial tolazo-
line infusion in peripheral arterial trauma. Surgery 1977;81:605-609.

Diebel LN, Wilson RF, Bennder J, Paules B: A comparison of passive and active
shunting for bypass of retrohepatic IVC. J Trauma 1991;31:987-990.

Dieter RA, Asselmeier GH, Hamouda F, et al: Traumatic disruption of the tho-
racic aorta: A community hospital experience. Mil Med 1983;148:502-506.

Dieux JJ, Milani H, Maillet P, Brahy R: A case of 2-stage traumatic rupture of
the abdominal aorta. Acta Chir Belg 1985;85:367-370.

Dillard BM, Nelson DL, Norman HG: Review of 85 major traumatic arterial
injuries. Surgery 1968;63:391-395.

Dillard BM, Staple TW: Bullet embolism from the aortic arch to the popliteal
artery. Arch Surg 1969;98:326-328.

Dillman RO, Crumb CK, Lidsky MJ: Lead poisoning from a gunshot wound.
Am J Med 1979;66:509-514.

DiMaio VJ, DiMaio DJ: Bullet embolism: Six cases and a review of the literature.
J Forens Sci 1972;17:394-398.

Dimond FC Jr, Rich NM: M-16 wounds in Vietnam. J Trauma 1967;7:618-
625.

Dingeldein GR Proctor HJ, Jaques PF: Traumatic aorto-caval-portal-duodenal
fistula: Case report. J Trauma 1977;17:474-476.

Diveley WL, Daniel RAJr, Scott HWJr: Surgical management of penetrating
injuries of the ascending aorta arch. J Thorac Cardiovasc Surg 1961;41:23-
33.

DiVincenti FC, Weber BB: Traumatic carotid artery injuries in civilian practice.
Am Surg 1974;40:277-280.

Dixon RG, McEwan P: Notes on a case of penetrating wound of the heart. Br
MedJ1916;l:755.

Doan E, Gorton ME: Traumatic disruption of the innominate and right pul-
monary arteries: Case report. J Trauma 19;43:701-702.

Dobell ARC, MacNaughton EA, Crutchlow EF: Successful early treatment of
subadventitial rupture of the thoracic aorta. N Engl J Med 1964;270:410-
412.

Dobrin PB: Mechanisms and prevention of arterial injuries caused by balloon
embolectomy. Surgery 1989;106:457-466.

Donahue TK, Strauch GO: Ligation as definitive management of injury to the
superior mesenteric vein. J Trauma 1988;28:541-543.

Donchin Y, Rivkind Al, Bar-ZivJ, et al: Utility of postmortem computed tomo-
graphy in trauma victims. J Trauma 1994;37:552-556.

Donell ST, Hudson MJK: Iatrogenic superior mesenteric arteriovenous fistula:
Report of a case. J Vase Surg 1988;8:335.

Donovan DL, Sharp WV: Blunt trauma to the axillary artery. J Vase Surg
1984;1:681-683.

Dorfman GS, Cronan ]J: Bayesian analysis of chest plain film finding in trau-
matic rupture of the aorta. Invest Radiol 1987;22:S4.

Dorion RP, Hamati HF, Landis B: Risk and clinical significance of developing
antibodies induced by topical thrombin preparations. Arch Pathol Lab
Med 1998;122:887-894.

RE.qxd 4/16/04 3:19 PM Page 565

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 565

Dosios TJ, Magoven GJ, Gay TC, Joyner CR: Cardiac tamponade complicating
percutaneous catheterization of subclavian vein. Surgery 1975;78:261-263.

Doty DB, Baker WH: Bypass of superior vena cava with spiral vein graft. Ann
Thorac Surg 1976;22:490-493.

Doty DB, Treiman RL, Rothschild PD, Gaspar MR: Prevention of gangrene due
to fractures. Surg Gynecol Obstet 1967;125:284-288.

Downs AR, MacDonald P: Popliteal artery injuries: Civilian experience with sixty-
three patients during a twenty-four year period. J Vase Surg 1986;4:55-62.

DorflerJ: Uber arteriennaht. Beitr Klin Chir 1889;25:781.

Dragojevic D, Hetzer R, Oelert H: Surgery for traumatic rupture of the tho-
racic aorta. Thorac Cardiovasc Surg 1980;28:436-440.

Dragon R, Saranchak H, Lakin P, Strauch G: Blunt injuries to the carotid ver-
tebral arteries. Am J Surg 1981;141:497-500.

Drapanas T, Hewitt RL, Weichert RF III, Smith AD: Civilian vascular injuries:
Acritical appraisal of three decades of management. Ann Surg 1970;172:351-
360.

Dronen SC, Stern SA, Wang X, Stanley M: A comparison of the response of
near fatal acute hemorrhage mode with and with out a vascular injury to
rapid volume expansion. Am J Emerg Med 1993;11:331-335.

Drost TF, Rosemurgy AS, Proctor D, Kearney RE: Outcome of treatment of
combined orthopedic and arterial trauma to the lower extremity. J Trauma
1989;29:1331-1334.

Drury JK, Scullion JE: Vascular complications of anterior dislocation of the
shoulder. Br J Surg 1980;67:579-581.

Dshanelidze II. Manuskript petrograd. 1922. Cited in: Lilianthal H: 1926.

Du Toit DF, Greeff M: Low-velocity gunshot injury of the abdominal aorta
managed by debridement and re-anastomosis. S Afr Med J 1986;18:139-
140.

Du Toit DF, Rademan F: Traumatic superior mesenteric arteriovenous fistula:
A case report. S Afr Med J 1987;71:587.

Dube P: Control of massive carotid hemorrhage by balloon catheter. Thorax
1973;28:399-400.

Dubinskiy MB: Suture of the abdominal aorta. Khirurgiya 1944;4:71.

Duhaylongsod FG, Glower DD, Wolfe WG: Acute traumatic aortic aneurysm:
The Duke experience from 1970 to 1990. J Vase Surg 1992;15:331-343.

Dula DJ, Hughes HG, Majernick T: Traumatic disruption of the brachiocephalic
artery. Ann Emerg Med 1983;12:639-641.

Dulchavsky SA, Geller ER, Iorio DA: Analysis of injuries following the crash of
Avianca flight 52. J Trauma 1993;34:282-284.

Duncan A, Scalea T, Sclafani SJ: Evaluation of occult cardiac injuries using sub-
xiphoid pericardial window. J Trauma 1989;29:955-960.

Durham LA, Richardson RJ, Wall MJ: Emergency center thoracotomy impact
of prehospital resuscitation. J Trauma 1992;32:775.

Earle AS, HorsleyJS, Villavicencio JL, Warren R: Replacement of venous defects
by venous autografts. Arch Surg 1960;80:119-124.

Eastcott HH: The management of arterial injuries. J Bone Joint Surg
1965;47B:394-398.

Eastcott HHG: Arterial Surgery. Philadelphia, JB Lippincott Co, 1969.

Eaves CC: Traumatic rupture of the thoracic aorta presenting as transient para-
plegia. J Emerg Med 1990;8:429-431.

EckNV: K voprosu o perevyazkie vorotnoisveni. Predvaritelnoye soobshtshjenye
(Ligature of the portal vein). Voen Med J 2001;130:1-2.

RE.qxd 4/16/04 3:19 PM Page 566

566 VI • THE RICH REFERENCE COLLECTION

Eddy AC, Misbach GA, Luna GK: Traumatic rupture of the thoracic aorta in

the pediatric patient. Pediatr Emerg Care 1989;8:429-431.
Eddy AC, Nance DR, Goldman MA, et al: Rapid diagnosis of thoracic aortic

transection using intravenous digital subtraction angiography. Am J Surg

1990;159:500-503.
Eddy AC, Rusch VW, Fligner CL, et al: The epidemiology of traumatic rupture

of the thoracic aorta in children: A 13-year review. J Trauma 1990;30:989-

992.
Eddy AC, Rusch VW, Marchioro T, et al: Treatment of traumatic rupture of the

thoracic aorta. Arch Surg 1990;125:1351-1356.
Edmundson K: Transfixion of the aorta. Br J Surg 1963;23:869-870.
Edwards WS, Lyons C: Traumatic arterial spasm and thrombosis. Ann Surg

1957;140:318-323.
Egan TJ, Neiman RJ, Malave SR, Sanders JH: Computed tomography in the

diagnosis of aortic aneurysm dissection or traumatic injury. Radiology

1980;136:141-146.
Eger M, Glocman L, Goldstein A, Hirsch M: The use of temporary shunt in the

management of arterial vascular injuries. Surg Gynecol Obstet 1971 ; 1 32:67-

70.
Eger M, Glocman L, Torok G, Hirsch M: Inadvertent arterial stripping in the

lower limb: Problems of management. Surgery 1973;73:23-27.
Eger M, Glocman L, Schmidt D, Hirsch M: Problems in the management of

popliteal artery injuries. Surg Gynecol Obstet 1973;134:921-926.
Eger M, Schmidt B, Torok G: Replantation of the upper extremities. Am J Surg

1974;4:47-50.
Ehrenfeld WK, Wilber BG, Olcott CN, Stoney RJ: Autogenous tissue recon-
struction in the management of infected prosthetic grafts. Surgery

1979;85:82-91.
Eifert S, Villavicencio JL, Kao TC, et al: Prevalence of deep venous anomalies

in congenital vascular malformations of venous predominance. J Vase Surg

2000;31:462-471.
Eiseman B, Rainer WG: Clinical management of post traumatic rupture of the

thoracic aorta. J Thorac Cardiovasc Surg 1958;35:347-358.
EisenbreyAB: Arteriovenous aneurysm of the superficial femoral vessels. JAMA

1913;61:2155-2157.
Ekbom B, Towne JB, Majewski JT, Woods JH: Intra-abdominal vascular trauma:

A need for prompt operation. J Trauma 1981;21:1040-1044.
Eklof B, GjoresJE, Thulesius O, Bergqvist D: Controversies in the Management

of Venous Disorders. Stoneham, Butterworths, 1989.
Elderding SC, Manart FD, Moore EE: A reappraisal of penetrating neck injury

management. J Trauma 1980;20:695-697.
Elford J, Burrell C, Roobottom C: Ultrasound guided percutaneous thrombin

injection for the treatment of iatrogenic pseudoaneurysms. Heart

1999;82:526-527.
Elkin DC: Diagnosis and treatment of cardiac trauma. Ann Surg 1941;114:169-

185.
Elkin DC: Vascular injuries of warfare. Ann Surg 1944;120:284-310.
Elkin DC: Wounds of the heart. Ann Surg 1944;120:817-821.
Elkin DC: Arteriovenous aneurysm. Surg Gynecol Obstet 1945;80:217-

224.
Elkin DC: Traumatic aneurysm: The Matas Operation 57years after. Surg Gynecol

Obstet 1946;82:1-12.

RE.qxd 4/16/04 3:19 PM Page 567

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 567

Elkin DC, Banner EA: Arteriovenous aneurysms following surgical operations.
JAMA 1946;131:1117-1119.

Elkin DC, Campbell RE: Cardiac tamponade: Treatment by aspiration. Ann
Surg 1941;133:623-630.

Elkin DC, DeBakey ME: Vascular surgery in World War II. Washington, DC, US
Government Printing Office, 1955.

Elkin DC, Harris MH: Arteriovenous aneurysm of the vertebral vessels. Ann
Surg 1946;124:934-951.

Elkin DC, Shumacker HB Jr: In Elkin DC, DeBakey ME (eds) : Vascular Surgery
in World War II. Washington, DC, US Government Printing Office, 1944.

Elkin DC, Woodhall B: Combined vascular and nerve injuries of warfare. Ann
Surg 1944;119:411-431.

Elkins RC, DeMeester TR, Brawl ey RK: Surgical exposure of the upper abdomi-
nal aorta and its branches. Surgery 1971;70:622-627.

Eller JL, Ziter FMH: Avulsion of the innominate artery from the aortic arch.
Radiology 1970;94:75-78.

Elliot JA: Acute arterial occlusion: An unusual cause. Surgery 1956;39:825-827.

Ellis F: Surgical repair of a traumatic rupture of the thoracic aorta. Br J Surg
1959;46:495-499.

Ellis J: Case of gunshot wound, attended with secondary hemorrhage in which
both carotid arteries were tied at an interval of four and a half days. N YJ
Med 1845;5:187.

Ellis J: A case of probable lead poisoning, resulting fatally from a bullet lodged
in the knee joint twelve years previously. Boston Med Surg J 1874;91:
472.

Ellison RG, Meares CH: Traumatically injured aortic arch repaired under pro-
found hypothermia and circulatory arrest. Am Surg 1977;43:298-302.

Elmore JR, Gloviczki P, Harper CM Jr, et al: Spinal cord injury in experimen-
tal thoracic aortic occlusion: Investigation of combined methods of pro-
tection. J Vase Surg 1992;15:789-799.

Enderson BL, Reath DB, Meadors J, Dallas W: The tertiary trauma survey: A
prospective study of missed injury. J Trauma 1990;30:666.

Enge I, Aakhus T, Evensen A: Angiography in vascular injuries of the extremi-
ties. Acta Radiol Diag 1975;16:193-199.

Engleman RM, Clements JM, Herrmann JB: Stab wounds and traumatic false
aneurysms in the extremities. J Trauma 1969;9:77-87.

Epstein BM, Bocchiola FC, AndrewsJC, Bester L: Traumatic arteriovenous fistula
involving the portal venous system. Clin Radiol 1987;38:91-93.

Ergin MA, O'Connor JV, Blanche C, Griepp RB: Use of stapling instruments
in surgery for aneurysms of the aorta. Ann Thorac Surg 1983;36:161-166.

Ernst CB, Daugherty ME, Bristow DL: Supraceliac pseudoaneurysm of abdomi-
nal aorta. Arch Surg 1975;110:211-225.

Ernst CB, Kaufer F: Fibulectomy-fasciotomy: An important adjunct in the man-
agement of lower extremity arterial trauma. J Trauma 1971;11:365.

Erskine JM: Case report: A true traumatic aneurysm of the radial artery at the
wrist successfully treated by resection and arterial repair. J Trauma
1964;4:530-534.

Escobar GA, Escobar SC, Marquez L, et al: Vascular trauma: Late sequelae and
treatment. J Cardiac Surg 1980;21:35-40.

Eshaghy B, Loeb HS, Miller SE, et al: Mediastinal and retropharyngeal hem-
orrhage. A complication of cardiac catheterization. JAMA 1973;226:427-
431.

RE.qxd 4/16/04 3:19 PM Page 568

568 VI • THE RICH REFERENCE COLLECTION

Esmarch F: The Surgeons Handbook of the Treatment of the Wounded in War.
New York, LW Schmidt, 1878.

Espada R, Wisennand HH, Mattox KL, Beall AC Jr: Surgical management of
penetrating injuries to the coronary arteries. Surgery 1975;78:755-760.

Espinoza R, Sonneborn R: Contusion of the abdominal aorta and massive
embolization from the use of a seat belt. Rev Med Chil 1990;118:1376-1379.

Esposito TJ, Jurkovich G, Rice CL: Reappraisal of emergency room thoraco-
tomy in a changing environment. J Trauma 1991;31:881-887.

Esterera AS, Pass LJ, Piatt MR: Systemic arterial air embolism in penetrating
lung injury. Ann Thorac Surg 1990;2:257.

EttienJT: Crutch-induced aneurysms of the axillary artery. Am Surg 1980;46:267-
269.

Evans J, Gray LA, Rayner A, Fulton RL: Principles for the management of pen-
etrating cardiac wounds. Ann Surg 1979;189:777-784.

Evans WE, Bernhard VM: Tibial artery bypass for ischemia resulting from frac-
tures. J Trauma 1971;11:999-1007.

Fabian TC, Turkleson ML, Connelly TL, Stone HH: Injury to the popliteal artery.
Am J Surg 1982;143:225-228.

Fabian TC, Mangiante EC, Patterson CR, et al: Myocardial contusion in blunt
trauma: Clinical characteristics, means of diagnosis and implications for
patient management. J Trauma 1988;28:50-57.

Fabian TC, George SM Jr, Croce MA, et al: Carotid artery trauma: Management
based on mechanism of injury. J Trauma 1990;30:953-963.

Fabian TC, Richardson JD, Croce MA, et al: Prospective study of blunt aortic
injury: Multicenter trial of the American Association for the Surgery of
Trauma. J Trauma 1997;42:748-755.

Fabian TC, Richardson JD, Croce MA, et al: Perspective study of blunt aortic
injury: Multicenter trial of the American Association for Surgery of Trauma.
J Trauma 1997;42:374-387.

Fakhry BM, Jaques FF, Proctor HJ: Cervical vessel injury after blunt trauma.
J Vase Surg 1988;8:501-508.

Falkmer L, Eriksson A, Arnerlov C, Domellof L: Arterial bullet embolism with
radiologic demonstration of vessel entrance site. World J Surg 1987;1 1:548-
558.

Fallahnejad M, Kutty ACK, Menut H: The importance of intra-aortic balloon
pumping in the management of coronary artery laceration. J Cardiac Surg
1983;23:426-428.

Fallahnejad M, Kutty ACK, Wallace HW: Secondary lesions of penetrating cardiac
injuries: A frequent complication. Ann Surg 1980;191:228-233.

Fallahnejad M, Wallace HW, Su CC, et al: Unusual manifestations of penetrat-
ing cardiac injuries. Arch Surg 1975;110:1357-1362.

Fallon G, Thomford NR: False aneurysm of the superficial femoral artery asso-
ciated with fracture of the femur. Angiology 1970;21:120-123.

Falor WH, Hansel JR, Williams GB: Gangrene of the hand: A complication of
radial artery cannulation. J Trauma 1976;16:713-716.

Fargally M, ChristensonJT: Combined aortic and inferior vena cava injury during
laminectomy. Vasa 1988;17:288-292.

Farhood A, McGuire GM, Manning AM, et al: Intercellular adhesion molecule
1 (ICAM-1) expression and its role in neutrophil induced ischemia-
reperfusion injury in rat liver. J Leukoc Biol 1995;57:368-374.

Farina C, Cavallaro A, Schultz RD, et al: Popliteal aneurysms. Surg Gynecol
Obstet 1989;169:7-13.

RE.qxd 4/16/04 3:19 PM Page 569

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 569

Faro RS, Monson DO, Weinberg M, Javid H: Disruption of aortic arch branches
due to nonpenetrating chest trauma. Arch Surg 1983;118:1333-1336.

Farret A, Da Ros CT, Fischer CA, et al: Suprarenal aorta reconstruction using
a saphenous spiral graft: A case relate? J Trauma 1994;37:114-118.

Fasol R, Irvine S, Zilla P: Vascular injuries caused by anti-personnel mines.
J Cardiac Surg 1989;30:467.

Fay R, Brosman S, Lidstrom R: Renal artery thrombosis: A successful revascu-
larization by autotransplantation. J Urol 1974;111:572.

Feczko JD, Lynch L, PlessJE, et al: An autopsy case review of 142 nonpene-
trating (blunt) injuries of the aorta. J Trauma 1992;33:846-849.

FeeJF, CavoyJM, Dainko EA: Pseudoaneurysm of the axillary artery following
a modified Bristow operation: A report of a case and review. Cardiovasc
Surg 1978;19:65-68.

Feigenbaum H, Waldhausen JA, Hyde LP: Ultrasonic diagnosis of pericardial
effusion. JAMA 1965;191:107.

Feigenbaum H, Zaky A, Waldhausen JA: Use of ultrasound in diagnosis of peri-
cardial effusion. Intern Med 1966;65:443.

Feliciano DV: Managing peripheral vascular trauma. Infect Surg 1986;5:659-
669.

Feliciano DV: Pitfalls in the management of peripheral vascular injuries. In
Roses D (ed): Problems in General Surgery. Philadelphia, JB Lippincott
Co, 1986, pp 101-113.

Feliciano DV: Vascular injuries. Adv Trauma 1987;179:206.

Feliciano DV: Abdominal gunshot wounds. Ann Surg 1988;208:362-370.

Feliciano DV: Approach to major abdominal vascular injury. J Vase Surg
1988;7:730-736.

Feliciano DV: Counterpoint. J Trauma 1992;32:553-554.

Feliciano DV: Abdominal vessels. In Ivatury R, Cayten C (eds): The Textbook
of Penetrating Trauma. Baltimore, Williams & Wilkins, 1996, pp 702-716.

Feliciano DV: Abdominal vascular injuries. Surg Clin North Am 2001;68:741.

Feliciano DV, Accola KD, BurchJM, Spjut-Patrinely V: Extra-anatomic bypass
for peripheral arterial injuries. Am J Surg 1989;158:505.

Feliciano DV, Bitondo CG, Mattox KL, et al: Civilian trauma in 1980s: A one-
year experience with 456 vascular and cardiac injuries. Ann Surg
1984;199:717-724.

Feliciano DV, Bitondo CG, Mattox KL, et al: Combined tracheoesophageal
injuries. Am J Surg 1985;150:710-715.

Feliciano DV, BurchJM, Graham JM: Abdominal vascular injury. In Mattox KL,
Feliciano DV, Moore EE (eds): Trauma. New York, McGraw-Hill, 1999, pp
783-805.

Feliciano DV, BurchJM, Mattox KL, et al: Balloon catheter tamponade in car-
diovascular wounds. Am J Surg 1990;160:583-587.

Feliciano DV, Cosseli JS, Bitondo CG: Bilateral external iliac artery injury from
a single missile. J Cardiac Surg 1986;27:46.

Feliciano DV, Cruse PA, BurchJM, Bitondo CF: Delayed diagnosis of arterial
injuries. Am J Surg 1987;154:579-584.

Feliciano DV, Cruse PA, Spjvi-Patrinely V, et al: Fasciotomy after trauma to the
extremities. Am J Surg 1988;156:533-536.

Feliciano DV, Gentry LO, Bitondo CG, et al: Single agent cephalosporin pro-
phylaxis for penetrating abdominal trauma. Am J Surg 1986;152:674-681.

Feliciano DV, Herskowitz K, O'Gorman RB: Management of vascular injuries
in lower extremities. J Trauma 1988;28:319-328.

RE.qxd 4/16/04 3:19 PM Page 570

570 VI • THE RICH REFERENCE COLLECTION

Feliciano DV, Mattox KL: Major complications of percutaneous subclavian vein
catheters. Am J Surg 1979;138:869-874.

Feliciano DV, Mattox KL, Graham JM, Bitondo CG: Five-year experience with
PTFE grafts in vascular wounds. J Trauma 1985;25:71-82.

Feller I: Surgical anatomy of the abdominal aorta. Ann Surg 1961;154:239.

Fellmeth BD, Roberts AC, Bookstein JJ: Postangiographic femoral artery injuries:
Nonsurgical repair with US-guided compression. Radiology 1991;178:671-
675.

Fenner MN, Fisher KS, Sergei NL, et al: Evaluation of possible traumatic tho-
racic aortic injury using aortography. Am Surg 1990;56:497-499.

Ferguson IA, Byrd WM, McAfee DK: Experiences in the management of arte-
rial injuries. Ann Surg 1961;153:980-986.

Ferguson WM: Arteriovenous aneurysm following osteotomy for genu valgum.
Lancet 1914;1:532.

Fernandez LG, Lain KY, Messersmith RN, et al: Transesophageal echocardio-
graphy for diagnosing aortic injury: A case report and summary of current
imaging techniques. J Trauma 1994;36:877-880.

Fernandez LG, Radhakrishnan J, Gordon RT, et al: Thoracic injuries in pedi-
atric patients. J Trauma 1995;38:384-388.

Ferriter P, Hirschy J, Kesseler H, Scott WN: Popliteal pseudoaneurysm: A case
report. J Bone Joint Surg 1983;65-A:695-697.

Finkelmeier BA, Mentzer RM Jr, Kaiseer DL, et al: Chronic traumatic thoracic
aneurysm: Influence of operative treatment on natural history: An analy-
sis of reported cases. J Thorac Cardiovasc Surg 1982;84:257-266.

Fish GDJr, Hockhauser M: Laceration of the popliteal artery due to blunt trauma.
AmJSurgl957;94:651.

Fisher GW: Acute arterial injuries treated by the United States Army Medical
Service in Vietnam, 1965-1966. J Trauma 1967;7:844-855.

Fisher RE), Rienhoff WF III: Subclavian artery laceration resulting from frac-
ture first rib. J Trauma 1966;6:579.

Fisher RG, Ben-Manachem Y: Penetrating injuries of the thoracic aorta and
brachiocephalic arteries: Angiographic finding in 18 cases. AJR Am J
Roentgenol 1987;149:607-611.

Fisher RG, Chasen MH, Lamki N: Diagnosis of injuries of the aorta and bra-
chiocephalic arteries caused by blunt chest trauma: CT vs aortography. AJR
Am J Roentgenol 1994;162:1047-1052.

Fisher RG, Oria RA, Mattox KL, et al: Conservative management of aortic
lacerations due to blunt trauma. J Trauma 1990;30:1562-1566.

Fisher RG, Ward RE, Ben-Manachem Y, et al: Arteriography and the fractured
first rib: Too much or too little? AJR Am J Roentgenol 1982;1 17:657-
661.

Fitchett VH, Pomerantz M, Butsch DW, et al: Penetrating wounds of the neck.
Arch Surg 1969;99:307-314.

Fitts CT, Barnett LT, Webb CM, et al: Perforating wounds of the heart caused
by central venous catheters. J Trauma 1970;10:764-769.

Fitzgerald EJ, Brumsler WG, Ruttley ST: False aneurysm of the femoral artery:
Computed tomography and ultrasound appearance. Clin Radiat
1986;37:585-588.

Fitzgerald JB, Crawford ES, DeBakey ME: Surgical consideration of non pene-
trating abdominal injuries. Am J Surg 1960;100:22-29.

Fitzgerald JF, KeatesJ: False aneurysm as a late complication of anterior dislo-
cation of the shoulder. Ann Surg 1975;181:785-786.

RE.qxd 4/16/04 3:19 PM Page 571

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 571

Fitzsimons LE, Garvey FK: Inferior vena caval injury: Case report. J Urol

1959;83:258-259.
Flanigan DP: Civilian Vascular Trauma. Philadelphia, Lea & Febiger, 1992.
Flanigan DP, Keifer TJ, Schuler JJ, et al: Experience with iatrogenic pediatric

vascular injuries: Incidence, etiology, management, and results. Ann Surg

1983;198:430-442.
Fleckenstein JL, Schultz SM, Miller RH: Serial aortography assesses stability of

"atypical" aortic arch ruptures. Cardiovasc Intervent Radiol 1987;10:194-

197.
Fleming A, Bishop M, Shoemaker W, et al: Prospective trial of supranormal

values as goals of resuscitation in severe trauma. Arch Surg 1992; 1 27: 11 75-

1181.
Fleming AW, Green DC: Traumatic aneurysms of the thoracic aorta: A report

of 43 patients. Ann Thorac Surg 1974;18:91-101.
Fleming JI: Case of rupture of the carotid artery and wound of several of its

branches successfully treated by tying off the common trunk of the carotid

itself. (Translated by Coley RW). Med ChirJ (Lond) 1817;3:2.
Fleming JFR, Petrie D: Traumatic thrombosis of the internal carotid artery with

delayed hemiplegia. CanJ Surg 1968;11:166-172.
Fleming WB: A case of attempted repair of the superior mesenteric vessels. Aust

N Z J Surg 1961;31:151-154.
Fletcher JP, Little JM: Injuries of branches of the aortic arch. Aust N Z J Surg

1988;58:217-219.
Flint LM: Arterial injuries with lower extremity fracture. Surgery 1983;93:

5-8.
Flint LM, Synder WH, Perry MO, Shires GT: Management of major vascular

injuries in the base of the neck: An 11-year experience with 146 cases. Arch

Surg 1973;106:407-413.
Fogarty TJ: Catheter technique for arterial embolectomy. Ann Surg 1965;161:325-

330.
Fogarty TJ, CranleyJJ, Strasser ES, Hafner CD: A method for extraction of arte-
rial emboli and thrombi. Surg Gynecol Obstet 1963;116:241-244.
Fogelman MJ, Stewart RD: Penetrating wounds of the neck. Am J Surg

1965;91:581-596.
FomonJJ, Warren WD: Complications of peripheral arterial injuries. Arch Surg

1965;91:610-616.
Foramitti KI: Wien Klin Wschr 1910;25:46-55. (Cited in Foramitti.H)
Forbes AD, Ashbaugh DG: Mechanical circulatory support during repair of tho-
racic aortic injuries improves morbidity and prevents spinal cord injury.

Arch Surg 1994;129:497-498.
Forbes HW, Thompson CQ, Smith JW: Mesenteric arteriovenous fistula after a

gunshot wound. J Trauma 1969;9:806.
Forrest CR, Pang CY, Zhong AG, Kreidstein ML: Efficacy of intravenous infu-
sion of prostacyclin (PG12) or prostaglandin Ej (PGEj) in augmentation

of skin flap blood flow and viability in the pig. Prostaglandins 1991;225:518-

527.
Forster DA: Letter to editor. J Trauma 1985;25:1115.
Foster JH, Carter JW, Grahamm CPJr, Edwards WH: Arterial injury secondary

to the use of the Fogarty catheter. Ann Surg 1970;171:971-978.
Foster RD, AlbrightJA: Acute compartment syndrome of the thigh: A case report.

J Trauma 1990;30:108-110.
Fouin A: Stir la sutre des vaisseaux. Presse Med 1908;16:233-236.

RE.qxd 4/16/04 3:19 PM Page 572

572 VI • THE RICH REFERENCE COLLECTION

Fox S, Pierce WS, Waldhausen JA: Acute hypertension: Its significance in trau-
matic aortic rupture. J Thorac Cardiovasc Surg 1979;77:622-625.

Fradet G, Nelems B, Meuller NL: Penetrating injury of the torso with impale-
ment of the thoracic aorta: Preoperative value of the computed tomographic
scan. Ann Thorac Surg 1988;45:680-681.

Frame SB, Timberlake GA, Rush DS, et al: Penetrating injuries of the abdomi-
nal aorta. Am Surg 1990;56:651-654.

Francis H III, Thai ER, Weigelt JA, Redman HC: Vascular proximity: Is it a valid
indication for arteriography in asymptomatic patients? J Trauma 1991;
31:512-514.

Frank MJ, Nadimi M, Lesniak LJ: Effects of cardiac tamponade on myocardial
performance blood flow and metabolism. Am J Physiol 1971;220:179-185.

Franz JL, Simpson CR, Penny RM, et al: Avulsion of the innominate artery after
blunt chest trauma. J Thorac Cardiovasc Surg 1974;67:478-480.

Fraser GA: Closed traumatic rupture of common femoral artery. Ann Surg
1965;161:539-544.

Freeark RJ: Role of angiography in the management of multiple injuries. Surg
Gynecol Obstet 1969;128:761-771.

Freeman NE: Secondary hemorrhage arising from gunshot wounds of the peri-
pheral blood vessels. Ann Surg 1945;122:631-640.

Freeman NE: Arterial repair in the treatment of aneurysms and arteriovenous
fistulae: A report of 18 successful restorations. Ann Surg 1946;124:888-919.

Freeman NE, Shumacker HB Jr: Vascular surgery. In Elkin DC, DeBakey ME
(eds): Washington, DC, US Government Printing Office, 1955.

Freidman AL, GertlerJP: Thoracoabdominal repair of post-traumatic aorta-
renal vein fistula following a previous transabdominal approach: A case
report. J Trauma 1991;31:287-289.

French BG, Hughes CF: Post-traumatic chromic false aneurysm of the ascend-
ing aorta with long-term survival. Aust N Z J Surg 1994;64:284-285.

Freshman SP, Wisner DH, Weber CJ: 2D echocardiography: Eemergent use in
the evaluation of penetrating precordial trauma. J Trauma 1991;31:902-
906.

Fried G, Salerno T, Burke D, et al: Management of the extremity with combined
neurovascular and musculoskeletal trauma. J Trauma 1978;18:481-484.

Friedman SG: A History of Vascular Surgery. Mt. Kisco, NY, Futura Publishing,
1989.

Fromm SH, Lucas CE: Obturator bypass for mycotic aneurysm in the drug addict.
Arch Surg 1970;100:82-83.

Fromm SH, Carrasquilla C, Lucas C: The management of gunshot wounds of
the aorta: The use of Dacron grafts to replace the injured aorta. Arch Surg
1970;101:388-390.

Fry RE, Fry WJ: Extracranial carotid artery injuries. Surgery 1980;88:581-587.

Frydenberg M, Royle JP, Hoare M: Blunt abdominal aortic trauma. Aust N Z J
Surg 1990;60:347-350.

Frykberg ER: Arteriography of the injured extremity: Are we in proximity to
an answer. J Trauma 1992;32:551-552.

Frykberg ER, Crump JM, Dennis JW, et al: Nonoperative observation of clini-
cally occult arterial injuries: Aprospective evaluation. Surgery 1991 ;1 09:85-
96.

Frykberg ER, Crump JM, Vines FS, et al: A reassessment of the role of arteri-
ography in assessing acute vascular injuries. J Trauma 1989;29:1041-
1052.

RE.qxd 4/16/04 3:19 PM Page 573

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 573

Frykberg ER, Crump JM, Vines FS, McLellan GL: A reassessment of the role
of arteriography in penetrating proximity extremity: A prospective study.
J Trauma 1989;29:1041-1052.

Frykberg ER, Dennis JW, Bishop K, et al: The reliability of physical examina-
tion in the evaluation of penetrating extremity trauma for vascular injury:
Results at one year. J Trauma 1991;31:502-511.

Frykberg ER, Vines FS, Alexander RH: The natural history of clinically occult
arterial injuries: A prospective evaluation. J Trauma 1989;29:577-583.

Fu WR: Angiography of Trauma. Springfield, 111, Charles C Thomas, 1972.

Fulda G, Rodriguez A, Turney SZ, Cowley RA: Blunt traumatic pericardial rupture:
A ten-year experience 1979-89. J Cardiac Surg 1990;31:525-530.

Fullen WD, Hunt J, Altemeier WA: The clinical spectrum of penetrating injury
to the superior mesenteric arterial circulation. J Trauma 1972;12:656-664.

Furman S, Vijaynagar R, McMullen M, Scher DJW: Lethal sequelae of intra-
aortic balloon rupture surgery. Surgery 1971;69:121-129.

Furnas DW, Saliblan AH, Achauer BM: Genesis of a replantation program. Am
J Surg 1978;136:21-25.

Gaddard P,Jones AG, WisheartJD: Self-inflicted stab wound causing aorto-right
ventricular fistula. Am HeartJ 1981;46:101-103.

Gage M: Traumatic injuries to the peripheral vessels in both civil and military
practice. Surgery 1942;11:983-986.

Gainor BJ, Metzler M: Humeral shaft fracture with brachial artery injury. Clin
Orthop Relat Res 1986;204:154-161.

Gale SS, Scissons RP, Jones L, Salles-Cunha SX: Femoral pseudoaneurysm throm-
binjection. Am J Surg 2001;181:379-383.

Gallen J, Wiss DA, Cantelmo N, Menzoian JO: Traumatic pseudoaneurysm of
the axillary artery: Report of three cases and literature review. J Trauma
1984;24:350-354.

Gammie JS, Katz WE, Swanson ER, Peitsman AB: Acute aortic dissection after
blunt chest trauma. J Trauma 1996;40:126-127.

GaramellaJJ, Schmidt WR, Jensen NK, Lynch MF: Traumatic aneurysms of the
thoracic aorta. Report of four cases, including one of spontaneous rupture
into the esophagus. N EnglJ Med 1962;266:1341-1348.

Garcia-Rinaldi R, Defore WW, Mattox KL, Beall ACJr: Unimpaired renal myocar-
dial and neurologic function after cross clamping of the thoracic aorta.
Surg Gynecol Obstet 1976;143:249-252.

Gardner C: Traumatic vasospasm and its complications. Am J Surg 1952;83:468-
470.

Gardner WJ, StorerJ: The use of the G Suit in control of intra-abdominal bleed-
ing. Surg Gynecol Obstet 1966;123:792.

Garrison RN, Richardson JD, Fry DE: Diagnostic transdiaphragmatic pericar-
diotomy in thoracoabdominal trauma. J Trauma 1982;22:147-149.

Garzon A, Gleidman ML: Peripheral embolization of bullet following perfora-
tion of the thoracic aorta. Am Surg 1964;160:901.

Caspar MR: Vascular injury secondary to drug abuse. In Ernst CB, Stanley JC
(eds) : Current Therapy in Vascular Surgery. Philadelphia, BC Decker, 1987.

Caspar MR, Hare RR: Gangrene due to intraarterial injection of drugs by drug
addicts. Surgery 1987;72:573-577.

Caspar MR, Treiman RL: The management of injuries to major veins. Am J
Surg 1960;100:171-175.

Caspar MR, Treiman RL, Payne JH, et al: Principles of treatment and special
problems in vascular trauma. Surg Clin North Am 1968;48:1355.

RE.qxd 4/16/04 3:19 PM Page 574

574 VI • THE RICH REFERENCE COLLECTION

Gaspard DJ, Caspar MR: Arteriovenous fistula after Fogarty catheter thrombec-
tomy. Arch Surg 1972;105:90-92.

Gasparini D, Lovaria A, Saccheri S: Percutaneous treatment of iliac aneurysms
and pseudoaneurysms with Cragg Endopro System 1 stent-grafts. Cardio-
vasc Intervent Radiol 1997;20:348-352.

Gates JD, Clair DG, Hechtman DH: Thoracic aortic dissection with renal artery
involvement following blunt thoracic trauma: Case report. J Trauma
1994;36:430-432.

Gates JD, Knox JB: Axillary artery injuries secondary to anterior dislocation of
the shoulder. J Trauma 1995;39:581-583.

Gauderer MW, Wolkoff JS, Izant RJ: Traumatic aneurysm of the suprarenal
abdominal aorta: Surgical reconstruction in a 7-year-old patient. J Pediatr
Surg 1982;17:940-945.

Gaudio KM, Taylor MR, Chaudry IH, et al: Accelerated recovery of single nephron
function by the postischemic infusion of ATP-MgC12. Kidney Int 1982;22:13-
20.

Gavant ML, Gold RE, Fabian TC, Tonkin LI: Vascular trauma to the extremi-
ties and lower neck: Initial assessment with intravenous digital subtraction
angiography. Radiology 1986;158:755-760.

Gay W: Blunt trauma to the heart and great vessels. Surgery 1982;91:507-509.

Gazzanaga AB, IKhuri EI, Mir-Sepasi HM, Bartlett RH: Rupture of the thoracic
aorta following blunt trauma. Arch Surg 1975;110:1119-1123.

Geer TM, Rich NM: Cardiac trauma in Vietnam: Unpublished data in the Vietnam
Vascular Registry. 1972.

Geer TM: Personal communication, 1972.

Geiran O, Solheim K: Cardiac and aortic injuries. Scand J Thorac Cardiovasc
Surg 1974;8:27-33.

GeisWP, Johnson CF, ZajtchukR, Kittle CF: Extrapericardial (mediastinal) cardiac
tamponade. Arch Surg 1970;100:305-306.

GelbermanRH, BlasingameJP, ArnostF, et al: Forearm arterial injuries. J Hand
Surg 1979;4:401-408.

Gelberman RH, Menon J, Fronek A: The peripheral pulse following arterial
injury. J Trauma 1980;20:948-950.

Gelberman RH, NunleyJA, Koman LA, et al: The results of radial and ulnar
arterial repair in the forearm. J Bone Joint Surg 1982;64:383-387.

Geller DA, Chia SH, Takahashi Y, et al: Protective role of the L-arginine-nitric
oxide synthase pathway on preservation injury after rat-liver transplanta-
tion. J Parenter Enter Nutr 2001;25:142-147.

Gensoul: Note sur les Bless es recus a l'Hotel Dieu de Lyon, pendant les trou-
bles de 1831. Gaz Med Paris 1883;297.

Gensoul: 1883 Cited in Simeone, et al. On the question of ligation of the con-
comitant vein when a major artery is interrupted. Surgery 1951;29:932-951.

Gentry LO, Feliciano DV, Lea AS, et al: Perioperative antibiotic therapy for
penetrating injuries of the abdomen. Ann Surg 1984;200:561-566.

George SM Jr, Croce MA, Fabian TC: Cervicothoracic arterial injuries: Recom-
mendations for diagnosis and management. WorldJ Surg 1991;15:134-140.

Ger R: The coverage of vascular repairs by muscle transposition. J Trauma
1976;16:974-978.

Gerbode F, Holman E, Dickenson EH, Spencer FC: Arteriovenous fistulas and
arterial aneurysms: The repair of major arteries injured in warfare, and
the treatment of an arterial aneurysm with a vein graft inlay. Surgery 1952;
32:259-274.

RE.qxd 4/16/04 3:19 PM Page 575

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 575

Gerbode F, Braimbridge M, Osborn JJ, et al: Traumatic thoracic aneurysms:

Treatment by resection and grafting with the use of an extracorporeal bypass.

Surgery 1957;42:975-985.
Gerlock AJ Jr: The use of pedal venous pressure (PVP) as a guide in evaluating

the patency of venous repairs. J Trauma 1977;17:108-110.
Gerlock AJ Jr, Mathis J, Goncharenko V, Maravilla A: Angiography of intimal

and intramural arterial injuries. Radiology 1978;129:357-361.
Gerlock AJJr, Muhletaler CA: Venography of peripheral venous injuries. Radi-
ology 1979;133:77-80.
Gerlock AJJr, Thai ER, Snyder WH III: Venography in penetrating injuries of

the extremities. AJR Am J Roentgenol 1976;126:1023-1027.
German DS, Shapiro MJ, Willman VL: Acute aortic valvular incompetence

following blunt thoracic deceleration injury: Case report. J Trauma

1990;30:1411-1412.
Gertsch P: Lesions vasculaires des blesses de guerre Afghans Traitees a

l'Hospital du CICR a Peshawar. Med Milit 1986;2:46.
Ger vin AS, Fischer CA: The importance of prompt transport in salvage of patients

with penetrating heart wounds. J Trauma 1982;22:443-448.
Getzen LC, Bellinger SB, Kendall LW: Should all neck, axillary, groin or popliteal

wounds be explored for possible vascular or visceral injuries. J Trauma

1972;12:906.
Geuder JW, Hobson RW II, Padberg FT Jr, et al: The role of contrast arterio-
graphy in suspected arterial injuries of the extremities. Am Surg 1985;51:89-

93.
Gewertz B, O'Brien C, Kirsh MM: Use of the intra-aortic balloon support

of refractory low cardiac output in myocardial contusion. J Trauma

1977;17:325-327.
Gewertz BL, Samson DS, Ditmore QM, Bone GE: Management of penetrating

injuries of the internal carotid artery at the base of the skull utilizing

extracranial-intracranial bypass. J Trauma 1980;20:365-369.
GibbonsJR: Treatment of missile injuries of the chest: Belfast experience. J Car-

diothorac Surg 1989;4:297.
Gibson JMC: Rupture of axillary artery. J Bone Joint Surg 1962;44B:114-

115.
Gielchinsky I, McNamara JJ: Cardiac wounds at a military evacuation hospital

in Vietnam: A review of one-year's experience. J Thorac Cardiovasc Surg

1970;60:603-606.
Gielchinsky I, McNamaraJJ: Flechette wounds of the heart. Surgery 1971;69:229-

231.
GigliaJS, Zelenock GB, D'Alecy L: Prevention of paraplegia during thoracic

aortic cross-clamping: Importance of patent internal mammary arteries.

J Vase Surg 1994;19:1044-1051.
Gill SS, Eggleston FC, Singh CM: Arterial injuries of the extremities. J Trauma

1976;16:766-772.
Gingrass RP, Cunningham DS, Paletta FX: Skin grafting of exposed arterial

grafts: A clinical and experimental study. J Trauma 1973;13:951-957.
Giraud RM: Arteriovenous fistula of the aortic arch complicating stab wound

of the neck. S Afr Med J 1965;12:474-476.
Glaser RL, McKellar D, Scher KS: Arteriovenous fistulas after cardiac catheter-
ization. Arch Surg 1989;124:1313-1315.
Gltick T: Uber zwei falle von aortenaneurysmen nebst bemerkungen uber die

naht der blutgefasse. Arch Klin Chir 1883;28:548.

RE.qxd 4/16/04 3:19 PM Page 576

576 VI • THE RICH REFERENCE COLLECTION

Gnanadev DA, Fandrich BL: Popliteal artery trauma: Update and recent advances
in management. Ann Vase Surg 1988;2:332-335.

Goff JB, Gillespie DL, Rich NM: Long-term follow-up of a superficial femoral
vein injury: A case report from the Vietnam Vascular Registry. J Trauma
1998;44:209-211.

Goff J, Gillespie D, Rich NM: Long-Term Follow-up of Military Superficial Femoral
Vein Injury: A Case Report from Vietnam Vascular Registry. 1996 Febru-
ary 23-25, San Diego. San Diego, American Venous Forum, 1996.

Gold AH, Lee GW: Upper extremity replantation: Current concepts and patient.
J Trauma 1981;21:551-557.

Goldberg BB, Ostrium BJ, Isard JJ: Ultrasonic determination of pericardial effu-
sion. JAMA 1967;202:103.

Goldberger M: Clinical experience with intra-aortic balloon counter pulsation
in 112 consecutive patients. Am Heart 1986;111:497-502.

Goldman BS, Firor WB, Key JA: The recognition and management of peri-
pheral arterial injuries. Can Med Assoc J 1965;92:1154-1160.

Goldman LI, Maier WP, Drezner AD: Another complication of subclavian punc-
ture: Arterial laceration. JAMA 1971;217:78.

Goldman MH, Kent S, Schaumburg E: Brachial artery injuries associated with
posterior elbow dislocation. Surg Gynecol Obstet 1987;164:95-97.

Goletti O, Ghiselli G, Lippolis PV, et al: The role of ultrasonography in blunt
abdominal trauma: Results in 250 consecutive cases. J Trauma 1994;36:1 78-
181.

Golman BS, Firor WB, KeyJA: The recognition and management of peripheral
arterial injuries. Can Med Assoc J 1965;92:1154-1160.

Golueke PJ, Goldstein AS, Sclanfani SJA, et al: Routine versus selective explo-
ration of penetrating neck injuries: A randomized, prospective study.
J Trauma 1984;24:1010-1014.

Golueke PJ, Sclanfani S, Phillips T, et al: Vertebral artery injury: Diagnosis and
management. J Trauma 1987;27:856-865.

Gomes MMR, Gernatz PE: Arteriovenous fistulas: A review and 10-year experi-
ence at the Mayo Clinc. Mayo Clin Proc 1970;45:81-102.

Gomez GA, RreisDJJr, RatnerL, etal: Suspected vascular trauma of the extrem-
ities: The role of arteriography in proximity injuries.JTraumal986;26:1005-
1008.

Gomez RL, Bole PV, Lande A, et al: Successful repair of two false aneurysms of
the abdominal aorta. Arch Surg 1973;107:91-94.

Goodman C: Suture of blood vessel from projectiles of war. Surg Gynecol Obstet
1918;27:528.

Goodman P, Jeffrey R, Brant-Zawadki M: Digital subtraction angiography in
extremity trauma. Radiology 1984;153:61-64.

Gordon RL, Landau RH, Shifrin E, Romanoff H: The use of a balloon catheter
in the treatment of an iatrogenic pseudoaneurysm of the subclavian artery.
J Cardiovasc Surg 1983;24:178-180.

GormanJF: Combat wounds of the popliteal artery. Ann Surg 1968;24:178-180.

Gorman JF: Combat arterial trauma: Analysis of 106 limb-threatening injuries.
Arch Surg 1969;98:160-164.

Gosselin RA, Yukka Siegberg CJ, Coupland R, Agerskov K: Outcome of arter-
ial repairs in 23 consecutive patients at the ICRC-Peshawar hospital for war
wounded. J Trauma 1993;34:373-376.

Gott VL: Heparinized shunts for thoracic vascular operations. Ann Thorac Surg
1972;14:219-220.

RE.qxd 4/16/04 3:19 PM Page 577

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 577

Goyanes J: Neuvos trabajos de chirurgial vascular: Substitution plastica de las
the arterias por las venas, o arterio-plastia venosa, aplicado, como neuvo
metodo, al traitamiento de los aneurismas. El Siglo Med 1906;53:546-
561.

Grablowsky OM, Weichert RF III, Goff JB, Schlegel JU: Renal artery
thrombosis following blunt trauma: Report of four cases. Surgery
1970;67:895.

Graeber GM, Clagett GR Wolf RE, et al: Alteration in serum creatine kinase
and lactate dehydrogenase: Association with abdominal aortic surgery,
myocardial infarction and bowel necrosis. Chest 1990;97:521-527.

Graham JM, Feliciano DV, Mattox KL: Combined brachial, axillary and sub-
clavian artery injuries of the same extremity: A case report. J Trauma
1980;20:899-901.

Graham JM, Feliciano DV, Mattox KL, Beall AC Jr: Innominate vascular injury.
J Trauma 1982;22:647-655.

Graham JM, Feliciano DV, Mattox KL, et al: Management of subclavian vascu-
lar injuries. J Trauma 1980;20:537-544.

Graham JM, Mattox KL: Right ventricular bullet embolectomy without car-
diopulmonary bypass. J Thorac Cardiovasc Surg 1981;82:310-313.

Graham JM, Mattox KL, Beall AC Jr: Portal venous system injuries. J Trauma
1978;18:419-422.

Graham JM, Mattox KL, Beall AC Jr, DeBakey ME: Traumatic injuries of the
inferior vena cava. Arch Surg 1978;113:413-418.

Graham JM, Mattox KL, Beall AC Jr, DeBakey ME: Injuries to the visceral arter-
ies. Surgery 1978;84:835-839.

Graham JM, Mattox KL, Feliciano DV, DeBakey ME: Vascular injuries of the
axilla. Ann Surg 1982;195:232-238.

Gray WA: Prehospital resuscitation: The good, the bad, and futile. JAMA
1993;22:1471-1472.

Green NE, Allen BL: Vascular injuries associated with dislocation of the knee.
J Bone Joint Surg 1977;59-A:236-239.

Greenfield LJ, Ebert PA: Technical considerations in the management of axil-
lobrachial arterial injuries. J Trauma 1967;7:606-612.

Greenfield LJ: Perforation of the inferior vena cava with aortic and vertebral
penetration by a suprarenal Greenfield filter. Radiology 1990;175:287.

Greenholz SK, Moore EE, Peterson NE, Moore GE: Traumatic bilateral renal
artery occlusion: Successful outcome with out surgical intervention. J Trauma
1986;26:941-944.

GreenoughJ: Operations on innominate artery: Report of a successful ligation.
Arch Surg 1929;19:1484-1544.

Griffen WO, BelinRP, Walder AL: Traumatic aneurysm of the abdominal aorta.
Surgery 1966;60:813-816.

Griffiths SJH: Traumatic rupture of the aorta. Br J Surg 1931;18:664-665.

Grimley RP, Ashton F, Slaney G, Batten RL: Popliteal artery injuries associated
with civilian knee trauma. Injury 1981;13:1-6.

Griswold RA, Maguire CH: Penetrating wounds of the heart in pericardium.
Surg Gynecol Obstet 1942;74:406-418.

Griswold RA, Drye JC: Cardiac wounds. Ann Surg 1954;139:783-785.

Groms GA, FlintLT: Repair of two traumatic aneurysms of the supraceliac abdomi-
nal aneurysm in a single patient. Surgery 1972;72:371-377.

Gross WS, Flanigan P, Kraft RO, Stanley JC: Chronic upper extremity arterial
insufficiency. Arch Surg 1978;113:419-423.

RE.qxd 4/16/04 3:19 PM Page 578

578 VI • THE RICH REFERENCE COLLECTION

Grossi EA, Krieger KH, Cunningham JN Jr, et al: Venoarterial bypass: A tech-
nique for spinal cord protection. J Thorac Cardiovasc Surg 1985;89:228-
234.

Grosso MA, Simson MA, Kobayaski K: Myocardial ischemia pattern determines
predisposition to ventricular arrhythmias. Surg Forum 1984;34:239-240.

Groves LK: Traumatic aneurysm of the thoracic aorta. N Engl J Med 1964;
270:220-224.

Gruber HE, Weisman WH: Aortic thrombosis during sigmoidoscopy in Behcet's
syndrome. Arch Intern Med 1983;143:343-345.

Gryska PF: Major vascular injuries: Principles of management in selected cases
of arterial and venous injuries. N Engl J Med 1962;266:381-385.

Gschaedler R, Dollfus P, LoebJP, et al: Traumatic rupture of the aorta and para-
plegia. Paraplegia 1978;16:123-127.

Gubler KD, Wisner DH, Blaisdell FW: Multiple vessel injury to branches of the
aortic arch: Case report. J Trauma 1991;31:1566-1568.

Guerriero WG, Carlton CE Jr, Scott R, Beall AC Jr: Renal pedical injuries.
J Trauma 1971;11:53-62.

Gugenheim S, Sanders RJ: Axillary artery rupture caused by shoulder disloca-
tion. Surgery 1984;95:55.

Guilfoil PH, Christiansen T: An unusual vascular complication of fractured clav-
icle. JAMA 1967;200:72-73.

Gundry SR, Willimams S, Burney RE, et al: Indications for aortography in blunt
thoracic trauma: A reassessment. J Trauma 1982;22:664-671.

Gundry SR, Burney RE, MacKenzieJR, et al: Clinical contact with the trauma
patient enhances accuracy of chest roentgenogram interpretation in pre-
dicting traumatic rupture of the aorta. J Cardiovasc Surg 1985;26:332-336.

Gunnlaugnson GH, Hallgrimsson JG, Sigurdsson JL, et al: Complete traumatic
avulsion of the innominate artery from the aortic arch with a unique mech-
anism of injury. J Thorac Cardiovasc Surg 1973;66:235-240.

Gupta BK, Khaneja SC, Flores L, et al: The role of intra-aortic balloon occlu-
sion in penetrating abdominal trauma. J Trauma 1989;29:861-865.

Gupta SK, Veith FJ: Management of juxtarenal aortic occlusion: Technique for
suprarenal clamp placement. Ann Vase Surg 1992;6:306-310.

Gurdjian ES, Hardy WG, Lindner DW, Thomas LM: Closed cervical cranial
trauma, associated with involvement of carotid and vertebral arteries. Neu-
rosurgery 1963;20:418.

GurriJA, Johnson GJr: Management of brachial artery occlusion after cardiac
catheterization. Am Surg 1980;46:233-235.

Guthrie CC: Blood Vessel Surgery. London, Edward Arnold & Company,
1912.

Guthrie CC: Blood Vessel Surgery and Its Application. New York, Longmans,
Green and Co, 1912.

Guthrie GJ: Disease and injuries of arteries. 1830.

Guvendik L, Davis NR, Starr A: Repair of traumatic aortic transection: A man-
agement protocol and review of 21 patients. J Thorac Cardiovasc Surg
1988;36:198-201.

Gwathmey O, Byrd CW: Clinical experience with acute traumatic rupture of
the thoracic aorta in a general hospital. Ann Surg 1964;159:846-857.

Hafez HM, Woolgar J, Robbs JV: Lower extremity artery injury: Results of 550
cases and review of risk factors associated with limb loss. J Vase Surg
2001;33:1212-1219.

Haimovici H: History of arterial grafting. J Cardiac Surg 1963;4:152-174.

RE.qxd 4/16/04 3:19 PM Page 579

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 579

Haimovici H: Iatrogenic acute arterial thrombosis: In Vascular Emergencies.
New York, Appleton-Century-Crofts, 1982, pp 225-232.

Haimovici H, Hoffert PW, Zinicola N, Steinman C: An experimental and clin-
ical evaluation of grafts in the venous system. Surg Gynecol Obstet
1970;131:1173-1186.

Hall RL, Anderson CA, Bickerstaff LK: Isolated vertebral artery injuries. Contemp
Surg 1986;29:57-62.

Haller JA: Bullet transection of both carotid arteries: Immediate repair with
recovery. Am J Surg 1962;103:532-535.

Hallowell. Extract of a letter from Mr. Lambert, surgeon at Newcastle upon
Tyne, to Dr. Hunter, giving an account of new method of treating an
aneurysm. Med Obser Inq 1762;30:360.

Halpern AA, Nagel DA: Anterior compartment pressures in patients with tibial
fractures. J Trauma 1980;20:786-790.

Halpern NB, Aldrete JS: Factors influencing mortality and morbidity from injuries
to the abdominal aorta and inferior vena cava. Am J Surg 1979;137:384-
388.

Halsted W: Ligation of the first portion of the left subclavian artery and exci-
sion of subclavico-axillary aneurysm. Bull Johns Hopkins Hosp 1892;3:93.

Halsted W: Discussion in Bernheim, BM. Bull Johns Hopkins Hosp 1916;27:93.

Halsted WS: The effect of ligation of the common iliac artery on the circula-
tion and function of lower extremity. Report of a cure of iliofemoral
aneurysm by their application of an aluminum band to the vessel. Bull
Johns Hopkins Hosp 1912;23:191-220.

Halsted WS: Ligation of the left subclavian artery in its first portion. Bull Johns
Hopkins Hosp 1924;21:1.

Hamerlijnck RP, Rutsaert RR, De Geest R, et al: Surgical correction of descend-
ing thoracic aortic aneurysms under simple aortic cross-clamping. J Vase
Surg 1989;9:568-573.

Hammond SL, Gomez ER, Coffey JA, et al: Involvement of the lymphatic system
in chronic venous insufficiency. In Bergan JJ, Yao JST (eds): Venous Dis-
orders. Philadelphia, WB Saunders, 1991.

Hamza N, Marath A, Al-Fakhry MR: The management of aneurysms and arte-
riovenous fistulae of the popliteal artery arising from war trauma: Empha-
sis on sigmoid operative approach. J Cardiovasc Surg 1990;31:457-461.

Hanobrugh JF, Narrod JA: Arteriovenous fistulas following central venous
catheterization. Care Med 1983;9:287-289.

Hansaker G: An ordeal in a snowdrift. The Evening Star 14 June 1971.

Harbison SP: Major vascular complications of intervertebral disc surgery. Ann
Surg 1954;140:342-348.

Hardin WD Jr, Adinolfi MF, O'Connell RC, Kerstein MD: Management of trau-
matic peripheral vein injuries: Primary repair or vein ligation. Am J Surg
1982;144:235-238.

Hardin CA: Bypass saphenous grafts for the relief of venous obstruction of the
extremity. Surg Gynecol Obstet 1962;115:709-712.

Hardin WD, O'Connell RC, Adinolfi MF, Kerstein MD: Traumatic arterial injuries
of the upper extremity: Determinants of disability. Am J Surg 1985; 150:266-
270.

Hardy JD, Raju S, Neely WA, Berry DW: Aortic and other arterial injuries. Ann
Surg 1975;181:640-653.

Hardy JD, Timmis HH: Repair of intracardiac gunshot injuries: Report of three
cases. Ann Surg 1969;169:906-913.

RE.qxd 4/16/04 3:19 PM Page 580

580 VI • THE RICH REFERENCE COLLECTION

Hardy JD, Williams RD: Penetrating heart wounds: Analysis of 12 consecutive
cases without morality. Ann Surg 1967;166:228-231.

Hare RR, Caspar MR: The intimal flap. Arch Surg 1971;102:552-555.

Harken DE: Foreign bodies in, and in relation to, the thoracic blood vessels
and heart: Techniques for approaching and removing foreign bodies from
the chambers of the heart. Surg Gynecol Obstet 1946;83:117-125.

Harken DE, Williams AC: Foreign bodies in and in relation to the thoracic
blood vessels and heart: Migratory foreign bodies within the blood vascu-
lar system. Am J Surg 1946;72:80-90.

Harken DE, Zoll PM: Foreign bodies in and in relation to the thoracic blood
vessels and heart: Indications for the removal of intracardiac foreign bodies
and the behavior of the heart during manipulation. Am HeartJ 1946;32:1-
19.

Harley DP, Mena I: Cardiac and vascular sequelae of sternal fractures. J Trauma
1986;26:553-555.

Harrington DP, Barth KH, Whit Rljr, Brawley RK: Traumatic pseudoaneurysm
of the thoracic aorta in close proximity ot the anterior spinal artery: A ther-
apeutic dilemma. Surgery 1980;87:153-156.

Harrington EB, Schwartz M, Jacobson JH II, et al: Aortocaval fistula: A clinical
spectrum. J Cardiovasc Surg 1989;30:579-583.

Harris JD: A case of arteriovenous fistula following closed fracture of tibia and
fibula. Br J Surg 1963;50:774-776.

Hart RJJr, Gregoratos G: Ventricular septal defects caused by stab wounds: Report
of two cases. Milit Med 1974;139:289-292.

Hartford JM, Fayer RL, Shaver TE, et al: Transection of the thoracic aorta:
Assessment of a trauma system. Am J Surg 1986;151:224-229.

Harding RP, McGahan JP, Lindfors KK: Letter. Radiology 1987;165:291-292.

Harding RP, McGahan JP, Blaisdell FW, Lindfors KK: Stab wounds to the extrem-
ities: Indications for arteriography. Radiology 1987;162:465-467.

Hartsuck JM, Moreland HJ, Williams GR: Surgical management of vascular
trauma distal to the popliteal artery. Arch Surg 1972;105:937-940.

Harvey EN, Butler EG, McMillenJH, Puckett WO: Mechanism of wounding.
War Med 1945;8:91-104.

Harvey EN, Korr IM, Oster G, McMillenJH: Secondary damage in wounding
due to pressure changes accompanying the passage of high velocity mis-
siles. Surgery 1947;21:218-239.

Harvey EN, McMillenJH: An experimental study of shock waves resulting from
the impact of high velocity missiles on animal tissues. J Exp Med 1947;
85:321-328.

Hashizume M, Yang Y, Gait S: Intimal response of saphenous vein to intralu-
minal trauma simulated angioscopic insertion. J Vase Surg 1987;5:862-868.

Hashmonai M, Schramek KA, Abrahamson J, et al: Acute vascular injuries of
the upper extremity. Isr J Med Sci 1974;10:599.

Haskell RJ, French WJ, Harley DP: Traumatic aorto-right ventricular fistula pre-
senting with a diastolic murmur. Am HeartJ 1985;109:1110-1112.

Hass GM: Types of internal injuries of personnel involved in aircraft accidents.
JAviatMedl944;15:77.

Hass L, Staple T: Arterial injures associated with fractures of the proximal tibia
following blunt trauma. South Med J 1969;62:1439.

Hassantash SA, Mock C, Maier RV: Traumatic visceral artery aneurysm: Pre-
sentation as massive hemorrhage from perforation into an adjacent hollow
viscus. J Trauma 1995;38:357-360.

RE.qxd 4/16/04 3:19 PM Page 581

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 581

Hasselgren PO, Eriksson B, Lukes P, Seeman T: False popliteal aneurysm caused
by exostosis of the femur. J Cardiovasc Surg 1983;24:540-542.

Hassett A, Moran J, Sabiston DC, Kisslo J: Utility of echocardiography in the
management of patients with penetrating missile wounds of the heart. Am
J Cardiol 1987;7:1151-1156.

Hawkes SZ: Traumatic rupture of the heart and intrapericardial structures. Am
J Surg 1935;27:503-507.

Hawkins ML, Carraway RP, Ross SE: Pulmonary artery disruption from blunt
thoracic trauma. Am Surg 1988;54:148-152.

Hayes JM, Vanwickle GN: Axillary artery injury with minimally displaced frac-
ture of the neck of the humerus. J Trauma 1983;23:431-433.

Heaton LD, Hughes CW, Rosegay H, et al: Military surgical practices of the
United States Army in Vietnam. In Current Problems in Surgery. Chicago,
Year Book Medical Publishers, 1966.

Heberer G: Ruptures and aneurysms of the thoracic aorta after blunt chest
trauma.J Cardiac Surg 1971;12:115-120.

Heberer G, Becker HM, Stelter WJ: Vascular injuries in polytrauma. World J
Surg 1983;7:68-79.

Hebra A, Roison JG, Elliott BM: Traumatic aneurysm associated with fibroin-
timal proliferation of the common carotid artery following blunt trauma:
Case report. J Trauma 1993;34:297-299.

Hegarty MM, Angorn IB, Gollogy J, Baker LW: Traumatic arteriovenous fistu-
lae. Injury 1975;7:20-28.

Heggtveit HA, Campbell JS, Hooper GD: Innominate arterial aneurysms occur-
ring after blunt trauma. Am J Clin Pathol 1974;42:69-74.

Heiberg E, Wolverson MK, Sundaram M, Shields JB: CT in aortic trauma. AJR
Am J Roentgenol 1983;140:1119-1124.

Heidenhain L: Uber naht von arterienwunden. Centralbl Chir 1895;22:1113-
1115.

Helfet DL, Howey T, Sanders R, Johansen K: Limb salvage versus amputation.
Preliminary results of the Mangled Extremity Severity Score. Clin Orthop
1990;256:80.

Helvie MA, Rubin JM, Silver TM, Kresowik TF: The distinction between femoral
artery pseudoaneurysms and other causes of groin masses: Value of duplex
doppler sonography. AJR 1988;150:1177-1180.

Henderson V, Nambisan R, Smith ME, et al: Angiographic yield in penetrating
extremity trauma. WesJ Med 1991;155:253.

Hennessy OF, Gibson RN, Allison DJ: Use of giant steel coils in the therapeu-
tic embolization of a superior mesenteric artery-portal vein fistula. Car-
diovasc Intervent Radiol 1986;9:42.

Henroteaux D, Thoorens P, Trotteur G: Rupture of the external iliac artery
after total hip replacement. J Beige Radiol 1989;72:518-519.

Heppenstall RB, Sapega AA, Izant T, et al: Compartment syndrome: A quanti-
tative study of high-energy phosphorus compounds using 31P-magnetic
resonance spectroscopy. J Trauma 1989;29:1113-1119.

HergetCH: Wound ballistics. In Bowers WB (ed): Surgery of Trauma. Philadel-
phia, JB Lippincott Co, 1956.

Herlyn KE: Erfahrungen auf dem gebiete von aneurysmen und arteriovenosen
fisteln. Atti della prima Riunione Internacionale de Angio-cardio-
Chirurgia. Milano: Casa Edetrice "Mellon," 1951.

Hermreck AS, Sifers TM, Reckling FW, et al: Traumatic vascular injuries: Methods
and results of repair. AmJ Surg 1974;128:813-817.

RE.qxd 4/16/04 3:19 PM Page 582

582 VI • THE RICH REFERENCE COLLECTION

Hershey FB. Secondary repair of arterial injuries. Am Surg 1961;27:33-41.

Hershey FB, Spencer AD: Surgical repair of civilian arterial injuries. Arch Surg
1960;80:953-962.

Hershey FB, Spencer AD: Autogenous vein grafts for repairs of arterial injuries.
Arch Surg 1963;86:836-845.

Herskowitz K, Sclafani S: Acute traumatic dissection of the common iliac arter-
ies with spontaneous healing: Case report. Cardiovasc Intervent Radiol
1990; 13:364.

Hertzer NR: Peripheral atheromatous embolization following blunt abdomi-
nal trauma. Surgery 1977;82:244-247.

Hess PJ, Howe HR, Robicsek F, et al: Traumatic tears of the thoracic aorta:
Improved results using the Bio-Medicus pump. Ann Thorac Surg 1989;48:6-
9.

Hessel SJ, Adams DF: Complication of angiography. Radiology 1981;138:273-
281.

Hewes RC, Smith DC, Lavine MH: Iatrogenic hydromediastinum simulating
aortic laceration. AJR Am J Roentgenol 1979;133:817-820.

Hewitt RL: Technical considerations in acute military vascular injuries of the
extremities. Milit Med 1969;134:617-621.

Hewitt RL, Collins DJ: Acute arteriovenous fistulas in war injuries. Ann Surg
1969;169:447-449.

Hewitt RL, Collins DJ,HamitHF: Arterial injuries at a surgical hospital in Vietnam.
Arch Surg 1969;98:313-316.

Hewitt RL, Grablowsky OM: Acute traumatic dissecting aneurysm of the abdom-
inal aorta. Ann Surg 1970;171:160-164.

Hewitt RL, Smith AD, Becker ML, et al: Penetrating injuries of the thoracic
outlet. Surgery 1974;76:715-722.

Hewitt RL, Smith AD, Drapanas T: Acute traumatic arteriovenous fistulas.
J Trauma 1973;13:901-906.

Hewitt RL, Smith AD Jr, Weichert RF, Drapanas T: Penetrating cardiac injuries:
Current trends in management. Arch Surg 1970;101:683-688.

Heyes FLP, Aukland A: Occlusion of the common femoral artery complicating
total hip arthroplasty. J Bone Joint Surg 1985;67:533-535.

HiattJR, Busuttil RW, Wilson SE: Impact of routine arteriography on manage-
ment of penetrating neck injuries. J Vase Surg 1984;1:860-866.

HiattJR, Yeatman LA, Child JB: The value of echocardiography in blunt chest
trauma. J Trauma 1988;28:914-922.

HiattJR, Martin NA, Machleder HI: The natural history of a traumatic verte-
bral artery aneurysm: Case report. J Trauma 1989;29:1592-1603.

Hiebert CA, Gregory FJ: Bullet embolism from the head to the heart. JAMA
1974;229:442-443.

Hierholzer C, Harbercht BG, Billiar TR, Tweardy DJ: Hypoxia-inducible factor-
1 activation and cyclo-oxygenase-2 induction are early reperfusion inde-
pendent inflammatory events in hemorrhagic shock. Arch Orthop Trauma
Surg 2001;121:219-222.

Hiertonn T, Lindberg K, Rob CG: Cystic degeneration of the popliteal artery.
Br J Surg 1957;44:348.

Hiertonn T, RybeckB: Traumatic Arterial Lesions. Stockholm, ForsvaretsForskn-
ingsanstalt, 1968.

Higgins RSD, SanchezJA, DeGuidis L: Mechanical circulatory support decreases
neurologic complications in the treatment of traumatic injuries of the tho-
racic aorta. Arch Surg 1992;127:516-519.

RE.qxd 4/16/04 3:19 PM Page 583

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 583

Highbloom RY, Koolpe H, Morris MC: Traumatic occlusion of two radiocephalic
fistulas: Case report and their management. J Trauma 1990;30:364-365.

Hilgenberg AD, Logan DL, Adkins CW, et al: Blunt injuries of the thoracic
aorta. Ann Thorac Surg 1992;53:233-239.

Hill LL: A report of a case of successful suturing of the heart, and a table of 37
other cases of suturing by different operators with various terminations
and conclusions drawn. Med Rec N Y2001;62:846.

Hillborn M, Downey D: Deep venous thrombosis complicating sonographically
guided compression repair of pseudoaneurysm of the common femoral
artery. AJR Am J Roentgenol 1993;161:1334-1335.

Hills MW, Delprado AM, Deane SA: Sternal fractures: Associated injuries and
management. J Trauma 1993;35:55-60.

Hills MW, Thomas SG, McDougall PA, et al: Traumatic thoracic aortic rupture:
Investigation determines outcome. Aust N Z J Surg 1994;64:312-318.

Hiratzka LF, Wright CB: Experimental and clinical results of grafts in the venous
system: A current review. J Surg Res 1978;25:542-561.

Hirsch B: Blood Vessel Surgery. London, Edward Arnold & Company, 1912.

Hirsch EF: Internal versus external fixation of fractures with concomitant vas-
cular injuries in Vietnam. J Trauma 1971;11:463-473.

Hirshberg A, Wall MJ, Allen MR: Double jeopardy: Thoracoabdominal injuries
requiring surgical intervention in both chest and abdomen. J Trauma
1995;39:225-231.

HixWR, Mills M: Management of esophageal wounds. Ann Surg 1970;1 72:1002-
1006.

Ho RM, Freed MM: Persistent hypertension in young spinal cord injured indi-
viduals resulting from aortic repair. Arch Phys Med Rehabil 1 991; 72: 743-
746.

Hobson RW II, Croom RD III, Rich NM: Influence of heparin and low molec-
ular weight dextran on the patency of autogenous vein grafts: Vein grafts
in the venous system. Ann Surg 1973;178:773-776.

Hobson RW II, Croom RD III, Swan KG: Hemodynamics of the distal arteri-
ovenous fistula in venous reconstruction. J Surg Res 1973;14:483-489.

Hobson RW II, Israel MR, Lynch TG: Axillosubclavian arterial aneurysms. New
York, Grune & Stratton, 1982.

Hobson RW II, Lee BC, Lynch TG, et al: Use of intermittent pneumatic com-
pression of the calf in femoral venous reconstruction. Surg Gynecol Obstet
1984;159:284-286.

Hobson RW II, Rich NM: Traumatismes veineux des membres inferieurs. In
Kieffer E (ed): Traumatismes Arteriels. Paris, AERCV, 1995.

Hobson RW II, Rich NM, Wright CB: Venous Trauma: Pathophysiology, Diag-
nosis and Surgical Management. Mt. Kisco, NY, Futura Publishing, 1983.

Hobson RW II, Rich NM, Wright CB: Complications of direct venous recon-
struction. In Complications of Vascular Surgery. Orlando, Grune &
Stratton, 1985, pp 351-367.

Hobson RW II, Howard EW, Wright CB, et al: Pathophysiology of venous liga-
tion: Significance in arterial/venous injuries. Surgery 1972;74:824.

Hobson RWII, Howard EW, Wright CB, et al: Hemodynamics of canine femoral
venous ligation: Significance in combined arterial and venous injuries.
Surgery 1973;74:824-829.

Hobson RW II, Wright CB: Peripheral side to side arteriovenous fistula: Hemo-
dynamics and application in venous reconstruction. Am J Surg 1973;126:411-
414.

RE.qxd 4/16/04 3:19 PM Page 584

584 VI • THE RICH REFERENCE COLLECTION

Hobson RWII, Wright CB, Rich NM, Collins GJJr: Assessment of colonic ischemia
during aortic surgery by Doppler ultrasound. J Surg Res 1976;20:231-235.

Hobson RW II, Wright CB, Swan KG, et al: Current status of venous injury and
reconstruction in the lower extremities. In BerganJJ, YaoJST (eds) : Venous
Problems. Chicago, Year Book Medical Publishers, 1978, pp 469-484.

Hobson RWII, Yeager RA, Lynch TG, et al: Femoral venous trauma: Techniques
for surgical management and early results. Am J Surg 1983;146:220-224.

Hoff SJ, Reilly MK, Merrill WH, et al: Analysis of blunt and penetrating injury
of the innominate and subclavian arteries. Am Surg 1994;60:151-154.

Hohf RP: Arterial injuries occurring during orthopaedic operations. Clin Orthop
1963;28:21.

Holcomb GW, Meacham PW, Dean RH: Penetrating popliteal artery injuries
in children. J Pediatr Surg 1988;23:859-861.

HollemanJH, Killebrew LH: Tibial artery injuries. Am J Surg 1982;144:362-364.

HollermanJH, Killebrew LH: Injury to the popliteal artery. Surg Gynecol Obstet
1981;153:392-394.

Hollier LH: Protecting the brain and spinal cord. J Vase Surg 1987;5:524-528.

Hollingsworth RK, Johnston WW, McCooeyJF: Traumatic saccular aneurysm
of the thoracic aorta. J Thorac Surg 1952;24:325-345.

Holman E: Arteriovenous Aneurysms: Abnormal Communication between the
Arterial and Venous Circulations. New York, Macmillan, 1937.

Holman E: Clinical and experimental observations on arteriovenous fistulae.
Ann Surg 1940;112:840-875.

Holman E: War injuries to arteries and their treatment. Surg Gynecol Obstet
1942;75:183-192.

Holman E: Contributions to cardiovascular physiology gleaned from clinical
and experimental observations of abnormal arteriovenous communica-
tions. J Cardiovasc Surg 1962;3:48-63.

Holman E: Abnormal arteriovenous communications: Great variability of effects
with particular reference to delayed development of cardiac failure. Cir-
culation 1965;32:1001-1009.

Holman E: Abnormal Arteriovenous Communications: Peripheral and Intrac-
ardiac, Acquired and Congenital, 2nd ed. Springfield, 111, Charles C Thomas,
1968.

Holman E, Sir William Osier, Halsted WS: Two contrasting personalities. Pharos
AOA 1971;34:134.

Holman EF: Physiology of an arteriovenous fistula. Arch Surg 1971;7:64-82.

Holmes TWJr, Netterville RE: Complications of first rib fracture including one
case each of tracheoesophageal fistula and aortic arch aneurysm. J Tho-
racic Surg 1956;32:74-91.

Holzer CE Jr: Gunshot wound involving the abdominal aorta. Surgery
1948;23:645-652.

Honigman B: Mast increase mortality 7 times with heart injury. JAMA 1991;266.

Hoover NW: Injuries of the popliteal artery associated with fractures and dis-
locations. Surg Clin North Am 1961;41:1099-1112.

Horowitz MD, Schultz CS, Stinson EB: Sensitivity and specificity of echocar-
diogram diagnosis of pericardial effusion. Circulation 1974;50:239-247.

Horsely V: The destructive effects of small projectiles. Nature 1894;1:104-108.

HorsleyJS: Surgery of the Blood Vessels. St. Louis, Mosby, 1915.

Horwitz JR, Black CT, Lally KP, Andrassy RJ: Venous bypass as an adjunct for
the management of a retrohepatic venous injury in a child. J Trauma
1995;39:584-585.

RE.qxd 4/16/04 3:19 PM Page 585

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 585

Hoshida S, Yamashita N, Otsu K, et al: Cholesterol feeding exacerbates myocar-
dial injury in Zucker diabetic fatty rats. Am J Physiol Heart Circ Physiol

2000;278:H256-H262.
Houck WS: Blunt trauma to the popliteal artery: Review and presentation of

four cases. Am Surg 1977;43:434-437.
Howanitz EP, Murray KD, Galbraith TA, Myerowitz PD: Peripheral venous bullet

embolization to the heart: Case report and review of the literature. J Vase

Surg 1988;8:55-58.
Howanitz EP, Buckley D, Galbraith TA, et al: Combine blunt traumatic rupture

of the heart and aorta: Two case reports and review of the literature.

J Trauma 1990;30:506-508.
Howard C, Thai ER, Redman HC, Gibson P: Intra-arterial digital subtraction

angiography in the evaluation of peripheral vascular trauma. Ann Surg

1989;210:108-111.
Howe HRJr, Poole GVJr, Hansen KJ, et al: Salvage of lower extremities fol-
lowing combined orthopaedic and vascular trauma: A predictive salvage

index. Am Surg 1987;53:205-208.
Howe HR, Pennell PC: A superior temporary shunt for management of vascu-
lar trauma of extremity. Arch Surg 1986;121:1212.
Hoyt DB, Shackford SR, Davis JW, et al: Thoracotomy during trauma resusci-
tations: An appraisal by board certified general surgeons. J Trauma

1989;29:1318-1321.
Huang MS, Liu M, Wu J, et al: Ultrasonography for the evaluation of hemo-

peritoneum during resuscitation: A simple scoring system. J Trauma

1994;36:173-177.
Huang P, Fong C, Radmaker A: Prediction of traumatic aortic rupture from

plain chest film findings using stepwise logistic regression. Ann Emerg Med

1987;16:1330-1333.
Hudson HM II, Woodson J, Hirsch E: The management of traumatic aortic tear

in the multiply-injured patient. Ann Vase Surg 1991;5:445-448.
Hughes CW: Acute vascular trauma in Korean War casualties: An analysis of

180 cases. Surg Gynec Obstet 1954;99:91-100.
Hughes CW: Use of intra-aortic balloon catheter tamponade for controlling

intra-abdominal hemorrhage in man. Surgery 1954;36:65-68.
Hughes CW: The primary repair of wounds of major arteries: An analysis of

experience in Korea in 1953. Ann Surg 1955;141:297-303.
Hughes CW: Arterial repair during the Korean War. Ann Surg 1958;147:555-

561.
Hughes CW: Vascular injuries in the orthopaedic patient. J Bone Joint Surg

1958;40A:1271.
Hughes CW: Vascular surgery in the armed forces. Milit Med 1959;124:30-46.
Hughes CW: Acute vascular injuries: Civilian and military. J Trauma 1971 ;1 1:1 89-

190.
Hughes CW, Bowers WF: Traumatic Lesions of Peripheral Vessels. Springfield,

111, Charles C Thomas, 1961.
Hughes CW, Cohen A: The repair of injured blood vessels. Surg Clin North Am

1958;38:1529-1543.
Hughes CW, Jahnke EJJr: The surgery of traumatic arteriovenous fistulas and

aneurysms: A five-year follow up study of 215 lesions. Surg Clin North Am

1958;148:790-797.
Hughes CW, Rich NM. The management of vascular injuries. South Med Bull

1969;57:36.

RE.qxd 4/16/04 3:19 PM Page 586

586 VI • THE RICH REFERENCE COLLECTION

Hugier: Anevrisme raterioso-veineux de l'artere femorale gauche. BullSoc Chir

Paris 1852;2:106.
Hugier (1848). Cited by Horsely. The destructive effects of small projectiles.

Nature 1894;1:104-108.
Huk I, Brovkovych V, Nanobashvili J, et al: Prostaglandin Ei reduces

ischemia/reperfusion injury by normalizing nitric oxide and superoxide

release. Shock 2000;14:234-242.
Hull DA, Hyde CL: Arterial injuries in civilian practice. J Kentucky Med Assoc

1967;65:975-978.
Hunink MG, BosJJ: Triage of patients to angiography for detection of aortic

rupture after blunt chest trauma: Cost-effectiveness analysis of using CT.

AJR 1995;165:27-36.
Hunt JP, Baker CC, Lentrz CW, et al: Thoracic aorta injuries: Management and

outcome of 144 patients. J Trauma 1996;40:547-556.
Hunt TK, Blaisdell FW, Okimoto J: Vascular injuries of the base of the neck.

Arch Surg 1969;98:586-590.
Hunt TK, Leeds FH, Wanebo HJ, Blaisdell FW: Arteriovenous fistulas of major

vessels of the abdomen. J Trauma 1971;11:483-493.
Hunter J: A Treatise on the Blood, Inflammation and Gunshot Wounds. London,

George Nicol, 1974.
Hunter JI: Cited in Power, D-Arcy. Hunter's operation for the cure of aneurysm.

Br J Surg 1929;17:193-196.
Hunter W: The history of an aneurysm of the aorta, with some remarks on

aneurysms in general. Med Obs Soc Phys Lond 1757;1:323.
Hunter W: Further observations upon a particular species of aneurysm. Med

Obs Soc Phys Lond 1762;2:390.
Hurwitt ES, Seidenberg B: The non operative management of two cases of catheter

perforation of the aorta. Am J Surg 1965;110:452-455.
Hurwitt E, Seidenberg B: Rupture of the heart during cardiac massage. Ann

Surg 1953;137:115-119.
HuttonJE Jr, Rich NM: Pathophysiology of wounding. In McAninch JW (ed):

Traumatic and Reconstructive Urology. Philadelphia, WB Saunders, 1995.
Iannettoni MD, McCurry KR, Rodriguez JL, et al: Simultaneous traumatic ascend-
ing and descending thoracic aortic rupture. Ann Thoracic Surg 1994;57:481-

484.
Ikard R, Merendino KA: Accidental excision of the superior mesenteric artery:

Technical and physiological considerations. Surg Clin North Am 1970;

50:1075-1085.
Ikeda Y, Young LH, Scalia R, Lefer AM: Cardioprotective effects of citrulline in

ischemia/reperfusion injury via a non-nitric oxide-mediated mechanism.

Methods Find Exp Clin Pharmacol 2000;22:563-571.
Imamoglou K, Read RC, Heubl HC: Cervicomediastinal vascular surgery. Surgery

1967;61:274-80.
Inahara T: Arterial injuries of the upper extremity. Surgery 1962;51:605-610.
Inberg MC, Laaksonen V, Scheinin TM, et al: Early repair of traumatic rupture

of the thoracic aorta: Report of two cases. ScandJ Thorac Cardiovasc Surg

1972;6:287.
Inoue T, Kawada K, Tanaka S, et al: Clinical application of the temporary long

external bypass method for cross-clamping of the descending thoracic aorta.

J Thorac Cardiovasc Surg 1972;63:787-793.
Inui FK, Shannon J, Howard JM: Arterial injuries in the Korean conflict: Expe-
riences with 111 consecutive injuries. Surgery 1955;37:850-857.

RE.qxd 4/16/04 3:19 PM Page 587

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 587

Isaacs JP: Sixty penetrating wounds of the heart: Clinical and experimental
observations. In Blalock A (ed): Recent Advances in Surgery. 1959,
p 696.

Isaacs JP, Swanson HS, Smith RA: Transient childhood strokes from internal
carotid stenosis. JAMA 1969;207:1859-1862.

Iskecelli OK: Bullet embolus of left femoral artery: Report of a case which
occurred after abdominal gunshot wound. Arch Surg 1962;85:184-185.

Iskersky V, Reines HD, Vujic I: Left-sided vena cava mimicking traumatic rup-
tured thoracic aorta. J Trauma 1987;27:797-799.

Israel. Cited in Murphy JB: Resection of arteries and veins injured in continu-
ity-end-to-end suture: Experimental clinical research. Med Rec 1897;51:
73.

Itani KM, BurchJM, Spjut-Patrinely V, et al: Emergency center arteriography.
J Trauma 1992;32:302-307.

Ivatury RR, Shah PM, Ho K, et al: Emergency room thoracotomy for the resus-
citation of patients with fatal penetrating injuries of the heart. Ann Thorac
Surg 1981;32:377-385.

Ivatury RR, Rohman M, Lankin DH, Stahl WM: Ultrasonography in the diag-
nosis and management of post-venorrhaphy thrombosis of the protal vein.
J Trauma 1985;25:362-365.

Ivatury RR, Nallanthambi M, Roberge RJ: Penetrating thoracic injuries: Stabi-
lization vs. prompt transport. J Trauma 1987;27:1066.

Ivatury RR, Nallanthambi M, Lankin DH, et al: Portal vein injuries: Noninva-
sive follow-up of venorrhaphy. Ann Surg 1987;206:733-737.

Jackson FE, Mazur J: Traumatic aortic aneurysms in neurological patients. Milit
Med 1965;130:878-886.

Jackson MR, Olson DW, Beckett WC Jr, et al: Abdominal vascular trauma: A
review of 106 injuries. Am Surg 1992;58:622-626.

Jackson MR, Brengman ML, Rich NM: Delayed presentation of 50 years after
a World War II vascular injury with intraoperative localization by duplex
ultrasound of a traumatic false aneurysm. J Trauma 1997;43:159-161.

Jacobs JP, Horowitz MD, Ladden DA: Intra-aortic balloon counterpulsation in
penetrating cardiac trauma. J Cardiovasc Surg 1992;33:38-40.

JacobsonJH, HaimovJ: Venous revascularization of the arm: Report of three
cases. Surgery 1977;81:599-604.

Jaeschke H: Mechanisms of reperfusion injury after warm ischemia of the liver.
Hepatobiliary Pancreat Surg 1998;5:402-408.

Jaggers RC, Feliciano DV, Mattox KL, et al: Injury to popliteal vessels. Arch Surg
1982;117:657-661.

Jahnke EJ Jr: The surgery of acute vascular injuries: A report of 77 cases. Milit
Surg 1953;112:249-251.

Jahnke EJJr: Late structural and functional results of arterial injuries primar-
ily repaired. Surgery 1958;43:175-183.

Jahnke EJJr, Fisher GW, Jones C: Acute traumatic rupture of the thoracic aorta:
Report of six consecutive cases of successful early repair. J Thorac Car-
diovasc Surg 1964;48:63-77.

Jahnke EJJr, Howard JM: Primary repair of major arterial wounds: Report of
58 battle casualties. Arch Surg 1953;66:646-649.

Jahnke EJJr, Hughes CW, Howard JM: The rationale of arterial repair on the
battlefield. Am J Surg 1954;87:396-401.

Jahnke EJJr, Seeley SF: Acute vascular injuries in the Korean War: An analysis
of 77 consecutive cases. Ann Surg 1953;138:158-177.

RE.qxd 4/16/04 3:19 PM Page 588

588 VI • THE RICH REFERENCE COLLECTION

Jain SP, Roubin GS, Iyer SS: Closure of an iatrogenic femoral artery pseudoa-
neurysm by transcutaneous coil embolization. Cathet Cardiovasc Diagn
1996;39:317-319.

Jamieson NV, Watson CJ, Dunn DC: Dissection of the abdominal aorta associ-
ated with traumatic aneurysms of the iliac vessels. Case report. Acta Chir
Scand 1986;152:473-475.

JamousMA, Silver JR, Baker JHE: Paraplegia and traumatic rupture of the aorta:
A disease process or surgical complication. Injury 1992;23:475-478.

Jarrar D, Chaudry IH, Wang P: Organ dysfunction following hemorrhage and
sepsis: Mechanisms and therapeutic approaches. IntJ Mol Med 1999;57:368-
374.

Jarrar D, Wang P, Chaudry IH: Hepatocellular dysfunction: Basic considera-
tions. In Holzheimer RG, MannickJA (eds) : Surgical Treatment Evidence-
based and Problem-oriented. Munich, Zuckschwerdt, 2001, pp 763-767.

Jarrar D, Wang P, Song GY, et al: Inhibition of tyrosine kinase signaling after
trauma-hemorrhage: A novel approach for improving organ function and
decreasing susceptibility to subsequent sepsis. Ann Surg 2000;231 :399-407.

Jarstfer BS, Rich NM: The challenge of arteriovenous fistula formation follow-
ing disk surgery: A collective review. J Trauma 1976;16:726-733.

JassinowskyA: Die arteriennhat: Eine experimentelle studie. InaugDissDorpat
1889.

Javid H: Vascular injuries of the neck. Clin Orthop 1963;28:70.

JayJB, French SW III: Traumatic rupture of the thoracic aorta: Review of lit-
erature and case report. Arch Surg 1954;68:657-662.

Jensen: Ueber circulare gefassutur. Arch Klin Chir 1903;69:938-998.

Jensen AR: Bullet wound of the abdominal aorta with survival. J Fla Med Assoc
1963;49:656-657.

Jensen BT: Fourteen years' survival with an untreated traumatic rupture of the
thoracal aorta. Am J Forens Med Pathol 1988;9:58-59.

Jeresaty RM, LissJP: Effects of brachial artery catheterization on arterial pulse
and blood pressure in 203 patients. Am Heart J 1968;76:481-485.

Jernigan WR, Gardner WC: Carotid artery injuries due to closed cervical trauma.
J Trauma 1971;11:429-435.

Jimenez E, Martin M, Krukenkamp I, Barrett J: Subxiphoid pericardiotomy
versus echocardiography: A prospective evaluation of the diagnosis of occult
penetrating cardiac injuries. Surgery 1990;108:676-680.

Jimenez F, Utrilla A, Cuesta C, et al: Popliteal artery and venous aneurysm as
a complication of arthroscopic meniscectomy.J Trauma 1988;28:1404-1405.

JohansenK, BandykD, ThieleB, Hansen STJr: Temporary intraluminal shunts:
Resolution of a management dilemma in complex vascular injuries.J Trauma
1982;22:395-402.

Johansen K, Daines M, Howey T, et al: Objective criteria accurately predict ampu-
tation following lower extremity trauma. J Trauma 1990;30:568-573.

Johansen K, Lynch K, Paun M, Copass M: Non-invasive vascular tests reliably
exclude occult arterial trauma in injured extremities.J Trauma 1991;31:515-
522.

Johns TNP: A comparison of suture and non-suture methods for the anasto-
mosis of veins. Surg Gynecol Obstet 1947;84:939-942.

Johnson GJr, Peters RM, Dart CH Jr: A study of cardiac vein negative pressure
in arterio-venous fistula. Surg Gynecol Obstet 1967;124:82-86.

Johnson GJr, Blythe WB: Hemodynamic effects of arteriovenous shunts used
for hemodialysis. Ann Surg 1970;171:715-723.

RE.qxd 4/16/04 3:19 PM Page 589

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 589

Johnson B, Thursby P: Subclavian artery injury caused by a screw in a clavicu-
lar compression plate. Cardiovasc Surg 1996;4:414-415.

Johnson GW, LowryJH: Rupture of the axillary artery complicating anterior
dislocation of the shoulder. J Bone Joint Surg 1962;44B:116.

Johnson RH, Wall MJ, Mattox KL: Innominate artery trauma: A thirty-year expe-
rience. J Vase Surg 1993;17:134-140.

Johnson SB, Kearney PA, Smith MD: Echocardiography in the evaluation of
thoracic aorta. Surg Clin North Am 1995;75:193-205.

Johnson V, Eiseman B: Evaluation of arteriovenous shunts to maintain patency
of venous autograft. Am J Surg 1969;1 18:915.

Johnston R, Wall M, Mattox K: Innominate artery trauma: A 30-year experi-
ence. J Vase Surg 1993;17:134-139.

Jones AM, Graham NJ, Looney JR: Arterial embolism of a high-velocity rifle
bullet after a hunting accident: Case report and literature review. Am J
Forsensic Med Pathol 1983;4:259-264.

Jones EW, HelmsworthJ: Penetrating wounds of the heart: Thirty years' expe-
rience. Arch Surg 1968;96:671-682.

Jones JC: Traumatic rupture of ascending aorta and left main bronchus. Ann
Thorac Surg 1989;47:484.

Jones JW, Hewitt RL, Drapanas T: Cardiac contusion: A capricious syndrome.
Ann Surg 1975;181:567-574.

Jones RE, Smith EC, Bone GE: Vascular and orthopaedic complications of knee
dislocation. Surg Gynecol Obstet 1979;149:554-558.

Jones RF, Terrell JC, Walyer FE: Penetrating wounds of the neck: An analysis of
274 cases. J Trauma 1967;7:228-234.

Jousi M, Leppaninemi A: Management and outcome of traumatic aortic injuries.
Ann Chirurgiae Gynaecol 2000:89.

Jurkovich GJ, Zingarelli W, Wallace J, Curreri PW: Penetrating neck trauma:
Diagnostic studies in the asymptomatic patients. J Trauma 1985;25:819-
822.

Jurkovich GJ, Hoyt DB, Moore FA, et al: Portal triad injuries. J Trauma 1995;
39:426-434.

Kadambi A, Skalak TC: Role of leukocytes and tissue-derived oxidants in short-
term skeletal muscle ischemia reperfusion injury. Am J Physiol Heart Circ
Physiol 2000;278:H435-H443.

Kaeffer N, Richard V, Thuillez C: Delayed coronary endothelial protection 24
hours after preconditioning: Role of free radicals. Circulation 1997;96:231 1-
2316.

Kahn AM, Joseph WL, Hughes RK: Traumatic aneurysms of the thoracic aorta:
Excision and repair without graft. Ann Thorac Surg 1967;4:175-181.

Kakkar W: The cephalic vein as a peripheral vascular graft. Surg Gynecol Obstet
1969;128:551-556.

Kakos GS, Williams TE Jr, Kilman JW, Kalssen KP: Traumatic left ventricular
aneurysms after penetrating chest injury. Ann Surg 1971;174:202-206.

Kalmar P, Otto CB, Rodewald G: Selection of proper time of operation of trau-
matic thoracic aortic aneurysms (TTA) .J Thorac Cardiovasc Surg 1982;36-
37.

Kam J, Jackson H, Ben-Menachem Y: Vascular injuries in blunt pelvic trauma.
Radiol Clin North Am 1981;19:171-186.

Kamiya H, Hanaki Y, Kojima S: Fistula between noncoronary sinus of Valsalva
and right atrium after blunt chest trauma. Am Heart J 1987;114:429-
431.

RE.qxd 4/16/04 3:19 PM Page 590

590 VI • THE RICH REFERENCE COLLECTION

Kang SS, Labropoulos N, Mansour MA, Baker WH: Percutaneous ultrasound
guided thrombin injection: A new method for treating postcatheterization
femoral pseudoaneurysms. J Vase Surg 1998;27:1032-1038.

Kang SS, Labropoulos N: Postcatheterization femoral pseudoaneurysms: Treat-
ment with ultrasound-guided thrombin injection. Vase Ultrasound Today
1998;3:125-140.

Kang SS, Labropoulos N, Mansour MA: Expanded indications for ultrasound-
guided thrombin injection of pseudoaneurysms. J Vase Surg 2000;31:289-
298.

Kapp JP, Gielchinsky I, Jelsma R: Metallic fragment embolization to the cere-
bral circulation. J Trauma 1973;13:256-261.

Kappes S, Towne J, Adams M: Perforation of the superior vena cava: A com-
plication of subclavian dialysis. JAMA 1983;249:2232-2233.

Karalis DE, Victor MF, Davis GA, et al: The role of echocardiography in blunt
chest trauma: A transthoracic and transesophageal echocardiographic study.
J Trauma 1994;36:53-58.

Karmody AM, Lempert N, Jarmolych J: The pathology of post-catheterization
brachial artery occlusion. J Surg Res 1976;20:601-606.

Karrell R, Shaffer MA, Franaszek JB: Emergency diagnosis, resuscitation, and
treatment of acute penetrating cardiac trauma. Ann Emerg Med
1982;11:504-517.

KashukJL, Moore EE, MillikanJS, MooreJB: Major abdominal vascular trauma:
A unified approach. J Trauma 1982;22:672-679.

Kassel BA, Pugkhem T, Schechter LS, ChassinJL: Traumatic rupture of distal
thoracic aorta. N YStateJ Med 1980;80:1615-1617.

Kato M, Matsuda T, Kaneko M: Experimental assessment of newly devised tran-
scatheter stent-graft for aortic dissection. Ann Thorac Surg 1995;59:908-
915.

Katz NM, Blackstone EH, Kirklin JW, Karp RM: Incremental risk factors for
spinal cord injury following operation for acute traumatic aortic transec-
tion. J Thorac Cardiovasc Surg 1981;81:669-674.

Katz S, Mullin R, Berger RL: Traumatic transection associated with retrograde
dissection and rupture of the aorta: Recognition and management. Ann
Thorac Surg 1974;17:273-276.

Kaufman JL, Dinerstein CR, Shah DM, et al: Renal artery intimal flaps after
blunt trauma: Indications for non-operative therapy. J Vase Surg 1988;8:33-
37.

Kaushik VS, Mandel AK, Awariefe OA, et al: Early thoracotomy for stab wounds
of the heart. J Cardiovasc Surg 1979;20:423-426.

Kavic SM, Atweh N, Ivy ME, et al: Celiac axis ligation after gunshot wound to
the abdomen: Case report and literature review. J Trauma 2001;50:738-
739.

Kawada T, Mieda T, Abe H, et al: Surgical experience with traumatic rupture
of the thoracic aorta. J Cardiovasc Surg 1990;31:359-363.

Kay JK, Dykstra PC, Tsuji HK: Retrograde ilioaortic dissection: A complication
of common femoral artery perfusion during open-heart surgery. Am J
Surgery 1966;111:464-468.

Kazui T, Komatsu S, Yokoyama H: Surgical treatment of aneurysms of the tho-
racic aorta with the aid of partial cardiopulmonary bypass: An analysis of
95 patients. Ann Thorac Surg 1987;43:622-627.

Kearney P, Smith D, Johnson S, et al: Use of transesophageal echocardiogra-
phy in the evaluation of traumatic aortic injury.J Trauma 1993;34:696-703.

RE.qxd 4/16/04 3:19 PM Page 591

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 591

KeeleyJL: A bullet embolus to the left femoral artery following a thoracic gunshot

wound: Probable entrance through thoracic aorta: Case report and resume

of peripheral arterial bullet emboli. J Thorac Surg 1951;21:608-620.
Keeley SB, Snyder WH III, Weigelt JA: Arterial injuries below the knee: Fifty-
one patients with eighty-two injuries. J Trauma 1983;23:285-290.
Kelly GL, Eiseman B: Civilian vascular injuries. J Trauma 1975;15:507-514.
Kelly GL, Eiseman B: Management of small arterial injuries: Clinical and exper-
imental studies. J Trauma 1976;16:681-685.
Kelly JJ, Reuter KL, Waite RJ: Vascular injury complicating lumbar diskectomy:

CT diagnosis. AJR Am J Roentgenol 1989;153:1233-1234.
Kemmerer WT, Eckert WG, Gathright JB, et al: Patterns of thoracic injuries in

fatal traffic accidents. J Trauma 1961;1:595-599.
Kennedy FR, Cornwell EE, Camel J: Aortoesophageal fistula due to gunshot

wounds: Report of two cases with one survivor. J Trauma 1995;38:971-

974.
KennedyJC: Complete dislocations of the knee. J Bone Joint Surg 1959;41:878.
Kennedy JC: Complete dislocation of the knee joint. J Bone Joint Surg

1963;45:889-904.
Keynes G: The Apologie and Treatise of Ambroise Pare. Chicago, University of

Chicago, 1952.
Khalil IM, Livingston DH: Intravascular shunts in complex lower limb trauma.

J Vase Surg 1986;4:582-587.
Khoury G, Sfeir R, Khalifeh M, et al: Penetrating trauma to the abdominal

vessels. Cardiovasc Surg 1996;4:405-407.
Kieny R, Charpentier A: Traumatic lesions of the thoracic aorta: A report of 73

cases. J Cardiovasc Surg 1991;32:613-619.
Kikta MJ, Meyer JP, Bishara RA, et al: Crush syndrome due to limb compres-
sion. Arch Surg 1987;122:1078-1081.
Kilburn P, Sweeney JG, Silk FF: Three cases of compound posterior dislocation

of the elbow with rupture of the brachial artery. J Bone Joint Surg

1962;44:119-121.
Killen DA: Injury of the superior mesenteric vessel secondary to non-penetrating

abdominal trauma. Am Surg 1964;30:306-312.
KillewichLA, Bedford GR, Beach KW, StrandnessDE: Diagnosis of deep venous

thrombosis: A prospective study comparing duplex scanning to contrast

venography. Circulation 1989;79:810-814.
Kim H, Hwan KK: Role of nitric oxide and mucus in ischemia/reperfusion-

induced gastric mucosal injury in rats. Pharmacology 2001;62:200-207.
KinmonthJB: A report on the physiology and relief of traumatic arterial spasm.

BrMedJ1952;l:59.
Kipfer B, Leupi F, Schuepbach P, et al: Acute traumatic rupture of the thoracic

aorta: Immediate or delayed surgical repair? Eur J Cardiothorac Surg

1994;8:30-33.
Kirkup JR: Major arterial injury complicating fracture of the femoral shaft.

J Bone Joint Surg 1963;45:337-343.
Kirsh MM, Behrendt DM, Orringer MB, et al: The treatment of acute traumatic

rupture of the aorta: A 10-year experience. Ann Surg 1976;184:308.
Kirsh MM, Crane J, Kahn DG, et al: Roentgenographic evaluation of trauma

rupture of the aorta. Surg Gynecol Obstet 1970;131:900-904.
Kirsh MM, Kahn DR, Crane JD, et al: Repair of acute traumatic rupture of the

aorta without extracorporeal circulation. Ann Thorac Surg 1970;10:227-

236.

RE.qxd 4/16/04 3:19 PM Page 592

592 VI • THE RICH REFERENCE COLLECTION

Kirshner R, Seltzer S, D'Orsi C, DeWeese JA: Upper rib fractures and medi-
astinal widening: Indications for aortography. Ann Thorac Surg 1983;35:450-
454.

Kitzmiller JW, Hertzer NR, Beven EG: Routine surgical management of brachial
artery occlusion after cardiac catheterization. ArchSurg 1982; 11 7:1066-1071.

Kizer KW, Boone HA, Heneveld E, Orozco JR: Nail gun injury to the heart.
J Trauma 1995;38:382-383.

Kjellstrom T, Risberg B: Vascular trauma: Review of 10 years' experience. Acta
Chir Scand 1980;146:261.

Klein MD, Coran AG, Whitehouse WMJr, et al: Management of iatrogenic arte-
rial injuries in infants and children. J Pediatr Surg 1982;17:933-939.

Klein SR, Bongard FS, White RA: Neurovascular injuries of the thoracic outlet
and axilla. Am J Surg 1988;156:115-118.

Klein SR, Baumgartner FJ, Bongard FS: Contemporary management strategy
of major inferior vena caval injuries. J Trauma 1991;31:1032.

Kleinert HE: Homograft patch repair of bullet wounds of the aorta: Experi-
mental study and report of a case. Arch Surg 1958;76:811-820.

Kleinert HE, Romero J: Blunt abdominal trauma. J Trauma 1961;1:226-240.

Kleinert HE, Kasdan ML: Restoration of blood flow in upper extremity injuries.
J Trauma 1963;3:461.

Kleinert HE, Kasdan ML, Romero JL: Small bloodvessel anastomosis for salvage
of severely injured upper extremity. J Bone Joint Surg 1963;45:788-
796.

Kleinert HE, Volianitis GJ: Thrombosis of the Palmar Arch and its tributaries:
Etiology and newer concepts in treatment. J Trauma 1965;5:447-457.

Kleinert HE: Vascular diseases. 1972 (unpublished paper).

Kleinert HE, Burget GC, Morgan JA, et al: Aneurysms of the hand. Arch Surg
1973;106:554-557.

Kleinsasser LJ: The removal of a wire lodged in the interventricular septum of
the heart. Surgery 1961;50:500-503.

Kline DG, Hackett ER: Reappraisal of timing for exploration of civilian peri-
pheral nerve injuries. Surgery 1975;78:54-65.

Kline RM, Hertzer NR, Beven EG, et al: Surgical treatment of brachial artery
injuries after cardiac catheterization. J Vase Surg 1990;12:20-24.

Klingensmith W, Oles P, Martinez H: Arterial injuries associated with disloca-
tion of the knee or fracture of the lower femur. Surg Gynecol Obstet
1965;120:961-964.

Klingensmith W, Oles P, Martinez H: Fractureswith associated bloodvessel injury.
Am J Surg 1965;110:849-852.

Kluger Y, Sagie B, Soffer D, et al: The use of hemorrhage occluder pins for con-
trolling paravertebral intercostal artery bleeding: Case report. J Trauma
1997;43:687.

Knott-Craig CJ, PrzybojewskiJZ, Barnard PM: Penetrating wounds of the heart
and great vessels: A new therapeutic approach. S Afr Med J 1982;62:316-
320.

Knott LH, Crawford FA, Grogan JB: Comparison of autogenous vein, Dacron
and Gore-Tex in infected wounds. J Surg Res 1978;24:288-293.

Knudson MM, Lewis FR, Atkinson K, Neuhaus A: The role of duplex ultrasound
arterial imaging in patients with penetrating extremity trauma. Arch Surg
1993;128:1033.

Kollmeyer KR, Hunt JL: Aortoazygous fistula from gunshot wounds to the
suprarenal abdominal aorta. J Trauma 1985;25:257-259.

RE.qxd 4/16/04 3:19 PM Page 593

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 593

Kootstra G, Schipper JJ, Klasen HJ, Binnendijk B: Femoral shaft fracture with

injury of the superficial femoral artery in civilian accidents. Surg Gynecol

Obstet 1976;142:399-403.
Kornblith BA: Gunshot wound through the abdominal aorta. Ann Surg

1941;113:637-640.
Kowalenko T, Stern S, Wang X, Dronen S: Improved outcome with "hypoten-
sive" resuscitation of uncontrolled hemorrhagic shock in the swine model.

J Trauma 1991;31:1032.
Kozloff L, Rich NM, BrottWH, et al: Vascular trauma secondary to diagnostic

and therapeutic procedures: Cardiopulmonary bypass and intra-aortic

balloon assist. Am J Surg 1980;140:302-305.
Kozlov AV, Sobhian B, Duvigneau C, et al: Organ specific formation of nitrosyl

complexes under intestinal ischemia/reperfusion in rats involves NOS-

independent mechanism (s). Shock 2001;15:366-371.
RrajewskiLP, Hertzer NR: Blunt carotid artery trauma. Ann Surg 1980;19 1:341-

346.
Rram HB, Appel PL, Shoemaker WC: Increased incidence of cardiac contu-
sion in patients with traumatic thoracic aortic rupture. Ann Surg

1988;208:615-618.
Rram HB, Appel PL, Wohlmuth DA, Shoemaker WC: Diagnosis of traumatic

thoracic aortic rupture: A ten-year retrospective analysis. Ann Thorac Surg

1989;47:282-286.
Rram HB, Wohlmuth DA, Appel PL, Shoemaker WC: Clinical and radiographic

indications for aortography in blunt chest trauma. J Vase Surg 1987;6:168-

176.
Rraus TW, Paetz B, Richter GM, Allenberg JR: The isolated posttraumatic

aneurysm of the brachiocephalic artery after blunt thoracic contusion.

Ann Vase Surg 1993;7:275-281.
Rrauss M: Studies in wound ballistics: Temporary cavity effects in soft tissues.

MilitMed 1957;120:221.
Rrige JEJ, Spence RAJ: Popliteal artery trauma: A high risk injury. Br J Surg

1987;74:91-94.
Rrishnasastry RV, Friedman SG, Deckoff SL, Doscher W: Traumatic juxtarenal

aortocaval fistula and pseudoaneurysm. Ann Vase Surg 1990;4:378-380.
Rronzon I: Diagnosis and treatment of iatrogenic femoral artery pseudoa-
neurysm: A review. J Am Soc Echocardiogr 1997;10:236-245.
Rropilak M, Satiani B: Combined superficial femoral artery and vein injury with

deep venous thrombosis: Elements of proper management. Contemp Surg

1988;32:24-28.
Rrosnick A: Death due to migration of the ball from an aortic-valve prosthesis.

JAMA 1965;191:1083-1084.
Rruse-Andersen S, LorentzenJE, Rohr N: Arterial injuries of the upper extrem-
ities. Acta Chir Scand 1983;149:473-477.
Rudok RA, Bongard F: Determinants of survival after vena caval injury. Arch

Surg 1984;119:1009-1012.
Rudsk R, Sheldon G, Lim R: Atrial-caval shunting (ACS) after trauma. J Trauma

1982;22:81-85.
Rudsk RA, Bongard F, Lim RC Jr: Determinants of survival after vena

caval injury: Analysis of a 14-year experience. Arch Surg 1984;119:1009-

1012.
Ruiper DH: Cardiac tamponade and death in a patient receiving total parenteral

nutrition. JAMA 1974;230:877.

RE.qxd 4/16/04 3:19 PM Page 594

594 VI • THE RICH REFERENCE COLLECTION

Kulick DL, Kotlewski A, Hurvitz RJ, et al: Aortic rupture following percutaneous
catheter balloon coarctoplasty in an adult. Am Heart J 1990;119:190-193.

Kulshrestha P, Iyer KS, Das B, et al: Chest injuries: A clinical and autopsy profile.
J Trauma 1988;28:844-847.

Kurtoglu M, Ertekin C, Bulut T, et al: Management of vascular injuries of the
extremities. One hundred and fifteen cases. Int Angiol 1991;10:95.

Kurzel RB, Edinger DD: Injury to the great vessels: A hazard of transabdomi-
nal endoscopy. South Med J 1983;76:656-657.

Kurzweg FT: Vascular injuries associated with penetrating wounds of the groin.
J Trauma 1980;20:214-217.

Kuzman M, Tomic B, Stevanovic R, et al: Fatalities in the war in Croatia, 1991
and 1992: Underlying and external causes of death. JAMA 1993;270:626-
628.

Kummel: Uber circulare naht der gefasse. Munch Med Wschr 1899;46:1398.

KwaanJHM, Connolly JE: Successful management of prosthetic graft infection
with continuous povidone-iodine irrigation. Arch Surg 1981;116:716-720.

Kyosola K, Jarvinen A: Abdominal aortic aneurysm and dissection after blunt
trauma. J Cardiovasc Surg 1987;28:737-739.

La BergeJM, Jeffrey RB: Aortic lacerations: Fatal complications of thoracic aor-
tography. Radiology 1987;165:367-369.

La Garde LA: Report of the Surgeon General of the Army to the Secretary of
War. Washington, DC, Government Printing Office, 1893.

La Garde LA: Gunshot Injuries (How They Are Inflicted, Their Complications
and Treatment). New York, William Wood & Company, 1916.

LacyJH, BoxJM, Connors D, et al: Pseudoaneurysm: Diagnosis with color Doppler
ultrasound. J Cardiovasc Surg 1990;31:727-730.

Lafani SJA, Shatzkes D, Scalea T: The removal of intravascular bullets by inter-
ventional radiology: The prevention of central migration by balloon occlu-
sion—Case report. J Trauma 1991;31:1423-1425.

Lagerstrom CF, Reed RL, Rowlands BJ, Fisher R: Early fasciotomy for acute clin-
ically evident posttraumatic compartment syndrome. AmJ Surg 1989;158:36-
39.

Lai MD, Hoffman HB, AdamkiewiczJJ: Dissecting aneurysm of internal carotid
artery after non-penetrating neck injury. Acta Radiol Diag 1966;5:290-295.

Lain KC, Williams GR: Arteriography in acute peripheral arterial injuries: An
experimental study. Surg Forum 1970;21:179-181.

Lam CR, Mclntyre R: Air-pistol injury of pulmonary artery and aorta. Report
of a case with peripheral embolization of pellet and residual aorticopul-
monary fistula. J Thorac Cardiovasc Surg 1970;59:729-732.

Lamb RK, Pawade A, Prior AL: Intravascular missile: Apparent retrograde course
from the left ventricle. Thorax 1988;43:499-500.

Lancey RA, Davliakos GP, Vander Salm TJ: Simultaneous repair of multiple trau-
matic aortic tears. Ann Thorac Surg 1995;60:1120-1121.

Landreneau R, Mitchum P, Fry W: Iliac arterial transposition. Arch Surg
1989;124:978-981.

Lange R, Bach A, Hansen S, Johansen K: Open tibial fractures with associated
vascular injuries: Prognosis of limb salvage. J Trauma 1985;25:203-207.

Lange R: Limb reconstruction versus amputation decision making in massive
lower extremity trauma. Clin Orthop 1989;243:92-99.

Langenbeck B: Beitrage zur chirurgischen pathologie der venen. Arch Klin
Chirl861;l:l.

Langley G: Gunshotwound of the innominate artery. Br MedJ 1943;2:711-712.

RE.qxd 4/16/04 3:19 PM Page 595

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 595

LaRoque G: Penetrating bullet wound of the thoracic aorta followed by lodg-
ment of the bullet in the femoral artery. Ann Surg 1931;4:16.

Larrey D: Sur une blessure du pericorde suivie d'hydropericarde. Bull Sci Med
1810;6:1.

Larrey D: Clin Chir Paris 1829;2:284.

Lassonde J, Laurendeau F: Blunt injury of the abdominal aorta. Am Surg
1981;194:745-748.

Lassonde J, Morin M, Laurendeau F: Arterial injuries. Can J Surg 1984;27:343-
345.

Lau J, Mattox KL, Beall AC Jr, DeBakey ME: Use of substitute conduits in trau-
matic vascular injury. J Trauma 1977;17:541-546.

Launois B, Chateaubriant P, Rosat P, Kiroff G: Repair of suprahepatic caval
lesions under extracorporeal circulation in major trauma. J Trauma
1989;29:127-128.

Lavenson GJ, Rich NM, BaughJH: Value of ultrasonic flow detector in the man-
agement of peripheral vascular disease. Am J Surg 1970;120:522.

Lavenson GJ, Rich NM, Strandness DE Jr: Ultrasonic flow detector value in
combat vascular injuries. Arch Surg 1971;103:644-647.

Laverick MD, D'sa Barros, Kirk SJ, Mollan RAB: Management of blunt injuries
of the axillary and the neck of the humerus: Case report. J Trauma
1990;30:360-361.

Lawrence K, Shefts L, McDanielJ: Wounds of common carotid arteries: Report
of 17 cases from World War II. Am J Surg 1948;76:29-37.

Lawton R, Rossi N, Funk D: Intracardiac perforation. Arch Surg 1969;98:213-
216.

Layton T, Stroh A, Villella E: Missile embolus of the portal vein. J Trauma
1985;25:1111-1112.

Le Bret F, Ruel P, Rosier H, et al: Diagnosis of traumatic mediastinal hematoma
with transesophageal echocardiography. Chest 1994;105:373-376.

Learmonth J: Combined neuro-vascular lesions. Acta Chir Scand 1952;104:93-
99.

Learmonth J: An unusual type arteriovenous communication. Br J Surg
1945;32:321-323.

Learmonth J: Vascular injuries in war. Royal Soc Med 1946;39:488.

Leavitt B, Meyer J, Morton JR, et al: Survival following nonpenetrating trau-
matic rupture of cardiac chambers. Ann Thorac Surg 1987;44:532-535.

Leblanc J, Wood A, O'Shea M, Williams W: Peripheral arterial trauma in chil-
dren. J Cardiovasc Surg 1985;26:325-331.

Ledgerwood A, Lucas C: Survival following superior mesenteric artery occlu-
sion from trauma. J Trauma 1974;14:622-626.

Ledgerwood A, Lucas C: Biological dressings for exposed vascular grafts: A rea-
sonable alternative. J Trauma 1975;15:567-574.

Ledgerwood A, Kazmers M, Lucas C: The role of thoracic aortic occlusion for
massive hemoperitoneum. J Trauma 1976;16:610-615.

Ledgerwood A: The wandering bullet. Surg Clin North Am 1977;57:97-109.

Ledgerwood A, Mullins R, Lucas C: Primary repair vs ligation for carotid artery
injuries. Arch Surg 1980;115:488-493.

Lee F, Katzberg R, Gutierrez O, et al: Reevaluation of plain radiographic find-
ings in the diagnosis of aortic rupture: The role of inspiration and posi-
tioning on mediastinal width. J Emerg Med 1993;11:289-296.

Lee H, Beale LS: On the repair of arteries and veins after injury. Trans Med
Chir Soc 1865;50:477.

RE.qxd 4/16/04 3:19 PM Page 596

596 VI • THE RICH REFERENCE COLLECTION

Lee R, Stahlman G, Sharp K: Treatment priorities in patients with traumatic

rupture of the thoracic aorta. Am Surg 1992;58:37-43.
Lefer A, Lefer D: Pharmacology of the endothelium in ischemia-reperfusion

and circulatory shock. Ann Rev Pharmacol Toxicol 1993;33:71-90.
Lefer A: Endotoxin, Cytokines, and nitric oxide in shock. Shock 1994;1:79-80.
Lefer A: Role of the beta2-integrins and immunoglobulin superfamily members

in myocardial ischemia-reperfusion. Ann Thorac Surg 1999;68:1920-1923.
Lehr HA, Guhlmann A, Nolte D, et al: Leukotrienes as mediators in ischemia-
reperfusion injury in a microcirculation model in the hamster. J Clin Invest

1991;87:2036-2041.
LemaireJ, Dondelinger R: Percutaneous coil embolization of iatrogenic femoral

arteriovenous fistula or pseudo-aneurysm. Eur J Radiol 1994;18:96-100.
Lemos P, Okumura M, Azevedo AC, et al: Cardiac wounds: Experience based

on a series of 121 operated cases. J Cardiovasc Surg 1976;17:1-8.
Lennox A, Griffin M, Nicolaides A, Mansfield A: Percutaneous ultrasound guided

thrombin injection: A new method for treating postcatheterization femoral

pseudoaneurysms. J Vase Surg 1998;28:1120-1121.
Lennox.AF, Griffin M, Cheshire N: Treatment of an iatrogenic femoral artery

pseudoaneurysm with percutaneous duplex-guided injection of thrombin.

Circulation 1999;100:39-41.
Lennox.AF, Delis K, Szendro G: Duplex-guided thrombin injection for iatro-
genic femoral artery pseudoaneurysm is effective even in anticoagulated

patients. Br J Surg 2001;87:796-801.
Leppaniemi A, Wherry D, Pikoulis E, et al: Arterial and venous repair with vas-
cular clips: Comparison with suture closure. J Vase Surg 1997;26:24-28.
Leppaniemi A, Wherry D, Pikoulis E, et al: Common bile duct repair with tita-
nium staples: Comparison with suture closure. Surg Endosc 1997;11:714-

717.
Leppaniemi AK, Salo J, Haapiainen R: Civilian low velocity gunshot wounds of

the liver. Eur J Surg 1994;160:663-668.
Leppaniemi AK, Savolainen H, Salo J: Traumatic inferior vena caval injuries.

Scand J Thorac Cardiovasc Surg 1994;28:103-108.
Leppaniemi AK, Rich NM, Pikoulis E, et al: Sutureless vascular reconstruction

with titanium clips. Int Angiol 2000;19:69-74.
Lester J: Arteriovenous fistula after percutaneous vertebral angiography. Acta

Radiol Diag 1966;5:337-340.
Letsou G, GertlerJ, Baker CC, Hammond G: Blunt innominate injury: A report

of three cases. J Trauma 1989;29:104-108.
Letsou G, Gusberg R: Isolated bilateral renal artery thrombosis: An unusual

consequence of blunt abdominal trauma — Case report. J Trauma

1990;30:509-511.
Lev El A, Adar R, Rubinstein Z: Axillary artery injury in erect dislocation of the

shoulder. J Trauma 1981;21:323-324.
LeVeen H, Cerruti M: Surgery of large inaccessible arteriovenous fistulas. Ann

Surg 1963;158:285-289.
Levin A, Gover P, Nance F: Surgical restraint in the management of hepatic

injury: A review of the Charity Hospital experience. J Trauma 1978;18:399-

404.
Levin L, Goldner R, Urbaniak J, et al: Management of severe musculoskeletal

injuries of the upper extremity. J Orthop Trauma 1990;4:432.
Levin P, Rich NM, Hutton JE Jr, et al: Role of arteriovenous shunts in venous

reconstruction. Am J Surg 1971;122:183-191.

RE.qxd 4/16/04 3:19 PM Page 597

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 597

Levin P, Rich NM, Hutton JE Jr: The role of collateral circulation in arterial

injuries. Arch Surg 1971;102:392-398.
Levin P, Rich NM, Hutton JE Jr: Patency of venous grafts in the venous system.

J Cardiovasc Surg (Torino) 1972;13:421-427.
Levine E, Alverdy JC: Carotid-esophageal fistula following a penetrating neck

injury: Case report. J Trauma 1990;30:1588-1590.
Levitsky S, James P, Anderson RW, Hardeway RI: Vascular trauma in Vietnam

battle casualties: An analysis of 55 consecutive cases. Ann Surg 1968;1 68:831-

836.
Lewis D, Davies A, Irvine C: Compression ultrasonography for false femoral

artery aneurysms: Hypocoagulability is a cause of failure. Eur J Vase Surg

1998;16:427-428.
Lewis T: The adjustment of blood flow to the affected limb in arteriovenous

fistula. Clin Sci 1940;4:277-285.
LewtasJ: Traumatic subclavian aneurysm: Ligature of innominate and carotid

arteries: Recovery. Br Med J 1889;2:312.
Lexer E: Die ideale operation des arteriellen und des arteriell-venosen

aneurysma. Arch Klin Chir 1907;83:459-477.
Liau C, Ho F, Chen M, Lee Y: Treatment of iatrogenic femoral artery pseudoa-

neurysm with percutaneous thrombin injection. J Vase Surg 1997;26:18-

23.
Lichtenstein M: Acute injuries involving the large blood vessels in the neck.

Surg Gynecol Obstet 1947;85:165-175.
Lichti E, Erickson T: Traumatic arteriovenous fistula: Clinical evaluation and

intraoperative monitoring with the Doppler ultrasonic flowmeter. Am J

Surg 1974;127:333-335.
Liddicoat J, Bekassy SM, Daniell M, DeBakey ME: Inadvertent femoral artery

"stripping": Surgical management. Surgery 1975;77:318-320.
LiekwegW, Greenfield L: Management of penetrating carotid arterial injuries.

Ann Surg 1966;188:587-592.
Lilienthal H: Thoracic surgery: The surgical treatment of thoracic disease.

Philadelphia: WB Saunders Company, 1926.
Lillehei K, Robinson M: A critical analysis of the fatal injuries resulting from

the Continental flight 1713 airline disaster: Evidence in favor of improved

passenger restraint system. J Trauma 1994;37:826-830.
Lim LT, Michuda M, Flanigan DP, Pankovich A: Popliteal artery trauma: 31 con-
secutive cases without amputation. Arch Surg 1980;115:1307-1313.
Lim LT, SalettaJ, Flanigan DP: Subclavian and innominate artery trauma. Surgery

1979;86:890-897.
Lim RC, Glickman M, Hunt TK: Angiography in patients with bunt trauma to

the chest and abdomen. Surg Clin North Am 1972;52:551-565.
Lim RC, Miller S: Management of acute civilian vascular injuries. Surg Clin

North Am 1982;62:113-119.
Lim RC, Trunkey DD, Blaisdell FW: Acute abdominal aortic injury: An analy-
sis of operative and post-operative management. Arch Surg 1974;109:706-

712.
Linberg E: Bullet wound of the thoracic aorta with survival. Maryland State

MedJ 1959;8:285-286.
LindenJ: Molecular approach to adenosine receptors: Receptor-mediated mech-
anisms of tissue protection. Ann Rev Pharmacol Toxicol 2001;41:775-787.
Lindenauer S, Thompson N, Kraft R: Late complications of traumatic arteri-
ovenous fistulas. Surg Gynecol Obstet 1969;129:525-532.

RE.qxd 4/16/04 3:19 PM Page 598

598 VI • THE RICH REFERENCE COLLECTION

Lindenbaum B: Complications of knee joint arthroscopy. Clin Orthop Rel Res

1981;160:157.
Lindenbaum G, Jacobs L, Morris M: Perioperative surface and transesophageal

color-flow Doppler evaluation of posttraumatic intracardiac shunt. Am Heart

J 1990;119:193-196.
Lindskog G: The surgery of the innominate artery. N Engl J Med 1946;235:71-

76.
Lindskog G, Liebow A, Glenn W: Thoracic and Cardiovascular Surgery with

Related Pathology. New York, Appleton-Century-Crofts, 1962.
Linker R, Crawford FJr, Rittenbury M, Barton M: Traumatic aortocaval fistula:

case report. J Trauma 1989;29:255-257.
Linson M: Axillary artery thrombosis after fracture of the humerus. J Bonejoint

Surg 1980;62-A:1214-1215.
Linton R: Injuries to major arteries and their treatment. N YJ Med 1949;49:2039.
Linton R: Arterial injuries associated with fractures of the extremity. J Bone

Joint Surg 1964;46:575-576.
Lipscomb P, Burleson R: Vascular and neural complications in the supracondylar

fractures of the humerus in children. J Bonejoint Surg 1955;37:487-497.
Litchford B, Okies JE, Sugimura S, Starr A: Acute aortic dissection from cross

clamp injury. J Thorac Cardiovasc Surg 1976;72:709-713.
Little J, Ferguson D: The incidence of hypothenar hammer syndrome. Arch

Surg 1972;105:684.
Lizama V, Zerbini M, Gagliardi R, Howell L: Popliteal vein thrombosis and

popliteal artery pseudoaneurysm complicating osteochondroma of the

femur. AJR Am J Roentgenol 1987;148:783-784.
Lloyd J: Traumatic peripheral aneurysms. Am J Surg 1987;93:755-764.
LockJ, Huffman A, Johnson R: Blunt trauma to the abdominal aorta. J Trauma

1987;27:674-677.
Loello F, Nunn D: False aneurysm of the inferior epigastric artery as a com-
plication of abdominal retention sutures. Surgery 1973;74:460.
LohseJ, Botham RJ, Waters R: Traumatic bilateral renal artery thrombosis. J

Urol 1982;127:522.
Loose H, Haslam P: The management of peripheral arterial aneurysms using

percutaneous injection of fibrin adhesive. BrJ Radial 1998;17:1255-1259.
Lopez-Viegro M, SynderWH, Clagett GP: Penetrating abdominal aortic trauma:

A review of 129 patients. J Vase Surg 1992;15:247-248.
Lord JW, Stone P, Clouthier W, Breidenbach L: Major blood vessel injury during

elective surgery. Arch Surg 1958;77:282.
Lord R, Ehrenfeld W, Wylie EJ: Arterial injury from the Fogarty catheter. Med

J Aust 1968;2:70-71.
Lord R, Irana C: Assessment of arterial injury in limb trauma. J Trauma

1974;14:1042-1053.
Lorenz P, Steinmetz B, Lieberman J: Emergency thoracotomy: Survival corre-
lates with physiologic status. J Trauma 1992;32:780.
Louridas G, Perry MO: Basic data related to vascular trauma. Ann Vase Surg

1989;3:397.
Love C, Evans S: Gunshot wound of the abdominal aorta and anoxic cardiac

arrest: Report of a survival. Ann Surg 1963;158:131-132.
Love L, Braun T: Arteriography of peripheral vascular trauma. AJR Am J

Roentgenol 1968;102:431-440.
Lovric Z: Reconstruction of major arteries of extremities after war injuries.

J Cardiovasc Surg (Turin) 1993;34:33-37.

RE.qxd 4/16/04 3:19 PM Page 599

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 599

Lovric Z, Wertheimer B, Candric K, et al: Reconstruction of the popliteal artery

after war injury. Unfallchirurg 1993;97:375-377.
Lovric Z, Wertheimer B, Candric K, et al: War injuries of major extremity vessels.

J Trauma 1994;36:248-251.
Lowen H, Fink S, Helpern M: Transfixion of the heart by embedded ice pick

blade with eight months' survival. Circulation 1950;2:426-433.
Lozman H, Beaufils AT, Rossi G, et al: Vascular trauma observed at an urban

hospital center. Surg Gynecol Obstet 1978;146:237-240.
Lozman H, Robbins H: Injury to the superior gluteal artery as a complication

of total hip replacement arthroplasty: A case report. J Bone Joint Surg

1983;65:268-269.
Lucas A, Richardson JD, Flint LM, Polk H: Traumatic injury of the proximal

superior mesenteric artery. Ann Surg 1981;193:30-34.
Lucas R, Tumacder O, Wilson G: Hepatic artery occlusion following hepatic

artery catheterization. Ann Surg 1971;173:238-243.
Ludewig RM, Wangensteen S: Aortic bleeding and the effect of external counter

pressure. Surg Gynecol Obstet 1969;128:252-258.
Luetic V, Sosa T, Tonkovic I, et al: Military vascular injuries in Croatia. Cardio-

vasc Surg 1993;1:3-6.
Luke J: Arterial trauma. J Cardiovasc Surg 1962;3:165-168.
Lumpkin M, Logan W, Couves C, Howard JM: Arteriography as an aid in the

diagnosis and localization of acute arterial injuries. Ann Surg 1958; 147:353-

358.
Lumsden A, Miller J, Kosinski A: A prospective evaluation of surgically treated

groin complications following percutaneous cardiac procedures. Am Surg

1994;60:132-137.
Lundell C, Quinn M, Finck E: Traumatic laceration of the ascending aorta:

Angiographic assessment. AJR Am J Roentgenol 1985;145:715-719.
Lupetin A, Beckman I, Daffner R: CT diagnosis of traumatic abdominal aortic

rupture. J Comput Assist Tomogr 1990;14:313-314.
Lynch K, Johansen K: Can Doppler pressure measurement replace "exclusion"

arteriography in extremity trauma? Ann Surg 1991;214:737-741.
Lynch K, Johansen K: Can non-invasive vascular tests replace screening arteri-
ography in extremity trauma? J Vase Surg 9999.
Lyons C, Perkins R: Cardiac stab wounds. Am Surg 1957;23:507.
Macbeth A, Malone J, Norton L, Peltier L: Paralysis and aortic thrombosis fol-
lowing blunt abdominal trauma. J Trauma 1982;22:591-594.
MacDonell J: Traumatic aortic aneurysm. Can Med Assoc J 1956;75:581-

584.
MacGowan W: Acute ischemia complicating limb trauma. J Bone Joint Surg

1968;50-B:472-484.
Machiedo G, Jain K, Swan KG, et al: Traumatic aortocaval fistula. J Trauma

1983;23:243-247.
Machle W: Lead absorption from bullets lodged in tissues: Report of two cases.

JAMA1940;115:1536.
Machleder HI, SweeneyJ, Barker WF: Pulseless arm after brachial artery catheter-
ization. Lancet 1972;1:407.
MacLachlin A, Carroll S, Meades G, Amacher AL: Valve replacement in the

recanalized incompetent superficial femoral vein in dogs. Ann Surg

1965;162:446.
MacLean L: The diagnosis and treatment of arterial injuries. Can Med Assoc J

1963;88:1091-1101.

RE.qxd 4/16/04 3:19PM PageSOO

600 VI • THE RICH REFERENCE COLLECTION

MacLean L, Flam R, Petersen D: Diagnosis and treatment of arterial injuries.

Minn Med 1961;44:133-142.
Maggisano R, Nathans A, Alexandrova NA, et al: Traumatic rupture of the tho-
racic aorta: Should one always operate immediately? Ann Vase Surg 1995;9:

44-52.
Magilligan D, DavilaJ: Innominate artery disruption due to blunt trauma. Arch

Surg 1979;114:307-309.
Mahoney B, Gerdes D, Roller B, Ruiz E: Aortic compressor for aortic occlusion

in hemorrhagic shock. Ann Emerg Med 1984;13:11-16.
MajeskiJA, Gants A: A management of peripheral arterial vascular injuries with

Javid shunt. Am J Surg 1979;138:324-345.
Makins G: Blessures des vaisseaux. Comptes-endus conference Chirurgicale

Interalliee pour l'etude des Plaies de Guerre. Arch Med Pharm Mil

1917;68:341.
Makins G: Influence exerted by military experience of John Hunter himself

and the military surgeon of today. Lancet 1917;1:249-254.
Makins G: Gunshot injuries to the blood vessels. Bristol, England, John Wright

and Sons, 1919.
Makins G: Injuries to the blood vessels. Official History of the Great War Medical

Service. Surgery of the War, vol 2. London, His Majesty's Stationary Office,

1922, pp 170-296.
Makins G: Specimen showing the effects of gunshot injury on the heart and

blood vessels. Now on exhibit in the museum of the Royal College of Sur-
geons of England. Br J Surg 1977;18:141-146.
Makins G, Howard JM, Green R: Arterial injuries complicating fractures and

dislocations: The necessity for a more aggressive approach. Surgery

1966;59:203-209.
Maleux G, Soula P, Otal P, et al: Traumatic aortobiliac dissection treated by

kissing-stent placement. J Trauma 1997;43:706-708.
Malt R, McKhann C: A report on replantation of severed arms. JAMA

1964;189:716-722.
Man B, Kraus L, Shachor D: Self-inflicted stab wound of the abdominal aorta.

J Cardiovasc Surg 1978;19:503-505.
Mandal A, Boitano MA: Reappraisal of low-velocity gunshot wounds of the

aorta and inferior vena cava in civilian practice. J Trauma 1978;18:580-

585.
Mandal A, Oparah S: Unusually low mortality of penetrating wounds of

the chest: Twelve years experience. J Thorac Cardiovasc Surg 1989;1:

119.
Mandelbaum I, Kalsbeck J: Extrinsic compression of internal carotid artery.

Ann Surg 1970;171:434-437.
Manlove G, Quattlebaum F, Flom R, LaFaveJ: Gunshot wounds of the abdom-
inal aorta. Am J Surg 1960;99:941-944.
Mansberger A, Linberg E: First rib resection for distal exposure of subclavian

vessels. Surg Gynecol Obstet 1965;120:579.
Mansour MA, Moore FA, Moore EE: Hypogastric arterial embolization in pelvic

fracture hemorrhage: Case report. J Trauma 1990;30:1417-1418.
Marcove R, Lindeque B, Silane M: Pseudoaneurysm of the popliteal artery with

an unusual arteriographic presentation. Clin Orthop Related Res

1988;234:142-144.
Margolies M, Ring E, Waltman A: Arteriography in the management of hem-
orrhage from pelvic fractures. N Engl J Med 1972;287:317-321.

RE.qxd 4/16/04 3:19PM Page SOI

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 601

Marin M, Veith F, CynamonJ, et al: Initial experience with transluminally placed

endovascular grafts for the treatment of complex vascular lesions. J Vase

Surg 1995;222:449-465.
Marin M, Veith F, Panetta T: Transluminally placed endovascular stented graft

repair for arterial trauma. J Vase Surg 1994;20:466-473.
Marin M, Veith F, Panetta T, et al: Percutaneous transfemoral insertion of a

stented graft to repair a traumatic femoral arteriovenous fistula. J Vase Surg

1993;18:299-302.
Markey JJ, Hines J, Nance C: Penetrating neck wounds: A review of 218 cases.

Am Surg 1975;41:77-83.
Marnocha K, Maglinte D: Plain-film criteria for excluding aortic rupture in

blunt chest trauma. AJR Am J Roentgenol 1985;144:19-21.
Marnocha K, Maglinte D, Woods J, et al: Blunt chest trauma and suspected

aortic rupture: Reliability of chest radiographs finds. Ann Emerg Med

1985;14:644-649.
Marsh C, Moore R: Deceleration trauma. Am J Surg 1957;93:623.
Marsh D, Sturm J: Traumatic aortic rupture: Roentgenographic indications for

angiography. Ann Thorac Surg 1976;21:337-340.
Martin L, McKenney M, SosaJ, et al: Management of lower extremity arterial

trauma. J Trauma 1994;37:591-599.
Martin RR, Mattox KL, Burch JM, Richardson R: Advances in treatment of vas-
cular injuries from blunt and penetrating limb trauma. World J Surg

1992;16:930-937.
Martin R, Flynn T, Rowlands G: Blunt cardiac rupture. J Trauma 1984;24:287-

290.
Marts B, Durham R, Shapiro M, et al: Computed tomography in the diagnosis

of blunt thoracic injury. Am J Surg 1994;168:688-692.
Marty-Ane C, Alric P, Prudhomme M, et al: Intravascular stenting of traumatic

abdominal dissection. J Vase Surg 1996;23:156-161.
Marty-Ane C, Serres-Cousine O, Laborde J, et al: Endovascular stent for use in

acute aortic dissection: An experimental study. Ann Vase Surg 1994;8:434-

442.
Marvasti M, Meyer J, Ford B, Parker FJ: Spinal cord ischemia following opera-
tion for traumatic aortic transection. Ann Thorac Surg 1986;42:425-428.
Marvasti M, Parker FJ, Bredenberg CE: Injury to arterial branches of aortic

arch. J Thorac Cardiovasc Surg 1984;32:293-298.
Marymont J, Coder H, Harris JJ, et al: Posterior hip dislocation associated with

acute traumatic injury of the thoracic aorta: A previously unrecognized

injury complex. J Orthop Trauma 1990;4:383-387.
MarzelleJ, Nottin R, Dartevelle P, et al: Combined ascending aorta rupture and

left main bronchus disruption from blunt chest trauma. Ann Thorac Surg

1989;1989:769-771.
Massberg S, Enders G, Matos F, et al: Fibrinogen deposition at the postischemic

vessel wall promotes platelet adhesion during ischemia-reperfusion in vivo.

Blood 1999;94:3829-838.
Massberg S, Messmer K: The nature of ischemia/reperfusion injury. Transplant

Proc 1998;30:4217-4223.
Massberg S, Sausbier M, Klatt P, et al: Increased adhesion and aggregation of

platelets lacking cyclic guanosine 3',5'-monophosphate kinase I.J Exp Med

1999;189:1255-1264.
Matas R: Traumatic aneurysm of the left brachial artery — Incision and partial

excision of sac: Recovery. Phil Med News 1888;53:462-466.

RE.qxd 4/16/04 3:19PM PageS02

602 VI • THE RICH REFERENCE COLLECTION

Matas R: Traumatisms and traumatic aneurysms of the vertebral artery and

their surgical treatment. Ann Surg 1893;18:477-521.
Matas R: Traumatic arteriovenous aneurysms of the subclavian vessels, with an

analytical study of fifteen reported cases, including one operated. Trans

Am Surg Assoc 1901;19:237.
Matas R: An operation for radical cure of aneurysm based on arteriography.

Ann Surg 1903;37:161-196.
Matas R: Recent advances in the technique of thoracotomy and pericardiotomy

for wounds of the heart. South Med J 1908;1:75-81.
Matas R: Surgery of the vascular system. In Keen WW, DaCosta JC (eds) :

Philadelphia, WB Saunders, 1909, p 67.
Matas R: Testing the efficiency of the collateral circulation as a preliminary to

the occlusion of the great surgical arteries. Ann Surg 1911;53:1-43.
Matas R: Testing the efficiency of the collateral circulation as a preliminary to

the occlusion of the great surgical arteries. JAMA 1914;68:1441-1447.
Matas R: Endoaneurysmorrhaphy, I: Statistics of operation of endoaneurysm-

orrhaphy, II: Personal experiences and observations on the treatment of

arteriovenous aneurysms by the intravascular method of suture: With special

references to the transvenous route. Surg Gynecol Obstet 1920;30:456-458.
Matas R: Military Surgery of the Vascular System. Philadelphia, WB Saunders,

1921.
Mathieu D, Wattel F, Bouachour G, et al: Post-traumatic limb ischemia: Pre-
diction of final outcome by transcutaneous oxygen measurements in hyper-
baric oxygen. J Trauma 1990;30:307-314.
Mathur A, Pochaczevsky R, Levotitz B, Feraru F: Fogarty balloon catheter for

removal of catheter fragment in subclavian vein. JAMA 1971;217:481.
Matloff D, Morton J: Acute trauma to the subclavian arteries. Am J Surg

1968;115:675-680.
Matolo M, Danto L, Wolfman E. Traumatic aneurysm of the abdominal aorta:

Report of two cases and review of the literature. Arch Surg 1974;108:867-

869.
MatsubaraJ, Seko T, Ohta T, et al: Traumatic aneurysm of the abdominal aorta

with acute thrombosis of bilateral iliac arteries. Arch Surg 1983;1 18:1337-

1339.
Mattox KL: Comparison of techniques of autotransfusion. Surgery 1978;84:700-

702.
Mattox KL: Emergency department thoracotomy. JACEP 1978;7:455.
Mattox KL: Abdominal venous injuries. Surgery 1982;91:497-501.
Mattox KL: CPR: Not for everyone. Emerg Med 1983;15:147-150.
Mattox KL: Thoracic great vessel injury. Surg Clin North Am 1988;68:693-

703.
Mattox KL: Thoracic vascular trauma. J Vase Surg 1988;7:725-729.
Mattox KL: Approaches to trauma involving the major vessels of the thorax.

Surg Clin North Am 1989;69:77-92.
Mattox KL: Fact and Fiction about management of aortic transection. Ann Thorac

Surg 1989;48:1-3.
Mattox KL: Indications for thoracotomy: Deciding to operate. Surg Clin North

Am 1989;1:47.
Mattox KL: Invited editorial comment: What drives the need for new technol-
ogy? J Trauma 1992;32:761-768.
Mattox KL: The abbreviated injury scale, 1985 revision: A condensed chart for

clinical use. J Trauma 1997;42:353-368.

RE.qxd 4/16/04 3:19PM PageS03

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 603

Mattox KL, Allen MK: Penetrating wounds of the thorax. Injury 1986;174:313-

317.
Mattox KL, Beall AC Jr, Ennix C, DeBakey ME: Intravascular migratory bullets.

Am J Surg 1979;137:192-195.
Mattox KL, Beall AC Jr, Jordan GLJr, DeBakey ME: Cardiorrhaphy in the emer-
gency center. J Thorac Cardiovasc Surg 1974;68:886-895.
Mattox KL, Bickell W, Pepe PE, et al: Prospective MAST study in 911 patients.

J Trauma 1989;20:1104.
Mattox KL, Bickell WH, Pepe PE, Mangelsdorff A: Prospective randomized

evaluation of antishock MAST in posttraumatic hypotension. J Trauma

1986;26:779-786.
Mattox KL, BurchJM, Richardson R, Martin RR: Retroperitoneal vascular injury.

Surg Clin North Am 1990;70:635-653.
Mattox KL, Espada R, Beall AC Jr: Performing thoracotomy in the emergency

center. J Am Coll Emerg Phys 1974;3:13-17.
Mattox KL, Espada R, Beall ACJr: Traumatic injury to the portal vein. Ann Surg

1975;181:519-522.
Mattox KL, Feliciano DV: Role of external cardiac compression in truncal trauma.

J Trauma 1982;22:934-935.
Mattox KL, Feliciano DV, Burch J, et al: Five thousand seven hundred sixty car-
diovascular injuries in 4459 patients: Epidemiologic evolution 1958 to 1987.

Ann Surg 1989;209:698-707.
Mattox KL, Holzman M, Pickard LR, et al: Clamp /repair: A safe technique for

treatment of blunt injury to the descending thoracic aorta. Ann Thorac

Surg 1985;40:456-465.
Mattox KL, Limacher M, Feliciano D: Cardiac evaluation following heart injury.

J Trauma 1985;25:758-765.
Mattox KL, Maningas P, Moore EE, et al: Prehospital hypertonic saline/dextran

infusion for post-traumatic hypotension. The USA multicenter trial. Ann

Surg 1991;213:482-491.
Mattox KL, McCollum W, Beall ACJr, et al: Management of penetrating injuries

of the suprarenal aorta. J Trauma 1975;15:808-815.
Mattox KL, McCollum W, Jordan GLJr, et al: Management of upper abdomi-
nal vascular trauma. Am Surg 1974;128:823-828.
Mattox KL, Moore EE, Feliciano DV: Trauma. East Norwalk, Conn, Appleton

& Lange, 1988, pp 519-536.
Mattox KL, Pickard L, Allen MK: Emergency thoracotomy for injury. Injury

1986;17:327-331.
Mattox KL, Pickard L, Allen MK, Garcia-Rinaldi R: Suspecting thoracic aortic

transection. JACEP 1978;7:12-15.
Mattox KL, Rea J, Ennix C, et al: Penetrating injuries to the iliac arteries. Am

J Surg 1978;136:663-667.
Mattox KL, Von Koch L, Beall AC Jr, DeBakey ME: Logistic and technical

considerations in the treatment of the wounded heart. Circulation

1975;51(suppl I) and 52:210-214.
Mattox KL, Whisennand H, Espada R, Beall ACJr: Management of acute com-
bined injuries to the aorta and inferior vena cava. AmJ Surg 1975;130:720-

724.
Maughon J: An inquiry into the nature of wounds resulting in killed in action

in Vietnam. Milit Med 1970;135:8-13.
Mavroudis C, Roon A, Baker CC, Thomas AN: Management of acute cervi-

cothoracic vascular injuries. J Thorac Cardiovasc Surg 1980;80:342-349.

RE.qxd 4/16/04 3:19PM PageS04

604 VI • THE RICH REFERENCE COLLECTION

May A, Lipchik E, DeWeeseJA: Repair of hepatic and superior mesenteric artery
injury: Patency demonstrated by aortography. Ann Surg 1965;162:869-872.

McBride L, Tidik S, StothertJ, et al: Primary repair of traumatic aortic disrup-
tion. Ann Thorac Surg 1987;43:65-67.

McBurney R, Vaughn R: Rupture of the aorta due to nonpenetrating trauma.
Ann Surg 1961;153:670-679.

McBurney R, Gegan E: Blunt trauma to the aorta and major arteries. JAMA
1962;180:330.

McCabe C, Ferguson C, Ottinger L: Improved limb salvage in popliteal artery
injuries. J Trauma 1983;23:982-985.

McCann W: Successful wound repair of a stab wound of the ascending aorta.
NYStateJMed 1958;58:3177-3178.

McCarthy W, Yao JST, Schafer M, et al: Upper extremity arterial injury in ath-
letes. J Vase Surg 1989;9:317-327.

McCollum C, Mavor E: Brachial artery injury after cardiac catheterization.
J Vase Surg 1986;4:355-359.

McCordJ: Oxygen-derived free radicals in postischemic tissue injury. N Engl J
Med 1985;312:159-163.

McCorkell S, Harley J, Morishima M, Cummings D: Indications for angiogra-
phy in extremity trauma. AJR 1985;145:1245-1247.

McCormack L, Cauldwell E, Anson BJ: Brachial and antebrachial arterial pat-
terns: a study of 750 extremities. Surg Gynecol Obstet 1953;96:43-54.

McCormick T, Burch B: Routine angiographic evaluation of neck and extrem-
ity injuries. J Trauma 1979;19:384-387.

McCreadyR: Upper extremity vascular injuries. Surg Clin North Am 1988;68:725-
740.

McCready R, Logan N, Daugherty M: Long-term results with autogenous tissue
repair of traumatic extremity vascular injuries. Ann Surg 1987;206:804-
808.

McCready R, Procter C, Hyde GL: Subclavian-axillary vascular trauma. J Vase
Surg 1986;3:24-31.

McCroskey B, Moore EE, Moore FA, Abernathy CM: A unified approach to the
torn thoracic aorta. Am J Surg 1991;162:473-476.

McCroskey B, Moore EE, Pearce W, et al: Traumatic arterial injuries of the
upper extremity: Determinants of disability. Am J Surg 1988;156:553-
555.

McCroskey B, Moore EE, Rutherford R: Vascular Trauma. The Surgical Clinics
of North America. Philadelphia, WB Saunders, 1988.

McCullough J, Hollier L, Nugent M: Paraplegia after thoracic aorta occlusion:
Influence of cerebrospinal fluid drainage. Experimental and early clinical
results. J Vase Surg 1988;7:153-160.

McCutchan J, Gillham N: Injury to the popliteal artery associated with dislo-
cation of the knee: Palpable distal pulses do not negate the requirement
for arteriography. Injury 1989;20:307-310.

McDonald E, Goodman P, Weinstock D: Clinical indications for arteriography
in trauma to the extremity: A review of 114 cases. Radiology 1975;166:45-
47.

McDonald M, Mota-Filipe H, Paul A, et al: Calpain inhibitor I reduces the acti-
vation of nuclear factor-kappaB and organ injury/dysfunction in hemor-
rhagic shock. FASEBJ 2001;15:171-186.

McDonough J, Altemeier WA: Subclavian venous thrombosis secondary to
indwelling catheters. Surg Gynecol Obstet 1971;133:397-400.

RE.qxd 4/16/04 3:19PM PageS05

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 605

McFadden P, Jones J, Ochsner JL: The fuzzy foreign body fragment: A subtle

roentgenograph^ clue to mediastinal vascular injury. Am J Surg 1985;

149:809-811.
McFadden D, Lawelor B, Ali I: Portal vein injury. Can J Surg 1987;30:91.
McGough E, Helfrich L, Hughes R: Traumatic in timal prolapse of the common

carotid artery. Am J Surg 1972;123:724-75.
Mcllduff J, Foster E, Alley RD : Traumatic aortic rupture: An additional roentgen o-

graphic sign. Ann Thorac Surg 1977;24:77-79.
Mclntyre RJ, Moore EE, Read R, et al: Transesophageal echocardiography in

the evolution of a transmediastinal gunshot wound: Case report. J Trauma

1994;36:125-127.
McKenzie A, Sinclair A: Axillary artery occlusion complicating shoulder dislo-
cation: A report of two cases. Ann Surg 1958;148:139-144.
McKnightJ, Meyer J, Neville JJ: Nonpenetrating traumatic rupture of the tho-
racic aorta. Ann Surg 1964;160:1069-1072.
McLaughlin JS, Suherlis H, Yeager G: Sterile pericarditis from foreign body:

Acute tamponade one month following gunshot wound. Ann Thorac Surg

1967;3:52-56.
McLean T, McManus R: Penetrating trauma involving the innominate artery.

Ann Thorac Surg 1991;51:113-115.
McMillan R, Landreneau M, McCormic G, McDonald J: Major vascular injuries

of the torso. South Med J 1992;85:375-377.
McNab A, Fabinyi G, Miline P: Blunt trauma to the carotid artery. Aust N Z J

Surg 1988;58:651-656.
McNally W: Lead poisoning caused by a bullet embedded for twenty-seven years.

IndustMedl949;18:77.
McNalley M, Sugg W: Traumatic communication between the aorta, right atrium,

and left atrium. J Thorac Cardiovasc Surg 1967;54:150-152.
McNamaraJJ, Brief DK, Beasley W, WrightJ: Vascular injury in Vietnam combat

casualties: Results of treatment at the 24th Evacuation Hospital, ljuly 1967

to 12 August 1969. Ann Surg 1973;178:143-147.
McNamaraJJ, Brief DK, Stremple J, WrightJ: Management of fractures with

associated arterial injury in combat casualties. J Trauma 1973;13:17-19.
McNutt R, Seabrook G, Schmitt D, Aprahamian C: Blunt tibial artery trauma:

predicting the irretrievable extremity. J Trauma 1989;29:1624.
McQuillan W, Nolan B: Ischaemia complicating injury: A report of thirty-seven

cases. J Bone Joint Surg 1968;50-B:482-492.
McSwain NE Jr: Pneumatic trousers and the management of shock. J Trauma

1977;17:719-724.
McSwain NE Jr: PASG—Holding on for dear life. Emergency 1990.
Meagher DJ, Defore W, Mattox KL, Harberg F: Vascular trauma in infants and

children. J Trauma 1979;19:532-536.
Meek A, Robbs J: Vascular injury with associated bone and joint trauma. Br J

Surg 1984;71:341-344.
Meissner M, Paun M, Johansen K: Duplex sonography for arterial trauma. Am

JSurgl991;161:552.
MelkiJ, Tabley A, BessouJP, Soyer R: Chronic false aneurysm of the sub-renal

abdominal aorta after abdominal contusion (French) . J Maladies Vascu-

laires 1990;15:377-379.
Melton S, Croce MA, Patton JJ, et al: Popliteal artery trauma: Systemic antico-
agulation and intraoperative thrombolysis improve limb salvage. Ann Surg

1997;225:518-527.

RE.qxd 4/16/04 3:19PM PageS06

606 VI • THE RICH REFERENCE COLLECTION

Menger MD, Kerger H, Geisweid A, et al: Leukocyte-endothelium interaction
in the microvasculature of postischemic striated muscle. Adv Exp Med Biol
1994;361:541-545.

Menger MD, Pelikan S, Steiner D, Messmer K: Microvascular ischemia-
reperfusion injury in striated muscle: Significance of "reflow paradox."
Am J Physiol 1992;263:H1901-H1906.

Menger MD, Rucker M, Vollmar B: Capillary dysfunction in striated muscle
ischemia/reperfusion: On the mechanisms of capillary "no reflow." Shock
1997;8:2-7.

Menger MD, Vollmar B: In vivo analysis of microvascular reperfusion injury in
striated muscle and skin. Microsurgery 1994;15:383-389.

Mengoli L: Aneurysmorrhaphy of the internal carotid artery utilizing intralu-
minal distal control. Am J Surg 1969;117:397-399.

Menzoian J, Doyle J, Cantelmo N, et al: A comprehensive approach to extrem-
ity vascular trauma. Arch Surg 1985;120:801-805.

Menzoian J, Doyle J, Logerfo F, et al: Evaluation and management of vascular
injuries of the extremities. Arch Surg 1983;118:93-95.

Menzoian J, Logerfo F, Doyle J, et al: Management of vascular injuries to the
leg. Am J Surg 1981;144:231-234.

Meredith J, O'Neil E, Snow D, Hansen K: Femoral vein catheter related deep
venous thrombosis: A perspective evaluation with venous duplex sonog-
raphy. J Trauma 1991;31:1034.

Merin G, Bitran D, Donchin Y, et al: Traumatic rupture of the thoracic aorta
during pregnancy. Surgical considerations. Chest 1981;79:99-100.

Merine D, Brody W: Role of CT in excluding major arterial injury after blunt
thoracic trauma. Invest Radiol 1989;24:733-734.

Merrill W, Lee R, HammonJJ, et al: Surgical treatment of acute traumatic tear
of the thoracic aorta. Ann Surg 1988;207:699-706.

Messina L, Brothers T, Wakefield T: Clinical characteristics and surgical man-
agement of vascular complications in patients undergoing cardiac catheter-
ization: Interventional versus diagnostic procedures. J Vase Surg 1991;
13:593-600.

Metzdroff M, Hill J, Matar A, et al: Use of sutureless intraluminal aortic pros-
theses in traumatic rupture of the aorta. J Trauma 1986;26:691-694.

Metzger D, Hamilton R, Stephenson D: Mesenteric arteriovenous fistula:
Unusual cause of distal gastrointestinal bleeding. Am J Surg 1972;124:
767.

Meyer D, Jessen M, Grayburn P: Use of echocardiography to detect occult cardiac
injury after penetrating thoracic trauma: A prospective study. J Trauma
1995;39:902-909.

Meyer JP, Lim LT, Schuler J, et al: Peripheral vascular trauma from close-range
shotgun injuries. Arch Surg 1985;120:1126-1131.

Meyer JP, Walsh J, Barrett J, et al: Analysis of 18 recent cases of penetrating
injuries to common and internal carotid arteries. Am J Surg 1988;156:96-
99.

Meyer JP, Walsh J, Schuler J: The early fate of venous repair following civilian
vascular trauma: A clinical hemodynamic and venographic assessment. Ann
Surg 1987;206:458-464.

Meyer JP, Goldfaden D, BarrettJ, et al: Subclavian and innominate artery trauma:
A recent experience with nine patients. J Cardiovasc Surg 1988;29:283-289.

Meyer J, Neville JJ, Hansen W: Traumatic rupture of the aorta in a child. JAMA
1969;208:527-529.

RE.qxd 4/16/04 3:19PM PageS07

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 607

Meyer TJ, Slager R: False aneurysm following subtrochanteric osteotomy. J Bone
Joint Surg 1964;46:581-582.

Michaels A, Gerndt S, Taheri P, et al: Blunt force injury to the abdominal aorta.
J Trauma 1996;41:105-109.

Michaels J: Choice of material for above-knee femoropopliteal bypass graft. Br
J Surg 1989;76:7-14.

Michaud P, ChassignolleJ, Termet H, et al: Traumatic aneurysms of the aorta.
Analysis of 11 observations. J Cardiovasc Surg 1971;12:121-130.

Michelassi F, Pietrabissa A, Ferrari M, et al: Bullet emboli to the systemic and
venous circulation. Surgery 1990;107:239-245.

Midgley F, Behrendt DM: Surgical repair of chronic post-traumatic aneurysm
of the aortic arch. J Thorac Cardiovasc Surg 1974;67:229-232.

Mikulin T, Walker E: False aneurysm following blunt trauma. Injury 1984; 15:309-
310.

Miller D: Gangrene from arterial injuries associated with fractures and dislo-
cations of the leg in the young and in adults with normal circulation. Am
J Surg 1957;93:367-375.

Miller D, Freeark R: Injuries to the popliteal artery among the young. Am J
Surg 1962;104:633-639.

Miller F, Bond SJ, Shumate C: Diagnostic pericardial window: A safe alterna-
tive to exploratory thoracotomy for suspected heart injuries. Arch Surg
1987;122:605-609.

Miller F, Richardson JD, Thomas H, et al: Role of CT in diagnosis of major arte-
rial injury after blunt thoracic trauma. Surgery 1988;106:596-602.

Miller F, Seward J, Gersh B, Tajik A: Two-dimensional echocardiographic find-
ings in cardiac trauma. Am J Cardiol 1982;50:1022-1027.

Miller F, Shumate C, Richardson JD: Myocardial contusion: when can the diag-
nosis be eliminated? Arch Surg 1989;124:805-808.

Miller H, Welch C: Quantitative studies on time factor in arterial injuries. Ann
Surg 1949;130:428-438.

Millham F, Grindlinger G: Survival determinants in patients undergoing emer-
gency room thoracotomy for penetrating chest injury. J Trauma 1993;34:332-
336.

Millikan JS, Moore EE, Cogbill TH: Inferior vena cava injuries: A continuing
challenge. J Trauma 1983;23:207-212.

Millikan JS, Moore EE, Van Way G, Kelly GL: Vascular trauma in the groin: Con-
trast between iliac and femoral injuries. Am J Surg 1981;142:695-698.

Millikan JS, Moore EE: Outcome of resuscitative thoracotomy and descending
aortic occlusion. J Trauma 1984;24:387-392.

Millikan JS, Moore EE: Critical factors in determining mortality from abdom-
inal aortic trauma. Surg Gynecol Obstet 1985;160:313-316.

Mills J, Wiedeman J, Robison JG, Hallett JJ: Minimizing mortality and morbid-
ity from iatrogenic arterial injuries: The need for early recognition and
prompt repair. J Vase Surg 1986;4:22-27.

Mirvis S, Kostrubiak I, Whitley N, et al: Role of CT in excluding major arterial
injury after blunt thoracic trauma. AJR Am J Roentgenol 1987;149:601-
605.

Mitchell D, Needlemon L, Bezzi M, et al: Femoral artery pseudoaneurysm: Diag-
nosis with conventional duplex and color Doppler. Radiology 1987;165:687-
690.

Mitchell FI, Thai E: Results of venous interposition grafts in arterial injuries.
J Trauma 1990;30:336-339.

RE.qxd 4/16/04 3:19 PM Page 608

608 VI • THE RICH REFERENCE COLLECTION

Mitchell R, Enright L: The surgical management of acute and chronic injuries
of the thoracic aorta. Surg Gynecol Obstet 1983;157:1-4.

Mittal A, May I, Samson P: Traumatic aneurysm of the aortic arch. Ann Thorac
Surg 1972;13:494-498.

Corrected

Monson D, Saletta J, Freeark R: Carotid vertebral trauma. J Trauma 1969;9:987-
999.

Montales E, Yao S, Silva Y: Management of traumatic peripheral arteriovenous
fistulas. J Trauma 1973;13:161-165.

Montgomery M: Effect of therapeutic venous ligation on blood flow in cases of
arterial occlusion. Proc Soc Exp Biol Med 1929;27:178.

Montgomery M: Therapeutic venous occlusion: Its effect on blood flow in the
extremity in acute obstruction. Arch Surg 1932;24:1016-1027.

Moon M, Dake M, Pelc L, et al: Intravascular stenting of acute experimental
type B dissections. J Surg Res 1993;54:381-388.

Moore C, Cohen A: Combined arterial, venous and ureteral injury complicat-
ing lumbar disc surgery. Am J Surg 1968;115:574-577.

Moore C, Wolma F, Brown R, Derrick J: Vascular trauma: A review of 250 cases.
Am J Surg 1971;122:576-578.

Moore EE, Burch JM, Franciose RJ, et al: Staged physiologic restoration and
damage control surgery. World J Surg 1998;22:1184.

Moore EE, Cogbill TH, Jurkovich GJ: Organ injury scaling III: Chest wall, abdom-
inal vascular, ureter, bladder and urethra. J Trauma 1992;33:337-339.

Moore EE, Cogbill TH, Malangoni M, et al: Organ injury scaling. Surg Clin
North Am 1995;75:293-303.

Moore EE, Malangoni M, Cogbill TH: Organ Injury Scaling IV: Thoracic, vas-
cular, lung, cardiac, and diaphragm. J Trauma 1994;36:229-300.

Moore E, Webb W, Verrier E, et al: MRI of chronic posttraumatic aneurysms of
the thoracic aorta. AJR Am J Roentgenol 1984;143:1195-1196.

Moore HJ, Nyhus L, Kanar E, Harkins H: Gunshot wounds of the major arter-
ies: An experimental study with clinical implications. Surg Gynecol Obstet
1954;98:129-147.

Moore T: Acute arterial obstruction due to the traumatic circumferential intimal
fracture. Ann Surg 1958;148:111-114.

Moore T, Peters M: Thru-and-thru gunshot penetration of the abdominal aorta
in a 4-year-old child managed by aortic transection, debridement and reanas-
tomosis with survival. J Trauma 1979;19:537-539.

Moore W: Vascular Surgery. Orlando, Grune & Stratton, 1986.

Morano J, Burkhalter J, Daniel CJr: Bilateral popliteal arteriovenous fistulas.
J Trauma 1987;27:577-578.

Moreno C, Moore EE, Majune J: Pericardial tamponade. A critical determinant
for survival following penetrating cardiac wounds. J Trauma 1986;26:
821.

Moreno C, Moore EE, Rosenberger A, Cleveland H: Hemorrhage associated
with major pelvic fracture: Amultispecialty challenge. J Trauma 1986;26:987-
994.

Morgan P, Goodman L, Aprahamian C, et al: Evaluation of traumatic aortic
injury: Does dynamic contrast-enhanced CT ply a role? Radiology
1992;182:661-666.

Morin J, Provan J, Jewett M, Ameli FM: Vascular injury and repair associated
with retroperitoneal lymphadenectomy for nonseminomatous germinal
cell tumours of the testis. Can J Surg 1992;35:253-256.

RE.qxd 4/16/04 3:19PM PageS09

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 609

Morin R, Wright CB, Dunn E, et al: Vascular trauma. In James E, Corry R, Perry
JFJr (eds): Basic Surgical practice. St. Louis, Hanley & Belfus, 1987, pp
521-523.

Morris GC Jr, Beall AC Jr, Berry WB, et al: Anatomical studies of the distal
popliteal artery and its branches. Surg Forum 1960;10:498-502.

Morris GC Jr, Beall AC Jr, Roof WR, DeBakey ME: Surgical experience with 220
acute arterial injuries in civilian practice. Am J Surg 1960;99:775-781.

Morris GCJr, Creech O Jr, DeBakey ME: Acute arterial injuries in civilian prac-
tice. Am J Surg 1957;93:565-572.

Morton J, Southgate W, DeWeeseJA: Arterial injuries of the extremities. Surg
Gynecol Obstet 1966;123:611-627.

Morton JR, Crawford ES: Bilateral traumatic renal artery thrombosis. Ann Surg
1972;176:62-67.

Morton JR, Reul GJ, Arbegast NR, et al: Bullet embolus to the right ventricle:
Report of three cases. Am J Surg 1971;122:584-590.

Moss A, Bruhn F: The echocardiogram. An ultrasound technic for the detec-
tion of pericardial effusion. N Engl J Med 1996;274:380.

Moss C, Veith F, Jason R, Rudavsky A: Screening isotope angiography in arter-
ial trauma. Surgery 1969;86:881-889.

Motsay G, Manlove C, PerryJF: Major venous injury with pelvic fracture.J Trauma
1969;9:343-346.

Mott V: Reflections on securing in a ligature the arteria innominata. Med Surg
1918;1:9.

Moure P: Les Greffes Vasculaires. Paris, Doin, 1914.

Moya J, de Pablo C, Sanchez M, et al: Diagnosis by Doppler echocardiography.
Chest 1990;98:1016-1017.

Mozingo J, Denton I: The neurologic deficit associated with sudden occlusion
of the abdominal aorta due to blunt trauma. Surgery 1975;77:118-125.

Mubarak S, Owen C: Double-incision fasciotomy of the leg for decompression
in compartment syndromes. J Bone Joint Surg 1977;59A:184.

Mucha PJ, Olivier HJ, Pairolero P, Farnell M: Blunt thoracic aortic injury: A
reappraisal. J Trauma 1983;23:652.

Mucha PJ, Schaff H, Pairolero P: Clamp/repair of traumatic transection of
descending aorta. Ann Thorac Surg 1987;43:351-352.

Mufti M, LaGuerre J, Pochaczevsky R, et al: Diagnostic value of hematoma in
penetrating arterial wounds of the extremities. Arch Surg 1970;101:562-
569.

Mulder D, GrollmanJJ: Traumatic disruption of the thoracic aorta. Am J Surg
1969;118:311-316.

Muller WJ, Goodwin W: Renal arteriovenous fistula following nephrectomy.
Ann Surg 1956;144:240-244.

Mullins R, Lucas C, Ledgerwood A: The natural history following venous liga-
tion for civilian injuries. J Trauma 1980;20:737-743.

Munda R, Bole PV, Lande A, Clauss RH: The use of an external Dacron shunt
in repair of a supraceliac abdominal aortic traumatic aneurysm. J Cardio-
vasc Surg 1977;18:141-146.

Murdock C: Traumatic rupture of the thoracic aorta. Arch Surg 1957;74:589-
592.

MurphyJ: Resection of arteries and veins injured in continuity end-to-end suture.
Exp Clin Res Med Rec 1897;51:73-104.

MurphyJ: Myositis; ischemic myositis; infiltration myositis; cicatricial muscular
or tendon fixation in forearm; internal, external and combined compression

RE.qxd 4/16/04 3:19 PM Page 610

610 VI • THE RICH REFERENCE COLLECTION

myositis, with subsequent musculotendinous shortening. JAMA 1914;

63:1249-1255.
Murphy T, Dorfman G, Segall M: Iatrogenic arterial dissection: Treatment by

percutaneous transluminal angioplasty. Cardiovasc Intervent Radiol

1991;14:302.
Murphy T, Piper C, Anderson CL: Complications of left heart catheterization.

Am Surg 1971;37:472-475.
Murray D: Posttraumatic thrombosis of the internal carotid and vertebral

arteries after non-penetrating injuries of the neck. Br J Surg 1957;44:

556.
Murray E, Minami K, Kortke H, et al: Traumatic sinus of Valsalva fistula and

aortic valve rupture. Ann Thorac Surg 1993;55:760-761.
Murray G: Heparin in thrombosis and embolism. Br J Surg 1940;27:567-

598.
Murray G: Surgical repair of injuries to main arteries. Am J Surg 1952;83:480.
Murray G, Brawley RK, Gott V: Reconstruction of the innominate artery by

means of a temporary heparin-coated shunt bypass. J Thorac Cardiovasc

Surg 1971;62:34-41.
Murray G, Janes J: Prevention of acute failure of circulation following injuries

to large arteries: Experiments with glass cannulae kept patent by admin-
istration of heparin. Br Med J 1940;2:6-7.
Mustard W, Bull C: A reliable method for relief of traumatic vascular spasm.

Ann Surg 1962;155:339-344.
Myers S, Reed M, Black CT, et al: Noniatrogenic pediatric vascular trauma. J

Vase Surg 1989;10:258-265.
Myers S, Harward T, Cagle L: Isolated subclavian artery dissection after blunt

trauma. Surgery 1991;109:336.
Myers SI, Harward TRS, Maher DP, et al: Complex upper extremity vascular

trauma in an urban population. J Vase Surg 1990;12:305-309.
Myers W, Lawton B, Sautter R: An operation for tracheal-innominate artery

fistula. Arch Surg 1972;105:269-274.
Myles R, Yellin AE: Traumatic injuries of the abdominal aorta. Am J Surg

1979;138:273-277.
Nabatoff R, Blum L, Touroff A: Long-term sequelae of common femoral vein

ligation in the treatment of thromboembolic disease. Surgery 1970;67:272-

276.
Nachbur B, Meyer R, Verkkala K, Zurcher R: The mechanisms of severe arter-
ial injury in surgery of the hip joint. Clin Orthop 1979;141:122-133.
Naclerio E: Penetrating wounds of the heart: Experience with 249 patients. Dis

Chest 1964;46:1-22.
Nakano J, DeSchryver C: Effects of arteriovenous fistula on systemic and pul-
monary circulations. Am J Physiol 1964;207:1319.
Napoli P, Meade P, Adams CW: Primary aortoenteric fistula from a post trau-
matic pseudoaneurysm. J Trauma 1996;41:149-152.
Nashef S, Talwalkar N, Janieson M: Aortic arch rupture in a child following

minor blunt trauma. J Thorac Cardiovasc Surg 1987;35:240-241.
NataliJ, Lacombe M, Bruchou P, Vinardi G: Les traumatismes arteriels vus tar-

divement conduite a tenir en leur presence. Presse Med 1964;72:2273.
NataliJ, Maraval M, Kieffer E, Petrovic P: Fractures of a clavicle and injuries of

the subclavian artery: Report of 10 cases. J Cardiovasc Surg 1975;16:541.
Natali J, Benhemori AC: Iatrogenic vascular injuries. J Cardiovasc Surg

1979;20:169-176.

RE.qxd 4/16/04 3:19 PM Page 611

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 61 1

Naude G, Back M, Perry MO, Bongard FS: Blunt disruption of the abdominal

aorta: Report of a case and review of the literature. J Vase Surg 1997;25:931-

935.
Navarre J, Cardillo P: Vascular trauma in children and adolescents. Am J Surg

1982;143:229-231.
Neagu S: Abdomino-thoracic shooting wound with multivisceral involvement

including injury of abdominal aorta in the supra-mesocolic segment. Acta

Chir Belg 1993;93:107-109.
NeelS: Army aeromedical evacuation procedures in Vietnam.JAMA 1968;204:99-

103.
Neely W, Hardy JD, Artz CP: Arterial injuries in civilian practice: A current reap-
praisal with analysis of 43 cases. J Trauma 1961;1:424-439.
Neville R, Franco C, Anderson RJ, et al: Popliteal artery agenesis: a new anatomic

variant. J Vase Surg 1990;12:573-576.
Neville R, Hobson R, Wantanabe B: A prospective evaluation of arterial intimal

injuries in an experimental model. J Trauma 1991;31:669-675.
Neville R, Yasuhara H, Watanabe B: Endovascular management of arterial intimal

defects: An experimental comparison by arteriography, angioscopy, and

intravascular ultrasonography. J Vase Surg 1991;13:496-502.
Nghiem D, Boland JP: Four-compartment fasciotomy of the lower extremity

without fibulectomy: A new approach. Am Surg 1980;46:414-417.
Ngu V, Konstam PG: Traumatic dissecting aneurysm of the abdominal aorta.

Br J Surg 1965;52:981-982.
Nguyen L, LewinJ: Angiographic demonstration of fistula between abdominal

aorta and thoracic duct. JAMA 1970;211:499-500.
Nicholas G, Lane F: Traumatic superior mesenteric artery-superior mesenteric

vein fistula. J Trauma 1974;14:344.
Nicholas G, DeMuth WE Jr: Long-term results of brachial thrombectomy fol-
lowing cardiac catheterization. Ann Surg 1976;183:436-438.
Nichols J, Svoboda J, Parks S: Use of temporary intravascular shunts in selected

peripheral arterial injuries. J Trauma 1986;26:1094-1096.
Nichols J, Lillehei K: Nerve injury associated with acute vascular trauma. Surg

Clin North Am 1988;68:837-852.
Nicholson J, Foster R, Heath R: Bryant's traction: A provocative cause of cir-
culatory complication. JAMA 1955;157:415-418.
Nicoladoni C: Phlebarteriectasie der rechten oberen extremitat. Arch Klin Chir

1875;18:252.
Nizzero A, Miles J: Blunt trauma of the abdominal aorta. Can Med Assoc J

1986;135:219-220.
Nolan B, McQuillan N: A study of acute traumatic limb ischaemia. Br J Surg

1965;52:559-565.
Nolan B: Vascular injuries. J Royal Coll Surg 1968;13:72.
Nolte D, Lehr HA, Messmer K: Adenosine inhibits postischemic leukocyte-

endothelium interaction in postcapillary venules of the hamster. Am J

Physiol 1991;261:H651-H655.
Nolte D, Hecht R, Schmid P, et al: Role of Mac-1 and ICAM-1 in ischemia-

reperfusion injury in a microcirculation model of BALB/C mice. Am J

Physiol 1994;267:H295-H930.
Noon G, Boulafendis D, Beall AC Jr: Rupture of the heart secondary to blunt

trauma.J Trauma 1971;11:122-128.
Nordestgaard A, Bodily KC, Osborne RJ, ButtorffJ: Major vascular injuries during

laparoscopic procedures. Am J Surg 1995;169:543-545.

RE.qxd 4/16/04 3:19 PM Page 612

612 VI • THE RICH REFERENCE COLLECTION

Norotsky M, Rogers F, Shackford S: Delayed presentation of splenic artery
pseudoaneurysms following blunt abdominal trauma: Case reports. J Trauma
1995;38:444-447.

Norris C, Zlotnick R, Silva W, Wheeler H: Traumatic pseudoaneurysm follow-
ing blunt trauma. J Trauma 1986;28:480-482.

Norris G: Varicose aneurysm at the bend of the arm: Ligature of the artery
above and below the sac; Secondary hemorrhages with a return of the
aneurysm thrill on the tenth day; Cure. Am J Med Sci 1843;5:17.

North C, Ahmadi J, Segall H, Zee C: Penetrating vascular injuries of the face
and neck: Clinical and angiographic correlation. AJR Am J Roentgenol
1986;147:995-999.

Norton L, Spencer FC: Long-term comparison of vein patch with direct suture.
Arch Surg 1964;89:1083.

Noth P: Electrocardiographic patterns in penetrating wounds of the heart. Am
HeartJ 1946;32:713.

NunleyD: Radiographic diagnosis of aortic injury. Ann Thorac Surg 1984;38:424-
425.

NunleyJ, Roman L, UrbaniakJ: Arterial shunting as an adjunct to major limb
revascularization. Ann Surg 1981;193:271-273.

Nunn D: Abdominal aortic dissection following non-penetrating abdominal
trauma. Am Surg 1973;39:117-179.

Nypaver T, SchulerJ, McDonnell P: Long-term results of venous reconstruc-
tion after trauma in civilian practice. J Vase Surg 1992;16:762-768.

O'DonnellV, AtikM, Pick Revaluation and management of penetrating wounds
of the neck. Am J Surg 1979;138:309-314.

O'Donnell TJ, Brewster DC, Darling RC, et al: Arterial injuries associated with
fractures and/or dislocations of the knee. J Trauma 1977;17:775-784.

O'Gorman R, Feliciano DV: Arteriography performed in the emergency center.
Am J Surg 1986;152:323-325.

O'Gorman R, Feliciano DV, Bitondo CG, et al: Emergency center arteriogra-
phy in the evaluation of suspected peripheral vascular injuries. Arch Surg
1984;119:568-573.

O'Neill JJ: Traumatic vascular lesions in infants and children. In Dean RH,
O'Neill ]J (eds): Vascular Disorders of Childhood. Philadelphia, Lea &
Febiger, 1983, pp 181-193.

O'Neill JJ, Killen DA: Autogenous vein graft for repair of acute tibial artery
injury. Ann Surg 1965;162:218-220.

O'Neill MJ, MyersJ, Brown G, et al: Avulsion of the innominate artery from the
aortic arch associated with a posterior tracheal tear. J Trauma 1982;22:56-
59.

O'Reilly M, Hood J, Livingston RH, IrwinJ: Penetrating injuries of the popliteal
vein: A report on 34 cases. Br J Surg 1980;67:337-340.

O'Sullivan M, Folkerth T, Morgan J, Fosburg R: Posttraumatic thoracic aortic
aneurysm: Recognition and treatment. Arch Surg 1972;105:14-18.

Ochsner JL, Crawford ES, DeBakey ME: Injuries of the vena cava caused by
external trauma. Surgery 1961;49:397-405.

Ochsner M, Harviel J, Stafford P, et al: Development and organization for casu-
alty management on a 1 ,000-bed hospital ship in the Persian Gulf. J Trauma
1992;32:501-513.

Ochsner M, Hoffman A, DiPasquale D, et al: Associated aortic rupture-pelvic
fracture: An alert for orthopaedic and general surgeons. J Trauma 1992;33:
429-434.

RE.qxd 4/16/04 3:19 PM Page 613

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 613

Ochsner MJ, Champion HR, Chambers R, Harviel J: Pelvic fracture as an indi-
cator of increased risk of thoracic rupture. J Trauma 1980;29:1376-1379.

Odekwu P, Oiler D: Hematemesis as initial presentation of traumatic paraceliac
pseudoaneurysm of the abdominal aorta. Cardiovasc Surg 1994;2:781-782.

Odom C: Causes of amputations of battle injuries with emphasis on vascular
injuries. Surgery 1946;19:562.

Ogilvie W: War surgery in Africa. Br J Surg 1944;31:313.

Ohkawa M, Clemens M, Chaudry IH: Studies on the mechanism of beneficial
effects of ATP-MgC12 following hepatic ischemia. Am J Physiol
1983;244:R695-R702.

Ohkawa M, Chaudry IH, Clemens M, Baue AE: ATP-MgCL produces sustained
improvementin hepatic mitochondrial function and blood flow after hepatic
ischemia. J Surg Res 1984;37:226-234.

Okubo S, Bernardo NL, Elliot G, et al: Tyrosine kinase signaling in action poten-
tial shortening and expression of HSP72 in late preconditioning. Physiol
Heart Circ Physiol 2000;279:H2269-H2276.

Olinde A: Letters to the editors: Traumatic subclavian-axillary aneurysm. J Vase
Surg 1990;11:848-849.

Oiler D, Rutledge R, Thomason M, et al: Vascular injuries in a rural state: A
review of 940 patients from state trauma registry. J Trauma 1991;31:1036.

Oiler D, Rutledge R, Clancey T, et al: Vascular injuries in a rural state: A review
of 978 patients from a state trauma registry. J Trauma 1992;32:740-746.

Orcutt M, Levine B, Gaskill H III, Sirinek K: Iatrogenic vascular injury: A reducible
problem. Arch Surg 1985;120:384-385.

Orcutt M, Levine B, Gaskill H III, Sirinek K: Civilian vascular trauma of the
upper extremity. J Trauma 1986;26:63-67.

Orcutt M, Levine B, Root H, Sirinek K: The continuing challenge of popliteal
vascular injuries. Am J Surg 1983;146:758-761.

Ordog G, Albin D, Wasserberger J, Balasubramanium S: Shotgun "birdshot"
wounds to the neck. J Trauma 1988;28:491-497.

Orringer M, Kirsh MM: Primary repair of acute traumatic aortic disruption.
Ann Thorac Surg 1983;35:672-675.

Ortner A, Berg HF, Ledbendiger A: Limb salvage through small-vessel surgery.
Arch Surg 1961;83:414-421.

Osier T, Baker SP, Long W: A modification of the injury severity score that both
improves accuracy and simplifies scoring. J Trauma 1997;43:922-926.

Osier W: Case of arteriovenous aneurysm of the axillary artery and vein of 14
years duration. Ann Surg 1893;17:37-40.

Osier W: Report of a case of arteriovenous aneurysm of the thigh.Johns Hopkins
HospBulll905;16:119.

Osier W: An arteriovenous aneurysm of the axillary vessels of 30 years dura-
tion. Lancet 1913;2:1248.

Osier W: Remarks on arteriovenous aneurysm. Lancet 1915;1:949.

Ottolenghi C: Vascular complications in injuries about the kneejoint. Clin Orthop
1982;165:148-156.

Ouchi H, Ohara I, Kijima M: Intraluminal protrusion of completely disrupted
intima: An unusual form of acute arterial injury. Surgery 1965;57:220-224.

Overbeck W, Gruenagel N, Krauss H: Eisensplitterverletzung der intraprikar-
dialen aorta. Thoraxchirurgie 1968;16:274.

Oweida S, Roubin G, Smith RI, Salam A: Postcatheterization vascular compli-
cations associated with percutaneous transluminal coronary angioplasty.
J Vase Surg 1990;12:310-315.

RE.qxd 4/16/04 3:19 PM Page 614

614 VI • THE RICH REFERENCE COLLECTION

Owen D, Hodgson P: Control of hemorrhage following missile wound to the
pelvis. J Trauma 1980;20:906-908.

OwensJ: The management of arterial trauma. Surg Clin North Am 1963;43:371-
385.

Owens T, Watson W, Prough D, et al: Limiting initial resuscitation of uncon-
trolled hemorrhage reduces internal bleeding and subsequent volume
requirements. J Trauma 1995;39:200-207.

Pachter H, Spencer F, Hofsetter S: Experience with the finger fracture tech-
nique to achieve intra-hepatic hemostasis in 75 patients with severe injuries
of the liver. Ann Surg 1978;197:771-777.

Pachter H, Spencer FC, Hofsetter S, et al: The management of juxtahepatic
venous injuries without an atriocaval shunt: Preliminary clinical observa-
tions. Surgery 1986;99:569-575.

Padar S: Air gun pellet embolizing the intracranial internal carotid artery: Case
report. J Neurosurg 1975;43:222-224.

Padberg FT, RubelowskyJ, Hernandez-Maldonado J, et al: Infrapopliteal arte-
rial injury: Prompt revascularization affords optimal limb salvage. J Vase
Surg 1992;16:877-886.

Page C, Hagood C, Kremmerer W: Management of catheterization brachial
artery thrombosis. Surgery 1982;72:619-623.

Paget S: The Surgery of the Chest. London, John Wright and Company, 1896.

Pairolero P, Walls J, Payne W, et al: Subclavian-axillary artery aneurysms. Surgery
1981;90:757-763.

Palma E, Esperon R: Vein transplants and graft in the surgical treatment of the
post-phlebitic syndrome. J Cardiovasc Surg 1960;1:94-107.

Pan M, Medina A, Suarez de Lezo J: Obliteration of femoral pseudoaneurysm
complicating coronary intervention by direct puncture and permanent or
removable coil insertion. Am J Cardiol 1997;80:786-788.

Panes J, Kurose I, Rodriguez-Vaca D, et al: Diabetes exacerbates inflammatory
responses to ischemia-reperfusion. Circulation 1996;93:161-167.

Panetta T, Sclafani S, Goldstein A, et al: Percutaneous transcatheter emboliza-
tion for massive bleeding from pelvic fractures. J Trauma 1985;25:1021-
1029.

Panetta T, Bottiurai VS, Batson RC: Nonreversed translocated saphenous vein
bypass for arterial trauma. J Trauma 1988;28:1065-1070.

Panetta T, Hunt J, Buechter K: A blind, randomized canine study of duplex
scanning and arteriography for the diagnosis of arterial injury. J Trauma
9999.

Panetta TF, Hunt JP, Buechter KJ, et al: Duplex ultrasonography versus arteri-
ography in the diagnosis of arterial injury: An experimental study.J Trauma
1992;33:627-636.

Panetta T, Hunt J, Buechter K, et al: Duplex ultrasonography versus arteriog-
raphy in the diagnosis of arterial injury: An experimental study.J Trauma
1992;33:627-636.

Pappas P, Haser P, Teehan E, et al: Outcome of Complex Venous Reconstruc-
tions in Trauma Patients: Proceedings of the Eight American Venous Forum,
1996 February 23-25: San Diego. San Diego, American Venous Forum,
1996.

Parkinson D, West M: Traumatic intracranial aneurysms.J Neurosurg 1980;52:11-
20.

Parks T: Surgical management of gunshot injures of the large intestine. J R Soc
Med 1979;72:412-416.

RE.qxd 4/16/04 3:19 PM Page 615

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 615

Parmley L, Mattingly T, Manion W, Jahnke EJ Jr: Non-penetrating traumatic
injury of the aorta. Circulation 1958;17:1086-1101.

Parmley L, Mattingly T, Manion W: Penetrating wounds of the heart and aorta.
Circulation 1958;17:953-973.

Parmley LJ, Orbison J, Hughes CW, Mattingly T: Acquired arteriovenous fistu-
las complicated by endarteritis and endocarditis lenta due to streptococ-
cus faecalis. N Engl J Med 1954;250:305-309.

ParodiJ: Endovascular repair of abdominal aortic aneurysms and other arter-
ial lesions. J Vase Surg 1995;21:556-557.

ParodiJ: Endovascular repair of aortic aneurysms, arteriovenous fistulas, and
false aneurysms. World J Surg 1996;20:655-663.

Partap V, Cassoff J: Ultrasound-guided percutaneous thrombin injection for
treatment of femoral pseudoaneurysms: Technical note. Can Assoc Radiol
J 1999;50:182-184.

Pasch AR, Bishara RA, Lim LT, et al: Optimal limb salvage in penetrating civil-
ian vascular trauma. J Vase Surg 1986;3:189-195.

Pasch AR, Rashad A, Bishara RA, et al: Results of venous reconstruction after
civilian vascular trauma. Arch Surg 1986;121:607-611.

Passaro EJ, Pace W: Traumatic rupture of the aorta. Surgery 1959;46:787-791.

Pate J: Traumatic rupture of the aorta: Emergency operation. Ann Thorac Surg
1985;39:531-537.

Pate J, Butterick O, Richardson R: Traumatic rupture of the thoracic aorta.
JAMA 1968;203:1022-1024.

Pate J, Cole F, Walker W, Fabian TC: Penetrating injuries of the aorta arch and
its branches. Ann Thorac Surg 1993;55:586-592.

Pate J, Fabian TC, Walker W: Acute traumatic rupture of the aortic isthmus:
Repair with cardiopulmonary bypass. Ann Thorac Surg 1995;59:90-99.

Pate J, Fabian TC, Walker W: Traumatic rupture of the aortic isthmus: An emer-
gency? World J Surg 1995;19:119-125.

PateJ, Richardson RJ: Penetratingwounds of cardiac valves.JAMA 1969;207:309-
311.

PateJ, Sherman R, Jackson T, Wilson H: Cardiac failure following traumatic
arteriovenous fistula: A report of 14 cases. J Trauma 1965;5:398-403.

PateJ, Wilson H: Arterial injuries of the base of the neck. Arch Surg 1964;89:1 106-
1110.

Patel A, Marin M, Veith F, et al: Endovascular graft repair of penetrating sub-
clavian artery injuries. J Endovasc Surg 1996;3:383-388.

Patel K, Kulkarni S, Babu S, Clauss RH: Abdominal vascular trauma. Dis Chest
1987;30:13-23.

Patel K, Cortes LE, Semel L, et al: Bullet embolism.J Cardiovasc Surg 1989;30:584-
590.

Patel N, Mann F, Jurkovich GJ: Penetrating ulcer of the descending aorta
mimicking a traumatic aortic laceration. AJR Am J Roentgenol 1996;166:
20.

Pathria M, Zlatkin M, Sartoris D, et al: Ultrasonography of the popliteal fossa
and lower extremities. Radiol Clin North Am 1988;26:77-85.

Patman R, Poulos E, Shires G: The management of civilian arterial injuries.
Surg Gynecol Obstet 1964;118:725-738.

Patman R, Thompson J: Fasciotomy in peripheral vascular surgery: Report of
164 patients. Arch Surg 1970;101:633-672.

Patman R: Indications and technique. In Rutherford R (ed): Vascular Surgery.
Philadelphia, WB Saunders, 1984.

RE.qxd 4/16/04 3:19PM PageS16

616 VI • THE RICH REFERENCE COLLECTION

Paton B, Elliot D, Taubman J, Owens J: Acute treatment of traumatic aortic

rupture. J Trauma 1971;11:1-14.
Patt A, McCroskey B, Moore EE: Hypothermia-induced coagulopathies in trauma.

Surg Clin North Am 1988;64:775-785.
Patterson F, Morton K: The cause of death on fractures of the pelvis: With a

note on treatment by ligation of the hypogastric (internal iliac) artery.

J Trauma 1973;13:849-856.
Patterson R, Burns W, Jannotta F: Rupture of the thoracic aorta: Complication

of resuscitation. JAMA 1973;226:197.
Patton A, Guyton S, Lawson D: Treatment of severe arterial injuries. Am J Surg

1981;141:465-471.
Payne S, Snell M: Traumatic renal artery dissection. Urology 1988;16:335-337.
Peacock J, Proctor HJ: Factors limiting extremity function following vascular

injury. J Trauma 1977;17:532-534.
Pearlman A: Transesophageal echocardiography: Sound diagnostic technique

or two edged sword? N Engl J Med 1991;324:841-843.
Peck C: The operative treatment of heart wounds. Ann Surg 1909;50:100-134.
Peck J, Eastmen A, Bergan JJ, Sedwitz M: Popliteal vascular trauma: A commu-
nity experience. Arch Surg 1990;120:1339-1344.
Pecunia R, Raves J: A technique for evaluation of the injured extremity with a

single film exclusion arteriography. Surg Gynecol Obstet 1990;1 70:448.
Peiper H: Significance of traumatology in abdominal and vascular surgery. Jpn

J Surg 1985;15:93-102.
Pemberton J, Seefeld P, Barker NW: Traumatic arteriovenous fistula involving

the abdominal aorta and the inferior vena cava. Ann Surg 1946;123:580-

586.
Penn I: The vascular complications of fractures of the clavicle. J Trauma

1964;4:819-831.
Pennington D, Dranpanas T: Acute post-traumatic coarctation of the abdomi-
nal aorta. Surgery 1975;78:538-542.
Pepe PE, Bass RR, Mattox KL: Clinical trail of the pneumatic antishock garment

in the urban prehospital setting. Ann Emerg Med 1986;15:1407-1410.
Perchinsky M, LongWB, HillJ, et al: Extracorporeal cardiopulmonary life support

with heparin-bonded circuitry in the resuscitation of massively injured

trauma patients. Am J Surg 1995;169:488-491.
Perdue GJ, Smith RI: Intra-abdominal vascular injury. Surgery 1968;64:562-

568.
Perkins R, Elchos T: Stab wound of the aortic arch. Ann Surg 1958;147:83-86.
Perler B, McCabe C, Abbott WM, Buckley MJ: Vascular complications of intra-

aortic balloon counterpulsation. Arch Surg 1983;118:957-9562.
Perry MO: The Management of Acute Vascular Injuries. Baltimore, Williams &

Wilkins, 1981.
Perry M: Metabolic consequences of vascular trauma. Contemp Surg 1981 ;1 8:39-

46.
Perry MO: Iatrogenic injuries of arteries in infants. Surg Gynecol Obstet

1983;157:415-418.
Perry MO: Compartment syndromes and reperfusion injury. Surg Clin North

Am 1988;68:853-864.
Perry MO, Synder W, Thai E: Carotid artery injuries caused by blunt trauma.

Ann Surg 1980;192:74-77.
Perry MO, Thai E, Shires G: Management of arterial injuries. Ann Surg

1971;173:403-408.

RE.qxd 4/16/04 3:19 PM Page 617

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 617

Peterson A, Williams D, Rodriguez J, Francis I: Percutaneous treatment of a

traumatic aortic dissection by balloon fenestration and stent placement.

AJR Am J Roentgenol 1996;164:1274-1276.
Peterson H, Greenspan J, Ory H: Death following puncture of the aorta during

laparoscopic sterilization. Obstet Gynecol 1982;59:133-134.
Peterson N: Traumatic bilateral renal infraction. J Trauma 1989;29:158-161.
Petit-Dutaillis D, Janet H, Thiebaut F, Guillaumat L: Effets d'une inversion cir-

culatoire par anastomose carotido-jugulaire sure une hemiplegie droit avec

aphasie due a una thrombose de la carotide interne d'Origine inconnue

chez tin adolescent de 13 ans. Rev Neurol 1949;81:75.
Petrovsky B, Milinov O: "Arterialization" and "venization" of vessels involved in

traumatic arteriovenous fistulae: Aetiology and pathogenesis (an experi-
mental study). J Cardiovasc Surg 1967;8:396-407.
Petty S, Parker L, Mauro M, et al: Chronic posttraumatic aortic pseudoaneurysm:

Recognition before rupture. Postgrad Med 1991;89:177-178.
Pezzella A, Todd E, Dillon M, et al: Early diagnosis and individualized treat-
ment of blunt thoracic aortic trauma. Am Surg 1978;44:699-703.
Pezzella A, Griffen W, Ernst CB: Superior mesenteric artery injury following

blunt abdominal trauma: Case report with successful primary repair.

J Trauma 1978;18:472-474.
Phifer T, Gerlock A, Vekovius W, et al: Amputation risk factors in concomitant

superficial femoral artery and vein injuries. Ann Surg 1984;199:241-

243.
Phifer T, Gerlock A, Rich NM, McDonaldJ: Long-term patency of venous repairs

demonstrated by venography. J Trauma 1985;25:342-346.
Phillips C, Jacobsen D, Brayton DF, Bloch JH: Central vessel trauma. Am Surg

1979;45:517-530.
Phillips E, Rogers W, Caspar MR: First rib fractures: Incidence of vascular injury

and indications for angiography. Surgery 1981;89:42-47.
Pick T: On partial rupture of arteries from external violence. St George's Hosp

Rep (Lond) 1873;6:161.
Pick T: A clinical lecture of a case of arteriovenous aneurysm. Lond Med Times

Gaz 1883;2:677.
Pickard L, Mattox KL, Espada R, et al: Transection of the descending thoracic

aorta secondary to blunt trauma. J Trauma 1977;17:749-754.
Pickelmann S, Nolte D, Leiderer R, et al: Attenuation of postischemic reper-

fusion injury in striated skin muscle by diaspirin-cross-linked Hb. Am J

Physiol 1998;275:H361-H368.
Pietri P, Alagni G, Settembrini P: Iatrogenic vascular lesions. Int Surg

1981;66:213-216.
Pikoulis E, Rhee P, Nishibe T, et al: Arterial repair with synthetic patch by using

titanium clips. J Trauma 2000;48:292-295.
Pisters P, Heslin M, Riles T: Abdominal aortic pseudoaneurysm after blunt trauma.

J Vase Surg 1993;18:307-309.
Pitner S: Carotid thrombosis due to intraoral trauma: An unusual complica-
tion of a common childhood accident. N Engl J Med 1966;274:764-

767.
Piwnica A, Chetochine F, Soyer R, Winckler C: Traumatic rupture of the aortic

arch with disinsertion of the innominate artery. J Thorac Cardiovasc Surg

1971;61:246-252.
Plume S, DeWeese JA: Traumatic rupture of the thoracic aorta. Arch Surg

1979;114:240-243.

RE.qxd 4/16/04 3:19PM PageS18

618 VI • THE RICH REFERENCE COLLECTION

Plummer D, Bunette D, Asinger R, Ruiz E: Emergency department echocar-
diography improves outcome in penetrating cardiac injury. Ann Emerg

Med 1992;21:709-712.
Pochaczevsky R, Mufti M, LaGuerre J: Arteriography of penetrating wound of

the extremities: Help or hindrance? J Canad Assoc Radiol 1973;24:354-

361.
Pomerantz M, Hutchison D: Traumaticwounds of the heart.J Trauma 1969;9:135-

139.
Pontius G, Kilbourne B, Paul E: Non-penetrating abdominal trauma. Arch Surg

1957;72:800.
Pool E: Treatment of heart wounds. Ann Surg 1912;55:485-512.
Poole G: Fracture of the upper ribs and injury to the greatvessels. Surg Gynecol

Obstet 1989;169:275-282.
Pope M, Johnston K: Anaphylaxis after thrombin injection of a femoral pseudoa-

neurysm: Recommendations for prevention. J Vase Surg 2000;32:190-191.
Porter W, Bigger IA: Stab wounds of the heart and great vessels: A study of

seventeen cases. Trans Am Clin Climatol Asoc 1939;54:96-104.
Posner M, Moore EE, Greenholz S, et al: Natural history of untreated inferior

vena cava injury and assessment of venous access. J Trauma 1986;26:698-

701.
PostempskiP: La sutura deivasi sanguigni. Arch Socltal Chir Roma 1886;3:391.
Potts R, Alguire PC: Pseudoaneurysm of the abdominal aorta: A case report

and review of the literature. Am J Med Sci 1991;301:265-268.
Pouyanne H, Arne L, Loiseau P, Mouton L: Considerations sur deux cas de

thrombose de la carotide interne chez l'enfant. Rev Neurol 1957;97:525.
Power D-A: Hunter's operation for the cure of aneurysm. BrJ Surg 1929;17:193.
Pradham D, Juanteguy J, Wilder R: Arterial injuries of extremities associated

with fractures. Arch Surg 1972;105:582-585.
Prat A, Warembourg HJ, Watel A, et al: Chronic traumatic aneurysm of the

descending thoracic aorta (19 cases). J Cardiovasc Surg 1986;27:268-272.
Pratt G: Importance of a knowledge of vascular surgery in World War II. Am J

Surg 1942;56:335.
Prean G, Aragon GE: Arterial embolism from a bullet: A case report. Am Surg

1976;42:863-865.
Preston A: Arterial injuries of warfare: Complications and management. Surgery

1946;20:786.
Pretre R, Kursteiner K, Khatchatourian G, Faidutti B: Traumatic occlusion of

the left anterior descending artery and rupture of the aortic isthmus. J

Trauma 1995;39:388-390.
Pretre R, LaHarpe R, Cheretakis A: Blunt injury to the ascending aorta: Three

patterns of presentation. Surgery 1996;119:603-610.
Pridgen W, Jacobs J: Postoperative arteriovenous fistula. Surgery 1962;51:205.
Pritchard D, MaloneyJ, Barnhorst DA, Spittel JJ: Traumatic popliteal arteri-
ovenous fistulas. Arch Surg 1977;112:849-852.
Proudfoot R, Harris M, Victor D, Bennett S: Arterial bullet embolism. J Ky Med

Assoc 1989;87:17-18.
Puckett W: The wounding effect of small high velocity fragments as revealed

by high speed radiography. J Elisha Mitchell Sci Soc 1946;62:59.
Puijlaert C: Roentgen diagnosis of traumatic rupture of the aorta. Radiol Clin

North Am 1976;45:217-235.
Puri R, Clark J, Corkey P: Axillary artery damage following a closed fracture of

the neck of the humerus: A case report. Injury 1985;16:426-427.

RE.qxd 4/16/04 3:19 PM Page 619

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 619

Qinyao W, Weijin S, Youren Z: New concepts in severe presacral hemorrhage

during proctectomy. Arch Surg 1982;19:1013-1020.
Quast D, Shirkey AL, Fitzgerald J, et al: Surgical correction of injuries to the

vena cava: An analysis of sixty-one cases. J Trauma 1965;5:1-10.
Queral L, Flinn W, Yao JST, Bergan JJ: Management of peripheral arterial

aneurysms. Surg Clin North Am 1979;59:693-706.
Quigley M, Bret PM: Occult pseudoaneurysm of the abdominal aorta follow-
ing gunshot wound: The importance of plain film findings. J Trauma

1995;38:269-273.
Rabhan N, Guillebeau J, Brackney EL: Arteriovenous fistula of the superior

mesenteric vessels after a gunshot wound. N Engl J Med 1962;266:603.
Rabinowitz R, Goldfarb D: Surgical treatment of axillosubclavian venous throm-
bosis: A case report. Surgery 1971;70:703.
Rabinsky I, Sidhu G, Wagner R: Mid-descending aortic traumatic aneurysms.

Ann Thorac Surg 1990;50:155-160.
Raffa H, Sorefan A: Repair of torn aortic root with the left atrial appendage.

Jpn Heart J 1992;33:265-269.
Rahat M, Lahat N, Smollar J, et al: Divergent effects of ischemia/reperfusion

and nitric oxide donor on TNF-alpha mRNA accumulation in rat organs.

Shock 2001;15:312-317.
Ramakantan R, Shah P: False aneurysm secondary to aortic cannulation: Rupture

into lung with fatal hemoptysis during aortography. J Thorac Cardiovasc

Surg 1989;37:322-323.
Ramanathan T, Somasundaram K, Yong N: Successful repair of penetrating

wound of the thoracic aorta. Thorax 1975;30:348-351.
Rana M, Singh G, Wang P, et al: Protective effects of preheparinization on the

microvasculature during and after hemorrhagic shock. J Trauma

1992;32:420-426.
Randhawa MJ, Menzoian J: Seat belt aorta. Ann Vase Surg 1990;4:370-377.
Ransdell H, Glass HJ: Gunshot wounds of the heart: A review of 20 cases. Am J

Surg 1960;999:788-797.
Ranshoff J: Arteriovenous aneurysm of the superior thyroid artery and vein.

Surg Gynecol Obstet 1935;61:816.
Rapoport S, Sniderman U, Morse S, et al: Pseudoaneurysm: A complication of

faulty technique in femoral artery puncture. Radiology 1985;154:529-530.
Rau S, Carner D: Brachial plexus compression. Arch Surg 1981;116:175-178.
Rautio J, Paavolainen P: Afghan war wounded: Experience with 200 cases.

J Trauma 1988;28:523.
Ravikumar S, Stahl WM: Intraluminal balloon catheter occlusion for major vena

cava injuries. J Trauma 1985;25:458-460.
Razek M, Mnaymneh W, Yacoubian HD: Injuries of peripheral arteries with

associated bone and soft tissue injuries. J Trauma 1973;13:907.
RazzoukA, Gundry S, WangN, etal: Pseudoaneurysms of the aorta after cardiac

surgery or chest trauma. Am Surg 1993;59:818-823.
Rea W, Sugg W, Wilson L, et al: Coronary artery lacerations: An analysis of 22

patients. Ann Thorac Surg 1969;7:518-528.
Read R, Moore EE, Moore FA, et al: Intravascular ultrasound for the diagnosis

of traumatic aortic disruption: A case report. Surgery 1993;114:624-628.
Read R, Moore EE, Moore FA, Haenel J: Partial left heart bypass for thoracic

aorta repair. Arch Surg 1993;128:746-752.
Reckling F, Peltier L: Acute knee dislocations and their complications. J Trauma

1969;9:181-191.

RE.qxd 4/16/04 3:19PM PageS20

620 VI • THE RICH REFERENCE COLLECTION

Redman H: Thoracic, abdominal, and peripheral trauma: Evaluation with angio-
graphy. JAMA 1977;237:2415-2418.

Reed J, McGinn R, Gorman JF: Traumatic mesenteric arteriovenous fistula
presenting as the superior mesenteric artery syndrome. Arch Surg
1986;121:1209.

Rees R, Bonneval M, Batson R, Hollier L: Angiography in extremity trauma: A
prospective study. Am Surg 1978;44:661-663.

Rehn L: Ueber penetrirende herzwunden und hernalt. Arch Klin Chir
1897;55:56-60.

Rehr R, Mack M, Firth B: Aortic regurgitation and sinus of Valsalva-right atrial
fistula after blunt thoracic trauma. Br Heart J 1982;48:410-412.

Reichle F, Golsorkhi M: Diagnosis and management of penetrating arterial and
venous injuries in the extremities. Am J Surg 1980;140:365-367.

Reid C, Kawanishi D, Rahimtoola SH, Chandraratna P: Chest trauma: Evalua-
tion by two-dimensional echocardiography. Am Heart J 1987;113:971-
976.

Reid J, Redman H, WeigeltJA, et al: Wounds of the extremities in proximity to
major arteries: Value of angiography in the detection of arterial injury. AJR
1988;151:1053-1059.

Reid J, WeigeltJA: Forty-three cases of vertebral trauma. J Trauma 1988;28:1007-
1012.

Reid J, WeigeltJA, Thai E, Francis H III: Assessment of proximity of a wound
to major vascular structures as an indication for arteriography. Arch Surg
1988;123:942-946.

Reid M: The effect of arteriovenous fistula upon the heart and blood vessels:
An experiment and clinical study. Bull Johns Hopkins Hosp 1920;31:43-
50.

Reid M: Abnormal arteriovenous communications. Acquired and congenital,
II. The origin and nature of arteriovenous aneurysms, cirsoid aneurysms
and simple angiomas. Arch Surg (Chicago) 1925;10:996-1009.

Reid M, McGuire J: Arteriovenous aneurysm. Ann Surg 1938;108:643-693.

Reiley M, Bond D, Branick RI, Wilson E: Vascular complications following total
hip arthroplasty: A review of the literature and a report of two cases. Clin
Orthop 1984;186:23-28.

Reilly PM, Rotondo MF, Carpenter JP, et al: Temporary vascular continuity during
damage control: Intraluminal shunting for proximal superior mesenteric
artery injury. J Trauma 1996;39:757-760.

Reilly L, Ramos T, Murray S, et al: Optimal exposure of the proximal abdomi-
nal aorta: A critical appraisal of transabdominal medial visceral rotation.
J Vase Surg 1994;19:375-389.

Reines HD, Dill L, Saad S: Neurogenic pulmonary edema and missile emboli.
J Trauma 1980;20:698-701.

Reisman J, Morgan A: Analysis of 46 intra-abdominal aortic injuries from blunt
trauma: Case reports and literature review. J Trauma 1990;30:1294-
1297.

Reissman P, Rivkind A, Jurim O, Simon D: Case report: The management of
penetrating cardiac trauma with major coronary artery injury — Is car-
diopulmonary bypass essential? J Trauma 1992;33:773-775.

Requena R, Cherukuri R, Lerner R: A logical approach in the management of
intraabdominal vascular trauma. Contemp Surg 1983;23:31.

Reul GJ, Beall AC Jr, Jordan GLJr, Mattox KL: The early operative manage-
ment of injuries to the great vessels. Surgery 1973;74:862-873.

RE.qxd 4/16/04 3:19PM PageS21

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 621

Reul GJ, Mattox KL, Beall AC Jr, Jordan GLJr: Recent advances in the opera-
tive management of massive chest trauma. Ann Thorac Surg 1973;16:521-

662.
Reul GJ, Rubio P, Beall ACJr: The surgical management of acute injury to the

thoracic aorta. J Thorac Cardiovasc Surg 1974;67:272-281.
Reyes L, Rubio P, Korompai F, Guinn G: Successful treatment of transection of

aortic arch and innominate artery. Ann Thorac Surg 1975;19:468-471.
Reynolds B, Balsano NA: Venography in pelvic fractures: A clinical evaluation.

Ann Surg 1971;173:104-106.
Reynolds R, McDowell H, Diethelm A: The surgical treatment of blunt and

penetrating injuries of the popliteal artery. Am Surg 1983;49:405-410.
Reynolds R, McDowell H, Diethelm A: The surgical treatment of arterial injuries

in the civilian population. Am Surg 1979;189:700-708.
Rhee PM, Acosta J, Bridgeman A, et al: Survival after emergency department

thoracotomy: Review of published data from the past 25 years. J Am Coll

Surg 2000;190:288-298.
Rhee P, Talon E, Eifert S, et al: Induced hypothermia during emergency depart-
ment thoracotomy: An animal model. J Trauma 2000;48:439-447.
Rhodes G, Cox C, Silver D: Arteriovenous fistula and false aneurysm as the

cause of consumption coagulopathy. Surgery 1973;73:535-540.
Riccen E, Dickens P: Traumatic aneurysm of the abdominal aorta of 27 years

duration: Case report. US Nav Med Bull 1942;40:692-694.
Rice W, Wittstruck K: Acute hypertension and delayed traumatic rupture of the

aorta. JAMA 1951;147:915-917.
Rich NM: Vietnam missile wounds evaluated in 750 patients. Milit Med 1968; 1 33:9-

22.
Rich NM: Wounding power of various ammunition. Resident Physician

1968;14:72.
Rich NM: Missile wound evaluation at the 2nd Surgical Hospital in Vietnam.

In GeorjiadeN (ed) : Plastic and Maxillofacial Trauma Symposium. St. Louis,

CVMosby, 1969.
Rich NM: Vascular trauma in Vietnam. J Cardiovasc Surg 1970;11:368-377.
Rich NM: Surgery for arterial trauma. In Dale WA (ed): Management of

Arterial Occlusive Disease. Chicago, Year Book Medical Publishers,

1971.
Rich NM: Complications of operations for vascular trauma. In Beebe HG (ed) :

Complications in Vascular Surgery. Philadelphia, JB Lippincott Co,

1973.
Rich NM: Vascular trauma. Surg Clin North Am 1973;53:1367-1392.
Rich NM: Vascular injuries. In Whelan TJ (ed) : Emergency War Surgery: NATO

Handbook. Washington, DC, Government Printing Office, 1975.
Rich NM: Weapons and wounds. J Trauma 1975;15:464-465.
Rich NM: Bullets and blood vessels. Surg Clin North Am 1978;58:995-1003.
Rich NM: Principles and indications for primary venous repair. Surgery

1982;91:492-496.
Rich NM: Vascular injuries. In Cameron J (ed) : Current Surgical Therapy.

Philadelphia, BC Decker, 1984.
Rich NM: The management of trauma to the carotid-vertebral system. In

Robicsek F (ed): Extracranial Cerebrovascular Disease Diagnosis and

Management. New York, Macmillan Publishing, 1986.
Rich NM: Venous injuries. In Sabiston DJ (ed): Textbook of Surgery.

Philadelphia, WB Saunders, 1986, pp 2009-2018.

RE.qxd 4/16/04 3:19PM PageS22

622 VI • THE RICH REFERENCE COLLECTION

Rich NM: Arterial injuries associated with fracture, dislocation, and extensive
soft tissue trauma. In Ernst CB, Stanley JC (eds): Current Therapy in Vas-
cular Surgery. Philadelphia, BC Decker, 1987.

Rich NM: Management of venous trauma. Surg Clin North Am 1988;68:809-
821.

Rich NM: Gunshot wound to the groin. In Brewster DC (ed): Common Prob-
lems in Vascular Surgery. Chicago, Year Book Medical Publishers, 1989,
pp 305-308.

Rich NM: Mechanism and reversibility of proximal arterial dilatation with large
arteriovenous fistulas. In Veith F (ed): Current Critical Problems in Vas-
cular Surgery. St. Louis, Quality Medical Publishing, 1989.

Rich NM: Current status of lower extremity venous repair. In Veith F (ed) : Current
Critical Problems in Vascular Surgery. St. Louis, Quality Medical Publish-
ing, 1990.

Rich NM: Trauma: Responsibility, resources, and responsiveness (Scudder
Oration). ACS Bull 1990;76:6-13.

Rich NM: Brief history of vascular trauma. Trauma Q 1991;7:1-5.

Rich NM: Vascular trauma: Abrief military perspective. WorldJ Surg 1992;16:938-
939.

Rich NM: History of vascular trauma. In Flanigan DP, Schuler J, Meyer JP (eds) :
Civilian Vascular Trauma. Philadelphia, Lea & Febiger, 1992, pp 3-7.

Rich NM: Military vascular injuries in Croatia. Cardiovasc Surg 1993;1:2.

Rich NM: Surgeon's response to battlefield vascular trauma (Hume Memorial
Lecture). Am J Surg 1993;166:91-96.

Rich NM: Venous injuries. In Sabiston DJ (ed): Textbook of Surgery.
Philadelphia, WB Saunders, 1995.

Rich NM: Commentary. In Ivatury RR, Cayten C (eds): The Textbook of
Penetrating Trauma. Philadelphia, Williams & Wilkins, 1996.

Rich NM, Amato JJ, Billy LJ: Arterial thrombosis secondary to temporary cavi-
tation. Surg Dig 197l;6:12.

Rich NM, Andersen CA, Ricotta J, et al: Arterial trauma: A remaining problem
of increasing magnitude. Milit Med 1977;141:847-852.

Rich NM, Baugh JH, Hughes CW: Popliteal artery injuries in Vietnam. Am J
Surg 1969;118:531-534.

Rich NM, Baugh JH, Hughes CW: Acute arterial injuries in Vietnam: 1,000
cases. J Trauma 1970;10:359-369.

Rich NM, Baugh JH, Hughes CW: Significance of complications associated
with vascular repairs performed in Vietnam. Arch Surg 1970;100:646-
651.

Rich NM, Clagett GP, Salander J, Piscevic S: The Matas/Soubbotitch connec-
tion. Surgery 1983;93:17-19.

Rich NM, Clarke J, Baugh JH: Successful repair of a traumatic aneurysm of the
abdominal aorta. Surgery 1969;66:492-496.

Rich NM, Collins GJ Jr, Andersen CA, et al: Venous trauma: Successful venous
reconstruction remains an interesting challenge. Am J Surg 1977;134:226-
230.

Rich NM, Collins GJJr, Andersen CA, et al: Missile emboli. J Trauma 1978;
18:236-239.

Rich NM, Collins GJ, Andersen CA, McDonald P: Autogenous venous interpo-
sition grafts in repair of major venous injuries. J Trauma 1977;17:512-520.

Rich NM, Collins GJJr, Hobson RW II, et al: Carotid-axillary bypass: Clinical
and experimental evaluation. Am J Surg 1977;134:805-808.

RE.qxd 4/16/04 3:19PM PageS23

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 623

Rich NM, Collins GJJr, YoukeyJR: Cervical and Thoracic Outlet Venous Injuries.

Surgery of the Veins. New York, Grune & Stratton, 1985.
Rich NM, Gomez ER, Coffey JA, et al: Long-term follow-up of venous recon-
struction following trauma. In Bergan JJ, Yao JST (eds) : Venous Disorders.

Philadelphia, WB Saunders, 1991.
Rich NM, Gomez ER, Jackson MR: Pulsating hematomas and pseudoaneurysms:

Should they be managed by noninvasive compression under duplex control?

In Veith F (ed): Current Critical Problems in Vascular Surgery. St. Louis,

Quality Medical Publishing, 1994, pp 319-323.
Rich NM, Hobson RW II: Historical background of repair venous injuries. In

Witkin E (ed) : Venous Diseases, Medical and Surgical Management. Hague,

the Netherlands, Mouton, 1974.
Rich NM, Hobson RW II: Trauma to the venous system. In Swan KG, Hobson

RWII, Reynolds D, etal (eds): Symposium on Venous Surgery in the Lower

Extremities. St. Louis, Green Publishers, 1975.
Rich NM, Hobson RW II: Venous trauma: Emphasis for repair is indicated.

J Cardiovasc Surg 1975; special issue:571.
Rich NM, Hobson RW II, Collins GJJr: Traumatic arteriovenous fistulas and

false aneurysms: A review of 558 lesions. Surgery 1975;78:817-828.
Rich NM, Hobson RW II, Collins GJJr: Elective vascular reconstruction after

trauma. Am J Surg 1975;130:712-719.
Rich NM, Hobson RWII, Collins GJJr, Anderson CA: The effect of acute popliteal

venous interruption. Ann Surg 1976;183:365-368.
Rich NM, Hobson RW II, Fedde C: Vascular trauma secondary to diagnostic

and therapeutic procedures. Am J Surg 1974;128:715-721.
Rich NM, Hobson RW II, Fedde C, Collins GJJr: Acute common femoral arte-
rial trauma. J Trauma 1975;15:628-637.
Rich NM, Hobson R II, Hutton JE Jr: Arterial trauma: Lessons of the Vietnam

war. Paper presented at: Annual International Vascular Meeting, Paris,

France, 1995.
Rich NM, Hobson RW II, Hutton JE Jr: Traumatismes arteriels: les lecons de la

guerre du Vietnam. In Kieffer E (ed) : Traumatismes Arteriels. Paris, AERCV,

1995.
Rich NM, Hobson RWIIJarstfer B, Geer TM: Subclavian artery trauma.J Trauma

1973;13:485-496.
Rich NM, Hobson RWII, Wright CB: Historical aspects of direct venous recon-
struction. In Bergan JJ, Yao JST (eds) : Symposium on Venous Problems in

Honor of Geza de Takats. Chicago: Year Book Medical Publishers, 1978.
RichNM, Hobson RWII, Wright CB, Fedde C: Repair of lower extremity venous

trauma: A more aggressive approach required. J Trauma 1974;14:639-652.
Rich NM, Hobson RW II, Wright CB, Swan KG: Techniques of venous repair.

In Swan KG, Hobson RWII, Reynolds D, etal (eds): Symposium on Venous

Surgery in the Lower Extremities. St. Louis, Warren H Green Publishers,

1975.
Rich NM, Hughes CW: Vietnam Vascular Registry: A preliminary report. Surgery

1969;65:218-226.
Rich NM, Hughes CW: Stistiques sur les plaies vasculaires au Vietnam (4500

Cas). Social Med Chir 1970;9:805-809.
Rich NM, Hughes CW: Rapport sur les plais vasculaires au Vietnam (Transla-
tion, D. Rignault). Revue des corps de Sante 1971;12:673.
Rich NM, Hughes CW: Fifty years' progress in vascular surgery. Bull Am Coll

Surg 1972;57:35.

RE.qxd 4/16/04 3:19PM PageS24

624 VI • THE RICH REFERENCE COLLECTION

Rich NM, Hughes CW: The fate of prosthetic material used to repair vascular
injuries in contaminated wounds. J Trauma 1972;12:459-467.

Rich NM, Hughes CW, Baugh JH: Management of venous injuries. Ann Surg
1970;171:724-730.

Rich NM, Jarstfer B, Geer TM: Popliteal artery repair failure: Causes and pos-
sible prevention. J Cardiovasc Surg 1974;15:340-351.

Rich NM, Jarstfer B, Geer TM: Concomitant popliteal arterial and venous trauma.
In Swan KG, Hobson RWII, Reynolds D, et al (eds): Symposium on venous
surgery in the lower extremities. St. Louis, Warren H Green Publishers,
1975, pp 29-40.

Rich NM, Johnson E, Dimond FJr: Wounding power of missiles used in the
Republic of Vietnam. JAMA 1967;199:157.

Rich NM, Levin P, HuttonJEJr: Effect of distal arteriovenous fistulas on venous
graft patency. In Swan KG, Hobson RW II, Reynolds D, et al (eds) : Sym-
posium on Venous Surgery in the Lower Extremities. St. Louis, Warren H
Green Publishers, 1975.

Rich NM, Manion W, Hughes CW: Surgical and pathological evaluation of vas-
cular injuries in Vietnam. J Trauma 1969;9:279-291.

Rich NM, Metz CJ, HuttonJEJr, et al: Internal versus external fixation of frac-
tures with concomitant vascular injuries in Vietnam. J Trauma 1971 ;1 1:463-
473.

Rich NM, Rhee P: An historical tour of vascular injury management: From its
inception to the new millennium. Surg Clin North Am 2001;81:1199-1215.

Rich NM, Rob CG: Ischemia-induced myonecrosis, myoglobinuria and secondary
renal failure. In Ernst CB, Stanley JC (eds): Current Therapy in Vascular
Surgery. Philadelphia, BC Decker, 1990.

Rich NM, Salander J, Orecchia P, et al: Venous injuries. In Bergan JJ, Yao JST
(eds): Vascular Surgical Emergencies. Orlando, Grune & Stratton, 1987,
pp 275-282.

Rich NM, Shumacker HB Jr: Cold injury. In Ernst CB, StanleyJC (eds) : Current
Therapy in Vascular Surgery. Philadelphia, BC Decker, 1990.

Rich NM, Spencer FC: Vascular Trauma. Philadelphia, WB Saunders, 1978.

Rich NM, Sullivan W: Clinical recanalization of an autogenous vein graft in the
popliteal vein. J Trauma 1972;12:919-920.

Richards AJ, Lamis PJ, Rogers JJ, Bradham GB: Laceration of abdominal aorta
and study of intact abdominal wall as tamponade: Report of survival and
literature review. Ann Surg 1966;164:321-324.

Richardson D, Shina M, Miller F, Bergamini TM: Peripheral vascular compli-
cations of coronary angioplasty. Am Surg 1989;55:675-680.

Richardson JD: Indications for thoracotomy in thoracic trauma. Curr Surg
1985;42:361-364.

Richardson JD, Fallat M, Nagaraj H, et al: Arterial injuries in children. Arch
Surg 1981;116:685-690.

Richardson JD, Simpson C, Miller F: Management of carotid artery trauma.
Surgery 1988;104:673-680.

RichardsonJD , Vitale G, Flint LM: Penetrating arterial trauma: Analysis of missed
vascular injuries. Arch Surg 1987;122:678-683.

Richardson JJ, Jurkovich GJ, Walker G, et al: A temporary arteriovenous shunt
in the management of traumatic venous injuries of the lower extremity
(Scribner). J Trauma 1986;26:503-509.

Richardson R, Khandeadar A, Moseley P: Traumatic rupture of the thoracic
aorta. South Med J 1979;72:300-302.

RE.qxd 4/16/04 3:19PM PageS25

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 625

Ricketts R, Finck E, Yellin AE: Management of major arteriovenous fistulas by

arteriography techniques. Arch Surg 1978;113:1153.
Ricks R, Howell J, Beall AC Jr, DeBakey ME: Gunshot wounds of the heart: A

review of 31 cases. Surgery 1965;57:787-790.
Rielly J, Brandt ML, Mattox KL, Pokorny W: Thoracic trauma in children.

J Trauma 1993;34:329-331.
Risely T, McClerkin W: Bullet transection of both carotid arteries: Delayed repair

with recovery. Am J Surg 1971;121:385-386.
Rittenhouse E, Dillard D, Winterscheid L, Merendino K: Traumatic rupture of

the thoracic aorta: A review of the literature and a report of five cases with

attention to special problems in early management. Ann Surg 1969;1 70:87-

100.
Ritter D, Chang F: Delayed hemothorax resulting form stab wounds to the inter-
nal mammary artery. J Trauma 1995;39:586-589.
Rob CG: Diagnosis of abdominal trauma in warfare. Surg Gynecol Obstet

1947;85:147-154.
Rob CG: Reconstruction of a stenosed internal carotid artery. Br Med J

1956;2:1265.
Rob CG: Die indikationstellung zur operativen widerherstellung der aorta

und der groesseren arterien. Arch and Deutschen Zt J Chir 1957;287:

305.
Rob CG: Obliterations of the aortic bifurcation (Leriche's syndrome). Car-

dioangiologica 1957;5:1.
Rob CG: Arterial wounds, acute ischemia of the limbs. J Cardiovasc Surg

1963;4:249-252.
Rob CG: A history of arterial surgery. Arch Surg 1972;105:821-823.
Rob CG: Military surgery, our debt to our patients and predecessors. J R Army

Med Corps 1986;132:11-15.
Rob CG, Battle S: Arteriovenous fistula following the use of the Fogarty balloon

catheter. Arch Surg 1971;102:144-145.
Rob CG, Standeven A: Closed traumatic lesions of the axillary and brachial

arteries. Lancet 1956;1:597-599.
RobbsJ, Baker LW: Subclavian and axillary artery injury. S Afr MedJ 1977;51 :227-

231.
Robbs J, Baker LW: Arterial trauma involving the lower limb. J Trauma

1978;18:324-328.
RobbsJ, Baker LW: Major arterial trauma: Review of experience with 267 injuries.

Br J Surg 1978;65:532-538.
RobbsJ, Baker LW: Cardiovascular trauma. Curr Prob Surg 1984;21:7-87.
RobbsJ, Baker LW, Human R, et al: Cervicomediastinal arterial injuries. Arch

Surg 1981;116:663-668.
RobbsJ, Naidoo K: Nerve compression injuries due to traumatic false aneurysm.

Ann Surg 1984;200:80-82.
RobbsJ, Reddy E: Management options for penetrating injuries to the great

veins of the neck and superior mediastinum. Surg Gynecol Obstet

1987;165:323-326.
Roberson G: Combined stab wounds of the aorta and vena cava of the abdomen.

Arch Surg 1967;95:12-15.
Roberts R, String T: Arterial injuries in extremity shotgun wounds: Requisite

factors for successful management. Surgery 1984;96:902-907.
Roberts S, Main D, PindertonJ: Surgical therapy of femoral artery pseudoa-

neurysm after angioplasty. Am J Surg 1987;10:676-680.

RE.qxd 4/16/04 3:19PM PageS26

626 VI • THE RICH REFERENCE COLLECTION

Robinson J, Moyer C: Comparison of late sequelae of common and superficial

femoral vein ligations. Surgery 1954;35:690-697.
Robinson N, Flotte C: Traumatic aneurysm of the carotid arteries. Am Surg

1974;40:121-124.
Robison R, Brown J, Caldwell R, Stone K: Management of asymptomatic intrac-
ardiac missiles using echocardiography. J Trauma 1988;28:1402-1403.
Roche K, Genieser N, Berger DK, Ambrosino MM: Traumatic abdominal pseudoa-

neurysm secondary to child abuse. Pediatr Radiol 1995;25:S247-S248.
Roe B: Cardiac trauma including injury of great vessels. Surg Clin North Am

1972;52:573-583.
Rohman M, Ivatury RR, Steichen F, et al: Emergency room thoracotomy for

penetrating cardiac injuries. J Trauma 1983;23:570-576.
Rohrer M, Cardullo P, Pappas A, et al: Axillary artery compression and throm-
bosis in throwing athletes. J Vase Surg 1990;11:761-769.
Rojas R, Levitsky S, Stansel HCJr: Acute traumatic subclavian Steal Syndrome.

J Thorac Cardiovasc Surg 1966;51:113-115.
Rollins D, Bernhard VM, TowneJB: Fasciotomy: An appraisal of controversial

issues. Arch Surg 1981;116:1474-1481.
Romanoff H, Goldberger S: Major peripheral vein injuries. Vase Surg

1976;10:157-163.
Roostar L: Indications for surgery in penetrating chest injuries. Ann Chirur-

giae Gynaecol 1993;82:177-181.
Roper B, Provan J: Late thrombosis of the femoral artery complicating fracture

of the femur. J Bone Joint Surg 1965;47:510-513.
Roques X, Bourdeaudhui A, Collet D, et al: Traumatic rupture and aneurysm

of the aortic isthmus: Late results of repair by direct suture. Ann Vase Surg

1989;3:47-51.
Rose S, Moore EE: Angiography in patients with arterial trauma: Correlations

between angiographic abnormalities, operative findings and clinical

outcome. AJR Am J Roentgenol 1987;149:613-619.
Rose S, Moore EE: Emergency trauma angiography: Accuracy, safety, and pit-
falls. AJR Am J Roentgenol 1987;148:1243-1246.
Rose S, Moore EE: Trauma angiography: The use of clinical findings to improve

patient selection and case preparation. J Trauma 1988;28:240-245.
Rosemurgy AS, Norris P, Olson S, et al: Prehospital traumatic cardiac arrest:

The cost of futility. J Trauma 1993;35:468-474.
RosenbergJ, Bredenberg CE, Marvasti M, et al: Blunt injuries to the aortic arch

vessels. Ann Thorac Surg 1989;48:508-513.
Rosenblatt M, Lemer J, Best LA: Thoracic wounds in Israeli battle casualties

during the 1982 evacuation of wounded from Lebanon. J Trauma

1985;4:350.
Rosenbloom M, Fellows B: Chronic pseudoaneurysm of the popliteal artery

after blunt trauma. J Vase Surg 1989;10:187-189.
Rosensweig J, Simon MA: Traumatic aneurysm of the axillary artery: A golf

hazard. Can Med Assoc J 1965;93:165-167.
Rosenthal D, Ellison R, Luke J: Traumatic superior mesenteric arteriovenous

fistula: Report of a case and review of the literature. J Vase Surg 1987;5:486-

491.
Rosenthal J, Caspar MR, Gjerdrum T, Newman J: Vascular injuries associated

with fractures of the femur. Arch Surg 1975;110:494-499.
Ross S, Ransom K, Shatney C: The management of venous injuries in blunt

extremity trauma. J Trauma 1985;25:150-153.

RE.qxd 4/16/04 3:19PM PageS27

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 627

Roth S, Wheeler J, Gregory R, et al: Blunt injury of the abdominal aorta: A
review. J Trauma 1997;42:748-755.

Rothlin M, Naf R, Amgwerd M, et al: Ultrasound in blunt abdominal and tho-
racic trauma. J Trauma 1993;34:488-495.

Rotondo M, Schwab CW, McGonigal MD, et al: "Damage control": An approach
for improved survival in exsanguinating penetrating abdominal injury.
J Trauma 1993;35:375-383.

Rovito P: Arterial caval shunting in blunt hepatic vascular injury. Ann Surg
1987;205:318-321.

Roy-Shapira A, Levi I, Khoda J: Sternal fractures: A red flag or a red herring?
J Trauma 1994;37:59-61.

Rozin L, Perper J: Spontaneous fatal perforation of aorta and vena cava by
Mobin-Uddin umbrella. Am J Forensic Med Pathol 1989;10:149-151.

Rozycki G, Ochsner M, Schmidt J, et al: A prospective study of surgeon-per-
formed ultrasound as the primary adjuvant modality for injured patient
assessment. J Trauma 1995;39:492-500.

Rozycki G, Kraut E: Isolated blunt rupture of the infrarenal inferior vena cava:
The role of ultrasound and computed tomography in an occult injury.
J Trauma 1995;38:402-405.

Rpatopoulos V, Sheiman R, Phillips D, et al: Traumatic aortic tear: Screening
with chest CT. Radiology 1992;182:667-673.

Ruberti U, Odero A, Arpesani A, et al: Acute ruptures of the thoracic aorta.
Personal experience. J Cardiovasc Surg 1987;28:81-84.

Ruberti U, Odero A, Arperani A, et al: Surgical treatment of thoracic aortic
aneurysms: Personal experience. J Cardiovasc Surg 1988;29:245-256.

Rubio P, Reul GJ, Beall AC Jr, et al: Acute carotid artery injury: 25 years' expe-
rience. J Trauma 1974;14:967-973.

Rubio P, Reul GJ: Penetrating cardiac injury by wire thrown from a lawn mower.
Int Surg 1979;64:9-10.

Rudich M, Rowland M, Seibel R, Border J: Survival following a gunshot wound
of the abdominal aorta and inferior vena cava. J Trauma 1978;18:548-549.

Rush D, Frame S, Bell RM, Berg EE: Does open fasciotomy contribute to mor-
bidity and mortality after acute lower extremity ischemia and revascular-
ization? J Vase Surg 1989;10:343.

Ruskey J, Lieberman M, Shaikh K, Talucci R: Unusual subclavian artery lacer-
ations resulting from lap-shoulder seatbelt trauma: Case reports. J Trauma
1989;29:1598-1600.

Russell W, Sailors D, Whittle T, et al: Limb salvage versus traumatic amputation:
A decision based on a seven part predictive index. Ann Surg 1991;213:473.

Russo P, Orszulak T, Arnold PG, et al: Concomitant repair of a chronic trau-
matic aortic aneurysm with tracheal erosion. Ann Thorac Surg 1987;43:559-
560.

Rutherford R: Diagnostic evaluation of extremity vascular injuries. Surg Clin
North Am 1988;68:683-691.

Rutherford R, Baue AE: Extraanatomic bypass. In Rutherford R (ed) : Vascular
Surgery. Philadelphia, WB Saunders, 1989, pp 705-716.

Rutsaert R, Van Schil P, Martens C, et al: Occlusion of the left common femoral
artery after total hip replacement. Report of a case and review of the lit-
erature. J Cardiovasc Surg 1988;29:216-218.

Ryan J, Cooper G, Haywood I, Milner S: Field surgery on a future conventional
battlefield: Strategy and wound management. Ann R Coll Surg Engl
1991;73:13.

RE.qxd 4/16/04 3:19PM PageS28

628 VI • THE RICH REFERENCE COLLECTION

Ryan W, Snyder WH III, Bell T, Hunt J: Penetrating injuries of the iliac vessels:
Early recognition and management. Am J Surg 1982;144:642-645.

Rybeck B: Missile wounding and hemodynamic effects of energy absorption.
Acta Chir Scand 1974,450:1.

RybuckJ, Thomford N: Acute occlusion of the infrarenal aorta from blunt trauma.
Am Surg 1969;36:444-447.

Saaman H: The hazards of radial artery pressure monitoring. J Cardiovasc Surg
1971;12:342.

Sachtello C, Ernst CB, Griffen WJ: The acute ischemic upper extremity: Selected
management. Surgery 1974;76:1002.

Sadow S, Murray C, Wilson R, et al: Traumatic rupture of ascending aorta and
left main bronchus. Ann Thorac Surg 1988;45:682-683.

Sagalowski A, McConnell J, Peters P: Renal trauma requiring surgery: An analy-
sis of 185 cases. J Trauma 1983;23:128-131.

Sahler O, Jaretzki AJ: Thrombosis of the abdominal aorta: Its production by
ureteral compression during intravenous pyelography. Arch Surg
1968;96:76-77.

Sako Y, Varco R: Arteriovenous fistula: Results of management of congenital
and acquired forms, blood flow measurements and observations on proxi-
mal arterial degeneration. Surgery 1970;67:40-61.

Salam A, Stewart M: New approach to wounds of the aortic bifurcation and infe-
rior vena cava. Surgery 1985;98:105-108.

Salander J, YoukeyJ, Rich NM, et al: Vascular injury related to lumbar disk
surgery. J Trauma 1984;24:628-631.

Salas A, PanesJ, Rosenbloom C, etal: Differential effects of a nitric oxide donor
on reperfusion-induced microvascular dysfunction in diabetic and non-
diabetic rats. Diabetologia 1999;42:1350-1358.

Saletta J, Freeark R: The partially severed artery. Arch Surg 1968;97:198-
205.

Saletta J, Freeark R: Vascular injuries associated with fractures. Orthop Clin
North Am 1970;1:93.

SalettaJ, Freeark R: Injuries to the profunda femoris artery. J Trauma 1972;12:
778.

SalettaJ, Lowe RLL: Penetrating trauma of the neck. J Trauma 1976;16:579-
587.

Saletta S, Lederman E, Fein S, et al: Transesophageal echocardiography for the
initial evaluation of the widened mediastinum in trauma patients. J Trauma
1995;39:137-141.

Samaan H: Vascular injuries of the upper thorax and the root of the neck. Br
J Surg 1971;58:881-886.

Samson P: Two unusual cases of war wounds of the heart. Surgery 1946;20:373.

Samson P: Battle wounds and injuries of the heart and pericardium: Experi-
ences in forward hospitals. Ann Surg 1948;127:1127.

Samson R, Pasternak B: Traumatic arterial spasm: Rarity or nonentity. J Trauma
1980;20:607-609.

Samson R, Sprayregen S, Veith F, et al: Management of angioplasty complica-
tions, unsuccessful procedures and early and late failures. Ann Surg
1984;199:234-240.

Santanello S, Barnes S, Price J, Falcone R: Below the belt: Seat belt related
injuries. Contemp Surg 1991;39:29-32.

Sato O, Tada Y, Sudo K, et al: Arteriovenous fistula following central venous
catheterization. Arch Surg 1986;121:729-731.

RE.qxd 4/16/04 3:19PM PageS29

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 629

Saueracker A, McCroskey B, Moore EE: Intraoperative hypogastric artery
embolization for life-threatening pelvic hemorrhage: Apreliminary report.
J Trauma 1987;27:1127-1129.

Sauerbruch: Uber die Verwendbarkeit der pneumatischen Kammer fur die Her-
schirurgie. Centralbl Chir 1907;34:44.

Saunders M, Riberi A, Massullo E: Delayed traumatic superior mesenteric arte-
riovenous fistula after a stab wound: Case report. J Trauma 1992;32:101-
106.

Savage R: Popliteal artery injury associated with knee dislocation: Improved
outlook? Am Surg 1980;46:627-632.

Saylam A, Melo J, Ahmad A, et al: Early surgical repair in traumatic rupture of
the thoracic aorta. (Report of 9 cases and review of the current concepts) .
J Cardiovasc Surg 1980;21:295-302.

Scalea T, Sclafani S: Angiographically placed balloons for arterial control: A
description of a technique. J Trauma 1991;31:1671-1677.

Schaff H, Brawley RK: Operative management of penetrating vascular injuries
of the thoracic outlet. Surgery 1977;82:182-191.

Schede M: Zur frage von derjodoformvergiftung. Zentralb Chir Beil 1882;9:33-
38.

Scheerlinck T, Van den Brande P: Post-traumatic intima dissection and throm-
bosis of the external iliac artery in a sportsman. SurgJ Vase Surg 1994;8:645.

Schenk WJ, Bahn RA, Cordell A, Stephens J: The regional hemodynamics of
acute experimental arteriovenous fistulas. Surg Gynecol Obstet
1957;105:733.

Schenk WJ, MartinJ, Leslie M, Portin B: The regional hemodynamics of chronic
arteriovenous fistulas. Surg Gynecol Obstet 1960;110:44-50.

Schlosser W, Spillner G, Breymann T, UrbayniB: Vascular injuries in orthopaedic
surgery. J Cardiovasc Surg 1982;23:323-327.

Schmidt C, JacobsonJ: Thoracic aortic injury: A ten-year experience. Arch Surg
1984;119:1244-1246.

Schmitt H, Armstrong RC: Wounds causing loss of limb. Surg Gynecol Obstet
1970;130:682-684.

Schoenfeld H: Heart Injuries with suture. Ann Surg 2001;87:823-828.

Schonholtz G, Jahnke EJJr: Occult injury of the thoracic aorta associated with
orthopaedic trauma. J Bone Joint Surg 1964;46A:1421.

Schorn B, Reitmeier F, Falk V, et al: True aneurysm of the superior gluteal
artery: Case report and review of the literature. J Vase Surg 1995;21:851.

Schott U, Lindbom L, Sjostrand U: Hemodynamic effects of colloid concen-
tration in experimental hemorrhage: A comparison of Ringer's acetate,
3% dextran-60 and 6% dextran-70. Crit Care Med 1998;16:346-352.

Schramek A, Hashmonai M: Distal arteriovenous fistula for the prevention of
occlusion of venous interposition grafts to veins. J Cardiovasc Surg
1974;15:392-395.

Schramek A, Hashmonai M, Farbstein J, Adler O: Reconstructive surgery in
major vein injuries in the extremities. J Trauma 1975;15:816-822.

Schramek A, Hashmonai M: Vascular injuries in the extremities in battle casu-
alties. Br J Surg 1977;64:644-648.

Schwab C, Lawson R, Lind J, Garland L: Aortic injury: Comparison of supine
and upright portable chest films to evaluate the widened mediastinum.
Ann Emerg Med 1984;13:896-899.

Schwab C, Adcock OT, Max H: Emergency department thoracotomy (EDT) : A
26-month experience using an "agonal" protocol. Am Surg 1986;52:20-28.

RE.qxd 4/16/04 3:19 PM Page 630

630 VI • THE RICH REFERENCE COLLECTION

Schwab C, McMahan D, Phillips G, Pentecost M: Aortic balloon control of a

traumatic aortoenteric fistula after damage control laparotomy: A case

report. J Trauma 1996;40:1021-1023.
Schwartz A: The historical development of methods of hemostasis. Surgery

1958;44:604.
Schwartz D, Haller JAJr: Open anterior hip dislocation with femoral vessel tran-
section in a child. J Trauma 1974;14:1054.
Schwartz L,McCannR: Traumatic false aneurysm of the common carotid artery

presenting as a mediastinal mass: A case report. J Vase Surg 1989;10:281-

284.
Schwartz ML, Fisher R, Sako Y, et al: Posttraumatic aneurysms of the thoracic

aorta. Surgery 1975;78:589-593.
Sclafani SJ, Panetta T, Goldstein A, et al: The management of arterial injuries

caused by penetration of Zone III of the neck. J Trauma 1985;25:878-

881.
Sclafani S, Cooper R, Shaftan GW, et al: Arterial trauma: Diagnostic and ther-
apeutic angiography. Radiology 1986;161:165-172.
Sclafani S, Cavaliere G, Atweh N, et al: The role of angiography in penetrating

neck trauma. J Trauma 1991;31:557-563.
Scott C, Pinson W, Inahara T: Common femoral artery injury by blunt trauma:

A case report. Surgery 1984;96:122-125.
Scott R. Aspects of military surgery. Injury 1970;2:116.
Scultetus AH, Villavicencio JL, Rich NM: Historical review: Facts and fiction

surrounding the discovery of the venous valves. J Vase Surg 2001;33:435-

441.
Sechas M, Fotiadis C, Baramily B, Skalkeas G: Plaie des vaisseaux mesenteriques

superieurs a propos d'un cas. Ann Chir 1988;42:423-425.
Seeley S: Vascular surgery at Walter Reed Army Hospital. US Armed Forces

MedJ 1954;8.
Seeley S, Hughes CW, Cooke F, Elkin DC: Traumatic arteriovenous fistulas and

aneurysms in war wounded. Am J Surg 1952;83:471-479.
Seeley S, Hughes CW, Jahnke EJJr: Surgery of the popliteal artery. Ann Surg

1953;138:712-717.
Seeley S, Hughes CW, Jahnke EJJr: Major vessel damage in lumbar disc oper-
ation. Surgery 1954;35:421-429.
Sefczek D, Sefczek RJ, Deeb Z. Radiographic signs of acute traumatic

rupture of the thoracic aorta. AJR Am J Roentgenol 1983;141:1259-

1262.
Segar R, Palmisano D: Repair of gunshot wounds of the aorta and vena cava.

Ohio State MedJ 1969;65:501-505.
Seguin J, Bouillon P, Aubry P, et al: Aorto-right ventricular shunt and associ-
ated aortic valve injury resulting from a penetrating wound of the heart.

Thorac Cardiovasc Surg 1984;32:386-388.
Seidenberg B, Hurwitt E: Retrograde femoral-Seldinger-aortography: Surgical

complications in twenty-six cases. Ann Surg 1966;163:221-226.
Seiler JI, Richardson JD: Amputation after extremity injury. Am J Surg

1986;152:260-264.
Seltzer S, D'Orsi C, Kirshner R, DeWeese JA: Traumatic aortic rupture: Plain

radiographic findings. AJR 1981;137:1011-1014.
Sencert L: Les Blessures des Vaisseaux. Paris, Masson & Cie, 1917.
Sethi G, Scott S, Takaro T: False aneurysm of the abdominal aorta due to blunt

trauma. Ann Surg 1975;182:33-36.

RE.qxd 4/16/04 3:19 PM Page 631

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 631

Sethi G, Scott S, Bhayana J, Takaro T: Traumatic avulsion of the innominate

artery: Report of a case and review of literature. J Cardiovasc Surg

1975;16:171-175.
Sethi G, Scott S: Subclavian artery laceration due to migration of a Hagie Pin.

Surgery 1976;80:644.
Shackford SR, Sise MJ: Renal and mesenteric vascular trauma: In Vascular Injuries

in Surgical Practice. In Bongard FS, Wilson SE, Perry MO (eds) : Norwalk,

Conn, San Mateo, Appleton & Lange, 1991, pp 173-184.
Shadow S, Murray CI, Wilson R, et al: Traumatic rupture of ascending aorta

and left main bronchus. Ann Thorac Surg 1988;45:682-683.
Shaftan GW, Chiu C, Dennis C, Harris B: Fundamentals of physiologic control

of arterial hemorrhage. Surgery 1965;58:851-856.
Shah D, Leather R, Corson J, Karmody A: Polytetrafluoraethylene grafts in the

rapid reconstruction of acute contaminated peripheral vascular injuries.

Am J Surg 1984;148:229-233.
Shah D, Naraynsingh V, Leather R, et al: Advances in the management of acute

popliteal vascular blunt injuries. J Trauma 1985;25:793-797.
Shah D, Corson J, Karmody A, et al: Optimal management of tibial arterial

trauma. J Trauma 1988;28:228-234.
Shah PM, Ito K, Clauss RH, et al: Expanded microporous polytetrafluroethyl-

ene (PTFE) grafts in contaminated wounds: Experimental and clinical study.

J Trauma 1983;23:1030-1033.
Shah PM, Mackey R, Babu SC, et al: Pseudoaneurysm of anterior tibial artery

after occlusion from blunt trauma: Nonoperative management. J Trauma

1985;25:656-658.
Shah PM, Agarwal N, Babu SC, et al: Causes of limb loss in civilian arterial

injuries. J Cardiovasc Surg 1986;27:278-281.
Shah PM, Ivatury RR, Babu SC, et al: Is limb loss avoidable in civilian vascular

injuries? Am J Surg 1987;154:202-205.
Shaker I, White J, Signer R, et al: Special problems of vascular injuries in chil-
dren. J Trauma 1976;16:863-867.
Shamoun J, Barraza KR, Jurkovich GJ, Salley R: In extreme use of staples for

cardiorrhaphy in penetrating cardiac trauma: Case report. J Trauma

1989;29:1589-1591.
Shandall A, Leopold P, Shah D, et al: Visceral aortic aneurysm in 4 1/2 year old

child: An unusual complication of umbilical artery catheterization. Surgery

1986;100:928-931.
Shannon J, Vo N, Stanton P: Peripheral arterial missile embolization. J Vase

Surg 1987;5:773-778.
ShanthakumarRE,ZwavelingJH, WaterbolkTW, GirbesARJ: Aorto-esophageal

fistula: An "early" complication following rupture of the thoracic aorta.

2001.
Sharar S, Winn R, Murry C, et al: A CD18 monoclonal antibody increases the

incidence and severity of subcutaneous abscess formation after high-dose

Staphylococcus aureus injection in rabbits. Surgery 1991;110:213-220.
Sharma P, Babu SC, Shah PM, Clauss RH: Changing patterns in civilian arter-
ial injuries. J Cardiovasc Surg 1985;26:7-11.
Sharma P, Ivatury RR, Simon R, Vinzons A: Central and regional hemodynamics

determine optimal management of major venous injuries. J Vase Surg

1992;16:887-894.
Sharma P, Shah PM, Vinzons A, et al: Meticulously restored lumina of injured

veins remain patent. Surgery 1992;112:928-932.

RE.qxd 4/16/04 3:19 PM Page 632

632 VI • THE RICH REFERENCE COLLECTION

Shauna R, Main D, PinkertonJ: Surgical therapy of femoral artery pseudoa-
neurysm after angiography. Am J Surg 1987;154:676-680.

Sheikh A, Culbertson C: Emergency department thoracotomy in children: Ratio-
nale for selective application. J Trauma 1993;34:323-328.

Sheiman R, Brophy D, Perry L, Akbari C: Thrombin injection for the repair of
brachal artery pseudoaneurysms. AJR Am J Roentgenol 1999;173:1029-
1030.

Sheldon G, Lim RC, Yee E, Petersen S: Management of injuries to the porta
hepatis. Ann Surg 1985;202:539-542.

Sheldon P, Oglevie S, Kaplan L: Prolonged generalized urticarial reaction after
percutaneous thrombin injection for treatment of a femoral artery
pseudoaneurysm.JVIR 2000;11:759-761.

Shepard G, Rich NM, Dimond F Jr: Punji stick wounds: Experience with 342
wounds in 324 patients in Vietnam. Ann Surg 1967;166:902-907.

Sher M: Principles in the management of arterial injuries associated with frac-
ture/dislocations. Ann Surg 1975;182:630-636.

Sherman M, Saini V, Yarnox M, et al: Management of penetrating heart wounds.
Am J Surg 1978;135:553-558.

Shield CI, Richardson JD, Buckley C, Hagood C: Pseudyaneurysm of the bra-
chiocephalic arteries: A complication of percutaneous internaljugular vein
catheterization. Surgery 1975;78:190-194.

Shih F, Wang S, Dang K, et al: Successful management of traumatic mesenteric
arteriovenous fistula after failure of steel coil embolization: Case report.
J Trauma 1994;37:682-686.

Shin D, Wall MJ Jr, Mattox KL: Combined penetrating injury of the innomi-
nate artery, left common carotid artery, trachea, and esophagus. J Trauma
2000;49:780-783.

Shirkey AL, Quast DC, Jordan GL: Superior mesenteric artery division and intesti-
nal function. J Trauma 1967;7:7-24.

Shoemaker WC, Carey J, Yao S: Hemodynamic alterations in acute cardiac tam-
ponade after penetrating injuries of the heart. Surgery 1970;67:754-764.

Shoemaker WC, CareyJ, Yao S: Hemodynamic monitoring for physiologic eval-
uation, diagnosis, and therapy of acute hemopericardial tamponade from
penetrating wounds. J Trauma 1973;13:36-44.

Shoenfeld N, Stuchin S, Pearl R, Haveson S: The management of vascular injuries
associated with total hip arthroplasty. J Vase Surg 1990;11:549-555.

Shorr R, Crittenden M, Indeck M, et al: Blunt thoracic trauma. Analysis of 515
patients. Ann Surg 1987;206:200-205.

Shrock T, Blaisdell FW, Mathewson CJ: Management of blunt trauma to the
liver and hepatic veins. Arch Surg 1968;96:698-704.

Shuck J, Trump D: Nonpenetrating abdominal trauma with injuries to blood
vessels. Am Surg 1961;27:693-697.

ShuckJ, Omer GJLCJ: Arterial obstruction due to intimal disruption in extrem-
ity fractures. J Trauma 1972;12:481-489.

Shumacker HBJr: Incisions in surgery of aneurysm: With special reference to
explorations in the antecubital and popliteal fossae. Ann Surg 1946;124:586-
598.

Shumacker HBJr: Resection of the clavicle with particular reference to the use
of bone chips in the periosteal bed. Surg Gynecol Obstet 1947;84:245-248.

Shumacker HBJr: Surgical cure of innominate aneurysm: Report of a case with
comments on applicability of surgical measures. Surgery 1947;22:729-
739.

RE.qxd 4/16/04 3:19 PM Page 633

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 633

Shumacker HBJr: Operative exposure of the blood vessels in the superior ante-
rior mediastinum. Am Surg 1948;127:464-475.

Shumacker HBJr: Problem of maintaining the continuity of artery in surgery
of aneurysms and arteriovenous fistulae: Notes on the development and
clinical application of methods of arterial suture. Ann Surg 1948;127:207-
230.

Shumacker HBJr: Arterial aneurysms and arterialvenous fistulas. Spontaneous
problems. Cures in Surgery. In Elkin DC, DeBakey ME (eds): World War
II, Vascular Surgery. Washington, DC: US Government Printing Office,
OTSG, Department of the Army, 1955: 361-374.

Shumacker HBJr: Arterial suture techniques and grafts: Past, present and future.
Surgery 1969;66:419-433.

Shumacker HBJr: Book review: Vascular disorders of the upper extremity. Ann
Surg 1984;199:249.

Shumacker HBJr: Ramuald Weglowski: Neglected pioneer in vascular surgery.
J Vase Surg 2001;6:95-97.

Shumacker HBJr, Carter K: Arteriovenous fistulas and false aneurysms in mil-
itary personnel. Surgery 1946;20:9-25.

Shumacker HBJr, Stahl N: A study of the cardiac frontal area in patients with
arteriovenous fistulas. Surgery 1949;26:928-944.

Shumacker HBJr, Stokes G: Studies of combined vascular and neurologic injuries.
Ann Surg 1950;132:386-393.

Shumacker HB Jr, Wayson E: Spontaneous cure of aneurysms and arteriove-
nous fistulas, with some notes on intrasaccular thrombosis. Am J Surg
1950;79:532-544.

Siavelis H, Marsan R, Marshall W, Maull K: Aortoventricular fistula secondary
to blunt trauma: A case report and review of the literature. J Trauma
1997;43:713-715.

Sibbitt R, Palmaz J, Garcia F, Reuter S: Trauma to the extremities: Prospective
comparison of digital and conventional angiography. Radiology
1986;160:179-182.

SiegelR: Galen on surgery of the pericardium: An early record of therapy based
on anatomical and experimental studies. Am J Cardiol 1970;26:524-527.

Siegmeth A, Gaebler C, Sandbach G, Vecsei V: Arare case of a traumatic aneurysm
of the inferior thyroid artery. J Vase Surg 1995;22:812-813.

Sigel B, Popky G, Wagner D, et al: Comparison of clinical and Doppler ultra-
sound evaluation of confirmed lower extremity venous disease. Surgery
1968;64:332-338.

Sigler L, Gutierrez-Carreho R, Martinez-Lopez, et al: Aortocaval fistula: Expe-
rience with five patients. Vase Surg 2001;35:207-212.

Silen W, Spieker D: Fatal hemorrhage from the innominate artery after tra-
cheostomy. Ann Surg 1965;162:1005-1012.

Simeone F, Grillo H, Rundle F: On the question of ligation of the concomitant
vein when a major artery is interrupted. Surgery 1951;29:932-951.

Simmons K: Defense against free radicals has therapeutic implications. JAMA
1984;251:2187-2192.

Simstein N, Poole GV Jr, Nelson L: Perforation of the intrapericardial aorta
during subclavian catheterization. South Med J 1984;77:1605.

Sinclair T, Stephenson HJ: Survival following abdominal aortic rupture from
blunt trauma: Case report. Mo Med 1972;69:271-272.

Singh I, Gorman JF: Vascular injuries in closed fractures near junction of middle
and lower thirds of the tibia. J Trauma 1972;12:592-598.

RE.qxd 4/16/04 3:19 PM Page 634

634 VI • THE RICH REFERENCE COLLECTION

Sinkler W, Spencer A: The importance of early exploration of vascular injuries.
Surg Gynecol Obstet 1958;107:228-234.

Sinkler W, Spencer A: The value of peripheral arteriography in assessing acute
vascular injuries. Arch Surg 1960;80:300-304.

Sirinek KR, Levine BA: Trauma injury to the proximal superior mesenteric
vessels. Surgery 1985;98:831-835.

Sirinek K, Levine B, Gaskill H III, Root H: Reassessment of the role of routine
operative exploration in vascular trauma. J Trauma 1981;21:339-344.

Sirinek K, Gaskill H, Root H: Visceral vascular injury: Factors influencing sur-
vival. J Trauma 1982;22:641.

Sirinek K, Gaskill H III, Dittman W, Levine B: Exclusion angiography for patients
with possible vascular injuries of the extremities: A better use of trauma
center resources. Surgery 1983;94:598-603.

Sirinek K, Gaskill H III, Root H, Levine B: Truncal vascular injury: Factors influ-
encing survival. J Trauma 1983;23:372-377.

SitzmannJ, Ernst CB: Management of arm arterial injuries. Surgery 1984;96:895-
901.

SkillmanJ, Ducksoo K, Bain DS: Vascular complications of percutaneous femoral
cardiac interventions: Incidence and operative repair. Arch Surg
1988;123:1207-1212.

Skinner D: Traumatic renal artery thrombosis: A successful thrombectomy and
revascularization. Ann Surg 1973;177:264-267.

Skipper R, Debski R: Intramyocardial shotgun pellets diagnosed on initial emer-
gency room chest x-ray: Case report. J Trauma 1990;30:1609-1610.

Skyhar M, Hargens A, Strauss M, et al: Hyperbaric oxygen reduces edema and
necrosis of skeletal muscle in compartment syndromes associated with hem-
orrhagic hypotension. J Bone Joint Surg 1986;68:1218-1224.

Slaney G, Ashton F, Abrams LD: Traumatic rupture of the aorta. Br J Surg
1966;53:361-364.

Slater R, Edge A, Salman A: Delayed arterial injury after hip replacement. J
Bone Joint Surg 1989;71:699.

Sloop R, Robertson K: Non-penetrating traumas of the abdominal aorta due
to blunt trauma. Ann Surg 1975;182:33-36.

Sloop R, Robertson K: Nonpenetrating trauma of the abdominal aorta with
partial vessel occlusion: Report of two cases. Am Surg 1975;41:555-559.

Smejkal R, Izaznt T, Born C, et al: Pelvic crush injuries with occlusion of the
iliac artery. J Trauma 1988;28:1479-1482.

Smith C, Green R: Pediatric vascular injuries. Surgery 1981;90:20-31.

Smith G, Northrop C: Stab wound causing mesenteric-portal arteriovenous fistula:
An unusual case with a spontaneous closure. J Trauma 1976;16:408.

Smith K, Ben-Menachem B, Duke J, Hill G: The superior gluteal: An artery at
risk in blunt pelvic trauma. J Trauma 1976;16:273-279.

Smith L, Foran R, Gaspar MR: Acute arterial injuries of the upper extremity.
Am J Surg 1963;106:144-151.

Smith M, CassidyJ, Souther S, et al: Transesophageal echocardiography in the
diagnosis of traumatic rupture of the aorta. N Engl Med J 1995;332:356-
362.

Smith P, Lim W, Ferris E, Casali R: Emergency arteriography in extremity trauma:
Assessment of indications. AJR Am J Roentgenol 1981;137:803-807.

Smith R, Perdue GJ, Walker LJ, Israel P: Posttraumatic aneurysm of the abdom-
inal aorta with recurrent emboli of the superior mesenteric artery: A case
report. Surgery 1968;64:736-742.

RE.qxd 4/16/04 3:19 PM Page 635

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 635

Smith RI, Stone H: Traumatic fistulas involving the portal venous system. Am
JSurgl970;119:570.

Smith R, Szilagyi D, Pfeifer J: A study of arterial trauma. Arch Surg 1963;86:825-
835.

Smith R, Szilagyi D, Elliott J Jr: Fracture of long bones with arterial injury due
to blunt trauma. Arch Surg 1969;99:315-324.

Smith R, Elliot J, Hageman J: Acute penetrating arterial injuries of the neck
and limbs. Arch Surg 1974;109:198-205.

Smith R, Chang F: Traumatic rupture of the aorta: Still a lethal injury. Am J
Surg 1986;152:660-663.

Smith V, Hughes CW, Sapp O, et al: High-output circulatory failure due to arte-
riovenous fistula: complication of intervertebral-disk surgery. AMA Arch
IntMed 1957;100:833-841.

Smith W: Cardiorraphy in acute injuries. Ann Surg 1923;78:696-710.

Smyth E: Major arterial injury in closed fracture of the neck of the humerus:
Report of a case. J Bone Joint Surg 1969;51:B:508.

Snyder WH III: Vascular injuries near the knee: An updated series and overview
of the problem. Surgery 1982;91:502-506.

Snyder III WH: Popliteal and shank arterial injury. Surg Clin North Am
1988;68:787-807.

Snyder WH III, Thai E, Bridges RA, et al: The validity of normal arteriography
in penetrating trauma: A review of 114 cases. Arch Surg 1978;113:424-428.

Snyder III WH, Thai E, Perry MO. Vascular injuries of the extremities. In Vas-
cular Surgery. In Rutherford R (ed) : Philadelphia, PA: WB Saunders, 1989:
613-637.

Snyder WH III, Watkins W, Whiddon L: Civilian popliteal artery trauma: An 1 1-
year experience with 83 injuries. Surgery 1979;85:101-108.

Soldano S, Rich NM, Collins GJ, et al: Long-term follow-up of penetrating abdom-
inal aortic injuries after 15 years. J Trauma 1988;28:1358-1362.

Solovei G, Alame A, Bardoux JL: Paraplegia and dissection of the abdominal
aorta after closed trauma: A proposal of a case. Current review of the lit-
erature (1982-1993) [inFrench] JChirurgie 1994;131:236-244.

Sondenaa K, Tveit B, Kordt K, et al: Traumatic rupture of the thoracic aorta:
A clinicopathological study. Acta Chir Scand 1990;156:137-143.

Soots G, Warembourg HJ, Pratt A, Roux J: Acute traumatic rupture of the tho-
racic aorta: Place of delayed surgical repair.J Cardiovasc Surg 1989;30:173-
177.

Sotta R: Vascular problems in the proximal upper extremity. Clin Sports Med
1990;9:379.

Soubbotitch V: Military experiences of traumatic aneurysms. Lancet 1913;2:720-
721.

Soyer R, Brunet A, Piwnica A, et al: Traumatic rupture of the thoracic aorta
with reference to 34 operated cases. J Cardiovasc Surg 1981;22:103-108.

Soyer R, Bessou JP, Bouchart F, et al: Long-term results of surgical treatment
of traumatic rupture of the thoracic aorta: 47 cases. J Cardiovasc Surg
1990;31(suppl):102.

Speechly-Dick M, Grover G, Yellon D: Does ischemic preconditioning in the
human involve protein kinase C and the ATP dependent K+ channel? Circ
Res 1995;77:1030-1035.

Spellman M, Mandal A, Freeman HP: Successful repair of an arteriovenous
fistula between the superior mesenteric vessels secondary to a gunshot
wound. Ann Surg 1967;165:458.

RE.qxd 4/16/04 3:19 PM Page 636

636 VI • THE RICH REFERENCE COLLECTION

Spence R, DelRossi AJ, CilleyJ, Civil I: Exsanguinating upper extremity vascu-
lar injury: Is an initial approach by clavicular resection adequate? J Car-
diovasc Surg 1989;30:450.

Spencer A: The reliability of signs of peripheral vascular injury. Surg Gynec
Obstet 1962;114:490-494.

Spencer FC: The use of optical magnification in coronary bypass grafting.
J Thorac Cardiovasc Surg 1970.

Spencer FC, Grewe R: The management of acute arterial injuries in battle casu-
alties. Ann Surg 1955;141:304-313.

Spencer FC, Tompkins R: Management of acute arterial injuries. Postgrad Med
1960;28:476-481.

Spencer FC, Guerin P, Blake HA, Bahnson HT: A report of fifteen patients with
traumatic rupture of the thoracic aorta. J Thorac Cardiovasc Surg
1961;41:1-22.

Spirnak J, Resnick M: Revascularization of traumatic thrombosis of the renal
artery. Surg Gynec Obstet 1987;164:22-26.

Sponge A, Borrows PE, Armstrong D, Daneman A: Traumatic aortic rupture
in the pediatric population: Role of plain film, CT, and angiography in the
diagnosis. Pediatr Radiat 1991;21:324-328.

Stables D, Fouche R, de Villiers van Niekerek J, et al: Traumatic renal artery
occlusion: 21 cases. J Urol 1976;115:229.

Stafford G, O'Brien M: Traumatic rupture of the thoracic aorta. AustNZJ Surg
1977;47:175-179.

Stain SC, Yellin AE, Weaver FA, Pentecost M: Selective management of nonoc-
clusive arterial injuries. Arch Surg 1989;124:1136-1141.

Stain SC, Weaver FA, Yellin AE: Extra-anatomic bypass of failed traumatic arte-
rial repairs. J Trauma 1991;31:575-578.

Starnes BW, O'Donnell SD, Gillespie DL, et al: Endovascular management of
renal ischemia in a patient with acute aortic dissection and renovascular
hypertension. Ann Vase Surg 2002.

Starzl T, Kaupp HJ, Beheler EM: The treatment of penetrating wounds to the
inferior vena cava. Surgery 1962;51:195-204.

StavensB, Hasim S, Hammond G, et al: Optimal methods of repair of descend-
ing thoracic aortic transections and aneurysms. Am J Surg 1983;145:508-
513.

Steenburg R, Ravitch MM: Cervico-thoracic approach for subclavian vessel injury
from compound fracture of the clavicle: Consideration of subclavian-
axillary exposure. Ann Surg 1963;15j7:839-846.

Steichen F, Dargan E, Efron G, et al: A graded approach to the management
of penetrating wounds of the heart. Arch Surg 1971;103:574-580.

Stein AJ: Arterial injury in orthopaedic surgery. J Bone Joint Surg 1956;38:669.

Stein L, Shubin H, Weil M: Recognition in management of pericardial
tamponade. JAMA 1973;225:503.

Stein M, Mirvis S, Wiles CI: Delayed embolization of a shotgun pellet from the
chest to the middle cerebral artery. J Trauma 1995;39:1006-1009.

Stein R, Bono J, Korn J, Wolff W: Axillary artery injury in closed fracture of the
neck of the scapular: A case report. J Trauma 1971;11:528-531.

Steinbauer M, Harris A, Leiderer R, et al: Impact of dextran on microvascular
disturbances and tissue injury following ischemia/reperfusion in striated
muscle. Shock 1998;9:345-351.

Stelzner V, Horatz K: Correction of gunshot wounds of extrapericardial ascend-
ing aorta. Thoraxchirurgie 1963;10:632.

RE.qxd 4/16/04 3:19 PM Page 637

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 637

Stemmer E, Oliver C, CareyJ, Connolly JE: Fatal complications of tracheotomy.

Am J Surg 1976;131:288-290.
Stewart F: Arteriovenous aneurysm treated by angiography (angiorrhaphy).

Abb Surg 1913;57:247-254.
Stich R: Ueber gefaess und organ transplantationen mittelst gefaessnaht. Ergeon

ChirOrth 1910;1:1.
Stiles Q, Cohlmia G, Smith J, et al: Management of injuries of the thoracic and

abdominal aorta. Am J Surg 1985;150:132-140.
Stinnett D, Graham JM, Edwards W: Fibromuscular dysplasia and thrombosed

aneurysm of the popliteal artery in a child. J Vase Surg 1987;5:769-772.
Stipa S, Vollmar J: Arterial Trauma. Rome, Italy, Ares-Serono Symposia, 1986.
Stokes J, McAfee C: Increasing limb survival in vascular injury with fracture.

J Trauma 1965;5:162.
Stollone R, Ecker R, Samson P: Management of major acute thoracic vascular

injuries. Am J Surg 1974;128:249-254.
Stone H, Oxford W, Austin JT: Penetrating wounds of the abdominal aorta.

South Med J 1973;66:1351-1355.
Stone H, Fabian TC, Turkleson M: Wounds of the portal venous system. World

J Surg 1982;6:335-341.
Stone K, Walshaw R, Sugiyama G, et al: Polytetrafluoroethylene versus autoge-
nous vein grafts for vascular reconstruction in contaminated wounds. Am

J Surg 1984;147:692-695.
Stone W: Observations on the treatment of wounded arteries, with cases. New

Orleans Med SurgJ 1857;2:168.
Stoney R, Roe B, RedingtonJ: Rupture of the thoracic aorta due to closed chest

trauma. Arch Surg 1964;89:840-847.
Storey C, Nardi G, Sewell W: Traumatic aneurysms of the thoracic aorta: Report

of two cases, one successfully treated by resection and graft replacement

with the aid of a shunt. Ann Surg 1956;144:69-78.
Stothert JJ, McBride L, Tidik S, et al: Multiple aortic tears treated by primary

suture repair. J Trauma 1987;27:955-956.
Strandness DE Jr: Collateral Circulation in Clinical Surgery. Philadelphia, WB

Saunders, 1969.
Strandness DE Jr, Bell JW: Peripheral vascular disease: Diagnosis and objective

evaluation using a mercury strain gauge. Ann Surg 1965;161 (suppl 1):3-

35.
Strassmann G: Traumatic rupture of the aorta. Am Heart J 1947;33:508-515.
Straus R: Pulmonary embolism caused by a lead bullet following a gunshot

wound of the abdomen. Arch Pathol 1942;33:63-68.
Stringer W, Kelly DJ: Traumatic dissection of the extracranial internal carotid

artery. Neurosurgery 1980;6:123-130.
Strodel W, Eckhauser F, Lemmer J: Presentation and perioperative manage-
ment of arterioportal fistulas. Arch Surg 1987;122:563.
Stromberg B: Symptomatic lead toxicity secondary to retained shotgun pellets:

Case report. J Trauma 1990;30:356-357.
Stubbs D, Dorner D, Johnson R: Thrombosis of the iliofemoral artery during

revision of a total hip replacement: A case report. J Bone Joint Surg [Am]

1986;68:454-455.
Sturm J, Strate R, Mowlem A, et al: Blunt trauma to the subclavian artery. Surg

Gynec Obstet 1974;138:915-918.
Sturm J, Perry JJ, Cass AS: Renal artery and vein injury following blunt trauma.

Ann Surg 1975;182:696.

RE.qxd 4/16/04 3:19 PM Page 638

638 VI • THE RICH REFERENCE COLLECTION

Sturm J, Marsh D, Bodily KC: Ruptured thoracic aorta: Evolving radiological
concepts. Surgery 1979;85:363-367.

Sturm J, Bodily KC, Rothenberger D, Perry JF: Arterial injuries of the extrem-
ities following blunt trauma. J Trauma 1980;20:933-936.

Sturm J, Cicero J: The clinical diagnosis of ruptured subclavian artery follow-
ing blunt thoracic trauma. Ann Emerg Med 1983;12:17-19.

Sturm J, Perry JFJr, Olson F, Cicero J: Significance of symptoms and signs in
patients with traumatic aortic rupture. Ann Emerg Med 1984;13:876-
878.

Sturm J, Billiar TR, DorseyJ, et al: Risk factors for survival following treatment
of traumatic aortic rupture. Ann Thorac Surg 1985;39:418-421.

Sturm J, Perry JJ: Brachial plexus injuries form blunt thoracic trauma: A
harbinger of vascular and thoracic injury. Ann Emerg Med 1987; 16:404-
406.

Sturm J, Billiar TR, Luxenberg M, Perry JF: Risk factors for the development
of renal failure following the surgical treatment of traumatic aortic rupture.
Ann Thorac Surg 1987;43:425-427.

Sturm J, McGee M, Luxenberg M: An analysis of risk factors for death at the
scene following traumatic aortic rupture. J Trauma 1988;28:1578-1580.

Suarez C, Bernstein DM, Goldberger J, et al: The role of nuclear scanning in
the evaluation of arterial injuries. Am Surg 1983;49:209-210.

Sugg S, Gerndt S, Hamilton B, et al: Pseudoaneurysms of the intraparenchy-
mal splenic artery after blunt abdominal trauma: A complication of non-
operative therapy and its management. J Trauma 1995;39:593-595.

Sugg W, Rea W, Ecker R: Penetrating wounds of the heart: An analysis of 459
cases. J Thorac Cardiovasc Surg 1986;56:531-545.

Sullivan M: Rupture of the brachial artery from posterior discoloration of the
elbow treated by vein graft. Br J Surg 1971;58:470-471.

Sullivan M, Smalley R, Banowsky LH: Renal artery occlusion secondary to blunt
abdominal trauma. J Trauma 1972;12:509-515.

Sullivan W, Thorton F, Baker LH, et al: Early influence of popliteal vein repair
in the treatment of popliteal vessel injuries. Am J Surg 1971;122:528-531.

Summerall C, Lee WJ, Boone JA: Intracardiac shunts after penetrating wounds
of the heart. N Engl J Med 1965;272:240-242.

Sumpio G, Gusberg R: Aortic thrombosis with paraplegia: An unusual conse-
quence of blunt abdominal trauma. J Vase Surg 1987;6:412-414.

Sutorius D, Schreiber J, HelmsworthJ: Traumatic disruption of the thoracic
aorta. J Trauma 1973;13:583-590.

Svane H, Ottosen T: Traumatic vascular lesions. J Cardiovasc Surg 1963;4:303-
305.

Svensson L, Antunes MDJ, Kinsley R: Traumatic rupture of the thoracic aorta:
A report of 14 cases and a review of the literature. S Afr Med J 1985;67:853-
857.

Swan KG, HobsonRWII, Reynolds D, etal: Venous surgery in the lower extrem-
ities. In Swan KG, Hobson R, Reynolds D, et al (eds): St Louis, Warren H
Green Publishers, 1975.

Sweetman W: Subclavian steal syndrome following trauma: Case report. Am
Surg 1965;31:463-466.

Swetnam J, Hardin WD, Kerstein MD: Successful management of trifurcation
injuries. Am Surg 1986;52:585-587.

Symbas P, Vlasis-Hale S, Picone A: Missiles in the heart. Ann Thorac Surg
1989;48:192-194.

RE.qxd 4/16/04 3:19 PM Page 639

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 639

Symbas P, Pourhamidi A, Levin J: Traumatic rupture of the aortic arch between

the left common carotid and left subclavian arteries and avulsion of the

left subclavian artery. Ann Surg 1969;170:152-156.
Symbas P, Sehdeva J, Abbott OA, et al: Penetrating wounds of the thoracic aorta

and great arteries. South Med J 1970;63:853-857.
Symbas P, Sehdeva J: Penetrating wounds of the thoracic aorta. Ann Surg

1970;171:441-450.
Symbas P, Tyras D, Ware R, Hatcher CJ: Rupture of the aorta. Ann Thorac Surg

1973;15:405-410.
Symbas P, Tyras D, Ware R, Diroio D: Traumatic rupture of the aorta. Ann Surg

1973;178:6-12.
Symbas P, Kourias E, Tyras D, Hatcher CJ: Penetrating wounds of great vessels.

Ann Surg 1974;179:757-762.
Symbas P, Harlaftis N, Waldo W: Penetrating cardiac wounds: A comparison of

different therapeutic methods. Ann Surg 1976;183:377-381.
Symbas P, Harlaftis N: Bullet emboli in the pulmonary and systemic arteries.

Am Surg 1977;185:318-320.
SymesJ, Eadie D, Maclean A: Traumatic aorto-caval fistula associated with horse-
shoe kidney. J Trauma 1974;14:402-408.
Symonds F, Games A, Porter V, Crikelair G: Pitfalls in the management of

penetrating injuries of the forearm. J Trauma 1971;11:47-52.
Synder C, Eyer S: Blunt chest trauma with transection of the azygos vein: Case

report. J Trauma 1989;29:889-890.
Synder S, Wheeler J, Gregory R, etal: Freshly harvested cadaveric venous homo-
grafts as arterial conduits in infected fields. Surgery 1987;101:283-291.
Syracuse D, Seaver PRJr, Amato JJ: Aortic gunshot injury and paraplegia: Pre-
operative definition with arteriography and computerized axial tomogra-
phy. J Trauma 1985;25:271-273.
Szentpetery S, Lower R: Changing concepts in the treatment of penetrating

cardiac injuries. J Trauma 1977;17:457-461.
Szentpetery S: Management of aortic cannulation site blowouts. Ann Thorac

Surg 1992;54:582-583.
Szilagyi D: Discussion on "Choice of vascular graft material for patients." In

Wesolowski S, Dennis C (eds): Fundamentals of Vascular Grafting. New

York, McGraw-Hill, 1963, pp 397-419.
Szilagyi D: Spinal cord damage in surgery of the abdominal aorta. Surgery

1978;83:38-56.
Szuchmacher P, Freed J: Immediate revascularization of the popliteal artery

and vein: Report of a case. J Trauma 1978;18:142-144.
Tailor A, Granger D: Role of adhesion molecules in vascular regulation and

damage. Curr Hyperten Rep 2000;2:78-83.
Takeuchi M, Maruyama K, Nakamura M, et al: Posttraumatic inferior vena caval

thrombosis: Case report and review of the literature.J Trauma 1995;39:605-

608.
Tamim W, Arbid EJ, Andrews LS, Arous EJ: Percutaneous induced thrombosis

of iatrogenic femoral pseudoaneurysms following catheterization. Ann Vase

Surg 2000;14:254-259.
Tarlow S, Achterman CA, Hayhurst J, Ovadia D: Acute compartment syndrome

in the thigh complicating fracture of the femur: A report of three cases.

J Bone Joint Surg 1986;68:1439-1443.
Tassi A, DaviesA: Pericardial tamponade due to penetrating fragment wounds

of the heart. Am J Surg 1969;118:535-538.

RE.qxd 4/16/04 3:19 PM Page 640

640 VI • THE RICH REFERENCE COLLECTION

Tawes RJ, Etheredge S, Webb R, et al: Popliteal artery injury complicating arthro-
scopic meniscectomy. Am J Surg 1988;156:136-138.

Taylor B, Rhee R, Muluk S: Thrombin injection versus compression of femoral
artery pseudoaneurysms. J Vase Surg 1999;30:1052-1059.

Taylor LJ, Troutman R, Feliciano P, et al: Late complications after femoral artery
catheterization in children less than five years of age. J Vase Surg
1990;11:297-306.

Taylor TKF, Wardill JC: Successful primary repair of rupture of the popliteal
artery in association with compound dislocation of the knee-joint. Br Surg
1964;51:163-166.

Tector A, Reuben C, Hoffman J, et al: Coronary artery wounds treated with
saphenous vein bypass grafts. JAMA 1973;225:282-284.

Tector A, Worman L, Romer J, et al: Unusual injury to the aortic arch: A case
report. J Thorac Cardiovasc Surg 1974;67:547-552.

Tegner Y, Bergdahl L, Ekestrom S: Traumatic disruption of the thoracic aorta.
Acta Chir Scand 1984;150:635-638.

TepasJ, Alexander RH, Snyder J: Real time ultrasonography as a diagnostic
screen in experimental arterial injury. J Trauma 1985;25:720.

Thai E, Perry MO, Crighton J: Traumatic abdominal aortic occlusion. South
MedJ 1971;64:653-656.

ThalE, Snyder WH III, Hays R, Perry MO: Management of carotid artery injuries.
Surgery 1974;76:955-962.

Theodorides T, de Keizer G: Injuries of the axillary artery caused by fractures
of the neck of the humerus. Injury 1976;8:120-123.

Theunis P, Coenen L, BrouwersJ: Traumatic injuries to the porta hepatis. Injury
1989;20:152.

Thevenet A, DuCailiar C: Chronic traumatic aneurysms of the thoracic aorta.
World J Surg 1989;13:112-116.

Thio R: False Aneurysm of the ulnar artery after surgery employing a tourni-
quet. Am J Surg 1972;123:604-605.

Thio R, Stanton P, Logan W: Simultaneous avulsion of the innominate and left
intrathoracic subclavian arteries. J Thorac Cardiovasc Surg 1973;66:96-
98.

Thomas A, Goodman P, Roon A: Role of angiography in cervicothoracic trauma.
J Thorac Cardiovasc Surg 1978;76:633-638.

Thomas CJ, Carter J, Lowder S: Pericardial tamponade from central venous
catheters. Arch Surg 1969;98:217-218.

Thomas D, Wilson R, Wieneck R: Vascular Injury about the knee: Improved
outcome. Ann Surg 1989;55:370-377.

Thomas T: Management of cardiac and intrathoracic great vessel injuries. Surg
Gynecol Obstet 1967;125:997-1002.

Thomford N, Curtiss P, Marable S: Injuries of the iliac and femoral arteries asso-
ciated with blunt skeletal trauma. J Trauma 1969;9:126-134.

Thomford N, Pace W, Meckstroth C: Traumatic rupture of the thoracic artery.
Am Surg 1969;35:244-249.

Thorlacius H, Vollmar B, Westermann S, et al: Effects of local cooling on microvas-
cular hemodynamics and leukocyte adhesion in the striated muscle of ham-
sters. J Trauma 1998;45:715-719.

Tilney N, McLamb J: Leg trauma with posterior tibial artery tear. J Trauma
1967;7:807.

Timberlake G, O'Connell RC, Kerstein MD: Venous Injuries, to repair or ligate,
the dilemma. J Vase Surg 1986;4:533-538.

RE.qxd 4/16/04 3:19 PM Page 641

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 641

Timberlake G, Adinolfi MF, McSwain N Jr: Problem: Rupture of the thoracic

aorta. Emerg Med 1987;19:45-49.
Timberlake G, Kerstein MD, McSwain N Jr: Penetrating thoracic aortic injuries:

Rare but potentially salvageable sequelae of urban warfare. South Med J

1989;82:970-972.
Timberlake G, Kerstein MD: Venous injury: To repair or litigate, the dilemma

revisited. Am Surgeon 1995;61:139-145.
Tipton W, D 'Ambrosia R: Vascular Impairment as a result of fracture-
dislocation of the ankle. J Trauma 1975;15:524-527.
Tisnado J, Tsai F, Als A, Roach J: A new radiographic sign of acute traumatic

rupture of the thoracic aorta: Displacement of the nasogastric tube to the

right. Radiology 1977;125:603-608.
Todd G, Bregman D, Voorhees A, Reemtsma K: Vascular Complications asso-
ciated with percutaneous intra-aortic balloon pumping. ArchSurg

1983;118:963-964.
Toguri A, Liu T, Bayliss C: Traumatic bilateral renal artery thrombosis. J Urol

1974;112:430.
Toivio I, Karlsson B: Treatment of ischemia of extremity caused by a shotgun

blast. Ann Med Milit Fenn 1975;4:159.
Tomatis L, Doornobs F, Beard JA: Circumferential intimal tear of the aorta with

complete occlusion due to blunt trauma. J Trauma 1968;8:1096-1101.
Tomiak M, Rosenblum J, Messersmith R, Zarins C: Use of CT for diagnosis of

traumatic rupture of the thoracic aorta. Ann Vase Surg 1993;7:130-

139.
Toursarkissian B, Allen BT, Petrinec D: Spontaneous closure of selected iatro-
genic pseudoaneurysms and arteriovenous fistulae. J Vase Surg 1997;25:803-

809.
Towne JB, Delbert D, Smith J: Thrombosis of the internal carotid artery fol-
lowing blunt cervical trauma. Arch Surg 1972;104:565-568.
Townsend R, Colella J, Diamond D: Traumatic rupture of the aorta: Critical

decisions for trauma surgeons. J Trauma 1990;30:1169-1174.
Traber D: Nitric oxide synthase and tissue injury. Shock 2000;14:243-244.
Trask A, Richards F, Schwartzbach C, Kurtzke R: Massive orthopedic, vascular,

and soft tissue wounds from military type assault weapons: A case report.

J Trauma 1995;30:1169-1174.
Travers B, Cooper A: On wounds and ligature of veins. Surgical Essays (Lond)

1818;1:243.
Treiman G, Yellin AE, Weaver FA, et al: Examination of a patient with a knee

dislocation: The case for selective angiography. Arch Surg 1992;127:1056-

1063.
Treiman R, Doty D, Caspar MR: Acute vascular trauma: A fifteen year study.

Am Surg 1966;111:469-473.
Trent M, Parsonnet V, Shoenfeld R: A balloon expandable-intravascular stent

for obliterating aortic dissection. J Vase Surg 1990;11:707-717.
Tribble C, Crosby I: Traumatic rupture of the thoracic aorta. South Med J

1988;81:963-968.
Trimble C: Arterial bullet embolism following thoracic gunshot wounds. Ann

Surg 1968;168:911-916.
Trinkle JK, Marcos J, Grover FL, Cuello L: Management of the wounded heart.

Ann Thorac Surg 1974;38:181-182.
Trinkle JK, Toon R, Franz J, et al: Affairs of the wounded heart: Penetrating

cardiac wounds. J Trauma 1979;19:467-472.

RE.qxd 4/16/04 3:19 PM Page 642

642 VI • THE RICH REFERENCE COLLECTION

Trinkle JK: Penetrating heart wounds: Difficulty in evaluating clinical series
(editorial) . Ann Thorac Surg 1984;38:181-182.

Trueblood H, Wuerflein R, Angell WW: Blunt trauma rupture of the heart.
Ann Surg 1973;177:66-69.

Trunkey DD,BlaisdellFW: Abdominal vascular injuries. WestJ Med 1975;123:321-
324.

Trunkey DD: Trauma: Accidental and intentional injuries account for more
years of life loss in the U.S. than cancer and heart disease. Among the pre-
scribed remedies are improved prevention efforts, speedier surgery and
further research. Sci Am 1983;249:28-35.

Tse D, Slabaugh P, Carlson P: Injury to the axillary artery by a closed fracture
of the clavicle. J Bone Joint Surg 1980;62:1372-1373.

Tuffier M: Contemporary French surgery. Br J Surg 1915;3:100-112.

Turner G: Gunshotwounds of the heart. War Medicine, a Symposium. In Pingh
WS (ed): Podolsky Edward, 1942.

Turney SZ, Attar S, Ayella R, et al: Traumatic rupture of the aorta: A five-year
experience. J Thorac Cardiovasc Surg 1976;72:727-734.

Turney SZ, Attar S, Ayella R, et al: Is arteriography necessary in the manage-
ment of vascular trauma of the extremities? Surgery 1978;84:557-562.

Turney SZ, Rodriguez A, Attar S: Repair of traumatic thoracic aortic rupture:
Risk factors of paraplegia. J Cardiovasc Surg 1990;31:107.

Turpin I, State D, Schwartz A: Injuries to the inferior vena cava and their man-
agement. Am J Surg 1977;134:25-34.

Tuzeo S, Saad S, Hastings O, Swan KG: Management of brachial artery injuries.
Surg Gynec Obstet 1978;146:21-24.

TyburskiJG, Wilson RF, Dente C, et al: Factors affecting mortality rates in patients
with abdominal vascular injuries. J Trauma 2001;50:1020-1026.

Uhlmann D, Uhlmann S, Spiegel H: Endothelin/nitric oxide balance influ-
ences hepatic ischemia-reperfusion injury. J Cardiovasc Pharmacol
2000;36:S212-S214.

Ulflacker R, SaadiJ: Transcatheter embolization of superior mesenteric arte-
riovenous fistula. AJR Am J Roentgenol 1982;139:1212.

Ulvestad L: Repair of laceration of superior mesenteric artery acquired by non-
penetrating injury to the abdomen. Ann Surg 1954;140:752-754.

UtleyJ, Singer M, Roe B, et al: Definitive management of innominate artery
hemorrhage complicating tracheostomy. JAMA 1972;220:577-579.

Valle A: War injuries of heart and mediastinum. Arch Surg 1955;70:398-
404.

Van De Wal H, Draaisma J, Vincent J, Goris R: Rupture of the supradiaphrag-
matic inferior vena cava by blunt decelerating trauma: Case report.J Trauma
1990;30:111-113.

Van Gilder J, Coxe W: Shotgun Pellet embolus of the middle cerebral artery.
Neurosurgery 1970;32:711-714.

van Leeuwen J, Broos P, Rommens P, Nevelsteen A: Combined blunt rupture
of the diaphragm and the thoracic artery. Injury 1990;21:117-119.

Van NiekerkJ, Heijstraten F, Goris R, et al: Spinal cord injury following surgery
for acute traumatic rupture of the thoracic aorta. Thorac Cardiovasc Surg
1986;34:30-34.

Van Way C: Intrathoracic and intravascular migratory foreign bodies. Surg Clin
North Am 1989;69:125-133.

Varner J, Oliver R: Superior mesenteric arteriovenous fistula. Ann Surg
1969;170:862.

RE.qxd 4/16/04 3:19PM PageS43

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 643

VaskoJ, Raess D, Williams TEJr: Non-penetrating trauma to the thoracic aorta.

Surgery 1977;82:400-406.
Vaughan G, Mattox KL, Feliciano DV, et al: Surgical experience with expanded

polytetrafluorethylene (PTFE) as a replacement graft for traumatized vessels.

J Trauma 1979;19:403-408.
VautheyJ, Maddern G, Balsiger D, et al: Superselective embolization of supe-
rior gluteal artery pseudoaneurysms following intramuscular injection: Case

report. J Trauma 1991;31:1174.
Veith F, Gupta S, Daly V: Technique for occluding the supraceliac aorta through

the abdomen. Surg Gynec Obstet 1980;151:426-428.
Veith F, Ascer E, Gupta S, Wengerter K: Lateral approach to the popliteal artery.

JVascSurgl987;6:119.
Verdant A, Mercier C, Page A, et al: Major mediastinal vascular injuries. Can J

Surg 1983;26:38-42.
Verdant A, CossetteR, DontignyL, etal: Acute and chronic traumatic aneurysms

of the descending thoracic aorta: A 10-year experience with a single method

of aortic shunting. J Trauma 1985;25:601-607.
Verdant A: Major mediastinal vessel injury: An underestimated lesion. Can J

Surg 1987;30:402-404.
Verdant A: Traumatic rupture of the thoracic aorta. Ann Thorac Surg

1990;49:686-687.
Veterans Administration Cooperative Study Group 141: Comparative

evaluation of prosthetic, reversed, and in situ vein bypass grafts in

distal popliteal and tibioperoneal revascularization. Arch Surg 1988;123:434-

438.
Vignon P, Gueret P, Vedrinne J, et al: Role to transesophageal echocardiogra-
phy in the diagnosis and management of traumatic aortic disruption. Cir-
culation 1995;92:2959-2968.
Vrj D, Simoni E, Smith R: Resuscitative thoracotomy for patients with traumatic

injury. Surgery 1983;94:554-561.
Vincent K, Blair WF: A false aneurysm of the ulnar artery after a forearm com-
partment syndrome. Orthopedics 1984;7:1834-1836.
Visser P, Hermreck A, Pierce G, et al: Prognosis of nerve injuries incurred during

acute trauma to peripheral arteries. Am J Surg 1980;140:596-599.
Vitale G, Richardson JD, George SMJr, Miller F: Fasciotomy for severe, blunt,

and penetrating trauma of the extremity. Surg Gynecol Obstet 1988; 166:397-

401.
Vitelli C, Scalea T, Phillips T, et al: A technique for controlling injuries of the

iliac vein in the patient with trauma. Surg Gynecol Obstet 1988;166:551-

552.
Vollmar J, Krumhaar D: Surgical experience with 200 traumatic arteriovenous

fistulae. In Hiertonn T, Rybeck B (eds) : Traumatic Arterial Lesions.

Stockholm, Forsvarets Forskningsanstalt, 1968.
Vollmar J: Surgical experience with 197 traumatic arterial lesions (1953-66).

In Hiertonn T, Rybeck B (eds): Traumatic Arterial Lesions. Stockholm,

Forsvarets Forskningsanstalt, 1968.
Vollmar J: Knochenbruch und Gefassverletzung. Langenbecks Arch Chir

2001;339:473-477.
von Horoch C: Die Gefassnaht. Allg Wien Med Ztg 1888;33:263-279.
von Oppell U, Beningfield SJ, Odel J, Reichart B: Cardiac rupture caused by

blunt trauma as well as false angiographic aortic rupture: A case report. S

Afr Med J 1988;74:519-520.

RE.qxd 4/16/04 3:19 PM Page 644

644 VI • THE RICH REFERENCE COLLECTION

von Oppell U, Dunne T, DeGroot M, Zilla P: Traumatic aortic rupture: Twenty

year metaanalysis of mortality and risk of paraplegia. Ann Thorac Surg

1994;58:585-593.
Von Zoege-Manteuffel: Demonstration eines Praparates von aneurysma arte-

riosovenosum ossificans der art femoralis profunda. Verhandl Deutsch

Gesellsch Chir 1895;24:167-170.
Vorwerk D, Gtinther R, Wendt G: Chronic aortoiliac dissection treated by

self-expanding stent placement. Cardiovasc Intervent Radiol 1995;18:

43.
Vosloo S, Reichart B: Inflow occlusion in the surgical management of a pene-
trating aortic arch injury: Case report. J Trauma 1990;30:514-515.
Waddell J, Lenczer E: Arterial injury associated with skeletal trauma. Injury

1974;6:28-32.
Waddell W, Vogelfanger I, Prudhomme P, et al: Venous valve transplantation.

Arch Surg 1964;88:5-15.
Wagner W, Calkins E, Weaver FA: Blunt popliteal artery trauma: 100 consecu-
tive cases injuries. J Vase Surg 1988;7:736-748.
Wagner W, Calkins E, Weaver FA, et al: Blunt popliteal artery trauma: One

hundred consecutive injures. J Vase Surg 1988;5:736-743.
Wagner W, Yellin AE, Weaver FA, et al: Acute treatment of penetrating popliteal

artery trauma: The importance of soft tissue injury. Ann Vase Surg

1994;8:557-565.
Waibel P, Ludin H: Unusual sources for peripheral arterial embolization: A case

report. Arch Surg 1966;92:105-106.
WaigandJ, Uhlich F, Gross C: Percutaneous treatment of pseudoaneurysms and

arteriovenous fistulas after invasive vascular procedures. Catheter Cardio-
vasc Interv 1999;47:157-164.
Walden R, Lynn M, Golan M, Garniek A: Plastic bullet arterial embolization

following gunshot injury to the heart: Case report and review of the liter-

ature.J Cardiovasc Surg 1990;31:482-485.
Walker A, Walker R: Traumatic thrombosis of the aorta. Br Med J 1961;5238:

1514.
Walker M, PoindexterJ, Stovall I: Principles of management of shotgun wounds.

Surg Gynecol Obstet 1990;170:97-106.
Walker P, Dake M, Mitchell R, Miller D: The use of endovascular techniques

for the treatment of complications of aortic dissection. J Vase Surg

1993;18:1042-1051.
Walker T, Geller S, Brewster DC: Transcatheter occlusion of a profunda femoral

artery pseudoaneurysm using thrombin. AJRAmJ Roentgenol 1987;149:185-

186.
Walker W, Pate J: Medical management of acute traumatic rupture of the aorta.

Ann Thorac Surg 1990;50:965-967.
Walker W, Cooley DA, Duncan J, et al: The management of aortoduodenal

fistula by in situ replacement of the infected abdominal aortic graft. Ann

Surg 1987;205:727-732.
Wall MJ Jr, Pape PE, Martin RR, et al: Immediate versus delayed fluid resusci-
tation for hypotensive patients with penetrating torso injuries. N Engl J

Med 1994;331:1105-1109.
Wall MJJr, Granchi T, Liscum K, Mattox KL: Penetrating thoracic vascular injuries.

Surg Clin North Am 1996;76:749-761.
Wallenhaupt S, Huspeth A, Mills S, et al: Current treatment of traumatic aortic

disruptions. Am Surg 1989;55:316-320.

RE.qxd 4/16/04 3:19PM PageS45

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 645

Waller B, Girod D, DillionJ: Transverse aortic wall in infants after balloon angio-
plasty for aortic valve stenosis: Relation of aortic wall damage to diameter
of inflated angioplasty balloon and aortic lumen in seven necropsy cases.
J Am Coll Cardio 1984;4:1235-1241.

Walls J, Curtis J, Boley T: Sarns centrifugal pump for repair of thoracic aortic
injury: Case report. J Trauma 1989;29:1283-1285.

Walls J, Boley TM, Curtis J, Schmaltz R: Experience with four surgical tech-
niques to repair traumatic aortic pseudoaneurysm. J Thorac Cardiovasc
Surg 1993;106:283-287.

Walsh J, Meyer JR Rosenbloom M: Production and treatment of mechanically
induced arterial vasospasm in a rabbit model. Surg Fo 1987;38:313-314.

Wand J, Zuckerman J: Delayed rupture of false aneurysm following a femoral
fracture. J Bone Joint Surg 1989;7lB:700.

Wang N, Sparks S, Bailey LL: Staged repair using omentum for posttraumatic
aortoesophageal fistula. Ann Thorac Surg 1994;58:557-559.

Wang P, Singh G, Rana M, et al: Preheparinization improves organ function
after hemorrhage and resuscitation. Am J Physiol 1990;259:R645-R650.

Wang P, Ba ZF, Chaudry IH: Endothelial cell dysfunction occurs after hemor-
rhage in nonheparinized but not in preheparinized models. J Surg Res
1993;54:499-506.

Wang P, Tait S, Ba ZF, Chaudry IH: ATP-MgC12 administration normalizes
macrophage cAMP and beta-adrenergic receptors after Hhemorrhage and
resuscitation. J Physiol 1994;267:G52-G58.

Wang P, Ba ZF, Chaudry IH: Chemically modified heparin improves hepato-
cellular function, cardiac output, and microcirculation after trauma: Hem-
orrhage and resuscitation. Surgery 1994;116:169-175.

Wang P, Ba ZF, Chaudry IH: Nitric oxide. To block or enhance its production
during sepsis? Arch Surg 1994;129:1137-1142.

Wang P, Ba ZF, Chaudry IH: ATP-MgC12 restores depressed endothelial cell
function after hemorrhagic shock and resuscitation. Am J Physiol
1995;268:H1390-H1396.

Wang P, Ba ZF, Chaudry IH: Endothelium-dependent relaxation is depressed
at the macro- and microcirculatory levels during sepsis. Am J Physiol
1995;269:R988-R994.

Wang P, Ba ZF, Stepp K, Chaudry IH: Pentoxifylline attenuates the depressed
endothelial cell function and vascular muscle contractility following trauma
and hemorrhagic shock. J Trauma 1995;39:121-126.

Wang P, Ba ZF, Reich S, et al: Effects of nonanticoagulant heparin on cardio-
vascular and hepatocellular function after hemorrhagic shock. Am J Physiol
1996;270:H1294-H1302.

Wang P, Ba ZF, Cioffi W, et al: Salutary effects of ATP-MgCl 2 on the depressed
endothelium-dependent relaxation during hyperdynamic sepsis. Crit Care
Med 1999;27:959-964.

Ward P, Suzuki A: Gunshot wound of the heart with peripheral embolization.
J Thorac Cardiovasc Surg 1974;68:440.

Warren R: Report to the Surgeon General. Washington, DC, Department of
the Army, 1952.

Warren R, Akins CW, Conn A, et al: Acute traumatic disruption of the thoracic
aorta: Emergency department management. Ann Emerg Med 1992;21 :39 1-
396.

Warrian R, Shoenut J, Iannicello C, et al: Seatbelt injury to the abdominal aorta.
J Trauma 1988;28:1505-1507.

RE.qxd 4/16/04 3:19PM PageS46

646 VI • THE RICH REFERENCE COLLECTION

Wascher R, Gwinn B: Air rifle pellet injury to the heart with retrograde caval
migration. J Trauma 1995;38:379-381.

Watson W, Silverstone S: Ligature of the common carotid artery in cancer of
head and neck. Ann Surg 1939;109:1-27.

Waxman K, Soliman M, Braunstein P, et al: Diagnosis of traumatic cardiac con-
tusion. Arch Surg 1986;121:689-692.

Waxman K: Shock: Ischemia, reperfusion, and inflammation. New Horiz
1996;4:153-160.

Weaver FA, Rosenthal R, Waterhouse G, Adkins RB: Combined skeletal and vas-
cular injuries of the lower extremities. Am Surg 1984;50:189-197.

Weaver FA, Yellin AE, Wagner W, et al: The role of arterial reconstruction in
penetrating carotid injuries. Arch Surg 1988;123:1106-1111.

Weaver FA, Suda R, Stiles G, Yellin AE: Injuries to the ascending aorta, aortic
arch and great vessels. Surg Gynecol Obstet 1989;169:27-31.

Weaver FA, Yellin AE, Bauer MAP, et al: Is arterial proximity a valid indication
for arteriography in penetrating extremity trauma? A perspective analysis.
Arch Surg 1990;125:1256-1260.

Weber T, Dent T, Lindenaur S: Viable vein graft preservation. J Surg Res
1975;18:247-255.

Wei J, Chang C, Chang Y: Traumatic sinus of Valsalva fistula. Ann Thorac Surg
1991;52:852-854.

Weiland A, Robinson H, FutrellJ: External stabilization of a replanted upper
extremity: Case report. J Trauma 1976;16:239-241.

Weimann S, San Nicolo M, Sandbichler P, et al: Civilian popliteal artery trauma.
J Cardiovasc Surg 1987;28:145-151.

Weinstein M, Golding A: Temporary external shunt bypass in the traumatically
amputated upper extremity. J Trauma 1975;15:912-915.

Weisberg D, Goetz R: Necrosis of arterial wall following application of methyl-
2-cyanoacrylate. Surg Gynecol Obstet 1964;119:1248.

Weiser M, Gibbs S, Valeri C, et al: Anti-selectin therapy modifies skeletal muscle
ischemia and reperfusion injury. Shock 1996;5:402-407.

Weiss J, Bernadine HB, Hutchins G, Mason S: Two-dimensional echocardio-
graphy recognition of myocardial injury in man: Comparison with post-
mortem studies. Circulation 1981;63:401-408.

Welborn MJ, Sas J: Acute abdominal aortic occlusion due to nonpenetrating
trauma. Am J Surg 1969;118:112-116.

Welling R, Kakkasseril J, Cranley J: Complete dislocations of the knee with
popliteal vascular injury. J Trauma 1981;21:450-453.

Welling R, Rremchek T, Rath R, et al: Blunt arterial injuries associated with mul-
tiple trauma. Ann Vase Surg 1989;3:345-350.

Werne C, Sagraves S, Costa C: Mitral and tricuspid valve rupture from blunt
trauma sustained during a motor vehicle collision. J Trauma 1989;29:113-
115.

Wernly J, Campbell C, Replogle R: Traumatic avulsion of the innominate and
left carotid arteries. J Thorac Cardiovasc Surg 1982;84:392-397.

Wexler L, Silverman J: Traumatic rupture of the innominate artery: A seat belt
injury. N Engl J Med 1970;282:1186-1187.

Whelan TJ, Baugh JH: Non-Atherosclerotic Arterial Lesions and Their Man-
agement: Current Problems in Surgery. Chicago, Year Book Medical Pub-
lishers, 1967.

White GH, White RA, Kopchok G, Wilson SE: Angioscopic thromboembolec-
tomy: Preliminary observations with a recent technique. J Vase Surg
1988;7:318-325.

RE.qxd 4/16/04 3:19 PM Page 647

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 647

White GH, White RA, Kopchok G: Endoscopic intravascular surgery removes

intraluminal flaps, dissections and thrombus. J Vase Surg 1990;11:280-299.
White J: Shark attack in Natal. Injury 1975;6:187-197.

White J, Talbert J, Haller JAJr: Peripheral arterial injury in infants and chil-
dren. Ann Surg 1968;167:757-766.
Whitehouse W, Coran A, Stanley JC: Pediatric vascular trauma. Arch Surg

1976;111:1269-1275.
Whitesides T, Haney T, Morimoto K: Tissue pressure measurement as a deter-
minant for the need for fasciotomy. Clin Orthop 1975;113:43-51.
Whitman G, McCroskey B, Moore EE, et al: Traumatic popliteal and trifurca-

tion vascular injuries: Determinants of functional limb salvage. Am J Surg

1987;154:681-684.
Wholey M, Bocher J: Angiography in musculoskeletal trauma. Surg Gynecol

Obstet 1967;125:730-736.
Wholey M, Bocher J: Angiographic features of aortic and peripheral arterial

trauma. Arch Surg 1968;97:68-74.
Whye D, Barish R, Alquist T, et al: Echocardiographic diagnosis of acute peri-
cardial affusion in penetrating chest trauma. Am J Emerg Med 1988;6:2T

23.
Wiechert R, Hewitt RL: Injuries to the vena cava: Report of 35 cases. J Trauma

1970;10:649-657.
Wiedeman J, Mills J, Robison JG: Special problems after iatrogenic vascular

injuries. Surg Gynecol Obstet 1988;166:323-326.
Wiencek R, Wilson R: Abdominal venous injuries. J Trauma 1986;26:771-778.
Wiencek R, Wilson R: Injuries to the abdominal vascular system: How much

does aggressive resuscitation and prelaparotomy really help. Surgery

1987;102:731-736.
Wiener I, Flye M: Traumatic false aneurysm of the vertebral artery. J Trauma

1984;24:346-349.
Wigle R, Morgan J: Spontaneous healing of a traumatic thoracic aortic tear:

Case report. J Trauma 1991;31:280-283.
Wildegans H: Verletzungen der aorta. Deutsch Med Wchnschr 1926;52:1810-

1812.
Williams C, Brenowitz JB: Sequential aortic and inferior caval clamping for

control of suprarenal vena caval injuries: Case report.J Trauma 1977; 17:1 64-

167.
Williams C, Robinson D: Traumatic abdominal aorta-inferior vena cava fistula

with immediate repair. Ann Surg 1961;154:998-1000.
Williams D: Stab wound of the heart and pericardium-recovery-patient alive

three years afterward. Medical Record 1897;51:437-439.
Williams D: Embolization of a bullet to the posterior tibial artery following a

gunshot wound of the thorax. J Trauma 1964;4:258-265.
Williams D, Brothers T, Messina L: Relief of mesenteric ischemia in type III

aortic dissection with percutaneous fenestration of aortic septum. Radiol-
ogy 1990;171:450-452.
Williams G: Peripheral vascular trauma: Report of 90 cases. Am J Surg

1968;116:725-730.
Williams G, CrumplerJ, Campbell G: Effect of sympathectomy on the severely

traumatized artery. Arch Surg 1970;101:704-707.
Williams J, Silver D, Laws H: Successful management of heart rupture from

blunt trauma. J Trauma 1981;21:534-537.
Williams J, Graff J, Uku JM, SteinigJ: Aortic injury in vehicular trauma. Ann

Thorac Surg 1994;57:726-730.

RE.qxd 4/16/04 3:19PM PageS48

648 VI • THE RICH REFERENCE COLLECTION

Williams J, Sherman R: Penetrating wounds of the neck: Surgical management.
J Trauma 1973;13:435-442.

Williams T, Knopp R, EllysonJ: Compartment syndrome after anti-shock trouser
use without lower extremity trauma. J Trauma 1982;22:595-597.

Wilson C: Aortic bypass graft in a child. Am J Surg 1974;128:797-798.

Wilson J: Fracture of the pelvis complicated by ischemia of the lower limb.
J Bone Joint Surg 1952;34-B:68-69.

Wilson L: Dispersion of bullet energy in relation to wound effects. Milit Surg
1921;49:241-251.

Wilson R, Bassett JS: Penetrating wounds of the pericardium or its contents.
JAMA 1966;195:513-518.

Wilson R, Arbulu A, BassetJS: Acute mediastinal widening following blunt chest
trauma: Critical decisions. Arch Surg 1972;104:551-558.

Wilson R, Wiencek R, Balog M: Predicting and preventing infection after abdom-
inal vascular injuries. J Trauma 1989;29:1371-1375.

Wilson R, Wiencek R, Balog M: Factors affecting mortality rate with iliac vein
injuries. J Trauma 1990;30:320-323.

Wilson SE, Veith F, Hobson RW II, Williams R: Noninvasive Diagnosis of Venous
Obstruction and Insuficency. New York, McGraw-Hill, 1987.

Wilson S, Au FC: In extreme use of a Foley catheter in a cardiac stab wound.
J Trauma 1986;26:400-402.

Wind G, Finley R, Rich NM: Three-dimensional computer graphic modeling
of ballistic injuries. J Trauma 1988;28:S16-S20.

Wiser E, Cheek R, Britt L: Gunshot wounds of the suprarenal abdominal aorta.
Am Surg 1976;42:430-435.

Witte C, Smith C: Single anastomosis vein bypass for subclavian vein obstruc-
tion. Arch Surg 1966;93:664-666.

Wixon C, PhilpottJ, Bogey WM, Powell C: Duplex-directed thrombin injection
as a method to treat femoral artery pseudoaneurysms. J Am Coll Surg
1998;187:464-466.

Wolf R, Berry RE: Transaxillary intra-aortic balloon tamponade in trauma.
J Vase Surg 1986;4:95-97.

Wolf Y, Reyna T, Schropp K, Harmel R: Arterial trauma of the upper extrem-
ity in children. J Trauma 1990;30:903-905.

Wolfel G, Moore EE, Cogbill TH: Severe thoracic and abdominal injuries asso-
ciated with lap-harness seatbelts. J Trauma 1984;24:166-167.

Wood J, Fabian TC, Mangiante E: Penetrating neck injuries: recommendations
for selective management. J Trauma 1989;29:602-605.

Wood M, Nykamp P: Traumatic arteriovenous fistula of the superior mesen-
teric vessels. J Trauma 1980;20:378.

Woodhall B, Nulsen F: Peripheral nerve wounds. In Bowers WF (ed): Surgery
of Trauma. Philadelphia, JB Lippincott Co, 1953.

Woodhurst W, Robertson W, Thompson G: Carotid injury due to intraoral
trauma: Case report and review of the literature. Neurosurgery 1980;6:559-
563.

WoodringJ, Fried A, Hatfield D, et al: Fractures of first and second ribs: Pre-
dictive value for arterial and bronchial injury. AJR Am J Roentgenol
1982;138:211-215.

Woodruff C: The cases of the explosive effect of modern small caliber bullets.
NYJMed 1898;67:593.

Woodson G, Kendrick B: Laryngeal paralysis as the presenting sign of aortic
trauma. Arch Otol Head Neck Surg 1989;115:1100-1102.

RE.qxd 4/16/04 3:19 PM Page 649

26 • RICH'S HISTORIC COLLECTION OF VASCULAR REFERENCES 649

Woolsey R: Aortic laceration after anterior spinal fusion. Surg Neurol
1986;25:267-268.

Wright CB, Swan KG: Hemodynamics of venous occlusion in the canine hindlimb.
Surgery 1973;73:141-146.

Wright CB, Swan KG: Hemodynamics of venous repair in the canine hind limb.
J Thorac Cardiovasc Surg 1973;65:195-199.

Wright CB, Hobson R: Hemodynamic effects of femoral occlusion in the sub-
human primate. Surgery 1974;75:453-460.

Wright CB, Hobson RW II, Swan KG, Rich NM: Extremity venous ligation:
Clinical and hemodynamic correlation. Am Surg 1975;41:203-208.

Wright CB, Hobson RW II: Prediction of intestinal viability using Doppler ultra-
sound techniques. Am J Surg 1975;129:642-645.

Wright CB, Hobson RW II, Giordano J, et al: Acute femoral venous occlusion:
Management by segmental venous replacement. J Cardiovasc Surg
1977;18:523-529.

Wright CB, Hiratzka L, Hobson RWII, et al: Management of vena caval injuries:
The Vietnam Vascular Registry review. J Cardiovasc Surg 1981;22:203-212.

Wright R, Edwards W: Manifestations and management of acute arterial injuries.
J Trauma 1973;463-468.

Wyatt D, Kellum CD, Joob A, Daniel T: Isolated injury of the proximal verte-
bral artery associated with blunt chest trauma. J Vase Surg 1986;4:196-198.

Yajko R, Trimble C: Arterial bullet embolism following abdominal gunshot
wounds. J Trauma 1974;14:200-211.

Yamada S, Kindt G, Youmans J: Carotid artery occlusion due to nonpenetrat-
ing trauma. J Trauma 1967;7:333-342.

Yamada T, Sato H, Seki M, et al: Successful salvage of aortoesophageal fistula
caused by a fish bone. Ann Thorac Surg 1996;61:1843-1845.

Yamaguchi Y, Matsumura F, Liang J, et al: Neutrophil elastase and oxygen
radicals enhance monocyte chemoattractant protein-expression after
ischemia/reperfusion in rat liver. Transplantation 1999;68:1459-1468.

Yao JST, Vanecko RM, Printen K, Shoemaker WC: Penetrating wounds of the
heart: A review of 80 cases. Ann Surg 1968;168:67-78.

Yao J, Suri R, Patt N, et al: An unusual subclavian artery injury. J Trauma
1970;10:176-180.

Yarbrough DR III, Grooms G, Flint L: Repair of two traumatic aneurysms of
the supraceliac abdominal aorta in a single patient. Surgery 1972;72:371-
377.

Yaw P, Van Beek A, Glover JL: Successful repair of a gunshot wound to the first
part of the superior mesenteric artery. J Trauma 1974;14:885.

Yeager RA, Hobson RW II, Lynch TG, et al: Popliteal and infrapopliteal arter-
ial injuries: Differential management and amputation rates. Am Surg
1984;50:155-158.

Yee L, Olcott E, Knudson M, Lim RC Jr: Extraluminal, transluminal, and obser-
vational treatment for vertebral artery injuries. J Trauma 1995;39:480-486.

Yellin A, Golan M, Klein E: Penetrating thoracic wounds caused by plastic bullets.
Thorac Cardiovasc Surg 1992;2:381.

Yellin AE, Shore E: Surgical management of arterial occlusion following per-
cutaneous femoral angiography. Surgery 1973;73:772-777.

Yellin AE, Lundell C, Finck E: Diagnosis and control of post-traumatic pelvic
hemorrhage. Arch Surg 1983;118:1378-1388.

Yelon J, Scalea T: Venous injuries of the lower extremities and pelvis: Repair
versus ligation. J Trauma 1992;33:532-538.

RE.qxd 4/16/04 3:19PM PageS50

650 VI • THE RICH REFERENCE COLLECTION

Yelon J, Barrett L, Evans J: Distal innominate artery transection and cervical
spine injury. J Trauma 1995;39:590-592.

Yeo M, DomanskisE, BartlettRH, Gazzaniga A: Penetrating injuries of the abdom-
inal aorta. Arch Surg 1974;108:839-844.

Yoder R, Merck D: Innocuous appearing stab wounds to the neck: Is explo-
ration always indicated? South MedJ 1969;62:113-114.

Yoshioka H, Seibel R, Pillai K, Luchette F: Shotgun wounds and pellet emboli:
Case reports and review of the literature. J Trauma 1995;39:596-601.

Yosowitz P, Hobson RWII, Rich NM: Iliac vein laceration caused by blunt trauma
to the pelvis. Am J Surg 1972;124:91-93.

Youkey J, Clagett GP, Rich NM, et al: Vascular trauma secondary to diagnostic
and therapeutic procedures: 1974 through 1982. Am J Surg 1983;146:788-
791.

Young J, Stallone R, Iverson L, et al: Surgical management of traumatic dis-
ruption of the descending aorta. West J Med 1989;150:662-664.

Young P: Following microdiskectomy: Laceration of the abdominal aorta and
vena cava. IMJ 1988;174:93-94.

Zabin A: Cholecystectomy complicated by hemorrhage from the inferior vena
cava. N YJ Med 1950;50:1500.

Zakharia AT: Cardiovascular and thoracic battle injuries in the Lebanon war.
J Thorac Cardiovasc Surg 1985;89:723.

Zakharia A: Thoracic battle injuries in the Lebanon war: Review of the early
operative approach in 1,992 patients. Ann Thorac Surg 1985;3:209-213.

Zehnder M: Delayed posttraumatic rupture of the aorta in a young healthy
individual after closed injury: Mechanical-etiological considerations. Angi-
ology 1956;7:252.

Zehntner MK, Petropoulos P, Burch HB: Arterial injuries associated with frac-
tures of the extremities. Proc of the First Mediterranean Congress of Angi-
ology 1988;223-226.

Zeiger M, Clark DE, Morton JR: Reappraisal of surgical treatment of traumatic
transection of the thoracic aorta. J Cardiovasc Surg 1990;31:607-610.

Zelenock G, Kazmers A, Whitehouse W: Extracranial internal carotid artery
dissections. Arch Surg 1982;117:425-432.

Zelenock G, Kazmers A, Graham L, et al: Nonpenetrating subclavian artery
injuries. Arch Surg 1985;120:685-692.

Zellweger R, Ayala A, Zhu X, et al: A novel nonanticoagulant heparin improves
splenocyte and peritoneal macrophage immune function after trauma:
Hemorrhage and resuscitation. J Surg Res 1995;59:211-218.

Zhou M, Wang P, Chaudry IH: Endothelial nitric oxide synthase is downregu-
lated during hyperdynamic sepsis. Biochim Biophys Acta 1997;1335:182-
190.

Zilkha A: Traumatic occlusion of the internal carotid artery. Radiology 1970;
97:543-548.

Ziperman H: Acute arterial injuries in the Korean War: A statistical study. Ann
Surg 1954;139:1-8.

Zuckerman J, Flugstad D, Teitz C, King H: Axillary artery injury as a compli-
cation of proximal humeral fractures. Clin Orthop 1984;189:234-237.

Zweifach S, Hargens A, Evans K, et al: Skeletal muscle necrosis in pressurized
compartments associated with hemorrhagic hypotension. J Trauma 1980;
20:941-947.

INDEX. qxd 4/16/04 3:18PM Page 651

INDEX

Abdominal aorta, 340

Abdominal aortic aneurysm (AAA), 207. See also

Endovascular grafts.
Abdominal aortic injury, 200
Abdominal compartment syndrome, 111, 444-445,

445-446, 448, 453
Abdominal injuries, 299-313

celiac trunk, 304-305

clinical presentation, 300-301

complications, 312

Huey Long rule, 310

incidence, 300

inframesocolic area (zone 1), 307-309

infrarenal abdominal aorta, 307-309

kidney compartment syndrome, 310

pathophysiology, 300

renal artery, 307, 309-312

renal revascularization, 310-311

superior mesenteric artery, 305-307

supramesocolic area (zone 1), 301-307

suprarenal abdominal aorta, 301-304

upper lateral retroperitoneum (zone 2), 302-312

zones, 371
Abdominal vascular injuries, 149-153, 200-201
Abductor pollicis longus muscle, 373f
Access, control and repair techniques, 137-164. See also

Surgical techniques.
Ace pressure monitor, 449
Acidosis, 105

Activated partial thromboplastin time (APTT), 108
Active core rewarming, 106
Active external rewarming, 106
Acute arterial insufficiency, 126
Acute arteriovenous fistula, 229
Acute lung injury (ALI), 108, 109
Acute respiratory distress syndrome (ARDS), 79,

109
Adenosine triphosphate (ATP), 75
Advanced trauma life support (ATLS) guidelines,

117
Aeneid (Virgil), 252
Afghanistan War, 27t
Air hammer, 54

Algorithms

DVT, 534f

extremity vascular injury, 129f

penetrating extremity injuries, 93f
ALI, 108, 109
Allopurinol, 78, 453
Amputation

axillary artery injury, 367

brachial artery injury, 371

combat extremity arterial injuries, 405t

combined extremity injuries, 406, 412-414

common femoral artery injury, 379

extremity vascular injury, 358

ligation of femoral arteries, 1 70

mangled lower extremity, 387

profunda femoral artery injury, 379

subclavian artery injury, 363

superficial femoral artery injury, 380
Anastomosis, 159-161
Anatomy. See Surgical anatomy.

Ancillary tests, 119-121. See also Imaging techniques.
Anderson, John T, 113
Anesthesia, 104
AneuRx grafts, 209
Aneurysmal abscess, 423
Angio-Seal device, 432, 432f
Angiogram /angiography

AV fistula, 465f, 470f, 474f, 483f, 484f, 498f

complications, 51t

contrast media-related risks, 181

CTA. SeeCT/CTK.

false aneurysm, 61f, 510f, 512f, 513f

findings, 184-192

follow-up angiogram, 60f

follow-up femoral angiogram, 62f

gold standard, as, 102, 182

gunshot wound (chest), 68f, 214f

iatrogenic AVF, 218f

iliac vessel injury, 342f, 344

indications/contraindications, 180-182

intra-arterial metallic fragment, 65f

MRA. S^MRA.

occlusion (right common iliac artery), 342f

651

INDEX. qxd 4/16/04 3:18PM Page 652

652 INDEX

Angiogram /angiography (Continued)

PE, 531

pelvis, 202

penetrating cervical injuries, 231-232

technical complications, 181-182
Angiographic catheter complications, 51t
Angiographically placed stents, 348-349
Anterior circumflex humeral artery, 364f
Anterior spinal artery, 448
Anterior spinal artery syndrome, 448
Anterior tibial artery, 381f, 382
Anterior tibial recurrent artery, 381f
Anterior ulnar recurrent artery, 372f
Anterolateral thoracotomy, 146, 147, 292
Anteroposterior chest radiograph, 255
Antibiotics, 110
Anticoagulation, 198
Antiplatelet therapy, 198
Antyllus, 499

Aortic compression device, 303f
Aortic occlusion, 292
Aortography

arch, 196f

blunt thoracic injury, 271

deficiencies, 271

pelvic, 202

"pullout" abdominal, 312

subtraction, 257f
API, 118-119
APTT, 108

Arch aortography, 196f
Archigenes, 5
ARDS, 79, 109
Arm, 447

Arm injury, 202-203

Armed Forces. See Military vascular trauma experience.
Arterial aneurysms, 502. See also Traumatic false

aneurysms.
Arterial closure devices, 431-435
Arterial injury

blunt, 103

hard/soft signs, lOOt

types, lOlf
Arterial pressure index (API), 118-119
Arterialization, 477
Arteriogram/arteriography

AV fistula, 472f, 473f, 474f, 494f, 498f

axillary artery injury, 365

bleeding (right hepatic artery), 194f

calf, 205

coil occlusion, 193f

combined extremity injuries, 407, 408f

common femoral artery injury, 377

completion, 162, 398, 411f, 416

contrast, 127, 132

elbow, 194f

external carotid artery, 198

extremity vascular injuries, 356

ICA injury, 198f

indications, 120t

intraoperative, 408f, 417

nonsuture anastomsis, 59f

Arteriogram/arteriography (Continued)

pelvis, 202

penetrating thoracic injury, 255-256

popliteal/ tibial artery injury, 383

posterior knee dislocation, 396

profunda femoral artery injury, 377

pseudoaneurysm (subclavian artery), 21 7f

vascular injury repair, 41 If
Arteriovenous (AV) fistula, 190f, 458-499

Branham-Nicoladoni sign, 478, 480

cardiac enlargement, 481, 482f, 484

clinical features, 480-481

clinical pathology, 478-480

diagnostic considerations, 481-484

edema, 479f

etiology, 470-475

follow-up, 497-498

historical overview, 458-461

incidence, 461-470

Korean conflict, 468t, 495t

Location, 465t, 466f, 467t, 468t, 469t

oscillometric studies, 493t

pathophysiology, 475-478

pressure flow, 477-478

pulsating venous lakes, 479f

results, 488-497

spontaneous cure, 486-488

surgical treatment, 484-486

types, 464f

vein transplantation, 492t

Vietnam Vascular Registry, 464t, 465t, 469t, 47lt,
495t, 496t, 497

World War II, 490t
Artery injury, 371-374
Artery of Adamkiewicz, 200-201
Ascending aorta injury, 262-263
Ascending lumbar vein, 3l7f
Ascending pharyngeal artery, 226f
Asensio, Juan A., 339
Asthma, 181
Athletic injuries, 53
ATLS guidelines, 117
ATP, 75
ATP-MgCl 2 , 80
Autogenous conduits, 162
Auto transfusion, 105

AV fistula. See Arteriovenous (AV) fistula.
Axillary artery, 365f
Axillary artery injuries, 148, 364-367
Axillary artery laceration with pseudoaneurysm, 357f
Axillary subclavian artery, 210f
Axillary vein, 364, 365f
Azygos vein injury, 147-148, 264

Babcock clamps, 322, 322f

Bailout procedure, 168, 169

Balkan Wars, 13-14, 488

Ballistics, 55-56

Balloon catheter tamponade, 140, 170, I7lf

Balloon occlusion, 200

Baseball players, 53

INDEX. qxd 4/16/04 3:18PM Page 653

INDEX

653

Basilar artery, 226f

Basilic vein, 368f

BCVL See Blunt cervical vascular trauma.

BCVI grading scale, 246, 247t

Bee de corbin, 6f

Beck's triad, 444

Below the knee medial incision, 156f

Bibliography, 537-649

Bicipital aponeurosis, 373f

Biffl, Walter L., 241

Bifurcation, 317, 320

Bilateral hypogastric angiography, 202

Blaisdell, R William, 113

Bleeding/bleeding control. See also

Hemorrhage/hemorrhage control.

BCVIs, 248

blood transfusion, 108

iliac vessel injury, 347-348

postoperative phase, 111

primary survey, 99

quantification of blood loss, 99t
Blood transfusion

autotransfusion, 105

complications, 108, 109b

perioperative care, 105

postoperative phase, 107
Blue toes, 437

Blunt abdominal vascular injuries, 102
Blunt arterial injuries, 103
Blunt cervical vascular trauma, 241-250

anatomic considerations, 242

clinical presentation, 244

diagnostic evaluation, 246

incidence, 245

injury grading, 246

mechanism of injury, 242-243

pathophysiology, 243

patient at risk, 245-246

screening, 245

summary and guidelines, 249-250

treatment/ outcome, 2246-249
Blunt thoracic aortic injury (BTAI). See Blunt thoracic

vascular trauma.
Blunt thoracic vascular trauma, 269-283

aortogram, 271-272

chest x-ray, 272-273

clamp-and-sew technique, 277-278

CT, 273-275

demographics/pattern of injury, 270-271

diagnosis, 271-276

DPL, 276

exposure, 279t

innominate artery, 278-279

preoperative management, 276-277

presentation, 271

primary repair vs. prosthetic graft, 278

pulmonary artery/vein, 280

shunt techniques, 278

subclavian artery, 279-280

surgical technique, 277-278

TRR, 275-276

vena cava, 280

Blunt trauma

cervical injuries, 241-250

concomitant injuries, 103-104

mechanism of injury, 53

thoracic injuries, 269-283
Bogota bag, 453
Boyden, Allen M., 17
Brachial artery, 367-368
Brachial artery injuries, 148-149, 182f, 202-203,

367-371
Brachialis muscle, 368f, 373f
Brachiocephalic artery, 359f
Brachiocephalic vessel injury, 130-132, 199-200
Brachioradialis muscle, 373f
Bradley, Kevin M., 315
Branham-Nicoladoni sign, 478, 480
BTAI, 269-283. See also Blunt thoracic vascular trauma.
Buckman, Robert R, Jr., 315
Bulldog clamps, 323
Bullet embolism, 119
Burch,JonM., 241
Butterfly fracture, 343

CABG, 294f

Calcium replacement, 108

Calf compartment syndrome, 385, 446

Calf injury, 205

Cannulation of large veins, 99

Cannulation of right subclavian vein, 435

Carbon dioxide, 181

Cardiac compressions, 292

Cardiac enlargement, 481, 482f, 484

Cardiac manipulation, 292

Cardiac septal injuries, 294-295

Cardiac trauma. See Wounds of the heart.

Cardiac valvular injury, 295

Cardiopulmonary bypass, 296

Carotid bulb, 225

Carotid/internal jugular vein fistula, 436f

Carotid sheath, 227f

Catheter-based angiography, 182. See also

Angiogram/angiography.
Cattell-Braasch maneuver, 152, 153f
Causalgia, 375-376
Caval bifurcation zone, 317, 320
Caval wounds. See Inferior vena cava injuries.
Cayne, NealS., 207
CD11/CD18, 76
Celiac artery, 340f
Celiac trunk injury, 304-305
Celsus, 5

Central venous access, 435
Cephalic vein, 368f
Cephalosporin, 104
Cerebral vasospasm, 229
Cervical injuries

blunt trauma, 241-250. See also Blunt cervical
vascular trauma.

neck injuries. See Neck injuries.

penetrating injuries, 223-240. See also Penetrating
cervical vascular injuries.

INDEX. qxd 4/16/04 3:18PM Page 654

654 INDEX

CFA, 204, 376

Chaudry, Irshad H., 73

Chest injuries, 146-148

Chest radiography, 255t, 257-258f

Chest tube sizes, 254t

Chest x-ray, 272-273

Chronic venous insufficiency, 47f

Circle of Willis, 225, 228f

Circumflex nerve, 365f

Citrate intoxication, 108

Civilian penetrating trauma, 115

Clamp-and-sew technique, 277-278

Clamping

cross, 296

innominate artery/vein, 261

IVC injuries, 322-323

surgical technique, 151, 154

walking the clamps, 154
Classification of injury, 114
cNOS, 78

Coagulation monitoring, 107-108
Cocaine, 425-426
Coil blockade, 202
Coil embolization, 193, 208
Coil occlusion, 193, 202
Coimbra, Raul, 97
Collagen plug, 432
Color flow duplex imaging. See Duplex

ultrasonography.
Colorectal operations, 437

Combined Kocher and Cattell-Brassch maneuver, 153f
Combined Palmaz stent/ ePTFE graft, 209, 211f, 214f,

21 7f, 218f
Combined vascular/ skeletal extremity trauma,
404-414

amputation, 405t, 412-414

diagnosis, 406-408

epidemiology/prognostic factors, 404-406

fracture management, 412

mechanism of injury, 406

treatment, 408-412
Common bile duct, 328f
Common carotid artery, 226f, 227f, 435f
Common femoral artery (CFA), 204, 376
Common femoral artery injury, 376-379
Common iliac veins, 340
Common interosseous artery, 373f
Compartment hypertension, 417
Compartment syndrome, 443-455

abdomen, 448

abdominal, 111, 444-445, 445-446, 448, 453

arm, 447

calf, 446

diagnosis, 448

diabetes, 446

extremity, 375, 385, 450-454

extremity compartment measurement, 449

hand, 447

laboratory evaluation, 450

lower extremity, 385

noninvasive assessment, 449-450

pathophysiology, 116, 117, 450

Compartment syndrome (Continued)

pericardial, 444

pericardium, 448

postoperative phase, 111-112

presentation, 445-446

prophylactic fasciotomy, 133

spinal, 444

spinal cord, 448

systemic diseases, 446

thigh, 446

treatment, 450-454

upper extremity, 375
Completion arteriography, 162, 398, 411f, 416. See also

Arteriogram/arteriography.
Complex repairs, 170
Complications

abdominal injuries, 312

angiographic procedures, 51t

angiography, 181-182

autogenous venous grafts, 45

blood transfusion, 108, 109b

elective operative procedures, 50t

extremity revascularization, 129-130

iliac vessel injury, 349-350

incidence, 51t

passive rewarming, 106

thromboembolic, 525-535. See also Thromboembolic
complications.
Computed tomography/computed tomographic

angiography. See CT/CTA.
Concomitant blunt thoracic/abdominal trauma, 103
Concomitant injuries, 103-104
Conduit occlusion, 193
Conklin, Lori D., 251
Constitutive NOS (cNOS), 78
Continuous anastomosis, 160
Contrast arteriography, 127, 132. See also

Arteriography.
Contrast media-related risks, 181
Contusion, 54f

Coracobrachialis muscle, 368f
Coronary artery bypass grafting (CABG) , 294f
Coronary artery injuries, 293-294
Coronary vein, 328f

Corvita endovascular graft, 209f, 211-212
Costocervical trunk, 200, 359f, 360f
Coverage, 163
Covered stents, 195
Crafoord clamps, 323
Cragg Endopro, 209f
Crawford, E. Stanley, 439
Croatia, 27t, 405t
Cross clamping, 296
Cross-matched blood, 105
Crutches, 53
Cryoprecipitate, 106
Crystalloids, 105
CT angiography. See CT/CTA.
CT/CTA, 182-184

arterial injury, 183f

BCVIs, 246

BTAI, 273-275

INDEX. qxd 4/16/04 3:18PM Page 655

INDEX

655

CT/CTA (Continued)
effectiveness, 131-132
extremity vascular trauma, 356
hepatic hilar arterial injury, 197f
iliac vessel injury, 343-344
laceration of liver, 194f
PE, 531, 532f

penetrating cervical injury, 232-233
penetrating thoracic injury, 256
radial and ulnar artery injury, 373
renal artery, 310
retroperitoneal hematoma, 432f

Cyclic hyper-resuscitation, 142

Dacron graft. SsePTFE (Dacron) graft.
Dacron substitute conduits, 162
Damage control, 165-176

acidosis, 168

coagulopathy, 168

historical overview, 166, 167t

hypothermia, 167-168

initial operation, 168-169

penetrating thoracic injury, 259-260

perioperative care, 104-105

phases, 168-170

physiologic envelope, 167-168

planned reoperation, 169, 173-174

postoperative limb ischemia, 172-173

repair, 170-171

resuscitation, 169

surgery, 157

temporary shunts, 171-172
De Takats, Geza, 14, 15f
Dead space, 184

DeBakey, Michael E., I7f, 18, 59, 443
Decompression, 451-453
Deep femoral artery, 377f
Deep mattress sutures, 293
Deep radial nerve, 373f
Deep venous thrombosis (DVT) . See also
Thromboembolic complications.

algorithm, 534f

diagnosis, 530

heparin, 531

iliac vessel injury, 350
Deferoxamine, 453
Demetriades, Demetrios, 339
Descending genicular artery, 377f, 381f
Descending hypoglossal nerve, 227f
Descending thoracic aortic injury, 263
Dextran, 388

Diabetes, compartment syndrome, 446
Diagnosis of vascular trauma, 113-14. See also Imaging
techniques.

ancillary tests, 119-122

classification, 114

compartment syndrome, 116-117

diagnosis, 117-122

hard/ soft signs, 118-119

history, 117-118

ischemia, 116

Diagnosis of vascular trauma (Continued)

mechanism, 115-116

pathophysiology, 114-117

physical examination, 118

reperfusion injury, 116
Diagnostic imaging. See Imaging techniques.
Diagnostic peritoneal lavage (DPL), 276
Diaphragmatic aorta, 301, 302f
DIC, 108

Die Chirgurie der Blutgefasse und des Herzens (Jeger), 16
Digital subtraction angiography, 271-272
Digital thoracotomy, 290
Direct balloon occlusion, 199
Dislocation of knee, 52-53

Disseminated intravascular coagulation (DIC), 108
Distal brachial artery injury, 149
Distal renal artery, 309
Distal superficial femoral artery, 155
Distal superficial femoral artery injury, 115f
Djanelidze, Yustin, 252
DopplerAPI, 127-128

Dorsal cutaneous branch ulnar nerve, 373f
Dorsal interosseous artery, 372f
Dorsal scapular artery, 359f, 360f
Double Pringle maneuver, 153
DPL, 276

Duett device, 433, 433f
Dum-dum bullet, 56
Duplex ultrasonography, 120, 121

axillary vein valve transfer, 64f

BCVIs, 246

brachial artery injury, 182f

cardiac trauma, 290

combined extremity injuries, 408

DVT, 530, 531f, 533t

effectiveness, 128-129, 131, 133

penetrating cervical injury, 232

popliteal/ tibial artery injury 382

venous injuries (lower extremity), 388

venous injury, 401, 404
DVT. See Deep venous thrombosis (DVT).

Early ALI/ARDS, 109

Early direct vascular reconstruction, 7-13

Eber's papyrus, 5

EC thoracotomy, 100, 254, 290

Echocardiography, 290, 295

Edema

AV fistula, 479f

incidence, 45t
Elbow dislocation, 410f
Elective operative procedures, vascular injury,

50t
Elliott, David C, 269
Embolization, 193-195

categories, 193

circumflex femoral arteries, 205

coil, 193, 208

empirical, 201

gelfoam, 194f

ICA injury, 196

INDEX. qxd 4/16/04 3:18PM Page 656

656 INDEX

Embolization (Continued)

iliac vessel injury, 349f

lumbar artery injury, 200, 201

pelvic injury, 201, 202

upper extremity injury, 203

vertebral artery injury, 198-199
Emergency center (EC) thoracotomy, 100, 254,

294
Empirical embolization, 201
End-to-end repair, 160-161

Endoaneurysmorrhaphy, 500, 501f, 515f, 516f, 518t
Endothelial and neuronal NOS, 78
Endovascular aortic aneurysm repair, 439-440
Endovascular grafts, 207-220

background, 208-211

lesions, location, characteristics, 210t

Montefiore experience, 211-218

types of devices, 209
Endovascular interventions, 192-196, 207-220

embolization, 193-195. See also Embolization.

grafts, 207-220. See also Traumatic vascular lesions.

stent/ stent grafts, 195-196

temporary hemostasis, 192

traumatic vascular lesions, 207-220

vascular bed occlusion, 195
Endovascular stent grafts, 199
Endovascular stenting, 256-259
ePTFE graft, 209, 211f, 214f, 2l7f, 218f
Esmarch, Freidrich van, 6
Etomidate, 104
Expanded PTFE (ePTFE) graft, 209, 211f, 214f, 2l7f,

218f
Exploratory laparotomy, 103
Exposure. See Incisions.
Extended Kocher maneuver, 152
Extensive Kocher maneuver, 302, 307
External carotid artery, 225, 226f
External carotid artery injury, 198
External compression, 54f
External iliac artery, 340, 377f
External iliac vein, 31 7f
Extra-anatomic bypass, 398, 424
Extravasation, 184, 185f

Extremity compartment measurements, 449
Extremity compartment syndrome, 111-112,

450-453
Extremity injuries, 78-79, 101-106

algorithm, 129f

diagnosis, 126-130

evaluation (flowchart), 122f

fractures, 103b

initial care, 102-103

lower extremity. See Lower extremity.

mangled extremities, 404. See also Combined
vascular/skeletal extremity trauma.

revascularization, 129-130

upper extremity. See Upper extremity.

vascular trauma. See Extremity vascular trauma.
Extremity revascularization, 129-130
Extremity vascular trauma, 353-389

axillary artery injuries, 364-367

brachial artery injuries, 367-371

Extremity vascular trauma (Continued)
clinical presentation, 355

compartment syndrome (upper extremity), 375
diagnosis, 355-356
hard/ soft signs, 356t
lower extremity vascular injuries, 376-389. See also

Lower extremity vascular injuries,
management, 359t
nonoperative management, 356-357
operative management, 357-359
post-traumatic causalgia, 375-376
radial/ulnar artery injury, 371-374
subclavian artery injuries, 359-364
venous injuries (upper extremity), 374-375

Facial artery, 226f

Failed repair of arterial injury, 416-417

False aneurysms. See Traumatic false aneurysms.

Farrier's (veterinarian's) stitch, 8f

Fasciotomy

combined extremity injuries, 412

compartment injury of upper extremity, 375

compartment syndrome, 444, 450-451

extremity vascular injury, 358

iliac vessel injury, 348

popliteal artery injury, 399

prophylactic, 130, 133

when needed, 163, 417
Feliciano, David V., 299
Femoral access site complications, 182
Femoral arteries, 204-205
Femoral artery, 21 Of
Femoral nerve, 376
Femoral-to-fe moral artery bypass, 424
Fentanyl, 104
FFP, 106

Flexor carpi radialis muscle, 373f
Flexor carpi radialis tendon, 373f
Flexor carpi ulnaris muscle, 373f, 44 7f
Flexor digitorum profundus muscle, 373f, 447f
Flexor digitorum sublimis muscle, 373f, 44 7f
Flexor digitorum superficialis tendons, 373f
Flexor pollicis longus muscle, 373f
Fogarty balloon catheter, 141, 157, 158b, 440
Fogarty catheterization, 425
Foley catheter balloon tamponade, 347f
Follow-up, 58-59. .SVe Vietnam Vascular Registry.
Follow-up angiogram, 60f
Follow-up femoral angiogram, 62f
Forearm, 447

Foreign body embolism, 265
Four-compartment decompression, 451f
Four-compartment fasciotomy, 41 2
Fracture, 103b
Fractures, 52
French sheaths, 428
Fresh frozen plasma (FFP), 106
Fresh fungus vegetations, 423
Frykberg, Eric R., 393
Fullen zone I injuries, 301, 306
Fullen zone II injuries, 301, 306

INDEX. qxd 4/16/04 3:18PM Page 657

INDEX

657

Gadolinium, 181
Galen, 5, 286
Garcia, Priscilla, 443
Gargiulo, Nicholas J., Ill, 207
Gelfoam

pelvic injury, 202

upper extremity injury, 202

vascular bed occlusion, 195
Gelfoam pledget embolization, 1943f
Gerota's fascia, 310, 448
Gluteal compartment syndrome, 446
Gott shunt, 278
Graft/grafting

Corvita stent graft, 209f, 211-212

endovascular grafts, 207-220

ePTFE graft, 209, 211f, 214f, 2l7f, 218f

interposition grafting, 310

IVC injury, 325, 326f

new devices, 209,212

patch grafting, 414

portal vein, 335f

prosthetic grafts, 414-415

PTFE graft. SeePTFE (Dacron) graft.

stent grafts. See Stent/ stent grafts.

substitute conduit, 161-162

vascular grafts, 414-416

vein graft, 209

wall graft, 196f, 211, 212
Granchi, Thomas S., 443
Grenada, 57

Groin injury, 154-155, 203-204
Gulf War, 57
Gunshot wound

abdominal aorta injury, 470f

ballistics, 55-56

chest, 68f, 214f, 215f

etiology, 38t, 39t

iliac vessel injury, 341 1

infrarenal abdominal aorta, 308

IVC injury, 318

location, 38t

minimal injury, 89t

neck, 233f, 238f

right media knee, 356f

thrombosis of superficial femoral artery, 191f
Gustilo III-C complex extremity crush injury, 413f

Haiti, 57
Hand, 447
Hard signs

arterial injury, lOOt

combined extremity injuries, 407

knee dislocation, 397t

vascular injury, 118-119, 356t
Heart. See Wounds of the heart.
Heliodorus, 5
Hemodilution, 168

Hemorrhage/hemorrhage control. See also
Bleeding/bleeding control.

cardiac trauma, 292-293

common femoral artery injury, 377

Hemorrhage /hemorrhage control (Continued)

high-risk injuries, 143b

infrahepatic IVC, 321-323

pelvic fracture, 201

penetrating thoracic injury, 266

percutaneous vascular access, 430-431

popliteal artery injury, 398

profunda femoral artery injury, 377

retrohepatic IVC, 320, 323-324

superficial femoral artery injury, 380

suprarenal abdominal aorta, 303

surgery, 139-142
Henry principle of extensile exposure, 149, 155
Heparin

BCVIs, 249t

cocaine, vascular injury from, 426

DVT/PE, 528-529, 531, 533t

perioperative care, 105

surgery, 157-159

thromboembolic complications, 528-529, 531,
533t
Heparin-bonded Gott shunt, 278
Hepatic hilar arterial injury, 197f
Heroin, 422
Herophilus, 5

High-risk orthopedic injuries, 94-95
Hip arthroplasty, 440
Hip injury, 203-204
Hirshberg, Asher, 137, 165
Historic classification of vascular injury, 54-55
Historic observations

iatrogenic injury, 48-52

mechanism of injury, 52-54

site of injury, 47-48
Historical overview, 3-72. See also Military vascular
trauma experience.

AVF, 458-461

Balkan Wars, 13-14

ballistics, 55-56

bee de corbin, 6f

civilian vascular injuries, 28-37

damage control, 166, 167t

diagnosis of extremity injury, 126-127

early direct vascular reconstruction, 7-13

Egyptians (1600 B.C.), 5

false aneurysms, 499-502

first end-to-end anastomosis, 9f, 1 If

heart, wounds of, 285-286

Korean Conflict. See Korean Conflict.

Military vascular trauma experience, 13-28

minimal injuries, 87-88

Pare, 6

penetrating cervical injuries, 224

penetrating thoracic injuries, 253

popliteal artery injuries, 394-395

post-Vietnam military armed conflict, 27-28, 57

reflections and projections, 56-68

site of injury, 47-48

tourniquet, 6

thromboembolic complications, 525-526

20th century, 37-46

venous injuries, 399-400

INDEX. qxd 4/16/04 3:18PM Page 65 8

658 INDEX

Historical overview (Continued)

Vietnam War, 23-27. See also Vietnam War.

World War I. See World War I.

World War II. See World War II.
Historical reflections and projections, 56-58
History, 117-118
HMS Tonnant, 6, 224
Hoyt, David B., 97
Huey's Long rule, 310
Hughes, Carl, 21-23
Hunter, John, 6

Hunter, William, 6, 458, 459t, 478, 499
Hyperkalemia, 108
Hypocalcemia, 108
Hypogastric arteriography, 202
Hypogastric vein, 3l7f
Hypothermia, 106, 167-168
Hypothermic circulatory arrest, 324
Hypoxia, 74

IABP, 435-437

Iatrogenic vascular trauma, 203, 427-442

arterial closure devices, 431-435

central venous access, 435

colorectal procedures, 437

hemorrhage, 430-431

historical overview, 48-52

IABP, 435-437

intraoperative vascular injuries, 437-441

laparoscopic procedures, 437-438

neurosurgery, 440-441

orthopedic surgery, 440

pancreatobiliary procedures, 437

percutaneous vascular access, 428-437

pseudoaneurysms, 429-430

vascular/ endovascular surgery, 438
ICA, 225, 226f
ICA injuries, 196-198
ICAM-1, 75, 76
Ideal conduit, 57
Iliac arterial injuries, 345-346
Iliac artery, 21 Of
Iliac vascular injury, 154
Iliac venous injury, 346-347
Iliac vessel injury, 339-351

anatomy, 340-341

angiography, 344

arterial injuries, 345-346

bleeding control, 347

clinical presentation, 342

complications, 349-350

CT, 343-344

diagnostic investigations, 342-344

fasciotomy, 348

incidence/epidemiology, 341

interventional radiology, 348-349

mortality, 351

operative management, 344-348

perioperative management, 348-351

radiographic studies, 342-343

venous injuries, 346-347

/^(Horner), 252

Illicit street drugs, 421-426

cocaine, 425-426

direct arterial injection, 422-423

mycotic aneurysms, 423-424, 425

perivascular hematoma/abscess, 421-422

vascular reconstruction, 424

venous aneurysms, 425
Imaging techniques

alternate, 182-184

ancillary tests, 119-121

angiography. .See Angiography

Aortography. See Aortography.

arteriography. See Arteriography.

best practices, 125-134

chest radiography, 255t, 257-258f

CTA. SeeCT/CTA.

MRA. SeeMRA.

most important role, 181

TCD studies, 132

TEE, 275-276

ultrasound. See Duplex ultrasonography.

venogram/venography, 43f, 44f, 400, 404

x-rays, 119
Incisions, 140b

antecubital fosca, 51 7f

anterior tibial injury, 386f

AV fistula, 485

below the knee medial, 156f

brachial artery injury, 370f

cardiac trauma, 291-292

common feinoral artery, 378f

compartment syndrome, 447f, 452f

false aneurysms, 5l7f

midline laparotomy, 149

neck, 143-144

out-of-favor techniques, 143b

popliteal exposure, 384f

profunda femoral artery, 378, 378f

radial and ulnar artery injury, 374f

radial/ulnar arteries, 447f

subclavian artery injury, 361

thoracic vascular injuries, 256t

venous injuries, 401
Incomplete transection, 54f
Inducible NOS (iNOS), 78
Inferior gluteal artery, 377f
Inferior lateral genicular artery, 381f
Inferior medial genicular artery, 381f
Inferior mesenteric vein, 328f
Inferior ulnar collateral artery, 372f
Inferior vena cava injuries, 264, 316-327

exposure and control, 319-324

hemorrhage control, 321-324

initial assessment and inanagement, 319

patterns of injury, 318-319

postoperative inanagement, 325-326

repair, 324-325

surgical anatomy, 317-318
Inferior vena cava repair, 324-325
Infrarenal abdominal aorta, 307-309
Initial anesthesia, 104

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INDEX

659

Initial care

abdominal vascular injuries, 102

concomitant injuries, 103-104

extremity injuries, 102-103

general guidelines, 98-100

neck vascular injuries, 101

primary survey, 98-100

secondary survey, 100

thoracic vascular injuries, 101-102
Innominate vein/artery

blunt thoracic injuries, 278-279

penetrating cervical injuries, 233

penetrating thoracic injuries, 261-262

thoracic outlet injury, 146
iNOS, 78

Intercostal artery injury, 264
Interior carotid artery, 226f
Interior iliac artery, 377f
Interior jugular vein, 227f
Interior thoracic artery, 359f, 360f
Internal carotid artery (ICA), 225, 226f
Internal carotid artery (ICA) injuries, 196-198
Internal iliac artery, 340
Internal jugular vein, 435, 435f
Internal thoracic injury, 264
Interosseous artery, 372f
Interosseous recurrent artery, 372f
Interposition grafting, 310, 414
Interventional radiology, 180, 348. See also

Endovascular interventions; Surgical techniques;
Surgical treatment.
Intimal flaps, 190

Intra-aortic balloon pump (IABP), 435-437
Intra-arterial metallic fragment, 65f
Intraluminal balloon control of arteries, 208
Intraluminal filling defects, 187, 187f, 189
Intraluminal shunting, 399
Intraluminal shunts, 171
Intraluminal thrombus, 189-190
Intraoperative arteriogram, 417
Intraoperative monitoring, 104
Intraoperative vascular injuries, 437-441

colorectal procedures, 437

laparoscopic procedures, 437-438

neurosurgery, 441-442

orthopedic surgery, 440

pancreatobiliary procedures, 437

vascular/ endovascular surgery, 438-440
Intrapericardial inferior vena cava injury,

295-296
Intrathoracic inferior vena cava injury, 264
Intravascular stents, 208
Introducer sheath, 434f
I /R injury. .S^Ischemia-reperfusion injury.
Ischemia

defined, 74

extremity vascular injury, 360

five Ps, 74

iliac arterial injuries, 346

pathophysiology, 116

postoperative limb, 172-173

signs, 74

Ischemic preconditioning, 80
Ischemia-reperfusion injury, 73-84

comorbidities, 79

endothelial cells, 76

inflammatory mediators, 79

ischemic preconditioning, 80

leukocyte-endothelial cell interaction, 76-77

leukocytes, 75

modifying factors, 80

NO, 75, 78-79

pathophysiologic changes, 78f

pharmacologic adjuncts, 80

platelets, 77-78
Israel, 27t, 405t
Ivatury, Rao R., 223
IVC injuries. See Inferior vena cava injuries.

Jarrar, Doraid, 73
Jeger, Ernst, 16
Jerome of Brunswick, 5
Johansen, Kaj, 125
Johnston, Albert Sidney, 394

Ketamine, 104

Kidney compartment syndrome, 310

Knee arthroplasty, 440

Knee dislocation, 397-399

Knee injury, 205

Knudson, M. Margaret, 525

Kocher maneuver

combined Kocher and Cattell-Brassch maneuver,
153f

extended, 152

extensive, 302, 307

wide, 331
Korean Conflict

acute vascular trauma, 41 1

amputation, 405t

AV fistula, 461,462, 468t

carotid artery injury, 229t

importance of venous repair, 46

location of injuries, 36t

major vessel lesions, 495t

MASH, 23f

popliteal artery injury, 394, 395t

renewal of interest in repair, 40

surgical heritage, 18-23

venous injury, 399

Laceration, 54f

Lactic acidosis, 168

Laparoscopic surgery, 437-438

Laparotomy, 168, 444

LateARDS, 109

Lateral aortorrhaphy, 303

Lateral arteriorrhaphy, 159, 398

Lateral circumflex femoral artery, 377f

Lateral circumflex iliac vein, 155

Lateral repair, 170

INDEX. qxd 4/16/04 3:18PM Page 66

660

INDEX

Lateral superior genicular artery, 377f

Lateral thoracic artery, 364f

Lateral venorrhaphy/arteriorrhaphy, 159

Lateral venorrhaphy, 401

LDUH, 528-529, 533t

Lebanon, 27t, 395t

Ledgerwood, Anna M., 421

Left anterolateral thoracotomy, 292

Left common carotid artery, 262, 359f

Left common iliac dissection, 429f

Left common iliac vein, 340

Left gastric vein, 328f

Left posterolateral thoracotomy, 139

Left renal vein, 340f

Left-sided medial mobilization maneuver, 301-302,

302f, 303f
Left subclavian artery, 359f
Lemaire, Scott A., 251
Lepore, Michael R., Jr., 427

Lesions, 210. See also Traumatic vascular lesions.
Ligation, 170
Limb ischemia, 172-173
Lingual artery, 226f
LMWH, 529, 533t

Local vascular occluding devices, 159
Low-molecular-weight heparin (LMWH), 529, 533t
Lower extremity. See also Extremity injuries.

compartment syndrome, 385

fracture, 103b

mangled, 385-387

treatment/repair, 154-155, 203-206

vascular injuries, 376-389. See also Lower extremity
vascular injuries.

venous injuries, 387-390
Lower extremity compartment syndrome, 385
Lower extremity vascular injuries, 376-389

common femoral/profunda femoral arteries,
376-379

lower extremity compartment syndrome, 385

mangled lower extremity, 385-387

popliteal and tibial arteries, 381-385

superficial femoral artery, 379-381

venous injuries, 387-389
Lucas, Charles E., 421
Lumbar artery injuries, 200-201
Lumbar disk surgery, 441
Lumbar veins, 31 7f
Luminal dilatation, 187, 188f
Luminal filling defects, 187, 189, 189f
Luminal narrowing, 184, 186f

Magnetic resonance. SeeMR/MRA.

Mainlining, 422

"Management of Venous Injuries: Clinical and

Experimental Evaluation," 46f
Mangled extremities, 404. See also Combined

vascular/skeletal extremity trauma.
Mangled lower extremity, 385-387
MASH, 23f

Massive hemothorax, 254
MAST suits, 252, 253

Mathewson, Carleton, Jr., 66, 67f
Mattox, Kenneth L., 137, 443
Mattox maneuver, 151, 152f
Mechanical prophylactic devices, 528
Mechanical ventilation, 108-110
Mechanism of injury, 115-116

athletic injuries, 53

BCVIs, 242-243

blunt trauma, 53

children, 53

civilian trauma, 36t

combined extremity injuries, 406

crutches, 53

extremity vascular injury, 360

fractures, 52

historic observations, 52-54

popliteal artery injury, 115f

posterior dislocation of knee, 52-53

radiation, 53-54

vibratory tools, 54
Medial distal thigh femoral incision, 155
Median nerve, 365f, 368f, 373f
Median sternotomy, 145, 264, 292
Mediastinal traverse injuries, 264-265
Mesenteric vein, 329
Mesocaval shunting, 334
Metallic fragment, 65
Michael DeBakey International Military Surgeons

Award, l7f
Microvascular bleeding, 108
Middle colic vein, 328f
Midline laparotomy incision, 149
Midline looping, 152
Midshaft femur fracture, 41 If

Military antishock trousers (MAST suits), 252, 253
Military vascular trauma experience, 13-28

Afghanistan War, 27t

Balkan Wars, 13-14,488

Bosnia, 57

Croatia, 27t, 405t

Grenada, 57

Gulf War, 57

Haiti, 57

Ireland, 395t

Israel, 27t, 405t

Korean Conflict, 18-23. See also Korean Conflict.

Lebanon, 27t, 395t

Panama, 57

Serbo-Bulgarian Wars, 488

Somalia, 57

Vietnam, 23-27. See also Vietnam Vascular Registry;
Vietnam War.

WWI, 14-16. See also World War I.

WWII, 16-18. See also World War II.
Minimal vascular injuries, 85-96

defined, 85-87

high-risk orthopedic injuries, 94-95

historical overview, 87-88

natural history, 88-91

penetrating neck injuries, 92-94

penetrating proximity extremity trauma, 91-92
Misregistration artifacts, 189

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INDEX 661

Mobile army surgical hospital (MASH), 23f

Mobile wad, 447

Money, Samuel R., 427

Monoclonal antibodies, 80

Monson's zones, 101, 131, 230, 231f

Montefiore Medical Center (endovascular grafts),

211-218
Moore, Ernest E., 241
MR/MRA, 184

BCVIs, 246

penetrating cervical injuries, 233
Mural thrombus, 187
Murphy,JohnB.,9-12
Murray, James A., 339
Musculocutaneous nerve, 365f
Mycotic aneurysms, 423-424
Mycotic aneurysms of carotid vessels, 425
Myoglobinuria, 450

Narrowing, 184

ND, 75, 78-79, 104

Near-infrared spectroscopy (NIRS), 449

Neck injuries. See also Cervical injuries.

external carotid artery, 198

gunshot wounds, 233f, 238f

ICA injury, 196-198

initial care, 101

minimal injuries, 92-94

penetrating injuries, 92-94, 101

treatment/repair, 143-144, 196-200

vertebral artery, 198-199

zones, 230, 231f
Nephrectomy, 311
Nephrotoxicity, 181
Neurosurgery, 440-441
NF-kB, 76
Nifedipine, 184
99m Tc-MIBI, 450
NIRS, 449

Nitric oxide (ND), 75, 78-79, 104
Noninvasive physiologic vascular tests, 127-129
Nonsuture method of bridging arterial defects, 19

Obliterative endoaneurysmorrhaphy, 501f, 515f, 518t
Occipital artery, 226f
Occlusion, 191f

angiogram, 342f

balloon, 199, 200, 214f

coil, 193f, 202

conduit, 193

defined, 191

parenchymal, 193

temporary balloon, 192f, 197

tissue bed, 193

vascular bed, 195
Occlusion balloon, 214f
Ohki,Takao, 207
Omohyoid muscle, 227f

Operating procedures. See Surgical techniques.
Orthopedic injuries, 103b

Orthopedic surgery, 440
Oxyhemoglobin saturation, 449

acute arterial insufficiency, 126b

ischemia, 74
Packing, 170-171
Palmar carpal ligament, 373f
Palmaris longus tendon, 373f
Palmaz stent, 209, 21 If, 214f, 21 7f, 218f
Panama, 57

Pancreaticoduodenal veins, 328f
Pancreatobiliary operations, 437
Paraplegia, 263

Pare, Ambroise, 6, 56, 224, 286
Parenchymal disruptions, 195
Parenchymal occlusion, 193
Parietal pleura, 141

Partial thromboplastic time (PTT), 106
Particulate embolization, 199
PASGs, 277

Passive external rewarming, 106
Patch angioplasty, 162
Patch grafting, 414
Pathak, Abhijit S., 315
Pathophysiology, 114-117

abdominal injuries, 300

AV fistula, 475-478

BCVIs, 243

classification, 114

compartment syndrome, 116-117, 450

heart, wounds of, 288-289

ischemia, 116

mechanism, 115-116

reperfusion injury, 116

thromboembolic complications, 526
Patient history, 117-118
Patient positioning, 138-139
PE. See Pulmonary embolism.
PECAM-1, 75, 76
Pectoralis minor muscle, 368f
Pedicle vascular injury, 201
PEEP, 109

Pelvic aortography, 202
Pelvic binder, 343
Pelvic injuries, 149-153, 201-202
Penetrating aortic arch injuries, 263
Penetrating cervical vascular injuries, 223-240. See also
Neck injuries.

angiography, 231-232

carotid artery injuries, 233-236

color flow Doppler, 232

CTA, 232-233

historical overview, 224

incidence/etiology, 228

initial evaluation/management, 229-300

innominate/subclavian vessel injuries, 233, 235f

MRA, 233

pathology, 228-229

physical examination, 230-231

surgical anatomy, 224-228

INDEX. qxd 4/16/04 3:18PM Page 662

662 INDEX

Penetrating cervical vascular injuries (Continued)

treatment, 233-237

venous injuries, 237

vertebral artery injuries, 236-237

zones of neck, 230, 231f
Penetrating injuries

cervical injuries, 223-240

concomitant injuries, 104

thoracic injuries, 251-267
Penetrating mechanisms, 115

Penetrating proximity extremity trauma, 91-92, 93f
Penetrating thoracic vascular trauma, 251-267

ascending aorta, 262-263

azygos vein, 264

catheter arteriography, 255-256

chest radiography, 255t, 257-258f

CTA, 256

damage control, 259-260

descending thoracic aorta, 263

diagnostic studies, 255-256

EC thoracotomy, 254

emergency center management, 253-255

endovascular stenting, 256-259

foreign air embolism, 265

history, 253

incisions, 256t

initial examination, 253

innominate artery/vein, 261-262

internal thoracic/intercostal arteries, 264

intravenous access/fluid administration, 253-254

left common carotid artery, 262

mediastinal traverse injuries, 264-265

pericardiocentesis, 254

physical examination, 255t

postoperative management, 265-267

prehospital management, 252-253

preoperative considerations, 259

primary survey, 253-254

pulmonary artery/vein, 263-264

secondary survey, 254-255

subclavian artery/vein, 260-261, 262f

surgical repair, 259-260

systemic air embolism, 265, 266f

thoracic aorta, 262-263

thoracic duct injury, 265

thoracic inlet, 260-262

thoracic vena cava, 264

transverse aortic arch, 263

treatment options, 256-260

tube thoracostomy, 254
Perclose device, 434, 434f
Percutaneous vascular access, 428-437

arterial closure devices, 431-435

central venous access, 435

hemorrhage, 430-431

IABP, 435-437

pseudoaneurysms, 429-430
Pericardial compartment syndrome, 444, 445
Pericardiocentesis, 254, 290
Pericardiotomy, 254
Pericardium, 141, 448
Periconduit infections, 162

Perigraft infections, 162
Perioperative blood transfusion, 107
Perioperative care, 104-107

damage control, 106-107

hypothermia, 106

initial anesthesia, 104

intraoperative monitoring, 80-81

volume therapy, 105-106
Peripheral vascular trauma. See Extremity vascular

trauma.
Peripheral venous injuries, 400
Perivascular hematoma/access, 421-423
Permissive hypercapnia, 109
Peroneal artery, 382
PFA injury, 204-205
Phrenic artery, 340f
Phrenic nerve, 227f
Physical examination, 118

brachial artery injury, 369

brachiocephalic vessels, 132

penetrating cervical injuries, 230-231

penetrating thoracic injury, 255t

perivascular hematoma, 422

scapulothoracic dissociation, 363
Physiologic envelope, 167-168
Planned reoperation, 169, 173-174
"Pinky", 421, 422
Platelet function, 108
Platelets, 106
Platysma, 224

Pneumatic antishock garments (PASGs), 277
Pneumatic tourniquet, 155
Pneumonectomy, 260
Popliteal artery, 381f, 387

Popliteal artery and branch injuries, 381-385,
394-399

diagnostic issues, 395-397

history/ epidemiology, 394-395

incision/access, 155, 156f

mechanism of injury, 115f

military experience, 395t

nonoperative observation, 399

posterior knee dislocation, 397-398

surgical adjuncts, 398

treatment, 205-206, 398-399
Porcine xenograft/homograft, 163
Portal vein, 327-328
Portal vein injuries, 327-335

associated injuries, 329-330

exposure/initial vascular control, 330-332

initial assessment and management, 330

multiple vascular injuries, 332

pancreatic division, 332

patterns of injury, 329-330

portal vein, 327-328

portal vein ligation, 333-334

postoperative management, 334-335

retropancreatic exposure, 332

retropancreatic wounds, 333

splenic vein, 328-329

stable hematoma, 330-331

superior mesenteric vein, 328-329

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INDEX 663

Portal vein injuries (Continued)

suprapancreatic exposure, 331-332

suprapancreatic wounds, 333

surgical anatomy, 327-329

treatment, 333-334
Portal vein ligation, 333-334, 335f
Portocaval shunting, 334

Post-Vietnam military armed conflict, 27-28, 57
Positioning, 138-139

Positive end-expiratory pressure (PEEP), 109
Posterior cerebral artery, 226f
Posterior circumflex humeral artery, 364f
Posterior communicating artery, 226f
Posterior dislocation of knee, 52-53
Posterior intrapericardial inferior vena cava, 296f
Posterior knee dislocation, 397-399
Posterior tibial artery, 381f, 382
Posterior ulnar recurrent artery, 372f
Postoperative limb ischemia, 172-173
Postoperative priorities, 107-112

antibiotics, 110

assessment/determination of take back,
110-112

blood transfusion, 107, 108, 109b

coagulation monitoring, 107-108

hemodynamic monitoring, 107

mechanical ventilation, 108-110
Preconditioning, 80
Prednisone, 181
Primary survey, 98-100
Principle of extensile exposure, 149, 155
Pringle maneuver, 153, 324
Procoagulant activity, 108
Profunda femoral artery, 204-205, 376
Profunda femoral artery injury, 376-379
Pronator teres muscle, 373f
Prone ventilation, 110
Prophylactic fasciotomy, 130, 133
Prophylactic inferior vena cava filters, 350
Prophylactic vena cava filters, 529-530, 533t
Prosthetic grafts, 414-415
Prosthetic vascular graft, 266
Prothrombin time (PT), 108
Proximal control, 140
Proximal embolization, 199
Proximal renal arteries, 307
Pseudoaneurysms, 429-430
PT, 108
PTFE (Dacron) graft

BTAI, 278, 279

common femoral artery injury, 378

effectiveness, 415

iliac arterial injuries, 345

infrarenal abdominal aorta, 308

profunda femoral artery injury, 378

substitute conduit, 161, 162

superficial femoral artery injury, 380

suprarenal abdominal aorta, 304

vascular reconstruction, 424
PTT, 106

Pullout abdominal aortogram, 312
Pulmonary artery/vein injury, 263-264

Pulmonary embolism. See also Thromboembolic
complications.

diagnosis, 531

heparin, 531

IVC injuries, 326
Pyloric vein, 328f

Quadrangulation method, 13f

Radial and ulnar artery injury, 371-374
Radial artery, 371, 372f, 373f
Radial collateral artery, 372f
Radial nerve, 365f, 368f, 373f
Radial recurrent artery, 372f

Repair principles/techniques, 156-163. See also Surgical
treatment.

ligation, 170

packing, 170-171

step 1 (control), 156

step 2 (explore the injury), 156

step 3 (enter the hematoma), 156-157

step 4 (vascular damage control), 157

step 5 (debridement), 157

step 6 (type of repair required), 157

step 7 (stay sutures), 157

step 8 (Fogarty catheters), 157, 158b

step 9 (heparin), 157-159

step 10 (local vascular occluding devices), 159

step 11a (simple repair techniques), 159-160

step lib (end-to-end repair), 160-161

step lie (substitute conduit), 161-162

step lid (patch angioplasty), 162

step 12 (flush), 162

step 13 (complete suture line/clamp removal), 162

step 14 (distal circulation), 163-164

step 15 (fasciotomy), 163

step 16 (coverage), 163
Radiation, 53-54

Radical hepatic mobilization, 321
Radiographic studies. See Imaging techniques.
Rapid infusion systems, 99
References, 537-649
Renal artery, 201
Renal artery injury, 307, 309-312
Renal revascularization, 310-311
Reperfusion injury, 116. See also Ischemia-reper fusion

injury.
Resuscitation, 99, 169
Resuscitative thoracotomy, 147

Retrohepatic vena caval injuries, 321, 323-324, 325
Retropancreatic confluence zone, 327
Retroperitoneal hematoma, 432f
Retroperitoneum, 431
Rewarming, 106
Rice, David, 285
Rich, Norman M., 3, 457
Right common carotid artery, 359f
Right common iliac artery, 340, 377f
Right common iliac vein, 340
Right decubitus position, 138f

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664 INDEX

Right gastroepiploic vein, 328f
Rob, Charles G., 2 If, 60f
Rodriguez, Aurelio, 269
Rufus of Ephesus, 5, 6

Sandbags, 182

Scalenus anticus muscle, 359f, 360f

Scalenus medius muscle, 359f, 360f

Scapulothoracic dissociation, 191f, 363-364

Scintigraphy, 450

Sclafani, Salvatore J. A., 179

Scoliosis, 441

Scott, Bradford G., 165

Screw tourniquet, 6

Secondary survey, 100

Seeley, Sam, 23

Segmental veins, 3l7f

Selective reconstructive endoaneurysmorrhaphy, 516f

Self-tamp on ade, 318

Septic phlebitis, 425

Serial venography, 42

Seven Ps of acute arterial insufficiency, 126

SFA, 204, 205, 377f, 379

SFA injury, 204, 205

Shackford, Steven R., 353

Sheaths, 428, 434f

Sherman, H. M., 286

Shotgun wound. See Gunshot wound.

Shumacker, Harris, 19f

Shunt/shunting

BTA1, 278

combined extremity injuries, 409

Gott shunt, 278

popliteal artery injury, 399

portal vein, 334

temporary shunts, 171-172
Silastic intraluminal shunts, 409
Simple vascular repair techniques, 159-160, 170
Sise, Michael J., 353
Site of injury, 47-48
Small branch injuries, 200
Soft signs

arterial injury, lOOt

vascular injury, 118-119, 229, 356t
Soltero, Ernesto, 285
Somalia, 57

Soubbotitch, V., 13, 14f
Spinal compartment syndrome, 444
Spinal cord, 448

Spiral computed tomographic angiography, 356
Splenic arteriography, 193f
Splenic artery, 201
Splenic vein, 328f, 329
Sponge stick, 154
Spontaneous cure

AVF, 486-488

false aneurysms, 520
Spontaneous tamponade, 318
Stab wound

cardiac trauma, 293, 294, 294f

etiology, 38t, 39t

Stab wound (Continued)

iliac vessel injury, 341 1

IVC injury, 318

location, 38t

minimal injury, 89t, 235
Stable hematoma, 330
Stay sutures, 157
Stent/ stent grafts, 195-196

brachiocephalic vessel injury, 200

ICA injury, 198

iliac vessel injury, 348-349

Palmaz stent, 209, 211f, 214f, 2l7f, 218f

penetrating thoracic injuries, 256-259

thoracic vascular injuries, 199

uncovered/ covered, 195
Steri-Strips, 453

Sternocleidomastoid muscle, 224, 227f
Sternohyoid muscle, 227f
Sternothyroid muscle, 227f
Stocking-glove distribution sensory deficit, 116
Stoner, Michael C., 223
Stretch injuries, 201
Stryker pressure monitor, 449
Subclavian artery, 436f
Subclavian vein, 436f
Subclavian vein/artery

arterial injuries, 359-364

balloon tamponade, 260f

blunt thoracic injuries, 279-280

mortality, 363

penetrating cervical injuries, 233, 235f

penetrating thoracic injuries, 260-261, 262f

results, 362-363

scapulothoracic dissociation, 363-364

surgical anatomy, 359-360

surgical treatment, 361-362
Subclavian vein/artery fistula, 436f
Subclavian venous access, 435
Subscapular artery, 364f
Substitute interposition conduit, 161-162
Subtraction angiography, 271-272
Subtraction aortography, 257f
Superficial epigastric artery, 377f
Superficial femoral artery (SFA), 204, 205, 377f, 379
Superficial femoral artery injury, 379-381
Superficial femoral vein, 379
Superficial iliac circumflex artery, 377f
Superficial radial nerve, 373f
Superficial temporal artery, 226f
Superficial volar branch radial artery, 372f
Superior collateral artery, 368f
Superior gluteal artery, 377f
Superior lateral genicular artery, 381f
Superior medial genicular artery, 381f
Superior mesenteric artery, 305-307
Superior mesenteric vein, 328f, 329
Superior thoracic artery, 364f
Superior thyroid artery, 226f, 227f
Superior ulnar collateral artery, 368, 368f, 372f
Superior vena cava injuries, 264
Superoxide, 78, 453
Supine decubitus position, 138f

INDEX. qxd 4/16/04 3:18PM Page 665

INDEX

665

Supraclavicular incision, 361
Suprahepatic vena cava, 280
Supramesocolic hematoma, 302
Suprapancreatic portal vein, 331-333
Suprarenal abdominal aorta, 301-304
Surgical anatomy

axillary artery injuries, 364

BCVIs, 242

brachial artery injuries, 367-368

common fern oral /profunda femoral arteries, 376,
377f

iliac vessel injuries, 340-341

IVC injuries, 317-318

penetrating cervical injuries, 224-228

popliteal/ tibial arteries, 381-382

portal vein injuries, 327-329

radial/ulnar artery injury, 371, 372f

subclavian artery injuries, 359-360

superficial femoral artery, 379

venous injuries (lower extremity), 387
Surgical techniques, 137-164. See also Surgical
treatment.

abdomen/pelvis, 149-153

axillary artery, 148

brachial artery, 148-149

Cattell-Braasch maneuver, 152, 153f

chest, 146-148

colorectal procedures, 437

decompression, 451-453

distal superficial femoral artery, 155

groin, 154-155

hemorrhage control, 139-142

high-risk injuries, 143b

incisions, 140b, 143b. See also Incisions.

laparoscopic procedures, 437-438

lower extremity, 154-155

Mattox maneuver, 151, 152f

neck, 143-144

neurosurgery, 441-442

orthopedic surgery, 440

pancreatobiliary procedures, 437

percutaneous vascular access, 428-437

popliteal artery, 155, 156f

positioning, 138-139

Pringle maneuver, 153

repair, 156-163. See also Repair
principles/techniques.

thoracic outlet, 144-146

upper extremity, 148-149

vascular/ endovascular surgery, 438-440
Surgical treatment. See also Repair

principles/techniques; Surgical techniques.

abdominal vascular injury, 200-201

arm injury, 202-203

AVF, 484-486

axillary artery injuries, 362t, 366-367

balloon catheter tamponade, 170, l7lf

BCVIs, 246-249

blunt thoracic injuries, 277-278

brachial artery injuries, 362t, 369-371

brachiocephalic vessels, 199-200

calf injury, 205

Surgical treatment (Continued)

clamp-and-sew technique, 277-278

combined extremity injuries, 408-412

common femoral/profunda femoral arteries,
378-379

extremity compartment syndrome, 450-453

external carotid artery injury, 198

extremity vascular trauma, 357-359

false aneurysms, 513-520

femoral arteries, 204-205

groin injury, 203-204

hip injury, 203-204

ICA injuries, 196-198

iliac vessel injuries, 344-348

knee injury, 205

lateral repair, 170

ligation, 170

lumbar artery injury, 200-201

lower extremity, 203-206

neck, 196-200

packing, 170-171

pedicle vascular injury, 201

pelvic injury, 201-202

penetrating cervical injuries, 233-237

penetrating thoracic injuries, 259-260

planned reoperation, 169, 173-174

popliteal artery & branches, 205-206

popliteal/tibial arteries, 383-385

portal vein ligation, 333-334

radial/ulnar artery injuries, 362t, 372-373

simple/complex repairs, 170

small branch injuries, 200

stretch injuries, 201

subclavian artery injuries, 361-362, 362t

superficial femoral artery, 380

thigh injury, 205

thoracic vascular injuries, 199-200

upper extremity, 202-203

vascular repair techniques, 170-171

venous injuries, 401-404

venous injuries (lower extremity), 388

venous ligation, 403-404

vertebral artery injury, 198-199
Swan-Ganz catheter, 107
Swan-Ganz monitoring, 265
Synthetic conduits, 162
Systemic air embolism, 265, 266f

""Tc-MIBI, 450

TCD studies, 132

Technetium-99 methoxyisobutyl isonitrile

( 99m Tc-MIBI),450
TEE, 275-276, 295

Temporary balloon occlusion, 192f, 197
Temporary hemostasis, 192
Temporary intraluminal arterial shunt, 66f
Temporary shunts, 171-172
10/30 rule, 107

Testicular (ovarian) artery, 340f
Testicular (ovarian) vein, 340f
Thigh compartment syndrome, 385, 446

INDEX. qxd 4/16/04 3:18PM Page 66 6

666 INDEX

Thigh injury, 205
Thoracic aorta injury, 262-263
Thoracic duct injury, 265
Thoracic injuries, 101-102

blunt injuries, 269-283. See also Blunt thoracic
vascular trauma.

operative principles, 146-148

penetrating injuries, 2521-267. See also Penetrating
thoracic vascular trauma.
Thoracic inlet, 2630-2632
Thoracic outlet injury, 144-146
Thoracic vascular injuries, 199-200
Thoracic vena cava, 280
Thoracic vena cava injury, 264
Thoracoabdominal aortic operations, 439
Thoracoabdominal exposure of aorta, 439f
Thoracoacromial artery, 364f
Thoracotomy

anterolateral, 146, 147, 292

digital, 290

EC, 100, 254, 290

left anterolateral, 292

left posterolateral, 139

resuscitative, 147
Thromboelastography, 108
Thromboembolic complications, 525-535

algorithm, 534f

clinical epidemiology/risk factor analysis, 526-527

diagnosis/ treatment, 530-533

historical overview, 525-526

LDUH, 528-529

LMWH, 529

mechanical prophylactic devices, 528

outcomes research, 532-533

pathophysiology, 526

prophylactic measures, 527-528

prophylactic vena cava filters, 529-530

recommendations/future directions, 533-535
Thyrocervical trunk, 200, 359f, 360f
Thyrohyoid muscle, 227f
Tibial arterial injuries, 381-385
Tibial artery, 382
Tissue bed occlusion, 193
Tissue manometry, 130
Topical hemostasis, 142
Total hip arthroplasty, 440
Total knee arthroplasty, 440
Tourniquet, 6
Trachea, 227f

Transcatheter embolization. See Embolization.
Transcranial Doppler (TCD) studies, 132
Transection, 54f

Transfusion. See Blood transfusion.
Transesophageal echocardiography (TEE), 275-276,

295
Transversalis fascia, 448
Transverse aortic arch, 263
Trauma surgery. See Surgical techniques; Surgical

treatment.
Traumatic false aneurysms, 54f, 484f, 499-521

Angiography, 61f, 510, 512f, 513f

clinical features, 510

Traumatic false aneurysms (Continued)

clinical pathology, 506-510

closed fractures, 504t

diagnostic considerations, 510-513

etiology, 503-506

follow-up, 520-521

historical overview, 499-502

incidence, 502-503

incisions, 51 7f

e n do aneurysm or rhaphy, 500, 501f, 515f, 516f,
518t

peripheral nerve lesions, 508t

spontaneous cure, 520

surgical treatment, 513-520

Vietnam Vascular Registry, 464t, 465t, 469t, 47lt,
495t, 496t, 508f

World War II, 51 7f, 518t, 519t
Traumatic hemothorax, 254
Traumatic vascular lesions, 207-220

background, 208-211

characteristics of lesions/outcome, 210f

coil embolization, 208

intraluminal balloon control of arteries, 208

intravascular stents, 208

Montefiore experience, 211-218
Treatment. See Surgical techniques; Surgical treatment.
Triangulation method of suturing, 12f
Tube thoracostomy, 254, 290

Ulnar artery, 371, 372f, 373f, 447f
Ulnar nerve, 365f, 368f, 44 7f
Ultrasound. See Duplex ultrasonography.
Ultrasound-guided pseudoaneurysm compression, 430
Uncovered stents, 195
Uncross-matched type O blood, 105
Unfractioned heparin (LDUH), 528-529, 533t
Upper extremity. See also Extremity injuries,
compartment syndrome, 375

fracture, 103b

treatment/repair, 148-149, 202-203

venous injury, 374-375
Ureter, 340f

Vagus nerve, 22 7f

Vascular anastomosis, 159-161

Vascular bed occlusion, 195

Vascular/ en dovascular surgery, 438-440

Vascular grafts, 414-416

Vascular patency, 111

VasoSeal device, 432, 433f

Vasospasm, 181, 184, 186f

Vein graft, 209

Vein transplantation, 492t

Veith, Frank J., 207

Vena cava filters, 326, 350, 529-530, 533t

Vena comitans, 368f

Venization, 477

Venogram/venography, 43f, 44f, 400, 404

Venous access, 435

Venous aneurysms, 425

INDEX. qxd 4/16/04 3:18PM Page 667

INDEX

667

Venous injuries, 399-404

diagnosis, 400-401

history/ epidemiology, 399-400

iliac vessel injuries, 346-347

ligation, 403-404

lower extremity, 387-389

penetrating cervical injuries, 237

treatment, 401-404

upper extremity, 374-375
Venous ligation, 403-404
Venous patency, 388
Venous repair, 401-404
Venovenous bypass, 324
Ventricular septal defects, 294, 295f
Veress needle, 438, 439f
Vertebral artery, 225, 226f, 359f, 360f
Vertebral artery injury, 198-199, 236-237
Veterinarian's stitch, 8f
Vibratory tools, 54

Vietnam Vascular Registry, 24, 228, 458. See also
Vietnam War.

AV fistula, 464t, 465t, 469t, 47lt, 495t, 496t, 497

exhibit, 26f

extremity venous injuries, 27t

false aneurysm, 464t, 465t, 469t, 471 1, 495t, 496t, 508f

importance, 224

preliminary report, 26f, 41, 42t

pulmonary emboli, 46

studies, 43

venous ligation, 399

wrist pressure, 64f
Vietnam War

amputation, 405t

AV fistula, 461,462

cardiac trauma, 287, 287t

carotid artery injury, 229t

combined extremity injuries, 405, 412

follow-up. See Vietnam Vascular Registry.

interposition grafting, 414

location of injuries, 36t

popliteal artery injury, 394, 395t

prosthetic grafts, 414

surgical heritage, 25-27

venous injuries, 399, 400, 402
Virchow triad, 526
Visceral aorta, 301, 302f
Volar interosseous artery, 372f
Volkmann's ischemic contracture, 445
Volume therapy, 105-106

Walking the clamps, 154

Wall, Matthew J., Jr., 251, 285

Wallgraft, 196f, 211, 212

Wang, Ping, 73

War. See Military vascular trauma experience.

Wide Kocher maneuver, 331

World War I, 14-16

carotid artery injury, 229t

location of injuries, 36t

popliteal artery injury, 394, 395t

venous injury, 399
World War II, 16-18

AF fistula, 463t, 488-489, 490t

amputation, 405t

carotid artery injury, 229t

false aneurysm, 5l7f, 518t, 519t

location of injuries, 36t

Matas endoaneurysmorrhaphy, 518t

popliteal artery injury, 394, 395t

venous injury, 399
Wounds of the heart, 285-297

aortic occlusion, 292

cardiac manipulation, 292

cardiac septal injuries, 294-295

cardiac valvular injury, 295

clinical pathology, 287-288

complex injuries, 293-294

EC thoracotomy, 290-291

emergency center, 289-291

hemorrhage control, 292-293

historical overview, 285-286

incidence, 286-287

incisions, 291-292

i n trap eri cardial inferior vena cava injury,
295-296

operative management, 291-296

pathophysiology, 288-289

prehospital management, 289

X-rays, 119

Xanthine oxidase-derived oxidants, 78

Xanthine oxidase inhibitors, 453

Zone I neck wounds, 131, 230, 231f
Zone II neck wounds, 101, 131, 230, 231f
Zone III neck wounds, 101, 131, 230, 231f

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